male pattern baldness

男性型脱毛症

WordNet

1. for or pertaining to or composed of men or boys; "the male lead"; "the male population"
2. an animal that produces gametes (spermatozoa) that can fertilize female gametes (ova)
3. a person who belongs to the sex that cannot have babies (同)male person
4. characteristic of a man; "a deep male voice"; "manly sports" (同)manful, manlike, manly, virile
5. being the sex (of plant or animal) that produces gametes (spermatozoa) that perform the fertilizing function in generation; "a male infant"; "a male holly tree"
6. form a pattern; "These sentences pattern like the ones we studied before"
7. a model considered worthy of imitation; "the American constitution has provided a pattern for many republics"
8. make light, rapid and repeated sounds; "gently pattering rain" (同)pitter-patter
9. a quick succession of light rapid sounds; "the patter of mice"; "the patter of tiny feet"
10. the condition of having no hair on the top of the head (同)phalacrosis
11. informal terms for a mother (同)mama, mamma, mom, momma, mommy, mammy, mum, mummy

PrepTutorEJDIC

1. 『男性の』,男の;(動物が)雄の,(植物が)雄性の / 《名詞の前にのみ用いて》(機械・器具などが)雄の差し込み口のある / 『男性』;(動物の)雄,雄性植物
2. (壁紙・織物などの)『模様』,柄,デザイン / 『模範』,手本 / 『原型』,ひな型 / (行動・性資の)『型』,様式パターン / (…の型)・手本に従って)…‘を'型どる,作る,まねる《+『名』+『upon』(『on, after』)+『名』》 / …‘を'模様をつける
3. 〈雨などが〉パラパラ降る / 〈子供・動物などが〉パタパタ走る / (…の)パラパラ(パタパタ)イウ音《+『of』+『名』》
4. 《時にa~》早口ぺらぺらしゃべること…早口のせりふ / おしゃべり,むだ話 / (ある職業・階級の)仲間言葉,符ちょう / 早口に話す,ぺらぺらしゃべる / 〈祈り・詩など〉‘を'早口に唱える
5. はげていること;はげ / 単調さ,飾りのなさ;ありのまま,露骨
6. 《M-》《話》おかあちゃん(mamma)

Wikipedia preview

出典(authority):フリー百科事典『ウィキペディア（Wikipedia）』「2013/01/21 01:30:26」(JST)

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Androgenic alopecia
Classification and external resources
Male androgenic alopecia
ICD-10	L64
DiseasesDB	7773
MedlinePlus	001177
eMedicine	derm/21
MeSH	D000505

Androgenic alopecia (also known as androgenetic alopecia, alopecia androgenetica, male pattern baldness) is loss of hair 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 lifetime. Men typically present with hairline recession at the temples and vertex balding while women normally diffusely thin 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 has been colloquially referred to as 'female pattern baldness', although its characteristics can occur in males as well. 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.

Human hair
List of hairstyles List of facial hairstyles
By type
Lanugo · Androgenic Terminal · Vellus
Facial hair
Beard · Chin curtain · Chinstrap · Goatee · Handlebar moustache · Moustache · Neckbeard · Shenandoah · Sideburns · Soul patch · Stubble · Toothbrush moustache · Van Dyke
Other areas
Head · Nose · Ear · Underarm · Chest Abdominal · Pubic · Leg
Hair loss
Baldness · Glabrousness Hair removal (waxing · threading · laser IPL · chemical · electric · Plucking) Shaving (head · leg) Razor
Related topics
Hairstyle · Hairdresser · Barber Hair length · Hair color · Hair coloring Hair fetishism · Pubic hair fetishism

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 Macaca arctoides), of which the macaques demonstrate the greatest incidence and most prominent hair loss.

Hormonal etiology

Androgens can interact with the Wnt signalling pathway to cause to hair loss.

Researchers assert 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 SHBG, FSH, 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 IGF 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. Type 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 was found to inhibit elongation of hair follicles in vitro with abnormal morphology and cell death in the bulb matrix.

Studies look at 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 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 have 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 nitric oxide synthase usually occurs in an oxidative environment, where 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 anti-microbial and anti-tumor activities as part of the oxidative burst of macrophages. The gene coding for nitric oxide synthase is on human chromosome 17.

Hair follicle and mesenchymal dermal papilla, labelled at top.

There is also crosstalk 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.

Genetics

Individual pilosebaceous unit.

Since androgens and androgen receptors (AR) are the cause of androgenic alopecia, their genetic corollaries are a subject of much research. Some involved genes are 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, however, 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 which 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 non-androgenic 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 non-androgenic alopecias.

Age effect

Two men practicing Tahtib, one of them with androgenic alopecia, on an Ostraca from Ancient Egypt, Louvre

Androgens stimulate growth of facial hair, but can suppress scalp hair, a condition which 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:

1. Decrease in testosterone
2. Decrease in DHT and 5-alpha reductase
3. Decrease 3AAG, a peripheral marker of DHT metabolism,
4. Increase in SHBG.
5. Decrease in androgen receptors in the scalp with age.

This decrease in androgens, 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 anti-androgens such as finasteride.

Free testosterone decreases in men by age 80 to levels double that of a woman at age 20. 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. It has been theorized that the testicular secretion of testosterone "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 2nd decade, for example, causes slow progression of androgenic alopecia over many years, while testosterone late in life causes rapid hair loss within a month.

An example of premature age effect is Werner's syndrome, a condition of accelerated aging from low fidelity copying of mRNA. Affected children display premature androgenic alopecia.

Androgenic impact of exercise

The impact of aerobic exercise on hair loss is different in acute and chronic settings.

Exercise can impact androgenic hair loss by affecting androgen and estrogen levels. The Rancho Bernardo Study, a large cross sectional examination of a community in southern California based on self report, found that among both genders there was no significant difference in premature graying or balding status related to alcohol, smoking, exercise, appropriate use of calcium supplements, diuretics, or thyroid medication. In women with androgenic alopecia, there was an increased association with corticosteroid and estrogen use. Self reports typically have less strength in the context of evidence based medicine and hormonal indices were not measured in this study.

Quantification of androgen indices in response to exercise can be understood in four categories: short versus long term, and anaerobic versus aerobic. These are indirect assays of exercise impact on hair loss, although the ability of exogenous androgen to worsen or precipitate miniaturization in the genetically predisposed is well documented. Investigations have been either self-report, or cross-sectional and cohort studies with exercise and serum hormonal indices, but no phase III clinical trials. In some studies, conflicting results are thought related to differences in exercise mode, volume, or physical condition of subjects.

In cross-sectional analyses, aerobic exercisers have lower basal total and free testosterone compared to the sedentary. Anaerobic exercisers also have lower testosterone compared to the sedentary with slight increase in basal testosterone in resistance training over time. There is some correlation between testosterone and physical activity in the middle aged and elderly. Acutely, testosterone briefly increases when comparing aerobic, anaerobic and mixed forms of exercise. A study assessed men who were resistance trained, endurance trained, or sedentary in which they either rested, ran or did a resistance session. Androgens increased in response to exercise, particularly resistance, while cortisol only increased with resistance. DHEA increased with resistance exercise and remained elevated during recovery in resistance-trained subjects. After initial post-exercise increase, there was decline in free and total testosterone during resistance recovery, particularly in resistance-trained subjects. Endurance-trained subjects showed less change in hormone levels in response to exercise than resistance-trained subjects. Another study have found relative short term effects of aerobic, anaerobic and combined anaerobic-aerobic exercise protocols on hormone levels to not be different. It showed increases in testosterone and cortisol immediately after exercise that returned to baseline in 2 hours.

Aerobic

In trained long term aerobic exercisers, basal levels are unchanged, or decreased. Acutely, endurance based aerobic efforts cause testosterone to rise.

A year long, moderate-intensity aerobic exercise program increased DHT and SHBG in sedentary men age 40-75, but had no effect on other androgens. Both DHT and SHBG increased 14% in exercisers at 3 months, and at 12 months they remained 9% above baseline. SHBG is protective against DHT as it binds free androgen. In acute assessment of hormone levels in soccer players before, during and after a game, DHT and testosterone increased during the match, but returned to baseline after 45 minutes rest. Aerobic exercise in Japanese rats done on a rodent treadmill doubled local concentrations of DHT in calf muscles as assessed by protein assay. After intense aerobic effort, high endurance athletes were also found to have lower free testosterone the next day. In prolonged endurance exercise, such as a marathon, levels ultimately decrease. Similarly, DHT drops, while adrenal androgen and cortisol will increase with the stress response.

Anaerobic

Effects of anaerobic exercise also vary with length of time.

It is unknown if anaerobic training changes individual hormone profiles, or if conditioned athletes in studies self-selected because of physiologic predisposition to physical conditioning. There is variation of response to anaerobic stress depending on exercise intensity, age, gender, length of time studied, and time at which serum indices were drawn. Most studies report that testosterone increases or is unchanged acutely, though some even report it to decrease. Anaerobic exercisers have testosterone levels below sedentary controls in cross sectional analysis. Over months to years, levels vary with intensity of training cycle in specific protocols, although follow up at two years has found baseline levels slightly increased.

The ratio of testosterone to cortisol can both increase and decrease during resistance training, depending on intensity of exercise. A study comparing young and old subjects showed acute increases in GH and testosterone for both, although the latter increased less in older men. Testosterone rises in late hours of sleep after anaerobic exercise. Androgen receptor expression increases with acute exercise in correlation to free testosterone. When comparing men and women in the 30, 50 and 70 year age groups, young and middle aged men showed increased testosterone after exercise, with the latter also having increased cortisol. Elderly men showed no change. Other studies have also shown with age there is a downtrend of testosterone and attenuated growth hormone response. Young men have shown no acute change in testosterone with resistance training, with increase in cortisol and growth hormone depending on intensity. One study in young men showed testosterone acutely stable, with increase in GH and IGF-1. Similarly, a study showed testosterone did not increase in young men, women, and pubescent boys unaccustomed to weight training when corrected for plasma volume. Extreme intensity of strength training may trigger the stress response, resulting in lower testosterone levels, an effect accentuated by energy deprivation. A separate study comparing different ages, however, found no difference in acute testosterone and cortisol levels between groups, but attenuated growth hormone response in the elderly. Acutely, other studies have shown testosterone to increase. In a small group of anaerobically trained athletes, stressful training acutely even decreased serum testosterone and its ratio to cortisol and SHBG, with an increase in LH. With subsequent decompensation, testosterone was stable, but cortisol and SHBG decreased. Another case control showed with intense training followed by rest, testosterone dropped and LH increased initially.

Interval and quality of exercise also affect hormonal response. Sessions of moderate to high intensity with multiple sets and short time intervals, during which energy is derived from glycolytic lactate metabolism, appear to be the greatest stimulus for steroid hormone response. Hormonal response in young men varies with the number of sets in the exercise session. However, when the number increased from 4 to 6, anabolic levels stabilized and cortisol continued to rise, suggesting that alterations in anaerobic volume could alter anabolic and catabolic hormonal balance. When sets are performed at maximum repetitions, interval has no influence at a certain intensity range, with no acute hormone response difference between protocols at 10 maximum reps with 2- and 5-minute intervals. There is a higher total testosterone response in hypertrophy protocols compared to those for strength and power, despite equalization of total work load (defined as load x sets x repetitions). There is a 27% greater testosterone response using protocols with simultaneous use of all four limbs. Androgenic response was also noted in protocols using upper and lower limbs separately to a lesser degree.

A number of studies have looked at effects of anaerobic exercise over months to years, showing it to be constant or slightly increased. A small case-control of anaerobic training in young untrained males over six weeks found decline in free testosterone of 17 percent. With men in their 60s, resistive training over 16 weeks did not affect baseline anabolic hormone levels, although GH increased acutely with exercise. A study over 21 weeks in male strength athletes showed basal hormone levels to be constant, despite strength increase. A follow up study looked at a larger group of weight trainers over 24 weeks, with 12 week decompensation. Training caused no change in total testosterone, but there were decreases in free testosterone, progesterone, androstendione, DHEA, cortisol, transcortin, and in the cortisol:CBG ratio, suggesting androgen turnover increased with training intensity, without change in total testosterone. A study looking at young men and resistance training over 48 weeks found increases in baseline serum testosterone from 20 ± 5 to 25 ± 5 nmol/l, and an increase in testosterone:SHBG ratio, LH and FSH.

Combined training

One study showed GH increase with anaerobic effort to be blunted in those who performed aerobic training for 60 minutes prior to strength training. Testosterone levels remained high only at the end of the training session with aerobic training followed by strength training, a phenomenon not seen with weight training done before aerobics. In an 11 week soccer training program focusing on combined vertical jumps, short sprints, and submaximal endurance running, total testosterone increased, but SHBG rose in parallel, maintaining a constant free androgen index.

Female androgenic alopecia

A recent cross sectional study on female monozygotic twins provided insight into female alopecia.

Female androgenic alopecia, clinically known as 'female pattern hair loss,' (FPHL) more often causes diffuse thinning without hairline recession. Approximately 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 regrowth include finasteride, the androgen-independent growth promoter minoxidil, or 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 statistically significant (p < 0.05) were as follows:

• 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 (p = 0.001) and longer sleep duration (p = 0.011) as risk factors, but also included PCOS (p = 0.002), lack of hat use (p = 0.017), smoking (p = 0.021), high income (p = 0.023), diabetes mellitus (p = 0.023), stress (p = 0.034), and multiple marriages (p = 0.043).

Statistically significant causes of vertex hair loss were: lack of sun protection (p = 0.020), less caffeine (p = 0.040), and a history of skin disease (p = 0.048). Higher testosterone levels were associated with increased temporal and vertex hair loss patterns (p < 0.039). Stress, smoking, more children, and a history of hypertension or cancer were associated with increased hair thinning (p < 0.05). 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 that 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.

Male homologue to PCOS

A number of studies have found a link between androgenic alopecia and metabolic syndrome, suggesting the combination as a male homologue to PCOS.

Multiple cross sectional studies have found association 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. It has been suggested that premature androgenic alopecia and insulin resistance are 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 post exercise.

Measurement of subcutaneous and visceral adipose stores by MRI, demonstrated inverse association between visceral adipose 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 insulin Growth Factor-1 (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 GH (growth hormone). Methods of increasing IGF include exercise, hypoglycemia, low fatty acids, deep sleep (stage IV REM), estrogens, and consumption of amino acids like 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.

Evolutionary biology

Certain studies have suggested androgenetic alopecia conveys survival advantage.

Some studies have suggested a survival advantage with androgenic alopecia. Psychologists have noted when showing subjects people with difference appearances, decrease in cranial hair was associated with social maturity, appeasement, older age, and decreased attractiveness and aggressiveness.

A study from South Korea showed most people rated balding men less attractive. Men and women viewed six male models with different levels of facial and cranial hair, and participants rated each combination on 32 adjectives related to social perception. 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 full heads of hair were seen as more aggressive, while baldness was associated with social maturity.

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

Psychological effects

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.

Diagnosis

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.

Treatment

Main article: Management of androgenic alopecia

Conventional medicine

Early stages of hair loss can be slowed or reversed with medication, with FDA approved drugs being minoxidil and finasteride. Topical formulations of finasteride have 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 systemic options include the longer acting dutasteride and spironolactone, the latter of which has a high rate of feminizing side effects.^{[citation needed]}

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.

Alternative and future therapies

The field of research to prevent and treat androgenic hair loss is vast, with systemic and topical therapies with varying degrees of efficacy. In the United States alone, it is a multi-billion dollar industry. Low-level laser therapy (LLLT) claims to stimulate hair growth through "photo-biostimulation" of hair follicles, but has limited evidence of benefit or safety. L-Carnitine induces hair growth in vitro. TRX2, a hair loss supplement, includes it as the main ingredient. It is technically a dietary supplement, and not approved by the Food and Drug Administration. Consumption of grateloupia elliptica, a red seaweed in Jeju Island, South Korea, has the potential to treat androgenic alopecia and alopecia areata. Topical IGF in a liposomal vehicle thickens and elongates hair in transgenic mice with androgenic alopecia. The enzyme prostaglandin D2 (PGD2) was present in the scalp of balding men at higher levels than those with hair, and prevented hair follicle maturation, with the possibility of treatment based on this research by 2014.

See also

• Baldness
• Dihydrotestosterone
• Hamilton-Norwood scale
• Ludwig scale
• Management of baldness
• Noncicatricial alopecia

References

External links

• NLM- Genetics Home Reference
• Scow, Dean Thomas; Nolte, Robert S.; Shaugnessy, Allen F. (April 1999). "Medical treatments for balding in men". American family physician 59 (8): 2189–2194, 2196. PMID 10221304. http://www.aafp.org/afp/990415ap/2189.html.
• Kabai, P (2008). "Androgenic alopecia may have come about to protect men from prostate cancer by increasing skin exposure to ultraviolet radiation". Medical Hypotheses 70 (5): 1038–1040. doi:10.1016/j.mehy.2007.07.044. PMID 17910907.
• How Hair Replacement Works Covers oral medications, hair transplant surgery, and topical treatments.
• Male Pattern Baldness Genetics
• Article examining the impact of baldness on career success from USA Today

UpToDate Contents

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• 1. 男性における男性型脱毛症の治療 treatment of androgenetic alopecia in men
• 2. 男性における男性型脱毛症：病因、臨床的特徴、および診断 androgenetic alopecia in men pathogenesis clinical features and diagnosis
• 3. 脱毛の評価および診断 evaluation and diagnosis of hair loss
• 4. 女性型脱毛症（女性のアンドロゲン性脱毛症）：治療および予後 female pattern hair loss androgenetic alopecia in women treatment and prognosis
• 5. 卵巣莢膜細胞過形成 ovarian hyperthecosis

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• Histological assessment of follicular delivery of flutamide by solid lipid nanoparticles: potential tool for the treatment of androgenic alopecia.

• Hamishehkar H1, Ghanbarzadeh S1,2, Sepehran S3, Javadzadeh Y4, Adib ZM5, Kouhsoltani M6.
• Drug development and industrial pharmacy.Drug Dev Ind Pharm.2016 Jun;42(6):846-53. doi: 10.3109/03639045.2015.1062896. Epub 2015 Jul 7.
• CONTEXT: Flutamide is a potent anti-androgen with the several unwanted side effects in systemic administration, therefore, it has attracted special interest in the development of topically applied formulations for the treatment of androgenic alopecia.OBJECTIVE: The purpose of this study was to prepa
• PMID 26154267

• Applications of platelet-rich plasma in dermatology: A critical appraisal of the literature.

• Lynch MD1, Bashir S1.
• The Journal of dermatological treatment.J Dermatolog Treat.2016 Jun;27(3):285-9. doi: 10.3109/09546634.2015.1094178. Epub 2015 Oct 14.
• Platelet-rich plasma (PRP) is an autologous blood-derived product enriched in platelets, growth factors, chemokines and cytokines. Initial applications were predominantly in musculoskeletal and maxillofacial fields, however in recent years, it has been used for a range of dermatological indications
• PMID 26466811

Japanese Journal

• 英語でNATURE(第78回)男性型脱毛症の原因についての手がかり

• Phillips Melissa Lee
• Natureダイジェスト : 日本語で読む世界の最新科学ニュース 9(7), 38-40, 2012-07
• NAID 40019380946

• 毛髪再生とアンチエイジング

• 小友 進
• Drug delivery system 24(2), 109-116, 2009-03-13
• 加齢に伴う脱毛は，老人性脱毛と男性型脱毛である．老人性脱毛は，老化による毛包の消失によるもので，一定の脱毛パターンをつくらない．一方，男性型脱毛は，男性ホルモンによって起こる第二次性徴として定義され，その発症は主に毛サイクルの成長期が，男性ホルモンによって短縮して起こる毛包の矮小化で，特徴ある脱毛パターンを形成する．外観上も心理的にも関心と重要性が大きいのは後者で，そのためのアンチエイジングとして …
• NAID 10024781214

• Male-pattern baldness susceptibility locus at 20p11

• RICHARDS J. B.
• Nat Genet 40, 1282-1284, 2008
• NAID 80019845146

Related Links

• Male pattern baldness: MedlinePlus Medical Encyclopedia

Male pattern baldness is related to your genes and male sex hormones. It usually follows a pattern of receding hairline and hair thinning on the crown, and is caused by hormones and genetic predisposition. Each strand ...

• What Is Male Pattern Baldness? - WebMD - Better ...

An overview of male hair loss, which affects most men at some point in their life. ... The male pattern baldness (MPB) form of androgenetic alopecia (there is also a female pattern baldness) accounts for more than 95% ...

Related Pictures

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★リンクテーブル★

リンク元	「男性型脱毛症」「androgenetic alopecia」
関連記事	「pattern」「male」「baldness」「patterning」「males」

「男性型脱毛症」

　　[★]

英

male pattern alopecia, androgenetic alopecia AGA、male pattern baldness

関

脱毛症、壮年性脱毛症

「androgenetic alopecia」

　　[★]

• 男性型脱毛症

関

AGA、alopecia、baldness、male pattern baldness

「pattern」

　　[★]

• n.

• パターン、様式、型、種類

• v.

• パターン形成する

関

class、fashion、form、kind、manner、modal、modality、mode、pattern formation、patterning、sort、type、typed

　 　 　

「male」

　　[★]

• n.

• オス、男性

• adj.

• 雄性の、男の

関

female、glycogen synthase kinase 3 beta、male sex、males、man、men

　 　 　 　 　 　

「baldness」

　　[★]

• 脱毛症、禿頭症

関

alopecia、androgenetic alopecia、decalvant、male pattern baldness

関

Alopecia

　 　

「patterning」

　　[★]

• n.

• パターン形成、パターニング、パターンニング、パターン化

関

pattern、pattern formation

「males」

　　[★]

• np.

• オス、男

関

male