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"Rejuvenate" redirects here. For the album by Ralph Moore, see Rejuvenate!
Medical discipline focused on the practical reversal of the aging process
Rejuvenation is a medical discipline focused on the practical reversal of the aging process.[1]
Rejuvenation is distinct from life extension. Life extension strategies often study the causes of aging and try to oppose those causes to slow aging. Rejuvenation is the reversal of aging and thus requires a different strategy, namely repair of the damage that is associated with aging or replacement of damaged tissue with new tissue. Rejuvenation can be a means of life extension, but most life extension strategies do not involve rejuvenation.
Various myths tell the stories about the quest for rejuvenation. It was believed that magic or intervention of a supernatural power can bring back youth and many mythical adventurers set out on a journey to do that, for themselves, their relatives or some authority that sent them anonymously.
An ancient Chinese emperor sent out ships of young men and women to find a pearl that would rejuvenate him. This led to a myth among modern Chinese that Japan was founded by these people.
In some religions, people were to be rejuvenated after death prior to placing them in heaven.
The stories continued well into the 16th century. The Spanish explorer Juan Ponce de León led an expedition around the Caribbean islands and into Florida to find the Fountain of Youth. Led by the rumors, the expedition continued the search and many perished. The Fountain was nowhere to be found as locals were unaware of its exact location.
Since the emergence of philosophy, sages and self-proclaimed wizards always made enormous efforts to find the secret of youth, both for themselves and their noble patrons and sponsors. It was widely believed that some potions may restore the youth.
Another commonly cited approach was attempting to transfer the essence of youth from young people to old. Some examples of this approach were sleeping with virgins or children (sometimes literally sleeping, not necessarily having sex),[2] bathing in or drinking their blood.
The quest for rejuvenation reached its height with alchemy. All around Europe, and also beyond, alchemists were looking for the Philosopher's Stone, the mythical substance that, as it was believed, could not only turn lead into gold, but also prolong life and restore youth. Although the set goal was not achieved, alchemy paved the way to the scientific method and so to the medical advances of today.[citation needed]
Serge Abrahamovitch Voronoff was a French surgeon born in Russia who gained fame for his technique of grafting monkey testicle tissue on to the testicles of men while working in France in the 1920s and 1930s. This was one of the first medically accepted rejuvenation therapies (before he was proved to be wrong around 1930–1940). The technique brought him a great deal of money, although he was already independently wealthy. As his work fell out of favor, he went from being a highly respected surgeon to a subject of ridicule. By the early 1930s, over 500 men had been treated in France by his rejuvenation technique, and thousands more around the world, such as in a special clinic set up in Algiers.[3] Noteworthy people who had the surgery included Harold McCormick, chairman of the board of International Harvester Company,[4] and the aging premier of Turkey.[5]
Rejuvenation technology and its effects on individuals and society have long been a subject of science fiction. The Misspent Youth and Commonwealth Saga by Peter F. Hamilton are among the most well known examples of this, dealing with the short- and long-term effects of a near perfect 80-year-old to 20-year-old body change with mind intact. The less perfect rejuvenation featured in the Mars trilogy by Kim Stanley Robinson results in long-term memory loss and sheer boredom that comes with extreme age. The post-mortal characters in the Revelation Space series have long-term or essentially infinite lifespans, and sheer boredom induces them to undertake activities of extreme risk.
Aging is the accumulation of damage to macromolecules, cells, tissues and organs in and on the body which, when it can no longer be tolerated by an organism, ultimately leads to its death. If any of that damage can be repaired, the result is rejuvenation.
There have been many experiments which have been shown to increase the maximum life span of laboratory animals,[citation needed] thereby achieving life extension. A few experimental methods such as replacing hormones to youthful levels have had considerable success in partially rejuvenating laboratory animals and humans. A 2011 experiment involved breeding genetically manipulated mice that lacked an enzyme called telomerase, causing the mice to age prematurely and suffer ailments. When the mice were given injections to reactivate the enzyme, it repaired the damaged tissues and reversed the signs of aging.[6] There are at least eight important hormones that decline with age: 1. human growth hormone (HGH); 2. the sexual hormones: testosterone or oestrogen/progesterone; 3. erythropoietin (EPO); 4. insulin; 5. DHEA; 6. melatonin; 7. thyroid; 8. pregnenolone. In theory, if all or some of these hormones are replaced, the body will respond to them as it did when it was younger, thus repairing and restoring many body functions. In line with this, recent experiments show that heterochronic parabiosis, i.e. connecting the circulatory systems of young and old animal, leads to the rejuvenation of the old animal, including restoration of proper stem cell function. Similar experiments show that grafting old muscles into young hosts leads to their complete restoration, whereas grafting young muscles into old hosts does not. These experiments show that aging is mediated by systemic environment, rather than being an intrinsic cell property.[citation needed] Clinical trials based on transfusion of young blood were scheduled to begin in 2014.[7] Another intervention that is gaining popularity is epigenetic reprogramming.[8] Through the use of Yamanaka factors, aged cells can revert to a younger state. It has been demonstrated that reprogramming induces a youthful epigenetic state and can restore vision after injury.[9] Only through reprogramming were stochastic epigenetic variations, which accumulate with age, successfully reversed, as demonstrated by a stochastic data-based clock.[10]
Most attempts at genetic repair have traditionally involved the use of a retrovirus to insert a new gene into a random position on a chromosome. But by attaching zinc fingers (which determine where transcription factors bind) to endonucleases (which break DNA strands), homologous recombination can be induced to correct and replace defective (or undesired) DNA sequences. The first applications of this technology are to isolate stem cells from the bone marrow of patients having blood disease mutations, to correct those mutations in laboratory dishes using zinc finger endonucleases and to transplant the stem cells back into the patients.[11] More recent efforts leverage CRISPR-Cas systems or adeno-associated viruses (AAVs).
Yet another option involves cosmetic changes to the individual to create the appearance of youth. These are generally superficial and do little to make the person healthier or live longer, but the real improvement in a person's appearance may elevate their mood and have positive side effects normally correlated with happiness. Cosmetic surgery is a large industry offering treatments such as removal of wrinkles ("face lift"), removal of extra fat (liposuction) and reshaping or augmentation of various body parts (abdomen, breasts, face).
There are also, as commonly found throughout history, many fake rejuvenation products that have been shown to be ineffective. Chief among these are powders, sprays, gels, and homeopathic substances that claim to contain growth hormones. Authentic growth hormones are only effective when injected, mainly due to the fact that the 191-amino acid protein is too large to be absorbed through the mucous membranes, and would be broken up in the stomach if swallowed.
The Mprize scientific competition is under way to deliver on the mission of extending healthy human life. It directly accelerates the development of revolutionary new life extension therapies by awarding two cash prizes: one to the research team that breaks the world record for the oldest-ever mouse; and one to the team that develops the most successful late-onset rejuvenation. Current Mprize winner for rejuvenation is Steven Spindler. Caloric restriction (CR), the consumption of fewer calories while avoiding malnutrition, was applied as a robust method of decelerating aging and the development of age-related diseases.[14]
The biomedical gerontologistAubrey de Grey has initiated a project, strategies for engineered negligible senescence (SENS), to study how to reverse the damage caused by aging. He has proposed seven strategies for what he calls the seven deadly sins of aging:[16]
Senescent cells can be removed by activating the immune system against them. Or they can be destroyed by gene therapy to introduce "suicide genes" that only kill senescent cells.
Proteincross-linking can largely be reversed by drugs that break the links. But to break some of the cross-links we may need to develop enzymatic methods.
For intracellular junk we need to introduce new enzymes, possibly enzymes from soil bacteria, that can degrade the junk (lipofuscin) that our own natural enzymes cannot degrade.
For mitochondrial mutations the plan is not to repair them but to prevent harm from the mutations by putting suitably modified copies of the mitochondrial genes into the cell nucleus by gene therapy. The mitochondrial DNA experiences a high degree of mutagenic damage because most free radicals are generated in the mitochondria. A copy of the mitochondrial DNA located in the nucleus will be better protected from free radicals, and there will be better DNA repair when damage occurs. All mitochondrial proteins would then be imported into the mitochondria.
For cancer (the most lethal consequence of mutations) the strategy is to use gene therapy to delete the genes for telomerase and to eliminate telomerase-independent mechanisms of turning normal cells into "immortal" cancer cells. To compensate for the loss of telomerase in stem cells we would introduce new stem cells every decade or so.
In 2009, Aubrey de Grey co-founded the SENS Foundation to expedite progress in the above-listed areas.
^Common, Laura. (April 25, 2000) The Medical Post[1]Great balls of fire: from prehistory, men have tried implants and extracts from macho animals to cure impotence, but it was only relatively recently that they began to understand why they did so.
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 and 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] The condition is caused by a combination of male sex hormones (balding never occurs in castrated men) and genetic factors.[4]
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).[12][13][14]
By the age of 50, pattern hair loss 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[16] and younger male patients of early onset AGA (before the age of 35) had a higher likelihood of metabolic syndrome (MetS)[17][18][19][20] and insulin resistance.[21] With younger males, studies found metabolic syndrome to be at approximately a 4× increased frequency, which is deemed clinically significant.[22][23] Abdominal obesity, hypertension, and lowered high density lipoprotein were also significantly higher for younger groups.[24]
Hair follicle and mesenchymal dermal papilla, labelled at top
Pattern hair loss is classified as a form of non-scarring hair loss.[citation needed]
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.[25]
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.[26] 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.[27]
In most cases, receding hairline is the first starting point; the hairline starts moving backwards from the front of the head and the sides.[28]
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.[citation needed]
KRT37 is the only keratin that is regulated by androgens.[29] 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.[29]
Although it is generally accepted that male pattern baldness follows a pattern of autosomal dominant inheritance, more recent research has shown that approximately 80% of bald men have bald fathers. This is greater than would be expected if pattern balding were a purely autosomal trait, and may suggest that there is an important paternal route of inheritance, either through a Y-chromosome gene or a paternal imprinting effect.[30]
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'.[34]
Men with androgenic alopecia typically have higher 5α-reductase, higher total testosterone, higher unbound/free testosterone, and higher free androgens, including DHT.[35] 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.[36] The genetic corollary that codes for this enzyme has been discovered.[37]Prolactin has also been suggested to have different effects on the hair follicle across gender.[38]
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 enzymeprostaglandin 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 mesenchymal dermal papillae.[40]Types 1 and 2 5α reductase enzymes are present at pilosebaceous units in papillae of individual hair follicles.[41] They catalyze formation of the androgen dihydrotestosterone from testosterone, which in turn regulate hair growth.[34] 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.[34] Hair follicles in anaphase express four different caspases. Significant levels of inflammatory infiltrate have been found in transitional hair follicles.[42] Interleukin 1 is suspected to be a cytokine mediator that promotes hair loss.[43]
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]
Multiple cross-sectional studies have found associations between early androgenic alopecia, insulin resistance, and metabolic syndrome,[45][46] with low HDL being the component of metabolic syndrome with highest association.[47] Linolenic and linoleic acids, two major dietary sources of HDL, are 5 alpha reductase inhibitors.[48] Premature androgenic alopecia and insulin resistance may be a clinical constellation that represents the male homologue, or phenotype, of polycystic ovary syndrome.[49] Others have found a higher rate of hyperinsulinemia in family members of women with polycystic ovarian syndrome.[50] 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.[51]
In support of the association, finasteride improves glucose metabolism and decreases glycated hemoglobin HbA1c, a surrogate marker for diabetes mellitus.[52] The low SHBG seen with premature androgenic alopecia is also associated with, and likely contributory to, insulin resistance,[53] and for which it still is used as an assay for pediatric diabetes mellitus.[54]
Obesity leads to upregulation of insulin production and decrease in SHBG. Further reinforcing the relationship, SHBG is downregulated by insulinin vitro, although SHBG levels do not appear to affect insulin production.[55]In vivo, insulin stimulates both testosterone production and SHBG inhibition in normal and obese men.[56] 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.[57] Patients with Laron syndrome, with resultant deficient IGF, demonstrate varying degrees of alopecia and structural defects in hair follicles when examined microscopically.[58]
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.[11] Measurement of subcutaneous and visceral adipose stores by MRI, demonstrated inverse association between visceraladipose tissue and testosterone/DHT, while subcutaneous adipose correlated negatively with SHBG and positively with estrogen.[59] 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.[60]
Female patients with mineralocorticoid resistance present with androgenic alopecia.[61]
IGF levels have been found lower in those with metabolic syndrome.[62] Circulating serum levels of IGF-1 are increased with vertex balding, although this study did not look at mRNA expression at the follicle itself.[63] 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.[64]
The expression of insulin resistance and metabolic syndrome, AGA is related to being an increased risk factor for cardiovascular diseases, glucose metabolism disorders,[65]type 2 diabetes,[66][67] and enlargement of the prostate.[68]
Decrease in androgen receptors, 5-alpha reductase type I and II activity, and aromatase in the scalp[69][70]
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.[71]
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.[72] 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.[73]
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.[74]
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.[75]Trichoscopy can be used for further evaluation.[76] Biopsy may be needed to exclude other causes of hair loss,[77] and histology would demonstrate perifollicular fibrosis.[78][79] The Hamilton–Norwood scale has been developed to grade androgenic alopecia in males by severity.[citation needed]
Finasteride is a medication of the 5α-reductase inhibitors (5-ARIs) class.[83] By inhibiting type II 5-AR, finasteride prevents the conversion of testosterone to dihydrotestosterone in various tissues including the scalp.[83][84] 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.[84] 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.[84]
Dutasteride is a medication in the same class as finasteride but inhibits both type I and type II 5-alpha reductase.[84] Dutasteride is approved for the treatment of male-pattern hair loss in Korea and Japan, but not in the United States.[84] However, it is commonly used off-label to treat male-pattern hair loss.[84]
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.[91] Finasteride was shown to be no more effective than placebo based on low-quality studies.[91] The effectiveness of laser-based therapies is unclear.[91]Bicalutamide, an antiandrogen, is another option for the treatment of female pattern hair loss.[92][5][93]
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.[86] 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.[94][95] Cosmetic scalp tattoos can also mimic the appearance of a short, buzzed haircut.
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.[citation needed]
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,[96] with more emphasis to be placed on lasers compared to LEDs.[97] Ultraviolet and infrared light are more effective for alopecia areata, while red light and infrared light is more effective for androgenetic alopecia.[98]
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.[99][81][100]
Using ones own cells and tissues and without harsh side effects, PRP is beneficial for alopecia areata[101] and androgenetic alopecia and can be used as an alternative to minoxidil or finasteride.[102] It has been documented to improve hair density and thickness in both genders.[103] 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.[104] Factors that determine efficacy include amount of sessions, double versus single centrifugation, age and gender, and where the PRP is inserted.[105]
Future larger randomized controlled trials and other high quality studies are still recommended to be carried out and published for a stronger consensus.[99][103][106] Further development of a standardized practice for procedure is also recommended.[101]
Many people use unproven treatments.[107] Regarding female pattern alopecia, there is no evidence for vitamins, minerals, or other dietary supplements.[108] As of 2008, there is little evidence to support the use of lasers to treat male-pattern hair loss.[109] The same applies to special lights.[108] Dietary supplements are not typically recommended.[109] 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.[110][111]
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.[112]
Androgenic alopecia is typically experienced as a "moderately stressful condition that diminishes body image satisfaction".[113] However, although most men regard baldness as an unwanted and distressing experience, they usually are able to cope and retain integrity of personality.[114]
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.[115]
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.[116]
For male androgenic alopecia, by the age of 50 30-50% of men have it, hereditarily there is an 80% predisposition.[117] Notably, the link between androgenetic alopecia and metabolic syndrome is strongest in non-obese men.[118]
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,[119] a 2002 survey of Welsh women found that they rated bald and gray-haired men quite desirable.[120] 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.[15]
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.[121]
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.[citation needed]
Weight training and other types of physical activity cause baldness
Because it increases testosterone levels, many Internet forums[which?] 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.[122][123] 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.[citation needed]
Baldness can be caused by emotional stress, sleep deprivation, etc.
Emotional stress has been shown to accelerate baldness in genetically susceptible individuals.[124] Stress due to sleep deprivation in military recruits lowered testosterone levels, but is not noted to have affected SHBG.[125] 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.[126][127]
Animal models of androgenic alopecia occur naturally and have been developed in transgenic mice;[128]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.[129][130]
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.[131]
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]
^ abcdefghVary 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. PMID26476248.
^Randall VA (2012-07-26). "Androgens and hair: a biological paradox with clinical consequences". Testosterone. Cambridge University Press. pp. 154–176. doi:10.1017/cbo9781139003353.008. ISBN978-1-139-00335-3. Male pattern baldness is androgen dependent, since it does not occur in castrates, unless they are given testosterone (Hamilton 1942), nor in XY individuals with androgen insensitivity due to non-functional androgen receptors (see Chapter 3). The genetic involvement in androgenetic alopecia is also pronounced.
^ abMeyer-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. hdl:11585/863826. PMID34668238. S2CID239029062.
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