Male-pattern hair loss
|Male-pattern hair loss|
Male androgenic alopecia
|Classification and external resources|
|Specialty||Dermatology, plastic surgery|
Male-pattern hair loss, also known as androgenic alopecia and male pattern baldness (MPB), is hair loss that occurs due to an underlying susceptibility of hair follicles to androgenic miniaturization. It is the most common cause of hair loss and will affect up to 70% of men and 40% of women at some point in their lifetimes. Men typically present with hairline recession at the temples and vertex balding, while women normally thin diffusely over the top of their scalps. Both genetic and environmental factors play a role, and many etiologies remain unknown.
Classic androgenic hair loss in males begins above the temples and vertex, or calvaria, of the scalp. As it progresses, a rim of hair at the sides and rear of the head remains. This has been referred to as a 'Hippocratic wreath', and rarely progresses to complete baldness. The Hamilton-Norwood scale has been developed to grade androgenic alopecia in males.
Female androgenic alopecia is known colloquially as "female pattern baldness", although its characteristics can also occur in males. It more often causes diffuse thinning without hairline recession; and, like its male counterpart, rarely leads to total hair loss. The Ludwig scale grades severity of androgenic alopecia in females.
Animal models of androgenic alopecia occur naturally and have been developed in transgenic mice; chimpanzees (Pan troglodytes); bald uakaris (Cacajao rubicundus); and stump-tailed macaques (Macaca speciosa and M. arctoides). Of these, macaques have demonstrated the greatest incidence and most prominent degrees of hair loss.
- 1 Effects
- 2 Causes
- 3 Diagnosis
- 4 Management
- 5 Society and culture
- 6 Other animals
- 7 References
- 8 External links
Androgenic alopecia is typically experienced as a "moderately stressful condition that diminishes body image satisfaction". However, although most men regard baldness as an unwanted and distressing experience, they usually are able to cope and retain integrity of personality.
Research indicates that the initial programming of pilosebaceous units begins in utero. The physiology is primarily androgenic, with dihydrotestosterone (DHT) the major contributor at the dermal papillae. Below-normal values of sex hormone-binding globulin, follicle-stimulating hormone, testosterone, and epitestosterone are present in men with premature androgenic alopecia compared to normal controls. Although follicles were previously thought permanently gone in areas of complete hair loss, they are more likely dormant, as recent studies have shown the scalp contains the stem cell progenitors from which the follicles arose.
Transgenic studies have shown that growth and dormancy of hair follicles are related to the activity of insulin-like growth factor at the dermal papillae, which is affected by DHT. Androgens are important in male sexual development around birth and at puberty. They regulate sebaceous glands, apocrine hair growth, and libido. With increasing age, androgens stimulate hair growth on the face, but suppress it at the temples and scalp vertex, a condition that has been referred to as the 'androgen paradox'.
These observations have led to study at the level of the mesenchymal dermal papillae. Types 1 and 2 5α reductase enzymes are present at pilosebaceous units in papillae of individual hair follicles. They catalyze formation of the androgens testosterone and DHT, which in turn regulate hair growth. Androgens have different effects at different follicles: they stimulate IGF-1 at facial hair, leading to growth, but stimulate TGF β1, TGF β2, dickkopf1, and IL-6 at the scalp, leading to catagenic miniaturization. Hair follicles in anaphase express four different caspases. Tumor necrosis factor inhibits elongation of hair follicles in vitro with abnormal morphology and cell death in the bulb matrix.
Studies of serum levels of IGF-1 show it to be increased with vertex balding. Earlier work looking at in vitro administration of IGF had no effect on hair follicles when insulin was present, but when absent, caused follicle growth. The effects on hair of IGF-I were found to be greater than IGF-II. Later work also showed IGF-1 signalling controls the hair growth cycle and differentiation of hair shafts, possibly having an anti-apoptotic effect during the catagen phase. In situ hybridization in adult human skin has shown morphogenic and mitogenic actions of IGF-1. Mutations of the gene encoding IGF-1 result in shortened and morphologically bizarre hair growth and alopecia. IGF-1 is modulated by IGF binding protein, which is produced in the dermal papilla.
DHT inhibits IGF-1 at the dermal papillae. Extracellular histones inhibit hair shaft elongation and promote regression of hair follicles by decreasing IGF and alkaline phosphatase in transgenic mice. Silencing P-cadherin, a hair follicle protein at adherens junctions, decreases IGF-1, and increases TGF beta 2, although neutralizing TGF decreased catagenesis caused by loss of cadherin, suggesting additional molecular targets for therapy. P-cadherin mutants have short, sparse hair.
At the occipital scalp, androgens enhance inducible nitric oxide synthase (iNOS), which catalyzes production of nitric oxide from L-arginine. The induction of iNOS usually occurs in an oxidative environment, where the high levels of nitric oxide produced interact with superoxide, leading to peroxynitrite formation and cell toxicity. iNOS has been suggested to play a role in host immunity by participating in antimicrobial and antitumor activities as part of the oxidative burst of macrophages. The gene coding for nitric oxide synthase is on human chromosome 17.
Also, crosstalk occurs between androgens and the Wnt-beta-catenin signaling pathway that leads to hair loss. At the level of the somatic stem cell, androgens promote differentiation of facial hair dermal papillae, but inhibit it at the scalp. Other research suggests the enzyme prostaglandin D2 synthase and its product prostaglandin D2 (PGD2) in hair follicles as contributive.
Men with androgenic alopecia typically have higher 5-alpha-reductase, lower total testosterone, higher unbound/free testosterone, and higher free androgens, including DHT. 5-alpha-reductase converts free testosterone into DHT, and is highest in the scalp and prostate. DHT is most commonly formed at the tissue level by 5α-reduction of testosterone. The genetic corollary that codes for this enzyme has been discovered.
Prolactin has also been suggested to have different effects on the hair follicle across gender. It seasonally modulates and can delay hair growth in animal models. In vitro models show it inhibits hair follicle growth. In vivo it can inhibit facial hair growth in humans. Researchers have suggested it works through paracrine action.
Balding is multifactorial, with several lines of evidence suggesting it most likely functions by a genetic predisposition (diathesis). Since androgens and androgen receptors (AR) are the initiating cause of androgenic alopecia, their genetic corollaries are a subject of much research. Some involved genes are not X-linked, with men whose fathers show hair loss 2.5 times more likely to experience it themselves regardless of maternal report. The maternal line is crucial as well, as it contains the androgen receptor gene, which provides the necessary diathesis for androgenic alopecia.
The specific variant of the AR for baldness is on a recessive allele, so a woman would need two X chromosomes with the defect to show male pattern hair loss. The EDA2R gene on the X chromosome at Xq11-q12, close to the area that codes for the androgen receptor gene, has been suggested by some researchers as specific to androgenic alopecia. An allele on chromosome 3 at 3q26 also contributes.
Genetic causes of hair texture and nonandrogenic hair loss have been discovered, as well. One is P2RY5, mutations of which affect hair structure and woolly hair. Variants at this site can lead to baldness. Other research identified the gene SOX21, Y-linked, as related to certain nonandrogenic alopecias.
Much research has gone into the genetic component of male pattern baldness, or androgenetic alopecia (AGA). Susceptibility to premature male pattern baldness is largely the cause of sex-influenced inheritance (because males can pass on the trait to their sons, which would be impossible if it were X-linked). Other genes that are not sex-linked are also involved.
Researchers from the University of Bonn in Germany indicate the androgen receptor gene as the cardinal prerequisite for balding. 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. This gene is recessive and a female would need two X chromosomes for 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 suggests another gene on the X chromosome that lies close to the androgen receptor gene is important 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 mostly associated with AGA. This finding has been replicated in at least three following independent studies.
Other genes involved with hair loss have been found, including a gene located at 3q26. This gene is also involved in a type of baldness associated with mental retardation. It is recessive.
Research confirmed the X-linked androgen receptor as the most important gene, with a gene on chromosome 20 being the second-most important determinant gene (snpedia). This research suggests that heredity of AGA is X-linked; however, research has also shown that a person with a balding father has a significantly greater chance of experiencing hair loss. Men whose fathers had experienced hair loss were 2.5 times more likely to experience hair loss themselves, regardless of the mother's side of the family, which may suggest Y-linked heredity plays a role.
Androgens stimulate growth of facial hair, but can suppress scalp hair, a condition that has been called the 'androgen paradox'. The American Academy of Dermatology reports that in adult men, the incidence of androgenic alopecia is roughly equivalent to chronological age, with half of men experiencing hair loss by age 50.
A number of hormonal changes occur with aging:
- Decrease in testosterone
- Decrease in serum DHT and 5-alpha reductase
- Decrease 3AAG, a peripheral marker of DHT metabolism
- Increase in SHBG
- Decrease in androgen receptors, 5-alpha reductase type I and II activity, and aromatase in the scalp
This decrease in androgens and androgen receptors, and the increase in SHBG are opposite the increase in androgenic alopecia with aging. This is not intuitive, as testosterone and its peripheral metabolite, DHT, accelerate hair loss, and SHBG is thought to be protective. The ratio of T/SHBG, DHT/SHBG decreases by as much as 80% by age 80, in numeric parallel to hair loss, and approximates the pharmacology of antiandrogens such as finasteride.
Free testosterone decreases in men by age 80 to levels double that of a woman at age 20. About 30% of normal male testosterone level, the approximate level in females, is not enough to induce alopecia; 60%, closer to the amount found in elderly men, is sufficient. The testicular secretion of testosterone perhaps "sets the stage" for androgenic alopecia as a multifactorial diathesis stress model, related to hormonal predisposition, environment, and age. Supplementing eunuchs with testosterone during their second decade, for example, causes slow progression of androgenic alopecia over many years, while testosterone late in life causes rapid hair loss within a month.
Permanent hair-loss is a result of reduction of the number of living hair matrixes. Long-term of insufficiency of nutrition is an important cause for the death of hair matrixes. Misrepair-accumulation aging theory  suggests that dermal fibrosis is associated with the progressive hair-loss and hair-whitening in old people. With age, the dermal layer of the skin has progressive deposition of collagen fibers, and this is a result of accumulation of Misrepairs of derma. Fibrosis makes the derma stiff and makes the tissue have increased resistance to the walls of blood vessels. The tissue resistance to arteries will lead to the reduction of blood supply to the local tissue including the papillas. Dermal fibrosis is progressive; thus the insufficiency of nutrition to papillas is permanent. Senile hair-loss and hair-whitening are partially a consequence of the fibrosis of the skin.
Multiple cross-sectional studies have found associations between early androgenic alopecia, insulin resistance, and metabolic syndrome, with low HDL being the component of metabolic syndrome with highest association. Linolenic and linoleic acids, two major dietary sources of HDL, are 5 alpha reductase inhibitors. Premature androgenic alopecia and insulin resistance may be a clinical constellation that represents the male homologue, or phenotype, of polycystic ovary syndrome. Others have found a higher rate of hyperinsulinemia in family members of women with polycystic ovarian syndrome.
In support of the association, finasteride improves glucose metabolism and decreases glycosylated hemoglobin HbA1c, a surrogate marker for diabetes mellitus. The low SHBG seen with premature androgenic alopecia is also associated with, and likely contributory to, insulin resistance, and for which it still is used as an assay for pediatric diabetes mellitus.
Obesity leads to upregulation of insulin production and decrease in SHBG. Further reinforcing the relationship, SHBG is downregulated by insulin in vitro, although SHBG levels do not appear to affect insulin production. In vivo, insulin stimulates both testosterone production and SHBG inhibition in normal and obese men. The relationship between SHBG and insulin resistance has been known for some time; decades prior, ratios of SHBG and adiponectin were used before glucose to predict insulin resistance. Patients with Laron syndrome, with resultant deficient IGF, demonstrate varying degrees of alopecia and structural defects in hair follicles when examined microscopically.
Because of its association with metabolic syndrome and altered glucose metabolism, both men and women with early androgenic hair loss should be screened for impaired glucose tolerance and diabetes mellitus II. A low-fat and high-fiber diet combined with regular aerobic exercise increases SHBG and insulin sensitivity. Regarding androgenic impact of diet with exercise, a study found increased protein intake led to higher concentrations of free and total testosterone immediately after exercise.
Measurement of subcutaneous and visceral adipose stores by MRI, demonstrated inverse association between visceral adipose tissue and testosterone/DHT, while subcutaneous adipose correlated negatively with SHBG and positively with estrogen. Subcutaneous fat did not correlate with androgens once the SHBG relationship was taken into account. SHBG association with fasting blood glucose is most dependent on intrahepatic fat, which can be measured by MRI in and out of phase imaging sequences. Serum indices of hepatic function and surrogate markers for diabetes, previously used, show less correlation with SHBG by comparison.
Female patients with mineralocorticoid resistance present with androgenic alopecia.
IGF levels have been found lower in those with metabolic syndrome. Circulating serum levels of IGF-1 are increased with vertex balding, although this study did not look at mRNA expression at the follicle itself. Locally, IGF is mitogenic at the dermal papillae and promotes elongation of hair follicles. The major site of production of IGF is the liver, although local mRNA expression at hair follicles correlates with increase in hair growth. IGF release is stimulated by growth hormone (GH). Methods of increasing IGF include exercise, hypoglycemia, low fatty acids, deep sleep (stage IV REM), estrogens, and consumption of amino acids such as arginine and leucine. Obesity and hyperglycemia inhibit its release. IGF also circulates in the blood bound to a large protein whose production is also dependent on GH. GH release is dependent on normal thyroid hormone. During the sixth decade of life, GH decreases in production. Because growth hormone is pulsatile and peaks during sleep, serum IGF is used as an index of overall growth hormone secretion. The surge of androgens at puberty drives an accompanying surge in growth hormone.
Some studies have suggested a survival advantage with androgenic alopecia. It's difficult to gauge how society perceives balding men. One study has noted when showing subjects people with different appearances, decreased cranial hair was associated with social maturity, appeasement, older age, decreased attractiveness, and decreased aggressiveness. However, a more recent study has found that balding men are perceived as more masculine, taller and physically stronger.
Studies have been inconsistent and not stable across cultures how balding men rate on the attraction scale. While a study from South Korea showed most people rated balding men less attractive, a more recent survey of 1000 Welsh women rated bald and gray haired men quite desirable.
More theories include that baldness signaled dominance, social status, or longevity. Biologists have hypothesized the larger sunlight exposed area would allow more vitamin D to be synthesized, which might have been a "finely tuned mechanism to prevent prostate cancer", as the malignancy itself is also associated with higher levels of DHT.
No consensus has been reached regarding the details of the evolution of male pattern baldness. The assertion that MPB is intended to convey a social message is supported by the fact that the distribution of androgen receptors in the scalp differs between men and women, and older men or women with high androgen levels often exhibit diffuse thinning of hair as opposed to male pattern baldness.
MPB is mostly the result of a genetic event that causes DHT, a male hormone, to cause the hair follicles to atrophy. The hair produced is progressively smaller, until it is practically invisible (or may disappear completely). Other evolutionary hypotheses include genetic linkage to beneficial traits unrelated to hair loss, and genetic drift.
Female androgenic alopecia
Female androgenic alopecia, clinically known as 'female pattern hair loss,' (FPHL) more often causes diffuse thinning without hairline recession. About 30% of Caucasian adult females experience hair loss. Like its male counterpart, the condition rarely leads to total hair loss, although it is possible. Treatment options to arrest progression and stimulate growth include finasteride, the androgen-independent growth promoter minoxidil, and androgen receptor antagonists spironolactone and cyproterone acetate. These work best initiated early, and hair transplantation can be considered in more advanced cases.
A recently published study comparing monozygotic female twins found a number of factors associated with hair loss in women with varying degrees of statistical certainty, and stratified by pattern. Factors associated with increased temporal hair loss that were:
- more children (p = 0.005)
- longer sleep duration (p = 0.006)
- diabetes mellitus (p = 0.008)
- lack of exercise (p = 0.012)
- hypertension (p = 0.027)
- divorce or separation (p = 0.034)
- multiple marriages (p = 0.040)
Frontal hair loss, like temporal, included hypertension and longer sleep duration as risk factors, but also included polycystic ovarian syndrome, lack of hat use, smoking, high income, diabetes mellitus, stress, and multiple marriages.
Statistically significant causes of vertex hair loss were lack of sun protection, less caffeine, and a history of skin disease. Higher testosterone levels were associated with increased temporal and vertex hair loss patterns. Stress, smoking, more children, and a history of hypertension or cancer were associated with increased hair thinning. It is unknown to what degree factors contributing to female hair loss overlap with those in men. Later studies have found that prolactin is unrelated to female androgenic pattern hair loss, despite earlier in vitro studies suggesting it inhibited growth. Female patients with mineralocorticoid resistance present with androgenic alopecia. Older studies have found a slight relationship of prolactin with female androgenic hair loss.
Although baldness is not as common in women as in men, the psychological effects of hair loss tend to be much greater. Typically, the frontal hairline is preserved, but the density of hair is decreased on all areas of the scalp. Previously, it was believed to be caused by testosterone just as in male baldness, but most women who lose hair have normal testosterone levels.
However, female hair loss has become a growing problem that, according to the American Academy of Dermatology, affects around 30 million women in the United States. Although hair loss in females normally occurs after the age of 50 or even later when it does not follow events like pregnancy, chronic illness, crash diets, and stress among others, it is now occurring at earlier ages with reported cases in women as young as 15 or 16.
Causes of female hair loss may vary from those that affect men. In the case of androgenic alopecia, female hair loss occurs because of the action of androgens hormones (testosterone, androsteinedione, and DHT. These male hormones normally occur in small amounts in women.
However, androgenic alopecia is not the main cause of hair loss in women and dermatologists now prefer to call this condition female pattern hair loss (or Ludwig pattern baldness after the scale developed to diagnose it) instead of using the term androgenic alopecia. The female pattern is diffuse and goes around the whole top of the head and can affect women at any time.
The actions of hormones may also cause female hair loss in other instances. Some examples are pregnancy, menopause, presence of ovarian cysts, birth control pills with a high androgen index, and polycystic ovary syndrome. Thyroid disorders, anemia, chronic illness, and some medications can also cause female hair loss.
The diagnosis of androgenic alopecia can be usually established based on clinical presentation in men. In women, the diagnosis usually requires more complex diagnostic evaluation. Further evaluation of the differential requires exclusion of other causes of hair loss, and assessing for the typical progressive hair loss pattern of androgenic alopecia. Trichoscopy can be used for further evaluation. Biopsy may be needed to exclude other causes of hair loss, and histology would demonstrate perifollicular fibrosis.
Early stages of hair loss can be slowed or reversed with medication. FDA-approved drugs include minoxidil and finasteride. Finasteride is an oral medication taken at a standard daily dose of 1 mg for hair loss, and it works by reducing the level of DHT produced by the 5-alpha reductase type 2 enzyme (5ar-2) by 85-90% (DHT from 5ar-2 is the main causal factor responsible for androgenic alopecia in men), thereby protecting the hair follicles from further DHT damage. Dutasteride, a similar drug, is used off-label as a hair loss treatment. Dutasteride inhibits DHT production from 5ar-2 even more potently than Finasteride, and it also additionally inhibits DHT production from the 5ar type 1 enzyme (this enzyme, however, is believed to play little to no role in hair loss). Dutasteride is therefore, in theory, a more effective hair loss treatment than Finasteride. However, Dutasteride is not FDA-approved as a hair loss treatment, and its long-term side effects (including possible neurological damage due to 5ar-1 inhibition) are unknown. Minoxidil is a growth stimulant that stimulates already-damaged hair follicles to produce normal hair. Minoxidil does not, however, provide any protection to the follicles from further DHT damage, and when a follicle eventually becomes completely destroyed by DHT, minoxidil will no longer be able to have any more regrowth effects on that follicle. Topical formulations of finasteride have been argued to be of similar efficacy to systemic, though prostate weight and serum PSA levels were not measured to exclude systemic absorption of topical application as the cause of hair growth. Other treatment options include tretinoin combined with minoxidil, ketoconazole shampoo, and spironolactone.
More advanced cases may be resistant or unresponsive to medical therapy, and require hair transplantation. Naturally occurring units of one to four hairs, called follicular units, are excised and moved to areas of hair restoration. These follicular units are surgically implanted in the scalp in close proximity and in large numbers. The grafts are obtained from either follicular unit transplantation (FUT) or follicular unit extraction (FUE). In the former, a strip of skin with follicular units is extracted and dissected into individual follicular unit grafts. The surgeon then implants the grafts into small incisions, called recipient sites. Specialized scalp tattoos can also mimic the appearance of a short, buzzed haircut.
Many people use unproven treatments. There is little evidence for vitamins, minerals, or other dietary supplements. There is little evidence as of 2008 to support the use of lasers in hair loss. The same applies to special lights. Dietary supplements are not typically recommended.
Society and culture
Many myths are given regarding the possible causes of baldness and its relationship with one's virility, intelligence, ethnicity, job, social class, wealth, etc. While skepticism may be warranted in many cases due to a lack of scientific validation, some claims may have a degree of underlying truth and are supported by research.
|“||You inherit baldness from your mother's father.||”|
Research suggests the gene for the androgen receptor, which is significant in determining probability for hair loss, is located on the X chromosome, so is always inherited from the mother's side for men. A 50% chance exists for a person to share the same X chromosome as his maternal grandfather. Because women have two X chromosomes, they have two copies of the androgen receptor gene, while men only have one. However, a person with a balding father also has a significantly greater chance of experiencing hair loss. Men whose fathers had experienced hair loss were 2.5 times more likely to experience hair loss themselves, regardless of the mother's side of the family.
|“||Weight training and other types of physical activity cause baldness.||”|
Because it increases testosterone levels, many internet forums have put forward the idea that weight training and other forms of exercise increase hair loss in predisposed individuals. Although scientific studies do support a correlation between exercise and testosterone, no direct study has found a link between exercise and baldness. However, a few have found a relationship between a sedentary lifestyle and baldness, suggesting some exercise is beneficial. The type or quantity of exercise may influence hair loss. Testosterone levels are not a good marker of baldness, and many studies actually show paradoxical low testosterone in balding persons, although research on the implications is limited.
|“||Intellectual activity or psychological problems can cause baldness.||”|
This notion may have arisen because cholesterol is involved in the process of neurogenesis and is the base material from which the body ultimately manufactures DHT. While the notion that bald men are more intelligent may lack credibility in the modern world, in the ancient world, if a person were bald, he likely had an adequate amount of fat in his diet. Thus, his mental development was probably not stunted by malnutrition during his crucial formative years, and he was more likely to be wealthy and to have had access to a formal education. However, a sedentary lifestyle is less likely to correlate with intelligence in the modern world, and dietary fat content is not linked to economic class in modern developed countries. Another possibility is that for some people, social standing accrued through intelligence can compensate in mating for physical attractiveness lowered by hair loss and therefore produce male offspring who are prone to both high intellect and hair loss. However, by way of better socioeconomic standing and in turn more access to hair loss treatments, an association between intelligence and actual hair loss is less likely in recent times. Total testosterone exhibits a positive relation to tactual-spatial abilities and to the degree of lateralization. Total testosterone is negatively correlated with verbal fluency. Testosterone in the saliva is also significantly positively correlated to tactual-spatial test scores and, in addition, to field independence. DHT and the ratio DHT/total testosterone are positively related to verbal fluency and negatively to the degree of lateralization of tactual-spatial performance.
|“||Baldness can be caused by emotional stress, sleep deprivation, etc.||”|
Emotional stress has been shown to accelerate baldness in genetically susceptible individuals. Stress due to sleep deprivation in military recruits lowered testosterone levels, but is not noted to have affected SHBG. Thus, stress due to sleep deprivation in fit males is unlikely to elevate DHT, which causes male pattern baldness. Whether it can cause hair loss by some other mechanism is not clear.
|“||Bald men are more 'virile' or sexually active than others.||”|
Levels of free testosterone are strongly linked to libido and DHT levels, but unless free testosterone is virtually nonexistent, levels have not been shown to affect virility. Men with androgenic alopecia are more likely to have a higher baseline of free androgens. However, sexual activity is multifactoral, and androgenic profile is not the only determining factor in baldness. Additionally, because hair loss is progressive and free testosterone declines with age, a male's hairline may be more indicative of his past than his present disposition.
|“||Frequent ejaculation causes baldness.||”|
Many misconceptions exist about what can help prevent hair loss, one of these being that lack of sexual activity will automatically prevent hair loss. While a proven direct correlation exists between increased frequency of ejaculation and increased levels of DHT, as shown in a recent study by Harvard Medical School, the study suggests that ejaculation frequency may be a sign, rather than necessarily a cause, of higher DHT levels. Another study shows that although sexual arousal and masturbation-induced orgasm increase testosterone concentration around orgasm, they reduce testosterone concentration on average (especially before abstinence) and because about 5% of testosterone is converted to DHT, ejaculation does not elevate DHT levels.
The only published study to test correlation between ejaculation frequency and baldness was probably large enough to detect an association (1390 subjects) and found no correlation, although persons with only vertex androgenetic alopecia had had fewer female sexual partners than those of other androgenetic alopecia categories (such as frontal or both frontal and vertex). One study may not be enough especially in baldness, where there is a complex with age. Marital status has been shown in some studies to influence hair loss in cross-sectional studies (NHANES1).
Male pattern hair loss is also known as androgenic alopecia, androgenetic alopecia (AGA), alopecia androgenetica and male pattern baldness (MPB).
Baldness is not only a human trait. One possible case study is the maneless male Tsavo lion. The Tsavo lions' prides are unique in that they frequently have only a single male lion with usually seven or eight adult females, as opposed to four females in other lion prides. Tsavo males may have heightened levels of testosterone, which could explain their reputation for aggression and dominance, indicating that lack of mane may at one time have had an alpha correlation.
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