Androgenic alopecia: Wikis


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Androgenic alopecia
Classification and external resources

Androgenic alopecia (baldness) illustrated in a male.
ICD-10 L64.
DiseasesDB 7773
eMedicine derm/21

Androgenic alopecia (also known as androgenetic alopecia or alopecia androgenetica) is a common form of hair loss in both female and male humans, chimpanzees, and orangutans.[1] In male humans in particular, this condition is also commonly known as male pattern baldness. Hair is lost in a well-defined pattern, beginning above both temples. Hair also thins at the crown of the head. Often a rim of hair around the sides and rear of the head is left, or the condition may progress to complete baldness.

The pattern of hair loss in women differs from male pattern baldness. In women, the hair becomes thinner all over the head, and the hairline does not recede. Androgenic alopecia in women rarely leads to total baldness.



A variety of genetic and environmental factors likely play a role in causing androgenic alopecia. Although researchers are studying the factors that may contribute to this condition, most of these remain unknown. Researchers have determined that this form of hair loss is related to hormones called androgens, particularly an androgen called dihydrotestosterone (DHT). Androgens are important for normal male sexual development before birth and during puberty. Androgens also have other important functions in both males and females, such as regulating hair growth and sex drive.

Male pattern baldness is caused by a genetic sensitivity of hair follicles to DHT, which causes them to shrink when exposed to it. This shortens their lifespan and prevents them from producing hair normally.[2]

Hair loss and genetics

Much research has gone into the genetic component of male pattern baldness, or androgenic alopecia (AGA). Research indicates that susceptibility to premature male pattern baldness is largely X-linked. Other genes that aren’t sex linked are also involved.

Large studies in 2005 and 2007 stress the importance of the maternal line in the inheritance of male pattern baldness. German researchers name the androgen receptor gene as the cardinal prerequisite for balding.[3] They conclude that a certain variant of the androgen receptor is needed for AGA to develop. In the same year the results of this study were confirmed by other researchers.[4] This gene is recessive and a female would need two X chromosomes with the defect to show typical male pattern alopecia. Seeing that androgens and their interaction with the androgen receptor are the cause of AGA it seems logical that the androgen receptor gene plays an important part in its development.

Other research in 2007 suggests another gene on the X chromosome, that lies close to the androgen receptor gene, is an important gene in male pattern baldness. They found the region Xq11-q12 on the X-chromosome to be strongly associated with AGA in males. They point at the EDA2R gene as the gene that is mostly associated with AGA.

Other genes involved with hair loss have been found. One of them being a gene on chromosome 3. The gene is located at 3q26.[5] This gene is recessive.

There are also genes that are involved in hair loss, although not male pattern baldenss. In particular, three genes have been shown to both affect hair texture and also cause baldness in some people. One of these is P2RY5. Mutations in this gene affects hair structure"wooly hair".[6] Certain variants can lead to baldness.[7]

In May 2009, researchers in Japan identified a gene, Sox21, that appears to be responsible for hair loss in humans.[8]

Hormone levels correlated with androgenic alopecia

Men with androgenic alopecia typically have higher levels of 5-alpha-reductase, lower levels of total testosterone, higher levels of unbound/free testosterone, and higher levels of total free androgens including DHT.[9][10]

5-alpha-reductase is responsible for converting free testosterone into DHT. The genes for 5-alpha-reductase are known.[11] The enzymes are present predominantly in the scalp and prostate. Levels of 5alpha-reductase are one factor in determining levels of DHT in the scalp and drugs which interfere with 5alpha-reductase (such as finasteride, which inhibits the predominant type 2 isoform) have been approved by the FDA as treatments for hair loss.

Sex hormone binding globulin (SHBG), which is responsible for binding testosterone and preventing its bioavailability and conversion to DHT, is typically lower in individuals with high DHT. SHBG is downregulated by insulin.

Increased levels of Insulin Growth Factor-1 (IGF-1) have been correlated to vertex balding.[12]

High insulin levels seem the likely link between metabolic syndrome and baldness. Low levels of SHBG in men and non-pregnant women are also correlated with glucose intolerance and diabetes risk, though this correlation disappears during pregnancy.[13]

Hair loss and lifestyle

While genetic factors seem to play the principal role in the development and progression of androgenic alopecia, lifestyle also plays a minor role as demonstrated by the vast increase in male and female pattern baldness in Japan after World War II. Pattern baldness (androgenic alopecia) was either rare or non-existent among hunter-gatherer and other, less westernized societies eating in their traditional manner. [14]

One study did show that free testosterone is lower 24 hours after intense aerobic exercise in men who already have high endurance[15] but it was not investigated whether that level remains lowered beyond that point, or whether that lowering affects male pattern baldness in any way. It has been suggested that weight training may have a detrimental effect on hair by increasing testosterone levels; however, there is at least one study that indicates a decline in free testosterone as result of weight training.[16]

Evolutionary theories of Male Pattern Baldness

One theory, advanced by Muscarella and Cunningham, suggests baldness evolved in males through sexual selection as an enhanced signal of aging and social maturity, whereby aggression and risk-taking decrease and nurturing behaviours increase. This may have conveyed a male with enhanced social status but reduced physical threat, which could enhance ability to secure reproductive partners and raise offspring to adulthood.

In a study by Muscarella and Cunnhingham, males and females viewed 6 male models with different levels of facial hair (beard and mustache or none) and cranial hair (full head of hair, receding and bald). Participants rated each combination on 32 adjectives related to social perceptions. Males with facial hair and those with bald or receding hair were rated as being older than those who were clean shaven or had a full head of hair. Beards and a full head of hair were seen as being more aggressive and less socially mature, and baldness was associated with more social maturity. A review of social perceptions of male pattern baldness has been provided by Henss (2001).

The assertion that male pattern baldness is intended to convey a social message is supported by the fact that pattern baldness is also common in other primates, and is often used to convey increased status and maturity. Gorillas evolved anatomically enlarged foreheads for this reason. This suggests that baldness could have evolved to enhance the apparent size of the forehead, and increase the area of the face to be displayed. It should also be noted that most ancestry primates had a shorter life-span, and as baldness usually occurs at a later stage in life, baldness could have been a sign of survival and longevity. Premature baldness could also have evolved in younger males to convey this message, which correlates with studies suggesting men with bald or receding hairlines were rated as older than those with a full head of hair.

Other evolutionary hypotheses include genetic linkage to beneficial traits unrelated to hair loss and genetic drift.


Differential diagnosis involves eliminating other causes of hair loss (such as poisoning) and comparing the pattern of hair loss to a typical male pattern baldness progression.[17]


While many people with male pattern baldness choose to accept the condition as they accepted their hair color or shape, there are baldness treatments which can reduce or halt hair loss, and in early stages or in rare cases, reverse it entirely. Treatments include:

See also


  1. ^ "The latest on baldness cures" ( – Scholar search). Duke Health News. December 1994. Retrieved 2009-01-09.  
  2. ^
  3. ^ Hillmer AM, Hanneken S, Genetic variation in the human androgen receptor gene is the major determinant of common early-onset Androgenic Alopecia (AGA). Department of Genomics, Life and Brain Center, University of Bonn, Bonn, Germany.
  4. ^ Levy-Nissenbaum E, Bar-Natan M, Confirmation of the association between male pattern baldness and the androgen receptor genr Danek Gartner Institute of Human Genetics, Sheba Medical Center, Tel Hashomer, Israel
  5. ^ Hillmer AM, Flaquer A, Genome-wide scan and fine-mapping linkage study of AGA reveals a locus on chromosome 3q26. Department of Genomics, Life and Brain Center, University of Bonn, D-53127 Bonn, Germany.
  6. ^ Shimomura Y, Wajid M, Ishii Y, Shapiro L, Petukhova L, Gordon D, Christiano AM. (Mar 2008). "Disruption of P2RY5, an orphan G protein-coupled receptor, underlies autosomal recessive woolly hair.". Nat Genet. 40 (3): 335–9. doi:10.1038/ng.100. PMID 18297072.  
  7. ^ Petukhova L, Sousa EC Jr, Martinez-Mir A, Vitebsky A, Dos Santos LG, Shapiro L, Haynes C, Gordon D, Shimomura Y, Christiano AM. (Nov 2008). "Genome-wide linkage analysis of an autosomal recessive hypotrichosis identifies a novel P2RY5 mutation". Genomics 92 (5): 273–8. doi:10.1016/j.ygeno.2008.06.009. PMID 18692127.  
  8. ^ [1]
  9. ^ Stárka L, Cermáková I, Dusková M, Hill M, Dolezal M, Polácek V (2004). "Hormonal profile of men with premature balding". Exp. Clin. Endocrinol. Diabetes 112 (1): 24–8. doi:10.1055/s-2004-815723. PMID 14758568.  
  10. ^ Demark-Wahnefried W, Lesko SM, Conaway MR, et al. (1997). "Serum androgens: associations with prostate cancer risk and hair patterning". J. Androl. 18 (5): 495–500. PMID 9349747.  
  11. ^ Ellis JA, Panagiotopoulos S, Akdeniz A, Jerums G, Harrap SB (2005). "Androgenic correlates of genetic variation in the gene encoding 5alpha-reductase type 1". J. Hum. Genet. 50 (10): 534–7. doi:10.1007/s10038-005-0289-x. PMID 16155734.  
  12. ^ Signorello LB, Wuu J, Hsieh C, Tzonou A, Trichopoulos D, Mantzoros CS (1999). "Hormones and hair patterning in men: a role for insulin-like growth factor 1?". J. Am. Acad. Dermatol. 40 (2 Pt 1): 200–3. doi:10.1016/S0190-9622(99)70188-X. PMID 10025745.  
  13. ^ McElduff A, Hitchman R, McElduff P (2006). "Is sex hormone-binding globulin associated with glucose tolerance?". Diabet. Med. 23 (3): 306–12. doi:10.1111/j.1464-5491.2005.01780.x. PMID 16492215.  
  14. ^ Cordain L, Eades MR, Eades MD (2003). "Hyperinsulinemic diseases of civilization: more than just Syndrome X". Comp. Biochem. Physiol., Part a Mol. Integr. Physiol. 136 (1): 95–112. doi:10.1016/S1095-6433(03)00011-4. PMID 14527633.  
  15. ^ Daly W, Seegers CA, Rubin DA, Dobridge JD, Hackney AC (2005). "Relationship between stress hormones and testosterone with prolonged endurance exercise". Eur. J. Appl. Physiol. 93 (4): 375–80. doi:10.1007/s00421-004-1223-1. PMID 15618989.  
  16. ^ Ara, I.; Perez-Gomez, J.; Vicente-Rodriguez, G.; Chavarren, J.; Dorado, C.; Calbet, J. A. L. (2006). "Serum free testosterone, leptin and soluble leptin receptor changes in a 6-week strength-training programme." ( – Scholar search). British Journal of Nutrition 96 (6): 1053–9. doi:10.1017/BJN20061956. PMID 17181880.  
  17. ^
  18. ^
  19. ^ Fischer TW, Hipler UC, Elsner P (2007). "Effect of caffeine and testosterone on the proliferation of human hair follicles in vitro". Int. J. Dermatol. 46 (1): 27–35. doi:10.1111/j.1365-4632.2007.03119.x. PMID 17214716.  


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