Why am I balding like a female?

Bro you need to stop it at all costs even if it means trying fin imo
You are not masc enough
I'm currently taking Otezla, tofacitinib, doxycycline, and megadosing an anti-histamine

I am putting off Finasteride because there was a forum member who has the SAME type of diffuse hairloss I have from accutane, and when he inevitably tried finasteride his entire body crashed terribly.


You can see his original accutane hairloss posts on the following thread-


He ended up going bald, not even finasteride stopped his diffuse accutane hairloss. I'd bet he had Lichen Planopilaris also
 
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I'm currently taking Otezla, tofacitinib, doxycycline, and megadosing an anti-histamine

I am putting off Finasteride because there was a forum member who has the SAME type of diffuse hairloss I have from accutane, and when he inevitably tried finasteride his entire body crashed terribly.


You can see his original accutane hairloss posts on the following thread-


He ended up going bald, not even finasteride stopped his diffuse accutane hairloss. I'd bet he had Lichen Planopilaris also
Holy shit 😩
 
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He makes an autistic amount of dubious conclusions, that's for sure. It's obvious the guy has some good knowledge in inorganic chem, but some of his takes on MPB are very shaky and he uses a lot of "scientific" lingo to cover that up.

For example, from comment #8 "Cutting off that metabolic pathway (5AR) increases testosterone concentration and, subsequently, concentration of estrogens, but only for a short time due to negative hypothalamic feedback." The increase in T due to inhibited conversion to DHT after blocking 5-alpha-reductase is in the ballpark of 10% - if we take an average guy with ~800ng/dL, this would mean a rough increase of 80ng/dL. Interestingly, T levels naturally fluctuate more than that without suppressing the HPG, which effectively disproves his claim - "Observed peak-to-trough T concentration variation is estimated to be approximately 3.47 nmol/l (100 ng/dl) in young men." [1] Off to the next one.

From the same comment, a few lines further. "Cutting off 5AR results in higher serum levels of testosterone and estrogens, but LOWER levels of estrogens in the tissues where they belong." This, again, doesn't make a lot of sense - DHT is a known aromatase inhibitor, so lowering it should inevitably lead to higher estrogen concentrations, on top of that caused by the ~10% higher T. He speaks big words, not true ones. Off-topic but if there is one user at HLT that is worth following, it's pegasus2.

[1] - https://www.nature.com/articles/3901580

Pegasus2 is the smartest guy on the forum but he uses the most nuclear protocol I have ever seen
 
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Pegasus2 is the smartest guy on the forum but he uses the most nuclear protocol I have ever seen
Facts he must be a tranny by now
If I‘d blast that I wouldn’t be posting on hairlossforums anymore
 
Inb4 mrChibbs tells him it’s all in his thyroid and he will cure himself with warm milk aspirin and sunlight
 
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Will do, it will be long
Ok I will tag some high iq cels in the threads
There are some smart minds on each forum
but there is also lots of c0pe
 
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Facts he must be a tranny by now
If I‘d blast that I wouldn’t be posting on hairlossforums anymore
Tbh transitioning is less risky than the meds he uses - the cancer compounds are no joke.

They worked amazingly for him though - I do respect the grind
 
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Tbh transitioning is less risky than the meds he uses - the cancer compounds are no joke.

They worked amazingly for him though - I do respect the grind
Yeah especially the research chemical from curtis jfl
Imagine using that
 
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Tbh transitioning is less risky than the meds he uses - the cancer compounds are no joke.

They worked amazingly for him though - I do respect the grind
What is he taking? I always respect people who take this shit to the extremes
 
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What is he taking? I always respect people who take this shit to the extremes
 
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What is he taking? I always respect people who take this shit to the extremes

Hover over his name to see his massive regimen - afaik the SHH drugs are the scariest part of the regimen
 
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Beat me to it lol
 
I‘ll probably get a SAG, move to the mountainside and regrow all my hair for a month before succumbing to cancer
 
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I‘ll probably get a SAG, move to the mountainside and regrow all my hair for a month before succumbing to cancer
Ngl, inducing cancer would be good for suicideCels. Just induce cancer and die an apparent natural death theory
 
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Hover over his name to see his massive regimen - afaik the SHH drugs are the scariest part of the regimen
Do you know his norwood and what he looks like? Gyno etc
 
Do you know his norwood and what he looks like? Gyno etc

This is him

Looks like he just gets better and better

I don’t know how he deals with sides- I’m under the impression he is either extremely resistant to sides or is extremely resilient to their effects
 
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This is him

Looks like he just gets better and better

I don’t know how he deals with sides- I’m under the impression he is either extremely resistant to sides or is extremely resilient to their effects
Man i dont get the people taking all this shit to regrow to an ugly nw 3.5-4 when a shaved head looks better
If you do it at least get nw 2 or better
 
its literall called diffuse thinning, its not that uncommon

as long as you dont diffuse on side but still in the norwood range its probaly indeed male pattern baldness

example

diffuse-thinning.jpg
IMG_2910-2.jpg.16d27c3c14d504529ecbfedf3f7211e8.jpg
 
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its literall called diffuse thinning, its not that uncommon

as long as you dont diffuse on side but still in the norwood range its probaly indeed male pattern baldness

example

diffuse-thinning.jpg
IMG_2910-2.jpg.16d27c3c14d504529ecbfedf3f7211e8.jpg
im diffusing everywhere, even my eyebrows/eyelashes
 
Man i dont get the people taking all this shit to regrow to an ugly nw 3.5-4 when a shaved head looks better
If you do it at least get nw 2 or better
I made the thread on HLL under my username. If you wanna tag anyone that would be cool. I can add more information on the thread as people begin replying
 
im diffusing everywhere, even my eyebrows/eyelashes

get your thyroid checked, if you are diffusing beyond the norwood patttern (aka you also lose hair at the horseshoe) its proably sth else

norwood-7.png
 
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get your thyroid checked, if you are diffusing beyond the norwood patttern (aka you also lose hair at the horseshoe) its proably sth else

norwood-7.png
Lichen planopilaris sometimes causes full body hairloss, but my derm wants me to get my thyroid checked. She says I might have hypothyroidism, so your right
 
I made the thread on HLL under my username. If you wanna tag anyone that would be cool. I can add more information on the thread as people begin replying
Caged at the thread title
 
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get your thyroid checked, if you are diffusing beyond the norwood patttern (aka you also lose hair at the horseshoe) its proably sth else

norwood-7.png
I just found out from HLL that an itchy scalp is common with androgenetic alopecia. Shit, that's blackpilling. I've been coping that the itch is a sign I still have Lichen Planopilaris, but now I'm thinking my derm might have been wrong and I'm just diffuse balding MPB
 
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I just found out from HLL that an itchy scalp is common with androgenetic alopecia. Shit, that's blackpilling. I've been coping that the itch is a sign I still have Lichen Planopilaris, but now I'm thinking my derm might have been wrong and I'm just diffuse balding MPB
Probably. Accutane can trigger hair loss earlier
 
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Fuck fuck fuck. God damnit. Fuck accutane
Nah, If you had it coming it was coming. Maybe a year later at max
Check this thread regardless
 
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Nah, If you had it coming it was coming. Maybe a year later at max
Check this thread regardless

No way I had it coming. My hairline is literal child tier, and my testosterone is likely in the 100's. Accutane destroyed by future
 
No way I had it coming. My hairline is literal child tier, and my testosterone is likely in the 100's. Accutane destroyed by future
Look at the thread I sent. In gender checked Accutane like I checked Fin and SSRI but it’s part of the deadly trifecta
 
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Look at the thread I sent. In gender checked Accutane like I checked Fin and SSRI but it’s part of the deadly trifecta
Already read it before you sent it. I've read 1000's of forum posts' on this subject matter. My conclusion is that there is no conclusion
 
Already read it before you sent it. I've read 1000's of forum posts' on this subject matter. My conclusion is that there is no conclusion
Fuck man you are in a bad spot. If it’s not MPB and you take FIN you are fucked. If it is and you don’t take it you are fucked because it’s too late
If I was you I would risk it and wait to see if it passes
 
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Fuck man you are in a bad spot. If it’s not MPB and you take FIN you are fucked. If it is and you don’t take it you are fucked because it’s too late
If I was you I would risk it and wait to see if it passes
Exactly. There is actually someone who had severe diffuse hairloss from accutane just like me, who eventually went on finasteride. As fate would have it, finasteride fucked him even harder then accutane, you can read about it here
 
Exactly. There is actually someone who had severe diffuse hairloss from accutane just like me, who eventually went on finasteride. As fate would have it, finasteride fucked him even harder then accutane, you can read about it here
I literally don’t want to it’s too depressing. I wish you the best of luck dude. Better to keep the dick than hair
 
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from rpf:

Based on my theory this study backs up the idea why accutane cause hair-loss. It increases free fatty acids when there is too much retinol https://www.jlr.org/content/10/4/395.full.pdf


A case of type 1 diabetes represented by diabetic ketoacidosis after isotretinoin therapy: is it a result or coincidence? | ECE2013
I'll read the first paper in a bit, but the second link directly alligns with my belief that accutane can be a potential trigger of autoimmune disease. Please God let me have Lichen Planopilaris.

My theory of accutane triggering autoimmune disease is getting popular on propeciahelp-
 
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The below study is worth a read-
Frontal fibrosing alopecia: An update on the hypothesis of pathogenesis and treatment - ScienceDirect

"Frontal fibrosing alopecia (FFA) is a relatively new scarring alopecia that is considered a variant of lichen planopilaris (LPP) with no recognized promising treatments. In this study, we tried to clarify the underlying signaling pathwaysand their roles in the pathogenesis and progression of FFA. Because of several differences in clinical manifestations, response to treatments, and pathological findings, these two conditions could be differentiated from each other. Taking into account the already discussed signaling pathways and involved players such as T cells, mast cells, and sebaceous glands, different possible therapeutic options could be suggested. In addition to treatments supported by clinical evidence, such as 5 alpha-reductase inhibitors, topical calcineurin inhibitors, hydroxychloroquine, peroxisome proliferator-activated receptor gamma agonists, and oral retinoid agents, various other treatment strategies and drugs, such as phototherapy, Janus kinase inhibitors, dehydroepiandrosterone, sirolimus, cetirizine, and rituximab, could be suggested to mitigate disease progression. Of course, such lines of treatment need further evaluation in clinical trials"

"Inflammation around the hair follicles is suggested as the etiology of hair loss in primary scarring alopecia, but there is not enough detail about the pathogenesis of LPP and FFA"

"Unfortunately, currently available treatments are not very effective to stop hair loss, although the progression of the diseases can be slowed with 5 alpha-reductase inhibitors (5αRI; eg, dutasteride and finasteride), hydroxychloroquine (HCQ), and oral retinoid agents (MacDonald et al., 2012). Conversely, topical and systemic corticosteroids and immunosuppressive drugs, such as mycophenolate mofetil, do not halt the progression of FFA (Kossard et al., 1997, Tosti et al., 2005), which may be due to the difference in predominant immune responses and the involvement of different immune pathways in these diseases. Moreover, the differences in the targeted hair types (ie, vellus, intermediate, and terminal) need more discussion."

"Although eyebrow loss was reported in both men and women, women may be affected more frequently than men with FFA (Bolduc et al., 2016). Moreover, eyebrow loss as the initial clinical presentation was associated with mild forms of FFA (Bolduc et al., 2016). Interestingly, involvement of the eyebrows precedes a frontal recession without any sign of clinical inflammation"

"There are major differences related to the response to treatment by patients with FFA and LPP. LPP responds well to topical or intralesional injection of corticosteroid agents as well as some immunosuppressive therapies, but these treatments were not found effective for FFA (Lajevardi et al., 2015). On the other hand, there is growing evidence that FFA progression can be halted with 5αRI (eg, dutasteride and finasteride), oral retinoid agents, and peroxisome proliferator-activated receptor gamma(PPAR-γ) agonists (Chiang et al., 2010, Pedrosa et al., 2017, Pirmez et al., 2017, Rakowska et al., 2017, Samrao et al., 2010, Vano-Galvan et al., 2014). Of note, some treatments, such as HCQ, appear effective not only for FFA, but also in decreasing symptoms and signs of LPP"

"There is a growing body of evidence that fibrotic pathways and specifically epithelial-to-mesenchymal transition (EMT) are deeply involved in FFA. EMT is a physiologic feature during embryogenesis and wound healing, but it also occurs during fibrotic diseases, malignant transformation of epithelial cells, and metastasis (Nieto et al., 2016). During EMT, epithelial cells gradually represent fibroblast-like morphology (such as vimentin and fibronectinupregulation) as a result of E-cadherin suppression via E-box binding factors, such as SNAI1, SNAI2, and TWIST"

"In addition to PPAR-γ agonists, which have documented efficacy in hampering EMT (Burgess et al., 2005, Zafiriou et al., 2005), retinoid agents are well known to have proven inhibitory effects against fibrosis pathways and can act as an agonist of PPAR-γ (Rankin et al., 2013). Furthermore, new evidence supports the inhibitory effect of 5αRIs in the TGF-β1-fibrosis pathway for the treatment of various types of alopecia (Inui and Itami, 2011, Yoo et al., 2006). Also, there is evidence for the role of androgens, especially dehydroepiandrosterone (DHEA), in suppressing TGF-β1 and fibrosis"

"At first glance, considering the high prevalence of FFA in postmenopausal women, estrogen deficiency could be considered as a triggering factor of FFA initiation. Estrogen has many known effects on different parts of the immune system, and it has regulatory effects on the function and number of neutrophilsand macrophages (Hsieh et al., 2009, Kovats, 2015). Moreover, high levels of estrogen (eg, during pregnancy) can shift the immune response from Th1 to Th2 cells"
"Simultaneously, estrogen receptor-alpha (ERα)-mediated signaling upregulates the expression of FoxP3, programmed cell death protein 1, and CTLA-4. Thus, estrogen seems capable of promoting the expansion of Tregs, which are critical players in the downregulation of immune responses (Polanczyk et al., 2005). However, the serum levels of estrogen have been reported as normal in previous reports, and FFA has been reported in a man who received estrogen as part of neoadjuvant hormonal therapy for prostate cancer. These observations question the protective role of estrogen in FFA"

"The reported effectiveness of 5αRIs in FFA management can be justified with the microenvironmental estrogen deficiency theory. Aromatase is the responsible enzyme for the conversion of androgens (specifically testosterone) into estrogen, and it is found in many tissues including hair follicles. Both finasteride and dutasteride inhibit the conversion of testosterone into dihydrotestosterone, leading to higher levels of testosterone in the scalp. Subsequently, this accumulated testosterone is converted to estrogen by activated aromatase. Consequently, 5αRIs increase the estrogen level in the scalp microenvironment, which could implement many anti-inflammatory effects. However, considering the high prevalence of AGA in patients with FFA and the well-known effects of 5αRIs in the treatment of AGA. The efficacy of 5αRIs in FFA patients could probably conditioned by its effect on improving AGA rather than FFA"

"Second, a new growing concept is built on the basis of the low androgen level theory, which has been discussed very recently in the literature. Ranasinghe et al. (2017) reported that androgen deficiency (especially DHEA and DHEA sulphate) has been identified in many patients with FFA. DHEA and DHEA sulphate are the most abundant circulating steroid hormones in humans. Their production in women reaches the highest levels between the age of 25 and 30 years and starts decreasing at age 60 years, with only 10% to 20% of peak levels"

"In view of the biochemical effects, DHEA exhibits affinity to the androgen receptor (AR) and estrogen receptors (ERs) with a preference for ER-β (Chen et al., 2005)."

"Surprisingly, depending on the circulating testosterone and dihydrotestosterone levels, DHEA has been shown to behave as a partial agonistof AR, and therefore probably has an anti-androgen effect. On the other hand, DHEA is a full agonist of ERβ with similar or slightly greater effect than estradiol. As such, DHEA has been proposed to be an important and potentially major endogenous estrogen in the body (Webb et al., 2006). Thus, considering the anti-inflammatory, anti-fibrosis, anti-androgen, and estrogen-like effects, DHEA can be a potentially effective treatment for FFA. Of note, despite these theories on the role of DHEA, since FFA is occurs in postmenopausal women in > 90% of cases, the significantly lower serum levels of DHEA in the study by Ranasinghe et al. (2017) could be due to the higher mean age of the patients with FFA, and not necessarily a triggering factor for FFA"

"Lastly, the association of FFA with hypothyroidism and the effect of thyroid hormones on K15, CD200, and deiodinase 2 in cultured human K15-GFP + cells suggest a potential role of thyroid hormones in maintaining the stem cell niche/bulge immune privilege in FFA"
 
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I'll read the first paper in a bit, but the second link directly alligns with my belief that accutane can be a potential trigger of autoimmune disease. Please God let me have Lichen Planopilaris.

My theory of accutane triggering autoimmune disease is getting popular on propeciahelp-
jfl.

anyways im not even sure lichen is better than mpb tbh

there seems to be no cure for it either and its going to make you bald quicker
 
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jfl.

anyways im not even sure lichen is better than mpb tbh

there seems to be no cure for it either and its going to make you bald quicker
I'd rather have Lichen Planopilaris. I'm taking the most potent medicaiton for it. Just waiting for the drugs to fully kick in. MPB would be a death sentence as I would be out of options. But I can already envision myself going down the route of taking cancer inducing medications,
 
did you get lichen after accutane or while on it?

have you considered going back on it? i know some pfs people just go back on fin and do better than before lol

I have considered hopping back on accutane. Accutane is actually a treatment for Lichen Planopilaris jfl.

I got lichen exactly 4 months into the course, just like many others I've spoken to
 
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I have considered hopping back on accutane. Accutane is actually a treatment for Lichen Planopilaris jfl.

I got lichen exactly 4 months into the course, just like many others I've spoken to
praying for you ngl
you should talk with your parents about it and get professional help
 
praying for you ngl
you should talk with your parents about it and get professional help
I read on Nathan Hatch's book that he lost hair after supplenting vitamin a, which he strongly warns against as a supplement. He claims that synthetic A will release a huge amount of iron from the body tissues and this will cause hairloss. Accutane is a massive dose of synthetic vitamin a.

not me
 
Well, just eating kinda Peaty was enough for me it seems.
Fibrosis, Calcification, Having CO2 instead of NO heavy vasodilators and good metabolic rate/glucose oxidation; these are my focus.

I think the things which helped my hair most directly (despite general diet, avoiding PUFA (which I definitely have problems with) and proper energy levels) are following:

Doxycycline


Taurine


Thiamine
cba to find some references on it but I think its effect on mitchondria and CO2 may be positive for me​
As I said, I am taking microdose T3:T4 (1:3; 6mcg T3 like 3 times a day) and doing an IGF LR3 cycle for 4 weeks. They will most likely have a positive effect aswell.
I am still experimenting around but my focus will be to potentiate the things I am already doing/addressing. I dont need any specific hairloss drugs, I think I am fine now. Still trying around with CO2 (baking soda+ citric acid bathes or bag breathing but I havent found anything proper yet). I am happy and I will stick with it

Dream has come true and CH and pegasus are discussing
@Dr Shekelberg

ch sounds higher iq ngl but im easy to impress
 
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Dream has come true and CH and pegasus are discussing
@Dr Shekelberg

ch sounds higher iq ngl but im easy to impress
Screenshot 20210125 005405 Chrome

This Nigga is a walking pharmacy and probably still Norwood 3. So much arguing and no success, while Chad uses Beer which is poured over him at parties as topical and gets more hair follicles from it
 
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View attachment 944937
This Nigga is a walking pharmacy and probably still Norwood 3. So much arguing and no success, while Chad uses Beer which is poured over him at parties as topical and gets more hair follicles from it
Exactly
Probably bc chad tolerates the beer well
Chad tolerates anything
Elevated being
 

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