Why is male balding so common in comparison to female balding?

Why is male balding so common in comparison to female balding?

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I have heard that over 30% of men will be bald by 30, and that 60% will be bald by 50. However, I hardly ever see a bald woman unless it is a story about a cancer survivor or someone going through cancer, meaning that they lost their hair through chemotherapy rather than natural balding. I do not understand why this is. I do know that women tend to have longer hair than men, so maybe their follicles are more active, preventing them from going bald. If someone could correct my explanation, that'd be appreciated.

Let's start off by saying that "baldness" is a very broad term… it includes not only hair loss but also miniaturization, which accounts for the majority of the phenotypic "baldness" associated with alopecia areata. While alopecia areata is not the only cause of baldness, it accounts for 4 out of 5 cases in men, whereas in women it only accounts for half.

The reason that it's more frequent in males is the presence of 5α‐reductase in the sebacious glands and the dermal papilla - this enzyme mediates the metabolism of testosterone into dihydrotestosterone. Dihydrotestosterone, in its turn, binds to androgen receptors and affects gene expression, speeding up the anogen phase. Consequently more hairs are in the telogen phase, and the hair is shorter. In severe cases, miniaturization can become actual hair loss.

Because males higher levels of androgens, there is more testosterone available to be metabolized in the follicles. Therefore, the incidence of alopecia areata (and consequently baldness) is higher in men than in women.


  • Piraccini BM, Alessandrini A. Androgenetic alopecia. G Ital Dermatol Venereol. 2014 Feb;149(1):15-24. PMID: 24566563.

  • Randall VA, Thornton MJ, Messenger AG. Cultured dermal papilla cells from androgen-dependent human hair follicles (e.g. beard) contain more androgen receptors than those from non-balding areas of scalp. J Endocrinol. 1992 Apr;133(1):141-7. doi: 10.1677/joe.0.1330141. PMID: 1517703.

The genetics of baldness: More complex than you might think

From bald eagles to Bruce Willis, bald spots are a common sight and part of the fabric of our society. It’s often assumed that baldness has a genetic component to it, and that’s absolutely true it does. But it’s also commonly believed that baldness is inherited from your maternal grandfather. That part isn’t entirely true. As with many concepts in genetics, there’s a lot more to it than that!

Both men and women experience hair loss, but research has historically focused primarily on male subjects (and efforts to link the two have shown that female pattern hair loss is not predicted by the same genetic markers). Because of this, significantly less is known about female hair loss. We do know that approximately 30% of males experience some degree of hair loss (including simple hair thinning or a receding hairline) by the age of 30, 50% by the age of 50, and 80% by the age of 70 1 .

Like this article? Check out some of our other writings, including articles about the ways DNA may affect facial hair growth patterns and the genetics of hairlessness

Male pattern baldness (MPB) is a condition where hair loss occurs in multiple parts of the scalp, ultimately leading to a bald region surrounded by hair in a horseshoe-like pattern 3 .The process of going bald is more complex than simply hair falling out, though. For starters, individuals with MPB are known to have smaller hair follicles on their scalp. Hair follicles are made of multiple cell types, each one dedicated to a particular process in building hair, which is actually a long chain of proteins (mostly keratin, which you can read about here) outside those cells. These follicles are where hair gains its unique features like curliness and color. Individuals with MPB not only have smaller follicles, but those follicles produce less hair, which contributes to the hair thinning process. Eventually, these follicles die, which produces a bald spot 1-4 .

A condition thought only to affect women may cause male-pattern baldness

Polycystic ovary syndrome — as the name suggests — is a disease typically associated only with women, but it is time to think again.

The syndrome, also known as the acronym PCOS, affects women’s menstrual cycles, plays havoc with hormone levels, and can make the metabolism go awry. PCOS symptoms can include irregular periods, oily skin, erroneous facial hair, and difficulty getting pregnant, as well as weight problems, diabetes, and even cardiovascular issues. It affects as many as 10 percent of women during their reproductive years, and although the symptoms can be treated, there is no cure and scientists know little about what drives the syndrome.

So little, in fact, that they may have got one critical aspect of PCOS entirely wrong: Despite the name, a version of the syndrome can affect men, too.

What’s new — For the first time, researchers show that the primary cause of polycystic ovary syndrome may not depend on the ovaries at all. That’s according to preliminary evidence presented on Tuesday at ENDO2021, the Endocrine Society's annual meeting.

By testing male relatives of women with the syndrome, scientists found a genetic component to the condition which, in men, can lead to male pattern baldness, risk of obesity, diabetes, and heart problems. The lead researcher on the study Jia Zhu, who is a doctor at Boston Children's Hospital, tells Inverse the new evidence prompts a rethink about everything scientists thought they knew about this “women’s disease.”

“This tells us that men can have a PCOS-like condition that we still need to better understand and define,” she says.

Why it matters — The findings suggest PCOS is actually not an ovary-derived syndrome. In turn, they pave the way for better research into what causes the condition, and may enable scientists to develop a wider array of treatments — and maybe even find a cure.

“Our study really provides genetic evidence that PCOS is more than a disorder of female reproduction and has long-term health implications beyond the reproductive years for both women and men,” Zhu says.

These findings help better define PCOS, demonstrating that it may not be a disorder of female reproduction after all, but rather a cardiometabolic condition, caused by the disruption of biological pathways common to both women and men, independently of the reproductive organs.

How they did it — Zhu and her team used genetic data gleaned from the UK Biobank, a British biomedical database replete with the genetic information of half a million people. From these data, they analyzed 176,360 men’s genetic susceptibility for PCOS. Then, the researchers drilled down into the 20 percent of men with the highest genetic risk for PCOS and found their risk correlated with increased genetic risk for obesity, diabetes, cardiovascular disease, and male-pattern baldness.

“When it comes to the metabolic — type-2 diabetes, obesity, and cardiovascular disease — and hyperandrogenic — male-pattern baldness — complications of PCOS, women and men may have more in common than we thought,” Zhu says.

“Hyperandrogenic” here refers to a defining feature of PCOS, “hyperandrogenism,” which means atypically high levels of androgen hormones, which play important roles in the development and maintenance of “male” characteristics. Testosterone, for example, is an androgen hormone. In females with PCOS, atypically high androgen-hormone levels most often manifest as excessive body hair (think facial hair, back hair, chest hair, and leg hair), or, conversely, thinning or even balding hair on the head.

This mirrors the effects of high androgen levels in men: High levels of testosterone, for example, are associated with head hair loss and “male-pattern baldness.”

“That’s why we considered male-pattern baldness as a hyperandrogenic feature of PCOS associated with genetic risk factors for PCOS in men,” Zhu explains.

What’s next — The findings are preliminary, which means they need to be confirmed in further research and peer-reviewed. But they hint there may be multiple different causes for PCOS, and that there may be many different biological mechanisms involved, according to Zhu. Further genetic studies could help tease out the individual differences and how different genes play into risk for PCOS, both in men and in women.

“Genetic susceptibility of PCOS had been described in both men and women. The pathology of the syndrome includes insulin and/or gonadotropin-androgen pathways,” Anis Rehman, who is a researcher at Southern Illinois University, explains to Inverse. Rehman was not involved in the new study.

“It is still too early to change the general public health screening guidelines to identify cardiovascular and metabolic diseases based on this study. However, the study does point out the importance of PCOS in female family members on male family members’ health,” Rehman says. In other words, if you are a bald man, and have female family members who have PCOS, the two conditions may be more related than you think.

Polycystic ovary syndrome is an endocrinopathy that two researchers named Stein and Leventhal initially described in 1935, Rehman says. In light of these new findings, it could prompt a rethink on whether we should rename PCOS the “Stein-Leventhal syndrome.”

Broadly, Zhu says, the new work offers a hint at the discoveries awaiting scientists who seek genetic explanations for health conditions. By investigating what causes PCOS in women, scientists could unlock the biology behind how hormones shape our physiology — whether we are male or female.

“We hope our findings provide additional support for focusing and targeting the metabolic complications of PCOS in clinical practice and research in both women and men on the long term,” Zhu says.

Baldness cure may be coming after discovery of protein that fuels hair growth

CAMBRIDGE, Mass. — A scientific discovery may make the “comb over” a thing of the past for people losing their hair. Harvard researchers say a baldness cure is on the horizon after scientists uncovered a protein that fuels hair growth.

The breakthrough could lead to a cream that fuels an unlimited supply of locks for the follicly-challenged — a true baldness cure, rather than a temporary fix. In experiments, mice successfully sprouted three times as many hairs by surgically removing their adrenal glands. The small organs above each kidney release the stress hormone corticosterone, the rodent equivalent of cortisol. This stops the protein GAS6 in its tracks.

Stress reactions such as worry, anger, and anxiety have long been connected to male pattern baldness. Researchers even estimate about a quarter of COVID-19 survivors suffer hair loss due to the shock of infection.

“Stress hormones suppress growth in mice through the regulation of hair follicle stem cells,” says corresponding author Ya-Chieh Hsu, a professor of stem cell and regenerative biology, in a statement per SWNS.

The study, appearing in the journal Nature, identifies the process that underpins hair loss for the first time and reveals how to reverse it, allowing for a potential groundbreaking baldness cure.

“Chronic, sustained exposure to stressors can profoundly affect tissue homeostasis, although the mechanisms by which these changes occur are largely unknown,” researchers write in their report. “The stress hormone corticosterone—which is derived from the adrenal gland and is the rodent equivalent of cortisol in humans—regulates hair follicle stem cell (HFSC) quiescence and hair growth in mice.”

Turning back the clock on hair’s lifespan

Study authors explain the hormone regulates dormancy and activity of hair follicle stem cells (HFSCs) in mice. In the absence of systemic corticosterone, the little cavities where each hair grows enter substantially more rounds of the regeneration cycle throughout life.

“When corticosterone levels are elevated, hair follicles stay in an extended rest phase and fail to regenerate,” says Hsu. “Conversely, if corticosterone is depleted, hair follicle stem cells become activated and new hair growth occurs.”

An analysis discovered corticosterone suppresses production of GAS6. In the absence of the hormone, it boosts proliferation of hair follicles.

“Restoring the expression of GAS6 could overcome stress-induced inhibition of hair follicle stem cells – and might encourage regeneration of growth,” Hsu notes. “It might therefore be possible to exploit the ability of HFSCs to promote hair-follicle regeneration by modulating the corticosterone–GAS6 axis.”

Throughout a person’s lifespan, hair cycles through three stages, growth (or “anagen”), degeneration (“catagen”), and rest (“telogen”). During anagen, a follicle continuously pushes out a hair shaft. In catagen, growth stops and the lower portion shrinks, but the hair remains in place. During telogen, it remains dormant.

Under severe stress, many hair follicles enter this phase prematurely and the hair quickly falls out, leading to baldness. This lifespan is much shorter in the corticosterone-free mice than controls less than 20 days compared with two to three months.

‘Exciting findings’ in long-sought journey to baldness cure

Their follicles also engaged in hair growth roughly three times as often. However, researchers restored their normal hair cycle by feeding the subjects corticosterone. Interestingly, when they applied various mild stressors to the controls for nine weeks, corticosterone rose and hair stopped growing. These stressors included tilting their cage, isolation, crowding, damp bedding, rapid lighting changes, and restraining. Injecting GAS6 into their skin reinitiated hair growth with no side-effects.

“These exciting findings establish a foundation for exploring treatments for hair loss caused by chronic stress,” adds Prof. Rui Yi, a dermatalogist at Northwestern University who is not involved in the study.

The study also reveals GAS6 increases expression of genes involved in cell division in HFSCs.

“So, the authors might have uncovered a previously unknown mechanism that stimulates HFSC activation directly by promoting cell division,” Prof Yi continues. “In aging skin, most progenitor cells harbor DNA mutations – including harmful ones that are often found in skin cancers – without forming tumors.

“It will be crucial to see whether forced GAS6 expression could inadvertently unleash the growth potential of these quiescent but potentially mutation-containing HFSCs,” Yi concludes. “Modern life for humans is inevitably stressful. But perhaps, one day, it will prove possible to combat the negative impact of chronic stress on our hair, at least – by adding some GAS6.”


Large terminal follicles are shed and replaced by small vellus hairs in androgenetic alopecia. Three areas of the scalp are affected preferentially: the temples, vertex scalp and mid frontal scalp (Figure 2). Within these areas the process is strictly patterned. Bitemporal hair loss starts at the anterior hairline and moves posteriorly over the scalp. Hair loss over the vertex scalp begins centrally and radiates outwards circumferentially. Over the mid frontal scalp, hair follicle miniaturization leads to a pattern of hair loss reminiscent of a Christmas tree (75). These three zones are not affected equally leading to clinical variations in the pattern of hair loss, with some men balding more to the front while other bald more over the crown.

Figure 2

Areas of the scalp. F-Frontal / M - Mid frontal / T-Temple / V-Vertex

The 3 key features of MAA are alteration of hair cycle dynamics, follicular miniaturization and inflammation.

Hair Cycle Dynamics and Androgenetic Alopecia

Hair is lost and replaced cyclically. Follicles undergo corresponding cyclic phases of growth, involution, quiescence and regeneration (Figure 3). The growth phase (anagen) lasts for 3-5 years (76). As hair elongation is relatively constant at 1 cm per month, the duration of the growth phase is the primary determinant of the final hair length. At the end of anagen the involutional phase (catagen) lasts for a few weeks. The period of hair follicle quiescence (telogen) that follows lasts approximately 3 months (77). Hair follicle regeneration occurs in approximately the first week of anagen and once regenerated, the anagen phase continues until the hair reaches its final (possibly predetermined) length.

Figure 3 Normal hair cycle- Each telogen hair is replaced by a new anagen hair

Hair cycle in mammals has an intrinsic rhythmic behaviour and this is modified by systemic and local factors. Humans have an asynchronous hair cycle and the duration of anagen and the final length of hair differ between regions of the body. A number of molecular signals including growth factors, nuclear receptors, cytokines and intracellular signalling pathways are involved in controlling the hair cycle. Growth factors such as IGF-1, hepatocyte growth factor, keratinocyte growth factor and vascular endothelial growth factor (VEGF) promote anagen phase of the hair cycle. Similarly, transforming growth factor-beta (TGFbeta), interleukin 1-alpha and tumor necrosis factor-alpha promote onset of catagen (77).

In androgenetic alopecia, the duration of anagen decreases with each cycle, while the length of telogen remains constant or is prolonged this results in a reduction of the anagen to telogen ratio (36). Balding patients often describe periods of excessive hair shedding, most noticeable while combing or washing. This is due to the relative increase in numbers of follicles in telogen. As the hair growth rate remains relatively constant, the duration of anagen growth determines hair length. Thus, with each successively foreshortened hair cycle, the length of each hair shaft is reduced. Ultimately, anagen duration becomes so short that the growing hair fails to achieve sufficient length to reach the surface of the skin, leaving an empty follicular pore. Prolongation of the kenogen phase, the lag phase or the delayed replacement of telogen hair, seems to last longer in MAA leaving a higher percentage of empty hair follicles contributing to balding (78,79). Further, the kenogen (latent phase) is prolonged in MAA, reducing hair numbers and contributing to the balding process (78).

In MAA tiny, pale hairs gradually replace large, pigmented ones. Androgens appear to reduce alopecia hair colour by inhibiting dermal papilla stem cell factor (SCF) production, which is important in embryonic melanocyte migration and bulbar melanocyte pigmentation (80).

Hair Follicle Miniaturization

Hair follicle miniaturization is the histological hallmark of androgenetic alopecia (81). Hair follicles consist of mesenchymal and ectodermal components. The ectodermal part consists of an invagination of epidermis into the dermis and subcutaneous fat. The hair bulb contains the hair matrix which produces the hair shaft. The mesenchymal component is the dermal papilla, a small collection of specialised fibroblasts that is totally surrounded by the hair bulb.

In association with the changes in hair cycle dynamics, there is progressive, stepwise miniaturization of the entire follicular apparatus in MAA (Figure 4). The mesenchyme-derived dermal papilla, located in the middle of the hair bulb at the follicle base, regulates many aspects of the epithelial follicle and determines the type of hair produced (82,83). As the dermal papilla is central in the maintenance and control of hair growth, it is likely to be the target of androgen-mediated events leading to miniaturization and hair cycle changes (84-86). The constant geometric relationship between the dermal papilla size and the size of the hair matrix suggests that the size of the dermal papilla determines the size of the hair bulb and ultimately the hair shaft produced (87,88).

Figure 4 Progressive miniaturization of hair in each cycle

A greater than tenfold reduction in overall cell numbers is likely to account for the decrease in hair follicular size (89). The mechanism by which this decrease occurs is unexplained, and may be the result of either apoptotic cell death, decreased proliferation of keratinocytes (92), cell displacement with loss of cellular adhesion leading to dermal papilla fibroblasts dropping off into the dermis, or migration of dermal papilla cells into the dermal sheath associated with the outer root sheath of the hair follicle (88,90). In vitro studies demonstrate that human balding dermal papilla cells secrete inhibitory factors, which affect the growth of both human and rodent dermal papilla cells, and factors that delay the onset of anagen in mice in vivo. These inhibitory factor(s) probably cause the formation of smaller dermal papillae and smaller hairs in MAA (91). Insulin-like growth factor binding protein 3 (IGFBP3) has a demonstrated antagonistic effect on keratinocyte proliferation in the hair follicle in transgenic mice studies (92).

Smaller follicles result in finer hairs. The calibre of hair shafts reduces from 0.08mm to less than 0.06mm. On the balding scalp, transitional indeterminate hairs represent the bridge between full-sized and miniaturised terminal hairs (93). Traditional models of MAA show follicular miniaturization occurring in a stepwise fashion. This has recently been contested, and it is now believed that the transition from terminal to vellus hair occurs as an abrupt, large step process (96). Either way, the cross-sectional area of individual hair shafts remains constant throughout fully developed anagen (93), indicating that the hair follicle, and its dermal papilla, remains the same size. Therefore follicular miniaturization occurs between anagen cycles rather than within the anagen phase. This short window of androgen effect may also explain the lengthy delay experienced between clinical response and the commencement of therapy, as any pharmacological intervention will only have effect at the point of miniaturization (93).

Follicular miniaturization leaves behind stelae as dermal remnants of the full sized follicle. These stelae, also known as fibrous tracts or streamers, extend from the subcutaneous tissue up the old follicular tract to the miniaturized hair and mark the formal position of the original terminal follicle (94,95). Arao-Perkins bodies may be seen with elastic stains within the follicular stelae. An Arao-Perkins body begins as a small cluster of elastic fibres in the neck of the dermal papilla. These clump during catagen and remain situated at the lowest point of origin of the follicular stelae. With the progressive shortening of anagen hair seen in androgenetic alopecia, multiple elastic clumps may be found in a stela, like the rungs of a ladder (96).

In addition to the hair follicle miniaturization that leads to thin fibres in androgenetic alopecia, a reduction in anagen duration leads to shorter hair length, while an increase in telogen duration delays regeneration. This results in hairs so short and fine that they fail to achieve sufficient length to reach the surface of the scalp.

While miniaturized hairs are also seen in alopecia areata, that condition is potentially fully treatment reversible. In contrast, MAA is only partially reversible at its best. The mechanism for the difference may be related to the attachment of arrector pili muscle and the hair follicle, which will be discussed later in this chapter.

Pattern of Hair Loss

There are 2 concurrent patterns in the hair loss a macroscopic pattern and a microscopic pattern. The macroscopic pattern of hair loss is highly reproducible with certain zones of the scalp being affected preferentially. This is best seen over the vertex scalp where the baldness begins at a central focus and hair loss progresses radially in all directions. There are no-skip lesions. Hair transplantation studies have demonstrated that this pattern is not due to a local signal or a diffusible chemical but rather genetically imprinted in the follicle. The orderly and systematic progression of hair loss is retained even when follicles are relocated to distant sites.

The microscopic pattern of hair loss refers to the pattern of hair loss within scalp follicular units (97). In contrast to beard hairs, scalp hairs exist as compound follicles with between 2 and 5 hairs emerging from a single pore. Miniaturization within these follicular units is also ordered and leads to a reduction in the number of terminal hairs per follicular unit, which can be demonstrated via dermoscopy (Figure 5). This is perceived by the affected individual as a loss of hair volume. When all the hairs within a follicular unit have miniaturized, additional denuded scalp is visible and perceived by affected individuals as baldness.

Figure 5 Dermatoscopic images of scalp in different stages of alopecia

a. Normal scalp with 2-4 hairs in most follicular units

b. Early androgenetic alopecia with mixture of multiple and single hair in follicular units

c. Advanced androgenetic alopecia with thin and single hair in most follicular units


Studies suggest that inflammation is a feature in MAA even though its significance in the pathogenesis of the disease is controversial. Activated T-cells infiltrating about the lower portions of follicular infundibula have been demonstrated in scalp biopsies (98). A moderate perifollicular, lymphohistiocytic infiltrate, perhaps with concentric layers of perifollicular collagen deposition, is present in some 40% of cases of androgenetic alopecia, but only 10% of normal controls (95). Occasional eosinophils and mast cells can be seen. The cellular inflammatory changes also occur around lower follicles in some cases and occasionally involve follicular stelae. A considerable difference in the inflammatory infiltrate has been observed between balding and non-balding scalp (99).

A modest degree of chronic inflammation around the upper part of hair follicles has been well described by many investigators (96,99,100).


The possibility of a slow inflammatory scarring process has been suggested by the irreversibility of the hair loss, the histological evidence of fibrous tracts and the histological similarity seen between MAA and lichen planopilaris (101).

ELI5: Why do more men bald with age than women?

It seems like there’s a lot more bald/balding old men than old women. Why is that? I mean I’m sure there’s a fair share of women balding with age and hair does thin as well, but it seems like men just tend to be balder.

Men have more testosterone than women.

Testosterone gets converted to a more powerful form called DHT.

The more that DHT binds to your hair, the more likely it is to fall out.

So you're telling me that this luxurious head of hair I possess is only an intermediary step until I achieve my ultimate, hairless form?

I went bald at around 20 (i'm 32 now) do I still possess this ultimate form of testosterone? How can I use it to it's full extent!?

It can happen to women with screwed up hormones. I have female pattern baldness from having Polycystic Ovarian Syndrome which means I have more testosterone in my system. It sucks.

Women have two X chromosomes. A lot of the male dominated conditions (male pattern baldness, colorblindness) are usually to do with the fact that men only have one copy of a certain gene if it's on the X chromosome and a lot of these traits are probably recessive, meaning that a single working copy of a gene will stop the condition. If the gene in question is defective then they don't have a backup copy like a woman would. A female on the other hand would require two defective copies of a gene for any genetic condition to take effect making these genetic conditions far less likely.

Or a better question, if we know exactly why Men bald, why the fuck they can't stop that shit?

Actually, they can. The drug finasteride(Propecia) helps prevent the conversion of testosterone to DHT, and the drug dutasteride apparently does this even more effectively, so it can protect those hair follicles from being exposed to it.

Balding is generally determined by genetics.

Female pattern baldness was fairly well documented in the past. Afflicted women had less chance of reproducing, so the condition became less common over time.

There is a far more scientific explanation, but if you want my darwinian take, basically in every species one gender will be more "beautiful" looking in order to compete for a mate. In birds this is usually the male, in Humans it's the female. Long hair is an attractive trait that gives you an advantage over other women for reproducing. It signals higher estrogen, since one thing estrogen and testosterone regulate is hair growth, so long hair = more estrogen, more fertile and healthy and neotenous/feminine thus more attractive. Men are also selected for in terms of physical characteristics, but in a different way to women. With a man, it's more about what he can do than how he looks that makes him attractive, though having more muscle for example means he's gonna be better at defending you, at building and doing hard work, or in the past, hunting, etc.

TLDR: long hair is advantageous for women in order to attract a mate, in the same way a male peacock needs colourful feathers do to so, whereas in men, hair is less important (though I'm sure many women still have preferences).

Chapter 1 - The Biology of Hair Growth

This chapter reviews the functions of hair, its structure and the processes occurring during the hair growth cycle, the changes which can occur with the seasons, and the importance of the main regulator of human hair growth, the androgens. Its main focus lies on human hair growth. Mammalian skin produces hair everywhere except for the glabrous skin of the lips, palms, and soles. Although obvious in most mammals, human hair growth is so reduced with tiny, virtually colorless vellus hairs in many areas, that we are termed the “naked ape.” Externally hairs are thin, flexible tubes of dead, fully keratinised epithelial cells they vary in color, length, diameter, and cross-sectional shape. Inside the skin hairs are part of individual living hair follicles, cylindrical epithelial downgrowths into the dermis, and subcutaneous fat, which enlarge at the base into the hair bulb surrounding the mesenchyme-derived dermal papilla. Human hair's main functions are protection and communication it has virtually lost insulation and camouflage roles, although seasonal variation and hair erection when cold indicate the evolutionary history. Children's hairs are mainly protective eyebrows and eyelashes stop things entering the eyes, while scalp hair probably prevents sunlight, cold, and physical damage to the head and neck.

The Genetics of Balding

No one likes to go bald. Most people don't like to think that something about them caused it. So balding men come up with all kinds of explanations for why it is happening.

They aren't eating right. Their hair follicles are all clogged from their shampoo. Their blood doesn't circulate well on the scalp. Their mom's dad was bald.

Except for the last one, these are all bogus. And the last one is only partially true.

Most baldness comes
from genes people

Baldness happens because of the genes people inherit from both their mom and dad. Some studies show that 80% of balding is genetic.

A key gene can come from a maternal grandpa. But this gene doesn't explain all baldness. People are just as likely to be bald if their dad or their maternal grandfather is bald.

Two new studies have fingered a small region on chromosome 20 called 20p11 as being associated with balding. This sort of thing could explain people who are bald even though their mom's dad still has a full head of hair.

Scientists don't know how this DNA is involved or even what part is involved. All they know is that people who are bald tend to have a certain version of 20p11.

One study found that having this DNA could increase a man's chances of going bald up to 4 times. If men also have certain versions of another gene, then the odds go up as high as 7 times.

The other study found a different bit of 20p11 was involved. They concluded from their study that the increased risk was as high as 3 times.

These two bits of DNA are pretty close together and are probably pointing to the same part of chromosome 20 as being important. Unfortunately neither group found out why these bits of DNA increase someone's risk for hair loss. There aren't even any genes close by. So obviously there is still a lot of work to be done.

In the meantime, scientists might be able to use these findings as a way to look for treatments to give men before they go bald. The idea would be to screen people who are likely to go bald and to find treatments for them. Perhaps medicines that can prevent balding are easier to discover than those that can cure it.

Once researchers figure out how chromosome 20 is involved in balding, scientists might be able to use that information to come up with new balding treatments. One can only hope.

Finding a gene can be like
a treasure hunt.

At first it might seem weird that researchers found a bit of DNA involved in baldness but that they can't figure out why it is involved. The reason for this has to do with the way people find DNA involved in disease.

Human DNA is a long string of 3 billion letters (or bases). Each human is unique because these letters are arranged in a certain order*.

It is too expensive to figure out all of the bases of the DNA from the hundreds or thousands of people involved in a typical study. So what scientists have done is figured out millions of places in human DNA where these letters are often different between people. (This is called the HapMap.)

These differences or SNPs (single nucleotide polymorphisms) work like landmarks to help scientists find which part of the DNA to focus on. They are like clues on a treasure map.

The first part in using a treasure map is narrowing down what part of the world the treasure is in. Imagine the map shows that the treasure is in San Francisco. Then there might be clues that the treasure is near a certain hill or near an oddly shaped tree. Perhaps the treasure is buried near the tower on Mt. Sutro.

With this information, the treasure seekers can get digging. If they know a treasure is in San Francisco, they can't just dig up the whole city. But if they know it is near the tower on Mt. Sutro, then they can dig all over that area.

This is how DNA searches work too. Scientists use SNPs as landmarks to narrow down DNA regions to focus on.

Instead of a treasure map, scientists use the HapMap. They use this map to compare the DNA of people with and without the condition they are interested in. In these studies, scientists compared the DNA of balding and not balding men.

The first study looked at German men. One experiment in this study compared 296 balding men to 347 German men and women who were not seriously bald. The researchers looked at over 500,000 different spots on their DNA and found that bald people shared a number of landmarks in a 1.7 million base chunk of chromosome 20. They had narrowed it down to San Francisco.

More clues led them to a single letter difference that was shared by many of the balding men. A second experiment looked at 319 bald men and compared them to 234 men who weren't bald by the age of 60. This second experiment confirmed the results of the first one.

The second study was done similarly. They compared 578 Swiss men with male pattern baldness to 547 Swiss men who weren't balding. They found a different SNP near the one the first study found. They confirmed that this DNA difference as associated with baldness in over 3000 other individuals from a variety of Northern European countries.

So these two studies have narrowed down where the "treasure" is. They made it to Mt. Sutro. They know that something on a small section of chromosome 20 is partly responsible for balding in Northern European men.

The next steps will be to do some serious digging and to find the treasure. In other words, the researchers need to figure out what in this region is causing these men to bald early. And once they do that, they need to find out why these men go bald. With that information, they might be able to create medicines that can treat baldness.

Usually there is a gene nearby that researchers can investigate. In this case, there isn't. The SNPs are in the middle of nowhere with the nearest gene being at least 350,000 bases away. So researchers have their work cut out for them.

In doing these studies, the researchers also rediscovered the DNA difference that men can inherit from their mom's dad that can lead to early balding.

*The exception is identical twins who have essentially the same DNA but are still unique for environmental reasons.

The Unpredictable Genetics Of Male-Pattern Baldness

What are the genetics of male pattern baldness? originally appeared on Quora: the knowledge sharing network where compelling questions are answered by people with unique insights.

Answer by Adriana Heguy, Director of the NYUMC Genome Technology Center and Professor of Pathology, on Quora:

Unfortunately the genetics of androgenetic alopecia (male-pattern baldness) is not really well understood. The more complex the biology behind a phenomenon is, the more difficult is going to be to find all the genetic factors. Regulation of hair growth in mammals is extremely complicated and poorly understood, in spite of this subject being a very active area of research. Hair is very important to mammalian thermoregulation thus it makes sense for its biology to be very complex.

It is clear that male-pattern baldness is a highly heritable condition [1], although there is also some evidence for the involvement of epigenetic factors [2]. There are a few genes implicated in androgenetic alopecia from different studies [3]. Unsurprisingly, the androgen receptor (AR) gene is one of them, as it is well known that the condition is dependent on testosterone (an androgen). The androgen receptor is on the X chromosome, which is why some people propagate the myth that male-pattern baldness comes from the mother's side of the family (a male inherits the X chromosome from mom, the Y chromosome from dad). But it is not the only gene involved, or even the main gene involved. There are genes in basically all chromosomes that have been implicated in androgenetic alopecia, and this is what makes it so difficult to unravel, as we would have to examine the overall contribution that each gene variant (single nucleotide polymorphism, or SNP) play in hair loss, and also how these genes interact with each other and the environment to result in the phenotype.

Position of genes implicated in male pattern hair loss, from [4].

Some of these genes code for transcription factors or histone deacetylases. The Wnt pathway appears to be involved. Even though we know a fair amount about transcription factors, the Wnt pathway, etc., this still does not tell us much about what's actually going on in androgenetic alopecia and why the hair follicles shrink and die. The hope is that identifying these genes will provide targets for therapeutic intervention. But so far, we are still far from a definitive "cure" for androgenetic alopecia.

If there is any consolation for men (or at least, heterosexual men) distressed about hair loss, if it was a phenotype that was repulsive to females, the gene variants would have been weeded out a long time ago, by sexual selection. Many of us find bald heads very manly and attractive.

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Balding: Genes, Hormones & Age

While the cause of androgenetic hair loss is the same for all men (i.e., men whose hair loss is not caused by an underlying medical condition, drugs, or stress), there is significant variation in the age at which men start to go bald, as well as the extent of their balding. This wide variability is due to the fact that the expression of androgenetic hair loss is significantly affected by three related factors: genes, hormones, and age.

Let us explore each of these important contributors to male hair loss.

Genes in Hair Loss

Many people have heard that “hair loss comes from the mother’s side of the family,” but this is largely a myth: while there is a slightly higher frequency of inheritance from the mother’s side, male pattern hair loss is a genetic trait that can be inherited from either parent. Research suggests that it is a polygenic trait, involving more than one gene, and it is much more complicated than originally thought.

A little background on genetics: a gene is one small part of the chemically encoded hereditary instruction manual that consists of 23 different pairs of chromosomes. It is found in every cell of our body. Twenty-two of the pairs are called “autosomes” and the 23rd pair is a pair of sex chromosomes (the X or Y chromosome). In men, the sex chromosomes include an X chromosome and a Y chromosome, while in women the pair consists of two X chromosomes. These genetic instructions control everything from the development of a fetus to the color of your eyes. Genes may be “dominant,” in that the gene only needs to be present in one chromosome of a pair for the trait to show up, or “recessive,” in which the gene must be present in both chromosomes for that gene to be activated or “expressed.” The most important genes involved in androgenetic alopecia are felt to be dominant ones. It is felt that the genes governing common baldness are both sex-linked and autosomal.

An important androgen receptor gene is located on the X chromosome

Inheritance from the maternal side of the family may be slightly more common due to the presence of an important androgen receptor gene (AR) on the X chromosome. The Y chromosome is not believed to contain any genes that affect hair loss. Inheritance from the father’s side would be explained by the presence of an autosomal (non-sex) gene, but this gene has yet to be discovered.

Complicating the issue further, just having the genes for baldness in your genetic makeup, does not guarantee that the trait will manifest. The baldness genes need to be “turned on” or “expressed” in order for androgenetic alopecia to be apparent. Gene expression is related to a number of factors, the major ones being hormones and age, although stress and other factors can contribute to hair loss in some individuals.

It is of interest that, although genes for some types of hair loss have been mapped, the genes responsible for male pattern baldness have yet to be fully identified. This suggests that any kind of genetic engineering to prevent common baldness is still many, many years away.

In summary, Androgenetic alopecia is felt to be a “dominant” genetic trait that is passed down from your mother or father, but with a slight predisposition to the maternal side due to the presence of an important androgen receptor gene on the X chromosome. In order for hair loss to become apparent, the trait must be expressed – through changes in the production of hormones or changes due to the aging process.

Hormones in Hair Loss

Hormones are biochemical substances produced by various glands located throughout the body. These glands secrete hormones directly into the bloodstream, spreading the chemicals throughout the body. Hormones are very powerful minute amounts can have profound effects on your body.

Testosterone, the major male sex hormone, and other hormones that have masculinizing effects are made primarily in the testicles. It is not until after the testicles develop and enlarge during puberty that hormones can reach a level in the bloodstream sufficient to commence the balding process. In addition to the testicles, the adrenal glands, located above each kidney in men and women, produce androgenic hormones. In females, the ovaries are an additional source of hormones that can affect hair growth.

The hormone felt to be directly involved in androgenetic alopecia is a derivative of testosterone called dihydrotestosterone (DHT). DHT, formed by the action of the enzyme 5-a reductase on testosterone, binds to special receptor sites on the cells of genetically susceptible hair follicles causing miniaturization and eventual balding. (See the Miniaturization graphic).

In men, 5-a reductase activity is higher in the balding area, which leads to the development of patterned hair loss. It typically begins with a recession of the hairline and temples and/or thinning in the crown. It can start as early as adolescence or it can appear later in life. 5-alpha reductase Type II, the predominant form in hair follicles, is blocked by the hair loss medication finasteride (Propecia). The chemical finasteride binds to 5-alpha reductase molecules, preventing them from converting testosterone into DHT. The resulting decrease in the concentration of DHT results in the halting or reversal of the miniaturization process.

It is interesting to consider that while scalp hair growth is not dependent on androgens, scalp hair loss is androgen dependent.

Age in Hair Loss

Genes and hormones are not sufficient on their own to cause baldness. Even after a person has reached puberty, susceptible hair follicles must continually be exposed to DHT over time for hair loss to occur. The age at which these effects manifest varies from one individual to another and is related to a person’s genetic composition, the level of testosterone in the bloodstream, and the follicular sensitivity to the hormone.

Additionally, male hair loss does not occur all at once or in a steady, straight-line progression. Instead, it is characteristically irregular, with people losing their hair in alternating periods of slow and rapid hair loss, interspersed with periods of stability. The reasons that hair loss rates speed up and slow down are unknown, but we do know that with age, a person’s total hair volume will gradually decrease.

Even when there is no predisposition to genetic balding, as a man ages, some hairs in each follicular unit randomly begin to miniaturize. As a result, each group will contain both full terminal hairs and miniaturized hairs, making the area appear less full. Eventually, the miniaturized hairs are lost and the follicular units are reduced in number. In all adult patients, the entire scalp undergoes this aging process so that even the “Permanent Zone” is not truly permanent but will gradually thin, to some degree, over time. Fortunately, in most men, the permanent zone retains enough permanent hair so that hair transplantation remains a viable option for men well into their 70s.


Beek (1950)

Beek evaluated 1,000 Caucasian males with patterned hair loss and classified them into two types — frontal baldness and frontovertical baldness, based on the stage of evolution.[1] It was a simple classification, which described only two stages of hair loss and did not take into account the various evolutionary stages but is important as this was the first attempt to classify hair loss.

Hamilton (1951)

Hamilton, an anatomist, studied more than 300 males with hair loss and proposed a detailed classification system based on frontoparietal and frontal recessions and frontal thinning, which consisted of eight evolutionary aspects and three subgroups [ Figure 1 ]. The various categories of hair loss described by Hamilton include a) scalps, which are not bald (Types I-III) and b) scalps, which are bald (Types IV-VIII), which are defined as follows.

Hamilton classification of male pattern hair loss. Type III has not been included in this figure as a large variety of conditions were included in this type[2]

Type I: There is an absence of bilateral recessions along the anterior border of the hairline in the frontoparietal regions. In this, there is a variant form in which the entire anterior border of the hairline lies high on the forehead, which is referred to as Type IA.

Type II: The anterior border of the hairline in the frontoparietal regions has triangular areas of recession, which tend to be symmetrica1 and extend no farther posteriorly than a point 3 cm anterior to a line drawn in a coronal plane between the external auditory meatuses. Hair is also lost, or sparse, along the midfrontal border of the scalp but the depth of the affected area is much less than in the frontoparietal regions.

Type III: Borderline cases were listed separately as Type III, which also included scalps in which classification is rendered inaccurate due to scars, lateral asymmetry in denudation, unusual types of sparseness and thinning of the hair, and other factors.

Type IV: It represents the minimal hair loss considered sufficient to represent baldness. There are deep frontotemporal recessions, usually symmetrical, and are either bare or very sparsely covered by hair. These recessions extend farther posteriorly than a point, which lies 3 cm anterior to a coronal line drawn between the external auditory meatuses. If hair is sparse or lacking as a broad band along the entire anterior border of the hairline, it is classified as Type IVA.

Type V: It includes extensive frontoparietal and frontal recessions with a sparseness or absence of hair on the crown.

Type VI: In this type, the tonsural region of alopecia remains separated from more anteriorly located areas of denudation by a laterally-directed bar of scalp in which the hair is only slightly sparse. An island of hair lies in the midline anterior to this laterally-directed hairy bridge. In the variant pattern, Type VIA, the peninsula or island of mid-frontal hair is sparse or lost.

Type VII and VIII: In these types, the horseshoe-shaped area of sparse hair or of denudation is unbroken by any well-haired, laterally-directed bridge of scalp. These are a result of the spread and confluence of the tonsural and the anteriorly located regions of alopecia.[2]

Hamilton classification set a benchmark for future classifications of male patterned hair loss as it had elaborately described the various evolutionary stages of hair loss and had based the classification on them but it did not describe a few rare patterns of hair loss, which were later on added by Norwood to give the commonly used Hamilton-Norwood classification.

Ogata (1953)

Ogata distinguished 15 different subtypes of patterned hair loss and classified them into six different subtypes based on the study of Japanese men. The first column shows a normal hairline for Japanese men according to Ogata. The second, third, and fourth columns represent early, intermediate, and late stages of patterned baldness, respectively [ Figure 2 ]. The classification system is somewhat different from the classification systems produced based on Caucasian men, suggesting that the development of patterned baldness in Japanese men may be distinct from Caucasians.[3]