Pattern hair loss

Pattern hair loss (also known as androgenetic alopecia (AGA)[1]) is a hair loss condition that primarily affects the top and front of the scalp.[2][3] In male-pattern hair loss (MPHL), the hair loss typically presents itself as either a receding front hairline, loss of hair on the crown (vertex) of the scalp, or a combination of both. Female-pattern hair loss (FPHL) typically presents as a diffuse thinning of the hair across the entire scalp.[3]

Pattern hair loss
Other namesMale pattern baldness;
Female pattern baldness;
Androgenic alopecia;
Androgenetic alopecia;
alopecia androgenetica
Male-pattern hair loss shown on the vertex of the scalp
SpecialtyDermatology, plastic surgery

Male pattern hair loss seems to be due to a combination of oxidative stress,[4] the microbiome of the scalp,[5][6] genetics, and circulating androgens; particularly dihydrotestosterone (DHT).[3] Men with early onset androgenic alopecia (before the age of 35) have been deemed as the male phenotypic equivalent for polycystic ovary syndrome (PCOS).[7][8][9][10] As an early clinical expression of insulin resistance and metabolic syndrome, AGA is related to being an increased risk factor for cardiovascular diseases, glucose metabolism disorders,[11] type 2 diabetes,[12][13] and enlargement of the prostate.[14]

The cause in female pattern hair loss remains unclear,[3] androgenetic alopecia for women is associated with an increased risk of polycystic ovary syndrome (PCOS).[15][16][17]

Management may include simply accepting the condition[3] or shaving one's head to improve the aesthetic aspect of the condition.[18] Otherwise, common medical treatments include minoxidil, finasteride, dutasteride, or hair transplant surgery.[3] Use of finasteride and dutasteride in women is not well-studied and may result in birth defects if taken during pregnancy.[3]

Pattern hair loss by the age of 50 affects about half of males and a quarter of females.[3] It is the most common cause of hair loss. Both males aged 40–91 [19] and younger male patients of early onset AGA (before the age of 35), had a higher likelihood of metabolic syndrome (MetS) [20][21][22][23] and insulin resistance.[24] With younger males, studies found metabolic syndrome to be at approximately a 4x increased frequency which is clinically deemed as significant.[25][26] Abdominal obesity, hypertension and lowered high density lipoprotein were also significantly higher for younger groups.[27]

Signs and symptoms
Hair follicle and mesenchymal dermal papilla, labelled at top

Pattern hair loss is classified as a form of non-scarring hair loss.

Male-pattern hair loss begins above the temples and at the vertex (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.[28]

Female-pattern hair loss more often causes diffuse thinning without hairline recession; similar to its male counterpart, female androgenic alopecia rarely leads to total hair loss.[29] The Ludwig scale grades severity of female-pattern hair loss. These include Grades 1, 2, 3 of balding in women based on their scalp showing in the front due to thinning of hair.

In most cases, receding hairline is the first starting point; the hairline starts moving backwards from the front of the head and the sides.[30]

Causes

Hormones and genes

KRT37 is the only keratin that is regulated by androgens.[31] This sensitivity to androgens was acquired by Homo sapiens and is not shared with their great ape cousins. Although Winter et al. found that KRT37 is expressed in all the hair follices of chimpanzees, it was not detected in the head hair of modern humans. As androgens are known to grow hair on the body, but decrease it on the scalp, this lack of scalp KRT37 may help explain the paradoxical nature of Androgenic alopecia as well as the fact that head hair anagen cycles are extremely long.

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

The initial programming of pilosebaceous units of hair follicles begins in utero.[32] The physiology is primarily androgenic, with dihydrotestosterone (DHT) being the major contributor at the dermal papillae. Men with premature androgenic alopecia tend to have lower than normal values of sex hormone-binding globulin (SHBG), follicle stimulating hormone (FSH), testosterone, and epitestosterone when compared to men without pattern hair loss.[10] Although hair follicles were previously thought to be permanently gone in areas of complete hair loss, they are more likely dormant, as recent studies have shown the scalp contains the stem cell progenitor cells from which the follicles arose.[33][34]

Transgenic studies have shown that growth and dormancy of hair follicles are related to the activity of insulin-like growth factor (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 can suppress it at the temples and scalp vertex, a condition that has been referred to as the 'androgen paradox'.[35]

Men with androgenic alopecia typically have higher 5α-reductase, higher total testosterone, higher unbound/free testosterone, and higher free androgens, including DHT.[36] 5-alpha-reductase converts free testosterone into DHT, and is highest in the scalp and prostate gland. DHT is most commonly formed at the tissue level by 5α-reduction of testosterone.[37] The genetic corollary that codes for this enzyme has been discovered.[38] Prolactin has also been suggested to have different effects on the hair follicle across gender.[39]

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.[35] Other research suggests the enzyme prostaglandin D2 synthase and its product prostaglandin D2 (PGD2) in hair follicles as contributive.[40]

These observations have led to study at the level of the mesenchymal dermal papillae.[41] Types 1 and 2 5α reductase enzymes are present at pilosebaceous units in papillae of individual hair follicles.[42] They catalyze formation of the androgens testosterone and DHT, which in turn regulate hair growth.[35] Androgens have different effects at different follicles: they stimulate IGF-1 at facial hair, leading to growth, but can also stimulate TGF β1, TGF β2, dickkopf1, and IL-6 at the scalp, leading to catagenic miniaturization.[35] Hair follicles in anaphase express four different caspases. Significant levels of inflammatory infiltrate have been found in transitional hair follicles.[43] Interleukin 1 is suspected to be a cytokine mediator that promotes hair loss.[44]

The fact that hair loss is cumulative with age while androgen levels fall as well as the fact that finasteride does not reverse advanced stages of androgenetic alopecia remains a mystery, but possible explanations are higher conversion of testosterone to DHT locally with age as higher levels of 5-alpha reductase are noted in balding scalp, and higher levels of DNA damage in the dermal papilla as well as senescence of the dermal papilla due to androgen receptor activation and environmental stress.[45] The mechanism by which the androgen receptor triggers dermal papilla permanent senescence is not known, but may involve IL6, TGFB-1 and oxidative stress. Senescence of the dermal papilla is measured by lack of mobility, different size and shape, lower replication and altered output of molecules and different expression of markers. The dermal papilla is the primary location of androgen action and its migration towards the hair bulge and subsequent signaling and size increase are required to maintain the hair follicle so senescence via the androgen receptor explains much of the physiology.

Inheritance
X-linked recessive inheritance

Male pattern baldness is a complex genetic condition with a "particularly strong signals on the X chromosome".[46]

Metabolic syndrome

Multiple cross-sectional studies have found associations between early androgenic alopecia, insulin resistance, and metabolic syndrome,[47][48] with low HDL being the component of metabolic syndrome with highest association.[49] Linolenic and linoleic acids, two major dietary sources of HDL, are 5 alpha reductase inhibitors.[50] Premature androgenic alopecia and insulin resistance may be a clinical constellation that represents the male homologue, or phenotype, of polycystic ovary syndrome.[51] Others have found a higher rate of hyperinsulinemia in family members of women with polycystic ovarian syndrome.[52] With early-onset AGA having an increased risk of metabolic syndrome, poorer metabolic profiles are noticed in those with AGA, including metrics for body mass index, waist circumference, fasting glucose, blood lipids, and blood pressure.[53]

In support of the association, finasteride improves glucose metabolism and decreases glycosylated hemoglobin HbA1c, a surrogate marker for diabetes mellitus.[54] The low SHBG seen with premature androgenic alopecia is also associated with, and likely contributory to, insulin resistance,[55] and for which it still is used as an assay for pediatric diabetes mellitus.[56]

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.[57] In vivo, insulin stimulates both testosterone production and SHBG inhibition in normal and obese men.[58] 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.[59] Patients with Laron syndrome, with resultant deficient IGF, demonstrate varying degrees of alopecia and structural defects in hair follicles when examined microscopically.[60]

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.[10] 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.[61] 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.[62]

Female patients with mineralocorticoid resistance present with androgenic alopecia.[63]

IGF levels have been found lower in those with metabolic syndrome.[64] Circulating serum levels of IGF-1 are increased with vertex balding, although this study did not look at mRNA expression at the follicle itself.[65] 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.[66]

Age

A number of hormonal changes occur with aging:

  1. Decrease in testosterone
  2. Decrease in serum DHT and 5-alpha reductase
  3. Decrease 3AAG, a peripheral marker of DHT metabolism
  4. Increase in SHBG
  5. Decrease in androgen receptors, 5-alpha reductase type I and II activity, and aromatase in the scalp[67][68]

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.[69]

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.[70] 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.[71]

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.[72]

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 [73][74] suggests that dermal fibrosis is associated with the progressive hair-loss and hair-whitening in old people.[75] 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.

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.[76] Trichoscopy can be used for further evaluation.[77] Biopsy may be needed to exclude other causes of hair loss,[78] and histology would demonstrate perifollicular fibrosis.[79][80] The Hamilton–Norwood scale has been developed to grade androgenic alopecia in males by severity.

Treatment
Main article: Management of hair loss

Androgen-dependent

Finasteride is a medication of the 5α-reductase inhibitors (5-ARIs) class.[81] By inhibiting type II 5-AR, finasteride prevents the conversion of testosterone to dihydrotestosterone in various tissues including the scalp.[81][82] Increased hair on the scalp can be seen within three months of starting finasteride treatment and longer-term studies have demonstrated increased hair on the scalp at 24 and 48 months with continued use.[82] Treatment with finasteride more effectively treats male-pattern hair loss at the crown than male-pattern hair loss at the front of the head and temples.[82]

Dutasteride is a medication in the same class as finasteride but inhibits both type I and type II 5-alpha reductase.[82] Dutasteride is approved for the treatment of male-pattern hair loss in Korea and Japan, but not in the United States.[82] However, it is commonly used off-label to treat male-pattern hair loss.[82]

Androgen-independent

Minoxidil dilates small blood vessels; it is not clear how this causes hair to grow.[83] Other treatments include tretinoin combined with minoxidil, ketoconazole shampoo, dermarolling (Collagen induction therapy), spironolactone,[84] alfatradiol, topilutamide (fluridil),[81] topical melatonin,[85][86][87] and intradermal and intramuscular botulinum toxin injections to the scalp.[88]

Female pattern

There is evidence supporting the use of minoxidil as a safe and effective treatment for female pattern hair loss, and there is no significant difference in efficiency between 2% and 5% formulations.[89] Finasteride was shown to be no more effective than placebo based on low-quality studies.[89] The effectiveness of laser-based therapies is unclear.[89] Bicalutamide, an antiandrogen, is another option for the treatment of female pattern hair loss.[90][4][91]

Procedures

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.[84] 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, and in the latter individual hairs are extracted manually or robotically. The surgeon then implants the grafts into small incisions, called recipient sites.[92][93] Cosmetic scalp tattoos can also mimic the appearance of a short, buzzed haircut.

Alternative therapies

Many people use unproven treatments.[94] Regarding female pattern alopecia, there is no evidence for vitamins, minerals, or other dietary supplements.[95] As of 2008, there is little evidence to support the use of lasers to treat male-pattern hair loss.[96] The same applies to special lights.[95] Dietary supplements are not typically recommended.[96] A 2015 review found a growing number of papers in which plant extracts were studied but only one randomized controlled clinical trial, namely a study in 10 people of saw palmetto extract.[97][98]

Prognosis

Androgenic alopecia is typically experienced as a "moderately stressful condition that diminishes body image satisfaction".[99] However, although most men regard baldness as an unwanted and distressing experience, they usually are able to cope and retain integrity of personality.[100]

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.[101]

Epidemiology

Female androgenic alopecia 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.[102]

For male androgenic alopecia, by the age of 50 30-50% of men have it, hereditarily there is an 80% predisposition.[103] Notably, the link between androgenetic alopecia and metabolic syndrome is strongest in non-obese men.[104]

Society and culture
Certain studies have suggested androgenic alopecia conveys survival advantage

Studies have been inconsistent across cultures regarding how balding men rate on the attraction scale. While a 2001 South Korean study showed that most people rated balding men as less attractive,[105] a 2002 survey of Welsh women found that they rated bald and gray-haired men quite desirable.[106] One of the proposed social theories for male pattern hair loss is that men who embraced complete baldness by shaving their heads subsequently signaled dominance, high social status, and/or longevity.[18]

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.[107]

Myths
An ancient phenomenon: Greek philosophers with and without much hair (from left to right: Socrates, Antisthenes, Chrysippus, and Epicurus, fifth to third centuries BC)

Many myths exist regarding the possible causes of baldness and its relationship with one's virility, intelligence, ethnicity, job, social class, wealth, and many other characteristics.

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 life and baldness, suggesting exercise is causally relevant. The type or quantity of exercise may influence hair loss.[108][109] 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.

Baldness can be caused by emotional stress, sleep deprivation, etc.

Emotional stress has been shown to accelerate baldness in genetically susceptible individuals.[110] Stress due to sleep deprivation in military recruits lowered testosterone levels, but is not noted to have affected SHBG.[111] Thus, stress due to sleep deprivation in fit males is unlikely to elevate DHT, which is one cause of male pattern baldness. Whether sleep deprivation 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.[112][113]

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 a cause, of higher DHT levels.[114] Another study shows that although sexual arousal and masturbation-induced orgasm increase testosterone concentration around orgasm, they reduce testosterone concentration on average, and because about 5% of testosterone is converted to DHT, ejaculation does not elevate DHT levels.[115]

The only published study to test correlation between ejaculation frequency and baldness was probably large enough to detect an association (1,390 subjects) and found no correlation, although persons with only vertex androgenetic alopecia 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.[116]

Other animals

Animal models of androgenic alopecia occur naturally and have been developed in transgenic mice;[117] 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.[118][119]

Baldness is not a trait unique to human beings. One possible case study is about a maneless male lion in the Tsavo area. The Tsavo lion 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. Male lions 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.[120]

Although primates do not go bald, their hairlines do undergo recession. In infancy the hairline starts at the top of the supraorbital ridge, but slowly recedes after puberty to create the appearance of a small forehead.

References
  1. "Androgenetic alopecia". National Library of Medicine, Bethesda, Maryland, United States. 1 August 2015. Retrieved 3 April 2022.
  2. Wang EH, Monga I, Sallee BN, Chen JC, Abdelaziz AR, Perez-Lorenzo R, Bordone LA, Christiano AM (Jul 2022). "Primary cicatricial alopecias are characterized by dysregulation of shared gene expression pathways". PNAS Nexus. 1 (3): pgac111. doi:10.1093/pnasnexus/pgac111. PMC 9308563. PMID 35899069.
  3. Vary JC (November 2015). "Selected Disorders of Skin Appendages--Acne, Alopecia, Hyperhidrosis". The Medical Clinics of North America (Review). 99 (6): 1195–1211. doi:10.1016/j.mcna.2015.07.003. PMID 26476248.
  4. Meyer-Gonzalez T, Bacqueville D, Grimalt R, Mengeaud V, Piraccini BM, Rudnicka L, et al. (November 2021). "Current controversies in trichology: a European expert consensus statement". Journal of the European Academy of Dermatology and Venereology. 35 (Suppl 2): 3–11. doi:10.1111/jdv.17601. PMID 34668238. S2CID 239029062.
  5. Suzuki, K.; Inoue, M.; Cho, O.; Mizutani, R.; Shimizu, Y.; Nagahama, T.; Sugita, T. (2021). "Scalp Microbiome and Sebum Composition in Japanese Male Individuals with and without Androgenetic Alopecia". Microorganisms. 9 (10): 2132. doi:10.3390/microorganisms9102132. PMC 8536999. PMID 34683453.
  6. Huang, J.; Ran, Y.; Pradhan, S.; Yan, W.; Dai, Y. (2019). "Investigation on Microecology of Hair Root Fungi in Androgenetic Alopecia Patients". Mycopathologia. 184 (4): 505–515. doi:10.1007/s11046-019-00345-8. PMID 31240449. S2CID 195353938.
  7. Cannarella, Rossella; La Vignera, Sandro; Condorelli, Rosita A.; Calogero, Aldo E. (2017). "Glycolipid and Hormonal Profiles in Young Men with Early-Onset Androgenetic Alopecia: A meta-analysis". Scientific Reports. 7 (1): 7801. Bibcode:2017NatSR...7.7801C. doi:10.1038/s41598-017-08528-3. PMC 5552767. PMID 28798373.
  8. Sanke, S.; Chander, R.; Jain, A.; Garg, T.; Yadav, P. (2016). "A Comparison of the Hormonal Profile of Early Androgenetic Alopecia in Men with the Phenotypic Equivalent of Polycystic Ovarian Syndrome in Women". JAMA Dermatology. 152 (9): 986–991. doi:10.1001/jamadermatol.2016.1776. PMID 27304785. S2CID 26897074.
  9. Krysiak, R.; Kowalcze, K.; Okopień, B. (2022). "Impaired metabolic effects of metformin in men with early-onset androgenic alopecia". Pharmacological Reports. 74 (1): 216–228. doi:10.1007/s43440-021-00347-8. PMC 8786753. PMID 34897595.
  10. Starka L, Duskova M, Cermakova I, Vrbiková J, Hill M (December 2005). "Premature androgenic alopecia and insulin resistance. Male equivalent of polycystic ovary syndrome?". Endocrine Regulations. Slovak Academic Press. 39 (4): 127–131. PMID 16552990. Archived from the original (pdf) on March 8, 2019. Retrieved Mar 7, 2019.
  11. Duskova M, Starka L, Hill M, Dolezal M, Simunkova K, Cermakova I (2006). "Is there male androgenetic alopecia the sign of male equivalent of polycystic ovary syndrome or metabolic syndrome?". Endocrine Abstracts. 11 (11): 366. eISSN 1479-6848. ISSN 1470-3947.
  12. Cannarella, R.; Condorelli, R. A.; Mongioì, L. M.; La Vignera, S.; Calogero, A. E. (2018). "Does a male polycystic ovarian syndrome equivalent exist?". Journal of Endocrinological Investigation. 41 (1): 49–57. doi:10.1007/s40618-017-0728-5. PMID 28711970. S2CID 11255317.
  13. Rodríguez-Gutiérrez, R.; Salcido-Montenegro, A.; González-González, J. G. (2018). "Early Clinical Expressions of Insulin Resistance: The Real Enemy to Look for". Diabetes Therapy: Research, Treatment and Education of Diabetes and Related Disorders. 9 (1): 435–438. doi:10.1007/s13300-017-0348-2. PMC 5801234. PMID 29209995.
  14. Ramsamy, K.; Subramaniyan, R.; Patra, A. K. (2016). "An observational Study of the Association between Androgenetic Alopecia and Size of the Prostate". International Journal of Trichology. 8 (2): 62–66. doi:10.4103/0974-7753.188034. PMC 4989389. PMID 27601858.
  15. Goodman, N. F.; Cobin, R. H.; Futterweit, W.; Glueck, J. S.; Legro, R. S.; Carmina, E.; American Association of Clinical Endocrinologists (AACE); American College of Endocrinology (ACE); Androgen Excess PCOS Society (AES) (2015). "American Association of Clinical Endocrinologists, American College of Endocrinology, and Androgen Excess and Pcos Society Disease State Clinical Review: Guide to the Best Practices in the Evaluation and Treatment of Polycystic Ovary Syndrome--Part 1". Endocrine Practice. 21 (11): 1291–1500. doi:10.4158/EP15748.DSC. PMID 26509855.
  16. Camacho-Martínez, F. M. (2009). "Hair loss in women". Seminars in Cutaneous Medicine and Surgery. 28 (1): 19–32. doi:10.1016/j.sder.2009.01.001. PMID 19341939.
  17. Moura, H. H.; Costa, D. L.; Bagatin, E.; Sodré, C. T.; Manela-Azulay, M. (2011). "Polycystic ovary syndrome: A dermatologic approach". Anais Brasileiros de Dermatologia. 86 (1): 111–119. doi:10.1590/s0365-05962011000100015. PMID 21437531.
  18. Dunn R (2012). "Why haven't bald men gone extinct?". New Scientist. 214 (2869): 44–47. Bibcode:2012NewSc.214...44D. doi:10.1016/s0262-4079(12)61567-x. Retrieved Dec 16, 2012.
  19. Su, L. H.; Chen, T. H. (2010). "Association of androgenetic alopecia with metabolic syndrome in men: A community-based survey". The British Journal of Dermatology. 163 (2): 371–377. doi:10.1111/j.1365-2133.2010.09816.x. PMID 20426781. S2CID 23615726.
  20. Ertas, R.; Orscelik, O.; Kartal, D.; Dogan, A.; Ertas, S. K.; Aydogdu, E. G.; Ascioglu, O.; Borlu, M. (2016). "Androgenetic alopecia as an indicator of metabolic syndrome and cardiovascular risk". Blood Pressure. 25 (3): 141–148. doi:10.3109/08037051.2015.1111021. PMID 26585114. S2CID 12031777.
  21. Dharam Kumar, K. C.; Kishan Kumar, Y. H.; Neladimmanahally, V. (2018). "Association of Androgenetic Alopecia with Metabolic Syndrome: A Case-control Study on 100 Patients in a Tertiary Care Hospital in South India". Indian Journal of Endocrinology and Metabolism. 22 (2): 196–199. doi:10.4103/ijem.IJEM_650_17. PMC 5972473. PMID 29911030.
  22. Bakry, O. A.; Shoeib, M. A.; El Shafiee, M. K.; Hassan, A. (2014). "Androgenetic alopecia, metabolic syndrome, and insulin resistance: Is there any association? A case-control study". Indian Dermatology Online Journal. 5 (3): 276–281. doi:10.4103/2229-5178.137776. PMC 4144211. PMID 25165643.
  23. Banger, H. S.; Malhotra, S. K.; Singh, S.; Mahajan, M. (2015). "Is Early Onset Androgenic Alopecia a Marker of Metabolic Syndrome and Carotid Artery Atherosclerosis in Young Indian Male Patients?". International Journal of Trichology. 7 (4): 141–147. doi:10.4103/0974-7753.171566. PMC 4738480. PMID 26903742.
  24. Acibucu, F.; Kayatas, M.; Candan, F. (2010). "The association of insulin resistance and metabolic syndrome in early androgenetic alopecia". Singapore Medical Journal. 51 (12): 931–936. PMID 21221497.
  25. Sheikh, F. Z.; Butt, G.; Hafeez, R.; Maqsood, A.; Altaf, F.; Hussain, I. (2021). "Association of Early-onset Androgenetic Alopecia and Metabolic Syndrome". Journal of the College of Physicians and Surgeons (Pakistan). 31 (2): 123–127. doi:10.29271/jcpsp.2021.02.123. PMID 33645175. S2CID 232079822.
  26. Pengsalae, N.; Tanglertsampan, C.; Phichawong, T.; Lee, S. (2013). "Association of early-onset androgenetic alopecia and metabolic syndrome in Thai men: A case-control study". Journal of the Medical Association of Thailand = Chotmaihet Thangphaet. 96 (8): 947–951. PMID 23991602.
  27. Gopinath, H.; Upadya, G. M. (2016). "Metabolic syndrome in androgenic alopecia". Indian Journal of Dermatology, Venereology and Leprology. 82 (4): 404–408. doi:10.4103/0378-6323.174421. PMID 27279298. S2CID 24300999.
  28. "Hippocratic wreath (Baldness)". Britannica Online. Dec 15, 2012. Retrieved Dec 15, 2012.
  29. "Female pattern baldness". MedlinePlus. Dec 15, 2012. Retrieved Dec 15, 2012.
  30. Rammos CK, Mardini S (January 2016). "Endoscopic Browlift in the Receding Hairline Patient". The Journal of Craniofacial Surgery. 27 (1): 156–158. doi:10.1097/SCS.0000000000002266. PMID 26674899. S2CID 6206827.
  31. Jave-Suarez LF, Langbein L, Winter H, Praetzel S, Rogers MA, Schweizer J (March 2004). "Androgen regulation of the human hair follicle: the type I hair keratin hHa7 is a direct target gene in trichocytes". The Journal of Investigative Dermatology. 122 (3): 555–564. doi:10.1111/j.0022-202X.2004.22336.x. PMID 15086535.
  32. Alonso LC, Rosenfield RL (2003). "Molecular genetic and endocrine mechanisms of hair growth". Hormone Research. 60 (1): 1–13. doi:10.1159/000070821. PMID 12792148. S2CID 40910080.
  33. Garza LA, Yang CC, Zhao T, Blatt HB, Lee M, He H, et al. (February 2011). "Bald scalp in men with androgenetic alopecia retains hair follicle stem cells but lacks CD200-rich and CD34-positive hair follicle progenitor cells". The Journal of Clinical Investigation. 121 (2): 613–622. doi:10.1172/JCI44478. PMC 3026732. PMID 21206086.
  34. Rahmani W, Sinha S, Biernaskie J (2020-05-11). "Immune modulation of hair follicle regeneration". NPJ Regenerative Medicine. 5 (1): 9. doi:10.1038/s41536-020-0095-2. PMC 7214459. PMID 32411394.
  35. Inui S, Itami S (March 2013). "Androgen actions on the human hair follicle: perspectives". Experimental Dermatology. 22 (3): 168–171. doi:10.1111/exd.12024. PMID 23016593. S2CID 33521841.
  36. Zhang Y, Xu J, Jing J, Wu X, Lv Z (October 2018). "Serum Levels of Androgen-Associated Hormones Are Correlated with Curative Effect in Androgenic Alopecia in Young Men". Medical Science Monitor. 24: 7770–7777. doi:10.12659/MSM.913116. PMC 6223099. PMID 30376555.
  37. Kaufman JM, Vermeulen A (October 2005). "The decline of androgen levels in elderly men and its clinical and therapeutic implications". Endocrine Reviews. 26 (6): 833–876. doi:10.1210/er.2004-0013. PMID 15901667.
  38. Ellis JA, Panagiotopoulos S, Akdeniz A, Jerums G, Harrap SB (2005). "Androgenic correlates of genetic variation in the gene encoding 5alpha-reductase type 1". Journal of Human Genetics. 50 (10): 534–537. doi:10.1007/s10038-005-0289-x. PMID 16155734.
  39. Langan EA, Ramot Y, Goffin V, Griffiths CE, Foitzik K, Paus R (March 2010). "Mind the (gender) gap: does prolactin exert gender and/or site-specific effects on the human hair follicle?". The Journal of Investigative Dermatology. 130 (3): 886–891. doi:10.1038/jid.2009.340. PMID 19890346.
  40. Garza LA, Liu Y, Yang Z, Alagesan B, Lawson JA, Norberg SM, et al. (March 2012). "Prostaglandin D2 inhibits hair growth and is elevated in bald scalp of men with androgenetic alopecia". Science Translational Medicine. 4 (126): 126ra34. doi:10.1126/scitranslmed.3003122. PMC 3319975. PMID 22440736.
  41. Randall VA, Hibberts NA, Thornton MJ, Merrick AE, Hamada K, Kato S, et al. (2001). "Do androgens influence hair growth by altering the paracrine factors secreted by dermal papilla cells?". European Journal of Dermatology. 11 (4): 315–320. PMID 11399537.
  42. Bernard BA (1994). "[Molecular approach of hair biology]". Comptes Rendus des Séances de la Société de Biologie et de ses Filiales. 188 (3): 223–233. PMID 7834505.
  43. Jaworsky C, Kligman AM, Murphy GF (September 1992). "Characterization of inflammatory infiltrates in male pattern alopecia: implications for pathogenesis". The British Journal of Dermatology. 127 (3): 239–246. doi:10.1111/j.1365-2133.1992.tb00121.x. PMID 1390168. S2CID 11764980.
  44. Hoffmann R, Happle R (1995). "Does interleukin-1 induce hair loss?". Dermatology. 191 (4): 273–275. doi:10.1159/000246567. PMID 8573920.
  45. Yang YC, Fu HC, Wu CY, Wei KT, Huang KE, Kang HY (March 15, 2013). "Androgen receptor accelerates premature senescence of human dermal papilla cells in association with DNA damage". PLOS ONE. 8 (11): e79434. Bibcode:2013PLoSO...879434Y. doi:10.1371/journal.pone.0079434. PMC 3828374. PMID 24244503.
  46. Hagenaars, Saskia P.; Hill, W. David; Harris, Sarah E.; Ritchie, Stuart J.; Davies, Gail; Liewald, David C.; Gale, Catharine R.; Porteous, David J.; Deary, Ian J.; Marioni, Riccardo E. (2017-02-14). Noethen, Markus M. (ed.). "Genetic prediction of male pattern baldness". PLOS Genetics. 13 (2): e1006594. doi:10.1371/journal.pgen.1006594. ISSN 1553-7404. PMC 5308812. PMID 28196072.
  47. Acibucu, F.; Kayatas, M.; Candan, F. (2010). "The association of insulin resistance and metabolic syndrome in early androgenetic alopecia". Singapore Medical Journal. 51 (12): 931–936. PMID 21221497.
  48. González-González, J. G.; Mancillas-Adame, L. G.; Fernández-Reyes, M.; Gómez-Flores, M.; Lavalle-González, F. J.; Ocampo-Candiani, J.; Villarreal-Pérez, J. S. Z. A. (2009). "Androgenetic alopecia and insulin resistance in young men". Clinical Endocrinology. 71 (4): 494–499. doi:10.1111/j.1365-2265.2008.03508.x. PMID 19094069. S2CID 205285087.
  49. Su, L. H.; Chen, T. H. H. (2010). "Association of androgenetic alopecia with metabolic syndrome in men: A community-based survey". British Journal of Dermatology. 163 (2): 371–377. doi:10.1111/j.1365-2133.2010.09816.x. PMID 20426781. S2CID 23615726.
  50. Liang, T.; Liao, S. (1992). "Inhibition of steroid 5 alpha-reductase by specific aliphatic unsaturated fatty acids". The Biochemical Journal. 285 (Pt 2): 557–562. doi:10.1042/bj2850557. PMC 1132824. PMID 1637346.
  51. Legro, R. S. (2000). "Is there a male phenotype in polycystic ovary syndrome families?". Journal of Pediatric Endocrinology & Metabolism. 13 (Suppl 5): 1307–1309. PMID 11117676.
  52. Norman, R. J.; Masters, S.; Hague, W. (1996). "Hyperinsulinemia is common in family members of women with polycystic ovary syndrome". Fertility and Sterility. 66 (6): 942–947. doi:10.1016/s0015-0282(16)58687-7. PMID 8941059.
  53. Qiu, Y., Zhou, X., Fu, S., Luo, S., & Li, Y. (2022). Systematic Review and Meta-analysis of the Association Between Metabolic Syndrome and Androgenetic Alopecia. Acta dermato-venereologica, 102, adv00645. https://doi.org/10.2340/actadv.v101.1012
  54. Duskova, M.; Hill, M.; Starka, L. (2010). "Changes of metabolic profile in men treated for androgenetic alopecia with 1 mg finasteride". Endocrine Regulations. 44 (1): 3–8. doi:10.4149/endo_2010_01_3. PMID 20151762.
  55. Pugeat, M.; Crave, J. C.; Elmidani, M.; Nicolas, M. H.; Garoscio-Cholet, M.; Lejeune, H.; Déchaud, H.; Tourniaire, J. (1991). "Pathophysiology of sex hormone binding globulin (SHBG): Relation to insulin". The Journal of Steroid Biochemistry and Molecular Biology. 40 (4–6): 841–849. doi:10.1016/0960-0760(91)90310-2. PMID 1958579. S2CID 248035.
  56. Gascón, F.; Valle, M.; Martos, R.; Ruz, F. J.; Ríos, R.; Montilla, P.; Cañete, R. (2000). "Sex hormone-binding globulin as a marker for hyperinsulinemia and/or insulin resistance in obese children". European Journal of Endocrinology. 143 (1): 85–89. doi:10.1530/eje.0.1430085. PMID 10870035.
  57. Strain, G.; Zumoff, B.; Rosner, W.; Pi-Sunyer, X. (1994). "The relationship between serum levels of insulin and sex hormone-binding globulin in men: The effect of weight loss". The Journal of Clinical Endocrinology and Metabolism. 79 (4): 1173–1176. doi:10.1210/jcem.79.4.7962291. PMID 7962291.
  58. Pasquali, R.; Casimirri, F.; De Iasio, R.; Mesini, P.; Boschi, S.; Chierici, R.; Flamia, R.; Biscotti, M.; Vicennati, V. (1995). "Insulin regulates testosterone and sex hormone-binding globulin concentrations in adult normal weight and obese men". The Journal of Clinical Endocrinology and Metabolism. 80 (2): 654–658. doi:10.1210/jcem.80.2.7852532. PMID 7852532.
  59. Ducluzeau, P. H.; Cousin, P.; Malvoisin, E.; Bornet, H.; Vidal, H.; Laville, M.; Pugeat, M. (2003). "Glucose-to-insulin ratio rather than sex hormone-binding globulin and adiponectin levels is the best predictor of insulin resistance in nonobese women with polycystic ovary syndrome". The Journal of Clinical Endocrinology and Metabolism. 88 (8): 3626–3631. doi:10.1210/jc.2003-030219. PMID 12915646.
  60. Lurie, R.; Ben-Amitai, D.; Laron, Z. (2004). "Laron Syndrome (Primary Growth Hormone Insensitivity): A Unique Model to Explore the Effect of Insulin-Like Growth Factor 1 Deficiency on Human Hair". Dermatology. 208 (4): 314–318. doi:10.1159/000077839. PMID 15178913. S2CID 8285817.
  61. Nielsen, T. L.; Hagen, C.; Wraae, K.; Brixen, K.; Petersen, P. H.; Haug, E.; Larsen, R.; Andersen, M. (2007). "Visceral and Subcutaneous Adipose Tissue Assessed by Magnetic Resonance Imaging in Relation to Circulating Androgens, Sex Hormone-Binding Globulin, and Luteinizing Hormone in Young Men". Journal of Clinical Endocrinology & Metabolism. 92 (7): 2696–2705. doi:10.1210/jc.2006-1847. PMID 17426100.
  62. Bonnet, F.; Velayoudom Cephise, F. L. V.; Gautier, A.; Dubois, S. V.; Massart, C.; Camara, A.; Larifla, L.; Balkau, B.; Ducluzeau, P. H. (2012). "Role of sex steroids, intra-hepatic fat and liver enzymes in the association between SHBG and metabolic features". Clinical Endocrinology. 79 (4): 517–522. doi:10.1111/cen.12089. PMID 23121021. S2CID 24411342.
  63. Van Rossum, E. F. C.; Lamberts, S. W. J. (2006). "Glucocorticoid resistance syndrome: A diagnostic and therapeutic approach". Best Practice & Research Clinical Endocrinology & Metabolism. 20 (4): 611–626. doi:10.1016/j.beem.2006.09.005. PMID 17161335.
  64. Devarakonda, K.; Martha, S.; Pantam, N.; Thungathurthi, S.; Rao, V. (2008). "Study of insulin resistance in relation to serum IGF-I levels in subjects with different degrees of glucose tolerance". International Journal of Diabetes in Developing Countries. 28 (2): 54–59. doi:10.4103/0973-3930.43100. PMC 2772007. PMID 19902049.
  65. Signorello, L. B.; Wuu, J.; Hsieh, C.; Tzonou, A.; Trichopoulos, D.; Mantzoros, C. S. (1999). "Hormones and hair patterning in men: A role for insulin-like growth factor 1?". Journal of the American Academy of Dermatology. 40 (2 Pt 1): 200–203. doi:10.1016/s0190-9622(99)70188-x. PMID 10025745.
  66. Rosenfeld, Ron G. (Nov 9, 2010). The IGF System: Molecular Biology, Physiology, and Clinical Applications (Contemporary Endocrinology). umana Press. ISBN 978-1-61737-138-7.
  67. "Histology and hormonal activity in senescent thinning in males". European Hair Research Society - Abstract (Conference).
  68. Price, V.H. (2001). "Histology and Hormonal Activity in Senescent Thinning in Males". European Hair Research Society. Retrieved 20 October 2014.
  69. "The Bald Truth About Hair Loss In Young Men". Stephanie Whyche, InteliHealth News Service. Aug 8, 2002. Retrieved Dec 16, 2012.
  70. Hamilton, J. B. (1942). "Male hormone stimulation is prerequisite and an incitant in common baldness". American Journal of Anatomy. 71 (3): 451–480. doi:10.1002/aja.1000710306.
  71. Hamilton, J. B. (1951). "Patterned loss of hair in man; types and incidence". Annals of the New York Academy of Sciences. 53 (3): 708–728. Bibcode:1951NYASA..53..708H. doi:10.1111/j.1749-6632.1951.tb31971.x. PMID 14819896. S2CID 32685699.
  72. James, William; Berger, Timothy; Elston, Dirk (2005). Andrews' Diseases of the Skin: Clinical Dermatology. (10th ed.). Saunders. ISBN 0-7216-2921-0.
  73. Wang, Jicun; Michelitsch, Thomas; Wunderlin, Arne; Mahadeva, Ravi (2009). "Aging as a consequence of Misrepair –a novel theory of aging". arXiv:0904.0575 [q-bio.TO].
  74. Wang-Michelitsch, Jicun; Michelitsch, Thomas (2015). "Aging as a process of accumulation of Misrepairs". arXiv:1503.07163 [q-bio.TO].
  75. Wang-Michelitsch, Jicun; Michelitsch, Thomas (2015). "Tissue fibrosis: a principal evidence for the central role of Misrepairs in aging". arXiv:1505.01376 [q-bio.TO].
  76. Diagnosing Men's Hair Loss: Norwood Scale Chart. Webmd.com (2010-03-01). Retrieved on 2010-11-28.
  77. Rudnicka L, Olszewska M, Rakowska A, Kowalska-Oledzka E, Slowinska M (July 2008). "Trichoscopy: a new method for diagnosing hair loss". Journal of Drugs in Dermatology. 7 (7): 651–654. PMID 18664157.
  78. Mounsey AL, Reed SW (August 2009). "Diagnosing and treating hair loss". American Family Physician. 80 (4): 356–362. PMID 19678603.
  79. Yoo HG, Kim JS, Lee SR, Pyo HK, Moon HI, Lee JH, et al. (June 2006). "Perifollicular fibrosis: pathogenetic role in androgenetic alopecia". Biological & Pharmaceutical Bulletin. 29 (6): 1246–1250. doi:10.1248/bpb.29.1246. PMID 16755026.
  80. Rashid RM, Thomas V (August 2010). "Androgenic pattern presentation of scarring and inflammatory alopecia". Journal of the European Academy of Dermatology and Venereology. 24 (8): 979–980. doi:10.1111/j.1468-3083.2009.03557.x. PMID 20059630. S2CID 39272849.
  81. Varothai S, Bergfeld WF (July 2014). "Androgenetic alopecia: an evidence-based treatment update". American Journal of Clinical Dermatology. 15 (3): 217–230. doi:10.1007/s40257-014-0077-5. PMID 24848508. S2CID 31245042.
  82. Yim E, Nole KL, Tosti A (December 2014). "5α-Reductase inhibitors in androgenetic alopecia". Current Opinion in Endocrinology, Diabetes, and Obesity (Review). 21 (6): 493–498. doi:10.1097/MED.0000000000000112. PMID 25268732. S2CID 30008068.
  83. "Minoxidil solution". DermNet NZ. Dec 29, 2013. Retrieved Jan 29, 2014.
  84. Rogers NE, Avram MR (October 2008). "Medical treatments for male and female pattern hair loss". Journal of the American Academy of Dermatology. 59 (4): 547–566, quiz 566–8. doi:10.1016/j.jaad.2008.07.001. PMID 18793935.
  85. Fischer, TobiasW; Hänggi, Gabriella; Innocenti, Marcello; Elsner, Peter; Trüeb, RalphM (2012). "Topical Melatonin for Treatment of Androgenetic Alopecia". International Journal of Trichology. 4 (4): 236–245. doi:10.4103/0974-7753.111199. PMC 3681103. PMID 23766606.
  86. Hatem, Shymaa; Nasr, Maha; Moftah, Noha H; Ragai, Maha H; Geneidi, Ahmed S; Elkheshen, Seham A (3 October 2018). "Clinical cosmeceutical repurposing of melatonin in androgenic alopecia using nanostructured lipid carriers prepared with antioxidant oils". Expert Opinion on Drug Delivery. 15 (10): 927–935. doi:10.1080/17425247.2018.1517740. PMID 30169980. S2CID 52139971.
  87. Hatem, Shymaa; Nasr, Maha; Moftah, Noha H.; Ragai, Maha H.; Geneidi, Ahmed S.; Elkheshen, Seham A. (15 September 2018). "Melatonin vitamin C-based nanovesicles for treatment of androgenic alopecia: Design, characterization and clinical appraisal". European Journal of Pharmaceutical Sciences. 122: 246–253. doi:10.1016/j.ejps.2018.06.034. ISSN 1879-0720. PMID 29981403. S2CID 51600289.
  88. English, Robert S.; Ruiz, Sophia (March 2022). "Use of Botulinum Toxin for Androgenic Alopecia: A Systematic Review". Skin Appendage Disorders. 8 (2): 93–100. doi:10.1159/000518574. ISSN 2296-9195. PMC 8928186. PMID 35415183.
  89. van Zuuren EJ, Fedorowicz Z, Schoones J (May 2016). "Interventions for female pattern hair loss". The Cochrane Database of Systematic Reviews. 2016 (5): CD007628. doi:10.1002/14651858.CD007628.pub4. PMC 6457957. PMID 27225981.
  90. Carvalho RM, Santos LD, Ramos PM, Machado CJ, Acioly P, Frattini SC, et al. (January 2022). "Bicalutamide and the new perspectives for female pattern hair loss treatment: What dermatologists should know". Journal of Cosmetic Dermatology. doi:10.1111/jocd.14773. PMID 35032336.
  91. Nestor MS, Ablon G, Gade A, Han H, Fischer DL (December 2021). "Treatment options for androgenetic alopecia: Efficacy, side effects, compliance, financial considerations, and ethics". Journal of Cosmetic Dermatology. 20 (12): 3759–3781. doi:10.1111/jocd.14537. PMC 9298335. PMID 34741573. S2CID 243801494.
  92. Caroli S, Pathomvanich D, Amonpattana K, Kumar A (2011). "Current status of hair restoration surgery". International Surgery. 96 (4): 345–351. doi:10.9738/cc31.1. PMID 22808618.
  93. Rose PT (August 2011). "The latest innovations in hair transplantation". Facial Plastic Surgery. 27 (4): 366–377. doi:10.1055/s-0031-1283055. PMID 21792780.
  94. Banka N, Bunagan MJ, Shapiro J (January 2013). "Pattern hair loss in men: diagnosis and medical treatment". Dermatologic Clinics. 31 (1): 129–140. doi:10.1016/j.det.2012.08.003. PMID 23159182.
  95. Levy LL, Emer JJ (August 2013). "Female pattern alopecia: current perspectives". International Journal of Women's Health. 5: 541–556. doi:10.2147/IJWH.S49337. PMC 3769411. PMID 24039457.
  96. Rogers NE, Avram MR (October 2008). "Medical treatments for male and female pattern hair loss". Journal of the American Academy of Dermatology. 59 (4): 547–566, quiz 567–8. doi:10.1016/j.jaad.2008.07.001. PMID 18793935.
  97. Rondanelli M, Perna S, Peroni G, Guido D (June 2016). "A bibliometric study of scientific literature in Scopus on botanicals for treatment of androgenetic alopecia". Journal of Cosmetic Dermatology. 15 (2): 120–130. doi:10.1111/jocd.12198. PMID 26608588. S2CID 20224420.
  98. Prager N, Bickett K, French N, Marcovici G (April 2002). "A randomized, double-blind, placebo-controlled trial to determine the effectiveness of botanically derived inhibitors of 5-alpha-reductase in the treatment of androgenetic alopecia". Journal of Alternative and Complementary Medicine. 8 (2): 143–152. doi:10.1089/107555302317371433. PMID 12006122. S2CID 5866411.
  99. Cash TF (September 1999). "The psychosocial consequences of androgenetic alopecia: a review of the research literature". The British Journal of Dermatology. 141 (3): 398–405. doi:10.1046/j.1365-2133.1999.03030.x. PMID 10583042. S2CID 40583229.
  100. Cash TF (June 1992). "The psychological effects of androgenetic alopecia in men". Journal of the American Academy of Dermatology. 26 (6): 926–931. doi:10.1016/0190-9622(92)70134-2. PMID 1607410.
  101. Birch MP, Lalla SC, Messenger AG (July 2002). "Female pattern hair loss". Clinical and Experimental Dermatology. 27 (5): 383–388. doi:10.1046/j.1365-2230.2002.01085.x. PMID 12190638. S2CID 39467830.
  102. "Women and Hair Loss: The Causes". Archived from the original on 30 June 2010. Retrieved 2010-06-29.
  103. Cranwell, W.; et al. (2000). "Male Androgenetic Alopecia". Endotext. MDText.com. PMID 25905192.
  104. Thomas, T. L.; Patel, G. L. (1976). "Optimal conditions and specificity of interaction of a distinct class of nonhistone chromosomal proteins with DNA". Biochemistry. 15 (7): 1481–1489. doi:10.1021/bi00652a019. PMID 4089.
  105. Henss R (2001). "Social Perceptions of Male Pattern Baldness. A Review". Dermatology and Psychosomatics. 2 (2): 63–71. doi:10.1159/000049641. S2CID 143994546.
  106. Castle S (2002). "IT LOCKS LIKE GIRLS GO FOR DARKER HAIR; Bald men sexy too says survey". The Free Library.
  107. Kabai P (August 2010). "Might early baldness protect from prostate cancer by increasing skin exposure to ultraviolet radiation?". Cancer Epidemiology. 34 (4): 507. doi:10.1016/j.canep.2010.04.014. PMID 20451486.
  108. Lotufo PA, Chae CU, Ajani UA, Hennekens CH, Manson JE (January 2000). "Male pattern baldness and coronary heart disease: the Physicians' Health Study". Archives of Internal Medicine. 160 (2): 165–171. doi:10.1001/archinte.160.2.165. PMID 10647754.
  109. Gatherwright J, Amirlak B, Rowe D, Liu M, Gliniak C, Totonchi A, Guyuron B (2011). "The Relative Contribution of Endogenous and Exogenous Factors to Male Alopecia". Plastic and Reconstructive Surgery. 128: 14. doi:10.1097/01.prs.0000406222.54557.75. S2CID 74776022.
  110. Schmidt JB (1994). "Hormonal basis of male and female androgenic alopecia: clinical relevance". Skin Pharmacology. 7 (1–2): 61–66. doi:10.1159/000211275. PMID 8003325.
  111. Remes K, Kuoppasalmi K, Adlercreutz H (June 1985). "Effect of physical exercise and sleep deprivation on plasma androgen levels: modifying effect of physical fitness". International Journal of Sports Medicine. 6 (3): 131–135. doi:10.1055/s-2008-1025825. PMID 4040893.
  112. Toone BK, Wheeler M, Nanjee M, Fenwick P, Grant R (September 1983). "Sex hormones, sexual activity and plasma anticonvulsant levels in male epileptics". Journal of Neurology, Neurosurgery, and Psychiatry. 46 (9): 824–826. doi:10.1136/jnnp.46.9.824. PMC 1027564. PMID 6413659.
  113. Davidson JM, Kwan M, Greenleaf WJ (November 1982). "Hormonal replacement and sexuality in men". Clinics in Endocrinology and Metabolism. 11 (3): 599–623. doi:10.1016/S0300-595X(82)80003-0. PMID 6814798.
  114. Mantzoros CS, Georgiadis EI, Trichopoulos D (May 1995). "Contribution of dihydrotestosterone to male sexual behaviour". BMJ. 310 (6990): 1289–1291. doi:10.1136/bmj.310.6990.1289. PMC 2549675. PMID 7773040.
  115. Exton MS, Krüger TH, Bursch N, Haake P, Knapp W, Schedlowski M, Hartmann U (November 2001). "Endocrine response to masturbation-induced orgasm in healthy men following a 3-week sexual abstinence". World Journal of Urology. 19 (5): 377–382. doi:10.1007/s003450100222. PMID 11760788. S2CID 36314782.
  116. Severi G, Sinclair R, Hopper JL, English DR, McCredie MR, Boyle P, Giles GG (December 2003). "Androgenetic alopecia in men aged 40-69 years: prevalence and risk factors". The British Journal of Dermatology. 149 (6): 1207–1213. doi:10.1111/j.1365-2133.2003.05565.x. PMID 14674898. S2CID 12793476.
  117. Crabtree JS, Kilbourne EJ, Peano BJ, Chippari S, Kenney T, McNally C, et al. (May 2010). "A mouse model of androgenetic alopecia". Endocrinology. 151 (5): 2373–2380. doi:10.1210/en.2009-1474. PMID 20233794.
  118. Sundberg JP, King LE, Bascom C (2001). "Animal models for male pattern (androgenetic) alopecia". European Journal of Dermatology. 11 (4): 321–325. PMID 11399538.
  119. Sundberg JP, Beamer WG, Uno H, Van Neste D, King LE (October 1999). "Androgenetic alopecia: in vivo models". Experimental and Molecular Pathology. 67 (2): 118–130. doi:10.1006/exmp.1999.2276. PMID 10527763.
  120. Borzo G (2002). "Unique social system found in famous Tsavo lions". EurekAlert.
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