Tuesday, July 24, 2018

Does a fungus cause baldness?

Endgame for an ant (Wikicommons)

Is male pattern baldness (MPB) caused by a pathogen? The question may seem silly because the genetic causation is obvious. MPB is normally a male problem, and family background is important. If your male relatives go bald at an early age, the chances are good that you will too.

Genetic causation does not exclude environmental causation, however. I will argue here that a pathogen, specifically lipid-dependent yeasts of the Malassezia genus, has evolved the ability to accelerate the onset of MPB. I will also argue that this is not a side effect of infection. It is key, in fact, to the pathogen’s survival and reproduction.

The germ theory

MPB in young men was once widely blamed on a pathogen. This germ theory was first put forward by a French dermatologist, Raymond Sabouraud:

In recent years our knowledge of this subject has been much increased by the researches of Unna, Sabouraud, and others. These investigators would lead us to look upon all forms of baldness as parasitic in origin. They say that thinning of the hair, whether general or beginning on the crown or at the temples and forehead (alopecia pityrodes), can be produced by a micro- organism. [...] Sabouraud thinks the micro-bacillus of oily seborrhoea finds its way into the hair follicle and causes sebaceous hyper- secretion; then hypertrophy of the sebaceous glands; next, progressive papillary atrophy; finally, death of the hair. (Waldo 1883)

The identity of the pathogen was a matter of debate. Sabouraud attributed baldness to a bacterium and seborrhea to a yeast initially named Pityrosporum ovale and now classified as the genus Malassezia. Antimicrobials, particularly sulfur ointments and shampoos, became popular treatments for seborrhea and MPB.

This germ theory fell out of favor in the mid-20th century. Ainsworth (1956, p. 589), in his review of the literature, concluded that P. ovale was usually harmless:

During the nineteenth century it was widely held that P. ovale was responsible for the various disorders (and particularly seborrheic dermatitis) with which it is commonly associated. Sabouraud cautiously attributed pityriasis (dandruff) to P. ovale but modern opinion is even more sceptical and during the past two decades the view most generally accepted is that of Ota and Huang (1933) who after a careful experimental investigation and a study of the evidence obtained by others concluded that P. ovale is merely an inoffensive saprophyte of man.

Similarly, Ludwig (1968) wrote: "Due to a misinterpretation of the role of oil seborrhea, which so frequently accompanies the development of common baldness, Sabouraud came to the erroneous conclusion that common baldness results from a chronic infection of the scalp by his 'microbacilli'."

The medical community was in no mood to investigate Sabouraud’s germ theory any further. This was a time when causation of disease was increasingly framed in terms of genetics or lifestyle, rather than infection by a pathogen:

During the first half of the 20th century, researchers began to confront another major barrier of crypticity: long delays between the onset of infection and the onset of disease. Long delays make cause-effect linkages cryptic because other events that occur during the intervening time can form the basis of alternative causal explanations. As the delay in onset of symptoms increases, the number of such events and, hence, the number of alternative hypotheses of causation increases. The alternative hypotheses may focus on specific environmental insults, or may interpret delayed, persistent symptoms as natural wear and tear, particularly if infections are ubiquitous. (Cochran et al. 2000)

Since the turn of the millennium there has been a renewed interest in Malassezia and its role in seborrhea and MPB (Arash et al. 2002; Dawson 2007; Sastry 2004).

Going beyond the proximal cause

Today, there is a growing consensus that seborrhea is caused by the lipid-dependent yeast Malassezia, most likely the species M. globosa and M. restricta (Dawson 2007). The mode of action is less certain. Malassezia degrades sebum and releases unsaturated fatty acids, which may in turn stimulate sebum production (Dawson 2007). Alternatively, it may increase conversion of testosterone to the more active dihydrotestosterone (DHT), thus causing not only excessive sebum production but also MPB. This effect has been shown with acne, a skin condition that overlaps with seborrhea in many ways. When biopsies were taken from affected and unaffected areas in 32 subjects with acne, it was found that "acne bearing skin produced from 2 to 20 times more dihydrotestosterone than normal back skin" (Sansone and Reisner 1971).

What would Malassezia gain from DHT? We know that DHT boosts production of sebum, which contains the fat that this pathogen feeds on. Sebum may also help to shield it from the body's immune system.

There nonetheless remains one apparent flaw in this germ theory: Malassezia is common, yet only a minority of young men develop MPB. It seems, then, that some men are more genetically susceptible than others to MPB. This is part of the reason, but another reason is that some Malassezia species are better than others at altering the chemistry of the skin. The species most implicated in seborrhea are M. globosa and M. restricta (Dawson 2007). Studies of a related skin infection, Pityriasis versicolor, have found M. globosa to be more implicated than M. restricta (Saad et al 2013; Salah et al. 2005). In a review of the literature, Zarei-Mahmoudabadi et al. (2013) conclude that M. globosa is the main cause of seborrhea:

Different Malassezia species were reported as causative agents of SD in the different countries. Lee et al. (23) reported M. restricta as the most important species in Korean SD patients. In addition, Prohic (26) in a study from Bosnia and Herzegovina believes that M. restricta (27.5%) is the main agents of SD and M. globosa (17.5%) and M. slooffiae (15%) are the next agents. In a molecular study by Tajima et al. (11), M. restricta and M. globosa were detected as the predominate agents of SD. In contrast, in Hedayati et al. study in north of Iran M. globosa was reported as the most frequently agent on scalp and face lesions, whereas M. furfur had most frequency on trunk lesions (24). In the present study, out of the 110 scalp scales that were cultured on Dixons agar, 24.5% yielded Malassezia that the most frequently Malassezia species was M. globosa (40.7%), followed by M. pachydermatis (22.2%), M. furfur (11.1%) and M. restricta (7.4%).

Nine Malassezia species are found on human hosts (Dawson et al. 2018). It is likely that different species compete against each other for sites on the body surface. Colonization by an aggressively seborrheic species is thus probably impeded if another species is already present. Indeed, the relative distribution of these species varies from one ethnic group to another and from one geographical area to another (Dawson et al. 2018).

Is Malassezia sexually transmitted?

There may be another side to infection by Malassezia. It colonizes not only the scalp but also the male genital region, particularly if the man is uncircumcised:

Recently, several authors have noted Malassezia spp. as part of the microflora of healthy uncircumcised male genital regions in 49.2% of the population, in contrast to circumcised male patients, in which Malassezia spp. are identified in 22.4% of the population (2, 3). Mayser et al. assumed that Malassezia yeasts find favorable growth conditions in the lipid-rich milieu of the preputial area because of its free sebaceous glands (i.e., Tyson's glands seem to be important) (Khadar et al. 2008)

It is known that yeasts, like Malassezia, can spread from one person to another through sexual contact (Spinillo et al. 1992). The pathogen can thus enhance its own reproductive success by influencing its host's sexual behavior. Premature hair loss may therefore be one of its strategies for spreading to other hosts.

Keep in mind that men in pre-modern societies were divided into age classes, and the transition from one class to the next was determined by visible physical changes: the growth spurt of childhood, the appearance of body and facial hair in adolescence and, finally, the loss of head hair later in life. By making its host lose his head hair prematurely, the Malassezia pathogen reassigns him to a class of older men who, except for the rich and powerful, deal with sexual dissatisfaction not by divorcing and remarrying (or by finding a mistress) but rather by frequenting prostitutes. The possibilities for transmission to a new host are thus increased many times over.

Stranger things have happened

A fungal infection may actually cause sexual dissatisfaction. This kind of behavioral manipulation is not as fantastic as it may seem. Fungi are champions of such manipulation, both in overall prevalence and in sophistication:

The observation that, as a Kingdom, Fungi have many parasitic taxa [...] does not distinguish them from other major groups. Parasitism is a very common mode of life that has evolved repeatedly and probably more times than predation as a life history strategy [...]. What is notable is the apparently high frequency of parasitic fungi that have evolved not just to infect animals but also to adaptively manipulate animal behavior in ways that increase the fitness of the fungus. (Hughes et al. 2016)

You have probably heard about "zombie ants": a fungus infects an ant and reprograms its brain, causing it to leave its nest, climb up a plant, lock its jaws into the plant tissue, and die. A fruiting body then emerges from the ant's head and rains down spores on the forest floor below. There are other examples. In one case, the fungus keeps its host alive and controls its flight behavior so that the insect becomes a moving vehicle for spore release (Hughes et al. 2016).

What about humans? Greg Cochran has argued that an unknown pathogen can alter a man’s sexual orientation as a means to increase its opportunities for spreading to other hosts: "One possible route would be sexual, whereby homosexual behavior could facilitate spread because of the larger numbers of partners homosexual males may have on average, relative to heterosexual males" (Cochran et al. 2000).

Similarly, there may exist a pathogen that reverses male jealousy and makes its host desire cuckoldry, thereby gaining access to many more hosts (Frost 2013). Although many sexual fetishes are attested in the writings of ancient civilizations, cuckold envy does not seem to be one of them. The oldest references date back to 17th century England (Kuchar, 2011, pp. 18-19). The cause may thus be a sexually transmitted pathogen that entered England during the early days of the slave trade. Such a pathogen could have evolved in West Africa, where most women were in polygynous marriages, and where cuckoldry was the main route for transmission from one household to another.

We have never identified such pathogens largely because we have never bothered to look. They are also hard to find, given the delay between infection and behavioral change.


Ainsworth, G.C. (1958). Pathogenic yeasts. In A.H. Cook (Ed.) The Chemistry and Biology of Yeasts (pp. 587-602). New York: Academic Press.

Arash, J., F. Sorour, and A.M. Mokhtari. (2002). Evaluation of the coincidence of Male Pattern Baldness and Pityrosporum group of fungus in Iran. Indian Journal of Dermatology 47(4): 224-226.

Cochran, G.M., P.W. Ewald, and K.D. Cochran. (2000). Infectious causation of disease: an evolutionary perspective. Perspectives in Biology and Medicine 43(3): 406-448.

Dawson, T.L. (2007).  Malassezia globosa and restricta: Breakthrough Understanding of the Etiology and Treatment of Dandruff and Seborrheic Dermatitis through Whole-Genome Analysis. Journal of Investigative Dermatology Symposium Proceedings 12(2): 15-19

Dawson, T.L., C. Leong, J. Goh, and A. Irudayaswamy. (2018). Geographical and ethnic differences in Malassezia species distribution on healthy skin. Congress of the International Society for Human and Animal Mycology

Frost, P. (2013). First, sexual transmissibility and then ...? Evo and Proud, January 5

Hughes, D.P., J.P.M. Araujo, R.G. Loreto, L. Quevillon, C. de Bekker, and H.C. Evans. (2016). Chapter Eleven - From So Simple a Beginning: The Evolution of Behavioral Manipulation by Fungi. Advances in Genetics 94: 437-469.

Khadar, R.K., F. Cherif, R. Ben Hadid, M. Mokni, and A. Ben Osman. (2008). Penile shaft involvement in pityriasis versicolor. Acta Dermatovenerol Alp Pannonica Adriat. 17(2):86-9.

Kuchar, G. (2001). Rhetoric, Anxiety, and the Pleasures of Cuckoldry in the Drama of Ben Jonson and Thomas Middleton. Journal of Narrative Theory 31(1): 1-30.

Ludwig, E. (1968). The role of sexual hormones in pattern alopecia. In A. Baccaredda-Boy, G. Moretti G, and J.R. Frey (Eds). Biopathology of Pattern Alopecia. International Symposium, Rapallo, July 1967: Proceedings. Basel, Karger, pp 50-60.

Saad, M., T. Sugita, H. Saeed, and A. Ahmed. (2013). Molecular Epidemiology of Malassezia globosa and Malassezia restricta in Sudanese Patients with Pityriasis Versicolor. Mycopathologia 175(1-2): 69-74.

Ben Salah, S., F. Makni, S. Marrakchi, H. Sellami, F. Cheikhrouhou, S. Bouassida, A. Zahaf, A. Ayadi (2005). Identification of Malassezia species from Tunisian patients with pityriasis versicolor and normal subjects. Mycoses 48(4): 242-245

Sansone, G., and R.M. Reisner. (1971). Differential Rates of Conversion of Testosterone to Dihydrotestosterone in Acne and in Normal Human Skin—a Possible Pathogenic Factor in Acne. Journal of Investigative Dermatology 56(5): 366-372.

Sastry, P.S.R.K. (2004). Occult fungal infection is the underlying pathogenic cause of atherogenesis. Medical Hypotheses 63(4): 671-674.

Spinillo, A., L. Carratta, G. Pizzoli, G. Lombardi, C. Cavanna, G. Michelone, and S. Guaschino. (1992). Recurrent vaginal candidiasis. Results of a cohort study of sexual transmission and intestinal reservoir. Journal of Reproductive Medicine 37(4): 343-347.

Szasz, T.S., and A.M. Robertson. (1950). A theory of the pathogenesis of ordinary human baldness. Archives of Dermatology and Syphilology 61(1):34-48. https://doi.org/10.1001/archderm.1950.01530080040004   

Waldo, H. (1883). The causes and treatment of baldness. Bristol Med. Chir. J. 23(88): 107-113.

Zarei-Mahmoudabadi, A., M. Zarrin, and F. Mehdinezhad (2013). Seborrheic dermatitis due to Malassezia species in Ahvaz, Iran. Iranian Journal of Microbiology 5(3): 268-271.


Anonymous said...

I can't read Dawson, Leong, Goh and Irudayaswamy 2018: can anyone please illuminate their distribution?

John said...

interesting report in the daily telegraph

Johnny Caustic said...

This leads to the natural questions:

- Is there something we can put on our heads that kills Malassezia?

- Which bacterium did Sabouraud attribute baldness to?

Anonymous said...

Re: Motala and EDAR, after consideration I think it has to be connected to the arrival of the pressure blade technique in Finland and Norway, coming from north-western Russia dated to 11.3–7.7 kya.

When its compared to the earlier Mesolithic Karelians, Motala has similar connections to Mal'ta 1 and Afontova Gora 3 (ANE) but in Motala it is noticably weaker - not stronger. My guess is EDAR came in at low frequencies when the ANE component showed up, because as we know Mal'ta and Afontova Gora 3 had already gotten some mixture from Asian and Pacific populations. The derived EDAR mutation and ANE must've reached the Baltic any time before 9 and 8 kya. Presuming ANE people were in Siberia up till Mongoloids arrived with the derived EDAR mutation (compare: Baikal 8kya, Juelmun Korea 10kya) there must be no better explanation for Europoids/ANE picking it up.

Anonymous said...

Why does MPB leave the familiar horseshoe pattern of hair on the head? In hair transplants, they take hair follicles from the side and back to the top and front areas that are bald. Is the hair on the sides and back of a different type and resistant to baldness?

Wanda said...

By making its host lose his head hair prematurely, the Malassezia pathogen reassigns him to a class of older men who, except for the rich and powerful, deal with sexual dissatisfaction not by divorcing and remarrying (or by finding a mistress) but rather by frequenting prostitutes.

That's just speculation, right? It seems weak. I could buy it if most call-girl clients were baldies and baldies rarely had mistresses. But it is so easy to find examples of famous bald or balding men who had mistresses. Douglas MacArthur springs to mind, as does Dwight Eisenhower. Aren't both John McCain and Donald Trump balding? They've both divorced and remarried. Do tell-all books by prostitutes remark on how many baldies they entertained?
I do agree that a bald head ages a man. I recall working once with a man, stocky and bald, whom I assumed was in his mid-forties. It turned out he was 27.

Sean said...

"Do tell-all books by prostitutes remark on how many baldies they entertained?" They do remark on the lack of good looking 'Johns'. Syphilis does not usually, but can, cause 'moth-eaten alopecia. Al Capone was a bouncer in brothels and he had syphilis, and premature male pattern baldness (33 years' old). John von Neumann was prematurely bald, as are Jeff Bezos and Elon Musk. Its conceivable that high DHT in youth has some cognitive benefits.

Anonymous said...


MacArthur and Eisenhower were among the most famous and powerful men of their time.

John McCain is 82 years old. Trump had scalp reduction surgery, which moves the scalp and thus the receded hairline forward towards the forehead. Trump also takes Propecia.

One of the biggest effects of MPB seems to be psychological. Most balding men in real life will not reveal their true feelings about their MPB except to their close male friends. If you read discussion forums online dedicated to MPB or just men and men's issues in general, you will find that it is quite psychologically distressing and even tends to induce a mild depressive episode or intense anger and frustration in otherwise healthy men who are often at the peak of their lives. It is not just the negative impact on appearance and sexual competition, but the early reminder of mortality and lost youth that produces the psychological distress.

This sort of psychological distress has a negative effect on confidence, which tends to further hinder success in the sexual market. Generally it's only compensated by wealth, power, or fame. But even wealthy, powerful, and famous men like Trump and Elon Musk and countless others feel compelled to correct their MPB, which suggests how negative it is perceived to be.

Anonymous said...

McCain was from a prominent Navy family. His father and grandfather were 4 star Admirals. McCain also became famous when he returned from Vietnam after being a POW. He had 2 Senators as groomsmen when remarried. At any rate, I don't think he was very bald if at all when he remarried.

Anonymous said...

“...Because of his bald head and the hairiness of his body, he announced that it was a capital offence should anyone either look down on him [from above] as he passed, or to mention goats in any context in the emperor’s presence...” -- Suetonius

This goes back a long way - both the MPB and the mental distress it causes. I have no idea how anyone thought it might be "sexy" or evolved as a sign of authority, when it lacks such positive connotations either now or in antiquity.

Anonymous said...

Now with that said the familiar horseshoe pattern of hair on the head does sound genetic: can the fungal hypothesis really explain that?

Anonymous said...


What explains the particular pattern of MPB? Why does the pathogen appear to attack the temples, the front hairline, and the crown to produce the familiar pattern of MPB? I've noticed that babies' heads of hair when they start growing hair look like those of bald men.

Presumably women would be infected by the pathogen as frequently as men. What would explain why women appear to be immune to MPB style hair loss? Are men's scalps a better environment for the pathogen?

According to this site,


"By age 35, two-thirds of American men will have some degree of appreciable hair loss and by age 50 approximately 85% of men have significantly thinning hair. About 25% of men who suffer from male pattern baldness begin the painful process before they reach 21."

So if most men have at least some hair loss, does that suggest that most men are infected by the pathogen and differ in how they react to it or how their immune system handles it?

Or does this statistic obscure two different types of hair loss, one pathogenic MPB, and the other some sort of gradual hair loss due to aging, like other aging caused gradual declines in muscle mass, energy, etc.?

Peter Frost said...


I've contacted the author (Thomas Dawson) for a copy of his presentation.


T. gondii promotes risk-taking behavior. It's associated with risky driving, promiscuity, and a lot of other injurious behaviors. I suspect it disables mental algorithms that ensure caution and double checking.

Johny Caustic,

A topical treatment? I'm skeptical. The fungi in question infect the scalp at a deep level.

In the studies I've read, he calls it a "micro-bacillus." The following paper describes it as follows:

"it is a white coccus, quite characteristic in appearance, and suspected by Sabouraud of playing some part in the genesis of alopecia"


I'm not hostile to the idea of gene flow from East Asia to Europe. Clearly, that has happened both in history and in prehistory. If you go far enough back, however, you come to a common ancestral population. I believe that the Sami people broke away from this population during the last ice age and thus share common characteristics with the two other groups. But I don't think the Sami are a product of mixture.


The horseshoe pattern probably serves to identify a man's age class. Its shape seems too stereotypical to be the result of aging itself.


Ouch! It's partly speculation. I'm making a strong argument and a weak argument here. The strong argument is that the fungus stimulates DHT production as a means to stimulate sebum production (which provides the fat that it feeds on). This increase in DHT causes premature baldness and thus creates new opportunities for the fungus to spread to other hosts. My weak argument is that the fungus exploits these opportunities by further increasing DHT production and further colonizing the genital region. There is actually good evidence for sexual transmission of Malassezia. The only element of my argument that is pure speculation is the idea that Malassezia causes sexual dissatisfaction.

I've previously argued that the yeast responsible for vulvovaginal candidiasis manipulates sexual behavior to its own advantage.

Wealth and power can compensate for a lot of defects. For most young men premature baldness is a big minus on the dating scene.

The last few anons:

Men naturally lose hair with age. I strongly suspect that there have been evolutionary reasons to retire men from the mate market and invest in parenting and grandparenting. Premature baldness is not natural.

Anonymous said...


If the pathogenic theory is correct and Malassezia or something like it is responsible, then theoretically MPB would be relatively easy to cure, right?

Given the tremendous demand there'd be for a cure, why do you suppose researchers and companies have not pursued this angle?

Anonymous said...


I agree the Sami are of near-total Mesolithic descent: but I don't see how one can deny that they have some more recent Siberian/Mongoloid mixture than Motala times. The idea of a Europoid + Mongoloid clade fits better with the total evidence from cultural anthropology and linguistics than with the current concensus. It even fits with the cladistic analysis of human teeth by Chris Stringer and I hope you're right, but it doesn't match the autosomal DNA evidence which seems so concrete now.

Wanda said...

Thanks for the response. I've been reading a bit on the subject -- there certainly is a lot of interest in MPB! One of the papers I found interesting is Why we go bald: an evolutionary hypothesis by Jonathan Hausmann, which you may have read. He postulates inflammation as at least a partial cause.
Another study lumps male vertex balding in with other diseases caused by hyperinsulinemia (Hyperinsulinemic diseases of civilization: more than just Syndrome X.)
I was looking for when MPB might have evolved but have found nothing so far, though Anon's reference to Suetonius takes it back to at least the first century AD. If in hunter-gatherer days life-span was around 30 or so, just when MPB begins for most men, maybe it didn't matter. They would have done their mating rituals and reproduced years earlier, long before they began to go bald.
Regarding Anon's comment about John McCain, yes, that was a bad example on my part. I've found photos of him when he was in his early 30s and he had a full head of hair, and his father, as an old man, seems to have still had most of his hair.
Anyway, I never thought the subject of male baldness would be so interesting, but it leads down all sorts of curious by-ways. Thanks for bringing it up!

Sean said...

Inflammation makes you feel anorexic, sleepy, and depressed, as opposed to wanting to go out and spend money having sex with prostitutes, which carries risks apart from infection. Even though the men would be under thirty in many cases, the bug would have to amp up their sex drive.

Wanda said...

Speaking of curious by-ways, trying to get a hint as to whether Peter's suggestion that MPB sufferers lacking wealth and status tend to be more likely to seek succor in the arms of a lady of the evening rather than maintain a mistress, I've been browsing mugshots of those arrested in prostitution stings. Below is an example. At a quick glance, it looks like 10-15% or so are bald or balding. Of course, this and other similar collections are only a small sample, and only includes those who got caught.

MUG SHOTS: More than 100 arrested in Harris County prostitution sting

Peter Frost said...


No, it wouldn't be easy to cure. Fungal infections are notoriously difficult to eradicate, mainly because they infect the skin down to the stratum corneum.

Lots of people are interested in the commercial possibilities. That's why we have antifungal shampoos (Selsun, ketoconazole, etc.). But a treatment that works would be costly, lengthy, and definitely not over-the-counter. I suspect the eventual treatment will be a topical DHT blocker combined with an oral antifungal. Evidently you would have to get a doctor's prescription and have monthly blood tests to check for liver dysfunction.


The separation between Africans and non-Africans is usually set at 60,000 years ago. Most people set the European/East Asian separation at 30,000 years ago, but I favor a more recent separation, i.e., 20,000 to 15,000 years ago. Getting the right date through inferential methods is difficult. Ultimately, aDNA will settle this question.


Thanks for the Hausmann reference! There seems to be a consensus that various microbes on the skin stimulate sebum production as a way of increasing their food supply (since they feed on the fat in sebum). Some do this by stimulating DHT production, and in doing so they create new opportunities for themselves. If a microbe stimulates DHT too much, it causes premature baldness, which in turn impacts the host's sexual behavior. Certain yeasts, particularly some of the Malassezia species, have gone the farthest in manipulating sexual behavior as a means to maximize transmission to other hosts.

I suspect that most young single men, balding or otherwise, satisfy their sexual urges by consuming Internet porn. But that's a new development. The first time I saw a pornographic image on the Internet would be the late 1990s. Farther back in time even celluloid porn was not easily available. In the 1970s you could not buy Playboy anywhere in my hometown. You had to go to a drugstore in a town 15 kilometres away.


Simply by increasing DHT production it would also increase its host's sex drive. I see this evolutionary process as a step-by-step process where each new step opens up new possibilities for host manipulation.

Anonymous said...


Would this hypothesis be easy to test, by simply biopsying balding men's scalps?

Do you suppose most men who don't go bald simply don't have infected scalps? Or do you think that they're infected too, and there is some other reason they don't go bald, such as genes which inhibit sebum production?

Anonymous said...

I don't know; the Oase fossils are dated to 39-42 kya (and the similar but unsampled Nazlet Khater 2 is 42kya) and Ust'Ishim is 45 kya, and both are outside the Europoid + Mongoloid clade. But people have noted Mechtoid and therefore Europoid traits in the child from Taramsa, which is as old as 50 kya and associated with the Levallois Nubian. If true this would put back the split between Europoids and Mongoloids to >50 kya, but I have a few doubts about the affinities of Taramsa. Now Australians and Papuans are on the Mongoloid side, we need to consider that Greater Australia was peopled c. 50 kya by people with a Middle Paleolithic technology, which even more certainly dates the split to >50 kya. If you go with the alternative topology then Australia doesn't matter, and it depends on the interpretation of Taramsa - with the Aurignacians & Kostenki 14 as the first definite Europoids.

Peter Frost said...

Very first Anon,

Thomas Dawson sent me a PDF of that presentation. Here is the breakdown of the Malassezia species by region :

M. sympodialis - 48%
M. globosa - 30%
M. furfur - 8%

M. sympodialis - 69%
M. globosa - 12%

M. restricta - 44%
M. sympodialis - 39%
M. furfur - 11%
M. slooffia - 11%

M. sympodialis -38%
M. globosa - 37%
M. furfur - 21%

M. globosa - 42%
M. sympodialis -25%
M. furfur - 23%

M. furfur - 39%
M. sympodialis - 36%
M. globosa - 22%

M. globosa - 30%
M. furfur - 23%
M. restricta - 23%
M. sympodialis - 17%

If you send him an email, he will probably send you a PDF


All men are infected with Malassezia, but there are different species, and some are more virulent than others. I also suspect that there are genetic predispositions that make some men more resistant than others.

Macgyver said...

The 5 alpha reductase inhibitors such as finasteride or dutasteride, are NOT the solution, in fact today and after many years of research there is no solution, but YES, within the total uselessness of practically all treatments. Finasteride and minoxidil are the LEAST useless ..

Once again we are face to face with the complexity of the AGA (androgenetic alopecia), it is true what you say, it was calculated that the maximum peak of testosterone in a man is between 25 to 30, starting a very slight downward curve in the production of testosterone ( may vary according to male), but incongruent with the adrogenic theory, this fact does not stop or slow down the hair loss and progress of the AGA, sometimes even accelerates more .. concluding that more than 60% of males over 45 years suffer from AGA ..

if the production of testosterone decreases and therefore and in theory that of DHT, to that add the aromatization in estrogen, because the AGA follows its course as it is?

even knowing that with small concentrations of DHT and an inherited hypersensitivity is the only thing that requires the "process" AGA, SEE the case of women, only produce androgens by the adrenal glands, do not have testicles.

I am more inclined that androgens cause an over-expression of the mRNA of certain proteins and inhibitory factors of hair growth, fibrotic, inflammatory degenerative processes, and even at the level of signaling proteins with WNT or beta-catenin, which interact with the cells mother (stem cells), these become inoperative, at least in regard to the signaling of hair growth.

I give you an example, to collation of an interesting article that read the other day about the nitric oxide, the transforming growth factor beta (TGF-beta) and the process of collagen degeneration ..

I came to say that it has been observed in patients with angina pectoris, arteriosclerosis where the obstructed vessels were formed largely by collagen that covers the arterial wall, large samples had revealed large amounts of the TGF-beta as the cause, and as the oxide Nitric is an inhibitor of this factor TGF-beta:

conclusion: little nitric oxide leads to higher production of TGF-beta and fibrotic processes.

in the medline there are more than 2 and 4 articles that show how DHT encodes large amounts of TGF-beta at the level of the hair follicle.

Nowadays, those who deny that there are underlying inflammatory processes and fibrosis, OBSERVED by electron microscopes, should simply read and expand their knowledge.

As much as you lower the testosterone or DHT, the "damage" in the follicle is done, those processes are the only thing that they are going to do is to reduce the cellular activity of the papilla of the follicle, if the stem cells no longer give signals that it helps us to remove the DHT in one stroke, the degenerative inertia of the follicle is total.

that is why it is so extremely difficult to revert an AGA unless it is creating an embryonic-like semi-environment where the stem cells do re-give wnt or beta-catenin signals to form a new follicle.

Anonymous said...

Thanks for the data but its hard to draw a phylogenetic pattern from this: why would M. restricta be in Switzerland and Singapore, but not places near to either? Singapore has never been a colony of a country with a presence in the Alps. The species furfur, globosa and sympodialis are universal to Eurasian and colonial peoples; sloofia is local to the Alps and restricta has the weird distribution. Mmm...

Sean said...

Androgenic alopecia, a condition characterized by increased levels of DHT could have been selected for due to the benefits that prostaglandin D2 (PGD2) has on the prostate. A DHT metabolite can increase the transcription of prostaglandin D2 synthase through estrogen receptor beta. The increase of PGD2 can decrease the risk of prostate cancer and proliferation of prostate cancer cells. Therefore, the mechanisms behind male pattern baldness may also curtail the advancement of prostate cancer."

https://www.uni-bonn.de/news/068-2017 “We were thus able to identify 63 alterations in the human genome that increase the risk of premature hair loss,” explains Dr. Stefanie Heilmann-Heimbach. The human geneticist at the University of Bonn is one of the lead authors of the international study. “Some of these alterations were also found in connection with other characteristics and illnesses, such as reduced body size, earlier occurrence of puberty and various cancers.” The genetic findings thus also confirm the link between hair loss and an increased risk of prostate cancer. The link with heart disease is much more complicated. Genes that reduce the risk were found along with genes that increase the risk. “We have also found links to light skin color and increased bone density,” explains Prof. Markus Nöthen, Director of the Institute of Human Genetics at the University of Bonn. “These could indicate that men with hair loss are better able to use sunlight to synthesize vitamin D. They could also explain why white men in particular lose their hair prematurely.”

"It shows that a drug originally designed as a treatment for osteoporosis has a dramatic stimulatory effect on human hair follicles donated by patients undergoing hair transplantation surgery....a compound originally developed to treat osteoporosis, called WAY-316606, targets the same mechanism as CsA by specifically antagonising SFRP1."

Diagnostic Value of SFRP1 as a Favorable Predictive and Prognostic Biomarker in Patients with Prostate Cancer

Anonymous said...

I think baldness looks more like a side affect than in infection, and if there's 63 alterations it looks like more than one phenomenon. It looks like MPB correlates with both high and low risk for prostate cancer. Though I'm a bit skeptical of vitamin D synthesis hypotheses generally there seems to be a generic link to the prostate. Would that be important in Europe, esp. Med Europoids?

jamjam said...

Over evolutionary time, I think it's probable that sub-dominant males have often had very little ability to prevent higher ranking or more powerful males from having sex with 'their' mates whether that mate consents or not, and in such a circumstance, a possible strategy for the sub male to maximize his chances of being the father of his mate's children is to have sex with her himself as soon as he can. This is also a strategy to respond to the rape of a mate, and has been observed in pair-bonded Ducks where the female has been gang raped by a roving band of mateless males.

So I don't think it should surprise us if it turns out that being aroused by watching yourself being cuckolded has evolved to serve that strategy.

In a way it parallels arguments for why some women are aroused by rape fantasies: the lubrication and edema of arousal could sharply reduce injuries which could otherwise result from being raped.

Anonymous said...

Jamjam, elsewhere Peter argued that the cuckold fetish is new - something like 17th C onward - and came to Europe from polygynous cultures of Africa or the Middle East. My problem is that the cuck fetish would need to be more common among blacks or MENAs than West Euros: and as far as I can tell... it isn't.

Anonymous said...

Jamjam: another thing I noticed in Clements' Anime Encyclopedia is the number of Japanese porn anime feature a viewer substitute rescuing a girl from a rapist, and being invited to take advantage of her. What you described is one of those beta male fantasies taboo-ed in the west because its outright exploitative of vulnerable women, but over in Japan they are open about it.

Peter Frost said...

"My problem is that the cuck fetish would need to be more common among blacks or MENAs than West Euros: and as far as I can tell... it isn't."

If a pathogen can neutralize or even reverse male sexual jealousy, there would be very strong selection for males who are less vulnerable to this kind of mental tampering. Presumably this sort of selection has been going on longer in West Africa than in Europe.

Sean said...

@Anon@ me, The bit about reduced height and whiter skin indicates baldness is a result of sexual selection on women, confirmed by the major genes for it being on the X chromosome as long known. The bald caveman of La Marche dates from the Magdalenian when the eponymous girl had the first known impacted wisdom tooth, and there was a reduction in height too. Dental overcrowding with jammed back teeth just breaking the gum would have regularly led to catastrophic abscesses in prime reproductive age. Selection for more feminine features and skin tone, and selection for great hair equals Europeans. Blacks go bald relatively rarely I agree it has nothing to do with vitamin D, blacks have greater bone density. There does seem to be a connection between bone density, a full head of hair, and virility, but then most hormones are influenced by one's bones. Dihydrotestosterone (DHT) "has strong androgenic effects and very weak anabolic effects, as well as no estrogenic effects", so it is a good thing to have more of, once you reach the andropause per estrone from accumulating fat in your mid fifties; rising DHT is an anti cancer mechanism of late middle age so you can care for your grandchildren. Even if you are young, I would think very carefully before taking drugs that reduce DHT (Chinese athletes doped with DHT to set world records by the way, so it is not only there to stop you getting cancer and make your penis bigger). What do old men with a great head of hair do?; if J. Philippe Rushton is any guide they seduce women thirty years their junior.

What Peter is saying about baldness being a marker for a post reproductive stage of life, and baldness being hijacked by a fungus to make young men infect their peers via prostitutes makes a lot of sense.

Anonymous said...

Peter, I agree in theory but you use the word, "presumably".

Anonymous said...

Sean, it has been arguedn among other objections, that the La Marche cartoons look too modern to be Magdalenian.


Sean said...

Ice Age Art at the British Museum: 'Not even Leonardo surpassed this'

Anonymous said...


DHT typically isn't used by athletes because it's not very anabolic. Athletes usually use testosterone and human growth hormone, among others. Are you sure those Chinese athletes didn't take testosterone?

Does DHT really have anti-cancer properties? It's been implicated in prostate growth and possibly prostate cancer.

Peter Brimelow has retained a full, thick head of hair and married an intern almost 40 years his junior. He's a celebrity of sorts, but even with such status it's probably less likely he would have married a woman that much younger at his age if he had been bald or had the typical head of hair for his age.

You seem to be suggesting that baldness is caused by selection and a fungus, which seems inconsistent.

Sean said...

It seem plausible that where men contribute provisioning for their children and grandchildren, at a certain stage in male life muscles and having a full head of hair becomes less important to natural selection that a rapidly increasingly danger of getting cancer. Dihydrotestosterone was used by cheating Chinese avoiding the obvious drugs, DHT has an effect on the nervous system that is useful for athletes. Growth hormones (including estrogen) will grow cancer too, and as you note DHT isn't vary anabolic, it also does not get converted to estrogen unlike testosterone so DHT does not give you gynecomastia (it also makes your bones more dense by the way). Africans have a higher ratio of DHT to testosterone.

As I understand it, the fungus would not cause the common baldness of late middle age because Peter is arguing that MPB in older men is a result of and marker for a certain stage of latter life, one in which natural selection has programmed men to maximize their reproductive fitnesss. The fungus would only be responsible for premature baldness that strikes in prime reproducing years.

Macgyver said...

@Peter Frost,

1)These microorganisms are not the only cause to develop seborreheic dermatitis (DS)
2)Formerly it was believed that it was exclusively by a hypercolonization of Malassezia, has been found up a lot of types of malassezia, some lipid dependent and others not.
3)The amount of malassezia found on the skin of the scalp of people affected by DS is NOT GREATER than unaffected people.
4)Later, some type of "abnormal" autoimmune response was suggested to the exposure of normal levels of malassezia, this took place when it was observed that subjects affected by HIV were more predisposed to develop or develop dermatitis.
5)In some way or another, malassezia is a key factor for the suffering of this DS.This has been observed due to the efficacy for dermatitis of the use of fungicides that kill this and other microorganisms( such as ketoconazole)
6) Also hypothesized about an inflammation due to irritation caused by malassezia in some subjects, but we return to the same, we all have malassezia, because dont everyone develop DS?
7)Assuming that malassezia can increase DHT levels (ie through the possession of the enzyme 5-alpha reductase in its metabolism or whatever), if you have a follicle that is not genetically hypersensitive to DHT, the follicle will remain intact , it will not miniaturize (e.g hairs of the parietal, occipital region or belonging to any region in people without hypersensitivity
8) I mean, you can put tons of dht in a person without AGA/MPB, and he will not get to lose hair nor with cannon shot. So what does it matter if this yeast may or may not increase the testosteroran conversion to dht?
9)the cells of the dermal papilla inherit a hypersensitivity to DHT due to unknown polygenic factors. Or are you speculating that hypersensitivity in dht receptacles is also induced by yeast?
10)Why are there people with DS who do not have AGA/MBP?
11)I repeat, AGA / MBP is alopecia due to sensitivity to androgens, it has nothing to do with hirsutism, acne, or seborrhea...what is the problem?
12)that the same sensitivity of the cells of the dermal papilla of the hair follicles can be presented by the epidermal cells, as well as the cells of all the corporal hairs, knowing that the DHT causes miniaturization in the hair of the head but stimulates the growth of body hair ..

Santoculto said...

We already have a one strong pattern for male homossexuality in some cases, which i'm part of, birth order effect, so why suppose that it's not ''intrinsically biological'' but fundamentally environmentally-pathogenic**

Your text there are a lot of ''may''...

May, pathogen or some pathogen or whatever it is, increase sexual desire but i don't think it alter the nature of sexual desire per si..

I find ''my'' theory of sexual diversity much more easier, simple [simpler..] at priori, one of the biological laws ideologues hbd on the extreme right love to forget, DIVERSITY: almost traits varies, the case of sexuality.

Heterossexuals varies on personality, we have a real sexual-psychological spectrum between the extremes poles.

This is re-interpretation of over-binnarial ''gender''-theory.

Santoculto said...

"My problem is that the cuck fetish would need to be more common among blacks or MENAs than West Euros: and as far as I can tell... it isn't."


Seems ''weird'' sexual fetiches tend to be along with highly ''intelligent'' people's, just look at the japaneses.

Santoculto said...

Remember that very important lesson

Before to get with the hard theory, start with the easier...

Before jump to this pathogenetic ''theories'' try cultural co-evolutionary ones.

Anonymous said...

Santoculto, I agree that paraphilias are connected to people with a high IQ, although they tend to have lower-than-normal libido: this is perhaps because high IQ people are generally prone to boredom (therefore sexual boredom?) and they are more creative, allowing them to find ways to compensate. For example I remember reading Bailey and remembering what they had to say about fetishistic transsexuals having a higher than average IQ, whilst other transsexuals did not.

But there may exist no such connection between IQ and paedophilia:

With homosexuality a connection to IQ is questionable:

Ofc the paraphilic nature of both paedophilia and homosexuality has been questioned, but how much of that is politics? (A paraphilia is learned, an orientation is inborn.)

fumaco said...

Funnily enough, I noticed it a couple of years ago. I am using a shampoo called Nizoral because it is widely touted in male hair loss forums as the greatest thing since sliced bread. There's even one study on mice that buttresses this claim. Personally I'm pretty skeptical, but I have to use some shampoo anyway, so why not. Then I went to the US and realized it was marketed as an anti-dandruff (not anti-hair loss) shampoo, which basically means it kills fungus.

Then I had a friend who had fungal infection from unprotected sex with his wife, and you know what the doctor prescribed to him? The same brand (different format, though)! So with one bottle of shampoo you can wash yourself up there to prevent baldness and down there to prevent funny smells. BTW, I'm not pushing for this particular brand, I don't care and have no conflict of interest: I'm sure any off-the-shelf anti-fungal shampoo/lotion/cream would do just as well on both ends...

John said...

This comment is a bit late, but the topic is interesting. Not only does the fungus play a direct role, but there seem to be other variables that fit in alongside the idea. Excess iron encourages fungal infections, including malassezia. Iron also has a clear role in oxidative stress and mitochondrial health. Women have less iron and less hair loss. In the early 20th century, a doctor put forth the "ivory dome" idea from examining cadavers, stating that excess calcification and blood supply loss was the cause. Those things are all related. Excess iron, hypothyroidism, high parathyroid hormone, inflammation--they have overlapping, synergistic, downstream effects (both in hair loss and other health problems). There are many common interventions that defend against those problems and hence prevent the fungal infections and excess calcification: adequate calcium, aspirin, vitamin K2, blood donations, avoiding the sh*t seed oils...those are some.

Selina Julie said...

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