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.
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