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Pattern hair loss

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Pattern hair loss
SpecialtyDermatology Edit this on Wikidata

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.

The name "androgenic alopecia" derives from the old and false hypotesis that baldness was caused by androgens, later it was seen that it has nothing to do with these hormones (with the important exception of DHT), indeed bald men have lower testosterone levels than hairy people [2] [3]

Cause

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 many hormones like the deficiency of testosterone, GH and IGF-I and the excess of other hormones as cortisol, dihydrotestosterone (DHT) and somatostatine . 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, preventing diabetes mellitus, osteoporosis, dementia, erectile disfunction, depression, baldness (bald people tend to have lower testosterone levels compared than hairy people).

Male pattern baldness is worsen 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.[4]

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 are not 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.[5] 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.[6] 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 an allele on chromosome 3. The allele is located at 3q26.[7] This allele 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".[8] Certain variants can lead to baldness.[9]

In May 2009, researchers in Japan identified a gene, Sox21, that appears to be responsible for hair loss in humans.[10]

Hormone levels correlated with androgenic alopecia

Typically bald men have significantly lower testosterone levels than controls (non bald men) and they are more likely to have diabetes mellitus and higher insulin levels [11] [12]. Low testosterone levels are strongly associated with diabetes mellitus and metabolic syndrome [13].

5-alpha-reductase is responsible for converting free testosterone into DHT. The genes for 5-alpha-reductase are known.[14] 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 because they have lower total testosterone levels (SHBG levels are quite proportional to total testosterone levels). SHBG is downregulated by insulin.


High insulin levels seem the likely link between metabolic syndrome, baldness and hypogonadism. Low levels of SHBG in men and non-pregnant women are also correlated with low testosterone levels, glucose intolerance and diabetes risk, though this correlation disappears during pregnancy.[15]

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. [16]

Evolutionary theories of male pattern baldness

One theory, advanced by Muscarella and Cunningham,[citation needed] 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 six 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.[citation needed] 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 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. 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.

Diseases related to baldness

The baldness is caused by several endocrinopaties like cortisol excess (Cushing's syndrome), hypotyroidism, and testosterone deficiency (hypogonadism).

Since the bald men or women have low testosterone levels, they can easily have the typical symptoms of hypogonadism like diabetes mellitus, low muscle mass, metabolic syndrome, insulinresistance, osteoporosis, erectile disfunction [17]

Diagnosis

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.[18]

Treatments

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:

Gallery

See also

References

  1. ^ "The latest on baldness cures" ([dead link]Scholar search). Duke Health News. 1994. Retrieved 2009-01-09. {{cite journal}}: External link in |format= (help); Unknown parameter |month= ignored (help)
  2. ^ http://www3.interscience.wiley.com/cgi-bin/fulltext/121568539/PDFSTART?CRETRY=1&SRETRY=0
  3. ^ http://www.ncbi.nlm.nih.gov/pubmed/14758568
  4. ^ http://www.webmd.com/skin-problems-and-treatments/hair-loss/hair-loss-causes
  5. ^ 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.
  6. ^ 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
  7. ^ 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.
  8. ^ Shimomura Y, Wajid M, Ishii Y, Shapiro L, Petukhova L, Gordon D, Christiano AM. (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. {{cite journal}}: Unknown parameter |month= ignored (help)CS1 maint: multiple names: authors list (link)
  9. ^ Petukhova L, Sousa EC Jr, Martinez-Mir A, Vitebsky A, Dos Santos LG, Shapiro L, Haynes C, Gordon D, Shimomura Y, Christiano AM. (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. {{cite journal}}: Unknown parameter |month= ignored (help)CS1 maint: multiple names: authors list (link)
  10. ^ [1]
  11. ^ http://www3.interscience.wiley.com/cgi-bin/fulltext/121568539/PDFSTART?CRETRY=1&SRETRY=0
  12. ^ http://www.ncbi.nlm.nih.gov/pubmed/14758568
  13. ^ http://www.ncbi.nlm.nih.gov/pubmed/18772488
  14. ^ 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.{{cite journal}}: CS1 maint: multiple names: authors list (link)
  15. ^ 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.{{cite journal}}: CS1 maint: multiple names: authors list (link)
  16. ^ 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.{{cite journal}}: CS1 maint: multiple names: authors list (link)
  17. ^ http://www3.interscience.wiley.com/cgi-bin/fulltext/121568539/PDFSTART?CRETRY=1&SRETRY=0
  18. ^ http://www.webmd.com/a-to-z-guides/hair-loss-diagnosis
  19. ^ http://www.webmd.com/a-to-z-guides/hair-loss-treatments
  20. ^ 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.{{cite journal}}: CS1 maint: multiple names: authors list (link)

Bibliography

External links