Pattern hair loss
Pattern hair loss | |
---|---|
Other names | Male pattern baldness; female pattern baldness; androgenic alopecia; androgenetic alopecia; alopecia androgenetica |
Male-pattern hair loss shown on the vertex of the scalp | |
Specialty | Dermatology, plastic surgery |
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]
Genetic research has identified
Some research has found evidence for the role of oxidative stress in hair loss,[6] the microbiome of the scalp,[7][8] genetics, and circulating androgens; particularly dihydrotestosterone (DHT).[3] Men with early onset androgenic alopecia (before the age of 35) have been deemed the male phenotypic equivalent for polycystic ovary syndrome (PCOS).[9][10][11][12]
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).[13][14][15]
Management may include simply accepting the condition
By the age of 50, pattern hair loss affects about half of males and a quarter of females.
Signs and symptoms
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.[26]
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.[27] 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.[28]
In most cases, receding hairline is the first starting point; the hairline starts moving backwards from the front of the head and the sides.[29]
Causes
The cause of pattern hair loss is not yet fully understood. It appears to be the result of genetic changes that make the activity of hair follicles on the scalp become sensitive to the presence of androgenic hormones, cholesterol, and proteins such as insulin-like growth factor.
Hormones and genes
Male pattern hair loss appears to be undergoing positive sexual selection in European and Asian populations.
The initial programming of
]Men with androgenic alopecia typically have higher
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.[34] Other research suggests the enzyme prostaglandin D2 synthase and its product prostaglandin D2 (PGD2) in hair follicles as contributive.[39]
These observations have led to study at the level of the
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.[44]
Inheritance
Male pattern baldness is a complex genetic condition with "particularly strong signals on the X chromosome".[45]
Metabolic syndrome
Multiple cross-sectional studies have found associations between early androgenic alopecia,
In support of the association, finasteride improves glucose metabolism and decreases glycated hemoglobin
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.[56] In vivo, insulin stimulates both testosterone production and SHBG inhibition in normal and obese men.[57] 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.[58] Patients with Laron syndrome, with resultant deficient IGF, demonstrate varying degrees of alopecia and structural defects in hair follicles when examined microscopically.[59]
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.
Female patients with mineralocorticoid resistance present with androgenic alopecia.[62]
IGF levels have been found lower in those with metabolic syndrome.
The expression of insulin resistance and metabolic syndrome, AGA is related to being an increased risk factor for cardiovascular diseases, glucose metabolism disorders,[66] type 2 diabetes,[67][68] and enlargement of the prostate.[69]
Age
A number of hormonal changes occur with aging:
- Decrease in testosterone
- Decrease in serum DHT and 5-alpha reductase
- Decrease 3AAG, a peripheral marker of DHT metabolism
- Increase in SHBG
- Decrease in androgen receptors, 5-alpha reductase type I and II activity, and aromatase in the scalp[70][71]
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.[72]
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.
An example of premature age effect is
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 [76][77] suggests that dermal fibrosis is associated with the progressive hair-loss and hair-whitening in old people.[78] 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.[79] Trichoscopy can be used for further evaluation.[80] Biopsy may be needed to exclude other causes of hair loss,[81] and histology would demonstrate perifollicular fibrosis.[82][83] The Hamilton–Norwood scale has been developed to grade androgenic alopecia in males by severity.
Treatment
Combination therapy
Combinations of finasteride, minoxidil and ketoconazole are more effective than individual use.[84]
Combination therapy of LLLT or microneedling with finasteride[85] or minoxidil demonstrated substantive increases in hair count.[86]
Androgen-dependent
Finasteride is a medication of the 5α-reductase inhibitors (5-ARIs) class.[87] By inhibiting type II 5-AR, finasteride prevents the conversion of testosterone to dihydrotestosterone in various tissues including the scalp.[87][88] 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.[88] 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.[88]
Dutasteride is a medication in the same class as finasteride but inhibits both type I and type II 5-alpha reductase.[88] Dutasteride is approved for the treatment of male-pattern hair loss in Korea and Japan, but not in the United States.[88] However, it is commonly used off-label to treat male-pattern hair loss.[88]
Androgen-independent
Minoxidil dilates small blood vessels; it is not clear how this causes hair to grow.[89] Other treatments include tretinoin combined with minoxidil, ketoconazole shampoo, dermarolling (Collagen induction therapy), spironolactone,[90] alfatradiol, topilutamide (fluridil),[87] topical melatonin,[91][92][93] and intradermal and intramuscular botulinum toxin injections to the scalp.[94]
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.[95] Finasteride was shown to be no more effective than placebo based on low-quality studies.[95] The effectiveness of laser-based therapies is unclear.[95] Bicalutamide, an antiandrogen, is another option for the treatment of female pattern hair loss.[96][6][97]
Procedures
More advanced cases may be resistant or unresponsive to medical therapy and require
Technological treatments
Low-level laser therapy (LLLT)
Low-level laser therapy or photobiomodulation is also referred to as red light therapy and cold laser therapy. It is a non-invasive treatment option.
LLLT is shown to increase hair density and growth in both genders. The types of devices (hat, comb, helmet) and duration did not alter the effectiveness,[100] with more emphasis to be placed on lasers compared to LEDs.[101] Ultraviolet and infrared light are more effective for alopecia areata, while red light and infrared light is more effective for androgenetic alopecia.[102]
Medical reviews suggest that LLLT is as effective or potentially more than other non invasive and traditional therapies like minoxidil and finasteride but further studies such as RCTs, long term follow up studies, and larger double blinded trials need to be conducted to confirm the initial findings.[103][85][104]
Platelet-rich plasma (PRP)
Using ones own cells and tissues and without harsh side effects, PRP is beneficial for alopecia areata[105] and androgenetic alopecia and can be used as an alternative to minoxidil or finasteride.[106] It has been documented to improve hair density and thickness in both genders.[107] A minimum of 3 treatments, once a month for 3 months are recommended, and afterwards a 3-6 month period of continual appointments for maintenance.[108] Factors that determine efficacy include amount of sessions, double versus single centrifugation, age and gender, and where the PRP is inserted.[109]
Future larger randomized controlled trials and other high quality studies are still recommended to be carried out and published for a stronger consensus.[103][107][110] Further development of a standardized practice for procedure is also recommended.[105]
Alternative therapies
Many people use unproven treatments.[111] Regarding female pattern alopecia, there is no evidence for vitamins, minerals, or other dietary supplements.[112] As of 2008, there is little evidence to support the use of lasers to treat male-pattern hair loss.[113] The same applies to special lights.[112] Dietary supplements are not typically recommended.[113] 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.[114][115]
Research
A 2023 study on genetically engineered mice published in the journal PNAS found that increasing production of a particular microRNA in hair follicle stem cells, which naturally harden with age, softened the cells and stimulated hair growth. The authors of the study said the next research step is to introduce the microRNA into the stem cells using nanoparticles applied directly to the skin, with the goal of developing a similar topical application for humans.[116]
Prognosis
Androgenic alopecia is typically experienced as a "moderately stressful condition that diminishes body image satisfaction".[117] However, although most men regard baldness as an unwanted and distressing experience, they usually are able to cope and retain integrity of personality.[118]
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.[119]
Epidemiology
Female androgenic alopecia has become a growing problem that, according to the
For male androgenic alopecia, by the age of 50 30-50% of men have it, hereditarily there is an 80% predisposition.[121] Notably, the link between androgenetic alopecia and metabolic syndrome is strongest in non-obese men.[122]
Society and culture
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,[123] a 2002 survey of Welsh women found that they rated bald and gray-haired men quite desirable.[124] 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.[16]
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.[125]
Myths
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[
Baldness can be caused by emotional stress, sleep deprivation, etc.
Emotional
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.[130][131]
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.[132] 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.[133]
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.[134]
Other animals
Animal models of androgenic alopecia occur naturally and have been developed in
Baldness is not a trait unique to human beings. One possible case study is about a
Although nonhuman 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.[citation needed]
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The European AGA risk alleles, however, are fixed in the East Asian sample (including 57K) and their frequencies therefore do not correlate with the AGA frequencies. As AGA might be regarded as a secondary sexual characteristic, rather than a disorder, it is possible that the hair loss itself was under enhanced sexual selection by identifying the older male leader comparable to the silver-backed gorilla (Randall 2007). The reported lower prevalence of AGA in Africans might then be explained by the importance of scalp hair for the protection against the tropical sun which outweighed the enhanced sexual selection (Randall 2007). Since the causative variant has not yet been identified, the lower prevalence of AGA in Asia and presumably in Africa might indicate a higher frequency of the functional AGA allele in the European population, either due to its origin on a Europe-specific background or differences in population demography. Alleles of 21 SNPs between AR and EDA2R are more frequent in Europeans than in East Asians and Africans (Supplementary Table 1).
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