Balding is caused by DHT

Don't listen to my nigga @DR. NICKGA

plug a bit weird but chill
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I am now a racist against indian people
 
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He wants you to use tranny drugs (finasteride/dutasteride) to make you his own personal femboy :hnghn:
Alright dont project you fantasys nigga
 
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@Gengar
Can you edit the message and put this thread into section

"WHAT DR NICKGA!! DHT IS NEEDED FOR BONEMASS AND AND..... (yapping)"
 
@Gengar
Can you edit the message and put this thread into section

"WHAT DR NICKGA!! DHT IS NEEDED FOR BONEMASS AND AND..... (yapping)"
should make a anti dht mega thread no
 
Last edited:
should make a anti dht mega thread no cap. mine yours and other thread in 1
Yes but let me make it

I need the reps , i want this thread to get to botb

A megathread can have more chance indeed
 
Last edited:
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Yes but let me make it

I need the reps , i want this thread to get to botb

A megathread can have more chance indeed
Once this thread get into botb

The dht war will finally be over , we will purge the last dht lovers out with a another storm of anti dht threads

I only need 4 more reps and then staff need to agree
 
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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 which requires the presence of androgens. The official name is androgenetic alopecia (AGA), which is a compound word for androgens+genetics and hair loss, meaning that both of these are required for it to occur. It refers to the specific type of hair loss in the horseshoe (Norwood) pattern that is caused by androgens, specifically DHT, and a genetic predisposition. The onset and severity of baldness can be predicted with high accuracy based on your genes.[16] These are the facts, it is so accepted in the medical community that these are the two causes of AGA that the very name of the disease is derived from them. Twin and genomic studies estimate the heritability of AGA to be around 80% for early and late-onset, with genetic influence of clear-cut vertex balding reaching as high as 89% and frontal recession reaching 96%, in young individuals[7][8]. In a study of 553 men, 92% of older men with baldness had a polymoprhism in the Stu1 restriction site of the androgen receptor, while only 76.6% of men without hair loss had this polymorphism, while 98% of men with premature baldness had it. There was only one balding young man out of 52 who did not have it.[17] He may have had other polymorphisms of the AR, and/or a lot of risk alleles in genes that are causal downstream of the AR. The significance of this finding has been confirmed several times. This is just one of many SNPs regulating the AR gene, yet it has a significant predictive effect on baldness, highlighting the importance of androgens in the etiology of AGA, and the requirement for a genetic predisposition.

View attachment 3391498
This shows the difference that just a single SNP on a single gene (AR) makes on the probability of going bald.[17] You are more than twice as likely to develop any balding or severe balding if you have the risk allele for this SNP. There are many other genes which interact with the AR and pathways regulated by androgens that have a significant effect. The combined effect of all of these genes makes baldness highly heritable. There is some environmental component, which has a minor effect on the severity or age of onset, but it would not be possible to induce common baldness in someone who is not genetically predisposed to it. Native American men without admixture, for example, do not go bald regardless of their lifestyle, nor do they have significant body hair[18].

Men with Klinefelter syndrome, i.e. born with an extra X chromosome causing androgen deficiency, do not go bald[22]. Men with androgen insensitivity syndrome, caused by a mutation in the AR gene making them insensitive to androgens, also do not go bald, with two exceptions of FPHL in the literature[21][23]. Pseudohermaphrodites who have a genetic mutation blocking the production of 5-alpha reductase type II are immune to baldness[19][20][32]. This is the enzyme that converts testosterone into the more potent metabolite dihydrotestosterone (DHT). It was the observation of no baldness in these pseudohermaphrodites which prompted the development of Propecia (finasteride) to treat baldness. The drug binds to and blocks the action of the enzyme 5ar-II, which is produced by the gene SRD5A2. Genetic studies have also identified this gene as causal in the development of AGA. When controlling for age, ethnicity, etc., men with variants of this gene that increase production of the enzyme have a significantly higher risk of going bald[9].

The effects of DHT on the hair follicle are mediated by binding to its receptors, the androgen receptor, this allows the androgen receptor to translocate into the nucleus of the cell where it can bind DNA and regulate gene transcription. The AR, the gene that produces the androgen receptor, shows an even stronger genetic association with baldness than SRD5A2. Polymorphisms of this gene show the strongest association with baldness of any gene. There is a disease called Kennedy disease, which is caused by extended CAG repeats in the AR gene. Repeats reduce the sensitivity of the AR gene to activation. Men with this disease are protected against baldness. The more repeats they have the less likely they are to go bald.[1][9]The application of androgens to hair follicles ex vivo retards their growth.[25][26][27] Even when hair follicle cells are removed and exposed to androgens in vitro it reduces their proliferation, the effect of which is reversed by coculture with an androgen receptor antagonist. Only dermal papilla cells from human and macaque hair follicles which are subject to AGA show reduced hair cell proliferation in response to androgens. It does not affect hair follicles on the back of the head.[10][24] Removing the AR or DHT prevents the gene transcription changes that take place in frontal hair follicles.[2] Treatment with androgens inhibits differentiation of hair follicle stem cells by inhibiting the Wnt pathway.[28]

Bald scalp has higher levels of DHT, AR and SRD5A2 than healthy scalp.[3][4][15] In all primates, men do not go bald before reaching sexual maturity. Macaques go bald within months of reaching puberty when androgens are produced. Their baldness represents a hypoplastic change in the type of hair follicle from terminal to vellus similar ,but in the opposite direction, to the hypoplastic change androgens cause in body hair after puberty. [6][29]. This is due to the known differential growth responses that androgens have on genetically identical hair follicles, which varies due to site-specific epigenetic programming.[30] Men who were castrated as juveniles do not go bald, but when injected with testosterone they do. Cessation of testosterone treatment in eunuchs, or castration of balding men, prevents further baldness, but does not reverse baldness[5]. Finasteride prevents baldness in monkeys.[14] Finasteride and dutasteride are highly selective drugs that inhibit only the enzyme responsible for producing DHT. Finasteride, which reduces scalp DHT by 64%[31], prevents baldness in 86% of men after a 10 year follow up[11], and 99% of Japanese men[12]. The more potent dutasteride halted baldness in 94% of men after 5 year follow up[12]. Genetic knockout of SRD5A2 or AR would prevent it in all men who don’t have a rare mutation in one of the genes downstream of the AR.

1 https://academic.oup.com/bjd/article-abstract/157/2/290/66408662 https://www.nature.com/articles/s41597-022-01846-w3 https://academic.oup.com/jcem/article-abstract/39/6/1012/26855274 https://www.nature.com/articles/s41598-023-48942-45 https://onlinelibrary.wiley.com/doi/10.1002/aja.10007103066 https://link.springer.com/chapter/10.1007/978-3-642-74612-3_187 https://link.springer.com/chapter/10.1007/978-3-642-74612-3_188 https://pubmed.ncbi.nlm.nih.gov/16127116/9 https://www.nature.com/articles/s41467-017-01490-810 https://pubmed.ncbi.nlm.nih.gov/8977424/11 https://pubmed.ncbi.nlm.nih.gov/21910805/12 https://pubmed.ncbi.nlm.nih.gov/38321615/13 https://www.oatext.com/Long-term-(1...3-Japanese-men-with-androgenetic-alopecia.php14 https://pubmed.ncbi.nlm.nih.gov/1309834/15 https://academic.oup.com/jcem/article-abstract/38/5/811/26854011 6 https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4441445/17 https://link.springer.com/article/10.1007/s00439-006-0317-81 8 https://www.belgraviacentre.com/blog/native-americans-and-hair-loss19 https://pubmed.ncbi.nlm.nih.gov/25321150/ 20 https://www.science.org/doi/10.1126/science.186.4170.121321 https://www.ncbi.nlm.nih.gov/books/NBK430924/ 22 https://karger.com/sad/article/7/2/135/291539/Androgenetic-Alopecia-in-a-Patient-with 23 https://pubmed.ncbi.nlm.nih.gov/8092978/24 https://www.spandidos-publications.com/10.3892/mmr.2015.3478?text=fulltext 25 https://pubmed.ncbi.nlm.nih.gov/2078048/26https://www.eeose.com/UserFiles/Image/files/pdfler/caffeineno_b.pdf 27 https://www.ncbi.nlm.nih.gov/pmc/articles/PMC698966028 https://pubmed.ncbi.nlm.nih.gov/22283397/29 https://pubmed.ncbi.nlm.nih.gov/7035577/ 30 https://pubmed.ncbi.nlm.nih.gov/29046359/31https://www.sciencedirect.com/science/article/pii/S0022202X1552935732https://pubmed.ncbi.nlm.nih.gov/4432067/ (bewerkt)

5-alpha reductase (5AR) inhibitors have barely or no side effects
5ar inhibitors have no side effects
I sended many good studies including meta analyses (The highest level of scientific proof) supporting this claim in this excellent thread

The FDA even did a investigation and found out that 5AR inhibitors have no sexual or depressive side effects

Don’t be scared of the DHT lovers in this forum and their pseudoscientific theories (which lack solid scientific evidence)
Their theories simply don’t happen in reality—it’s just yapping. They simply don’t happen.


WHAT DR NICKGA!! DHT IS NEEDED FOR BONEMASS AND AND..... (yapping)
It already got debunked in this thread (which they stole some of my arguments hehehehehehe) and this debate i had with a disgusting dht lover


NO NOOO NOOOOO BALDING IS CAUSED BY PROLACTIN AND UHH FAPPING!!
We males experience androgenetic alopecia
Balding in males is 99% caused by DHT, ANDROGENS
BALDING IS CAUSED BY HIGH LEVEL OF DHT IN THE SCALP COMBINED WITH HIGH LEVEL OF ANDROGEN RECEPTOR IN THE SCALP

the scalp tension bloodflow theory, the estrogen theory (low estrogen = balding) , the faping theoryy (......) and more
It’s all utter nonsense by the dht lovers
View attachment 3391607
View attachment 3391610View attachment 3391614View attachment 3391620View attachment 3391622View attachment 3391608
THESE PEOPLE ARE IDIOTS , VERY VERY DUMB IN THE PICTURES, IMAGINES ABOVE
including @ConfusedBolivian and @Jonas2k7 who also blamed serum prolactin causing androgenetic alopecia??????

this picturess , imagines are 0.00001 of the Psuedoscience and stupidity in .org


@piec @halloweed @Hexmask @DR. NICKGA
@piec @halloweed @Hexmask @DR. NICKGA
?
 
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 which requires the presence of androgens. The official name is androgenetic alopecia (AGA), which is a compound word for androgens+genetics and hair loss, meaning that both of these are required for it to occur. It refers to the specific type of hair loss in the horseshoe (Norwood) pattern that is caused by androgens, specifically DHT, and a genetic predisposition. The onset and severity of baldness can be predicted with high accuracy based on your genes.[16] These are the facts, it is so accepted in the medical community that these are the two causes of AGA that the very name of the disease is derived from them. Twin and genomic studies estimate the heritability of AGA to be around 80% for early and late-onset, with genetic influence of clear-cut vertex balding reaching as high as 89% and frontal recession reaching 96%, in young individuals[7][8]. In a study of 553 men, 92% of older men with baldness had a polymoprhism in the Stu1 restriction site of the androgen receptor, while only 76.6% of men without hair loss had this polymorphism, while 98% of men with premature baldness had it. There was only one balding young man out of 52 who did not have it.[17] He may have had other polymorphisms of the AR, and/or a lot of risk alleles in genes that are causal downstream of the AR. The significance of this finding has been confirmed several times. This is just one of many SNPs regulating the AR gene, yet it has a significant predictive effect on baldness, highlighting the importance of androgens in the etiology of AGA, and the requirement for a genetic predisposition.

View attachment 3391498
This shows the difference that just a single SNP on a single gene (AR) makes on the probability of going bald.[17] You are more than twice as likely to develop any balding or severe balding if you have the risk allele for this SNP. There are many other genes which interact with the AR and pathways regulated by androgens that have a significant effect. The combined effect of all of these genes makes baldness highly heritable. There is some environmental component, which has a minor effect on the severity or age of onset, but it would not be possible to induce common baldness in someone who is not genetically predisposed to it. Native American men without admixture, for example, do not go bald regardless of their lifestyle, nor do they have significant body hair[18].

Men with Klinefelter syndrome, i.e. born with an extra X chromosome causing androgen deficiency, do not go bald[22]. Men with androgen insensitivity syndrome, caused by a mutation in the AR gene making them insensitive to androgens, also do not go bald, with two exceptions of FPHL in the literature[21][23]. Pseudohermaphrodites who have a genetic mutation blocking the production of 5-alpha reductase type II are immune to baldness[19][20][32]. This is the enzyme that converts testosterone into the more potent metabolite dihydrotestosterone (DHT). It was the observation of no baldness in these pseudohermaphrodites which prompted the development of Propecia (finasteride) to treat baldness. The drug binds to and blocks the action of the enzyme 5ar-II, which is produced by the gene SRD5A2. Genetic studies have also identified this gene as causal in the development of AGA. When controlling for age, ethnicity, etc., men with variants of this gene that increase production of the enzyme have a significantly higher risk of going bald[9].

The effects of DHT on the hair follicle are mediated by binding to its receptors, the androgen receptor, this allows the androgen receptor to translocate into the nucleus of the cell where it can bind DNA and regulate gene transcription. The AR, the gene that produces the androgen receptor, shows an even stronger genetic association with baldness than SRD5A2. Polymorphisms of this gene show the strongest association with baldness of any gene. There is a disease called Kennedy disease, which is caused by extended CAG repeats in the AR gene. Repeats reduce the sensitivity of the AR gene to activation. Men with this disease are protected against baldness. The more repeats they have the less likely they are to go bald.[1][9]The application of androgens to hair follicles ex vivo retards their growth.[25][26][27] Even when hair follicle cells are removed and exposed to androgens in vitro it reduces their proliferation, the effect of which is reversed by coculture with an androgen receptor antagonist. Only dermal papilla cells from human and macaque hair follicles which are subject to AGA show reduced hair cell proliferation in response to androgens. It does not affect hair follicles on the back of the head.[10][24] Removing the AR or DHT prevents the gene transcription changes that take place in frontal hair follicles.[2] Treatment with androgens inhibits differentiation of hair follicle stem cells by inhibiting the Wnt pathway.[28]

Bald scalp has higher levels of DHT, AR and SRD5A2 than healthy scalp.[3][4][15] In all primates, men do not go bald before reaching sexual maturity. Macaques go bald within months of reaching puberty when androgens are produced. Their baldness represents a hypoplastic change in the type of hair follicle from terminal to vellus similar ,but in the opposite direction, to the hypoplastic change androgens cause in body hair after puberty. [6][29]. This is due to the known differential growth responses that androgens have on genetically identical hair follicles, which varies due to site-specific epigenetic programming.[30] Men who were castrated as juveniles do not go bald, but when injected with testosterone they do. Cessation of testosterone treatment in eunuchs, or castration of balding men, prevents further baldness, but does not reverse baldness[5]. Finasteride prevents baldness in monkeys.[14] Finasteride and dutasteride are highly selective drugs that inhibit only the enzyme responsible for producing DHT. Finasteride, which reduces scalp DHT by 64%[31], prevents baldness in 86% of men after a 10 year follow up[11], and 99% of Japanese men[12]. The more potent dutasteride halted baldness in 94% of men after 5 year follow up[12]. Genetic knockout of SRD5A2 or AR would prevent it in all men who don’t have a rare mutation in one of the genes downstream of the AR.

1 https://academic.oup.com/bjd/article-abstract/157/2/290/66408662 https://www.nature.com/articles/s41597-022-01846-w3 https://academic.oup.com/jcem/article-abstract/39/6/1012/26855274 https://www.nature.com/articles/s41598-023-48942-45 https://onlinelibrary.wiley.com/doi/10.1002/aja.10007103066 https://link.springer.com/chapter/10.1007/978-3-642-74612-3_187 https://link.springer.com/chapter/10.1007/978-3-642-74612-3_188 https://pubmed.ncbi.nlm.nih.gov/16127116/9 https://www.nature.com/articles/s41467-017-01490-810 https://pubmed.ncbi.nlm.nih.gov/8977424/11 https://pubmed.ncbi.nlm.nih.gov/21910805/12 https://pubmed.ncbi.nlm.nih.gov/38321615/13 https://www.oatext.com/Long-term-(1...3-Japanese-men-with-androgenetic-alopecia.php14 https://pubmed.ncbi.nlm.nih.gov/1309834/15 https://academic.oup.com/jcem/article-abstract/38/5/811/26854011 6 https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4441445/17 https://link.springer.com/article/10.1007/s00439-006-0317-81 8 https://www.belgraviacentre.com/blog/native-americans-and-hair-loss19 https://pubmed.ncbi.nlm.nih.gov/25321150/ 20 https://www.science.org/doi/10.1126/science.186.4170.121321 https://www.ncbi.nlm.nih.gov/books/NBK430924/ 22 https://karger.com/sad/article/7/2/135/291539/Androgenetic-Alopecia-in-a-Patient-with 23 https://pubmed.ncbi.nlm.nih.gov/8092978/24 https://www.spandidos-publications.com/10.3892/mmr.2015.3478?text=fulltext 25 https://pubmed.ncbi.nlm.nih.gov/2078048/26https://www.eeose.com/UserFiles/Image/files/pdfler/caffeineno_b.pdf 27 https://www.ncbi.nlm.nih.gov/pmc/articles/PMC698966028 https://pubmed.ncbi.nlm.nih.gov/22283397/29 https://pubmed.ncbi.nlm.nih.gov/7035577/ 30 https://pubmed.ncbi.nlm.nih.gov/29046359/31https://www.sciencedirect.com/science/article/pii/S0022202X1552935732https://pubmed.ncbi.nlm.nih.gov/4432067/ (bewerkt)

5-alpha reductase (5AR) inhibitors have barely or no side effects
5ar inhibitors have no side effects
I sended many good studies including meta analyses (The highest level of scientific proof) supporting this claim in this excellent thread

The FDA even did a investigation and found out that 5AR inhibitors have no sexual or depressive side effects

Don’t be scared of the DHT lovers in this forum and their pseudoscientific theories (which lack solid scientific evidence)
Their theories simply don’t happen in reality—it’s just yapping. They simply don’t happen.


WHAT DR NICKGA!! DHT IS NEEDED FOR BONEMASS AND AND..... (yapping)
It already got debunked in this thread (which they stole some of my arguments hehehehehehe) and this debate i had with a disgusting dht lover


NO NOOO NOOOOO BALDING IS CAUSED BY PROLACTIN AND UHH FAPPING!!
We males experience androgenetic alopecia
Balding in males is 99% caused by DHT, ANDROGENS
BALDING IS CAUSED BY HIGH LEVEL OF DHT IN THE SCALP COMBINED WITH HIGH LEVEL OF ANDROGEN RECEPTOR IN THE SCALP

the scalp tension bloodflow theory, the estrogen theory (low estrogen = balding) , the faping theoryy (......) and more
It’s all utter nonsense by the dht lovers
View attachment 3391607
View attachment 3391610View attachment 3391614View attachment 3391620View attachment 3391622View attachment 3391608
THESE PEOPLE ARE IDIOTS , VERY VERY DUMB IN THE PICTURES, IMAGINES ABOVE
including @ConfusedBolivian and @Jonas2k7 who also blamed serum prolactin causing androgenetic alopecia??????

this picturess , imagines are 0.00001 of the Psuedoscience and stupidity in .org


@piec @halloweed @Hexmask @DR. NICKGA
@piec @halloweed @Hexmask @DR. NICKGA

Go rep me thread, and i will tell
Didn't I?
 
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So? How do you destroy scalp ARs?
You cannot destroy ANDROGEN RECEPTORS in the scalp, there is right now no good way of doing it
(Ar antogonists like RU dont work good)

there is only one medicine that is on development for this purpose

Its called GT20029
This medicine will degrade androgen receptors ot the scalp ("destroy them") . So dht cannot do his evil work
its now on clinical trails
bapry9aw8x8e1.png

dbzbxvv69x8e1.jpg

This are some results released
 
Last edited:
You cannot destroy ANDROGEN RECEPTORS in the scalp, there is right now no way of doing it
(Btw Ar antogonists like RU dont work good)

there is only one medicine that is on development for this purpose

Its called GT20029
This medicine will degrade androgen receptors on the scalp ("destroy them") . So dht cannot do his evil work
its now on clinical trails
bapry9aw8x8e1.png

dbzbxvv69x8e1.jpg

This are some results on the clinical trail
Btw chinese and diffuse thinners are in general hyper responders

Lets see if its work so good at other people
 
You cannot destroy ANDROGEN RECEPTORS in the scalp, there is right now no good way of doing it
(Ar antogonists like RU dont work good)

there is only one medicine that is on development for this purpose

Its called GT20029
This medicine will degrade androgen receptors ot the scalp ("destroy them") . So dht cannot do his evil work
its now on clinical trails
bapry9aw8x8e1.png

dbzbxvv69x8e1.jpg

This are some results released
This can also be used for people with acne
Since androgens are a factor in getting acne

excited-spin.gif
 
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Reactions: ectomorpher
@ectomorpher might aswel rep the thread, not the message at the thread
 
5AR inhibitors protect elastin. Enough said.

2.5mg duta>>>
 
just stop cooming and your hairfall will stop, its not complicated :soy:
 
You cannot destroy ANDROGEN RECEPTORS in the scalp, there is right now no good way of doing it
(Ar antogonists like RU dont work good)

there is only one medicine that is on development for this purpose

Its called GT20029
This medicine will degrade androgen receptors ot the scalp ("destroy them") . So dht cannot do his evil work
its now on clinical trails
bapry9aw8x8e1.png

dbzbxvv69x8e1.jpg

This are some results released
How many time until this sent by God product is available to people?
 
Yes you are kinda right

in people with insulin resistance, metabolic syndromes, their ar receptors can even upregulate in certain body tissues

those people that have those disseases have faster androgen receptors

Oh wel, you still need to use a 5ar inhibitor, you are not gonna suddenly recover the damage that dht did IF YOU become normal

genetics gonna overpower diet
 
Last edited:
Yes you are kinda right

in people with insulin resistance, metabolic syndromes, their ar receptors can even upregulate in certain body tissues

those people that have those disseases have faster androgen receptors

Oh wel, you still need to use a 5ar inhibitor, you are not gonna suddenly recover the damage that dht did IF YOU become normal

genetics gonna overpower diet
I don't disagree in the modern day, but why would it make any sense evolutionarily that half of under 35 year olds go bald.

Maybe people who go bald really early are poeple who are hyper responders to sugar in terms of their DHT increase.



Would it not also raise DHT by some unknown amount (not even talking about androgen receptors) .

Google ai seems pretty concrete on this idea, as in if you ask it does it go down, it will compile that it wont. although there are no studies specifically on the correlation of dht and sugar/insulin as insulin spikes other horemones too.

even a modest increase of 20% could ramp up a decade of your balding progress over the course of a lifetime, considering finasteride lowers serum by 60% and scalp by only 30% or so..

I believe baldness is less common in hunter gatherer populations (80% meat based.)

You could say genetics, but by that same token, if a novel disease were to strike a population (in this context carbohydrate diet) obviously some people will respond to it better than others as a result of their genetics. Could that not be what we are seeing in the modern day. There have yet to be studies like this that I can find at least, I am postulating that carbs =baldness and some people are more sensitive to an amount of dht that should never have been so high to conclude.

This goes with the idea that carbs=ugliness. carbs=illness. There are massive correlations to be drawn between all of these, and yet for some reason the scientific establishment must insist on their dogmatic genetic determinism spree.

It simply doesn't make sense that 200 odd people would be able to live together in harmony through the majority of european history. and more than 3/4 of the men are incels. it just wouldn't be a stable society. Perhaps such a society can only be sustained by a highly autocratic city like society, relying more on rules and scarcity of grain/ meat than familial and friendship based high trusty society,

RETURN TO EDEN
 
Last edited:
I don't disagree in the modern day, but why would it make any sense evolutionarily that half of under 35 year olds go bald
Evolutionary dont care about beauty

1000000 years ago in the wildernis
Do you know what matters then?
THE ONE WHO CAN GET THE RESOURCES

also baldness manifest years after puberty (3-8 years after)
before this years people already breed some kids, or just simple dead
Reproductions happens way before balding kicks in

8000 years ago, you were fighting 3 short neanderthals that is bashing you skull (but no worries you tribes members will come to help) Beauty did not matter
 
Evolutionary dont care about beauty

1000000 years ago in the wildernis
Do you know what matters then?
THE ONE WHO CAN GET THE RESOURCES

also baldness manifest years after puberty (3-8 years after)
before this years people already breed some kids, or just simple dead
Reproductions happens way before balding kicks in

8000 years ago, you were fighting 3 short neanderthals that is bashing you skull (but no worries you tribes members will come to help) Beauty did not matter
You misunderstand what hunter gatherer societies were like. and you failed to understand what im trying to convey to you and why it may not be all genetics in the way that you think it is.
 
  • +1
Reactions: aestheticsrespecter
You misunderstand what hunter gatherer societies were like. and you failed to understand what im trying to convey to you and why it may not be all genetics in the way that you think it is.
itv was probably just stable small settlements like in the bronze age, not that hard to understand. based around a pastoralist lifestyle as per the roman accounts. you simply do not know what you are talking about
 
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Reactions: aestheticsrespecter
Evolutionary dont care about beauty

1000000 years ago in the wildernis
Do you know what matters then?
THE ONE WHO CAN GET THE RESOURCES

also baldness manifest years after puberty (3-8 years after)
before this years people already breed some kids, or just simple dead
Reproductions happens way before balding kicks in

8000 years ago, you were fighting 3 short neanderthals that is bashing you skull (but no worries you tribes members will come to help) Beauty did not matter
also neanderthals died out way longer than 8000 years ago, proof im wasting my time..
 
  • +1
Reactions: aestheticsrespecter
Evolutionary dont care about beauty

1000000 years ago in the wildernis
Do you know what matters then?
THE ONE WHO CAN GET THE RESOURCES

also baldness manifest years after puberty (3-8 years after)
before this years people already breed some kids, or just simple dead
Reproductions happens way before balding kicks in

8000 years ago, you were fighting 3 short neanderthals that is bashing you skull (but no worries you tribes members will come to help) Beauty did not matter
evolution absolutely cares about beauty, because in europe, women were in very equal standing to men, unlike in other parts of the world (at least in bronze age north europe)
 
DHT is obviously involved but it's clear from the crazy results some people get from deep microneedling, botox scalp injections and hard scalp massages that in many cases Norwooding is caused by fibrosis, calcification restriction of blood supply and head shape mechanical tension etc. The stresses to the scalp and lower oxygen environment is a signal for excessive DHT to park itself there and do it's final kill shot on the hair follicles. Females having low DHT and high estrogen avoid that fate usually. I think estrogen is the only way a Norwood 6 has ever got their hair back - by doing a transvestite sex change.
 
my only concern is the effect on cognitive function by suppressing DHT in the brain which has a large amount of androgen receptors. Repped.
 
water but some still dont know or believe it
 

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