DR. NICKGA
Kraken
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- Apr 12, 2023
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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.
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.
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
looksmax.org
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
looksmax.org
looksmax.org
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
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
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.
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
How To Avoid Nocebo From Finasteride/Dutasteride
This will be a quick and simple guide to avoid nocebo effect when taking finasteride or dutasteride. What is nocebo? Per the dictionary: "when a patient's negative expectations about a medical treatment cause them to experience undesirable symptoms or illnesses, even though the treatment has no...
looksmax.org
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
Why DHT is fucking useless and should be NUKED TO THE GROUND
Why you should be actively nuking DHT to the absolute fucking ground. Everyone talks about, needing DHT for bone mass, and says DHT is what causes bone growth of the chin and brow ridge and frame for example. or increase height etc. This is complete fucking bro science, a complete myth...
looksmax.org
Does DHT actually inhibit aromatase?
I've been seeing a lot of people saying that it inhibits aromatase activity but I've seen no evidence of it being the case, the only thing I'm sure of is that it doesnt convert to estrogen, unlike testosterone. But does it really inhibit it? Looking for real answers (can't find any)
looksmax.org
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
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
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