Exposing the biggest org fraud that is @piec (balding cell gftih)

[DR. NICKGA]

These people are injecting rat piss and random research chemicals but are scared of Fin

Yes they are scared of a fda approved medicine named finasteride


Which has multiple studies on it, for example this meta analysis of 2 + million people
Meta analysis = multiple studies

Association of 5α-Reductase Inhibitors with Depression and Suicide: A Mini Systematic Review and Meta-analysis - PubMed

5α-Reductase inhibitors (5-ARIs) are widely prescribed for treatment of benign prostatic obstruction and androgenic alopecia. Several studies with controversial findings regarding 5-ARI exposure have been published over a number of years, and concerns were recently raised about the potential...

pubmed.ncbi.nlm.nih.gov

"SUMMARY: We reviewed study data for more than two million patients taking drugs called 5α-reductase inhibitors (5-ARIs), which are widely prescribed for urinary problems caused by benign prostate enlargement and for male-pattern hair loss. In a pooled analysis we found no evidence of an association between 5-ARI use and the risk of depression or suicide
Keywords: 5α-Reductase"

No depression or suicide risks, now this is one example of two side effects
I can give 1000+ more studies


The only people i see that got side effects are reddit users or users from a weird obscure hairloss community

its all Bullshit , finasteride and for sure dutasteride is pretty safe

 

[mog_or_be_mogged]

dnrd my dad has a full head of hair at 52

 

[solansigilknight]

Why Finasteride (or dut) is a fraud :



So debunking the claim is finasteride dangerous for you yes or no

their are some people who get the following effects from just microdosing fin :

• sexual dysfunction
• Anhedonia
• Depression
• Anxiety
• Lack of motivation
• Lack of focus

While other seems fine using it

Soooo It depends on your neural phenotypes

Some things like childhood trauma has a lot of gaba menergic signaling adrenaline cortisol levels ect….

And also different architectures of the brain (I might write a thread about it its really interesting how you can just look at someone genes pool and know if he has adhd bi polar ect….. if this thread anhilate the fraud that is piec i sure would write about it)

Now lets starts on why finasteride cause all of this sides :

When you use and 5ar inhibitor your not just inhibiting dht but also progesterone and alopregnolone and if you neealycompletely inhibit the enzyme (which you probably will cause most of the 5ar is type 1 and don’t get me started on dut that shit blocks everything) or nearly you have no progesterone and alopregonolone function in your body so back then i thought well you can just take progestene just to come to the conclusion its gonna do nothing for cause you totaly inhibited thw enzyme.

Suggestion : (keep in mind this is not the best approach I’m gonna get to the nest approach later but its still better than the fraud that is piec feel free to insult his ass in the comments)



Now lets talk about the sides :

Remember about the sides i talked about earlier it was due to allo pregnolone who acts as a innate benzo in your system (so basicaly the main inhibotory gaba system in your brain is the gabaergic system related to the hormone you name it “gaba” it has 2 receptors Gaba B fair enough it can be agonized with just phenibut so no need first allopregnolone its not in the sort of communication in the brain anyway (which mean less signaling)

then We have Gaba A

The only critical receptor and guess what the Gaba A receptor is modulated by allopregnolone which if you remember correctly you blocked earlier sp how do i explain it basicaly its like you took a reverse xanax so the average nigga is gonna have anhedonia exept of he is an outlier so now your fucking dependent on benzos who are super dangerous if you don’t wanna feel like shit

(Then some smart ass in the comment gonna write well then why dont you take alopregnolone well it has very short half life and it can’t be stored or kept so unless you want to be taking ng of allopregnolone every 5 minutes you should either feel like shit like that evil piec want you to be or be addicted to benzos for progesterone you can just take transdermal or micronuzed progesterone just make sure to be on hormones cause your at high risk of hypogonadism if you mess up your dosages)



(Also their are other alternatives so 1) way to get allopregnolone which in theory would work not sure 100% is your gonna take your progesterone and agnozed the tsp receptor you’ll end up with more neuro steroidgenisis so you have more alopregnolone just make sure to not get addicted to that shit might write a thread about how to never get addicted to compounds and how to get rid off any addiction but for that ill need you to support me and all insult piec parents for not putting on a rubber that sad night

Getting back to what i was saying their some research that seem mehh like ettyfoxine but that shit is too risky in my opinion

2) alternative is basicaly fuck modulating gaba receptors you just take sodium valproate kt basicaly make your brain a sink of gaba kinda like piec asshole after getting fucked by every dermatologist prescribing him fin

And its a hdac inhibitor so it have epigenetic change keep in mind that shit aint salt that a epilepsy drug and they are reliable 100% cause nigga imagine an epileptic go through withdrawal his gonna fucking die like piec pride after i finish writing this thread)

So to summarize a little :

Erectil dysfunction: is caused by low progesterone abdominal low dht

Anhedhonia : is cause by low alopregnolone levels

Anxiety : is caused because the amygdila have gaba receptors which when inhibited cause the amygdala to start tweaking like piec teading this right now well i hope finasteride would give you trauma and make you hyper vigilant to not with me next time keep in mind if it don’t happen to you it could just mean you had a gabaminergic deficit or your life so

you adapted your the exeption not the rule



Lack of focus : mainly because of low dht and progesterone youll need for that to increase your dopamenergic signaling (supposing you have average serotonorgic signaling) but you can use something like wellbutrin ritalin low dose in the morning 2x per week

(Wellbutrin do have bad effects on cholinergic system but supposing your an average dude and get a lot of choline in your diet your probably fine)



Here a Choline stack if anyone is interested i already writed it down wayback in the thread fix your life as a teenager :

1. Acetylcholine

a.1g CDP choline 2x per day

b.20 mg Donepezil upon rising

c.300 mg alpha gpc in the morning

d.500 mg Uridine monophosphate in the morning

e.1000 mg piracetam (5x per week$

f.30 mg Noopept



So your gonna ask me what could you do well you can use a topical dut in the hairline or balding areas (but good luck sourcing that)

(Before you ragebait in the comments i already thought about blocking the androgen receptor with Ru but to much side effects especially knowing the information I’m gonna reveal later)



The biggest lie ever said about hairloss :

is that dht cause hairloss if dht cause its mainly becuase it caus low estrogen who is responsible for the hairloss (just look at the guys who took tamoxifen who get hairloss look at the guys who take masteron who get hairloss which if you didn’t know is less androgenic than test its because of its serm effects look at rad 140 who is literraly 0 androgenic and still result in hairloss don’t forget rad 140 was intended to cute breast cancer so its all about estrogens)



If anything Dht increase hair growth :

https://pmc.ncbi.nlm.nih.gov/articles/PMC6989660/



We have seen the effects of blocking DHT. It SLOWS hair loss and some get a MILD regrowth at best with all the sides and complex protocols you should apply to counter act those side effects



The problem with the hairloss comunity is they often overlook the basics like what about hypogonadol nigga who got hairloss they don’t have high dht yet they are bald

So lets get to it the main reasons of hairloss :

• Low estrogen as said earlier
• Bad lifestyle habits
• Poor nutrition
• Lack of exercise

Then we have the most important ones :

• Insulin resistance
• Stress
• The main contributing factor of hairloss and the most overloked one is hypoxia you can try it yourself put on a hat on your hair for 12 hours your gonna feel your haur thinning if you think im coping

So my Definitive hairloss stack that I’ll reccomend :



Topical supplements:
-Ketoconazole cream. 1 to 2 times a day, every day. If price or convenience is an issue, the minimum this should be applied is before bed to balding areas. Ketoconazole has been shown to be just as effective as minoxidil in studies with the shampoo. And even stronger the cream has been shown to produce results with an overnight application.

-Emu oil. 1-2 times a day. One of the only proven items I’ve come across that increases skin and hair DNA synthesis, with studies showing hair regrowth.

-Peppermint oil. 1-2 times a day. Peppermint oil has been shown in studies to be equivalent to minoxidil, without the negative side effects that result in premature aging of the skin.

-Evening Primrose oil or Borage oil. Both shown to cause hair regrowth in studies. Just adding a little more fat topically which is absorbed via the skin. Also useful for GLA’s effect on prostaglandins for halting inflammation, hair loss, and aiding hair regrowth.

-Spironolactone cream. Spironolactone has been shown to restore a 60 year old males hairline to his teenage years hair line that he had lost decades ago. Although we use this item topically, it still has the same benefits locally as it is used for such issues as hair loss and hirsutism topically. However topically it does not go systematic as in studies it has been applied to patients whole backs without going systematic. Spironolactone blocks the binding of androgens to the androgen receptor and helps increase estrogen locally.



-BiEstro cream. E2 and E3 combo, Estradiol and Estriol. Apply once or twice a day to balding areas.

The amount used here is enough to cover balding thinning areas. Due to the area we are applying it studies have shown no real systematic absorption. And also to the fact of the dose we are using is quite low as well. None of the users nor myself could produce an estrogenic side on this when applied to the scalp. Some of us who would normally get estrogenic sides off testosterone use as low as 200 mg.

(You can add bold for E1 if you wanna maximize but kinda pain in the ass cause you have to do bloods and make sure your E1 doesn’t lower your E2 and E3 basicaly you should keep them in harmony)



We have also seen what adding estrogen does for hair, as the byproduct of the thousands of male to female sex changes. These individuals can regrow full heads of amazing hair, bringing back hair reminiscent of that which they had when they were teenagers.

Likely, the ones seeing any bit of regrowth from DHT blockers are as a result of the mild estrogen increase triggered by these compounds. Studies of topical estrogen, plain and simple, work. In both men and women. As a bonus, adding estrogen topically doesn’t just increase estrogen -it also the localized concentration of the aromatase enzyme.

(I’ve saw myself dozens of people on reedit i swear i dont know why i couldnt find them having resuts if anyone has it please write it down below)

(For the studies i linked so many in the ashwaganda and no body gave a fuck

So because of that here are some studies on mice :

https://pubmed.ncbi.nlm.nih.gov/14962083/

https://www.researchgate.net/figure...e-tenth-day-after-hair-shaving_fig1_229083213





View attachment 3261225

Here is someone who got hair growth using estriol and estradiol cream



=End justification for BiEstro Cream==

Rub this mixture on once or twice a day depending on your available time. Once a day is totally fine, and optimal for most, if you can apply it before bed. If not, and you must do it in the day, pick a time where you can leave it on for at least 1-2 hours before showering it out.



Supplements:

Minerals might be needed if severely deficient, some doses are based off studies and you may not need these doses. You must find your own dose.

-Zinc Picolinate. 100-150mg a day for 6-8 weeks, tops.

This depends on a few factors. Add up your dietary zinc content that you typically average, and then decide if zinc might be low and determine the dose that you want. This has been noted in studies to completely reverse hair loss and hypothyroid conditions that are due to a zinc deficiency. NOTE: You may not need this, use discretion. Too much zinc can lead to other problems.

-Taurine. 2.5 grams, 2x a day.

In regards to hair loss, Taurine has been shown to help combat fibrosis of the scalp, thus

increasing circulation and hair growth.



Black Currant Oil, 3g a day.

This is utilized for its Gamma Linoleic Acid (GLA) content, which has anti-inflammatory properties, the ability to increase hair growth prostaglandins (PGE), and the ability to inhibit hair loss prostaglandins (PGD). These prostaglandins are another contributing factor to hair loss/growth aside from the androgens.

Three items have been shown to decrease GLA – wheat, dairy, and trans fats – through inhibition of an enzyme called D6D. The typical western diet is full of these foods. Inhibition of the D6D enzyme prevents the conversion of Linoleic Acid (LA) into GLA. The inhibition of D6D also happens with age, and is likely one of the key contributors to balding getting worse with age. This is just about the only process that can link balding to aging that has not already been explored.

In taking a GLA supplement, we bypass the enzymatic conversion entirely and have the end product.

Black Currant oil was also shown in animal studies to prevent many of the negatives of excessive fructose intake, such as fatty liver.



Grapeseed Extract, 500-1000mg a day.
GSE has been shown in animal studies to improve insulin resistance as much as metformin. Studies have also shown GSE to double the number of hairs in the anagen (growth) phase. As far as I am aware, no other compound has been shown to have effects this potent.

(Note : i do not advise to take metformin or berberine for other reasons i would write a thread about it in the near future)



Chromium gtf is used for combating insulin resistance, which is seen as a contributing factor for hair loss as mentioned above when talking about GSE. Again, some may not need this. Chromium GTF has been shown in case studies with type 2 diabetics to remove all exogenous insulin dependency within a couple months of use i recommend using 1000mcg a day for about 6 weeks



And you want to be eating or supplementing with those :

Magnesium

B vitamins

Vitamin K2

You also wanna be getting fats in your diet (especially from Mufas and Pufas (just make sure your not getting it from seed oils because its processed that a whole other topic id advise to get from seeds)



but I assure you, PUFA fats are NOT bad for you. Getting them from healthy sources has countless proven health benefits: anti-carcinogenic, anti-inflammatory, pro-sleep, pro-thyroid, etc. The benefits of unheated PUFA fats are a very deep topic on their own.

The epidermis of your skin is made of 60 percent Omega-6 PUFA fats. Do not fall for the “Omega-3 must be higher than Omega-6” speech that has no proven benefits and multiple proven detriments. All of the studies linking PUFA fats to health issues look at the typical use for PUFA fats in the western diet: cooking, frying, and otherwise heating the fats. If we are to take the same controlled environment but introduce raw, unheated PUFA fats from seeds and nuts, the studies flip completely. Anti-cancer, anti-inflammatory, and all-around health marker improvement is marked.



Another issue found often in the bodybuilding and fitness realm is the “eating too clean” phenomenon. If you were to add up chicken, rice, broccoli, and some olive oil on your favorite diet app, I can guarantee that you’d see that it’s a struggle to reach even 15 percent of RDA requirements for PUFA fats. When this happens, the skin goes dry and wrinkles appear, hair becomes straw like and falls out, etc. Digestive issues ensue, and metabolism slows down. As PUFA fats are shown to increase thyroid hormone sensitivity by almost 20 percent, dieting becomes harder and fat accrual in a calorie surplus becomes far easier. This isn’t even rectifiable with exogenous thyroid hormones – take all the thyroid drugs you want, if your sensitivity isn’t up to par your metabolism will suffer.

(Fun fact : Studies have also shown that when consumed in equal quantities, monounsaturated and saturated fats cause fat gain. Saturated fat was shown to cause a decrease in insulin sensitivity as well. PUFA fat, on the other hand, caused barely any fat gain. The majority of weight gained was muscle, insulin sensitivity increased, and abdominal fat thickness decreased.)



Other Foods.

Pineapple is used as a general health food with documented anti-inflammatory benefits, contains an enzyme papaya if i can recall that aids in the digestion of protein, is a fantastic source of vitamins, and is a preferred fruit due to the lower-end fructose content. In regards to hair regrowth, the main benefit is its anti-inflammatory property.



Massage/Mechanical Manipulation:

Vigorously massage, brush, or pinch your scalp in the balding areas. 1-2 times a day, for whatever time frame you can manage; the longer the better. 3-5 minutes is great, 10 minutes is better. Use as much pressure as possible. Tissue manipulation like this increases circulation and has been proven in studies to aid hair growth. To assist in blood flow further, you can bend over and point your head toward the ground, allowing gravity to assist in delivering blood to the target area.



You could also look in the More plates more plates micro needling stuff :



Sources :



[1] Stoner, E. (1990). The clinical development of a 5α-reductase inhibitor, finasteride. The Journal of steroid biochemistry and molecular biology, 37(3), 375-378.



[2] Vuichoud, C., & Loughlin, K. R. (2015). Benign prostatic hyperplasia: epidemiology, economics and evaluation. Can J Urol, 22(Suppl 1), 1-6.



[3] Adil, A., & Godwin, M. (2017). The effectiveness of treatments for androgenetic alopecia: a systematic review and meta-analysis. Journal of the American Academy of



141.



[4] Schumacher, M., Hussain, R., Gago, N., Oudinet, J. P., Mattern, C., & Ghoumari, A. (2012). Progesterone synthesis in the nervous system: implications for myelination and myelin repair. Frontiers in neuroscience, 6, 10.



[5] Skeldon, S. C., Macdonald, E. M., Law, M. R., Huang, A., Paterson, J. M., Mamdani, M. M., & Juurlink, D. (2017). The cardiovascular safety of dutasteride. The Journal of urology, 197(5), 1309-1314.



[6] Lee, H. J., & Chang, C. (2003). Recent advances in androgen receptor action. Cellular and Molecular Life Sciences CMLS, 60(8), 1613-1622.



[7] Bolton, E. C., So, A. Y., Chaivorapol, C., Haqq, C. M., Li, H., & Yamamoto, K. R. (2007). Cell-and gene-specific regulation of primary target genes by the androgen receptor. Genes & development, 21(16), 2005-2017.



[8] Winiarska, A., Mandt, N., Kamp, H., Hossini, A., Seltmann, H., Zouboulis, C. C., & Blume-Peytavi, U. (2006). Effect of 5α-dihydrotestosterone and testosterone on apoptosis in human dermal papilla cells. Skin pharmacology and physiology, 19(6), 311-321.



[9] Chhipa, R. R., Halim, D., Cheng, J., Zhang, H. Y., Mohler, J. L., Ip, C., & Wu, Y. (2013). The direct inhibitory effect of dutasteride or finasteride on androgen receptor activity is cell line specific. The Prostate, 73(14), 1483-1494.



[10] Mella, J. M., Perret, M. C., Manzotti, M., Catalano, H. N., & Guyatt, G. (2010). Efficacy and safety of finasteride therapy for androgenetic alopecia: a systematic review. Archives of dermatology, 146(10), 1141-1150.



[11] Di Loreto, C., La Marra, F., Mazzon, G., Belgrano, E., Trombetta, C., & Cauci, S. (2014). Immunohistochemical evaluation of androgen receptor and nerve structure density in human prepuce from patients with persistent sexual side effects after finasteride use for androgenetic alopecia. PLoS One, 9(6).



[12] Overstreet, J. W., Fuh, V. L., Gould, J., Howards, S. S., Lieber, M. M., Hellstrom, W., ... & LEWIS, R. (1999). Chronic treatment with finasteride daily does not affect spermatogenesis or semen production in young men. The Journal of urology, 162(4), 1295-1300.



[13] Samplaski, M. K., Lo, K., Grober, E., & Jarvi, K. (2013). Finasteride use in the male infertility population: effects on semen and hormone parameters. Fertility and sterility, 100(6), 1542-1546.



[14] Amory, J. K., Wang, C., Swerdloff, R. S., Anawalt, B. D., Matsumoto, A. M., Bremner, W. J., ... & Clark, R. V. (2007). The effect of 5α-reductase inhibition with dutasteride and finasteride on semen parameters and serum hormones in healthy men. The Journal of Clinical Endocrinology & Metabolism, 92(5), 1659-1665.



[15] Traish, A. M. (2020). Health Risks Associated with Long-Term Finasteride and Dutasteride Use: It's Time to Sound the Alarm. The World Journal of Men's Health, 38.



[16] Traish, A., Haider, K. S., Doros, G., & Haider, A. (2017). Long-term dutasteride therapy in men with benign prostatic hyperplasia alters glucose and lipid profiles and increases severity of erectile dysfunction. Hormone molecular biology and clinical investigation, 30(3).



[17] Doulabi, S. R. S. M., Kavoussi, H., Isapour, D., Hashemian, A., & Taheriniya, A. (2013). Effect of finasteride on lipid profile in individuals with androgenetic alopecia. African Journal of Pharmacy and Pharmacology, 7(6), 315-317.



[18] Duskova, M., Hill, M., & Starka, L. (2010). Changes of metabolic profile in men treated for androgenetic alopecia with 1 mg finasteride. Endocr Regul, 44(1), 3-8.



[19] Gild, P., Cole, A. P., Krasnova, A., Dickerman, B. A., von Landenberg, N., Sun, M., ... & Kibel, A. S. (2018). Liver disease in men undergoing androgen deprivation therapy for prostate cancer. The Journal of urology, 200(3), 573-581.



[20] Mendenhall, C. L. (1968). Anabolic steroid therapy as an adjunct to diet in alcoholic hepatic steatosis. The American journal of digestive diseases, 13(9), 783-791.



[21] Jacqueson, A., Thevenin, M., Warnet, J. M., Claude, J. R., & Truhaut, R. (1978). Comparative Study of the Protective Effect of an Anabolic Steroid. In Toxicological Aspects of Food Safety (pp. 193-196). Springer, Berlin, Heidelberg.



[22] Kelly, D. M., Nettleship, J. E., Akhtar, S., Muraleedharan, V., Sellers, D. J., Brooke, J. C., ... & Jones, T. H. (2014). Testosterone suppresses the expression of regulatory enzymes of fatty acid synthesis and protects against hepatic steatosis in cholesterol-fed androgen deficient mice. Life sciences, 109(2), 95-103.



[23] Lin, H. Y., Yu, I. C., Wang, R. S., Chen, Y. T., Liu, N. C., Altuwaijri, S., ... & Yeh, S. (2008). Increased hepatic steatosis and insulin resistance in mice lacking hepatic androgen receptor. Hepatology, 47(6), 1924-1935.



[24] Völzke, H., Aumann, N., Krebs, A., Nauck, M., Steveling, A., Lerch, M. M., ... & Wallaschofski, H. (2010). Hepatic steatosis is associated with low serum testosterone and high serum DHEAS levels in men. International journal of andrology, 33(1), 45-53.



[25] Velazquez, I., & Alter, B. P. (2004). Androgens and liver tumors: Fanconi's anemia and non‐Fanconi's conditions. American journal of hematology, 77(3), 257-267.



[26] Di Loreto, C., La Marra, F., Mazzon, G., Belgrano, E., Trombetta, C., & Cauci, S. (2014). Immunohistochemical evaluation of androgen receptor and nerve structure density in human prepuce from patients with persistent sexual side effects after finasteride use for androgenetic alopecia. PLoS One, 9(6).



[27] Hsieh, J. T., Chen, S. C., Yu, H. J., & Chang, H. C. (2011). Finasteride upregulates expression of androgen receptor in hyperplastic prostate and LNCaP cells: implications for chemoprevention of prostate cancer. The Prostate, 71(10), 1115-1121.



[28] Pinsky, M. R., Gur, S., Tracey, A. J., Harbin, A., & Hellstrom, W. J. (2011). The effects of chronic 5‐alpha‐reductase inhibitor (dutasteride) treatment on rat erectile function. The journal of sexual medicine, 8(11), 3066-3074.



[29] Iacono, F., Prezioso, D., Ruffo, A., Illiano, E., Romis, L., Di Lauro, G., ... & Amato, B. (2012). Testosterone deficiency causes penile fibrosis and organic erectile dysfunction in aging men. Evaluating association among Age. BMC surgery, 12(S1), S24.



[30] Zhang, M. G., Wang, X. J., Shen, Z. J., & Gao, P. J. (2013). Long-term oral administration of 5α-reductase inhibitor attenuates erectile function by inhibiting autophagy and promoting apoptosis of smooth muscle cells in corpus cavernosum of aged rats. Urology, 82(3), 743-e9.



[31] Melcangi, R. C., Caruso, D., Abbiati, F., Giatti, S., Calabrese, D., Piazza, F., & Cavaletti, G. (2013). Neuroactive steroid levels are modified in cerebrospinal fluid and plasma of post‐finasteride patients showing persistent sexual side effects and anxious/depressive symptomatology. The journal of sexual medicine, 10(10), 2598-2603.



sexual medicine, 10(10), 2598-2603.



[32] Alanazi, N. (2016). Assessing the quality of life and health outcomes of Androgenic Alopecia patients using Propecia (Doctoral dissertation, Rutgers University-School of Health Related Professions).



[33] Melcangi, R. C., Caruso, D., Abbiati, F., Giatti, S., Calabrese, D., Piazza, F., & Cavaletti, G. (2013). Neuroactive steroid levels are modified in cerebrospinal fluid and plasma of post‐finasteride patients showing persistent sexual side effects and anxious/depressive symptomatology. The journal of sexual medicine, 10(10), 2598-2603.



[34] Caruso, D., Abbiati, F., Giatti, S., Romano, S., Fusco, L., Cavaletti, G., & Melcangi, R. C. (2015). Patients treated for male pattern hair with finasteride show, after discontinuation of the drug, altered levels of neuroactive steroids in cerebrospinal fluid and plasma. The Journal of steroid biochemistry and molecular biology, 146, 74-79.



[35] Melcangi, R. C., Santi, D., Spezzano, R., Grimoldi, M., Tabacchi, T., Fusco, M. L., ... & Simoni, M. (2017). Neuroactive steroid levels and psychiatric and andrological features in post-finasteride patients. The Journal of steroid biochemistry and molecular biology, 171, 229-235.



[36] Martinez, P. E., Rubinow, D. R., Nieman, L. K., Koziol, D. E., Morrow, A. L., Schiller, C. E., ... & Schmidt, P. J. (2016). 5α-reductase inhibition prevents the luteal phase increase in plasma allopregnanolone levels and mitigates symptoms in women with premenstrual dysphoric disorder. Neuropsychopharmacology, 41(4), 1093.



[37] Basaria, S., Jasuja, R., Huang, G., Wharton, W., Pan, H., Pencina, K., ... & Labrie, F. (2016). Characteristics of men who report persistent sexual symptoms after finasteride use for hair loss. The Journal of Clinical Endocrinology & Metabolism, 101(12), 4669-4680.



[38] Van Praag, H., Schinder, A. F., Christie, B. R., Toni, N., Palmer, T. D., & Gage, F. H. (2002). Functional neurogenesis in the adult hippocampus. Nature, 415(6875), 1030-1034.



[39] Stockmeier, C. A., Mahajan, G. J., Konick, L. C., Overholser, J. C., Jurjus, G. J., Meltzer, H. Y., ... & Rajkowska, G. (2004). Cellular changes in the postmortem hippocampus in major depression. Biological psychiatry, 56(9), 640-650.



[40] Jacobs, B. L., Van Praag, H., & Gage, F. H. (2000). Adult brain neurogenesis and psychiatry: a novel theory of depression. Molecular psychiatry, 5(3), 262-269.



[41] Römer, B., Pfeiffer, N., Lewicka, S., Ben-Abdallah, N., Vogt, M. A., Deuschle, M., ... & Gass, P. (2010). Finasteride treatment inhibits adult hippocampal neurogenesis in male mice. Pharmacopsychiatry, 43(05), 174-178.



[42] Samuels, B. A., & Hen, R. (2011). Neurogenesis and affective disorders. European Journal of Neuroscience, 33(6), 1152-1159.



[43] Romeo, E., Ströhle, A., Spalletta, G., Michele, F. D., Hermann, B., Holsboer, F., ... & Rupprecht, R. (1998). Effects of antidepressant treatment on neuroactive steroids in major depression. American Journal of Psychiatry, 155(7), 910-913.



[44] Uzunova, V., Sampson, L., & Uzunov, D. P. (2006). Relevance of endogenous 3α-reduced neurosteroids to depression and antidepressant action. Psychopharmacology, 186(3), 351-361.



[45] Uzunova, V., Sheline, Y., Davis, J. M., Rasmusson, A., Uzunov, D. P., Costa, E., & Guidotti, A. (1998). Increase in the cerebrospinal fluid content of neurosteroids in patients with unipolar major depression who are receiving fluoxetine or fluvoxamine. Proceedings of the National Academy of Sciences, 95(6), 3239-3244.



[46] Schüle, C., Nothdurfter, C., & Rupprecht, R. (2014). The role of allopregnanolone in depression and anxiety. Progress in neurobiology, 113, 79-87.



[47] Rasmusson, A. M., Pinna, G., Paliwal, P., Weisman, D., Gottschalk, C., Charney, D., ... & Guidotti, A. (2006). Decreased cerebrospinal fluid allopregnanolone levels in women with posttraumatic stress disorder. Biological psychiatry, 60(7), 704-713.



[48] Hellgren, C., Åkerud, H., Skalkidou, A., Bäckström, T., & Sundström-Poromaa, I. (2014). Low serum allopregnanolone is associated with symptoms of depression in late pregnancy. Neuropsychobiology, 69(3), 147-153.



[49] Schüle, C., Nothdurfter, C., & Rupprecht, R. (2014). The role of allopregnanolone in depression and anxiety. Progress in neurobiology, 113, 79-87.



[50] Murphy, B. P., Abbott, F. V., Allison, C. M., Watts, C., & Ghadirian, A. M. (2004). Elevated levels of some neuroactive progesterone metabolites, particularly isopregnanolone, in women with chronic fatigue syndrome. Psychoneuroendocrinology, 29(2), 245-268.



[51] Uzunova, V., Sheline, Y., Davis, J. M., Rasmusson, A., Uzunov, D. P., Costa, E., & Guidotti, A. (1998). Increase in the cerebrospinal fluid content of neurosteroids in patients with unipolar major depression who are receiving fluoxetine or fluvoxamine. Proceedings of the National Academy of Sciences, 95(6), 3239-3244.



[52] Romeo, E., Ströhle, A., Spalletta, G., Michele, F. D., Hermann, B., Holsboer, F., ... & Rupprecht, R. (1998). Effects of antidepressant treatment on neuroactive steroids in major depression. American Journal of Psychiatry, 155(7), 910-913.



[53] Li, L., Kang, Y. X., Ji, X. M., Li, Y. K., Li, S. C., Zhang, X. J., ... & Shi, G. M. (2018). Finasteride inhibited brain dopaminergic system and open‐field behaviors in adolescent male rats. CNS neuroscience & therapeutics, 24(2), 115-125.



[54] Litim, N., Bourque, M., Al Sweidi, S., Morissette, M., & Di Paolo, T. (2015). The 5α-reductase inhibitor Dutasteride but not Finasteride protects dopamine neurons in the MPTP mouse model of Parkinson's disease. Neuropharmacology, 97, 86-94.



[55] Dazzi, L., Serra, M., Seu, E., Cherchi, G., Pisu, M. G., Purdy, R. H., & Biggio, G. (2002). Progesterone enhances ethanol‐induced modulation of mesocortical dopamine neurons: antagonism by finasteride. Journal of neurochemistry, 83(5), 1103-1109



(Keep in mind i put a big emphazize on finasteride mainly because piec was promoting it)

Tags : @Clavicular
@piec
@MA_ascender
@Sapieeen
@NZb6Air
@Rigged
@´´´´´´´´
@Acne Victim
@DR. NICKGA
@cooldude1231

Dndr cracker

 

[Rigged]

Why Finasteride (or dut) is a fraud :



So debunking the claim is finasteride dangerous for you yes or no

their are some people who get the following effects from just microdosing fin :

• sexual dysfunction
• Anhedonia
• Depression
• Anxiety
• Lack of motivation
• Lack of focus

While other seems fine using it

Soooo It depends on your neural phenotypes

Some things like childhood trauma has a lot of gaba menergic signaling adrenaline cortisol levels ect….

And also different architectures of the brain (I might write a thread about it its really interesting how you can just look at someone genes pool and know if he has adhd bi polar ect….. if this thread anhilate the fraud that is piec i sure would write about it)

Now lets starts on why finasteride cause all of this sides :

When you use and 5ar inhibitor your not just inhibiting dht but also progesterone and alopregnolone and if you neealycompletely inhibit the enzyme (which you probably will cause most of the 5ar is type 1 and don’t get me started on dut that shit blocks everything) or nearly you have no progesterone and alopregonolone function in your body so back then i thought well you can just take progestene just to come to the conclusion its gonna do nothing for cause you totaly inhibited thw enzyme.

Suggestion : (keep in mind this is not the best approach I’m gonna get to the nest approach later but its still better than the fraud that is piec feel free to insult his ass in the comments)



Now lets talk about the sides :

Remember about the sides i talked about earlier it was due to allo pregnolone who acts as a innate benzo in your system (so basicaly the main inhibotory gaba system in your brain is the gabaergic system related to the hormone you name it “gaba” it has 2 receptors Gaba B fair enough it can be agonized with just phenibut so no need first allopregnolone its not in the sort of communication in the brain anyway (which mean less signaling)

then We have Gaba A

The only critical receptor and guess what the Gaba A receptor is modulated by allopregnolone which if you remember correctly you blocked earlier sp how do i explain it basicaly its like you took a reverse xanax so the average nigga is gonna have anhedonia exept of he is an outlier so now your fucking dependent on benzos who are super dangerous if you don’t wanna feel like shit

(Then some smart ass in the comment gonna write well then why dont you take alopregnolone well it has very short half life and it can’t be stored or kept so unless you want to be taking ng of allopregnolone every 5 minutes you should either feel like shit like that evil piec want you to be or be addicted to benzos for progesterone you can just take transdermal or micronuzed progesterone just make sure to be on hormones cause your at high risk of hypogonadism if you mess up your dosages)



(Also their are other alternatives so 1) way to get allopregnolone which in theory would work not sure 100% is your gonna take your progesterone and agnozed the tsp receptor you’ll end up with more neuro steroidgenisis so you have more alopregnolone just make sure to not get addicted to that shit might write a thread about how to never get addicted to compounds and how to get rid off any addiction but for that ill need you to support me and all insult piec parents for not putting on a rubber that sad night

Getting back to what i was saying their some research that seem mehh like ettyfoxine but that shit is too risky in my opinion

2) alternative is basicaly fuck modulating gaba receptors you just take sodium valproate kt basicaly make your brain a sink of gaba kinda like piec asshole after getting fucked by every dermatologist prescribing him fin

And its a hdac inhibitor so it have epigenetic change keep in mind that shit aint salt that a epilepsy drug and they are reliable 100% cause nigga imagine an epileptic go through withdrawal his gonna fucking die like piec pride after i finish writing this thread)

So to summarize a little :

Erectil dysfunction: is caused by low progesterone abdominal low dht

Anhedhonia : is cause by low alopregnolone levels

Anxiety : is caused because the amygdila have gaba receptors which when inhibited cause the amygdala to start tweaking like piec teading this right now well i hope finasteride would give you trauma and make you hyper vigilant to not with me next time keep in mind if it don’t happen to you it could just mean you had a gabaminergic deficit or your life so

you adapted your the exeption not the rule



Lack of focus : mainly because of low dht and progesterone youll need for that to increase your dopamenergic signaling (supposing you have average serotonorgic signaling) but you can use something like wellbutrin ritalin low dose in the morning 2x per week

(Wellbutrin do have bad effects on cholinergic system but supposing your an average dude and get a lot of choline in your diet your probably fine)



Here a Choline stack if anyone is interested i already writed it down wayback in the thread fix your life as a teenager :

1. Acetylcholine

a.1g CDP choline 2x per day

b.20 mg Donepezil upon rising

c.300 mg alpha gpc in the morning

d.500 mg Uridine monophosphate in the morning

e.1000 mg piracetam (5x per week$

f.30 mg Noopept



So your gonna ask me what could you do well you can use a topical dut in the hairline or balding areas (but good luck sourcing that)

(Before you ragebait in the comments i already thought about blocking the androgen receptor with Ru but to much side effects especially knowing the information I’m gonna reveal later)



The biggest lie ever said about hairloss :

is that dht cause hairloss if dht cause its mainly becuase it caus low estrogen who is responsible for the hairloss (just look at the guys who took tamoxifen who get hairloss look at the guys who take masteron who get hairloss which if you didn’t know is less androgenic than test its because of its serm effects look at rad 140 who is literraly 0 androgenic and still result in hairloss don’t forget rad 140 was intended to cute breast cancer so its all about estrogens)



If anything Dht increase hair growth :

https://pmc.ncbi.nlm.nih.gov/articles/PMC6989660/



We have seen the effects of blocking DHT. It SLOWS hair loss and some get a MILD regrowth at best with all the sides and complex protocols you should apply to counter act those side effects



The problem with the hairloss comunity is they often overlook the basics like what about hypogonadol nigga who got hairloss they don’t have high dht yet they are bald

So lets get to it the main reasons of hairloss :

• Low estrogen as said earlier
• Bad lifestyle habits
• Poor nutrition
• Lack of exercise

Then we have the most important ones :

• Insulin resistance
• Stress
• The main contributing factor of hairloss and the most overloked one is hypoxia you can try it yourself put on a hat on your hair for 12 hours your gonna feel your haur thinning if you think im coping

So my Definitive hairloss stack that I’ll reccomend :



Topical supplements:
-Ketoconazole cream. 1 to 2 times a day, every day. If price or convenience is an issue, the minimum this should be applied is before bed to balding areas. Ketoconazole has been shown to be just as effective as minoxidil in studies with the shampoo. And even stronger the cream has been shown to produce results with an overnight application.

-Emu oil. 1-2 times a day. One of the only proven items I’ve come across that increases skin and hair DNA synthesis, with studies showing hair regrowth.

-Peppermint oil. 1-2 times a day. Peppermint oil has been shown in studies to be equivalent to minoxidil, without the negative side effects that result in premature aging of the skin.

-Evening Primrose oil or Borage oil. Both shown to cause hair regrowth in studies. Just adding a little more fat topically which is absorbed via the skin. Also useful for GLA’s effect on prostaglandins for halting inflammation, hair loss, and aiding hair regrowth.

-Spironolactone cream. Spironolactone has been shown to restore a 60 year old males hairline to his teenage years hair line that he had lost decades ago. Although we use this item topically, it still has the same benefits locally as it is used for such issues as hair loss and hirsutism topically. However topically it does not go systematic as in studies it has been applied to patients whole backs without going systematic. Spironolactone blocks the binding of androgens to the androgen receptor and helps increase estrogen locally.



-BiEstro cream. E2 and E3 combo, Estradiol and Estriol. Apply once or twice a day to balding areas.

The amount used here is enough to cover balding thinning areas. Due to the area we are applying it studies have shown no real systematic absorption. And also to the fact of the dose we are using is quite low as well. None of the users nor myself could produce an estrogenic side on this when applied to the scalp. Some of us who would normally get estrogenic sides off testosterone use as low as 200 mg.

(You can add bold for E1 if you wanna maximize but kinda pain in the ass cause you have to do bloods and make sure your E1 doesn’t lower your E2 and E3 basicaly you should keep them in harmony)



We have also seen what adding estrogen does for hair, as the byproduct of the thousands of male to female sex changes. These individuals can regrow full heads of amazing hair, bringing back hair reminiscent of that which they had when they were teenagers.

Likely, the ones seeing any bit of regrowth from DHT blockers are as a result of the mild estrogen increase triggered by these compounds. Studies of topical estrogen, plain and simple, work. In both men and women. As a bonus, adding estrogen topically doesn’t just increase estrogen -it also the localized concentration of the aromatase enzyme.

(I’ve saw myself dozens of people on reedit i swear i dont know why i couldnt find them having resuts if anyone has it please write it down below)

(For the studies i linked so many in the ashwaganda and no body gave a fuck

So because of that here are some studies on mice :

https://pubmed.ncbi.nlm.nih.gov/14962083/

https://www.researchgate.net/figure...e-tenth-day-after-hair-shaving_fig1_229083213





View attachment 3261225

Here is someone who got hair growth using estriol and estradiol cream



=End justification for BiEstro Cream==

Rub this mixture on once or twice a day depending on your available time. Once a day is totally fine, and optimal for most, if you can apply it before bed. If not, and you must do it in the day, pick a time where you can leave it on for at least 1-2 hours before showering it out.



Supplements:

Minerals might be needed if severely deficient, some doses are based off studies and you may not need these doses. You must find your own dose.

-Zinc Picolinate. 100-150mg a day for 6-8 weeks, tops.

This depends on a few factors. Add up your dietary zinc content that you typically average, and then decide if zinc might be low and determine the dose that you want. This has been noted in studies to completely reverse hair loss and hypothyroid conditions that are due to a zinc deficiency. NOTE: You may not need this, use discretion. Too much zinc can lead to other problems.

-Taurine. 2.5 grams, 2x a day.

In regards to hair loss, Taurine has been shown to help combat fibrosis of the scalp, thus

increasing circulation and hair growth.



Black Currant Oil, 3g a day.

This is utilized for its Gamma Linoleic Acid (GLA) content, which has anti-inflammatory properties, the ability to increase hair growth prostaglandins (PGE), and the ability to inhibit hair loss prostaglandins (PGD). These prostaglandins are another contributing factor to hair loss/growth aside from the androgens.

Three items have been shown to decrease GLA – wheat, dairy, and trans fats – through inhibition of an enzyme called D6D. The typical western diet is full of these foods. Inhibition of the D6D enzyme prevents the conversion of Linoleic Acid (LA) into GLA. The inhibition of D6D also happens with age, and is likely one of the key contributors to balding getting worse with age. This is just about the only process that can link balding to aging that has not already been explored.

In taking a GLA supplement, we bypass the enzymatic conversion entirely and have the end product.

Black Currant oil was also shown in animal studies to prevent many of the negatives of excessive fructose intake, such as fatty liver.



Grapeseed Extract, 500-1000mg a day.
GSE has been shown in animal studies to improve insulin resistance as much as metformin. Studies have also shown GSE to double the number of hairs in the anagen (growth) phase. As far as I am aware, no other compound has been shown to have effects this potent.

(Note : i do not advise to take metformin or berberine for other reasons i would write a thread about it in the near future)



Chromium gtf is used for combating insulin resistance, which is seen as a contributing factor for hair loss as mentioned above when talking about GSE. Again, some may not need this. Chromium GTF has been shown in case studies with type 2 diabetics to remove all exogenous insulin dependency within a couple months of use i recommend using 1000mcg a day for about 6 weeks



And you want to be eating or supplementing with those :

Magnesium

B vitamins

Vitamin K2

You also wanna be getting fats in your diet (especially from Mufas and Pufas (just make sure your not getting it from seed oils because its processed that a whole other topic id advise to get from seeds)



but I assure you, PUFA fats are NOT bad for you. Getting them from healthy sources has countless proven health benefits: anti-carcinogenic, anti-inflammatory, pro-sleep, pro-thyroid, etc. The benefits of unheated PUFA fats are a very deep topic on their own.

The epidermis of your skin is made of 60 percent Omega-6 PUFA fats. Do not fall for the “Omega-3 must be higher than Omega-6” speech that has no proven benefits and multiple proven detriments. All of the studies linking PUFA fats to health issues look at the typical use for PUFA fats in the western diet: cooking, frying, and otherwise heating the fats. If we are to take the same controlled environment but introduce raw, unheated PUFA fats from seeds and nuts, the studies flip completely. Anti-cancer, anti-inflammatory, and all-around health marker improvement is marked.



Another issue found often in the bodybuilding and fitness realm is the “eating too clean” phenomenon. If you were to add up chicken, rice, broccoli, and some olive oil on your favorite diet app, I can guarantee that you’d see that it’s a struggle to reach even 15 percent of RDA requirements for PUFA fats. When this happens, the skin goes dry and wrinkles appear, hair becomes straw like and falls out, etc. Digestive issues ensue, and metabolism slows down. As PUFA fats are shown to increase thyroid hormone sensitivity by almost 20 percent, dieting becomes harder and fat accrual in a calorie surplus becomes far easier. This isn’t even rectifiable with exogenous thyroid hormones – take all the thyroid drugs you want, if your sensitivity isn’t up to par your metabolism will suffer.

(Fun fact : Studies have also shown that when consumed in equal quantities, monounsaturated and saturated fats cause fat gain. Saturated fat was shown to cause a decrease in insulin sensitivity as well. PUFA fat, on the other hand, caused barely any fat gain. The majority of weight gained was muscle, insulin sensitivity increased, and abdominal fat thickness decreased.)



Other Foods.

Pineapple is used as a general health food with documented anti-inflammatory benefits, contains an enzyme papaya if i can recall that aids in the digestion of protein, is a fantastic source of vitamins, and is a preferred fruit due to the lower-end fructose content. In regards to hair regrowth, the main benefit is its anti-inflammatory property.



Massage/Mechanical Manipulation:

Vigorously massage, brush, or pinch your scalp in the balding areas. 1-2 times a day, for whatever time frame you can manage; the longer the better. 3-5 minutes is great, 10 minutes is better. Use as much pressure as possible. Tissue manipulation like this increases circulation and has been proven in studies to aid hair growth. To assist in blood flow further, you can bend over and point your head toward the ground, allowing gravity to assist in delivering blood to the target area.



You could also look in the More plates more plates micro needling stuff :



Sources :



[1] Stoner, E. (1990). The clinical development of a 5α-reductase inhibitor, finasteride. The Journal of steroid biochemistry and molecular biology, 37(3), 375-378.



[2] Vuichoud, C., & Loughlin, K. R. (2015). Benign prostatic hyperplasia: epidemiology, economics and evaluation. Can J Urol, 22(Suppl 1), 1-6.



[3] Adil, A., & Godwin, M. (2017). The effectiveness of treatments for androgenetic alopecia: a systematic review and meta-analysis. Journal of the American Academy of



141.



[4] Schumacher, M., Hussain, R., Gago, N., Oudinet, J. P., Mattern, C., & Ghoumari, A. (2012). Progesterone synthesis in the nervous system: implications for myelination and myelin repair. Frontiers in neuroscience, 6, 10.



[5] Skeldon, S. C., Macdonald, E. M., Law, M. R., Huang, A., Paterson, J. M., Mamdani, M. M., & Juurlink, D. (2017). The cardiovascular safety of dutasteride. The Journal of urology, 197(5), 1309-1314.



[6] Lee, H. J., & Chang, C. (2003). Recent advances in androgen receptor action. Cellular and Molecular Life Sciences CMLS, 60(8), 1613-1622.



[7] Bolton, E. C., So, A. Y., Chaivorapol, C., Haqq, C. M., Li, H., & Yamamoto, K. R. (2007). Cell-and gene-specific regulation of primary target genes by the androgen receptor. Genes & development, 21(16), 2005-2017.



[8] Winiarska, A., Mandt, N., Kamp, H., Hossini, A., Seltmann, H., Zouboulis, C. C., & Blume-Peytavi, U. (2006). Effect of 5α-dihydrotestosterone and testosterone on apoptosis in human dermal papilla cells. Skin pharmacology and physiology, 19(6), 311-321.



[9] Chhipa, R. R., Halim, D., Cheng, J., Zhang, H. Y., Mohler, J. L., Ip, C., & Wu, Y. (2013). The direct inhibitory effect of dutasteride or finasteride on androgen receptor activity is cell line specific. The Prostate, 73(14), 1483-1494.



[10] Mella, J. M., Perret, M. C., Manzotti, M., Catalano, H. N., & Guyatt, G. (2010). Efficacy and safety of finasteride therapy for androgenetic alopecia: a systematic review. Archives of dermatology, 146(10), 1141-1150.



[11] Di Loreto, C., La Marra, F., Mazzon, G., Belgrano, E., Trombetta, C., & Cauci, S. (2014). Immunohistochemical evaluation of androgen receptor and nerve structure density in human prepuce from patients with persistent sexual side effects after finasteride use for androgenetic alopecia. PLoS One, 9(6).



[12] Overstreet, J. W., Fuh, V. L., Gould, J., Howards, S. S., Lieber, M. M., Hellstrom, W., ... & LEWIS, R. (1999). Chronic treatment with finasteride daily does not affect spermatogenesis or semen production in young men. The Journal of urology, 162(4), 1295-1300.



[13] Samplaski, M. K., Lo, K., Grober, E., & Jarvi, K. (2013). Finasteride use in the male infertility population: effects on semen and hormone parameters. Fertility and sterility, 100(6), 1542-1546.



[14] Amory, J. K., Wang, C., Swerdloff, R. S., Anawalt, B. D., Matsumoto, A. M., Bremner, W. J., ... & Clark, R. V. (2007). The effect of 5α-reductase inhibition with dutasteride and finasteride on semen parameters and serum hormones in healthy men. The Journal of Clinical Endocrinology & Metabolism, 92(5), 1659-1665.



[15] Traish, A. M. (2020). Health Risks Associated with Long-Term Finasteride and Dutasteride Use: It's Time to Sound the Alarm. The World Journal of Men's Health, 38.



[16] Traish, A., Haider, K. S., Doros, G., & Haider, A. (2017). Long-term dutasteride therapy in men with benign prostatic hyperplasia alters glucose and lipid profiles and increases severity of erectile dysfunction. Hormone molecular biology and clinical investigation, 30(3).



[17] Doulabi, S. R. S. M., Kavoussi, H., Isapour, D., Hashemian, A., & Taheriniya, A. (2013). Effect of finasteride on lipid profile in individuals with androgenetic alopecia. African Journal of Pharmacy and Pharmacology, 7(6), 315-317.



[18] Duskova, M., Hill, M., & Starka, L. (2010). Changes of metabolic profile in men treated for androgenetic alopecia with 1 mg finasteride. Endocr Regul, 44(1), 3-8.



[19] Gild, P., Cole, A. P., Krasnova, A., Dickerman, B. A., von Landenberg, N., Sun, M., ... & Kibel, A. S. (2018). Liver disease in men undergoing androgen deprivation therapy for prostate cancer. The Journal of urology, 200(3), 573-581.



[20] Mendenhall, C. L. (1968). Anabolic steroid therapy as an adjunct to diet in alcoholic hepatic steatosis. The American journal of digestive diseases, 13(9), 783-791.



[21] Jacqueson, A., Thevenin, M., Warnet, J. M., Claude, J. R., & Truhaut, R. (1978). Comparative Study of the Protective Effect of an Anabolic Steroid. In Toxicological Aspects of Food Safety (pp. 193-196). Springer, Berlin, Heidelberg.



[22] Kelly, D. M., Nettleship, J. E., Akhtar, S., Muraleedharan, V., Sellers, D. J., Brooke, J. C., ... & Jones, T. H. (2014). Testosterone suppresses the expression of regulatory enzymes of fatty acid synthesis and protects against hepatic steatosis in cholesterol-fed androgen deficient mice. Life sciences, 109(2), 95-103.



[23] Lin, H. Y., Yu, I. C., Wang, R. S., Chen, Y. T., Liu, N. C., Altuwaijri, S., ... & Yeh, S. (2008). Increased hepatic steatosis and insulin resistance in mice lacking hepatic androgen receptor. Hepatology, 47(6), 1924-1935.



[24] Völzke, H., Aumann, N., Krebs, A., Nauck, M., Steveling, A., Lerch, M. M., ... & Wallaschofski, H. (2010). Hepatic steatosis is associated with low serum testosterone and high serum DHEAS levels in men. International journal of andrology, 33(1), 45-53.



[25] Velazquez, I., & Alter, B. P. (2004). Androgens and liver tumors: Fanconi's anemia and non‐Fanconi's conditions. American journal of hematology, 77(3), 257-267.



[26] Di Loreto, C., La Marra, F., Mazzon, G., Belgrano, E., Trombetta, C., & Cauci, S. (2014). Immunohistochemical evaluation of androgen receptor and nerve structure density in human prepuce from patients with persistent sexual side effects after finasteride use for androgenetic alopecia. PLoS One, 9(6).



[27] Hsieh, J. T., Chen, S. C., Yu, H. J., & Chang, H. C. (2011). Finasteride upregulates expression of androgen receptor in hyperplastic prostate and LNCaP cells: implications for chemoprevention of prostate cancer. The Prostate, 71(10), 1115-1121.



[28] Pinsky, M. R., Gur, S., Tracey, A. J., Harbin, A., & Hellstrom, W. J. (2011). The effects of chronic 5‐alpha‐reductase inhibitor (dutasteride) treatment on rat erectile function. The journal of sexual medicine, 8(11), 3066-3074.



[29] Iacono, F., Prezioso, D., Ruffo, A., Illiano, E., Romis, L., Di Lauro, G., ... & Amato, B. (2012). Testosterone deficiency causes penile fibrosis and organic erectile dysfunction in aging men. Evaluating association among Age. BMC surgery, 12(S1), S24.



[30] Zhang, M. G., Wang, X. J., Shen, Z. J., & Gao, P. J. (2013). Long-term oral administration of 5α-reductase inhibitor attenuates erectile function by inhibiting autophagy and promoting apoptosis of smooth muscle cells in corpus cavernosum of aged rats. Urology, 82(3), 743-e9.



[31] Melcangi, R. C., Caruso, D., Abbiati, F., Giatti, S., Calabrese, D., Piazza, F., & Cavaletti, G. (2013). Neuroactive steroid levels are modified in cerebrospinal fluid and plasma of post‐finasteride patients showing persistent sexual side effects and anxious/depressive symptomatology. The journal of sexual medicine, 10(10), 2598-2603.



sexual medicine, 10(10), 2598-2603.



[32] Alanazi, N. (2016). Assessing the quality of life and health outcomes of Androgenic Alopecia patients using Propecia (Doctoral dissertation, Rutgers University-School of Health Related Professions).



[33] Melcangi, R. C., Caruso, D., Abbiati, F., Giatti, S., Calabrese, D., Piazza, F., & Cavaletti, G. (2013). Neuroactive steroid levels are modified in cerebrospinal fluid and plasma of post‐finasteride patients showing persistent sexual side effects and anxious/depressive symptomatology. The journal of sexual medicine, 10(10), 2598-2603.



[34] Caruso, D., Abbiati, F., Giatti, S., Romano, S., Fusco, L., Cavaletti, G., & Melcangi, R. C. (2015). Patients treated for male pattern hair with finasteride show, after discontinuation of the drug, altered levels of neuroactive steroids in cerebrospinal fluid and plasma. The Journal of steroid biochemistry and molecular biology, 146, 74-79.



[35] Melcangi, R. C., Santi, D., Spezzano, R., Grimoldi, M., Tabacchi, T., Fusco, M. L., ... & Simoni, M. (2017). Neuroactive steroid levels and psychiatric and andrological features in post-finasteride patients. The Journal of steroid biochemistry and molecular biology, 171, 229-235.



[36] Martinez, P. E., Rubinow, D. R., Nieman, L. K., Koziol, D. E., Morrow, A. L., Schiller, C. E., ... & Schmidt, P. J. (2016). 5α-reductase inhibition prevents the luteal phase increase in plasma allopregnanolone levels and mitigates symptoms in women with premenstrual dysphoric disorder. Neuropsychopharmacology, 41(4), 1093.



[37] Basaria, S., Jasuja, R., Huang, G., Wharton, W., Pan, H., Pencina, K., ... & Labrie, F. (2016). Characteristics of men who report persistent sexual symptoms after finasteride use for hair loss. The Journal of Clinical Endocrinology & Metabolism, 101(12), 4669-4680.



[38] Van Praag, H., Schinder, A. F., Christie, B. R., Toni, N., Palmer, T. D., & Gage, F. H. (2002). Functional neurogenesis in the adult hippocampus. Nature, 415(6875), 1030-1034.



[39] Stockmeier, C. A., Mahajan, G. J., Konick, L. C., Overholser, J. C., Jurjus, G. J., Meltzer, H. Y., ... & Rajkowska, G. (2004). Cellular changes in the postmortem hippocampus in major depression. Biological psychiatry, 56(9), 640-650.



[40] Jacobs, B. L., Van Praag, H., & Gage, F. H. (2000). Adult brain neurogenesis and psychiatry: a novel theory of depression. Molecular psychiatry, 5(3), 262-269.



[41] Römer, B., Pfeiffer, N., Lewicka, S., Ben-Abdallah, N., Vogt, M. A., Deuschle, M., ... & Gass, P. (2010). Finasteride treatment inhibits adult hippocampal neurogenesis in male mice. Pharmacopsychiatry, 43(05), 174-178.



[42] Samuels, B. A., & Hen, R. (2011). Neurogenesis and affective disorders. European Journal of Neuroscience, 33(6), 1152-1159.



[43] Romeo, E., Ströhle, A., Spalletta, G., Michele, F. D., Hermann, B., Holsboer, F., ... & Rupprecht, R. (1998). Effects of antidepressant treatment on neuroactive steroids in major depression. American Journal of Psychiatry, 155(7), 910-913.



[44] Uzunova, V., Sampson, L., & Uzunov, D. P. (2006). Relevance of endogenous 3α-reduced neurosteroids to depression and antidepressant action. Psychopharmacology, 186(3), 351-361.



[45] Uzunova, V., Sheline, Y., Davis, J. M., Rasmusson, A., Uzunov, D. P., Costa, E., & Guidotti, A. (1998). Increase in the cerebrospinal fluid content of neurosteroids in patients with unipolar major depression who are receiving fluoxetine or fluvoxamine. Proceedings of the National Academy of Sciences, 95(6), 3239-3244.



[46] Schüle, C., Nothdurfter, C., & Rupprecht, R. (2014). The role of allopregnanolone in depression and anxiety. Progress in neurobiology, 113, 79-87.



[47] Rasmusson, A. M., Pinna, G., Paliwal, P., Weisman, D., Gottschalk, C., Charney, D., ... & Guidotti, A. (2006). Decreased cerebrospinal fluid allopregnanolone levels in women with posttraumatic stress disorder. Biological psychiatry, 60(7), 704-713.



[48] Hellgren, C., Åkerud, H., Skalkidou, A., Bäckström, T., & Sundström-Poromaa, I. (2014). Low serum allopregnanolone is associated with symptoms of depression in late pregnancy. Neuropsychobiology, 69(3), 147-153.



[49] Schüle, C., Nothdurfter, C., & Rupprecht, R. (2014). The role of allopregnanolone in depression and anxiety. Progress in neurobiology, 113, 79-87.



[50] Murphy, B. P., Abbott, F. V., Allison, C. M., Watts, C., & Ghadirian, A. M. (2004). Elevated levels of some neuroactive progesterone metabolites, particularly isopregnanolone, in women with chronic fatigue syndrome. Psychoneuroendocrinology, 29(2), 245-268.



[51] Uzunova, V., Sheline, Y., Davis, J. M., Rasmusson, A., Uzunov, D. P., Costa, E., & Guidotti, A. (1998). Increase in the cerebrospinal fluid content of neurosteroids in patients with unipolar major depression who are receiving fluoxetine or fluvoxamine. Proceedings of the National Academy of Sciences, 95(6), 3239-3244.



[52] Romeo, E., Ströhle, A., Spalletta, G., Michele, F. D., Hermann, B., Holsboer, F., ... & Rupprecht, R. (1998). Effects of antidepressant treatment on neuroactive steroids in major depression. American Journal of Psychiatry, 155(7), 910-913.



[53] Li, L., Kang, Y. X., Ji, X. M., Li, Y. K., Li, S. C., Zhang, X. J., ... & Shi, G. M. (2018). Finasteride inhibited brain dopaminergic system and open‐field behaviors in adolescent male rats. CNS neuroscience & therapeutics, 24(2), 115-125.



[54] Litim, N., Bourque, M., Al Sweidi, S., Morissette, M., & Di Paolo, T. (2015). The 5α-reductase inhibitor Dutasteride but not Finasteride protects dopamine neurons in the MPTP mouse model of Parkinson's disease. Neuropharmacology, 97, 86-94.



[55] Dazzi, L., Serra, M., Seu, E., Cherchi, G., Pisu, M. G., Purdy, R. H., & Biggio, G. (2002). Progesterone enhances ethanol‐induced modulation of mesocortical dopamine neurons: antagonism by finasteride. Journal of neurochemistry, 83(5), 1103-1109



(Keep in mind i put a big emphazize on finasteride mainly because piec was promoting it)

Tags : @Clavicular
@piec
@MA_ascender
@Sapieeen
@NZb6Air
@Rigged
@´´´´´´´´
@Acne Victim
@DR. NICKGA
@cooldude1231

Glad we both agree that uncs a fraud

 

[Deleted member 77820]

High effort low medicine understanding.
Recommending spirinolactone too youngsters is crazy.

Low medicine understanding
Nigga im reccomending it for oldcells what are the odds that a 16 yo suffers from extreme hairloss while on 500 aas of gear total

 

[Deleted member 77820]

High effort low medicine understanding.
Recommending spirinolactone too youngsters is crazy.

Low medicine understanding
Nigga im reccomending it for oldcells what are the odds that a 16 yo suffers from extreme hairloss while on 500 aas of gear total

 

[Deleted member 98369]

Holy shit thread, duta or ldar

Real question bro why does your face look puffy even when ur super lean, do u eat too much sodium or sum shit? Either way that sucks

 

[IOS]

Why Finasteride (or dut) is a fraud :



So debunking the claim is finasteride dangerous for you yes or no

their are some people who get the following effects from just microdosing fin :

• sexual dysfunction
• Anhedonia
• Depression
• Anxiety
• Lack of motivation
• Lack of focus

While other seems fine using it

Soooo It depends on your neural phenotypes

Some things like childhood trauma has a lot of gaba menergic signaling adrenaline cortisol levels ect….

And also different architectures of the brain (I might write a thread about it its really interesting how you can just look at someone genes pool and know if he has adhd bi polar ect….. if this thread anhilate the fraud that is piec i sure would write about it)

Now lets starts on why finasteride cause all of this sides :

When you use and 5ar inhibitor your not just inhibiting dht but also progesterone and alopregnolone and if you neealycompletely inhibit the enzyme (which you probably will cause most of the 5ar is type 1 and don’t get me started on dut that shit blocks everything) or nearly you have no progesterone and alopregonolone function in your body so back then i thought well you can just take progestene just to come to the conclusion its gonna do nothing for cause you totaly inhibited thw enzyme.

Suggestion : (keep in mind this is not the best approach I’m gonna get to the nest approach later but its still better than the fraud that is piec feel free to insult his ass in the comments)



Now lets talk about the sides :

Remember about the sides i talked about earlier it was due to allo pregnolone who acts as a innate benzo in your system (so basicaly the main inhibotory gaba system in your brain is the gabaergic system related to the hormone you name it “gaba” it has 2 receptors Gaba B fair enough it can be agonized with just phenibut so no need first allopregnolone its not in the sort of communication in the brain anyway (which mean less signaling)

then We have Gaba A

The only critical receptor and guess what the Gaba A receptor is modulated by allopregnolone which if you remember correctly you blocked earlier sp how do i explain it basicaly its like you took a reverse xanax so the average nigga is gonna have anhedonia exept of he is an outlier so now your fucking dependent on benzos who are super dangerous if you don’t wanna feel like shit

(Then some smart ass in the comment gonna write well then why dont you take alopregnolone well it has very short half life and it can’t be stored or kept so unless you want to be taking ng of allopregnolone every 5 minutes you should either feel like shit like that evil piec want you to be or be addicted to benzos for progesterone you can just take transdermal or micronuzed progesterone just make sure to be on hormones cause your at high risk of hypogonadism if you mess up your dosages)



(Also their are other alternatives so 1) way to get allopregnolone which in theory would work not sure 100% is your gonna take your progesterone and agnozed the tsp receptor you’ll end up with more neuro steroidgenisis so you have more alopregnolone just make sure to not get addicted to that shit might write a thread about how to never get addicted to compounds and how to get rid off any addiction but for that ill need you to support me and all insult piec parents for not putting on a rubber that sad night

Getting back to what i was saying their some research that seem mehh like ettyfoxine but that shit is too risky in my opinion

2) alternative is basicaly fuck modulating gaba receptors you just take sodium valproate kt basicaly make your brain a sink of gaba kinda like piec asshole after getting fucked by every dermatologist prescribing him fin

And its a hdac inhibitor so it have epigenetic change keep in mind that shit aint salt that a epilepsy drug and they are reliable 100% cause nigga imagine an epileptic go through withdrawal his gonna fucking die like piec pride after i finish writing this thread)

So to summarize a little :

Erectil dysfunction: is caused by low progesterone abdominal low dht

Anhedhonia : is cause by low alopregnolone levels

Anxiety : is caused because the amygdila have gaba receptors which when inhibited cause the amygdala to start tweaking like piec teading this right now well i hope finasteride would give you trauma and make you hyper vigilant to not with me next time keep in mind if it don’t happen to you it could just mean you had a gabaminergic deficit or your life so

you adapted your the exeption not the rule



Lack of focus : mainly because of low dht and progesterone youll need for that to increase your dopamenergic signaling (supposing you have average serotonorgic signaling) but you can use something like wellbutrin ritalin low dose in the morning 2x per week

(Wellbutrin do have bad effects on cholinergic system but supposing your an average dude and get a lot of choline in your diet your probably fine)



Here a Choline stack if anyone is interested i already writed it down wayback in the thread fix your life as a teenager :

1. Acetylcholine

a.1g CDP choline 2x per day

b.20 mg Donepezil upon rising

c.300 mg alpha gpc in the morning

d.500 mg Uridine monophosphate in the morning

e.1000 mg piracetam (5x per week$

f.30 mg Noopept



So your gonna ask me what could you do well you can use a topical dut in the hairline or balding areas (but good luck sourcing that)

(Before you ragebait in the comments i already thought about blocking the androgen receptor with Ru but to much side effects especially knowing the information I’m gonna reveal later)



The biggest lie ever said about hairloss :

is that dht cause hairloss if dht cause its mainly becuase it caus low estrogen who is responsible for the hairloss (just look at the guys who took tamoxifen who get hairloss look at the guys who take masteron who get hairloss which if you didn’t know is less androgenic than test its because of its serm effects look at rad 140 who is literraly 0 androgenic and still result in hairloss don’t forget rad 140 was intended to cute breast cancer so its all about estrogens)



If anything Dht increase hair growth :

https://pmc.ncbi.nlm.nih.gov/articles/PMC6989660/



We have seen the effects of blocking DHT. It SLOWS hair loss and some get a MILD regrowth at best with all the sides and complex protocols you should apply to counter act those side effects



The problem with the hairloss comunity is they often overlook the basics like what about hypogonadol nigga who got hairloss they don’t have high dht yet they are bald

So lets get to it the main reasons of hairloss :

• Low estrogen as said earlier
• Bad lifestyle habits
• Poor nutrition
• Lack of exercise

Then we have the most important ones :

• Insulin resistance
• Stress
• The main contributing factor of hairloss and the most overloked one is hypoxia you can try it yourself put on a hat on your hair for 12 hours your gonna feel your haur thinning if you think im coping

So my Definitive hairloss stack that I’ll reccomend :



Topical supplements:
-Ketoconazole cream. 1 to 2 times a day, every day. If price or convenience is an issue, the minimum this should be applied is before bed to balding areas. Ketoconazole has been shown to be just as effective as minoxidil in studies with the shampoo. And even stronger the cream has been shown to produce results with an overnight application.

-Emu oil. 1-2 times a day. One of the only proven items I’ve come across that increases skin and hair DNA synthesis, with studies showing hair regrowth.

-Peppermint oil. 1-2 times a day. Peppermint oil has been shown in studies to be equivalent to minoxidil, without the negative side effects that result in premature aging of the skin.

-Evening Primrose oil or Borage oil. Both shown to cause hair regrowth in studies. Just adding a little more fat topically which is absorbed via the skin. Also useful for GLA’s effect on prostaglandins for halting inflammation, hair loss, and aiding hair regrowth.

-Spironolactone cream. Spironolactone has been shown to restore a 60 year old males hairline to his teenage years hair line that he had lost decades ago. Although we use this item topically, it still has the same benefits locally as it is used for such issues as hair loss and hirsutism topically. However topically it does not go systematic as in studies it has been applied to patients whole backs without going systematic. Spironolactone blocks the binding of androgens to the androgen receptor and helps increase estrogen locally.



-BiEstro cream. E2 and E3 combo, Estradiol and Estriol. Apply once or twice a day to balding areas.

The amount used here is enough to cover balding thinning areas. Due to the area we are applying it studies have shown no real systematic absorption. And also to the fact of the dose we are using is quite low as well. None of the users nor myself could produce an estrogenic side on this when applied to the scalp. Some of us who would normally get estrogenic sides off testosterone use as low as 200 mg.

(You can add bold for E1 if you wanna maximize but kinda pain in the ass cause you have to do bloods and make sure your E1 doesn’t lower your E2 and E3 basicaly you should keep them in harmony)



We have also seen what adding estrogen does for hair, as the byproduct of the thousands of male to female sex changes. These individuals can regrow full heads of amazing hair, bringing back hair reminiscent of that which they had when they were teenagers.

Likely, the ones seeing any bit of regrowth from DHT blockers are as a result of the mild estrogen increase triggered by these compounds. Studies of topical estrogen, plain and simple, work. In both men and women. As a bonus, adding estrogen topically doesn’t just increase estrogen -it also the localized concentration of the aromatase enzyme.

(I’ve saw myself dozens of people on reedit i swear i dont know why i couldnt find them having resuts if anyone has it please write it down below)

(For the studies i linked so many in the ashwaganda and no body gave a fuck

So because of that here are some studies on mice :

https://pubmed.ncbi.nlm.nih.gov/14962083/

https://www.researchgate.net/figure...e-tenth-day-after-hair-shaving_fig1_229083213





View attachment 3261225

Here is someone who got hair growth using estriol and estradiol cream



=End justification for BiEstro Cream==

Rub this mixture on once or twice a day depending on your available time. Once a day is totally fine, and optimal for most, if you can apply it before bed. If not, and you must do it in the day, pick a time where you can leave it on for at least 1-2 hours before showering it out.



Supplements:

Minerals might be needed if severely deficient, some doses are based off studies and you may not need these doses. You must find your own dose.

-Zinc Picolinate. 100-150mg a day for 6-8 weeks, tops.

This depends on a few factors. Add up your dietary zinc content that you typically average, and then decide if zinc might be low and determine the dose that you want. This has been noted in studies to completely reverse hair loss and hypothyroid conditions that are due to a zinc deficiency. NOTE: You may not need this, use discretion. Too much zinc can lead to other problems.

-Taurine. 2.5 grams, 2x a day.

In regards to hair loss, Taurine has been shown to help combat fibrosis of the scalp, thus

increasing circulation and hair growth.



Black Currant Oil, 3g a day.

This is utilized for its Gamma Linoleic Acid (GLA) content, which has anti-inflammatory properties, the ability to increase hair growth prostaglandins (PGE), and the ability to inhibit hair loss prostaglandins (PGD). These prostaglandins are another contributing factor to hair loss/growth aside from the androgens.

Three items have been shown to decrease GLA – wheat, dairy, and trans fats – through inhibition of an enzyme called D6D. The typical western diet is full of these foods. Inhibition of the D6D enzyme prevents the conversion of Linoleic Acid (LA) into GLA. The inhibition of D6D also happens with age, and is likely one of the key contributors to balding getting worse with age. This is just about the only process that can link balding to aging that has not already been explored.

In taking a GLA supplement, we bypass the enzymatic conversion entirely and have the end product.

Black Currant oil was also shown in animal studies to prevent many of the negatives of excessive fructose intake, such as fatty liver.



Grapeseed Extract, 500-1000mg a day.
GSE has been shown in animal studies to improve insulin resistance as much as metformin. Studies have also shown GSE to double the number of hairs in the anagen (growth) phase. As far as I am aware, no other compound has been shown to have effects this potent.

(Note : i do not advise to take metformin or berberine for other reasons i would write a thread about it in the near future)



Chromium gtf is used for combating insulin resistance, which is seen as a contributing factor for hair loss as mentioned above when talking about GSE. Again, some may not need this. Chromium GTF has been shown in case studies with type 2 diabetics to remove all exogenous insulin dependency within a couple months of use i recommend using 1000mcg a day for about 6 weeks



And you want to be eating or supplementing with those :

Magnesium

B vitamins

Vitamin K2

You also wanna be getting fats in your diet (especially from Mufas and Pufas (just make sure your not getting it from seed oils because its processed that a whole other topic id advise to get from seeds)



but I assure you, PUFA fats are NOT bad for you. Getting them from healthy sources has countless proven health benefits: anti-carcinogenic, anti-inflammatory, pro-sleep, pro-thyroid, etc. The benefits of unheated PUFA fats are a very deep topic on their own.

The epidermis of your skin is made of 60 percent Omega-6 PUFA fats. Do not fall for the “Omega-3 must be higher than Omega-6” speech that has no proven benefits and multiple proven detriments. All of the studies linking PUFA fats to health issues look at the typical use for PUFA fats in the western diet: cooking, frying, and otherwise heating the fats. If we are to take the same controlled environment but introduce raw, unheated PUFA fats from seeds and nuts, the studies flip completely. Anti-cancer, anti-inflammatory, and all-around health marker improvement is marked.



Another issue found often in the bodybuilding and fitness realm is the “eating too clean” phenomenon. If you were to add up chicken, rice, broccoli, and some olive oil on your favorite diet app, I can guarantee that you’d see that it’s a struggle to reach even 15 percent of RDA requirements for PUFA fats. When this happens, the skin goes dry and wrinkles appear, hair becomes straw like and falls out, etc. Digestive issues ensue, and metabolism slows down. As PUFA fats are shown to increase thyroid hormone sensitivity by almost 20 percent, dieting becomes harder and fat accrual in a calorie surplus becomes far easier. This isn’t even rectifiable with exogenous thyroid hormones – take all the thyroid drugs you want, if your sensitivity isn’t up to par your metabolism will suffer.

(Fun fact : Studies have also shown that when consumed in equal quantities, monounsaturated and saturated fats cause fat gain. Saturated fat was shown to cause a decrease in insulin sensitivity as well. PUFA fat, on the other hand, caused barely any fat gain. The majority of weight gained was muscle, insulin sensitivity increased, and abdominal fat thickness decreased.)



Other Foods.

Pineapple is used as a general health food with documented anti-inflammatory benefits, contains an enzyme papaya if i can recall that aids in the digestion of protein, is a fantastic source of vitamins, and is a preferred fruit due to the lower-end fructose content. In regards to hair regrowth, the main benefit is its anti-inflammatory property.



Massage/Mechanical Manipulation:

Vigorously massage, brush, or pinch your scalp in the balding areas. 1-2 times a day, for whatever time frame you can manage; the longer the better. 3-5 minutes is great, 10 minutes is better. Use as much pressure as possible. Tissue manipulation like this increases circulation and has been proven in studies to aid hair growth. To assist in blood flow further, you can bend over and point your head toward the ground, allowing gravity to assist in delivering blood to the target area.



You could also look in the More plates more plates micro needling stuff :



Sources :



[1] Stoner, E. (1990). The clinical development of a 5α-reductase inhibitor, finasteride. The Journal of steroid biochemistry and molecular biology, 37(3), 375-378.



[2] Vuichoud, C., & Loughlin, K. R. (2015). Benign prostatic hyperplasia: epidemiology, economics and evaluation. Can J Urol, 22(Suppl 1), 1-6.



[3] Adil, A., & Godwin, M. (2017). The effectiveness of treatments for androgenetic alopecia: a systematic review and meta-analysis. Journal of the American Academy of



141.



[4] Schumacher, M., Hussain, R., Gago, N., Oudinet, J. P., Mattern, C., & Ghoumari, A. (2012). Progesterone synthesis in the nervous system: implications for myelination and myelin repair. Frontiers in neuroscience, 6, 10.



[5] Skeldon, S. C., Macdonald, E. M., Law, M. R., Huang, A., Paterson, J. M., Mamdani, M. M., & Juurlink, D. (2017). The cardiovascular safety of dutasteride. The Journal of urology, 197(5), 1309-1314.



[6] Lee, H. J., & Chang, C. (2003). Recent advances in androgen receptor action. Cellular and Molecular Life Sciences CMLS, 60(8), 1613-1622.



[7] Bolton, E. C., So, A. Y., Chaivorapol, C., Haqq, C. M., Li, H., & Yamamoto, K. R. (2007). Cell-and gene-specific regulation of primary target genes by the androgen receptor. Genes & development, 21(16), 2005-2017.



[8] Winiarska, A., Mandt, N., Kamp, H., Hossini, A., Seltmann, H., Zouboulis, C. C., & Blume-Peytavi, U. (2006). Effect of 5α-dihydrotestosterone and testosterone on apoptosis in human dermal papilla cells. Skin pharmacology and physiology, 19(6), 311-321.



[9] Chhipa, R. R., Halim, D., Cheng, J., Zhang, H. Y., Mohler, J. L., Ip, C., & Wu, Y. (2013). The direct inhibitory effect of dutasteride or finasteride on androgen receptor activity is cell line specific. The Prostate, 73(14), 1483-1494.



[10] Mella, J. M., Perret, M. C., Manzotti, M., Catalano, H. N., & Guyatt, G. (2010). Efficacy and safety of finasteride therapy for androgenetic alopecia: a systematic review. Archives of dermatology, 146(10), 1141-1150.



[11] Di Loreto, C., La Marra, F., Mazzon, G., Belgrano, E., Trombetta, C., & Cauci, S. (2014). Immunohistochemical evaluation of androgen receptor and nerve structure density in human prepuce from patients with persistent sexual side effects after finasteride use for androgenetic alopecia. PLoS One, 9(6).



[12] Overstreet, J. W., Fuh, V. L., Gould, J., Howards, S. S., Lieber, M. M., Hellstrom, W., ... & LEWIS, R. (1999). Chronic treatment with finasteride daily does not affect spermatogenesis or semen production in young men. The Journal of urology, 162(4), 1295-1300.



[13] Samplaski, M. K., Lo, K., Grober, E., & Jarvi, K. (2013). Finasteride use in the male infertility population: effects on semen and hormone parameters. Fertility and sterility, 100(6), 1542-1546.



[14] Amory, J. K., Wang, C., Swerdloff, R. S., Anawalt, B. D., Matsumoto, A. M., Bremner, W. J., ... & Clark, R. V. (2007). The effect of 5α-reductase inhibition with dutasteride and finasteride on semen parameters and serum hormones in healthy men. The Journal of Clinical Endocrinology & Metabolism, 92(5), 1659-1665.



[15] Traish, A. M. (2020). Health Risks Associated with Long-Term Finasteride and Dutasteride Use: It's Time to Sound the Alarm. The World Journal of Men's Health, 38.



[16] Traish, A., Haider, K. S., Doros, G., & Haider, A. (2017). Long-term dutasteride therapy in men with benign prostatic hyperplasia alters glucose and lipid profiles and increases severity of erectile dysfunction. Hormone molecular biology and clinical investigation, 30(3).



[17] Doulabi, S. R. S. M., Kavoussi, H., Isapour, D., Hashemian, A., & Taheriniya, A. (2013). Effect of finasteride on lipid profile in individuals with androgenetic alopecia. African Journal of Pharmacy and Pharmacology, 7(6), 315-317.



[18] Duskova, M., Hill, M., & Starka, L. (2010). Changes of metabolic profile in men treated for androgenetic alopecia with 1 mg finasteride. Endocr Regul, 44(1), 3-8.



[19] Gild, P., Cole, A. P., Krasnova, A., Dickerman, B. A., von Landenberg, N., Sun, M., ... & Kibel, A. S. (2018). Liver disease in men undergoing androgen deprivation therapy for prostate cancer. The Journal of urology, 200(3), 573-581.



[20] Mendenhall, C. L. (1968). Anabolic steroid therapy as an adjunct to diet in alcoholic hepatic steatosis. The American journal of digestive diseases, 13(9), 783-791.



[21] Jacqueson, A., Thevenin, M., Warnet, J. M., Claude, J. R., & Truhaut, R. (1978). Comparative Study of the Protective Effect of an Anabolic Steroid. In Toxicological Aspects of Food Safety (pp. 193-196). Springer, Berlin, Heidelberg.



[22] Kelly, D. M., Nettleship, J. E., Akhtar, S., Muraleedharan, V., Sellers, D. J., Brooke, J. C., ... & Jones, T. H. (2014). Testosterone suppresses the expression of regulatory enzymes of fatty acid synthesis and protects against hepatic steatosis in cholesterol-fed androgen deficient mice. Life sciences, 109(2), 95-103.



[23] Lin, H. Y., Yu, I. C., Wang, R. S., Chen, Y. T., Liu, N. C., Altuwaijri, S., ... & Yeh, S. (2008). Increased hepatic steatosis and insulin resistance in mice lacking hepatic androgen receptor. Hepatology, 47(6), 1924-1935.



[24] Völzke, H., Aumann, N., Krebs, A., Nauck, M., Steveling, A., Lerch, M. M., ... & Wallaschofski, H. (2010). Hepatic steatosis is associated with low serum testosterone and high serum DHEAS levels in men. International journal of andrology, 33(1), 45-53.



[25] Velazquez, I., & Alter, B. P. (2004). Androgens and liver tumors: Fanconi's anemia and non‐Fanconi's conditions. American journal of hematology, 77(3), 257-267.



[26] Di Loreto, C., La Marra, F., Mazzon, G., Belgrano, E., Trombetta, C., & Cauci, S. (2014). Immunohistochemical evaluation of androgen receptor and nerve structure density in human prepuce from patients with persistent sexual side effects after finasteride use for androgenetic alopecia. PLoS One, 9(6).



[27] Hsieh, J. T., Chen, S. C., Yu, H. J., & Chang, H. C. (2011). Finasteride upregulates expression of androgen receptor in hyperplastic prostate and LNCaP cells: implications for chemoprevention of prostate cancer. The Prostate, 71(10), 1115-1121.



[28] Pinsky, M. R., Gur, S., Tracey, A. J., Harbin, A., & Hellstrom, W. J. (2011). The effects of chronic 5‐alpha‐reductase inhibitor (dutasteride) treatment on rat erectile function. The journal of sexual medicine, 8(11), 3066-3074.



[29] Iacono, F., Prezioso, D., Ruffo, A., Illiano, E., Romis, L., Di Lauro, G., ... & Amato, B. (2012). Testosterone deficiency causes penile fibrosis and organic erectile dysfunction in aging men. Evaluating association among Age. BMC surgery, 12(S1), S24.



[30] Zhang, M. G., Wang, X. J., Shen, Z. J., & Gao, P. J. (2013). Long-term oral administration of 5α-reductase inhibitor attenuates erectile function by inhibiting autophagy and promoting apoptosis of smooth muscle cells in corpus cavernosum of aged rats. Urology, 82(3), 743-e9.



[31] Melcangi, R. C., Caruso, D., Abbiati, F., Giatti, S., Calabrese, D., Piazza, F., & Cavaletti, G. (2013). Neuroactive steroid levels are modified in cerebrospinal fluid and plasma of post‐finasteride patients showing persistent sexual side effects and anxious/depressive symptomatology. The journal of sexual medicine, 10(10), 2598-2603.



sexual medicine, 10(10), 2598-2603.



[32] Alanazi, N. (2016). Assessing the quality of life and health outcomes of Androgenic Alopecia patients using Propecia (Doctoral dissertation, Rutgers University-School of Health Related Professions).



[33] Melcangi, R. C., Caruso, D., Abbiati, F., Giatti, S., Calabrese, D., Piazza, F., & Cavaletti, G. (2013). Neuroactive steroid levels are modified in cerebrospinal fluid and plasma of post‐finasteride patients showing persistent sexual side effects and anxious/depressive symptomatology. The journal of sexual medicine, 10(10), 2598-2603.



[34] Caruso, D., Abbiati, F., Giatti, S., Romano, S., Fusco, L., Cavaletti, G., & Melcangi, R. C. (2015). Patients treated for male pattern hair with finasteride show, after discontinuation of the drug, altered levels of neuroactive steroids in cerebrospinal fluid and plasma. The Journal of steroid biochemistry and molecular biology, 146, 74-79.



[35] Melcangi, R. C., Santi, D., Spezzano, R., Grimoldi, M., Tabacchi, T., Fusco, M. L., ... & Simoni, M. (2017). Neuroactive steroid levels and psychiatric and andrological features in post-finasteride patients. The Journal of steroid biochemistry and molecular biology, 171, 229-235.



[36] Martinez, P. E., Rubinow, D. R., Nieman, L. K., Koziol, D. E., Morrow, A. L., Schiller, C. E., ... & Schmidt, P. J. (2016). 5α-reductase inhibition prevents the luteal phase increase in plasma allopregnanolone levels and mitigates symptoms in women with premenstrual dysphoric disorder. Neuropsychopharmacology, 41(4), 1093.



[37] Basaria, S., Jasuja, R., Huang, G., Wharton, W., Pan, H., Pencina, K., ... & Labrie, F. (2016). Characteristics of men who report persistent sexual symptoms after finasteride use for hair loss. The Journal of Clinical Endocrinology & Metabolism, 101(12), 4669-4680.



[38] Van Praag, H., Schinder, A. F., Christie, B. R., Toni, N., Palmer, T. D., & Gage, F. H. (2002). Functional neurogenesis in the adult hippocampus. Nature, 415(6875), 1030-1034.



[39] Stockmeier, C. A., Mahajan, G. J., Konick, L. C., Overholser, J. C., Jurjus, G. J., Meltzer, H. Y., ... & Rajkowska, G. (2004). Cellular changes in the postmortem hippocampus in major depression. Biological psychiatry, 56(9), 640-650.



[40] Jacobs, B. L., Van Praag, H., & Gage, F. H. (2000). Adult brain neurogenesis and psychiatry: a novel theory of depression. Molecular psychiatry, 5(3), 262-269.



[41] Römer, B., Pfeiffer, N., Lewicka, S., Ben-Abdallah, N., Vogt, M. A., Deuschle, M., ... & Gass, P. (2010). Finasteride treatment inhibits adult hippocampal neurogenesis in male mice. Pharmacopsychiatry, 43(05), 174-178.



[42] Samuels, B. A., & Hen, R. (2011). Neurogenesis and affective disorders. European Journal of Neuroscience, 33(6), 1152-1159.



[43] Romeo, E., Ströhle, A., Spalletta, G., Michele, F. D., Hermann, B., Holsboer, F., ... & Rupprecht, R. (1998). Effects of antidepressant treatment on neuroactive steroids in major depression. American Journal of Psychiatry, 155(7), 910-913.



[44] Uzunova, V., Sampson, L., & Uzunov, D. P. (2006). Relevance of endogenous 3α-reduced neurosteroids to depression and antidepressant action. Psychopharmacology, 186(3), 351-361.



[45] Uzunova, V., Sheline, Y., Davis, J. M., Rasmusson, A., Uzunov, D. P., Costa, E., & Guidotti, A. (1998). Increase in the cerebrospinal fluid content of neurosteroids in patients with unipolar major depression who are receiving fluoxetine or fluvoxamine. Proceedings of the National Academy of Sciences, 95(6), 3239-3244.



[46] Schüle, C., Nothdurfter, C., & Rupprecht, R. (2014). The role of allopregnanolone in depression and anxiety. Progress in neurobiology, 113, 79-87.



[47] Rasmusson, A. M., Pinna, G., Paliwal, P., Weisman, D., Gottschalk, C., Charney, D., ... & Guidotti, A. (2006). Decreased cerebrospinal fluid allopregnanolone levels in women with posttraumatic stress disorder. Biological psychiatry, 60(7), 704-713.



[48] Hellgren, C., Åkerud, H., Skalkidou, A., Bäckström, T., & Sundström-Poromaa, I. (2014). Low serum allopregnanolone is associated with symptoms of depression in late pregnancy. Neuropsychobiology, 69(3), 147-153.



[49] Schüle, C., Nothdurfter, C., & Rupprecht, R. (2014). The role of allopregnanolone in depression and anxiety. Progress in neurobiology, 113, 79-87.



[50] Murphy, B. P., Abbott, F. V., Allison, C. M., Watts, C., & Ghadirian, A. M. (2004). Elevated levels of some neuroactive progesterone metabolites, particularly isopregnanolone, in women with chronic fatigue syndrome. Psychoneuroendocrinology, 29(2), 245-268.



[51] Uzunova, V., Sheline, Y., Davis, J. M., Rasmusson, A., Uzunov, D. P., Costa, E., & Guidotti, A. (1998). Increase in the cerebrospinal fluid content of neurosteroids in patients with unipolar major depression who are receiving fluoxetine or fluvoxamine. Proceedings of the National Academy of Sciences, 95(6), 3239-3244.



[52] Romeo, E., Ströhle, A., Spalletta, G., Michele, F. D., Hermann, B., Holsboer, F., ... & Rupprecht, R. (1998). Effects of antidepressant treatment on neuroactive steroids in major depression. American Journal of Psychiatry, 155(7), 910-913.



[53] Li, L., Kang, Y. X., Ji, X. M., Li, Y. K., Li, S. C., Zhang, X. J., ... & Shi, G. M. (2018). Finasteride inhibited brain dopaminergic system and open‐field behaviors in adolescent male rats. CNS neuroscience & therapeutics, 24(2), 115-125.



[54] Litim, N., Bourque, M., Al Sweidi, S., Morissette, M., & Di Paolo, T. (2015). The 5α-reductase inhibitor Dutasteride but not Finasteride protects dopamine neurons in the MPTP mouse model of Parkinson's disease. Neuropharmacology, 97, 86-94.



[55] Dazzi, L., Serra, M., Seu, E., Cherchi, G., Pisu, M. G., Purdy, R. H., & Biggio, G. (2002). Progesterone enhances ethanol‐induced modulation of mesocortical dopamine neurons: antagonism by finasteride. Journal of neurochemistry, 83(5), 1103-1109



(Keep in mind i put a big emphazize on finasteride mainly because piec was promoting it)

Tags : @Clavicular
@piec
@MA_ascender
@Sapieeen
@NZb6Air
@Rigged
@´´´´´´´´
@Acne Victim
@DR. NICKGA
@cooldude1231

saved for later,bookmarked..
looks intresting

 

[Deleted member 76870]

Real question bro why does your face look puffy even when ur super lean, do u eat too much sodium or sum shit? Either way that sucks

That's just how his face looks like

 

[Deleted member 98369]

That's just how his face looks like

brootal, at least he's got other good features

 

[mfk]

idiot newcel farming reps through spending his time writing unnecessarily long threads on homeopathic bullshit

dht is shit after puberty

 

[true_volcel]

Why Finasteride (or dut) is a fraud :



So debunking the claim is finasteride dangerous for you yes or no

their are some people who get the following effects from just microdosing fin :

• sexual dysfunction
• Anhedonia
• Depression
• Anxiety
• Lack of motivation
• Lack of focus

While other seems fine using it

Soooo It depends on your neural phenotypes

Some things like childhood trauma has a lot of gaba menergic signaling adrenaline cortisol levels ect….

And also different architectures of the brain (I might write a thread about it its really interesting how you can just look at someone genes pool and know if he has adhd bi polar ect….. if this thread anhilate the fraud that is piec i sure would write about it)

Now lets starts on why finasteride cause all of this sides :

When you use and 5ar inhibitor your not just inhibiting dht but also progesterone and alopregnolone and if you neealycompletely inhibit the enzyme (which you probably will cause most of the 5ar is type 1 and don’t get me started on dut that shit blocks everything) or nearly you have no progesterone and alopregonolone function in your body so back then i thought well you can just take progestene just to come to the conclusion its gonna do nothing for cause you totaly inhibited thw enzyme.

Suggestion : (keep in mind this is not the best approach I’m gonna get to the nest approach later but its still better than the fraud that is piec feel free to insult his ass in the comments)



Now lets talk about the sides :

Remember about the sides i talked about earlier it was due to allo pregnolone who acts as a innate benzo in your system (so basicaly the main inhibotory gaba system in your brain is the gabaergic system related to the hormone you name it “gaba” it has 2 receptors Gaba B fair enough it can be agonized with just phenibut so no need first allopregnolone its not in the sort of communication in the brain anyway (which mean less signaling)

then We have Gaba A

The only critical receptor and guess what the Gaba A receptor is modulated by allopregnolone which if you remember correctly you blocked earlier sp how do i explain it basicaly its like you took a reverse xanax so the average nigga is gonna have anhedonia exept of he is an outlier so now your fucking dependent on benzos who are super dangerous if you don’t wanna feel like shit

(Then some smart ass in the comment gonna write well then why dont you take alopregnolone well it has very short half life and it can’t be stored or kept so unless you want to be taking ng of allopregnolone every 5 minutes you should either feel like shit like that evil piec want you to be or be addicted to benzos for progesterone you can just take transdermal or micronuzed progesterone just make sure to be on hormones cause your at high risk of hypogonadism if you mess up your dosages)



(Also their are other alternatives so 1) way to get allopregnolone which in theory would work not sure 100% is your gonna take your progesterone and agnozed the tsp receptor you’ll end up with more neuro steroidgenisis so you have more alopregnolone just make sure to not get addicted to that shit might write a thread about how to never get addicted to compounds and how to get rid off any addiction but for that ill need you to support me and all insult piec parents for not putting on a rubber that sad night

Getting back to what i was saying their some research that seem mehh like ettyfoxine but that shit is too risky in my opinion

2) alternative is basicaly fuck modulating gaba receptors you just take sodium valproate kt basicaly make your brain a sink of gaba kinda like piec asshole after getting fucked by every dermatologist prescribing him fin

And its a hdac inhibitor so it have epigenetic change keep in mind that shit aint salt that a epilepsy drug and they are reliable 100% cause nigga imagine an epileptic go through withdrawal his gonna fucking die like piec pride after i finish writing this thread)

So to summarize a little :

Erectil dysfunction: is caused by low progesterone abdominal low dht

Anhedhonia : is cause by low alopregnolone levels

Anxiety : is caused because the amygdila have gaba receptors which when inhibited cause the amygdala to start tweaking like piec teading this right now well i hope finasteride would give you trauma and make you hyper vigilant to not with me next time keep in mind if it don’t happen to you it could just mean you had a gabaminergic deficit or your life so

you adapted your the exeption not the rule



Lack of focus : mainly because of low dht and progesterone youll need for that to increase your dopamenergic signaling (supposing you have average serotonorgic signaling) but you can use something like wellbutrin ritalin low dose in the morning 2x per week

(Wellbutrin do have bad effects on cholinergic system but supposing your an average dude and get a lot of choline in your diet your probably fine)



Here a Choline stack if anyone is interested i already writed it down wayback in the thread fix your life as a teenager :

1. Acetylcholine

a.1g CDP choline 2x per day

b.20 mg Donepezil upon rising

c.300 mg alpha gpc in the morning

d.500 mg Uridine monophosphate in the morning

e.1000 mg piracetam (5x per week$

f.30 mg Noopept



So your gonna ask me what could you do well you can use a topical dut in the hairline or balding areas (but good luck sourcing that)

(Before you ragebait in the comments i already thought about blocking the androgen receptor with Ru but to much side effects especially knowing the information I’m gonna reveal later)



The biggest lie ever said about hairloss :

is that dht cause hairloss if dht cause its mainly becuase it caus low estrogen who is responsible for the hairloss (just look at the guys who took tamoxifen who get hairloss look at the guys who take masteron who get hairloss which if you didn’t know is less androgenic than test its because of its serm effects look at rad 140 who is literraly 0 androgenic and still result in hairloss don’t forget rad 140 was intended to cute breast cancer so its all about estrogens)



If anything Dht increase hair growth :

https://pmc.ncbi.nlm.nih.gov/articles/PMC6989660/



We have seen the effects of blocking DHT. It SLOWS hair loss and some get a MILD regrowth at best with all the sides and complex protocols you should apply to counter act those side effects



The problem with the hairloss comunity is they often overlook the basics like what about hypogonadol nigga who got hairloss they don’t have high dht yet they are bald

So lets get to it the main reasons of hairloss :

• Low estrogen as said earlier
• Bad lifestyle habits
• Poor nutrition
• Lack of exercise

Then we have the most important ones :

• Insulin resistance
• Stress
• The main contributing factor of hairloss and the most overloked one is hypoxia you can try it yourself put on a hat on your hair for 12 hours your gonna feel your haur thinning if you think im coping

So my Definitive hairloss stack that I’ll reccomend :



Topical supplements:
-Ketoconazole cream. 1 to 2 times a day, every day. If price or convenience is an issue, the minimum this should be applied is before bed to balding areas. Ketoconazole has been shown to be just as effective as minoxidil in studies with the shampoo. And even stronger the cream has been shown to produce results with an overnight application.

-Emu oil. 1-2 times a day. One of the only proven items I’ve come across that increases skin and hair DNA synthesis, with studies showing hair regrowth.

-Peppermint oil. 1-2 times a day. Peppermint oil has been shown in studies to be equivalent to minoxidil, without the negative side effects that result in premature aging of the skin.

-Evening Primrose oil or Borage oil. Both shown to cause hair regrowth in studies. Just adding a little more fat topically which is absorbed via the skin. Also useful for GLA’s effect on prostaglandins for halting inflammation, hair loss, and aiding hair regrowth.

-Spironolactone cream. Spironolactone has been shown to restore a 60 year old males hairline to his teenage years hair line that he had lost decades ago. Although we use this item topically, it still has the same benefits locally as it is used for such issues as hair loss and hirsutism topically. However topically it does not go systematic as in studies it has been applied to patients whole backs without going systematic. Spironolactone blocks the binding of androgens to the androgen receptor and helps increase estrogen locally.



-BiEstro cream. E2 and E3 combo, Estradiol and Estriol. Apply once or twice a day to balding areas.

The amount used here is enough to cover balding thinning areas. Due to the area we are applying it studies have shown no real systematic absorption. And also to the fact of the dose we are using is quite low as well. None of the users nor myself could produce an estrogenic side on this when applied to the scalp. Some of us who would normally get estrogenic sides off testosterone use as low as 200 mg.

(You can add bold for E1 if you wanna maximize but kinda pain in the ass cause you have to do bloods and make sure your E1 doesn’t lower your E2 and E3 basicaly you should keep them in harmony)



We have also seen what adding estrogen does for hair, as the byproduct of the thousands of male to female sex changes. These individuals can regrow full heads of amazing hair, bringing back hair reminiscent of that which they had when they were teenagers.

Likely, the ones seeing any bit of regrowth from DHT blockers are as a result of the mild estrogen increase triggered by these compounds. Studies of topical estrogen, plain and simple, work. In both men and women. As a bonus, adding estrogen topically doesn’t just increase estrogen -it also the localized concentration of the aromatase enzyme.

(I’ve saw myself dozens of people on reedit i swear i dont know why i couldnt find them having resuts if anyone has it please write it down below)

(For the studies i linked so many in the ashwaganda and no body gave a fuck

So because of that here are some studies on mice :

https://pubmed.ncbi.nlm.nih.gov/14962083/

https://www.researchgate.net/figure...e-tenth-day-after-hair-shaving_fig1_229083213





View attachment 3261225

Here is someone who got hair growth using estriol and estradiol cream



=End justification for BiEstro Cream==

Rub this mixture on once or twice a day depending on your available time. Once a day is totally fine, and optimal for most, if you can apply it before bed. If not, and you must do it in the day, pick a time where you can leave it on for at least 1-2 hours before showering it out.



Supplements:

Minerals might be needed if severely deficient, some doses are based off studies and you may not need these doses. You must find your own dose.

-Zinc Picolinate. 100-150mg a day for 6-8 weeks, tops.

This depends on a few factors. Add up your dietary zinc content that you typically average, and then decide if zinc might be low and determine the dose that you want. This has been noted in studies to completely reverse hair loss and hypothyroid conditions that are due to a zinc deficiency. NOTE: You may not need this, use discretion. Too much zinc can lead to other problems.

-Taurine. 2.5 grams, 2x a day.

In regards to hair loss, Taurine has been shown to help combat fibrosis of the scalp, thus

increasing circulation and hair growth.



Black Currant Oil, 3g a day.

This is utilized for its Gamma Linoleic Acid (GLA) content, which has anti-inflammatory properties, the ability to increase hair growth prostaglandins (PGE), and the ability to inhibit hair loss prostaglandins (PGD). These prostaglandins are another contributing factor to hair loss/growth aside from the androgens.

Three items have been shown to decrease GLA – wheat, dairy, and trans fats – through inhibition of an enzyme called D6D. The typical western diet is full of these foods. Inhibition of the D6D enzyme prevents the conversion of Linoleic Acid (LA) into GLA. The inhibition of D6D also happens with age, and is likely one of the key contributors to balding getting worse with age. This is just about the only process that can link balding to aging that has not already been explored.

In taking a GLA supplement, we bypass the enzymatic conversion entirely and have the end product.

Black Currant oil was also shown in animal studies to prevent many of the negatives of excessive fructose intake, such as fatty liver.



Grapeseed Extract, 500-1000mg a day.
GSE has been shown in animal studies to improve insulin resistance as much as metformin. Studies have also shown GSE to double the number of hairs in the anagen (growth) phase. As far as I am aware, no other compound has been shown to have effects this potent.

(Note : i do not advise to take metformin or berberine for other reasons i would write a thread about it in the near future)



Chromium gtf is used for combating insulin resistance, which is seen as a contributing factor for hair loss as mentioned above when talking about GSE. Again, some may not need this. Chromium GTF has been shown in case studies with type 2 diabetics to remove all exogenous insulin dependency within a couple months of use i recommend using 1000mcg a day for about 6 weeks



And you want to be eating or supplementing with those :

Magnesium

B vitamins

Vitamin K2

You also wanna be getting fats in your diet (especially from Mufas and Pufas (just make sure your not getting it from seed oils because its processed that a whole other topic id advise to get from seeds)



but I assure you, PUFA fats are NOT bad for you. Getting them from healthy sources has countless proven health benefits: anti-carcinogenic, anti-inflammatory, pro-sleep, pro-thyroid, etc. The benefits of unheated PUFA fats are a very deep topic on their own.

The epidermis of your skin is made of 60 percent Omega-6 PUFA fats. Do not fall for the “Omega-3 must be higher than Omega-6” speech that has no proven benefits and multiple proven detriments. All of the studies linking PUFA fats to health issues look at the typical use for PUFA fats in the western diet: cooking, frying, and otherwise heating the fats. If we are to take the same controlled environment but introduce raw, unheated PUFA fats from seeds and nuts, the studies flip completely. Anti-cancer, anti-inflammatory, and all-around health marker improvement is marked.



Another issue found often in the bodybuilding and fitness realm is the “eating too clean” phenomenon. If you were to add up chicken, rice, broccoli, and some olive oil on your favorite diet app, I can guarantee that you’d see that it’s a struggle to reach even 15 percent of RDA requirements for PUFA fats. When this happens, the skin goes dry and wrinkles appear, hair becomes straw like and falls out, etc. Digestive issues ensue, and metabolism slows down. As PUFA fats are shown to increase thyroid hormone sensitivity by almost 20 percent, dieting becomes harder and fat accrual in a calorie surplus becomes far easier. This isn’t even rectifiable with exogenous thyroid hormones – take all the thyroid drugs you want, if your sensitivity isn’t up to par your metabolism will suffer.

(Fun fact : Studies have also shown that when consumed in equal quantities, monounsaturated and saturated fats cause fat gain. Saturated fat was shown to cause a decrease in insulin sensitivity as well. PUFA fat, on the other hand, caused barely any fat gain. The majority of weight gained was muscle, insulin sensitivity increased, and abdominal fat thickness decreased.)



Other Foods.

Pineapple is used as a general health food with documented anti-inflammatory benefits, contains an enzyme papaya if i can recall that aids in the digestion of protein, is a fantastic source of vitamins, and is a preferred fruit due to the lower-end fructose content. In regards to hair regrowth, the main benefit is its anti-inflammatory property.



Massage/Mechanical Manipulation:

Vigorously massage, brush, or pinch your scalp in the balding areas. 1-2 times a day, for whatever time frame you can manage; the longer the better. 3-5 minutes is great, 10 minutes is better. Use as much pressure as possible. Tissue manipulation like this increases circulation and has been proven in studies to aid hair growth. To assist in blood flow further, you can bend over and point your head toward the ground, allowing gravity to assist in delivering blood to the target area.



You could also look in the More plates more plates micro needling stuff :



Sources :



[1] Stoner, E. (1990). The clinical development of a 5α-reductase inhibitor, finasteride. The Journal of steroid biochemistry and molecular biology, 37(3), 375-378.



[2] Vuichoud, C., & Loughlin, K. R. (2015). Benign prostatic hyperplasia: epidemiology, economics and evaluation. Can J Urol, 22(Suppl 1), 1-6.



[3] Adil, A., & Godwin, M. (2017). The effectiveness of treatments for androgenetic alopecia: a systematic review and meta-analysis. Journal of the American Academy of



141.



[4] Schumacher, M., Hussain, R., Gago, N., Oudinet, J. P., Mattern, C., & Ghoumari, A. (2012). Progesterone synthesis in the nervous system: implications for myelination and myelin repair. Frontiers in neuroscience, 6, 10.



[5] Skeldon, S. C., Macdonald, E. M., Law, M. R., Huang, A., Paterson, J. M., Mamdani, M. M., & Juurlink, D. (2017). The cardiovascular safety of dutasteride. The Journal of urology, 197(5), 1309-1314.



[6] Lee, H. J., & Chang, C. (2003). Recent advances in androgen receptor action. Cellular and Molecular Life Sciences CMLS, 60(8), 1613-1622.



[7] Bolton, E. C., So, A. Y., Chaivorapol, C., Haqq, C. M., Li, H., & Yamamoto, K. R. (2007). Cell-and gene-specific regulation of primary target genes by the androgen receptor. Genes & development, 21(16), 2005-2017.



[8] Winiarska, A., Mandt, N., Kamp, H., Hossini, A., Seltmann, H., Zouboulis, C. C., & Blume-Peytavi, U. (2006). Effect of 5α-dihydrotestosterone and testosterone on apoptosis in human dermal papilla cells. Skin pharmacology and physiology, 19(6), 311-321.



[9] Chhipa, R. R., Halim, D., Cheng, J., Zhang, H. Y., Mohler, J. L., Ip, C., & Wu, Y. (2013). The direct inhibitory effect of dutasteride or finasteride on androgen receptor activity is cell line specific. The Prostate, 73(14), 1483-1494.



[10] Mella, J. M., Perret, M. C., Manzotti, M., Catalano, H. N., & Guyatt, G. (2010). Efficacy and safety of finasteride therapy for androgenetic alopecia: a systematic review. Archives of dermatology, 146(10), 1141-1150.



[11] Di Loreto, C., La Marra, F., Mazzon, G., Belgrano, E., Trombetta, C., & Cauci, S. (2014). Immunohistochemical evaluation of androgen receptor and nerve structure density in human prepuce from patients with persistent sexual side effects after finasteride use for androgenetic alopecia. PLoS One, 9(6).



[12] Overstreet, J. W., Fuh, V. L., Gould, J., Howards, S. S., Lieber, M. M., Hellstrom, W., ... & LEWIS, R. (1999). Chronic treatment with finasteride daily does not affect spermatogenesis or semen production in young men. The Journal of urology, 162(4), 1295-1300.



[13] Samplaski, M. K., Lo, K., Grober, E., & Jarvi, K. (2013). Finasteride use in the male infertility population: effects on semen and hormone parameters. Fertility and sterility, 100(6), 1542-1546.



[14] Amory, J. K., Wang, C., Swerdloff, R. S., Anawalt, B. D., Matsumoto, A. M., Bremner, W. J., ... & Clark, R. V. (2007). The effect of 5α-reductase inhibition with dutasteride and finasteride on semen parameters and serum hormones in healthy men. The Journal of Clinical Endocrinology & Metabolism, 92(5), 1659-1665.



[15] Traish, A. M. (2020). Health Risks Associated with Long-Term Finasteride and Dutasteride Use: It's Time to Sound the Alarm. The World Journal of Men's Health, 38.



[16] Traish, A., Haider, K. S., Doros, G., & Haider, A. (2017). Long-term dutasteride therapy in men with benign prostatic hyperplasia alters glucose and lipid profiles and increases severity of erectile dysfunction. Hormone molecular biology and clinical investigation, 30(3).



[17] Doulabi, S. R. S. M., Kavoussi, H., Isapour, D., Hashemian, A., & Taheriniya, A. (2013). Effect of finasteride on lipid profile in individuals with androgenetic alopecia. African Journal of Pharmacy and Pharmacology, 7(6), 315-317.



[18] Duskova, M., Hill, M., & Starka, L. (2010). Changes of metabolic profile in men treated for androgenetic alopecia with 1 mg finasteride. Endocr Regul, 44(1), 3-8.



[19] Gild, P., Cole, A. P., Krasnova, A., Dickerman, B. A., von Landenberg, N., Sun, M., ... & Kibel, A. S. (2018). Liver disease in men undergoing androgen deprivation therapy for prostate cancer. The Journal of urology, 200(3), 573-581.



[20] Mendenhall, C. L. (1968). Anabolic steroid therapy as an adjunct to diet in alcoholic hepatic steatosis. The American journal of digestive diseases, 13(9), 783-791.



[21] Jacqueson, A., Thevenin, M., Warnet, J. M., Claude, J. R., & Truhaut, R. (1978). Comparative Study of the Protective Effect of an Anabolic Steroid. In Toxicological Aspects of Food Safety (pp. 193-196). Springer, Berlin, Heidelberg.



[22] Kelly, D. M., Nettleship, J. E., Akhtar, S., Muraleedharan, V., Sellers, D. J., Brooke, J. C., ... & Jones, T. H. (2014). Testosterone suppresses the expression of regulatory enzymes of fatty acid synthesis and protects against hepatic steatosis in cholesterol-fed androgen deficient mice. Life sciences, 109(2), 95-103.



[23] Lin, H. Y., Yu, I. C., Wang, R. S., Chen, Y. T., Liu, N. C., Altuwaijri, S., ... & Yeh, S. (2008). Increased hepatic steatosis and insulin resistance in mice lacking hepatic androgen receptor. Hepatology, 47(6), 1924-1935.



[24] Völzke, H., Aumann, N., Krebs, A., Nauck, M., Steveling, A., Lerch, M. M., ... & Wallaschofski, H. (2010). Hepatic steatosis is associated with low serum testosterone and high serum DHEAS levels in men. International journal of andrology, 33(1), 45-53.



[25] Velazquez, I., & Alter, B. P. (2004). Androgens and liver tumors: Fanconi's anemia and non‐Fanconi's conditions. American journal of hematology, 77(3), 257-267.



[26] Di Loreto, C., La Marra, F., Mazzon, G., Belgrano, E., Trombetta, C., & Cauci, S. (2014). Immunohistochemical evaluation of androgen receptor and nerve structure density in human prepuce from patients with persistent sexual side effects after finasteride use for androgenetic alopecia. PLoS One, 9(6).



[27] Hsieh, J. T., Chen, S. C., Yu, H. J., & Chang, H. C. (2011). Finasteride upregulates expression of androgen receptor in hyperplastic prostate and LNCaP cells: implications for chemoprevention of prostate cancer. The Prostate, 71(10), 1115-1121.



[28] Pinsky, M. R., Gur, S., Tracey, A. J., Harbin, A., & Hellstrom, W. J. (2011). The effects of chronic 5‐alpha‐reductase inhibitor (dutasteride) treatment on rat erectile function. The journal of sexual medicine, 8(11), 3066-3074.



[29] Iacono, F., Prezioso, D., Ruffo, A., Illiano, E., Romis, L., Di Lauro, G., ... & Amato, B. (2012). Testosterone deficiency causes penile fibrosis and organic erectile dysfunction in aging men. Evaluating association among Age. BMC surgery, 12(S1), S24.



[30] Zhang, M. G., Wang, X. J., Shen, Z. J., & Gao, P. J. (2013). Long-term oral administration of 5α-reductase inhibitor attenuates erectile function by inhibiting autophagy and promoting apoptosis of smooth muscle cells in corpus cavernosum of aged rats. Urology, 82(3), 743-e9.



[31] Melcangi, R. C., Caruso, D., Abbiati, F., Giatti, S., Calabrese, D., Piazza, F., & Cavaletti, G. (2013). Neuroactive steroid levels are modified in cerebrospinal fluid and plasma of post‐finasteride patients showing persistent sexual side effects and anxious/depressive symptomatology. The journal of sexual medicine, 10(10), 2598-2603.



sexual medicine, 10(10), 2598-2603.



[32] Alanazi, N. (2016). Assessing the quality of life and health outcomes of Androgenic Alopecia patients using Propecia (Doctoral dissertation, Rutgers University-School of Health Related Professions).



[33] Melcangi, R. C., Caruso, D., Abbiati, F., Giatti, S., Calabrese, D., Piazza, F., & Cavaletti, G. (2013). Neuroactive steroid levels are modified in cerebrospinal fluid and plasma of post‐finasteride patients showing persistent sexual side effects and anxious/depressive symptomatology. The journal of sexual medicine, 10(10), 2598-2603.



[34] Caruso, D., Abbiati, F., Giatti, S., Romano, S., Fusco, L., Cavaletti, G., & Melcangi, R. C. (2015). Patients treated for male pattern hair with finasteride show, after discontinuation of the drug, altered levels of neuroactive steroids in cerebrospinal fluid and plasma. The Journal of steroid biochemistry and molecular biology, 146, 74-79.



[35] Melcangi, R. C., Santi, D., Spezzano, R., Grimoldi, M., Tabacchi, T., Fusco, M. L., ... & Simoni, M. (2017). Neuroactive steroid levels and psychiatric and andrological features in post-finasteride patients. The Journal of steroid biochemistry and molecular biology, 171, 229-235.



[36] Martinez, P. E., Rubinow, D. R., Nieman, L. K., Koziol, D. E., Morrow, A. L., Schiller, C. E., ... & Schmidt, P. J. (2016). 5α-reductase inhibition prevents the luteal phase increase in plasma allopregnanolone levels and mitigates symptoms in women with premenstrual dysphoric disorder. Neuropsychopharmacology, 41(4), 1093.



[37] Basaria, S., Jasuja, R., Huang, G., Wharton, W., Pan, H., Pencina, K., ... & Labrie, F. (2016). Characteristics of men who report persistent sexual symptoms after finasteride use for hair loss. The Journal of Clinical Endocrinology & Metabolism, 101(12), 4669-4680.



[38] Van Praag, H., Schinder, A. F., Christie, B. R., Toni, N., Palmer, T. D., & Gage, F. H. (2002). Functional neurogenesis in the adult hippocampus. Nature, 415(6875), 1030-1034.



[39] Stockmeier, C. A., Mahajan, G. J., Konick, L. C., Overholser, J. C., Jurjus, G. J., Meltzer, H. Y., ... & Rajkowska, G. (2004). Cellular changes in the postmortem hippocampus in major depression. Biological psychiatry, 56(9), 640-650.



[40] Jacobs, B. L., Van Praag, H., & Gage, F. H. (2000). Adult brain neurogenesis and psychiatry: a novel theory of depression. Molecular psychiatry, 5(3), 262-269.



[41] Römer, B., Pfeiffer, N., Lewicka, S., Ben-Abdallah, N., Vogt, M. A., Deuschle, M., ... & Gass, P. (2010). Finasteride treatment inhibits adult hippocampal neurogenesis in male mice. Pharmacopsychiatry, 43(05), 174-178.



[42] Samuels, B. A., & Hen, R. (2011). Neurogenesis and affective disorders. European Journal of Neuroscience, 33(6), 1152-1159.



[43] Romeo, E., Ströhle, A., Spalletta, G., Michele, F. D., Hermann, B., Holsboer, F., ... & Rupprecht, R. (1998). Effects of antidepressant treatment on neuroactive steroids in major depression. American Journal of Psychiatry, 155(7), 910-913.



[44] Uzunova, V., Sampson, L., & Uzunov, D. P. (2006). Relevance of endogenous 3α-reduced neurosteroids to depression and antidepressant action. Psychopharmacology, 186(3), 351-361.



[45] Uzunova, V., Sheline, Y., Davis, J. M., Rasmusson, A., Uzunov, D. P., Costa, E., & Guidotti, A. (1998). Increase in the cerebrospinal fluid content of neurosteroids in patients with unipolar major depression who are receiving fluoxetine or fluvoxamine. Proceedings of the National Academy of Sciences, 95(6), 3239-3244.



[46] Schüle, C., Nothdurfter, C., & Rupprecht, R. (2014). The role of allopregnanolone in depression and anxiety. Progress in neurobiology, 113, 79-87.



[47] Rasmusson, A. M., Pinna, G., Paliwal, P., Weisman, D., Gottschalk, C., Charney, D., ... & Guidotti, A. (2006). Decreased cerebrospinal fluid allopregnanolone levels in women with posttraumatic stress disorder. Biological psychiatry, 60(7), 704-713.



[48] Hellgren, C., Åkerud, H., Skalkidou, A., Bäckström, T., & Sundström-Poromaa, I. (2014). Low serum allopregnanolone is associated with symptoms of depression in late pregnancy. Neuropsychobiology, 69(3), 147-153.



[49] Schüle, C., Nothdurfter, C., & Rupprecht, R. (2014). The role of allopregnanolone in depression and anxiety. Progress in neurobiology, 113, 79-87.



[50] Murphy, B. P., Abbott, F. V., Allison, C. M., Watts, C., & Ghadirian, A. M. (2004). Elevated levels of some neuroactive progesterone metabolites, particularly isopregnanolone, in women with chronic fatigue syndrome. Psychoneuroendocrinology, 29(2), 245-268.



[51] Uzunova, V., Sheline, Y., Davis, J. M., Rasmusson, A., Uzunov, D. P., Costa, E., & Guidotti, A. (1998). Increase in the cerebrospinal fluid content of neurosteroids in patients with unipolar major depression who are receiving fluoxetine or fluvoxamine. Proceedings of the National Academy of Sciences, 95(6), 3239-3244.



[52] Romeo, E., Ströhle, A., Spalletta, G., Michele, F. D., Hermann, B., Holsboer, F., ... & Rupprecht, R. (1998). Effects of antidepressant treatment on neuroactive steroids in major depression. American Journal of Psychiatry, 155(7), 910-913.



[53] Li, L., Kang, Y. X., Ji, X. M., Li, Y. K., Li, S. C., Zhang, X. J., ... & Shi, G. M. (2018). Finasteride inhibited brain dopaminergic system and open‐field behaviors in adolescent male rats. CNS neuroscience & therapeutics, 24(2), 115-125.



[54] Litim, N., Bourque, M., Al Sweidi, S., Morissette, M., & Di Paolo, T. (2015). The 5α-reductase inhibitor Dutasteride but not Finasteride protects dopamine neurons in the MPTP mouse model of Parkinson's disease. Neuropharmacology, 97, 86-94.



[55] Dazzi, L., Serra, M., Seu, E., Cherchi, G., Pisu, M. G., Purdy, R. H., & Biggio, G. (2002). Progesterone enhances ethanol‐induced modulation of mesocortical dopamine neurons: antagonism by finasteride. Journal of neurochemistry, 83(5), 1103-1109



(Keep in mind i put a big emphazize on finasteride mainly because piec was promoting it)

Tags : @Clavicular
@piec
@MA_ascender
@Sapieeen
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@Rigged
@´´´´´´´´
@Acne Victim
@DR. NICKGA
@cooldude1231

DNR. What is this sperg post?

 

[nuttheb]

Why Finasteride (or dut) is a fraud :



So debunking the claim is finasteride dangerous for you yes or no

their are some people who get the following effects from just microdosing fin :

• sexual dysfunction
• Anhedonia
• Depression
• Anxiety
• Lack of motivation
• Lack of focus

While other seems fine using it

Soooo It depends on your neural phenotypes

Some things like childhood trauma has a lot of gaba menergic signaling adrenaline cortisol levels ect….

And also different architectures of the brain (I might write a thread about it its really interesting how you can just look at someone genes pool and know if he has adhd bi polar ect….. if this thread anhilate the fraud that is piec i sure would write about it)

Now lets starts on why finasteride cause all of this sides :

When you use and 5ar inhibitor your not just inhibiting dht but also progesterone and alopregnolone and if you neealycompletely inhibit the enzyme (which you probably will cause most of the 5ar is type 1 and don’t get me started on dut that shit blocks everything) or nearly you have no progesterone and alopregonolone function in your body so back then i thought well you can just take progestene just to come to the conclusion its gonna do nothing for cause you totaly inhibited thw enzyme.

Suggestion : (keep in mind this is not the best approach I’m gonna get to the nest approach later but its still better than the fraud that is piec feel free to insult his ass in the comments)



Now lets talk about the sides :

Remember about the sides i talked about earlier it was due to allo pregnolone who acts as a innate benzo in your system (so basicaly the main inhibotory gaba system in your brain is the gabaergic system related to the hormone you name it “gaba” it has 2 receptors Gaba B fair enough it can be agonized with just phenibut so no need first allopregnolone its not in the sort of communication in the brain anyway (which mean less signaling)

then We have Gaba A

The only critical receptor and guess what the Gaba A receptor is modulated by allopregnolone which if you remember correctly you blocked earlier sp how do i explain it basicaly its like you took a reverse xanax so the average nigga is gonna have anhedonia exept of he is an outlier so now your fucking dependent on benzos who are super dangerous if you don’t wanna feel like shit

(Then some smart ass in the comment gonna write well then why dont you take alopregnolone well it has very short half life and it can’t be stored or kept so unless you want to be taking ng of allopregnolone every 5 minutes you should either feel like shit like that evil piec want you to be or be addicted to benzos for progesterone you can just take transdermal or micronuzed progesterone just make sure to be on hormones cause your at high risk of hypogonadism if you mess up your dosages)



(Also their are other alternatives so 1) way to get allopregnolone which in theory would work not sure 100% is your gonna take your progesterone and agnozed the tsp receptor you’ll end up with more neuro steroidgenisis so you have more alopregnolone just make sure to not get addicted to that shit might write a thread about how to never get addicted to compounds and how to get rid off any addiction but for that ill need you to support me and all insult piec parents for not putting on a rubber that sad night

Getting back to what i was saying their some research that seem mehh like ettyfoxine but that shit is too risky in my opinion

2) alternative is basicaly fuck modulating gaba receptors you just take sodium valproate kt basicaly make your brain a sink of gaba kinda like piec asshole after getting fucked by every dermatologist prescribing him fin

And its a hdac inhibitor so it have epigenetic change keep in mind that shit aint salt that a epilepsy drug and they are reliable 100% cause nigga imagine an epileptic go through withdrawal his gonna fucking die like piec pride after i finish writing this thread)

So to summarize a little :

Erectil dysfunction: is caused by low progesterone abdominal low dht

Anhedhonia : is cause by low alopregnolone levels

Anxiety : is caused because the amygdila have gaba receptors which when inhibited cause the amygdala to start tweaking like piec teading this right now well i hope finasteride would give you trauma and make you hyper vigilant to not with me next time keep in mind if it don’t happen to you it could just mean you had a gabaminergic deficit or your life so

you adapted your the exeption not the rule



Lack of focus : mainly because of low dht and progesterone youll need for that to increase your dopamenergic signaling (supposing you have average serotonorgic signaling) but you can use something like wellbutrin ritalin low dose in the morning 2x per week

(Wellbutrin do have bad effects on cholinergic system but supposing your an average dude and get a lot of choline in your diet your probably fine)



Here a Choline stack if anyone is interested i already writed it down wayback in the thread fix your life as a teenager :

1. Acetylcholine

a.1g CDP choline 2x per day

b.20 mg Donepezil upon rising

c.300 mg alpha gpc in the morning

d.500 mg Uridine monophosphate in the morning

e.1000 mg piracetam (5x per week$

f.30 mg Noopept



So your gonna ask me what could you do well you can use a topical dut in the hairline or balding areas (but good luck sourcing that)

(Before you ragebait in the comments i already thought about blocking the androgen receptor with Ru but to much side effects especially knowing the information I’m gonna reveal later)



The biggest lie ever said about hairloss :

is that dht cause hairloss if dht cause its mainly becuase it caus low estrogen who is responsible for the hairloss (just look at the guys who took tamoxifen who get hairloss look at the guys who take masteron who get hairloss which if you didn’t know is less androgenic than test its because of its serm effects look at rad 140 who is literraly 0 androgenic and still result in hairloss don’t forget rad 140 was intended to cute breast cancer so its all about estrogens)



If anything Dht increase hair growth :

https://pmc.ncbi.nlm.nih.gov/articles/PMC6989660/



We have seen the effects of blocking DHT. It SLOWS hair loss and some get a MILD regrowth at best with all the sides and complex protocols you should apply to counter act those side effects



The problem with the hairloss comunity is they often overlook the basics like what about hypogonadol nigga who got hairloss they don’t have high dht yet they are bald

So lets get to it the main reasons of hairloss :

• Low estrogen as said earlier
• Bad lifestyle habits
• Poor nutrition
• Lack of exercise

Then we have the most important ones :

• Insulin resistance
• Stress
• The main contributing factor of hairloss and the most overloked one is hypoxia you can try it yourself put on a hat on your hair for 12 hours your gonna feel your haur thinning if you think im coping

So my Definitive hairloss stack that I’ll reccomend :



Topical supplements:
-Ketoconazole cream. 1 to 2 times a day, every day. If price or convenience is an issue, the minimum this should be applied is before bed to balding areas. Ketoconazole has been shown to be just as effective as minoxidil in studies with the shampoo. And even stronger the cream has been shown to produce results with an overnight application.

-Emu oil. 1-2 times a day. One of the only proven items I’ve come across that increases skin and hair DNA synthesis, with studies showing hair regrowth.

-Peppermint oil. 1-2 times a day. Peppermint oil has been shown in studies to be equivalent to minoxidil, without the negative side effects that result in premature aging of the skin.

-Evening Primrose oil or Borage oil. Both shown to cause hair regrowth in studies. Just adding a little more fat topically which is absorbed via the skin. Also useful for GLA’s effect on prostaglandins for halting inflammation, hair loss, and aiding hair regrowth.

-Spironolactone cream. Spironolactone has been shown to restore a 60 year old males hairline to his teenage years hair line that he had lost decades ago. Although we use this item topically, it still has the same benefits locally as it is used for such issues as hair loss and hirsutism topically. However topically it does not go systematic as in studies it has been applied to patients whole backs without going systematic. Spironolactone blocks the binding of androgens to the androgen receptor and helps increase estrogen locally.



-BiEstro cream. E2 and E3 combo, Estradiol and Estriol. Apply once or twice a day to balding areas.

The amount used here is enough to cover balding thinning areas. Due to the area we are applying it studies have shown no real systematic absorption. And also to the fact of the dose we are using is quite low as well. None of the users nor myself could produce an estrogenic side on this when applied to the scalp. Some of us who would normally get estrogenic sides off testosterone use as low as 200 mg.

(You can add bold for E1 if you wanna maximize but kinda pain in the ass cause you have to do bloods and make sure your E1 doesn’t lower your E2 and E3 basicaly you should keep them in harmony)



We have also seen what adding estrogen does for hair, as the byproduct of the thousands of male to female sex changes. These individuals can regrow full heads of amazing hair, bringing back hair reminiscent of that which they had when they were teenagers.

Likely, the ones seeing any bit of regrowth from DHT blockers are as a result of the mild estrogen increase triggered by these compounds. Studies of topical estrogen, plain and simple, work. In both men and women. As a bonus, adding estrogen topically doesn’t just increase estrogen -it also the localized concentration of the aromatase enzyme.

(I’ve saw myself dozens of people on reedit i swear i dont know why i couldnt find them having resuts if anyone has it please write it down below)

(For the studies i linked so many in the ashwaganda and no body gave a fuck

So because of that here are some studies on mice :

https://pubmed.ncbi.nlm.nih.gov/14962083/

https://www.researchgate.net/figure...e-tenth-day-after-hair-shaving_fig1_229083213





View attachment 3261225

Here is someone who got hair growth using estriol and estradiol cream



=End justification for BiEstro Cream==

Rub this mixture on once or twice a day depending on your available time. Once a day is totally fine, and optimal for most, if you can apply it before bed. If not, and you must do it in the day, pick a time where you can leave it on for at least 1-2 hours before showering it out.



Supplements:

Minerals might be needed if severely deficient, some doses are based off studies and you may not need these doses. You must find your own dose.

-Zinc Picolinate. 100-150mg a day for 6-8 weeks, tops.

This depends on a few factors. Add up your dietary zinc content that you typically average, and then decide if zinc might be low and determine the dose that you want. This has been noted in studies to completely reverse hair loss and hypothyroid conditions that are due to a zinc deficiency. NOTE: You may not need this, use discretion. Too much zinc can lead to other problems.

-Taurine. 2.5 grams, 2x a day.

In regards to hair loss, Taurine has been shown to help combat fibrosis of the scalp, thus

increasing circulation and hair growth.



Black Currant Oil, 3g a day.

This is utilized for its Gamma Linoleic Acid (GLA) content, which has anti-inflammatory properties, the ability to increase hair growth prostaglandins (PGE), and the ability to inhibit hair loss prostaglandins (PGD). These prostaglandins are another contributing factor to hair loss/growth aside from the androgens.

Three items have been shown to decrease GLA – wheat, dairy, and trans fats – through inhibition of an enzyme called D6D. The typical western diet is full of these foods. Inhibition of the D6D enzyme prevents the conversion of Linoleic Acid (LA) into GLA. The inhibition of D6D also happens with age, and is likely one of the key contributors to balding getting worse with age. This is just about the only process that can link balding to aging that has not already been explored.

In taking a GLA supplement, we bypass the enzymatic conversion entirely and have the end product.

Black Currant oil was also shown in animal studies to prevent many of the negatives of excessive fructose intake, such as fatty liver.



Grapeseed Extract, 500-1000mg a day.
GSE has been shown in animal studies to improve insulin resistance as much as metformin. Studies have also shown GSE to double the number of hairs in the anagen (growth) phase. As far as I am aware, no other compound has been shown to have effects this potent.

(Note : i do not advise to take metformin or berberine for other reasons i would write a thread about it in the near future)



Chromium gtf is used for combating insulin resistance, which is seen as a contributing factor for hair loss as mentioned above when talking about GSE. Again, some may not need this. Chromium GTF has been shown in case studies with type 2 diabetics to remove all exogenous insulin dependency within a couple months of use i recommend using 1000mcg a day for about 6 weeks



And you want to be eating or supplementing with those :

Magnesium

B vitamins

Vitamin K2

You also wanna be getting fats in your diet (especially from Mufas and Pufas (just make sure your not getting it from seed oils because its processed that a whole other topic id advise to get from seeds)



but I assure you, PUFA fats are NOT bad for you. Getting them from healthy sources has countless proven health benefits: anti-carcinogenic, anti-inflammatory, pro-sleep, pro-thyroid, etc. The benefits of unheated PUFA fats are a very deep topic on their own.

The epidermis of your skin is made of 60 percent Omega-6 PUFA fats. Do not fall for the “Omega-3 must be higher than Omega-6” speech that has no proven benefits and multiple proven detriments. All of the studies linking PUFA fats to health issues look at the typical use for PUFA fats in the western diet: cooking, frying, and otherwise heating the fats. If we are to take the same controlled environment but introduce raw, unheated PUFA fats from seeds and nuts, the studies flip completely. Anti-cancer, anti-inflammatory, and all-around health marker improvement is marked.



Another issue found often in the bodybuilding and fitness realm is the “eating too clean” phenomenon. If you were to add up chicken, rice, broccoli, and some olive oil on your favorite diet app, I can guarantee that you’d see that it’s a struggle to reach even 15 percent of RDA requirements for PUFA fats. When this happens, the skin goes dry and wrinkles appear, hair becomes straw like and falls out, etc. Digestive issues ensue, and metabolism slows down. As PUFA fats are shown to increase thyroid hormone sensitivity by almost 20 percent, dieting becomes harder and fat accrual in a calorie surplus becomes far easier. This isn’t even rectifiable with exogenous thyroid hormones – take all the thyroid drugs you want, if your sensitivity isn’t up to par your metabolism will suffer.

(Fun fact : Studies have also shown that when consumed in equal quantities, monounsaturated and saturated fats cause fat gain. Saturated fat was shown to cause a decrease in insulin sensitivity as well. PUFA fat, on the other hand, caused barely any fat gain. The majority of weight gained was muscle, insulin sensitivity increased, and abdominal fat thickness decreased.)



Other Foods.

Pineapple is used as a general health food with documented anti-inflammatory benefits, contains an enzyme papaya if i can recall that aids in the digestion of protein, is a fantastic source of vitamins, and is a preferred fruit due to the lower-end fructose content. In regards to hair regrowth, the main benefit is its anti-inflammatory property.



Massage/Mechanical Manipulation:

Vigorously massage, brush, or pinch your scalp in the balding areas. 1-2 times a day, for whatever time frame you can manage; the longer the better. 3-5 minutes is great, 10 minutes is better. Use as much pressure as possible. Tissue manipulation like this increases circulation and has been proven in studies to aid hair growth. To assist in blood flow further, you can bend over and point your head toward the ground, allowing gravity to assist in delivering blood to the target area.



You could also look in the More plates more plates micro needling stuff :



Sources :



[1] Stoner, E. (1990). The clinical development of a 5α-reductase inhibitor, finasteride. The Journal of steroid biochemistry and molecular biology, 37(3), 375-378.



[2] Vuichoud, C., & Loughlin, K. R. (2015). Benign prostatic hyperplasia: epidemiology, economics and evaluation. Can J Urol, 22(Suppl 1), 1-6.



[3] Adil, A., & Godwin, M. (2017). The effectiveness of treatments for androgenetic alopecia: a systematic review and meta-analysis. Journal of the American Academy of



141.



[4] Schumacher, M., Hussain, R., Gago, N., Oudinet, J. P., Mattern, C., & Ghoumari, A. (2012). Progesterone synthesis in the nervous system: implications for myelination and myelin repair. Frontiers in neuroscience, 6, 10.



[5] Skeldon, S. C., Macdonald, E. M., Law, M. R., Huang, A., Paterson, J. M., Mamdani, M. M., & Juurlink, D. (2017). The cardiovascular safety of dutasteride. The Journal of urology, 197(5), 1309-1314.



[6] Lee, H. J., & Chang, C. (2003). Recent advances in androgen receptor action. Cellular and Molecular Life Sciences CMLS, 60(8), 1613-1622.



[7] Bolton, E. C., So, A. Y., Chaivorapol, C., Haqq, C. M., Li, H., & Yamamoto, K. R. (2007). Cell-and gene-specific regulation of primary target genes by the androgen receptor. Genes & development, 21(16), 2005-2017.



[8] Winiarska, A., Mandt, N., Kamp, H., Hossini, A., Seltmann, H., Zouboulis, C. C., & Blume-Peytavi, U. (2006). Effect of 5α-dihydrotestosterone and testosterone on apoptosis in human dermal papilla cells. Skin pharmacology and physiology, 19(6), 311-321.



[9] Chhipa, R. R., Halim, D., Cheng, J., Zhang, H. Y., Mohler, J. L., Ip, C., & Wu, Y. (2013). The direct inhibitory effect of dutasteride or finasteride on androgen receptor activity is cell line specific. The Prostate, 73(14), 1483-1494.



[10] Mella, J. M., Perret, M. C., Manzotti, M., Catalano, H. N., & Guyatt, G. (2010). Efficacy and safety of finasteride therapy for androgenetic alopecia: a systematic review. Archives of dermatology, 146(10), 1141-1150.



[11] Di Loreto, C., La Marra, F., Mazzon, G., Belgrano, E., Trombetta, C., & Cauci, S. (2014). Immunohistochemical evaluation of androgen receptor and nerve structure density in human prepuce from patients with persistent sexual side effects after finasteride use for androgenetic alopecia. PLoS One, 9(6).



[12] Overstreet, J. W., Fuh, V. L., Gould, J., Howards, S. S., Lieber, M. M., Hellstrom, W., ... & LEWIS, R. (1999). Chronic treatment with finasteride daily does not affect spermatogenesis or semen production in young men. The Journal of urology, 162(4), 1295-1300.



[13] Samplaski, M. K., Lo, K., Grober, E., & Jarvi, K. (2013). Finasteride use in the male infertility population: effects on semen and hormone parameters. Fertility and sterility, 100(6), 1542-1546.



[14] Amory, J. K., Wang, C., Swerdloff, R. S., Anawalt, B. D., Matsumoto, A. M., Bremner, W. J., ... & Clark, R. V. (2007). The effect of 5α-reductase inhibition with dutasteride and finasteride on semen parameters and serum hormones in healthy men. The Journal of Clinical Endocrinology & Metabolism, 92(5), 1659-1665.



[15] Traish, A. M. (2020). Health Risks Associated with Long-Term Finasteride and Dutasteride Use: It's Time to Sound the Alarm. The World Journal of Men's Health, 38.



[16] Traish, A., Haider, K. S., Doros, G., & Haider, A. (2017). Long-term dutasteride therapy in men with benign prostatic hyperplasia alters glucose and lipid profiles and increases severity of erectile dysfunction. Hormone molecular biology and clinical investigation, 30(3).



[17] Doulabi, S. R. S. M., Kavoussi, H., Isapour, D., Hashemian, A., & Taheriniya, A. (2013). Effect of finasteride on lipid profile in individuals with androgenetic alopecia. African Journal of Pharmacy and Pharmacology, 7(6), 315-317.



[18] Duskova, M., Hill, M., & Starka, L. (2010). Changes of metabolic profile in men treated for androgenetic alopecia with 1 mg finasteride. Endocr Regul, 44(1), 3-8.



[19] Gild, P., Cole, A. P., Krasnova, A., Dickerman, B. A., von Landenberg, N., Sun, M., ... & Kibel, A. S. (2018). Liver disease in men undergoing androgen deprivation therapy for prostate cancer. The Journal of urology, 200(3), 573-581.



[20] Mendenhall, C. L. (1968). Anabolic steroid therapy as an adjunct to diet in alcoholic hepatic steatosis. The American journal of digestive diseases, 13(9), 783-791.



[21] Jacqueson, A., Thevenin, M., Warnet, J. M., Claude, J. R., & Truhaut, R. (1978). Comparative Study of the Protective Effect of an Anabolic Steroid. In Toxicological Aspects of Food Safety (pp. 193-196). Springer, Berlin, Heidelberg.



[22] Kelly, D. M., Nettleship, J. E., Akhtar, S., Muraleedharan, V., Sellers, D. J., Brooke, J. C., ... & Jones, T. H. (2014). Testosterone suppresses the expression of regulatory enzymes of fatty acid synthesis and protects against hepatic steatosis in cholesterol-fed androgen deficient mice. Life sciences, 109(2), 95-103.



[23] Lin, H. Y., Yu, I. C., Wang, R. S., Chen, Y. T., Liu, N. C., Altuwaijri, S., ... & Yeh, S. (2008). Increased hepatic steatosis and insulin resistance in mice lacking hepatic androgen receptor. Hepatology, 47(6), 1924-1935.



[24] Völzke, H., Aumann, N., Krebs, A., Nauck, M., Steveling, A., Lerch, M. M., ... & Wallaschofski, H. (2010). Hepatic steatosis is associated with low serum testosterone and high serum DHEAS levels in men. International journal of andrology, 33(1), 45-53.



[25] Velazquez, I., & Alter, B. P. (2004). Androgens and liver tumors: Fanconi's anemia and non‐Fanconi's conditions. American journal of hematology, 77(3), 257-267.



[26] Di Loreto, C., La Marra, F., Mazzon, G., Belgrano, E., Trombetta, C., & Cauci, S. (2014). Immunohistochemical evaluation of androgen receptor and nerve structure density in human prepuce from patients with persistent sexual side effects after finasteride use for androgenetic alopecia. PLoS One, 9(6).



[27] Hsieh, J. T., Chen, S. C., Yu, H. J., & Chang, H. C. (2011). Finasteride upregulates expression of androgen receptor in hyperplastic prostate and LNCaP cells: implications for chemoprevention of prostate cancer. The Prostate, 71(10), 1115-1121.



[28] Pinsky, M. R., Gur, S., Tracey, A. J., Harbin, A., & Hellstrom, W. J. (2011). The effects of chronic 5‐alpha‐reductase inhibitor (dutasteride) treatment on rat erectile function. The journal of sexual medicine, 8(11), 3066-3074.



[29] Iacono, F., Prezioso, D., Ruffo, A., Illiano, E., Romis, L., Di Lauro, G., ... & Amato, B. (2012). Testosterone deficiency causes penile fibrosis and organic erectile dysfunction in aging men. Evaluating association among Age. BMC surgery, 12(S1), S24.



[30] Zhang, M. G., Wang, X. J., Shen, Z. J., & Gao, P. J. (2013). Long-term oral administration of 5α-reductase inhibitor attenuates erectile function by inhibiting autophagy and promoting apoptosis of smooth muscle cells in corpus cavernosum of aged rats. Urology, 82(3), 743-e9.



[31] Melcangi, R. C., Caruso, D., Abbiati, F., Giatti, S., Calabrese, D., Piazza, F., & Cavaletti, G. (2013). Neuroactive steroid levels are modified in cerebrospinal fluid and plasma of post‐finasteride patients showing persistent sexual side effects and anxious/depressive symptomatology. The journal of sexual medicine, 10(10), 2598-2603.



sexual medicine, 10(10), 2598-2603.



[32] Alanazi, N. (2016). Assessing the quality of life and health outcomes of Androgenic Alopecia patients using Propecia (Doctoral dissertation, Rutgers University-School of Health Related Professions).



[33] Melcangi, R. C., Caruso, D., Abbiati, F., Giatti, S., Calabrese, D., Piazza, F., & Cavaletti, G. (2013). Neuroactive steroid levels are modified in cerebrospinal fluid and plasma of post‐finasteride patients showing persistent sexual side effects and anxious/depressive symptomatology. The journal of sexual medicine, 10(10), 2598-2603.



[34] Caruso, D., Abbiati, F., Giatti, S., Romano, S., Fusco, L., Cavaletti, G., & Melcangi, R. C. (2015). Patients treated for male pattern hair with finasteride show, after discontinuation of the drug, altered levels of neuroactive steroids in cerebrospinal fluid and plasma. The Journal of steroid biochemistry and molecular biology, 146, 74-79.



[35] Melcangi, R. C., Santi, D., Spezzano, R., Grimoldi, M., Tabacchi, T., Fusco, M. L., ... & Simoni, M. (2017). Neuroactive steroid levels and psychiatric and andrological features in post-finasteride patients. The Journal of steroid biochemistry and molecular biology, 171, 229-235.



[36] Martinez, P. E., Rubinow, D. R., Nieman, L. K., Koziol, D. E., Morrow, A. L., Schiller, C. E., ... & Schmidt, P. J. (2016). 5α-reductase inhibition prevents the luteal phase increase in plasma allopregnanolone levels and mitigates symptoms in women with premenstrual dysphoric disorder. Neuropsychopharmacology, 41(4), 1093.



[37] Basaria, S., Jasuja, R., Huang, G., Wharton, W., Pan, H., Pencina, K., ... & Labrie, F. (2016). Characteristics of men who report persistent sexual symptoms after finasteride use for hair loss. The Journal of Clinical Endocrinology & Metabolism, 101(12), 4669-4680.



[38] Van Praag, H., Schinder, A. F., Christie, B. R., Toni, N., Palmer, T. D., & Gage, F. H. (2002). Functional neurogenesis in the adult hippocampus. Nature, 415(6875), 1030-1034.



[39] Stockmeier, C. A., Mahajan, G. J., Konick, L. C., Overholser, J. C., Jurjus, G. J., Meltzer, H. Y., ... & Rajkowska, G. (2004). Cellular changes in the postmortem hippocampus in major depression. Biological psychiatry, 56(9), 640-650.



[40] Jacobs, B. L., Van Praag, H., & Gage, F. H. (2000). Adult brain neurogenesis and psychiatry: a novel theory of depression. Molecular psychiatry, 5(3), 262-269.



[41] Römer, B., Pfeiffer, N., Lewicka, S., Ben-Abdallah, N., Vogt, M. A., Deuschle, M., ... & Gass, P. (2010). Finasteride treatment inhibits adult hippocampal neurogenesis in male mice. Pharmacopsychiatry, 43(05), 174-178.



[42] Samuels, B. A., & Hen, R. (2011). Neurogenesis and affective disorders. European Journal of Neuroscience, 33(6), 1152-1159.



[43] Romeo, E., Ströhle, A., Spalletta, G., Michele, F. D., Hermann, B., Holsboer, F., ... & Rupprecht, R. (1998). Effects of antidepressant treatment on neuroactive steroids in major depression. American Journal of Psychiatry, 155(7), 910-913.



[44] Uzunova, V., Sampson, L., & Uzunov, D. P. (2006). Relevance of endogenous 3α-reduced neurosteroids to depression and antidepressant action. Psychopharmacology, 186(3), 351-361.



[45] Uzunova, V., Sheline, Y., Davis, J. M., Rasmusson, A., Uzunov, D. P., Costa, E., & Guidotti, A. (1998). Increase in the cerebrospinal fluid content of neurosteroids in patients with unipolar major depression who are receiving fluoxetine or fluvoxamine. Proceedings of the National Academy of Sciences, 95(6), 3239-3244.



[46] Schüle, C., Nothdurfter, C., & Rupprecht, R. (2014). The role of allopregnanolone in depression and anxiety. Progress in neurobiology, 113, 79-87.



[47] Rasmusson, A. M., Pinna, G., Paliwal, P., Weisman, D., Gottschalk, C., Charney, D., ... & Guidotti, A. (2006). Decreased cerebrospinal fluid allopregnanolone levels in women with posttraumatic stress disorder. Biological psychiatry, 60(7), 704-713.



[48] Hellgren, C., Åkerud, H., Skalkidou, A., Bäckström, T., & Sundström-Poromaa, I. (2014). Low serum allopregnanolone is associated with symptoms of depression in late pregnancy. Neuropsychobiology, 69(3), 147-153.



[49] Schüle, C., Nothdurfter, C., & Rupprecht, R. (2014). The role of allopregnanolone in depression and anxiety. Progress in neurobiology, 113, 79-87.



[50] Murphy, B. P., Abbott, F. V., Allison, C. M., Watts, C., & Ghadirian, A. M. (2004). Elevated levels of some neuroactive progesterone metabolites, particularly isopregnanolone, in women with chronic fatigue syndrome. Psychoneuroendocrinology, 29(2), 245-268.



[51] Uzunova, V., Sheline, Y., Davis, J. M., Rasmusson, A., Uzunov, D. P., Costa, E., & Guidotti, A. (1998). Increase in the cerebrospinal fluid content of neurosteroids in patients with unipolar major depression who are receiving fluoxetine or fluvoxamine. Proceedings of the National Academy of Sciences, 95(6), 3239-3244.



[52] Romeo, E., Ströhle, A., Spalletta, G., Michele, F. D., Hermann, B., Holsboer, F., ... & Rupprecht, R. (1998). Effects of antidepressant treatment on neuroactive steroids in major depression. American Journal of Psychiatry, 155(7), 910-913.



[53] Li, L., Kang, Y. X., Ji, X. M., Li, Y. K., Li, S. C., Zhang, X. J., ... & Shi, G. M. (2018). Finasteride inhibited brain dopaminergic system and open‐field behaviors in adolescent male rats. CNS neuroscience & therapeutics, 24(2), 115-125.



[54] Litim, N., Bourque, M., Al Sweidi, S., Morissette, M., & Di Paolo, T. (2015). The 5α-reductase inhibitor Dutasteride but not Finasteride protects dopamine neurons in the MPTP mouse model of Parkinson's disease. Neuropharmacology, 97, 86-94.



[55] Dazzi, L., Serra, M., Seu, E., Cherchi, G., Pisu, M. G., Purdy, R. H., & Biggio, G. (2002). Progesterone enhances ethanol‐induced modulation of mesocortical dopamine neurons: antagonism by finasteride. Journal of neurochemistry, 83(5), 1103-1109



(Keep in mind i put a big emphazize on finasteride mainly because piec was promoting it)

Tags : @Clavicular
@piec
@MA_ascender
@Sapieeen
@NZb6Air
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@´´´´´´´´
@Acne Victim
@DR. NICKGA
@cooldude1231

you have the highest iq on this forum

 

[anonym20000]

So what's the cure to post finasteride syndrome from your research bud

it's cope

 

[jefty]

Why Finasteride (or dut) is a fraud :



So debunking the claim is finasteride dangerous for you yes or no

their are some people who get the following effects from just microdosing fin :

• sexual dysfunction
• Anhedonia
• Depression
• Anxiety
• Lack of motivation
• Lack of focus

While other seems fine using it

Soooo It depends on your neural phenotypes

Some things like childhood trauma has a lot of gaba menergic signaling adrenaline cortisol levels ect….

And also different architectures of the brain (I might write a thread about it its really interesting how you can just look at someone genes pool and know if he has adhd bi polar ect….. if this thread anhilate the fraud that is piec i sure would write about it)

Now lets starts on why finasteride cause all of this sides :

When you use and 5ar inhibitor your not just inhibiting dht but also progesterone and alopregnolone and if you neealycompletely inhibit the enzyme (which you probably will cause most of the 5ar is type 1 and don’t get me started on dut that shit blocks everything) or nearly you have no progesterone and alopregonolone function in your body so back then i thought well you can just take progestene just to come to the conclusion its gonna do nothing for cause you totaly inhibited thw enzyme.

Suggestion : (keep in mind this is not the best approach I’m gonna get to the nest approach later but its still better than the fraud that is piec feel free to insult his ass in the comments)



Now lets talk about the sides :

Remember about the sides i talked about earlier it was due to allo pregnolone who acts as a innate benzo in your system (so basicaly the main inhibotory gaba system in your brain is the gabaergic system related to the hormone you name it “gaba” it has 2 receptors Gaba B fair enough it can be agonized with just phenibut so no need first allopregnolone its not in the sort of communication in the brain anyway (which mean less signaling)

then We have Gaba A

The only critical receptor and guess what the Gaba A receptor is modulated by allopregnolone which if you remember correctly you blocked earlier sp how do i explain it basicaly its like you took a reverse xanax so the average nigga is gonna have anhedonia exept of he is an outlier so now your fucking dependent on benzos who are super dangerous if you don’t wanna feel like shit

(Then some smart ass in the comment gonna write well then why dont you take alopregnolone well it has very short half life and it can’t be stored or kept so unless you want to be taking ng of allopregnolone every 5 minutes you should either feel like shit like that evil piec want you to be or be addicted to benzos for progesterone you can just take transdermal or micronuzed progesterone just make sure to be on hormones cause your at high risk of hypogonadism if you mess up your dosages)



(Also their are other alternatives so 1) way to get allopregnolone which in theory would work not sure 100% is your gonna take your progesterone and agnozed the tsp receptor you’ll end up with more neuro steroidgenisis so you have more alopregnolone just make sure to not get addicted to that shit might write a thread about how to never get addicted to compounds and how to get rid off any addiction but for that ill need you to support me and all insult piec parents for not putting on a rubber that sad night

Getting back to what i was saying their some research that seem mehh like ettyfoxine but that shit is too risky in my opinion

2) alternative is basicaly fuck modulating gaba receptors you just take sodium valproate kt basicaly make your brain a sink of gaba kinda like piec asshole after getting fucked by every dermatologist prescribing him fin

And its a hdac inhibitor so it have epigenetic change keep in mind that shit aint salt that a epilepsy drug and they are reliable 100% cause nigga imagine an epileptic go through withdrawal his gonna fucking die like piec pride after i finish writing this thread)

So to summarize a little :

Erectil dysfunction: is caused by low progesterone abdominal low dht

Anhedhonia : is cause by low alopregnolone levels

Anxiety : is caused because the amygdila have gaba receptors which when inhibited cause the amygdala to start tweaking like piec teading this right now well i hope finasteride would give you trauma and make you hyper vigilant to not with me next time keep in mind if it don’t happen to you it could just mean you had a gabaminergic deficit or your life so

you adapted your the exeption not the rule



Lack of focus : mainly because of low dht and progesterone youll need for that to increase your dopamenergic signaling (supposing you have average serotonorgic signaling) but you can use something like wellbutrin ritalin low dose in the morning 2x per week

(Wellbutrin do have bad effects on cholinergic system but supposing your an average dude and get a lot of choline in your diet your probably fine)



Here a Choline stack if anyone is interested i already writed it down wayback in the thread fix your life as a teenager :

1. Acetylcholine

a.1g CDP choline 2x per day

b.20 mg Donepezil upon rising

c.300 mg alpha gpc in the morning

d.500 mg Uridine monophosphate in the morning

e.1000 mg piracetam (5x per week$

f.30 mg Noopept



So your gonna ask me what could you do well you can use a topical dut in the hairline or balding areas (but good luck sourcing that)

(Before you ragebait in the comments i already thought about blocking the androgen receptor with Ru but to much side effects especially knowing the information I’m gonna reveal later)



The biggest lie ever said about hairloss :

is that dht cause hairloss if dht cause its mainly becuase it caus low estrogen who is responsible for the hairloss (just look at the guys who took tamoxifen who get hairloss look at the guys who take masteron who get hairloss which if you didn’t know is less androgenic than test its because of its serm effects look at rad 140 who is literraly 0 androgenic and still result in hairloss don’t forget rad 140 was intended to cute breast cancer so its all about estrogens)



If anything Dht increase hair growth :

https://pmc.ncbi.nlm.nih.gov/articles/PMC6989660/



We have seen the effects of blocking DHT. It SLOWS hair loss and some get a MILD regrowth at best with all the sides and complex protocols you should apply to counter act those side effects



The problem with the hairloss comunity is they often overlook the basics like what about hypogonadol nigga who got hairloss they don’t have high dht yet they are bald

So lets get to it the main reasons of hairloss :

• Low estrogen as said earlier
• Bad lifestyle habits
• Poor nutrition
• Lack of exercise

Then we have the most important ones :

• Insulin resistance
• Stress
• The main contributing factor of hairloss and the most overloked one is hypoxia you can try it yourself put on a hat on your hair for 12 hours your gonna feel your haur thinning if you think im coping

So my Definitive hairloss stack that I’ll reccomend :



Topical supplements:
-Ketoconazole cream. 1 to 2 times a day, every day. If price or convenience is an issue, the minimum this should be applied is before bed to balding areas. Ketoconazole has been shown to be just as effective as minoxidil in studies with the shampoo. And even stronger the cream has been shown to produce results with an overnight application.

-Emu oil. 1-2 times a day. One of the only proven items I’ve come across that increases skin and hair DNA synthesis, with studies showing hair regrowth.

-Peppermint oil. 1-2 times a day. Peppermint oil has been shown in studies to be equivalent to minoxidil, without the negative side effects that result in premature aging of the skin.

-Evening Primrose oil or Borage oil. Both shown to cause hair regrowth in studies. Just adding a little more fat topically which is absorbed via the skin. Also useful for GLA’s effect on prostaglandins for halting inflammation, hair loss, and aiding hair regrowth.

-Spironolactone cream. Spironolactone has been shown to restore a 60 year old males hairline to his teenage years hair line that he had lost decades ago. Although we use this item topically, it still has the same benefits locally as it is used for such issues as hair loss and hirsutism topically. However topically it does not go systematic as in studies it has been applied to patients whole backs without going systematic. Spironolactone blocks the binding of androgens to the androgen receptor and helps increase estrogen locally.



-BiEstro cream. E2 and E3 combo, Estradiol and Estriol. Apply once or twice a day to balding areas.

The amount used here is enough to cover balding thinning areas. Due to the area we are applying it studies have shown no real systematic absorption. And also to the fact of the dose we are using is quite low as well. None of the users nor myself could produce an estrogenic side on this when applied to the scalp. Some of us who would normally get estrogenic sides off testosterone use as low as 200 mg.

(You can add bold for E1 if you wanna maximize but kinda pain in the ass cause you have to do bloods and make sure your E1 doesn’t lower your E2 and E3 basicaly you should keep them in harmony)



We have also seen what adding estrogen does for hair, as the byproduct of the thousands of male to female sex changes. These individuals can regrow full heads of amazing hair, bringing back hair reminiscent of that which they had when they were teenagers.

Likely, the ones seeing any bit of regrowth from DHT blockers are as a result of the mild estrogen increase triggered by these compounds. Studies of topical estrogen, plain and simple, work. In both men and women. As a bonus, adding estrogen topically doesn’t just increase estrogen -it also the localized concentration of the aromatase enzyme.

(I’ve saw myself dozens of people on reedit i swear i dont know why i couldnt find them having resuts if anyone has it please write it down below)

(For the studies i linked so many in the ashwaganda and no body gave a fuck

So because of that here are some studies on mice :

https://pubmed.ncbi.nlm.nih.gov/14962083/

https://www.researchgate.net/figure...e-tenth-day-after-hair-shaving_fig1_229083213





View attachment 3261225

Here is someone who got hair growth using estriol and estradiol cream



=End justification for BiEstro Cream==

Rub this mixture on once or twice a day depending on your available time. Once a day is totally fine, and optimal for most, if you can apply it before bed. If not, and you must do it in the day, pick a time where you can leave it on for at least 1-2 hours before showering it out.



Supplements:

Minerals might be needed if severely deficient, some doses are based off studies and you may not need these doses. You must find your own dose.

-Zinc Picolinate. 100-150mg a day for 6-8 weeks, tops.

This depends on a few factors. Add up your dietary zinc content that you typically average, and then decide if zinc might be low and determine the dose that you want. This has been noted in studies to completely reverse hair loss and hypothyroid conditions that are due to a zinc deficiency. NOTE: You may not need this, use discretion. Too much zinc can lead to other problems.

-Taurine. 2.5 grams, 2x a day.

In regards to hair loss, Taurine has been shown to help combat fibrosis of the scalp, thus

increasing circulation and hair growth.



Black Currant Oil, 3g a day.

This is utilized for its Gamma Linoleic Acid (GLA) content, which has anti-inflammatory properties, the ability to increase hair growth prostaglandins (PGE), and the ability to inhibit hair loss prostaglandins (PGD). These prostaglandins are another contributing factor to hair loss/growth aside from the androgens.

Three items have been shown to decrease GLA – wheat, dairy, and trans fats – through inhibition of an enzyme called D6D. The typical western diet is full of these foods. Inhibition of the D6D enzyme prevents the conversion of Linoleic Acid (LA) into GLA. The inhibition of D6D also happens with age, and is likely one of the key contributors to balding getting worse with age. This is just about the only process that can link balding to aging that has not already been explored.

In taking a GLA supplement, we bypass the enzymatic conversion entirely and have the end product.

Black Currant oil was also shown in animal studies to prevent many of the negatives of excessive fructose intake, such as fatty liver.



Grapeseed Extract, 500-1000mg a day.
GSE has been shown in animal studies to improve insulin resistance as much as metformin. Studies have also shown GSE to double the number of hairs in the anagen (growth) phase. As far as I am aware, no other compound has been shown to have effects this potent.

(Note : i do not advise to take metformin or berberine for other reasons i would write a thread about it in the near future)



Chromium gtf is used for combating insulin resistance, which is seen as a contributing factor for hair loss as mentioned above when talking about GSE. Again, some may not need this. Chromium GTF has been shown in case studies with type 2 diabetics to remove all exogenous insulin dependency within a couple months of use i recommend using 1000mcg a day for about 6 weeks



And you want to be eating or supplementing with those :

Magnesium

B vitamins

Vitamin K2

You also wanna be getting fats in your diet (especially from Mufas and Pufas (just make sure your not getting it from seed oils because its processed that a whole other topic id advise to get from seeds)



but I assure you, PUFA fats are NOT bad for you. Getting them from healthy sources has countless proven health benefits: anti-carcinogenic, anti-inflammatory, pro-sleep, pro-thyroid, etc. The benefits of unheated PUFA fats are a very deep topic on their own.

The epidermis of your skin is made of 60 percent Omega-6 PUFA fats. Do not fall for the “Omega-3 must be higher than Omega-6” speech that has no proven benefits and multiple proven detriments. All of the studies linking PUFA fats to health issues look at the typical use for PUFA fats in the western diet: cooking, frying, and otherwise heating the fats. If we are to take the same controlled environment but introduce raw, unheated PUFA fats from seeds and nuts, the studies flip completely. Anti-cancer, anti-inflammatory, and all-around health marker improvement is marked.



Another issue found often in the bodybuilding and fitness realm is the “eating too clean” phenomenon. If you were to add up chicken, rice, broccoli, and some olive oil on your favorite diet app, I can guarantee that you’d see that it’s a struggle to reach even 15 percent of RDA requirements for PUFA fats. When this happens, the skin goes dry and wrinkles appear, hair becomes straw like and falls out, etc. Digestive issues ensue, and metabolism slows down. As PUFA fats are shown to increase thyroid hormone sensitivity by almost 20 percent, dieting becomes harder and fat accrual in a calorie surplus becomes far easier. This isn’t even rectifiable with exogenous thyroid hormones – take all the thyroid drugs you want, if your sensitivity isn’t up to par your metabolism will suffer.

(Fun fact : Studies have also shown that when consumed in equal quantities, monounsaturated and saturated fats cause fat gain. Saturated fat was shown to cause a decrease in insulin sensitivity as well. PUFA fat, on the other hand, caused barely any fat gain. The majority of weight gained was muscle, insulin sensitivity increased, and abdominal fat thickness decreased.)



Other Foods.

Pineapple is used as a general health food with documented anti-inflammatory benefits, contains an enzyme papaya if i can recall that aids in the digestion of protein, is a fantastic source of vitamins, and is a preferred fruit due to the lower-end fructose content. In regards to hair regrowth, the main benefit is its anti-inflammatory property.



Massage/Mechanical Manipulation:

Vigorously massage, brush, or pinch your scalp in the balding areas. 1-2 times a day, for whatever time frame you can manage; the longer the better. 3-5 minutes is great, 10 minutes is better. Use as much pressure as possible. Tissue manipulation like this increases circulation and has been proven in studies to aid hair growth. To assist in blood flow further, you can bend over and point your head toward the ground, allowing gravity to assist in delivering blood to the target area.



You could also look in the More plates more plates micro needling stuff :



Sources :



[1] Stoner, E. (1990). The clinical development of a 5α-reductase inhibitor, finasteride. The Journal of steroid biochemistry and molecular biology, 37(3), 375-378.



[2] Vuichoud, C., & Loughlin, K. R. (2015). Benign prostatic hyperplasia: epidemiology, economics and evaluation. Can J Urol, 22(Suppl 1), 1-6.



[3] Adil, A., & Godwin, M. (2017). The effectiveness of treatments for androgenetic alopecia: a systematic review and meta-analysis. Journal of the American Academy of



141.



[4] Schumacher, M., Hussain, R., Gago, N., Oudinet, J. P., Mattern, C., & Ghoumari, A. (2012). Progesterone synthesis in the nervous system: implications for myelination and myelin repair. Frontiers in neuroscience, 6, 10.



[5] Skeldon, S. C., Macdonald, E. M., Law, M. R., Huang, A., Paterson, J. M., Mamdani, M. M., & Juurlink, D. (2017). The cardiovascular safety of dutasteride. The Journal of urology, 197(5), 1309-1314.



[6] Lee, H. J., & Chang, C. (2003). Recent advances in androgen receptor action. Cellular and Molecular Life Sciences CMLS, 60(8), 1613-1622.



[7] Bolton, E. C., So, A. Y., Chaivorapol, C., Haqq, C. M., Li, H., & Yamamoto, K. R. (2007). Cell-and gene-specific regulation of primary target genes by the androgen receptor. Genes & development, 21(16), 2005-2017.



[8] Winiarska, A., Mandt, N., Kamp, H., Hossini, A., Seltmann, H., Zouboulis, C. C., & Blume-Peytavi, U. (2006). Effect of 5α-dihydrotestosterone and testosterone on apoptosis in human dermal papilla cells. Skin pharmacology and physiology, 19(6), 311-321.



[9] Chhipa, R. R., Halim, D., Cheng, J., Zhang, H. Y., Mohler, J. L., Ip, C., & Wu, Y. (2013). The direct inhibitory effect of dutasteride or finasteride on androgen receptor activity is cell line specific. The Prostate, 73(14), 1483-1494.



[10] Mella, J. M., Perret, M. C., Manzotti, M., Catalano, H. N., & Guyatt, G. (2010). Efficacy and safety of finasteride therapy for androgenetic alopecia: a systematic review. Archives of dermatology, 146(10), 1141-1150.



[11] Di Loreto, C., La Marra, F., Mazzon, G., Belgrano, E., Trombetta, C., & Cauci, S. (2014). Immunohistochemical evaluation of androgen receptor and nerve structure density in human prepuce from patients with persistent sexual side effects after finasteride use for androgenetic alopecia. PLoS One, 9(6).



[12] Overstreet, J. W., Fuh, V. L., Gould, J., Howards, S. S., Lieber, M. M., Hellstrom, W., ... & LEWIS, R. (1999). Chronic treatment with finasteride daily does not affect spermatogenesis or semen production in young men. The Journal of urology, 162(4), 1295-1300.



[13] Samplaski, M. K., Lo, K., Grober, E., & Jarvi, K. (2013). Finasteride use in the male infertility population: effects on semen and hormone parameters. Fertility and sterility, 100(6), 1542-1546.



[14] Amory, J. K., Wang, C., Swerdloff, R. S., Anawalt, B. D., Matsumoto, A. M., Bremner, W. J., ... & Clark, R. V. (2007). The effect of 5α-reductase inhibition with dutasteride and finasteride on semen parameters and serum hormones in healthy men. The Journal of Clinical Endocrinology & Metabolism, 92(5), 1659-1665.



[15] Traish, A. M. (2020). Health Risks Associated with Long-Term Finasteride and Dutasteride Use: It's Time to Sound the Alarm. The World Journal of Men's Health, 38.



[16] Traish, A., Haider, K. S., Doros, G., & Haider, A. (2017). Long-term dutasteride therapy in men with benign prostatic hyperplasia alters glucose and lipid profiles and increases severity of erectile dysfunction. Hormone molecular biology and clinical investigation, 30(3).



[17] Doulabi, S. R. S. M., Kavoussi, H., Isapour, D., Hashemian, A., & Taheriniya, A. (2013). Effect of finasteride on lipid profile in individuals with androgenetic alopecia. African Journal of Pharmacy and Pharmacology, 7(6), 315-317.



[18] Duskova, M., Hill, M., & Starka, L. (2010). Changes of metabolic profile in men treated for androgenetic alopecia with 1 mg finasteride. Endocr Regul, 44(1), 3-8.



[19] Gild, P., Cole, A. P., Krasnova, A., Dickerman, B. A., von Landenberg, N., Sun, M., ... & Kibel, A. S. (2018). Liver disease in men undergoing androgen deprivation therapy for prostate cancer. The Journal of urology, 200(3), 573-581.



[20] Mendenhall, C. L. (1968). Anabolic steroid therapy as an adjunct to diet in alcoholic hepatic steatosis. The American journal of digestive diseases, 13(9), 783-791.



[21] Jacqueson, A., Thevenin, M., Warnet, J. M., Claude, J. R., & Truhaut, R. (1978). Comparative Study of the Protective Effect of an Anabolic Steroid. In Toxicological Aspects of Food Safety (pp. 193-196). Springer, Berlin, Heidelberg.



[22] Kelly, D. M., Nettleship, J. E., Akhtar, S., Muraleedharan, V., Sellers, D. J., Brooke, J. C., ... & Jones, T. H. (2014). Testosterone suppresses the expression of regulatory enzymes of fatty acid synthesis and protects against hepatic steatosis in cholesterol-fed androgen deficient mice. Life sciences, 109(2), 95-103.



[23] Lin, H. Y., Yu, I. C., Wang, R. S., Chen, Y. T., Liu, N. C., Altuwaijri, S., ... & Yeh, S. (2008). Increased hepatic steatosis and insulin resistance in mice lacking hepatic androgen receptor. Hepatology, 47(6), 1924-1935.



[24] Völzke, H., Aumann, N., Krebs, A., Nauck, M., Steveling, A., Lerch, M. M., ... & Wallaschofski, H. (2010). Hepatic steatosis is associated with low serum testosterone and high serum DHEAS levels in men. International journal of andrology, 33(1), 45-53.



[25] Velazquez, I., & Alter, B. P. (2004). Androgens and liver tumors: Fanconi's anemia and non‐Fanconi's conditions. American journal of hematology, 77(3), 257-267.



[26] Di Loreto, C., La Marra, F., Mazzon, G., Belgrano, E., Trombetta, C., & Cauci, S. (2014). Immunohistochemical evaluation of androgen receptor and nerve structure density in human prepuce from patients with persistent sexual side effects after finasteride use for androgenetic alopecia. PLoS One, 9(6).



[27] Hsieh, J. T., Chen, S. C., Yu, H. J., & Chang, H. C. (2011). Finasteride upregulates expression of androgen receptor in hyperplastic prostate and LNCaP cells: implications for chemoprevention of prostate cancer. The Prostate, 71(10), 1115-1121.



[28] Pinsky, M. R., Gur, S., Tracey, A. J., Harbin, A., & Hellstrom, W. J. (2011). The effects of chronic 5‐alpha‐reductase inhibitor (dutasteride) treatment on rat erectile function. The journal of sexual medicine, 8(11), 3066-3074.



[29] Iacono, F., Prezioso, D., Ruffo, A., Illiano, E., Romis, L., Di Lauro, G., ... & Amato, B. (2012). Testosterone deficiency causes penile fibrosis and organic erectile dysfunction in aging men. Evaluating association among Age. BMC surgery, 12(S1), S24.



[30] Zhang, M. G., Wang, X. J., Shen, Z. J., & Gao, P. J. (2013). Long-term oral administration of 5α-reductase inhibitor attenuates erectile function by inhibiting autophagy and promoting apoptosis of smooth muscle cells in corpus cavernosum of aged rats. Urology, 82(3), 743-e9.



[31] Melcangi, R. C., Caruso, D., Abbiati, F., Giatti, S., Calabrese, D., Piazza, F., & Cavaletti, G. (2013). Neuroactive steroid levels are modified in cerebrospinal fluid and plasma of post‐finasteride patients showing persistent sexual side effects and anxious/depressive symptomatology. The journal of sexual medicine, 10(10), 2598-2603.



sexual medicine, 10(10), 2598-2603.



[32] Alanazi, N. (2016). Assessing the quality of life and health outcomes of Androgenic Alopecia patients using Propecia (Doctoral dissertation, Rutgers University-School of Health Related Professions).



[33] Melcangi, R. C., Caruso, D., Abbiati, F., Giatti, S., Calabrese, D., Piazza, F., & Cavaletti, G. (2013). Neuroactive steroid levels are modified in cerebrospinal fluid and plasma of post‐finasteride patients showing persistent sexual side effects and anxious/depressive symptomatology. The journal of sexual medicine, 10(10), 2598-2603.



[34] Caruso, D., Abbiati, F., Giatti, S., Romano, S., Fusco, L., Cavaletti, G., & Melcangi, R. C. (2015). Patients treated for male pattern hair with finasteride show, after discontinuation of the drug, altered levels of neuroactive steroids in cerebrospinal fluid and plasma. The Journal of steroid biochemistry and molecular biology, 146, 74-79.



[35] Melcangi, R. C., Santi, D., Spezzano, R., Grimoldi, M., Tabacchi, T., Fusco, M. L., ... & Simoni, M. (2017). Neuroactive steroid levels and psychiatric and andrological features in post-finasteride patients. The Journal of steroid biochemistry and molecular biology, 171, 229-235.



[36] Martinez, P. E., Rubinow, D. R., Nieman, L. K., Koziol, D. E., Morrow, A. L., Schiller, C. E., ... & Schmidt, P. J. (2016). 5α-reductase inhibition prevents the luteal phase increase in plasma allopregnanolone levels and mitigates symptoms in women with premenstrual dysphoric disorder. Neuropsychopharmacology, 41(4), 1093.



[37] Basaria, S., Jasuja, R., Huang, G., Wharton, W., Pan, H., Pencina, K., ... & Labrie, F. (2016). Characteristics of men who report persistent sexual symptoms after finasteride use for hair loss. The Journal of Clinical Endocrinology & Metabolism, 101(12), 4669-4680.



[38] Van Praag, H., Schinder, A. F., Christie, B. R., Toni, N., Palmer, T. D., & Gage, F. H. (2002). Functional neurogenesis in the adult hippocampus. Nature, 415(6875), 1030-1034.



[39] Stockmeier, C. A., Mahajan, G. J., Konick, L. C., Overholser, J. C., Jurjus, G. J., Meltzer, H. Y., ... & Rajkowska, G. (2004). Cellular changes in the postmortem hippocampus in major depression. Biological psychiatry, 56(9), 640-650.



[40] Jacobs, B. L., Van Praag, H., & Gage, F. H. (2000). Adult brain neurogenesis and psychiatry: a novel theory of depression. Molecular psychiatry, 5(3), 262-269.



[41] Römer, B., Pfeiffer, N., Lewicka, S., Ben-Abdallah, N., Vogt, M. A., Deuschle, M., ... & Gass, P. (2010). Finasteride treatment inhibits adult hippocampal neurogenesis in male mice. Pharmacopsychiatry, 43(05), 174-178.



[42] Samuels, B. A., & Hen, R. (2011). Neurogenesis and affective disorders. European Journal of Neuroscience, 33(6), 1152-1159.



[43] Romeo, E., Ströhle, A., Spalletta, G., Michele, F. D., Hermann, B., Holsboer, F., ... & Rupprecht, R. (1998). Effects of antidepressant treatment on neuroactive steroids in major depression. American Journal of Psychiatry, 155(7), 910-913.



[44] Uzunova, V., Sampson, L., & Uzunov, D. P. (2006). Relevance of endogenous 3α-reduced neurosteroids to depression and antidepressant action. Psychopharmacology, 186(3), 351-361.



[45] Uzunova, V., Sheline, Y., Davis, J. M., Rasmusson, A., Uzunov, D. P., Costa, E., & Guidotti, A. (1998). Increase in the cerebrospinal fluid content of neurosteroids in patients with unipolar major depression who are receiving fluoxetine or fluvoxamine. Proceedings of the National Academy of Sciences, 95(6), 3239-3244.



[46] Schüle, C., Nothdurfter, C., & Rupprecht, R. (2014). The role of allopregnanolone in depression and anxiety. Progress in neurobiology, 113, 79-87.



[47] Rasmusson, A. M., Pinna, G., Paliwal, P., Weisman, D., Gottschalk, C., Charney, D., ... & Guidotti, A. (2006). Decreased cerebrospinal fluid allopregnanolone levels in women with posttraumatic stress disorder. Biological psychiatry, 60(7), 704-713.



[48] Hellgren, C., Åkerud, H., Skalkidou, A., Bäckström, T., & Sundström-Poromaa, I. (2014). Low serum allopregnanolone is associated with symptoms of depression in late pregnancy. Neuropsychobiology, 69(3), 147-153.



[49] Schüle, C., Nothdurfter, C., & Rupprecht, R. (2014). The role of allopregnanolone in depression and anxiety. Progress in neurobiology, 113, 79-87.



[50] Murphy, B. P., Abbott, F. V., Allison, C. M., Watts, C., & Ghadirian, A. M. (2004). Elevated levels of some neuroactive progesterone metabolites, particularly isopregnanolone, in women with chronic fatigue syndrome. Psychoneuroendocrinology, 29(2), 245-268.



[51] Uzunova, V., Sheline, Y., Davis, J. M., Rasmusson, A., Uzunov, D. P., Costa, E., & Guidotti, A. (1998). Increase in the cerebrospinal fluid content of neurosteroids in patients with unipolar major depression who are receiving fluoxetine or fluvoxamine. Proceedings of the National Academy of Sciences, 95(6), 3239-3244.



[52] Romeo, E., Ströhle, A., Spalletta, G., Michele, F. D., Hermann, B., Holsboer, F., ... & Rupprecht, R. (1998). Effects of antidepressant treatment on neuroactive steroids in major depression. American Journal of Psychiatry, 155(7), 910-913.



[53] Li, L., Kang, Y. X., Ji, X. M., Li, Y. K., Li, S. C., Zhang, X. J., ... & Shi, G. M. (2018). Finasteride inhibited brain dopaminergic system and open‐field behaviors in adolescent male rats. CNS neuroscience & therapeutics, 24(2), 115-125.



[54] Litim, N., Bourque, M., Al Sweidi, S., Morissette, M., & Di Paolo, T. (2015). The 5α-reductase inhibitor Dutasteride but not Finasteride protects dopamine neurons in the MPTP mouse model of Parkinson's disease. Neuropharmacology, 97, 86-94.



[55] Dazzi, L., Serra, M., Seu, E., Cherchi, G., Pisu, M. G., Purdy, R. H., & Biggio, G. (2002). Progesterone enhances ethanol‐induced modulation of mesocortical dopamine neurons: antagonism by finasteride. Journal of neurochemistry, 83(5), 1103-1109



(Keep in mind i put a big emphazize on finasteride mainly because piec was promoting it)

Tags : @Clavicular
@piec
@MA_ascender
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like this guy

 

[AlphaLooksmaxxer666]

 

[Deleted member 77820]

idiot newcel farming reps through spending his time writing unnecessarily long threads on homeopathic bullshit

dht is shit after puberty

Are you Piec alternate ???

 

[mfk]

Are you Piec alternate ???

no?

and why are you searching for posts from people who critique you? i made this comment over 2 weeks ago

 

[Deleted member 109219]

Why Finasteride (or dut) is a fraud :



So debunking the claim is finasteride dangerous for you yes or no

their are some people who get the following effects from just microdosing fin :

• sexual dysfunction
• Anhedonia
• Depression
• Anxiety
• Lack of motivation
• Lack of focus

While other seems fine using it

Soooo It depends on your neural phenotypes

Some things like childhood trauma has a lot of gaba menergic signaling adrenaline cortisol levels ect….

And also different architectures of the brain (I might write a thread about it its really interesting how you can just look at someone genes pool and know if he has adhd bi polar ect….. if this thread anhilate the fraud that is piec i sure would write about it)

Now lets starts on why finasteride cause all of this sides :

When you use and 5ar inhibitor your not just inhibiting dht but also progesterone and alopregnolone and if you neealycompletely inhibit the enzyme (which you probably will cause most of the 5ar is type 1 and don’t get me started on dut that shit blocks everything) or nearly you have no progesterone and alopregonolone function in your body so back then i thought well you can just take progestene just to come to the conclusion its gonna do nothing for cause you totaly inhibited thw enzyme.

Suggestion : (keep in mind this is not the best approach I’m gonna get to the nest approach later but its still better than the fraud that is piec feel free to insult his ass in the comments)



Now lets talk about the sides :

Remember about the sides i talked about earlier it was due to allo pregnolone who acts as a innate benzo in your system (so basicaly the main inhibotory gaba system in your brain is the gabaergic system related to the hormone you name it “gaba” it has 2 receptors Gaba B fair enough it can be agonized with just phenibut so no need first allopregnolone its not in the sort of communication in the brain anyway (which mean less signaling)

then We have Gaba A

The only critical receptor and guess what the Gaba A receptor is modulated by allopregnolone which if you remember correctly you blocked earlier sp how do i explain it basicaly its like you took a reverse xanax so the average nigga is gonna have anhedonia exept of he is an outlier so now your fucking dependent on benzos who are super dangerous if you don’t wanna feel like shit

(Then some smart ass in the comment gonna write well then why dont you take alopregnolone well it has very short half life and it can’t be stored or kept so unless you want to be taking ng of allopregnolone every 5 minutes you should either feel like shit like that evil piec want you to be or be addicted to benzos for progesterone you can just take transdermal or micronuzed progesterone just make sure to be on hormones cause your at high risk of hypogonadism if you mess up your dosages)



(Also their are other alternatives so 1) way to get allopregnolone which in theory would work not sure 100% is your gonna take your progesterone and agnozed the tsp receptor you’ll end up with more neuro steroidgenisis so you have more alopregnolone just make sure to not get addicted to that shit might write a thread about how to never get addicted to compounds and how to get rid off any addiction but for that ill need you to support me and all insult piec parents for not putting on a rubber that sad night

Getting back to what i was saying their some research that seem mehh like ettyfoxine but that shit is too risky in my opinion

2) alternative is basicaly fuck modulating gaba receptors you just take sodium valproate kt basicaly make your brain a sink of gaba kinda like piec asshole after getting fucked by every dermatologist prescribing him fin

And its a hdac inhibitor so it have epigenetic change keep in mind that shit aint salt that a epilepsy drug and they are reliable 100% cause nigga imagine an epileptic go through withdrawal his gonna fucking die like piec pride after i finish writing this thread)

So to summarize a little :

Erectil dysfunction: is caused by low progesterone abdominal low dht

Anhedhonia : is cause by low alopregnolone levels

Anxiety : is caused because the amygdila have gaba receptors which when inhibited cause the amygdala to start tweaking like piec teading this right now well i hope finasteride would give you trauma and make you hyper vigilant to not with me next time keep in mind if it don’t happen to you it could just mean you had a gabaminergic deficit or your life so

you adapted your the exeption not the rule



Lack of focus : mainly because of low dht and progesterone youll need for that to increase your dopamenergic signaling (supposing you have average serotonorgic signaling) but you can use something like wellbutrin ritalin low dose in the morning 2x per week

(Wellbutrin do have bad effects on cholinergic system but supposing your an average dude and get a lot of choline in your diet your probably fine)



Here a Choline stack if anyone is interested i already writed it down wayback in the thread fix your life as a teenager :

1. Acetylcholine

a.1g CDP choline 2x per day

b.20 mg Donepezil upon rising

c.300 mg alpha gpc in the morning

d.500 mg Uridine monophosphate in the morning

e.1000 mg piracetam (5x per week$

f.30 mg Noopept



So your gonna ask me what could you do well you can use a topical dut in the hairline or balding areas (but good luck sourcing that)

(Before you ragebait in the comments i already thought about blocking the androgen receptor with Ru but to much side effects especially knowing the information I’m gonna reveal later)



The biggest lie ever said about hairloss :

is that dht cause hairloss if dht cause its mainly becuase it caus low estrogen who is responsible for the hairloss (just look at the guys who took tamoxifen who get hairloss look at the guys who take masteron who get hairloss which if you didn’t know is less androgenic than test its because of its serm effects look at rad 140 who is literraly 0 androgenic and still result in hairloss don’t forget rad 140 was intended to cute breast cancer so its all about estrogens)



If anything Dht increase hair growth :

https://pmc.ncbi.nlm.nih.gov/articles/PMC6989660/



We have seen the effects of blocking DHT. It SLOWS hair loss and some get a MILD regrowth at best with all the sides and complex protocols you should apply to counter act those side effects



The problem with the hairloss comunity is they often overlook the basics like what about hypogonadol nigga who got hairloss they don’t have high dht yet they are bald

So lets get to it the main reasons of hairloss :

• Low estrogen as said earlier
• Bad lifestyle habits
• Poor nutrition
• Lack of exercise

Then we have the most important ones :

• Insulin resistance
• Stress
• The main contributing factor of hairloss and the most overloked one is hypoxia you can try it yourself put on a hat on your hair for 12 hours your gonna feel your haur thinning if you think im coping

So my Definitive hairloss stack that I’ll reccomend :



Topical supplements:
-Ketoconazole cream. 1 to 2 times a day, every day. If price or convenience is an issue, the minimum this should be applied is before bed to balding areas. Ketoconazole has been shown to be just as effective as minoxidil in studies with the shampoo. And even stronger the cream has been shown to produce results with an overnight application.

-Emu oil. 1-2 times a day. One of the only proven items I’ve come across that increases skin and hair DNA synthesis, with studies showing hair regrowth.

-Peppermint oil. 1-2 times a day. Peppermint oil has been shown in studies to be equivalent to minoxidil, without the negative side effects that result in premature aging of the skin.

-Evening Primrose oil or Borage oil. Both shown to cause hair regrowth in studies. Just adding a little more fat topically which is absorbed via the skin. Also useful for GLA’s effect on prostaglandins for halting inflammation, hair loss, and aiding hair regrowth.

-Spironolactone cream. Spironolactone has been shown to restore a 60 year old males hairline to his teenage years hair line that he had lost decades ago. Although we use this item topically, it still has the same benefits locally as it is used for such issues as hair loss and hirsutism topically. However topically it does not go systematic as in studies it has been applied to patients whole backs without going systematic. Spironolactone blocks the binding of androgens to the androgen receptor and helps increase estrogen locally.



-BiEstro cream. E2 and E3 combo, Estradiol and Estriol. Apply once or twice a day to balding areas.

The amount used here is enough to cover balding thinning areas. Due to the area we are applying it studies have shown no real systematic absorption. And also to the fact of the dose we are using is quite low as well. None of the users nor myself could produce an estrogenic side on this when applied to the scalp. Some of us who would normally get estrogenic sides off testosterone use as low as 200 mg.

(You can add bold for E1 if you wanna maximize but kinda pain in the ass cause you have to do bloods and make sure your E1 doesn’t lower your E2 and E3 basicaly you should keep them in harmony)



We have also seen what adding estrogen does for hair, as the byproduct of the thousands of male to female sex changes. These individuals can regrow full heads of amazing hair, bringing back hair reminiscent of that which they had when they were teenagers.

Likely, the ones seeing any bit of regrowth from DHT blockers are as a result of the mild estrogen increase triggered by these compounds. Studies of topical estrogen, plain and simple, work. In both men and women. As a bonus, adding estrogen topically doesn’t just increase estrogen -it also the localized concentration of the aromatase enzyme.

(I’ve saw myself dozens of people on reedit i swear i dont know why i couldnt find them having resuts if anyone has it please write it down below)

(For the studies i linked so many in the ashwaganda and no body gave a fuck

So because of that here are some studies on mice :

https://pubmed.ncbi.nlm.nih.gov/14962083/

https://www.researchgate.net/figure...e-tenth-day-after-hair-shaving_fig1_229083213





View attachment 3261225

Here is someone who got hair growth using estriol and estradiol cream



=End justification for BiEstro Cream==

Rub this mixture on once or twice a day depending on your available time. Once a day is totally fine, and optimal for most, if you can apply it before bed. If not, and you must do it in the day, pick a time where you can leave it on for at least 1-2 hours before showering it out.



Supplements:

Minerals might be needed if severely deficient, some doses are based off studies and you may not need these doses. You must find your own dose.

-Zinc Picolinate. 100-150mg a day for 6-8 weeks, tops.

This depends on a few factors. Add up your dietary zinc content that you typically average, and then decide if zinc might be low and determine the dose that you want. This has been noted in studies to completely reverse hair loss and hypothyroid conditions that are due to a zinc deficiency. NOTE: You may not need this, use discretion. Too much zinc can lead to other problems.

-Taurine. 2.5 grams, 2x a day.

In regards to hair loss, Taurine has been shown to help combat fibrosis of the scalp, thus

increasing circulation and hair growth.



Black Currant Oil, 3g a day.

This is utilized for its Gamma Linoleic Acid (GLA) content, which has anti-inflammatory properties, the ability to increase hair growth prostaglandins (PGE), and the ability to inhibit hair loss prostaglandins (PGD). These prostaglandins are another contributing factor to hair loss/growth aside from the androgens.

Three items have been shown to decrease GLA – wheat, dairy, and trans fats – through inhibition of an enzyme called D6D. The typical western diet is full of these foods. Inhibition of the D6D enzyme prevents the conversion of Linoleic Acid (LA) into GLA. The inhibition of D6D also happens with age, and is likely one of the key contributors to balding getting worse with age. This is just about the only process that can link balding to aging that has not already been explored.

In taking a GLA supplement, we bypass the enzymatic conversion entirely and have the end product.

Black Currant oil was also shown in animal studies to prevent many of the negatives of excessive fructose intake, such as fatty liver.



Grapeseed Extract, 500-1000mg a day.
GSE has been shown in animal studies to improve insulin resistance as much as metformin. Studies have also shown GSE to double the number of hairs in the anagen (growth) phase. As far as I am aware, no other compound has been shown to have effects this potent.

(Note : i do not advise to take metformin or berberine for other reasons i would write a thread about it in the near future)



Chromium gtf is used for combating insulin resistance, which is seen as a contributing factor for hair loss as mentioned above when talking about GSE. Again, some may not need this. Chromium GTF has been shown in case studies with type 2 diabetics to remove all exogenous insulin dependency within a couple months of use i recommend using 1000mcg a day for about 6 weeks



And you want to be eating or supplementing with those :

Magnesium

B vitamins

Vitamin K2

You also wanna be getting fats in your diet (especially from Mufas and Pufas (just make sure your not getting it from seed oils because its processed that a whole other topic id advise to get from seeds)



but I assure you, PUFA fats are NOT bad for you. Getting them from healthy sources has countless proven health benefits: anti-carcinogenic, anti-inflammatory, pro-sleep, pro-thyroid, etc. The benefits of unheated PUFA fats are a very deep topic on their own.

The epidermis of your skin is made of 60 percent Omega-6 PUFA fats. Do not fall for the “Omega-3 must be higher than Omega-6” speech that has no proven benefits and multiple proven detriments. All of the studies linking PUFA fats to health issues look at the typical use for PUFA fats in the western diet: cooking, frying, and otherwise heating the fats. If we are to take the same controlled environment but introduce raw, unheated PUFA fats from seeds and nuts, the studies flip completely. Anti-cancer, anti-inflammatory, and all-around health marker improvement is marked.



Another issue found often in the bodybuilding and fitness realm is the “eating too clean” phenomenon. If you were to add up chicken, rice, broccoli, and some olive oil on your favorite diet app, I can guarantee that you’d see that it’s a struggle to reach even 15 percent of RDA requirements for PUFA fats. When this happens, the skin goes dry and wrinkles appear, hair becomes straw like and falls out, etc. Digestive issues ensue, and metabolism slows down. As PUFA fats are shown to increase thyroid hormone sensitivity by almost 20 percent, dieting becomes harder and fat accrual in a calorie surplus becomes far easier. This isn’t even rectifiable with exogenous thyroid hormones – take all the thyroid drugs you want, if your sensitivity isn’t up to par your metabolism will suffer.

(Fun fact : Studies have also shown that when consumed in equal quantities, monounsaturated and saturated fats cause fat gain. Saturated fat was shown to cause a decrease in insulin sensitivity as well. PUFA fat, on the other hand, caused barely any fat gain. The majority of weight gained was muscle, insulin sensitivity increased, and abdominal fat thickness decreased.)



Other Foods.

Pineapple is used as a general health food with documented anti-inflammatory benefits, contains an enzyme papaya if i can recall that aids in the digestion of protein, is a fantastic source of vitamins, and is a preferred fruit due to the lower-end fructose content. In regards to hair regrowth, the main benefit is its anti-inflammatory property.



Massage/Mechanical Manipulation:

Vigorously massage, brush, or pinch your scalp in the balding areas. 1-2 times a day, for whatever time frame you can manage; the longer the better. 3-5 minutes is great, 10 minutes is better. Use as much pressure as possible. Tissue manipulation like this increases circulation and has been proven in studies to aid hair growth. To assist in blood flow further, you can bend over and point your head toward the ground, allowing gravity to assist in delivering blood to the target area.



You could also look in the More plates more plates micro needling stuff :



Sources :



[1] Stoner, E. (1990). The clinical development of a 5α-reductase inhibitor, finasteride. The Journal of steroid biochemistry and molecular biology, 37(3), 375-378.



[2] Vuichoud, C., & Loughlin, K. R. (2015). Benign prostatic hyperplasia: epidemiology, economics and evaluation. Can J Urol, 22(Suppl 1), 1-6.



[3] Adil, A., & Godwin, M. (2017). The effectiveness of treatments for androgenetic alopecia: a systematic review and meta-analysis. Journal of the American Academy of



141.



[4] Schumacher, M., Hussain, R., Gago, N., Oudinet, J. P., Mattern, C., & Ghoumari, A. (2012). Progesterone synthesis in the nervous system: implications for myelination and myelin repair. Frontiers in neuroscience, 6, 10.



[5] Skeldon, S. C., Macdonald, E. M., Law, M. R., Huang, A., Paterson, J. M., Mamdani, M. M., & Juurlink, D. (2017). The cardiovascular safety of dutasteride. The Journal of urology, 197(5), 1309-1314.



[6] Lee, H. J., & Chang, C. (2003). Recent advances in androgen receptor action. Cellular and Molecular Life Sciences CMLS, 60(8), 1613-1622.



[7] Bolton, E. C., So, A. Y., Chaivorapol, C., Haqq, C. M., Li, H., & Yamamoto, K. R. (2007). Cell-and gene-specific regulation of primary target genes by the androgen receptor. Genes & development, 21(16), 2005-2017.



[8] Winiarska, A., Mandt, N., Kamp, H., Hossini, A., Seltmann, H., Zouboulis, C. C., & Blume-Peytavi, U. (2006). Effect of 5α-dihydrotestosterone and testosterone on apoptosis in human dermal papilla cells. Skin pharmacology and physiology, 19(6), 311-321.



[9] Chhipa, R. R., Halim, D., Cheng, J., Zhang, H. Y., Mohler, J. L., Ip, C., & Wu, Y. (2013). The direct inhibitory effect of dutasteride or finasteride on androgen receptor activity is cell line specific. The Prostate, 73(14), 1483-1494.



[10] Mella, J. M., Perret, M. C., Manzotti, M., Catalano, H. N., & Guyatt, G. (2010). Efficacy and safety of finasteride therapy for androgenetic alopecia: a systematic review. Archives of dermatology, 146(10), 1141-1150.



[11] Di Loreto, C., La Marra, F., Mazzon, G., Belgrano, E., Trombetta, C., & Cauci, S. (2014). Immunohistochemical evaluation of androgen receptor and nerve structure density in human prepuce from patients with persistent sexual side effects after finasteride use for androgenetic alopecia. PLoS One, 9(6).



[12] Overstreet, J. W., Fuh, V. L., Gould, J., Howards, S. S., Lieber, M. M., Hellstrom, W., ... & LEWIS, R. (1999). Chronic treatment with finasteride daily does not affect spermatogenesis or semen production in young men. The Journal of urology, 162(4), 1295-1300.



[13] Samplaski, M. K., Lo, K., Grober, E., & Jarvi, K. (2013). Finasteride use in the male infertility population: effects on semen and hormone parameters. Fertility and sterility, 100(6), 1542-1546.



[14] Amory, J. K., Wang, C., Swerdloff, R. S., Anawalt, B. D., Matsumoto, A. M., Bremner, W. J., ... & Clark, R. V. (2007). The effect of 5α-reductase inhibition with dutasteride and finasteride on semen parameters and serum hormones in healthy men. The Journal of Clinical Endocrinology & Metabolism, 92(5), 1659-1665.



[15] Traish, A. M. (2020). Health Risks Associated with Long-Term Finasteride and Dutasteride Use: It's Time to Sound the Alarm. The World Journal of Men's Health, 38.



[16] Traish, A., Haider, K. S., Doros, G., & Haider, A. (2017). Long-term dutasteride therapy in men with benign prostatic hyperplasia alters glucose and lipid profiles and increases severity of erectile dysfunction. Hormone molecular biology and clinical investigation, 30(3).



[17] Doulabi, S. R. S. M., Kavoussi, H., Isapour, D., Hashemian, A., & Taheriniya, A. (2013). Effect of finasteride on lipid profile in individuals with androgenetic alopecia. African Journal of Pharmacy and Pharmacology, 7(6), 315-317.



[18] Duskova, M., Hill, M., & Starka, L. (2010). Changes of metabolic profile in men treated for androgenetic alopecia with 1 mg finasteride. Endocr Regul, 44(1), 3-8.



[19] Gild, P., Cole, A. P., Krasnova, A., Dickerman, B. A., von Landenberg, N., Sun, M., ... & Kibel, A. S. (2018). Liver disease in men undergoing androgen deprivation therapy for prostate cancer. The Journal of urology, 200(3), 573-581.



[20] Mendenhall, C. L. (1968). Anabolic steroid therapy as an adjunct to diet in alcoholic hepatic steatosis. The American journal of digestive diseases, 13(9), 783-791.



[21] Jacqueson, A., Thevenin, M., Warnet, J. M., Claude, J. R., & Truhaut, R. (1978). Comparative Study of the Protective Effect of an Anabolic Steroid. In Toxicological Aspects of Food Safety (pp. 193-196). Springer, Berlin, Heidelberg.



[22] Kelly, D. M., Nettleship, J. E., Akhtar, S., Muraleedharan, V., Sellers, D. J., Brooke, J. C., ... & Jones, T. H. (2014). Testosterone suppresses the expression of regulatory enzymes of fatty acid synthesis and protects against hepatic steatosis in cholesterol-fed androgen deficient mice. Life sciences, 109(2), 95-103.



[23] Lin, H. Y., Yu, I. C., Wang, R. S., Chen, Y. T., Liu, N. C., Altuwaijri, S., ... & Yeh, S. (2008). Increased hepatic steatosis and insulin resistance in mice lacking hepatic androgen receptor. Hepatology, 47(6), 1924-1935.



[24] Völzke, H., Aumann, N., Krebs, A., Nauck, M., Steveling, A., Lerch, M. M., ... & Wallaschofski, H. (2010). Hepatic steatosis is associated with low serum testosterone and high serum DHEAS levels in men. International journal of andrology, 33(1), 45-53.



[25] Velazquez, I., & Alter, B. P. (2004). Androgens and liver tumors: Fanconi's anemia and non‐Fanconi's conditions. American journal of hematology, 77(3), 257-267.



[26] Di Loreto, C., La Marra, F., Mazzon, G., Belgrano, E., Trombetta, C., & Cauci, S. (2014). Immunohistochemical evaluation of androgen receptor and nerve structure density in human prepuce from patients with persistent sexual side effects after finasteride use for androgenetic alopecia. PLoS One, 9(6).



[27] Hsieh, J. T., Chen, S. C., Yu, H. J., & Chang, H. C. (2011). Finasteride upregulates expression of androgen receptor in hyperplastic prostate and LNCaP cells: implications for chemoprevention of prostate cancer. The Prostate, 71(10), 1115-1121.



[28] Pinsky, M. R., Gur, S., Tracey, A. J., Harbin, A., & Hellstrom, W. J. (2011). The effects of chronic 5‐alpha‐reductase inhibitor (dutasteride) treatment on rat erectile function. The journal of sexual medicine, 8(11), 3066-3074.



[29] Iacono, F., Prezioso, D., Ruffo, A., Illiano, E., Romis, L., Di Lauro, G., ... & Amato, B. (2012). Testosterone deficiency causes penile fibrosis and organic erectile dysfunction in aging men. Evaluating association among Age. BMC surgery, 12(S1), S24.



[30] Zhang, M. G., Wang, X. J., Shen, Z. J., & Gao, P. J. (2013). Long-term oral administration of 5α-reductase inhibitor attenuates erectile function by inhibiting autophagy and promoting apoptosis of smooth muscle cells in corpus cavernosum of aged rats. Urology, 82(3), 743-e9.



[31] Melcangi, R. C., Caruso, D., Abbiati, F., Giatti, S., Calabrese, D., Piazza, F., & Cavaletti, G. (2013). Neuroactive steroid levels are modified in cerebrospinal fluid and plasma of post‐finasteride patients showing persistent sexual side effects and anxious/depressive symptomatology. The journal of sexual medicine, 10(10), 2598-2603.



sexual medicine, 10(10), 2598-2603.



[32] Alanazi, N. (2016). Assessing the quality of life and health outcomes of Androgenic Alopecia patients using Propecia (Doctoral dissertation, Rutgers University-School of Health Related Professions).



[33] Melcangi, R. C., Caruso, D., Abbiati, F., Giatti, S., Calabrese, D., Piazza, F., & Cavaletti, G. (2013). Neuroactive steroid levels are modified in cerebrospinal fluid and plasma of post‐finasteride patients showing persistent sexual side effects and anxious/depressive symptomatology. The journal of sexual medicine, 10(10), 2598-2603.



[34] Caruso, D., Abbiati, F., Giatti, S., Romano, S., Fusco, L., Cavaletti, G., & Melcangi, R. C. (2015). Patients treated for male pattern hair with finasteride show, after discontinuation of the drug, altered levels of neuroactive steroids in cerebrospinal fluid and plasma. The Journal of steroid biochemistry and molecular biology, 146, 74-79.



[35] Melcangi, R. C., Santi, D., Spezzano, R., Grimoldi, M., Tabacchi, T., Fusco, M. L., ... & Simoni, M. (2017). Neuroactive steroid levels and psychiatric and andrological features in post-finasteride patients. The Journal of steroid biochemistry and molecular biology, 171, 229-235.



[36] Martinez, P. E., Rubinow, D. R., Nieman, L. K., Koziol, D. E., Morrow, A. L., Schiller, C. E., ... & Schmidt, P. J. (2016). 5α-reductase inhibition prevents the luteal phase increase in plasma allopregnanolone levels and mitigates symptoms in women with premenstrual dysphoric disorder. Neuropsychopharmacology, 41(4), 1093.



[37] Basaria, S., Jasuja, R., Huang, G., Wharton, W., Pan, H., Pencina, K., ... & Labrie, F. (2016). Characteristics of men who report persistent sexual symptoms after finasteride use for hair loss. The Journal of Clinical Endocrinology & Metabolism, 101(12), 4669-4680.



[38] Van Praag, H., Schinder, A. F., Christie, B. R., Toni, N., Palmer, T. D., & Gage, F. H. (2002). Functional neurogenesis in the adult hippocampus. Nature, 415(6875), 1030-1034.



[39] Stockmeier, C. A., Mahajan, G. J., Konick, L. C., Overholser, J. C., Jurjus, G. J., Meltzer, H. Y., ... & Rajkowska, G. (2004). Cellular changes in the postmortem hippocampus in major depression. Biological psychiatry, 56(9), 640-650.



[40] Jacobs, B. L., Van Praag, H., & Gage, F. H. (2000). Adult brain neurogenesis and psychiatry: a novel theory of depression. Molecular psychiatry, 5(3), 262-269.



[41] Römer, B., Pfeiffer, N., Lewicka, S., Ben-Abdallah, N., Vogt, M. A., Deuschle, M., ... & Gass, P. (2010). Finasteride treatment inhibits adult hippocampal neurogenesis in male mice. Pharmacopsychiatry, 43(05), 174-178.



[42] Samuels, B. A., & Hen, R. (2011). Neurogenesis and affective disorders. European Journal of Neuroscience, 33(6), 1152-1159.



[43] Romeo, E., Ströhle, A., Spalletta, G., Michele, F. D., Hermann, B., Holsboer, F., ... & Rupprecht, R. (1998). Effects of antidepressant treatment on neuroactive steroids in major depression. American Journal of Psychiatry, 155(7), 910-913.



[44] Uzunova, V., Sampson, L., & Uzunov, D. P. (2006). Relevance of endogenous 3α-reduced neurosteroids to depression and antidepressant action. Psychopharmacology, 186(3), 351-361.



[45] Uzunova, V., Sheline, Y., Davis, J. M., Rasmusson, A., Uzunov, D. P., Costa, E., & Guidotti, A. (1998). Increase in the cerebrospinal fluid content of neurosteroids in patients with unipolar major depression who are receiving fluoxetine or fluvoxamine. Proceedings of the National Academy of Sciences, 95(6), 3239-3244.



[46] Schüle, C., Nothdurfter, C., & Rupprecht, R. (2014). The role of allopregnanolone in depression and anxiety. Progress in neurobiology, 113, 79-87.



[47] Rasmusson, A. M., Pinna, G., Paliwal, P., Weisman, D., Gottschalk, C., Charney, D., ... & Guidotti, A. (2006). Decreased cerebrospinal fluid allopregnanolone levels in women with posttraumatic stress disorder. Biological psychiatry, 60(7), 704-713.



[48] Hellgren, C., Åkerud, H., Skalkidou, A., Bäckström, T., & Sundström-Poromaa, I. (2014). Low serum allopregnanolone is associated with symptoms of depression in late pregnancy. Neuropsychobiology, 69(3), 147-153.



[49] Schüle, C., Nothdurfter, C., & Rupprecht, R. (2014). The role of allopregnanolone in depression and anxiety. Progress in neurobiology, 113, 79-87.



[50] Murphy, B. P., Abbott, F. V., Allison, C. M., Watts, C., & Ghadirian, A. M. (2004). Elevated levels of some neuroactive progesterone metabolites, particularly isopregnanolone, in women with chronic fatigue syndrome. Psychoneuroendocrinology, 29(2), 245-268.



[51] Uzunova, V., Sheline, Y., Davis, J. M., Rasmusson, A., Uzunov, D. P., Costa, E., & Guidotti, A. (1998). Increase in the cerebrospinal fluid content of neurosteroids in patients with unipolar major depression who are receiving fluoxetine or fluvoxamine. Proceedings of the National Academy of Sciences, 95(6), 3239-3244.



[52] Romeo, E., Ströhle, A., Spalletta, G., Michele, F. D., Hermann, B., Holsboer, F., ... & Rupprecht, R. (1998). Effects of antidepressant treatment on neuroactive steroids in major depression. American Journal of Psychiatry, 155(7), 910-913.



[53] Li, L., Kang, Y. X., Ji, X. M., Li, Y. K., Li, S. C., Zhang, X. J., ... & Shi, G. M. (2018). Finasteride inhibited brain dopaminergic system and open‐field behaviors in adolescent male rats. CNS neuroscience & therapeutics, 24(2), 115-125.



[54] Litim, N., Bourque, M., Al Sweidi, S., Morissette, M., & Di Paolo, T. (2015). The 5α-reductase inhibitor Dutasteride but not Finasteride protects dopamine neurons in the MPTP mouse model of Parkinson's disease. Neuropharmacology, 97, 86-94.



[55] Dazzi, L., Serra, M., Seu, E., Cherchi, G., Pisu, M. G., Purdy, R. H., & Biggio, G. (2002). Progesterone enhances ethanol‐induced modulation of mesocortical dopamine neurons: antagonism by finasteride. Journal of neurochemistry, 83(5), 1103-1109



(Keep in mind i put a big emphazize on finasteride mainly because piec was promoting it)

Tags : @Clavicular
@piec
@MA_ascender
@Sapieeen
@NZb6Air
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@´´´´´´´´
@Acne Victim
@DR. NICKGA
@cooldude1231

you really need a job bro

 

[DR. NICKGA]

DHT: The last battle

Know the truth

Balding is caused by DHT

BALDING (ANDROGENETIC ALOPECIA) IS CAUSED BY DHT the strongest evidence I can think of right now.. If it's not enough to convince someone of the causal role of androgens in baldness then that person is brain dead or willfully ignorant. Common male pattern baldness is a highly heritable trait...

looksmax.org

 

[Deleted member 77820]

Why Finasteride (or dut) is a fraud :



So debunking the claim is finasteride dangerous for you yes or no

their are some people who get the following effects from just microdosing fin :

• sexual dysfunction
• Anhedonia
• Depression
• Anxiety
• Lack of motivation
• Lack of focus

While other seems fine using it

Soooo It depends on your neural phenotypes

Some things like childhood trauma has a lot of gaba menergic signaling adrenaline cortisol levels ect….

And also different architectures of the brain (I might write a thread about it its really interesting how you can just look at someone genes pool and know if he has adhd bi polar ect….. if this thread anhilate the fraud that is piec i sure would write about it)

Now lets starts on why finasteride cause all of this sides :

When you use and 5ar inhibitor your not just inhibiting dht but also progesterone and alopregnolone and if you neealycompletely inhibit the enzyme (which you probably will cause most of the 5ar is type 1 and don’t get me started on dut that shit blocks everything) or nearly you have no progesterone and alopregonolone function in your body so back then i thought well you can just take progestene just to come to the conclusion its gonna do nothing for cause you totaly inhibited thw enzyme.

Suggestion : (keep in mind this is not the best approach I’m gonna get to the nest approach later but its still better than the fraud that is piec feel free to insult his ass in the comments)



Now lets talk about the sides :

Remember about the sides i talked about earlier it was due to allo pregnolone who acts as a innate benzo in your system (so basicaly the main inhibotory gaba system in your brain is the gabaergic system related to the hormone you name it “gaba” it has 2 receptors Gaba B fair enough it can be agonized with just phenibut so no need first allopregnolone its not in the sort of communication in the brain anyway (which mean less signaling)

then We have Gaba A

The only critical receptor and guess what the Gaba A receptor is modulated by allopregnolone which if you remember correctly you blocked earlier sp how do i explain it basicaly its like you took a reverse xanax so the average nigga is gonna have anhedonia exept of he is an outlier so now your fucking dependent on benzos who are super dangerous if you don’t wanna feel like shit

(Then some smart ass in the comment gonna write well then why dont you take alopregnolone well it has very short half life and it can’t be stored or kept so unless you want to be taking ng of allopregnolone every 5 minutes you should either feel like shit like that evil piec want you to be or be addicted to benzos for progesterone you can just take transdermal or micronuzed progesterone just make sure to be on hormones cause your at high risk of hypogonadism if you mess up your dosages)



(Also their are other alternatives so 1) way to get allopregnolone which in theory would work not sure 100% is your gonna take your progesterone and agnozed the tsp receptor you’ll end up with more neuro steroidgenisis so you have more alopregnolone just make sure to not get addicted to that shit might write a thread about how to never get addicted to compounds and how to get rid off any addiction but for that ill need you to support me and all insult piec parents for not putting on a rubber that sad night

Getting back to what i was saying their some research that seem mehh like ettyfoxine but that shit is too risky in my opinion

2) alternative is basicaly fuck modulating gaba receptors you just take sodium valproate kt basicaly make your brain a sink of gaba kinda like piec asshole after getting fucked by every dermatologist prescribing him fin

And its a hdac inhibitor so it have epigenetic change keep in mind that shit aint salt that a epilepsy drug and they are reliable 100% cause nigga imagine an epileptic go through withdrawal his gonna fucking die like piec pride after i finish writing this thread)

So to summarize a little :

Erectil dysfunction: is caused by low progesterone abdominal low dht

Anhedhonia : is cause by low alopregnolone levels

Anxiety : is caused because the amygdila have gaba receptors which when inhibited cause the amygdala to start tweaking like piec teading this right now well i hope finasteride would give you trauma and make you hyper vigilant to not with me next time keep in mind if it don’t happen to you it could just mean you had a gabaminergic deficit or your life so

you adapted your the exeption not the rule



Lack of focus : mainly because of low dht and progesterone youll need for that to increase your dopamenergic signaling (supposing you have average serotonorgic signaling) but you can use something like wellbutrin ritalin low dose in the morning 2x per week

(Wellbutrin do have bad effects on cholinergic system but supposing your an average dude and get a lot of choline in your diet your probably fine)



Here a Choline stack if anyone is interested i already writed it down wayback in the thread fix your life as a teenager :

1. Acetylcholine

a.1g CDP choline 2x per day

b.20 mg Donepezil upon rising

c.300 mg alpha gpc in the morning

d.500 mg Uridine monophosphate in the morning

e.1000 mg piracetam (5x per week$

f.30 mg Noopept



So your gonna ask me what could you do well you can use a topical dut in the hairline or balding areas (but good luck sourcing that)

(Before you ragebait in the comments i already thought about blocking the androgen receptor with Ru but to much side effects especially knowing the information I’m gonna reveal later)



The biggest lie ever said about hairloss :

is that dht cause hairloss if dht cause its mainly becuase it caus low estrogen who is responsible for the hairloss (just look at the guys who took tamoxifen who get hairloss look at the guys who take masteron who get hairloss which if you didn’t know is less androgenic than test its because of its serm effects look at rad 140 who is literraly 0 androgenic and still result in hairloss don’t forget rad 140 was intended to cute breast cancer so its all about estrogens)



If anything Dht increase hair growth :

https://pmc.ncbi.nlm.nih.gov/articles/PMC6989660/



We have seen the effects of blocking DHT. It SLOWS hair loss and some get a MILD regrowth at best with all the sides and complex protocols you should apply to counter act those side effects



The problem with the hairloss comunity is they often overlook the basics like what about hypogonadol nigga who got hairloss they don’t have high dht yet they are bald

So lets get to it the main reasons of hairloss :

• Low estrogen as said earlier
• Bad lifestyle habits
• Poor nutrition
• Lack of exercise

Then we have the most important ones :

• Insulin resistance
• Stress
• The main contributing factor of hairloss and the most overloked one is hypoxia you can try it yourself put on a hat on your hair for 12 hours your gonna feel your haur thinning if you think im coping

So my Definitive hairloss stack that I’ll reccomend :



Topical supplements:
-Ketoconazole cream. 1 to 2 times a day, every day. If price or convenience is an issue, the minimum this should be applied is before bed to balding areas. Ketoconazole has been shown to be just as effective as minoxidil in studies with the shampoo. And even stronger the cream has been shown to produce results with an overnight application.

-Emu oil. 1-2 times a day. One of the only proven items I’ve come across that increases skin and hair DNA synthesis, with studies showing hair regrowth.

-Peppermint oil. 1-2 times a day. Peppermint oil has been shown in studies to be equivalent to minoxidil, without the negative side effects that result in premature aging of the skin.

-Evening Primrose oil or Borage oil. Both shown to cause hair regrowth in studies. Just adding a little more fat topically which is absorbed via the skin. Also useful for GLA’s effect on prostaglandins for halting inflammation, hair loss, and aiding hair regrowth.

-Spironolactone cream. Spironolactone has been shown to restore a 60 year old males hairline to his teenage years hair line that he had lost decades ago. Although we use this item topically, it still has the same benefits locally as it is used for such issues as hair loss and hirsutism topically. However topically it does not go systematic as in studies it has been applied to patients whole backs without going systematic. Spironolactone blocks the binding of androgens to the androgen receptor and helps increase estrogen locally.



-BiEstro cream. E2 and E3 combo, Estradiol and Estriol. Apply once or twice a day to balding areas.

The amount used here is enough to cover balding thinning areas. Due to the area we are applying it studies have shown no real systematic absorption. And also to the fact of the dose we are using is quite low as well. None of the users nor myself could produce an estrogenic side on this when applied to the scalp. Some of us who would normally get estrogenic sides off testosterone use as low as 200 mg.

(You can add bold for E1 if you wanna maximize but kinda pain in the ass cause you have to do bloods and make sure your E1 doesn’t lower your E2 and E3 basicaly you should keep them in harmony)



We have also seen what adding estrogen does for hair, as the byproduct of the thousands of male to female sex changes. These individuals can regrow full heads of amazing hair, bringing back hair reminiscent of that which they had when they were teenagers.

Likely, the ones seeing any bit of regrowth from DHT blockers are as a result of the mild estrogen increase triggered by these compounds. Studies of topical estrogen, plain and simple, work. In both men and women. As a bonus, adding estrogen topically doesn’t just increase estrogen -it also the localized concentration of the aromatase enzyme.

(I’ve saw myself dozens of people on reedit i swear i dont know why i couldnt find them having resuts if anyone has it please write it down below)

(For the studies i linked so many in the ashwaganda and no body gave a fuck

So because of that here are some studies on mice :

https://pubmed.ncbi.nlm.nih.gov/14962083/

https://www.researchgate.net/figure...e-tenth-day-after-hair-shaving_fig1_229083213





View attachment 3261225

Here is someone who got hair growth using estriol and estradiol cream



=End justification for BiEstro Cream==

Rub this mixture on once or twice a day depending on your available time. Once a day is totally fine, and optimal for most, if you can apply it before bed. If not, and you must do it in the day, pick a time where you can leave it on for at least 1-2 hours before showering it out.



Supplements:

Minerals might be needed if severely deficient, some doses are based off studies and you may not need these doses. You must find your own dose.

-Zinc Picolinate. 100-150mg a day for 6-8 weeks, tops.

This depends on a few factors. Add up your dietary zinc content that you typically average, and then decide if zinc might be low and determine the dose that you want. This has been noted in studies to completely reverse hair loss and hypothyroid conditions that are due to a zinc deficiency. NOTE: You may not need this, use discretion. Too much zinc can lead to other problems.

-Taurine. 2.5 grams, 2x a day.

In regards to hair loss, Taurine has been shown to help combat fibrosis of the scalp, thus

increasing circulation and hair growth.



Black Currant Oil, 3g a day.

This is utilized for its Gamma Linoleic Acid (GLA) content, which has anti-inflammatory properties, the ability to increase hair growth prostaglandins (PGE), and the ability to inhibit hair loss prostaglandins (PGD). These prostaglandins are another contributing factor to hair loss/growth aside from the androgens.

Three items have been shown to decrease GLA – wheat, dairy, and trans fats – through inhibition of an enzyme called D6D. The typical western diet is full of these foods. Inhibition of the D6D enzyme prevents the conversion of Linoleic Acid (LA) into GLA. The inhibition of D6D also happens with age, and is likely one of the key contributors to balding getting worse with age. This is just about the only process that can link balding to aging that has not already been explored.

In taking a GLA supplement, we bypass the enzymatic conversion entirely and have the end product.

Black Currant oil was also shown in animal studies to prevent many of the negatives of excessive fructose intake, such as fatty liver.



Grapeseed Extract, 500-1000mg a day.
GSE has been shown in animal studies to improve insulin resistance as much as metformin. Studies have also shown GSE to double the number of hairs in the anagen (growth) phase. As far as I am aware, no other compound has been shown to have effects this potent.

(Note : i do not advise to take metformin or berberine for other reasons i would write a thread about it in the near future)



Chromium gtf is used for combating insulin resistance, which is seen as a contributing factor for hair loss as mentioned above when talking about GSE. Again, some may not need this. Chromium GTF has been shown in case studies with type 2 diabetics to remove all exogenous insulin dependency within a couple months of use i recommend using 1000mcg a day for about 6 weeks



And you want to be eating or supplementing with those :

Magnesium

B vitamins

Vitamin K2

You also wanna be getting fats in your diet (especially from Mufas and Pufas (just make sure your not getting it from seed oils because its processed that a whole other topic id advise to get from seeds)



but I assure you, PUFA fats are NOT bad for you. Getting them from healthy sources has countless proven health benefits: anti-carcinogenic, anti-inflammatory, pro-sleep, pro-thyroid, etc. The benefits of unheated PUFA fats are a very deep topic on their own.

The epidermis of your skin is made of 60 percent Omega-6 PUFA fats. Do not fall for the “Omega-3 must be higher than Omega-6” speech that has no proven benefits and multiple proven detriments. All of the studies linking PUFA fats to health issues look at the typical use for PUFA fats in the western diet: cooking, frying, and otherwise heating the fats. If we are to take the same controlled environment but introduce raw, unheated PUFA fats from seeds and nuts, the studies flip completely. Anti-cancer, anti-inflammatory, and all-around health marker improvement is marked.



Another issue found often in the bodybuilding and fitness realm is the “eating too clean” phenomenon. If you were to add up chicken, rice, broccoli, and some olive oil on your favorite diet app, I can guarantee that you’d see that it’s a struggle to reach even 15 percent of RDA requirements for PUFA fats. When this happens, the skin goes dry and wrinkles appear, hair becomes straw like and falls out, etc. Digestive issues ensue, and metabolism slows down. As PUFA fats are shown to increase thyroid hormone sensitivity by almost 20 percent, dieting becomes harder and fat accrual in a calorie surplus becomes far easier. This isn’t even rectifiable with exogenous thyroid hormones – take all the thyroid drugs you want, if your sensitivity isn’t up to par your metabolism will suffer.

(Fun fact : Studies have also shown that when consumed in equal quantities, monounsaturated and saturated fats cause fat gain. Saturated fat was shown to cause a decrease in insulin sensitivity as well. PUFA fat, on the other hand, caused barely any fat gain. The majority of weight gained was muscle, insulin sensitivity increased, and abdominal fat thickness decreased.)



Other Foods.

Pineapple is used as a general health food with documented anti-inflammatory benefits, contains an enzyme papaya if i can recall that aids in the digestion of protein, is a fantastic source of vitamins, and is a preferred fruit due to the lower-end fructose content. In regards to hair regrowth, the main benefit is its anti-inflammatory property.



Massage/Mechanical Manipulation:

Vigorously massage, brush, or pinch your scalp in the balding areas. 1-2 times a day, for whatever time frame you can manage; the longer the better. 3-5 minutes is great, 10 minutes is better. Use as much pressure as possible. Tissue manipulation like this increases circulation and has been proven in studies to aid hair growth. To assist in blood flow further, you can bend over and point your head toward the ground, allowing gravity to assist in delivering blood to the target area.



You could also look in the More plates more plates micro needling stuff :



Sources :



[1] Stoner, E. (1990). The clinical development of a 5α-reductase inhibitor, finasteride. The Journal of steroid biochemistry and molecular biology, 37(3), 375-378.



[2] Vuichoud, C., & Loughlin, K. R. (2015). Benign prostatic hyperplasia: epidemiology, economics and evaluation. Can J Urol, 22(Suppl 1), 1-6.



[3] Adil, A., & Godwin, M. (2017). The effectiveness of treatments for androgenetic alopecia: a systematic review and meta-analysis. Journal of the American Academy of



141.



[4] Schumacher, M., Hussain, R., Gago, N., Oudinet, J. P., Mattern, C., & Ghoumari, A. (2012). Progesterone synthesis in the nervous system: implications for myelination and myelin repair. Frontiers in neuroscience, 6, 10.



[5] Skeldon, S. C., Macdonald, E. M., Law, M. R., Huang, A., Paterson, J. M., Mamdani, M. M., & Juurlink, D. (2017). The cardiovascular safety of dutasteride. The Journal of urology, 197(5), 1309-1314.



[6] Lee, H. J., & Chang, C. (2003). Recent advances in androgen receptor action. Cellular and Molecular Life Sciences CMLS, 60(8), 1613-1622.



[7] Bolton, E. C., So, A. Y., Chaivorapol, C., Haqq, C. M., Li, H., & Yamamoto, K. R. (2007). Cell-and gene-specific regulation of primary target genes by the androgen receptor. Genes & development, 21(16), 2005-2017.



[8] Winiarska, A., Mandt, N., Kamp, H., Hossini, A., Seltmann, H., Zouboulis, C. C., & Blume-Peytavi, U. (2006). Effect of 5α-dihydrotestosterone and testosterone on apoptosis in human dermal papilla cells. Skin pharmacology and physiology, 19(6), 311-321.



[9] Chhipa, R. R., Halim, D., Cheng, J., Zhang, H. Y., Mohler, J. L., Ip, C., & Wu, Y. (2013). The direct inhibitory effect of dutasteride or finasteride on androgen receptor activity is cell line specific. The Prostate, 73(14), 1483-1494.



[10] Mella, J. M., Perret, M. C., Manzotti, M., Catalano, H. N., & Guyatt, G. (2010). Efficacy and safety of finasteride therapy for androgenetic alopecia: a systematic review. Archives of dermatology, 146(10), 1141-1150.



[11] Di Loreto, C., La Marra, F., Mazzon, G., Belgrano, E., Trombetta, C., & Cauci, S. (2014). Immunohistochemical evaluation of androgen receptor and nerve structure density in human prepuce from patients with persistent sexual side effects after finasteride use for androgenetic alopecia. PLoS One, 9(6).



[12] Overstreet, J. W., Fuh, V. L., Gould, J., Howards, S. S., Lieber, M. M., Hellstrom, W., ... & LEWIS, R. (1999). Chronic treatment with finasteride daily does not affect spermatogenesis or semen production in young men. The Journal of urology, 162(4), 1295-1300.



[13] Samplaski, M. K., Lo, K., Grober, E., & Jarvi, K. (2013). Finasteride use in the male infertility population: effects on semen and hormone parameters. Fertility and sterility, 100(6), 1542-1546.



[14] Amory, J. K., Wang, C., Swerdloff, R. S., Anawalt, B. D., Matsumoto, A. M., Bremner, W. J., ... & Clark, R. V. (2007). The effect of 5α-reductase inhibition with dutasteride and finasteride on semen parameters and serum hormones in healthy men. The Journal of Clinical Endocrinology & Metabolism, 92(5), 1659-1665.



[15] Traish, A. M. (2020). Health Risks Associated with Long-Term Finasteride and Dutasteride Use: It's Time to Sound the Alarm. The World Journal of Men's Health, 38.



[16] Traish, A., Haider, K. S., Doros, G., & Haider, A. (2017). Long-term dutasteride therapy in men with benign prostatic hyperplasia alters glucose and lipid profiles and increases severity of erectile dysfunction. Hormone molecular biology and clinical investigation, 30(3).



[17] Doulabi, S. R. S. M., Kavoussi, H., Isapour, D., Hashemian, A., & Taheriniya, A. (2013). Effect of finasteride on lipid profile in individuals with androgenetic alopecia. African Journal of Pharmacy and Pharmacology, 7(6), 315-317.



[18] Duskova, M., Hill, M., & Starka, L. (2010). Changes of metabolic profile in men treated for androgenetic alopecia with 1 mg finasteride. Endocr Regul, 44(1), 3-8.



[19] Gild, P., Cole, A. P., Krasnova, A., Dickerman, B. A., von Landenberg, N., Sun, M., ... & Kibel, A. S. (2018). Liver disease in men undergoing androgen deprivation therapy for prostate cancer. The Journal of urology, 200(3), 573-581.



[20] Mendenhall, C. L. (1968). Anabolic steroid therapy as an adjunct to diet in alcoholic hepatic steatosis. The American journal of digestive diseases, 13(9), 783-791.



[21] Jacqueson, A., Thevenin, M., Warnet, J. M., Claude, J. R., & Truhaut, R. (1978). Comparative Study of the Protective Effect of an Anabolic Steroid. In Toxicological Aspects of Food Safety (pp. 193-196). Springer, Berlin, Heidelberg.



[22] Kelly, D. M., Nettleship, J. E., Akhtar, S., Muraleedharan, V., Sellers, D. J., Brooke, J. C., ... & Jones, T. H. (2014). Testosterone suppresses the expression of regulatory enzymes of fatty acid synthesis and protects against hepatic steatosis in cholesterol-fed androgen deficient mice. Life sciences, 109(2), 95-103.



[23] Lin, H. Y., Yu, I. C., Wang, R. S., Chen, Y. T., Liu, N. C., Altuwaijri, S., ... & Yeh, S. (2008). Increased hepatic steatosis and insulin resistance in mice lacking hepatic androgen receptor. Hepatology, 47(6), 1924-1935.



[24] Völzke, H., Aumann, N., Krebs, A., Nauck, M., Steveling, A., Lerch, M. M., ... & Wallaschofski, H. (2010). Hepatic steatosis is associated with low serum testosterone and high serum DHEAS levels in men. International journal of andrology, 33(1), 45-53.



[25] Velazquez, I., & Alter, B. P. (2004). Androgens and liver tumors: Fanconi's anemia and non‐Fanconi's conditions. American journal of hematology, 77(3), 257-267.



[26] Di Loreto, C., La Marra, F., Mazzon, G., Belgrano, E., Trombetta, C., & Cauci, S. (2014). Immunohistochemical evaluation of androgen receptor and nerve structure density in human prepuce from patients with persistent sexual side effects after finasteride use for androgenetic alopecia. PLoS One, 9(6).



[27] Hsieh, J. T., Chen, S. C., Yu, H. J., & Chang, H. C. (2011). Finasteride upregulates expression of androgen receptor in hyperplastic prostate and LNCaP cells: implications for chemoprevention of prostate cancer. The Prostate, 71(10), 1115-1121.



[28] Pinsky, M. R., Gur, S., Tracey, A. J., Harbin, A., & Hellstrom, W. J. (2011). The effects of chronic 5‐alpha‐reductase inhibitor (dutasteride) treatment on rat erectile function. The journal of sexual medicine, 8(11), 3066-3074.



[29] Iacono, F., Prezioso, D., Ruffo, A., Illiano, E., Romis, L., Di Lauro, G., ... & Amato, B. (2012). Testosterone deficiency causes penile fibrosis and organic erectile dysfunction in aging men. Evaluating association among Age. BMC surgery, 12(S1), S24.



[30] Zhang, M. G., Wang, X. J., Shen, Z. J., & Gao, P. J. (2013). Long-term oral administration of 5α-reductase inhibitor attenuates erectile function by inhibiting autophagy and promoting apoptosis of smooth muscle cells in corpus cavernosum of aged rats. Urology, 82(3), 743-e9.



[31] Melcangi, R. C., Caruso, D., Abbiati, F., Giatti, S., Calabrese, D., Piazza, F., & Cavaletti, G. (2013). Neuroactive steroid levels are modified in cerebrospinal fluid and plasma of post‐finasteride patients showing persistent sexual side effects and anxious/depressive symptomatology. The journal of sexual medicine, 10(10), 2598-2603.



sexual medicine, 10(10), 2598-2603.



[32] Alanazi, N. (2016). Assessing the quality of life and health outcomes of Androgenic Alopecia patients using Propecia (Doctoral dissertation, Rutgers University-School of Health Related Professions).



[33] Melcangi, R. C., Caruso, D., Abbiati, F., Giatti, S., Calabrese, D., Piazza, F., & Cavaletti, G. (2013). Neuroactive steroid levels are modified in cerebrospinal fluid and plasma of post‐finasteride patients showing persistent sexual side effects and anxious/depressive symptomatology. The journal of sexual medicine, 10(10), 2598-2603.



[34] Caruso, D., Abbiati, F., Giatti, S., Romano, S., Fusco, L., Cavaletti, G., & Melcangi, R. C. (2015). Patients treated for male pattern hair with finasteride show, after discontinuation of the drug, altered levels of neuroactive steroids in cerebrospinal fluid and plasma. The Journal of steroid biochemistry and molecular biology, 146, 74-79.



[35] Melcangi, R. C., Santi, D., Spezzano, R., Grimoldi, M., Tabacchi, T., Fusco, M. L., ... & Simoni, M. (2017). Neuroactive steroid levels and psychiatric and andrological features in post-finasteride patients. The Journal of steroid biochemistry and molecular biology, 171, 229-235.



[36] Martinez, P. E., Rubinow, D. R., Nieman, L. K., Koziol, D. E., Morrow, A. L., Schiller, C. E., ... & Schmidt, P. J. (2016). 5α-reductase inhibition prevents the luteal phase increase in plasma allopregnanolone levels and mitigates symptoms in women with premenstrual dysphoric disorder. Neuropsychopharmacology, 41(4), 1093.



[37] Basaria, S., Jasuja, R., Huang, G., Wharton, W., Pan, H., Pencina, K., ... & Labrie, F. (2016). Characteristics of men who report persistent sexual symptoms after finasteride use for hair loss. The Journal of Clinical Endocrinology & Metabolism, 101(12), 4669-4680.



[38] Van Praag, H., Schinder, A. F., Christie, B. R., Toni, N., Palmer, T. D., & Gage, F. H. (2002). Functional neurogenesis in the adult hippocampus. Nature, 415(6875), 1030-1034.



[39] Stockmeier, C. A., Mahajan, G. J., Konick, L. C., Overholser, J. C., Jurjus, G. J., Meltzer, H. Y., ... & Rajkowska, G. (2004). Cellular changes in the postmortem hippocampus in major depression. Biological psychiatry, 56(9), 640-650.



[40] Jacobs, B. L., Van Praag, H., & Gage, F. H. (2000). Adult brain neurogenesis and psychiatry: a novel theory of depression. Molecular psychiatry, 5(3), 262-269.



[41] Römer, B., Pfeiffer, N., Lewicka, S., Ben-Abdallah, N., Vogt, M. A., Deuschle, M., ... & Gass, P. (2010). Finasteride treatment inhibits adult hippocampal neurogenesis in male mice. Pharmacopsychiatry, 43(05), 174-178.



[42] Samuels, B. A., & Hen, R. (2011). Neurogenesis and affective disorders. European Journal of Neuroscience, 33(6), 1152-1159.



[43] Romeo, E., Ströhle, A., Spalletta, G., Michele, F. D., Hermann, B., Holsboer, F., ... & Rupprecht, R. (1998). Effects of antidepressant treatment on neuroactive steroids in major depression. American Journal of Psychiatry, 155(7), 910-913.



[44] Uzunova, V., Sampson, L., & Uzunov, D. P. (2006). Relevance of endogenous 3α-reduced neurosteroids to depression and antidepressant action. Psychopharmacology, 186(3), 351-361.



[45] Uzunova, V., Sheline, Y., Davis, J. M., Rasmusson, A., Uzunov, D. P., Costa, E., & Guidotti, A. (1998). Increase in the cerebrospinal fluid content of neurosteroids in patients with unipolar major depression who are receiving fluoxetine or fluvoxamine. Proceedings of the National Academy of Sciences, 95(6), 3239-3244.



[46] Schüle, C., Nothdurfter, C., & Rupprecht, R. (2014). The role of allopregnanolone in depression and anxiety. Progress in neurobiology, 113, 79-87.



[47] Rasmusson, A. M., Pinna, G., Paliwal, P., Weisman, D., Gottschalk, C., Charney, D., ... & Guidotti, A. (2006). Decreased cerebrospinal fluid allopregnanolone levels in women with posttraumatic stress disorder. Biological psychiatry, 60(7), 704-713.



[48] Hellgren, C., Åkerud, H., Skalkidou, A., Bäckström, T., & Sundström-Poromaa, I. (2014). Low serum allopregnanolone is associated with symptoms of depression in late pregnancy. Neuropsychobiology, 69(3), 147-153.



[49] Schüle, C., Nothdurfter, C., & Rupprecht, R. (2014). The role of allopregnanolone in depression and anxiety. Progress in neurobiology, 113, 79-87.



[50] Murphy, B. P., Abbott, F. V., Allison, C. M., Watts, C., & Ghadirian, A. M. (2004). Elevated levels of some neuroactive progesterone metabolites, particularly isopregnanolone, in women with chronic fatigue syndrome. Psychoneuroendocrinology, 29(2), 245-268.



[51] Uzunova, V., Sheline, Y., Davis, J. M., Rasmusson, A., Uzunov, D. P., Costa, E., & Guidotti, A. (1998). Increase in the cerebrospinal fluid content of neurosteroids in patients with unipolar major depression who are receiving fluoxetine or fluvoxamine. Proceedings of the National Academy of Sciences, 95(6), 3239-3244.



[52] Romeo, E., Ströhle, A., Spalletta, G., Michele, F. D., Hermann, B., Holsboer, F., ... & Rupprecht, R. (1998). Effects of antidepressant treatment on neuroactive steroids in major depression. American Journal of Psychiatry, 155(7), 910-913.



[53] Li, L., Kang, Y. X., Ji, X. M., Li, Y. K., Li, S. C., Zhang, X. J., ... & Shi, G. M. (2018). Finasteride inhibited brain dopaminergic system and open‐field behaviors in adolescent male rats. CNS neuroscience & therapeutics, 24(2), 115-125.



[54] Litim, N., Bourque, M., Al Sweidi, S., Morissette, M., & Di Paolo, T. (2015). The 5α-reductase inhibitor Dutasteride but not Finasteride protects dopamine neurons in the MPTP mouse model of Parkinson's disease. Neuropharmacology, 97, 86-94.



[55] Dazzi, L., Serra, M., Seu, E., Cherchi, G., Pisu, M. G., Purdy, R. H., & Biggio, G. (2002). Progesterone enhances ethanol‐induced modulation of mesocortical dopamine neurons: antagonism by finasteride. Journal of neurochemistry, 83(5), 1103-1109



(Keep in mind i put a big emphazize on finasteride mainly because piec was promoting it)

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Why Finasteride (or dut) is a fraud :



So debunking the claim is finasteride dangerous for you yes or no

their are some people who get the following effects from just microdosing fin :

• sexual dysfunction
• Anhedonia
• Depression
• Anxiety
• Lack of motivation
• Lack of focus

While other seems fine using it

Soooo It depends on your neural phenotypes

Some things like childhood trauma has a lot of gaba menergic signaling adrenaline cortisol levels ect….

And also different architectures of the brain (I might write a thread about it its really interesting how you can just look at someone genes pool and know if he has adhd bi polar ect….. if this thread anhilate the fraud that is piec i sure would write about it)

Now lets starts on why finasteride cause all of this sides :

When you use and 5ar inhibitor your not just inhibiting dht but also progesterone and alopregnolone and if you neealycompletely inhibit the enzyme (which you probably will cause most of the 5ar is type 1 and don’t get me started on dut that shit blocks everything) or nearly you have no progesterone and alopregonolone function in your body so back then i thought well you can just take progestene just to come to the conclusion its gonna do nothing for cause you totaly inhibited thw enzyme.

Suggestion : (keep in mind this is not the best approach I’m gonna get to the nest approach later but its still better than the fraud that is piec feel free to insult his ass in the comments)



Now lets talk about the sides :

Remember about the sides i talked about earlier it was due to allo pregnolone who acts as a innate benzo in your system (so basicaly the main inhibotory gaba system in your brain is the gabaergic system related to the hormone you name it “gaba” it has 2 receptors Gaba B fair enough it can be agonized with just phenibut so no need first allopregnolone its not in the sort of communication in the brain anyway (which mean less signaling)

then We have Gaba A

The only critical receptor and guess what the Gaba A receptor is modulated by allopregnolone which if you remember correctly you blocked earlier sp how do i explain it basicaly its like you took a reverse xanax so the average nigga is gonna have anhedonia exept of he is an outlier so now your fucking dependent on benzos who are super dangerous if you don’t wanna feel like shit

(Then some smart ass in the comment gonna write well then why dont you take alopregnolone well it has very short half life and it can’t be stored or kept so unless you want to be taking ng of allopregnolone every 5 minutes you should either feel like shit like that evil piec want you to be or be addicted to benzos for progesterone you can just take transdermal or micronuzed progesterone just make sure to be on hormones cause your at high risk of hypogonadism if you mess up your dosages)



(Also their are other alternatives so 1) way to get allopregnolone which in theory would work not sure 100% is your gonna take your progesterone and agnozed the tsp receptor you’ll end up with more neuro steroidgenisis so you have more alopregnolone just make sure to not get addicted to that shit might write a thread about how to never get addicted to compounds and how to get rid off any addiction but for that ill need you to support me and all insult piec parents for not putting on a rubber that sad night

Getting back to what i was saying their some research that seem mehh like ettyfoxine but that shit is too risky in my opinion

2) alternative is basicaly fuck modulating gaba receptors you just take sodium valproate kt basicaly make your brain a sink of gaba kinda like piec asshole after getting fucked by every dermatologist prescribing him fin

And its a hdac inhibitor so it have epigenetic change keep in mind that shit aint salt that a epilepsy drug and they are reliable 100% cause nigga imagine an epileptic go through withdrawal his gonna fucking die like piec pride after i finish writing this thread)

So to summarize a little :

Erectil dysfunction: is caused by low progesterone abdominal low dht

Anhedhonia : is cause by low alopregnolone levels

Anxiety : is caused because the amygdila have gaba receptors which when inhibited cause the amygdala to start tweaking like piec teading this right now well i hope finasteride would give you trauma and make you hyper vigilant to not with me next time keep in mind if it don’t happen to you it could just mean you had a gabaminergic deficit or your life so

you adapted your the exeption not the rule



Lack of focus : mainly because of low dht and progesterone youll need for that to increase your dopamenergic signaling (supposing you have average serotonorgic signaling) but you can use something like wellbutrin ritalin low dose in the morning 2x per week

(Wellbutrin do have bad effects on cholinergic system but supposing your an average dude and get a lot of choline in your diet your probably fine)



Here a Choline stack if anyone is interested i already writed it down wayback in the thread fix your life as a teenager :

1. Acetylcholine

a.1g CDP choline 2x per day

b.20 mg Donepezil upon rising

c.300 mg alpha gpc in the morning

d.500 mg Uridine monophosphate in the morning

e.1000 mg piracetam (5x per week$

f.30 mg Noopept



So your gonna ask me what could you do well you can use a topical dut in the hairline or balding areas (but good luck sourcing that)

(Before you ragebait in the comments i already thought about blocking the androgen receptor with Ru but to much side effects especially knowing the information I’m gonna reveal later)



The biggest lie ever said about hairloss :

is that dht cause hairloss if dht cause its mainly becuase it caus low estrogen who is responsible for the hairloss (just look at the guys who took tamoxifen who get hairloss look at the guys who take masteron who get hairloss which if you didn’t know is less androgenic than test its because of its serm effects look at rad 140 who is literraly 0 androgenic and still result in hairloss don’t forget rad 140 was intended to cute breast cancer so its all about estrogens)



If anything Dht increase hair growth :

https://pmc.ncbi.nlm.nih.gov/articles/PMC6989660/



We have seen the effects of blocking DHT. It SLOWS hair loss and some get a MILD regrowth at best with all the sides and complex protocols you should apply to counter act those side effects



The problem with the hairloss comunity is they often overlook the basics like what about hypogonadol nigga who got hairloss they don’t have high dht yet they are bald

So lets get to it the main reasons of hairloss :

• Low estrogen as said earlier
• Bad lifestyle habits
• Poor nutrition
• Lack of exercise

Then we have the most important ones :

• Insulin resistance
• Stress
• The main contributing factor of hairloss and the most overloked one is hypoxia you can try it yourself put on a hat on your hair for 12 hours your gonna feel your haur thinning if you think im coping

So my Definitive hairloss stack that I’ll reccomend :



Topical supplements:
-Ketoconazole cream. 1 to 2 times a day, every day. If price or convenience is an issue, the minimum this should be applied is before bed to balding areas. Ketoconazole has been shown to be just as effective as minoxidil in studies with the shampoo. And even stronger the cream has been shown to produce results with an overnight application.

-Emu oil. 1-2 times a day. One of the only proven items I’ve come across that increases skin and hair DNA synthesis, with studies showing hair regrowth.

-Peppermint oil. 1-2 times a day. Peppermint oil has been shown in studies to be equivalent to minoxidil, without the negative side effects that result in premature aging of the skin.

-Evening Primrose oil or Borage oil. Both shown to cause hair regrowth in studies. Just adding a little more fat topically which is absorbed via the skin. Also useful for GLA’s effect on prostaglandins for halting inflammation, hair loss, and aiding hair regrowth.

-Spironolactone cream. Spironolactone has been shown to restore a 60 year old males hairline to his teenage years hair line that he had lost decades ago. Although we use this item topically, it still has the same benefits locally as it is used for such issues as hair loss and hirsutism topically. However topically it does not go systematic as in studies it has been applied to patients whole backs without going systematic. Spironolactone blocks the binding of androgens to the androgen receptor and helps increase estrogen locally.



-BiEstro cream. E2 and E3 combo, Estradiol and Estriol. Apply once or twice a day to balding areas.

The amount used here is enough to cover balding thinning areas. Due to the area we are applying it studies have shown no real systematic absorption. And also to the fact of the dose we are using is quite low as well. None of the users nor myself could produce an estrogenic side on this when applied to the scalp. Some of us who would normally get estrogenic sides off testosterone use as low as 200 mg.

(You can add bold for E1 if you wanna maximize but kinda pain in the ass cause you have to do bloods and make sure your E1 doesn’t lower your E2 and E3 basicaly you should keep them in harmony)



We have also seen what adding estrogen does for hair, as the byproduct of the thousands of male to female sex changes. These individuals can regrow full heads of amazing hair, bringing back hair reminiscent of that which they had when they were teenagers.

Likely, the ones seeing any bit of regrowth from DHT blockers are as a result of the mild estrogen increase triggered by these compounds. Studies of topical estrogen, plain and simple, work. In both men and women. As a bonus, adding estrogen topically doesn’t just increase estrogen -it also the localized concentration of the aromatase enzyme.

(I’ve saw myself dozens of people on reedit i swear i dont know why i couldnt find them having resuts if anyone has it please write it down below)

(For the studies i linked so many in the ashwaganda and no body gave a fuck

So because of that here are some studies on mice :

https://pubmed.ncbi.nlm.nih.gov/14962083/

https://www.researchgate.net/figure...e-tenth-day-after-hair-shaving_fig1_229083213





View attachment 3261225

Here is someone who got hair growth using estriol and estradiol cream



=End justification for BiEstro Cream==

Rub this mixture on once or twice a day depending on your available time. Once a day is totally fine, and optimal for most, if you can apply it before bed. If not, and you must do it in the day, pick a time where you can leave it on for at least 1-2 hours before showering it out.



Supplements:

Minerals might be needed if severely deficient, some doses are based off studies and you may not need these doses. You must find your own dose.

-Zinc Picolinate. 100-150mg a day for 6-8 weeks, tops.

This depends on a few factors. Add up your dietary zinc content that you typically average, and then decide if zinc might be low and determine the dose that you want. This has been noted in studies to completely reverse hair loss and hypothyroid conditions that are due to a zinc deficiency. NOTE: You may not need this, use discretion. Too much zinc can lead to other problems.

-Taurine. 2.5 grams, 2x a day.

In regards to hair loss, Taurine has been shown to help combat fibrosis of the scalp, thus

increasing circulation and hair growth.



Black Currant Oil, 3g a day.

This is utilized for its Gamma Linoleic Acid (GLA) content, which has anti-inflammatory properties, the ability to increase hair growth prostaglandins (PGE), and the ability to inhibit hair loss prostaglandins (PGD). These prostaglandins are another contributing factor to hair loss/growth aside from the androgens.

Three items have been shown to decrease GLA – wheat, dairy, and trans fats – through inhibition of an enzyme called D6D. The typical western diet is full of these foods. Inhibition of the D6D enzyme prevents the conversion of Linoleic Acid (LA) into GLA. The inhibition of D6D also happens with age, and is likely one of the key contributors to balding getting worse with age. This is just about the only process that can link balding to aging that has not already been explored.

In taking a GLA supplement, we bypass the enzymatic conversion entirely and have the end product.

Black Currant oil was also shown in animal studies to prevent many of the negatives of excessive fructose intake, such as fatty liver.



Grapeseed Extract, 500-1000mg a day.
GSE has been shown in animal studies to improve insulin resistance as much as metformin. Studies have also shown GSE to double the number of hairs in the anagen (growth) phase. As far as I am aware, no other compound has been shown to have effects this potent.

(Note : i do not advise to take metformin or berberine for other reasons i would write a thread about it in the near future)



Chromium gtf is used for combating insulin resistance, which is seen as a contributing factor for hair loss as mentioned above when talking about GSE. Again, some may not need this. Chromium GTF has been shown in case studies with type 2 diabetics to remove all exogenous insulin dependency within a couple months of use i recommend using 1000mcg a day for about 6 weeks



And you want to be eating or supplementing with those :

Magnesium

B vitamins

Vitamin K2

You also wanna be getting fats in your diet (especially from Mufas and Pufas (just make sure your not getting it from seed oils because its processed that a whole other topic id advise to get from seeds)



but I assure you, PUFA fats are NOT bad for you. Getting them from healthy sources has countless proven health benefits: anti-carcinogenic, anti-inflammatory, pro-sleep, pro-thyroid, etc. The benefits of unheated PUFA fats are a very deep topic on their own.

The epidermis of your skin is made of 60 percent Omega-6 PUFA fats. Do not fall for the “Omega-3 must be higher than Omega-6” speech that has no proven benefits and multiple proven detriments. All of the studies linking PUFA fats to health issues look at the typical use for PUFA fats in the western diet: cooking, frying, and otherwise heating the fats. If we are to take the same controlled environment but introduce raw, unheated PUFA fats from seeds and nuts, the studies flip completely. Anti-cancer, anti-inflammatory, and all-around health marker improvement is marked.



Another issue found often in the bodybuilding and fitness realm is the “eating too clean” phenomenon. If you were to add up chicken, rice, broccoli, and some olive oil on your favorite diet app, I can guarantee that you’d see that it’s a struggle to reach even 15 percent of RDA requirements for PUFA fats. When this happens, the skin goes dry and wrinkles appear, hair becomes straw like and falls out, etc. Digestive issues ensue, and metabolism slows down. As PUFA fats are shown to increase thyroid hormone sensitivity by almost 20 percent, dieting becomes harder and fat accrual in a calorie surplus becomes far easier. This isn’t even rectifiable with exogenous thyroid hormones – take all the thyroid drugs you want, if your sensitivity isn’t up to par your metabolism will suffer.

(Fun fact : Studies have also shown that when consumed in equal quantities, monounsaturated and saturated fats cause fat gain. Saturated fat was shown to cause a decrease in insulin sensitivity as well. PUFA fat, on the other hand, caused barely any fat gain. The majority of weight gained was muscle, insulin sensitivity increased, and abdominal fat thickness decreased.)



Other Foods.

Pineapple is used as a general health food with documented anti-inflammatory benefits, contains an enzyme papaya if i can recall that aids in the digestion of protein, is a fantastic source of vitamins, and is a preferred fruit due to the lower-end fructose content. In regards to hair regrowth, the main benefit is its anti-inflammatory property.



Massage/Mechanical Manipulation:

Vigorously massage, brush, or pinch your scalp in the balding areas. 1-2 times a day, for whatever time frame you can manage; the longer the better. 3-5 minutes is great, 10 minutes is better. Use as much pressure as possible. Tissue manipulation like this increases circulation and has been proven in studies to aid hair growth. To assist in blood flow further, you can bend over and point your head toward the ground, allowing gravity to assist in delivering blood to the target area.



You could also look in the More plates more plates micro needling stuff :



Sources :



[1] Stoner, E. (1990). The clinical development of a 5α-reductase inhibitor, finasteride. The Journal of steroid biochemistry and molecular biology, 37(3), 375-378.



[2] Vuichoud, C., & Loughlin, K. R. (2015). Benign prostatic hyperplasia: epidemiology, economics and evaluation. Can J Urol, 22(Suppl 1), 1-6.



[3] Adil, A., & Godwin, M. (2017). The effectiveness of treatments for androgenetic alopecia: a systematic review and meta-analysis. Journal of the American Academy of



141.



[4] Schumacher, M., Hussain, R., Gago, N., Oudinet, J. P., Mattern, C., & Ghoumari, A. (2012). Progesterone synthesis in the nervous system: implications for myelination and myelin repair. Frontiers in neuroscience, 6, 10.



[5] Skeldon, S. C., Macdonald, E. M., Law, M. R., Huang, A., Paterson, J. M., Mamdani, M. M., & Juurlink, D. (2017). The cardiovascular safety of dutasteride. The Journal of urology, 197(5), 1309-1314.



[6] Lee, H. J., & Chang, C. (2003). Recent advances in androgen receptor action. Cellular and Molecular Life Sciences CMLS, 60(8), 1613-1622.



[7] Bolton, E. C., So, A. Y., Chaivorapol, C., Haqq, C. M., Li, H., & Yamamoto, K. R. (2007). Cell-and gene-specific regulation of primary target genes by the androgen receptor. Genes & development, 21(16), 2005-2017.



[8] Winiarska, A., Mandt, N., Kamp, H., Hossini, A., Seltmann, H., Zouboulis, C. C., & Blume-Peytavi, U. (2006). Effect of 5α-dihydrotestosterone and testosterone on apoptosis in human dermal papilla cells. Skin pharmacology and physiology, 19(6), 311-321.



[9] Chhipa, R. R., Halim, D., Cheng, J., Zhang, H. Y., Mohler, J. L., Ip, C., & Wu, Y. (2013). The direct inhibitory effect of dutasteride or finasteride on androgen receptor activity is cell line specific. The Prostate, 73(14), 1483-1494.



[10] Mella, J. M., Perret, M. C., Manzotti, M., Catalano, H. N., & Guyatt, G. (2010). Efficacy and safety of finasteride therapy for androgenetic alopecia: a systematic review. Archives of dermatology, 146(10), 1141-1150.



[11] Di Loreto, C., La Marra, F., Mazzon, G., Belgrano, E., Trombetta, C., & Cauci, S. (2014). Immunohistochemical evaluation of androgen receptor and nerve structure density in human prepuce from patients with persistent sexual side effects after finasteride use for androgenetic alopecia. PLoS One, 9(6).



[12] Overstreet, J. W., Fuh, V. L., Gould, J., Howards, S. S., Lieber, M. M., Hellstrom, W., ... & LEWIS, R. (1999). Chronic treatment with finasteride daily does not affect spermatogenesis or semen production in young men. The Journal of urology, 162(4), 1295-1300.



[13] Samplaski, M. K., Lo, K., Grober, E., & Jarvi, K. (2013). Finasteride use in the male infertility population: effects on semen and hormone parameters. Fertility and sterility, 100(6), 1542-1546.



[14] Amory, J. K., Wang, C., Swerdloff, R. S., Anawalt, B. D., Matsumoto, A. M., Bremner, W. J., ... & Clark, R. V. (2007). The effect of 5α-reductase inhibition with dutasteride and finasteride on semen parameters and serum hormones in healthy men. The Journal of Clinical Endocrinology & Metabolism, 92(5), 1659-1665.



[15] Traish, A. M. (2020). Health Risks Associated with Long-Term Finasteride and Dutasteride Use: It's Time to Sound the Alarm. The World Journal of Men's Health, 38.



[16] Traish, A., Haider, K. S., Doros, G., & Haider, A. (2017). Long-term dutasteride therapy in men with benign prostatic hyperplasia alters glucose and lipid profiles and increases severity of erectile dysfunction. Hormone molecular biology and clinical investigation, 30(3).



[17] Doulabi, S. R. S. M., Kavoussi, H., Isapour, D., Hashemian, A., & Taheriniya, A. (2013). Effect of finasteride on lipid profile in individuals with androgenetic alopecia. African Journal of Pharmacy and Pharmacology, 7(6), 315-317.



[18] Duskova, M., Hill, M., & Starka, L. (2010). Changes of metabolic profile in men treated for androgenetic alopecia with 1 mg finasteride. Endocr Regul, 44(1), 3-8.



[19] Gild, P., Cole, A. P., Krasnova, A., Dickerman, B. A., von Landenberg, N., Sun, M., ... & Kibel, A. S. (2018). Liver disease in men undergoing androgen deprivation therapy for prostate cancer. The Journal of urology, 200(3), 573-581.



[20] Mendenhall, C. L. (1968). Anabolic steroid therapy as an adjunct to diet in alcoholic hepatic steatosis. The American journal of digestive diseases, 13(9), 783-791.



[21] Jacqueson, A., Thevenin, M., Warnet, J. M., Claude, J. R., & Truhaut, R. (1978). Comparative Study of the Protective Effect of an Anabolic Steroid. In Toxicological Aspects of Food Safety (pp. 193-196). Springer, Berlin, Heidelberg.



[22] Kelly, D. M., Nettleship, J. E., Akhtar, S., Muraleedharan, V., Sellers, D. J., Brooke, J. C., ... & Jones, T. H. (2014). Testosterone suppresses the expression of regulatory enzymes of fatty acid synthesis and protects against hepatic steatosis in cholesterol-fed androgen deficient mice. Life sciences, 109(2), 95-103.



[23] Lin, H. Y., Yu, I. C., Wang, R. S., Chen, Y. T., Liu, N. C., Altuwaijri, S., ... & Yeh, S. (2008). Increased hepatic steatosis and insulin resistance in mice lacking hepatic androgen receptor. Hepatology, 47(6), 1924-1935.



[24] Völzke, H., Aumann, N., Krebs, A., Nauck, M., Steveling, A., Lerch, M. M., ... & Wallaschofski, H. (2010). Hepatic steatosis is associated with low serum testosterone and high serum DHEAS levels in men. International journal of andrology, 33(1), 45-53.



[25] Velazquez, I., & Alter, B. P. (2004). Androgens and liver tumors: Fanconi's anemia and non‐Fanconi's conditions. American journal of hematology, 77(3), 257-267.



[26] Di Loreto, C., La Marra, F., Mazzon, G., Belgrano, E., Trombetta, C., & Cauci, S. (2014). Immunohistochemical evaluation of androgen receptor and nerve structure density in human prepuce from patients with persistent sexual side effects after finasteride use for androgenetic alopecia. PLoS One, 9(6).



[27] Hsieh, J. T., Chen, S. C., Yu, H. J., & Chang, H. C. (2011). Finasteride upregulates expression of androgen receptor in hyperplastic prostate and LNCaP cells: implications for chemoprevention of prostate cancer. The Prostate, 71(10), 1115-1121.



[28] Pinsky, M. R., Gur, S., Tracey, A. J., Harbin, A., & Hellstrom, W. J. (2011). The effects of chronic 5‐alpha‐reductase inhibitor (dutasteride) treatment on rat erectile function. The journal of sexual medicine, 8(11), 3066-3074.



[29] Iacono, F., Prezioso, D., Ruffo, A., Illiano, E., Romis, L., Di Lauro, G., ... & Amato, B. (2012). Testosterone deficiency causes penile fibrosis and organic erectile dysfunction in aging men. Evaluating association among Age. BMC surgery, 12(S1), S24.



[30] Zhang, M. G., Wang, X. J., Shen, Z. J., & Gao, P. J. (2013). Long-term oral administration of 5α-reductase inhibitor attenuates erectile function by inhibiting autophagy and promoting apoptosis of smooth muscle cells in corpus cavernosum of aged rats. Urology, 82(3), 743-e9.



[31] Melcangi, R. C., Caruso, D., Abbiati, F., Giatti, S., Calabrese, D., Piazza, F., & Cavaletti, G. (2013). Neuroactive steroid levels are modified in cerebrospinal fluid and plasma of post‐finasteride patients showing persistent sexual side effects and anxious/depressive symptomatology. The journal of sexual medicine, 10(10), 2598-2603.



sexual medicine, 10(10), 2598-2603.



[32] Alanazi, N. (2016). Assessing the quality of life and health outcomes of Androgenic Alopecia patients using Propecia (Doctoral dissertation, Rutgers University-School of Health Related Professions).



[33] Melcangi, R. C., Caruso, D., Abbiati, F., Giatti, S., Calabrese, D., Piazza, F., & Cavaletti, G. (2013). Neuroactive steroid levels are modified in cerebrospinal fluid and plasma of post‐finasteride patients showing persistent sexual side effects and anxious/depressive symptomatology. The journal of sexual medicine, 10(10), 2598-2603.



[34] Caruso, D., Abbiati, F., Giatti, S., Romano, S., Fusco, L., Cavaletti, G., & Melcangi, R. C. (2015). Patients treated for male pattern hair with finasteride show, after discontinuation of the drug, altered levels of neuroactive steroids in cerebrospinal fluid and plasma. The Journal of steroid biochemistry and molecular biology, 146, 74-79.



[35] Melcangi, R. C., Santi, D., Spezzano, R., Grimoldi, M., Tabacchi, T., Fusco, M. L., ... & Simoni, M. (2017). Neuroactive steroid levels and psychiatric and andrological features in post-finasteride patients. The Journal of steroid biochemistry and molecular biology, 171, 229-235.



[36] Martinez, P. E., Rubinow, D. R., Nieman, L. K., Koziol, D. E., Morrow, A. L., Schiller, C. E., ... & Schmidt, P. J. (2016). 5α-reductase inhibition prevents the luteal phase increase in plasma allopregnanolone levels and mitigates symptoms in women with premenstrual dysphoric disorder. Neuropsychopharmacology, 41(4), 1093.



[37] Basaria, S., Jasuja, R., Huang, G., Wharton, W., Pan, H., Pencina, K., ... & Labrie, F. (2016). Characteristics of men who report persistent sexual symptoms after finasteride use for hair loss. The Journal of Clinical Endocrinology & Metabolism, 101(12), 4669-4680.



[38] Van Praag, H., Schinder, A. F., Christie, B. R., Toni, N., Palmer, T. D., & Gage, F. H. (2002). Functional neurogenesis in the adult hippocampus. Nature, 415(6875), 1030-1034.



[39] Stockmeier, C. A., Mahajan, G. J., Konick, L. C., Overholser, J. C., Jurjus, G. J., Meltzer, H. Y., ... & Rajkowska, G. (2004). Cellular changes in the postmortem hippocampus in major depression. Biological psychiatry, 56(9), 640-650.



[40] Jacobs, B. L., Van Praag, H., & Gage, F. H. (2000). Adult brain neurogenesis and psychiatry: a novel theory of depression. Molecular psychiatry, 5(3), 262-269.



[41] Römer, B., Pfeiffer, N., Lewicka, S., Ben-Abdallah, N., Vogt, M. A., Deuschle, M., ... & Gass, P. (2010). Finasteride treatment inhibits adult hippocampal neurogenesis in male mice. Pharmacopsychiatry, 43(05), 174-178.



[42] Samuels, B. A., & Hen, R. (2011). Neurogenesis and affective disorders. European Journal of Neuroscience, 33(6), 1152-1159.



[43] Romeo, E., Ströhle, A., Spalletta, G., Michele, F. D., Hermann, B., Holsboer, F., ... & Rupprecht, R. (1998). Effects of antidepressant treatment on neuroactive steroids in major depression. American Journal of Psychiatry, 155(7), 910-913.



[44] Uzunova, V., Sampson, L., & Uzunov, D. P. (2006). Relevance of endogenous 3α-reduced neurosteroids to depression and antidepressant action. Psychopharmacology, 186(3), 351-361.



[45] Uzunova, V., Sheline, Y., Davis, J. M., Rasmusson, A., Uzunov, D. P., Costa, E., & Guidotti, A. (1998). Increase in the cerebrospinal fluid content of neurosteroids in patients with unipolar major depression who are receiving fluoxetine or fluvoxamine. Proceedings of the National Academy of Sciences, 95(6), 3239-3244.



[46] Schüle, C., Nothdurfter, C., & Rupprecht, R. (2014). The role of allopregnanolone in depression and anxiety. Progress in neurobiology, 113, 79-87.



[47] Rasmusson, A. M., Pinna, G., Paliwal, P., Weisman, D., Gottschalk, C., Charney, D., ... & Guidotti, A. (2006). Decreased cerebrospinal fluid allopregnanolone levels in women with posttraumatic stress disorder. Biological psychiatry, 60(7), 704-713.



[48] Hellgren, C., Åkerud, H., Skalkidou, A., Bäckström, T., & Sundström-Poromaa, I. (2014). Low serum allopregnanolone is associated with symptoms of depression in late pregnancy. Neuropsychobiology, 69(3), 147-153.



[49] Schüle, C., Nothdurfter, C., & Rupprecht, R. (2014). The role of allopregnanolone in depression and anxiety. Progress in neurobiology, 113, 79-87.



[50] Murphy, B. P., Abbott, F. V., Allison, C. M., Watts, C., & Ghadirian, A. M. (2004). Elevated levels of some neuroactive progesterone metabolites, particularly isopregnanolone, in women with chronic fatigue syndrome. Psychoneuroendocrinology, 29(2), 245-268.



[51] Uzunova, V., Sheline, Y., Davis, J. M., Rasmusson, A., Uzunov, D. P., Costa, E., & Guidotti, A. (1998). Increase in the cerebrospinal fluid content of neurosteroids in patients with unipolar major depression who are receiving fluoxetine or fluvoxamine. Proceedings of the National Academy of Sciences, 95(6), 3239-3244.



[52] Romeo, E., Ströhle, A., Spalletta, G., Michele, F. D., Hermann, B., Holsboer, F., ... & Rupprecht, R. (1998). Effects of antidepressant treatment on neuroactive steroids in major depression. American Journal of Psychiatry, 155(7), 910-913.



[53] Li, L., Kang, Y. X., Ji, X. M., Li, Y. K., Li, S. C., Zhang, X. J., ... & Shi, G. M. (2018). Finasteride inhibited brain dopaminergic system and open‐field behaviors in adolescent male rats. CNS neuroscience & therapeutics, 24(2), 115-125.



[54] Litim, N., Bourque, M., Al Sweidi, S., Morissette, M., & Di Paolo, T. (2015). The 5α-reductase inhibitor Dutasteride but not Finasteride protects dopamine neurons in the MPTP mouse model of Parkinson's disease. Neuropharmacology, 97, 86-94.



[55] Dazzi, L., Serra, M., Seu, E., Cherchi, G., Pisu, M. G., Purdy, R. H., & Biggio, G. (2002). Progesterone enhances ethanol‐induced modulation of mesocortical dopamine neurons: antagonism by finasteride. Journal of neurochemistry, 83(5), 1103-1109



(Keep in mind i put a big emphazize on finasteride mainly because piec was promoting it)

Tags : @Clavicular
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Interesting thread (I mostly read everything)

I need to do more research on anti balding before giving a good reply to this

 

[Deleted member 77820]

Why Finasteride (or dut) is a fraud :



So debunking the claim is finasteride dangerous for you yes or no

their are some people who get the following effects from just microdosing fin :

• sexual dysfunction
• Anhedonia
• Depression
• Anxiety
• Lack of motivation
• Lack of focus

While other seems fine using it

Soooo It depends on your neural phenotypes

Some things like childhood trauma has a lot of gaba menergic signaling adrenaline cortisol levels ect….

And also different architectures of the brain (I might write a thread about it its really interesting how you can just look at someone genes pool and know if he has adhd bi polar ect….. if this thread anhilate the fraud that is piec i sure would write about it)

Now lets starts on why finasteride cause all of this sides :

When you use and 5ar inhibitor your not just inhibiting dht but also progesterone and alopregnolone and if you neealycompletely inhibit the enzyme (which you probably will cause most of the 5ar is type 1 and don’t get me started on dut that shit blocks everything) or nearly you have no progesterone and alopregonolone function in your body so back then i thought well you can just take progestene just to come to the conclusion its gonna do nothing for cause you totaly inhibited thw enzyme.

Suggestion : (keep in mind this is not the best approach I’m gonna get to the nest approach later but its still better than the fraud that is piec feel free to insult his ass in the comments)



Now lets talk about the sides :

Remember about the sides i talked about earlier it was due to allo pregnolone who acts as a innate benzo in your system (so basicaly the main inhibotory gaba system in your brain is the gabaergic system related to the hormone you name it “gaba” it has 2 receptors Gaba B fair enough it can be agonized with just phenibut so no need first allopregnolone its not in the sort of communication in the brain anyway (which mean less signaling)

then We have Gaba A

The only critical receptor and guess what the Gaba A receptor is modulated by allopregnolone which if you remember correctly you blocked earlier sp how do i explain it basicaly its like you took a reverse xanax so the average nigga is gonna have anhedonia exept of he is an outlier so now your fucking dependent on benzos who are super dangerous if you don’t wanna feel like shit

(Then some smart ass in the comment gonna write well then why dont you take alopregnolone well it has very short half life and it can’t be stored or kept so unless you want to be taking ng of allopregnolone every 5 minutes you should either feel like shit like that evil piec want you to be or be addicted to benzos for progesterone you can just take transdermal or micronuzed progesterone just make sure to be on hormones cause your at high risk of hypogonadism if you mess up your dosages)



(Also their are other alternatives so 1) way to get allopregnolone which in theory would work not sure 100% is your gonna take your progesterone and agnozed the tsp receptor you’ll end up with more neuro steroidgenisis so you have more alopregnolone just make sure to not get addicted to that shit might write a thread about how to never get addicted to compounds and how to get rid off any addiction but for that ill need you to support me and all insult piec parents for not putting on a rubber that sad night

Getting back to what i was saying their some research that seem mehh like ettyfoxine but that shit is too risky in my opinion

2) alternative is basicaly fuck modulating gaba receptors you just take sodium valproate kt basicaly make your brain a sink of gaba kinda like piec asshole after getting fucked by every dermatologist prescribing him fin

And its a hdac inhibitor so it have epigenetic change keep in mind that shit aint salt that a epilepsy drug and they are reliable 100% cause nigga imagine an epileptic go through withdrawal his gonna fucking die like piec pride after i finish writing this thread)

So to summarize a little :

Erectil dysfunction: is caused by low progesterone abdominal low dht

Anhedhonia : is cause by low alopregnolone levels

Anxiety : is caused because the amygdila have gaba receptors which when inhibited cause the amygdala to start tweaking like piec teading this right now well i hope finasteride would give you trauma and make you hyper vigilant to not with me next time keep in mind if it don’t happen to you it could just mean you had a gabaminergic deficit or your life so

you adapted your the exeption not the rule



Lack of focus : mainly because of low dht and progesterone youll need for that to increase your dopamenergic signaling (supposing you have average serotonorgic signaling) but you can use something like wellbutrin ritalin low dose in the morning 2x per week

(Wellbutrin do have bad effects on cholinergic system but supposing your an average dude and get a lot of choline in your diet your probably fine)



Here a Choline stack if anyone is interested i already writed it down wayback in the thread fix your life as a teenager :

1. Acetylcholine

a.1g CDP choline 2x per day

b.20 mg Donepezil upon rising

c.300 mg alpha gpc in the morning

d.500 mg Uridine monophosphate in the morning

e.1000 mg piracetam (5x per week$

f.30 mg Noopept



So your gonna ask me what could you do well you can use a topical dut in the hairline or balding areas (but good luck sourcing that)

(Before you ragebait in the comments i already thought about blocking the androgen receptor with Ru but to much side effects especially knowing the information I’m gonna reveal later)



The biggest lie ever said about hairloss :

is that dht cause hairloss if dht cause its mainly becuase it caus low estrogen who is responsible for the hairloss (just look at the guys who took tamoxifen who get hairloss look at the guys who take masteron who get hairloss which if you didn’t know is less androgenic than test its because of its serm effects look at rad 140 who is literraly 0 androgenic and still result in hairloss don’t forget rad 140 was intended to cute breast cancer so its all about estrogens)



If anything Dht increase hair growth :

https://pmc.ncbi.nlm.nih.gov/articles/PMC6989660/



We have seen the effects of blocking DHT. It SLOWS hair loss and some get a MILD regrowth at best with all the sides and complex protocols you should apply to counter act those side effects



The problem with the hairloss comunity is they often overlook the basics like what about hypogonadol nigga who got hairloss they don’t have high dht yet they are bald

So lets get to it the main reasons of hairloss :

• Low estrogen as said earlier
• Bad lifestyle habits
• Poor nutrition
• Lack of exercise

Then we have the most important ones :

• Insulin resistance
• Stress
• The main contributing factor of hairloss and the most overloked one is hypoxia you can try it yourself put on a hat on your hair for 12 hours your gonna feel your haur thinning if you think im coping

So my Definitive hairloss stack that I’ll reccomend :



Topical supplements:
-Ketoconazole cream. 1 to 2 times a day, every day. If price or convenience is an issue, the minimum this should be applied is before bed to balding areas. Ketoconazole has been shown to be just as effective as minoxidil in studies with the shampoo. And even stronger the cream has been shown to produce results with an overnight application.

-Emu oil. 1-2 times a day. One of the only proven items I’ve come across that increases skin and hair DNA synthesis, with studies showing hair regrowth.

-Peppermint oil. 1-2 times a day. Peppermint oil has been shown in studies to be equivalent to minoxidil, without the negative side effects that result in premature aging of the skin.

-Evening Primrose oil or Borage oil. Both shown to cause hair regrowth in studies. Just adding a little more fat topically which is absorbed via the skin. Also useful for GLA’s effect on prostaglandins for halting inflammation, hair loss, and aiding hair regrowth.

-Spironolactone cream. Spironolactone has been shown to restore a 60 year old males hairline to his teenage years hair line that he had lost decades ago. Although we use this item topically, it still has the same benefits locally as it is used for such issues as hair loss and hirsutism topically. However topically it does not go systematic as in studies it has been applied to patients whole backs without going systematic. Spironolactone blocks the binding of androgens to the androgen receptor and helps increase estrogen locally.



-BiEstro cream. E2 and E3 combo, Estradiol and Estriol. Apply once or twice a day to balding areas.

The amount used here is enough to cover balding thinning areas. Due to the area we are applying it studies have shown no real systematic absorption. And also to the fact of the dose we are using is quite low as well. None of the users nor myself could produce an estrogenic side on this when applied to the scalp. Some of us who would normally get estrogenic sides off testosterone use as low as 200 mg.

(You can add bold for E1 if you wanna maximize but kinda pain in the ass cause you have to do bloods and make sure your E1 doesn’t lower your E2 and E3 basicaly you should keep them in harmony)



We have also seen what adding estrogen does for hair, as the byproduct of the thousands of male to female sex changes. These individuals can regrow full heads of amazing hair, bringing back hair reminiscent of that which they had when they were teenagers.

Likely, the ones seeing any bit of regrowth from DHT blockers are as a result of the mild estrogen increase triggered by these compounds. Studies of topical estrogen, plain and simple, work. In both men and women. As a bonus, adding estrogen topically doesn’t just increase estrogen -it also the localized concentration of the aromatase enzyme.

(I’ve saw myself dozens of people on reedit i swear i dont know why i couldnt find them having resuts if anyone has it please write it down below)

(For the studies i linked so many in the ashwaganda and no body gave a fuck

So because of that here are some studies on mice :

https://pubmed.ncbi.nlm.nih.gov/14962083/

https://www.researchgate.net/figure...e-tenth-day-after-hair-shaving_fig1_229083213





View attachment 3261225

Here is someone who got hair growth using estriol and estradiol cream



=End justification for BiEstro Cream==

Rub this mixture on once or twice a day depending on your available time. Once a day is totally fine, and optimal for most, if you can apply it before bed. If not, and you must do it in the day, pick a time where you can leave it on for at least 1-2 hours before showering it out.



Supplements:

Minerals might be needed if severely deficient, some doses are based off studies and you may not need these doses. You must find your own dose.

-Zinc Picolinate. 100-150mg a day for 6-8 weeks, tops.

This depends on a few factors. Add up your dietary zinc content that you typically average, and then decide if zinc might be low and determine the dose that you want. This has been noted in studies to completely reverse hair loss and hypothyroid conditions that are due to a zinc deficiency. NOTE: You may not need this, use discretion. Too much zinc can lead to other problems.

-Taurine. 2.5 grams, 2x a day.

In regards to hair loss, Taurine has been shown to help combat fibrosis of the scalp, thus

increasing circulation and hair growth.



Black Currant Oil, 3g a day.

This is utilized for its Gamma Linoleic Acid (GLA) content, which has anti-inflammatory properties, the ability to increase hair growth prostaglandins (PGE), and the ability to inhibit hair loss prostaglandins (PGD). These prostaglandins are another contributing factor to hair loss/growth aside from the androgens.

Three items have been shown to decrease GLA – wheat, dairy, and trans fats – through inhibition of an enzyme called D6D. The typical western diet is full of these foods. Inhibition of the D6D enzyme prevents the conversion of Linoleic Acid (LA) into GLA. The inhibition of D6D also happens with age, and is likely one of the key contributors to balding getting worse with age. This is just about the only process that can link balding to aging that has not already been explored.

In taking a GLA supplement, we bypass the enzymatic conversion entirely and have the end product.

Black Currant oil was also shown in animal studies to prevent many of the negatives of excessive fructose intake, such as fatty liver.



Grapeseed Extract, 500-1000mg a day.
GSE has been shown in animal studies to improve insulin resistance as much as metformin. Studies have also shown GSE to double the number of hairs in the anagen (growth) phase. As far as I am aware, no other compound has been shown to have effects this potent.

(Note : i do not advise to take metformin or berberine for other reasons i would write a thread about it in the near future)



Chromium gtf is used for combating insulin resistance, which is seen as a contributing factor for hair loss as mentioned above when talking about GSE. Again, some may not need this. Chromium GTF has been shown in case studies with type 2 diabetics to remove all exogenous insulin dependency within a couple months of use i recommend using 1000mcg a day for about 6 weeks



And you want to be eating or supplementing with those :

Magnesium

B vitamins

Vitamin K2

You also wanna be getting fats in your diet (especially from Mufas and Pufas (just make sure your not getting it from seed oils because its processed that a whole other topic id advise to get from seeds)



but I assure you, PUFA fats are NOT bad for you. Getting them from healthy sources has countless proven health benefits: anti-carcinogenic, anti-inflammatory, pro-sleep, pro-thyroid, etc. The benefits of unheated PUFA fats are a very deep topic on their own.

The epidermis of your skin is made of 60 percent Omega-6 PUFA fats. Do not fall for the “Omega-3 must be higher than Omega-6” speech that has no proven benefits and multiple proven detriments. All of the studies linking PUFA fats to health issues look at the typical use for PUFA fats in the western diet: cooking, frying, and otherwise heating the fats. If we are to take the same controlled environment but introduce raw, unheated PUFA fats from seeds and nuts, the studies flip completely. Anti-cancer, anti-inflammatory, and all-around health marker improvement is marked.



Another issue found often in the bodybuilding and fitness realm is the “eating too clean” phenomenon. If you were to add up chicken, rice, broccoli, and some olive oil on your favorite diet app, I can guarantee that you’d see that it’s a struggle to reach even 15 percent of RDA requirements for PUFA fats. When this happens, the skin goes dry and wrinkles appear, hair becomes straw like and falls out, etc. Digestive issues ensue, and metabolism slows down. As PUFA fats are shown to increase thyroid hormone sensitivity by almost 20 percent, dieting becomes harder and fat accrual in a calorie surplus becomes far easier. This isn’t even rectifiable with exogenous thyroid hormones – take all the thyroid drugs you want, if your sensitivity isn’t up to par your metabolism will suffer.

(Fun fact : Studies have also shown that when consumed in equal quantities, monounsaturated and saturated fats cause fat gain. Saturated fat was shown to cause a decrease in insulin sensitivity as well. PUFA fat, on the other hand, caused barely any fat gain. The majority of weight gained was muscle, insulin sensitivity increased, and abdominal fat thickness decreased.)



Other Foods.

Pineapple is used as a general health food with documented anti-inflammatory benefits, contains an enzyme papaya if i can recall that aids in the digestion of protein, is a fantastic source of vitamins, and is a preferred fruit due to the lower-end fructose content. In regards to hair regrowth, the main benefit is its anti-inflammatory property.



Massage/Mechanical Manipulation:

Vigorously massage, brush, or pinch your scalp in the balding areas. 1-2 times a day, for whatever time frame you can manage; the longer the better. 3-5 minutes is great, 10 minutes is better. Use as much pressure as possible. Tissue manipulation like this increases circulation and has been proven in studies to aid hair growth. To assist in blood flow further, you can bend over and point your head toward the ground, allowing gravity to assist in delivering blood to the target area.



You could also look in the More plates more plates micro needling stuff :



Sources :



[1] Stoner, E. (1990). The clinical development of a 5α-reductase inhibitor, finasteride. The Journal of steroid biochemistry and molecular biology, 37(3), 375-378.



[2] Vuichoud, C., & Loughlin, K. R. (2015). Benign prostatic hyperplasia: epidemiology, economics and evaluation. Can J Urol, 22(Suppl 1), 1-6.



[3] Adil, A., & Godwin, M. (2017). The effectiveness of treatments for androgenetic alopecia: a systematic review and meta-analysis. Journal of the American Academy of



141.



[4] Schumacher, M., Hussain, R., Gago, N., Oudinet, J. P., Mattern, C., & Ghoumari, A. (2012). Progesterone synthesis in the nervous system: implications for myelination and myelin repair. Frontiers in neuroscience, 6, 10.



[5] Skeldon, S. C., Macdonald, E. M., Law, M. R., Huang, A., Paterson, J. M., Mamdani, M. M., & Juurlink, D. (2017). The cardiovascular safety of dutasteride. The Journal of urology, 197(5), 1309-1314.



[6] Lee, H. J., & Chang, C. (2003). Recent advances in androgen receptor action. Cellular and Molecular Life Sciences CMLS, 60(8), 1613-1622.



[7] Bolton, E. C., So, A. Y., Chaivorapol, C., Haqq, C. M., Li, H., & Yamamoto, K. R. (2007). Cell-and gene-specific regulation of primary target genes by the androgen receptor. Genes & development, 21(16), 2005-2017.



[8] Winiarska, A., Mandt, N., Kamp, H., Hossini, A., Seltmann, H., Zouboulis, C. C., & Blume-Peytavi, U. (2006). Effect of 5α-dihydrotestosterone and testosterone on apoptosis in human dermal papilla cells. Skin pharmacology and physiology, 19(6), 311-321.



[9] Chhipa, R. R., Halim, D., Cheng, J., Zhang, H. Y., Mohler, J. L., Ip, C., & Wu, Y. (2013). The direct inhibitory effect of dutasteride or finasteride on androgen receptor activity is cell line specific. The Prostate, 73(14), 1483-1494.



[10] Mella, J. M., Perret, M. C., Manzotti, M., Catalano, H. N., & Guyatt, G. (2010). Efficacy and safety of finasteride therapy for androgenetic alopecia: a systematic review. Archives of dermatology, 146(10), 1141-1150.



[11] Di Loreto, C., La Marra, F., Mazzon, G., Belgrano, E., Trombetta, C., & Cauci, S. (2014). Immunohistochemical evaluation of androgen receptor and nerve structure density in human prepuce from patients with persistent sexual side effects after finasteride use for androgenetic alopecia. PLoS One, 9(6).



[12] Overstreet, J. W., Fuh, V. L., Gould, J., Howards, S. S., Lieber, M. M., Hellstrom, W., ... & LEWIS, R. (1999). Chronic treatment with finasteride daily does not affect spermatogenesis or semen production in young men. The Journal of urology, 162(4), 1295-1300.



[13] Samplaski, M. K., Lo, K., Grober, E., & Jarvi, K. (2013). Finasteride use in the male infertility population: effects on semen and hormone parameters. Fertility and sterility, 100(6), 1542-1546.



[14] Amory, J. K., Wang, C., Swerdloff, R. S., Anawalt, B. D., Matsumoto, A. M., Bremner, W. J., ... & Clark, R. V. (2007). The effect of 5α-reductase inhibition with dutasteride and finasteride on semen parameters and serum hormones in healthy men. The Journal of Clinical Endocrinology & Metabolism, 92(5), 1659-1665.



[15] Traish, A. M. (2020). Health Risks Associated with Long-Term Finasteride and Dutasteride Use: It's Time to Sound the Alarm. The World Journal of Men's Health, 38.



[16] Traish, A., Haider, K. S., Doros, G., & Haider, A. (2017). Long-term dutasteride therapy in men with benign prostatic hyperplasia alters glucose and lipid profiles and increases severity of erectile dysfunction. Hormone molecular biology and clinical investigation, 30(3).



[17] Doulabi, S. R. S. M., Kavoussi, H., Isapour, D., Hashemian, A., & Taheriniya, A. (2013). Effect of finasteride on lipid profile in individuals with androgenetic alopecia. African Journal of Pharmacy and Pharmacology, 7(6), 315-317.



[18] Duskova, M., Hill, M., & Starka, L. (2010). Changes of metabolic profile in men treated for androgenetic alopecia with 1 mg finasteride. Endocr Regul, 44(1), 3-8.



[19] Gild, P., Cole, A. P., Krasnova, A., Dickerman, B. A., von Landenberg, N., Sun, M., ... & Kibel, A. S. (2018). Liver disease in men undergoing androgen deprivation therapy for prostate cancer. The Journal of urology, 200(3), 573-581.



[20] Mendenhall, C. L. (1968). Anabolic steroid therapy as an adjunct to diet in alcoholic hepatic steatosis. The American journal of digestive diseases, 13(9), 783-791.



[21] Jacqueson, A., Thevenin, M., Warnet, J. M., Claude, J. R., & Truhaut, R. (1978). Comparative Study of the Protective Effect of an Anabolic Steroid. In Toxicological Aspects of Food Safety (pp. 193-196). Springer, Berlin, Heidelberg.



[22] Kelly, D. M., Nettleship, J. E., Akhtar, S., Muraleedharan, V., Sellers, D. J., Brooke, J. C., ... & Jones, T. H. (2014). Testosterone suppresses the expression of regulatory enzymes of fatty acid synthesis and protects against hepatic steatosis in cholesterol-fed androgen deficient mice. Life sciences, 109(2), 95-103.



[23] Lin, H. Y., Yu, I. C., Wang, R. S., Chen, Y. T., Liu, N. C., Altuwaijri, S., ... & Yeh, S. (2008). Increased hepatic steatosis and insulin resistance in mice lacking hepatic androgen receptor. Hepatology, 47(6), 1924-1935.



[24] Völzke, H., Aumann, N., Krebs, A., Nauck, M., Steveling, A., Lerch, M. M., ... & Wallaschofski, H. (2010). Hepatic steatosis is associated with low serum testosterone and high serum DHEAS levels in men. International journal of andrology, 33(1), 45-53.



[25] Velazquez, I., & Alter, B. P. (2004). Androgens and liver tumors: Fanconi's anemia and non‐Fanconi's conditions. American journal of hematology, 77(3), 257-267.



[26] Di Loreto, C., La Marra, F., Mazzon, G., Belgrano, E., Trombetta, C., & Cauci, S. (2014). Immunohistochemical evaluation of androgen receptor and nerve structure density in human prepuce from patients with persistent sexual side effects after finasteride use for androgenetic alopecia. PLoS One, 9(6).



[27] Hsieh, J. T., Chen, S. C., Yu, H. J., & Chang, H. C. (2011). Finasteride upregulates expression of androgen receptor in hyperplastic prostate and LNCaP cells: implications for chemoprevention of prostate cancer. The Prostate, 71(10), 1115-1121.



[28] Pinsky, M. R., Gur, S., Tracey, A. J., Harbin, A., & Hellstrom, W. J. (2011). The effects of chronic 5‐alpha‐reductase inhibitor (dutasteride) treatment on rat erectile function. The journal of sexual medicine, 8(11), 3066-3074.



[29] Iacono, F., Prezioso, D., Ruffo, A., Illiano, E., Romis, L., Di Lauro, G., ... & Amato, B. (2012). Testosterone deficiency causes penile fibrosis and organic erectile dysfunction in aging men. Evaluating association among Age. BMC surgery, 12(S1), S24.



[30] Zhang, M. G., Wang, X. J., Shen, Z. J., & Gao, P. J. (2013). Long-term oral administration of 5α-reductase inhibitor attenuates erectile function by inhibiting autophagy and promoting apoptosis of smooth muscle cells in corpus cavernosum of aged rats. Urology, 82(3), 743-e9.



[31] Melcangi, R. C., Caruso, D., Abbiati, F., Giatti, S., Calabrese, D., Piazza, F., & Cavaletti, G. (2013). Neuroactive steroid levels are modified in cerebrospinal fluid and plasma of post‐finasteride patients showing persistent sexual side effects and anxious/depressive symptomatology. The journal of sexual medicine, 10(10), 2598-2603.



sexual medicine, 10(10), 2598-2603.



[32] Alanazi, N. (2016). Assessing the quality of life and health outcomes of Androgenic Alopecia patients using Propecia (Doctoral dissertation, Rutgers University-School of Health Related Professions).



[33] Melcangi, R. C., Caruso, D., Abbiati, F., Giatti, S., Calabrese, D., Piazza, F., & Cavaletti, G. (2013). Neuroactive steroid levels are modified in cerebrospinal fluid and plasma of post‐finasteride patients showing persistent sexual side effects and anxious/depressive symptomatology. The journal of sexual medicine, 10(10), 2598-2603.



[34] Caruso, D., Abbiati, F., Giatti, S., Romano, S., Fusco, L., Cavaletti, G., & Melcangi, R. C. (2015). Patients treated for male pattern hair with finasteride show, after discontinuation of the drug, altered levels of neuroactive steroids in cerebrospinal fluid and plasma. The Journal of steroid biochemistry and molecular biology, 146, 74-79.



[35] Melcangi, R. C., Santi, D., Spezzano, R., Grimoldi, M., Tabacchi, T., Fusco, M. L., ... & Simoni, M. (2017). Neuroactive steroid levels and psychiatric and andrological features in post-finasteride patients. The Journal of steroid biochemistry and molecular biology, 171, 229-235.



[36] Martinez, P. E., Rubinow, D. R., Nieman, L. K., Koziol, D. E., Morrow, A. L., Schiller, C. E., ... & Schmidt, P. J. (2016). 5α-reductase inhibition prevents the luteal phase increase in plasma allopregnanolone levels and mitigates symptoms in women with premenstrual dysphoric disorder. Neuropsychopharmacology, 41(4), 1093.



[37] Basaria, S., Jasuja, R., Huang, G., Wharton, W., Pan, H., Pencina, K., ... & Labrie, F. (2016). Characteristics of men who report persistent sexual symptoms after finasteride use for hair loss. The Journal of Clinical Endocrinology & Metabolism, 101(12), 4669-4680.



[38] Van Praag, H., Schinder, A. F., Christie, B. R., Toni, N., Palmer, T. D., & Gage, F. H. (2002). Functional neurogenesis in the adult hippocampus. Nature, 415(6875), 1030-1034.



[39] Stockmeier, C. A., Mahajan, G. J., Konick, L. C., Overholser, J. C., Jurjus, G. J., Meltzer, H. Y., ... & Rajkowska, G. (2004). Cellular changes in the postmortem hippocampus in major depression. Biological psychiatry, 56(9), 640-650.



[40] Jacobs, B. L., Van Praag, H., & Gage, F. H. (2000). Adult brain neurogenesis and psychiatry: a novel theory of depression. Molecular psychiatry, 5(3), 262-269.



[41] Römer, B., Pfeiffer, N., Lewicka, S., Ben-Abdallah, N., Vogt, M. A., Deuschle, M., ... & Gass, P. (2010). Finasteride treatment inhibits adult hippocampal neurogenesis in male mice. Pharmacopsychiatry, 43(05), 174-178.



[42] Samuels, B. A., & Hen, R. (2011). Neurogenesis and affective disorders. European Journal of Neuroscience, 33(6), 1152-1159.



[43] Romeo, E., Ströhle, A., Spalletta, G., Michele, F. D., Hermann, B., Holsboer, F., ... & Rupprecht, R. (1998). Effects of antidepressant treatment on neuroactive steroids in major depression. American Journal of Psychiatry, 155(7), 910-913.



[44] Uzunova, V., Sampson, L., & Uzunov, D. P. (2006). Relevance of endogenous 3α-reduced neurosteroids to depression and antidepressant action. Psychopharmacology, 186(3), 351-361.



[45] Uzunova, V., Sheline, Y., Davis, J. M., Rasmusson, A., Uzunov, D. P., Costa, E., & Guidotti, A. (1998). Increase in the cerebrospinal fluid content of neurosteroids in patients with unipolar major depression who are receiving fluoxetine or fluvoxamine. Proceedings of the National Academy of Sciences, 95(6), 3239-3244.



[46] Schüle, C., Nothdurfter, C., & Rupprecht, R. (2014). The role of allopregnanolone in depression and anxiety. Progress in neurobiology, 113, 79-87.



[47] Rasmusson, A. M., Pinna, G., Paliwal, P., Weisman, D., Gottschalk, C., Charney, D., ... & Guidotti, A. (2006). Decreased cerebrospinal fluid allopregnanolone levels in women with posttraumatic stress disorder. Biological psychiatry, 60(7), 704-713.



[48] Hellgren, C., Åkerud, H., Skalkidou, A., Bäckström, T., & Sundström-Poromaa, I. (2014). Low serum allopregnanolone is associated with symptoms of depression in late pregnancy. Neuropsychobiology, 69(3), 147-153.



[49] Schüle, C., Nothdurfter, C., & Rupprecht, R. (2014). The role of allopregnanolone in depression and anxiety. Progress in neurobiology, 113, 79-87.



[50] Murphy, B. P., Abbott, F. V., Allison, C. M., Watts, C., & Ghadirian, A. M. (2004). Elevated levels of some neuroactive progesterone metabolites, particularly isopregnanolone, in women with chronic fatigue syndrome. Psychoneuroendocrinology, 29(2), 245-268.



[51] Uzunova, V., Sheline, Y., Davis, J. M., Rasmusson, A., Uzunov, D. P., Costa, E., & Guidotti, A. (1998). Increase in the cerebrospinal fluid content of neurosteroids in patients with unipolar major depression who are receiving fluoxetine or fluvoxamine. Proceedings of the National Academy of Sciences, 95(6), 3239-3244.



[52] Romeo, E., Ströhle, A., Spalletta, G., Michele, F. D., Hermann, B., Holsboer, F., ... & Rupprecht, R. (1998). Effects of antidepressant treatment on neuroactive steroids in major depression. American Journal of Psychiatry, 155(7), 910-913.



[53] Li, L., Kang, Y. X., Ji, X. M., Li, Y. K., Li, S. C., Zhang, X. J., ... & Shi, G. M. (2018). Finasteride inhibited brain dopaminergic system and open‐field behaviors in adolescent male rats. CNS neuroscience & therapeutics, 24(2), 115-125.



[54] Litim, N., Bourque, M., Al Sweidi, S., Morissette, M., & Di Paolo, T. (2015). The 5α-reductase inhibitor Dutasteride but not Finasteride protects dopamine neurons in the MPTP mouse model of Parkinson's disease. Neuropharmacology, 97, 86-94.



[55] Dazzi, L., Serra, M., Seu, E., Cherchi, G., Pisu, M. G., Purdy, R. H., & Biggio, G. (2002). Progesterone enhances ethanol‐induced modulation of mesocortical dopamine neurons: antagonism by finasteride. Journal of neurochemistry, 83(5), 1103-1109



(Keep in mind i put a big emphazize on finasteride mainly because piec was promoting it)

Tags : @Clavicular
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[It'snotover]

that is the most retarded shit i have ever seen in my life

Imagine these kids thinking they know more than 3 decades of hair loss studies and research

 

[Deleted member 77820]

Imagine these kids thinking they know more than 3 decades of hair loss studies and research

What research did you even read the scientific literature ???

Its not because smth is working thay mean is optimal
Its not because working security make you win money that mean its the best job ever

Heck i could find you a study of basically any fckn fat applied to the scalp would lead to enhanced hair growth and yall nigga send me a study of oww look 5mg fi tesulted in hairgrowth

It not because your watched youtube videos that mean that your knowledgeable enough to actually critique people with no evidence to back your claim

Wanna debate write a thread im waiting for you lets see what that big brain of yours is capable of doing

 

[It'snotover]

Wanna debate write a thread im waiting for you lets see what that big brain of yours is capable of doing

Pretty useless for a water is wet topic like this but it's pretty clear that hairloss is caused by individual dht sensitivity of the hair follicles, you are right that many men that are balding don't have high dht levels but this is not important since all that matter is the follicles sensitivity to the trash hormone, some men can have the dht of a foid and still norwood hard because of shit genes. Peppermint, rosemary oil and zinc might help but only if you fix the androgenic cause of your hair loss, otherwise the reaper will continue doing its job. The fact that men that lack 5AR conversion never go bald tell us everything we need to know.

 

[Deleted member 77820]

Pretty useless for a water is wet topic like this but it's pretty clear that hairloss is caused by individual dht sensitivity of the hair follicles, you are right that many men that are balding don't have high dht levels but this is not important since all that matter is the follicles sensitivity to the trash hormone, some men can have the dht of a foid and still norwood hard because of shit genes. Peppermint, rosemary oil and zinc might help but only if you fix the androgenic cause of your hair loss, otherwise the reaper will continue doing its job. The fact that men that lack 5AR conversion never go bald tell us everything we need to know.

What about ketoconazole and spironolactone cream as an alternative
Both combined should atleast block 95% of dht in the scalp

Im not pro dht i seriously don’t care i believe all androgens are equal aslong doses are equated i just hate tf out of fin and Dut

 

[It'snotover]

What about ketoconazole and spironolactone cream as an alternative
Both combined should atleast block 95% of dht in the scalp

Keto is a good tool to keep dandruff and scalp inflammation away + some minor dht decrease but is it even worth it considering nizoral 2% just once per week is enough to reap all these benefits? And spiro topically has always been called a weak anti androgen in most hair loss forums, I have no idea how much dht it would block. With fin we know it's about 30- 40% and dut 50 to 80% since dut is dose dependent.

Im not pro dht i seriously don’t care i believe all androgens are equal aslong doses are equated i just hate tf out of fin and Dut

Pfs is not something most doctors think is even real, sure these meds aren't for everyone but the vast majority of men will be fine on them if their t and E have a decent balance, if possible bloods before starting treatment are a good idea. Meds like SSRIs have way higher chances of sides than fin/dut.

 

[Deleted member 77820]

Keto is a good tool to keep dandruff and scalp inflammation away + some minor dht decrease but is it even worth it considering nizoral 2% just once per week is enough to reap all these benefits? And spiro topically has always been called a weak anti androgen in most hair loss forums, I have no idea how much dht it would block. With fin we know it's about 30- 40% and dut 50 to 80% since dut is dose dependent.

Pfs is not something most doctors think is even real, sure these meds aren't for everyone but the vast majority of men will be fine on them if their t and E have a decent balance, if possible bloods before starting treatment are a good idea. Meds like SSRIs have way higher chances of sides than fin/dut.

1x per day jfl

But i Agree with you 100%

 

[AforB]

All of this just to get hairmogged by some Pakistani villager