Alzheimer's and African Americans

A village elder of Mogode, Cameroon (Wikicommons - W.E.A. van Beek). African Americans are more than twice as likely to develop Alzheimer's. They also more often have an allele that increases the risk of Alzheimer's in Western societies but not in sub-Saharan Africa. Why is this allele adaptive there but not here?

Alzheimer's disease (AD) is unusually common among African Americans. Demirovic et al. (2003) found it to be almost three times more frequent among African American men than among white non-Hispanic men (14.4% vs. 5.4 %). Tang et al. (2001) found it to be twice as common among African American and Caribbean Hispanic individuals. On the other hand, it is significantly less common among Yoruba in Nigeria than among age-matched African Americans (Hendrie et al. 2001).

This past year, new light has been shed on these differences. Weuve et al. (2018) analyzed data from ten thousand participants 65 years old and over (64% black, 36% white) who had been followed for up to 18 years. Compared to previous studies, this one had three times as many dementia assessments and dementia cases. It also had a wider range of data: tests of cognitive performance, specific diagnosis of Alzheimer's (as opposed to dementia in general), educational and socioeconomic data, and even genetic data—specifically whether the participant had the APOE e4 allele, a major risk factor for Alzheimer's.

The results confirmed previous findings ... with a few surprises.

Incidence

Alzheimer's was diagnosed in 19.9% of the African American participants, a proportion more than twice that of the Euro American participants (8.2%).

Cognitive performance and cognitive decline

Cognitive performance was lower in the African American participants. "The difference in global cognitive score, -0.83 standard units (95% confidence interval [CI], -0.88 to -0.78), was equivalent to the difference in scores between participants who were 12 years apart in age at baseline."

On the other hand, both groups had the same rate of cognitive decline with age. In fact, executive function deteriorated more slowly in African Americans. The authors suggest that the higher rate of dementia in elderly African Americans is due to their cognitive decline beginning at a lower level:

[…] on average, white individuals have "farther to fall" cognitively than black individuals before reaching the functional threshold of clinical dementia, so that even if both groups have the same rate of cognitive decline, blacks have poorer cognitive function and disproportionately develop dementia. (Weuve et al. 2018)

Interaction with education.

Differences in educational attainment, i.e., years of education, explained about a third of the cognitive difference between the two groups of participants:

Educational attainment, as measured by years of education, appeared to mediate a substantial fraction but not the totality of the racial differences in baseline cognitive score and AD risk (Table 5). Under the hypothetical scenario in which education was "controlled" such that each black participant's educational level took on the level it would have been had the participant been white, all covariates being equal, black participants' baseline global cognitive scores were an average of 0.45 standard units lower than whites' scores (95% CI, -0.49 to -0.41), a difference smaller than without controlling years of education (-0.69; Table 5), and translating to about 35% of the total effect of race on cognitive performance mediated through years of education. (Weuve et al. 2018)

While educational attainment explains 35% of the cognitive difference between African Americans and Euro Americans, we should keep in mind that educational attainment itself is influenced by genetic factors. These genetic factors vary among African Americans, just as they vary between African Americans and other human populations.

APOE e4 allele

This allele was more common in the African American participants. It contributed to their higher risk of Alzheimer's but not to their lower cognitive score.

Black participants were more likely than white participants to carry an APOE e4 allele (37% vs 26%; Table 1). In analyses restricted to participants with APOE data, racial differences in baseline scores or cognitive decline did not vary by e4 carriership (all Pinteraction > 0.16). Furthermore, adjustment for e4 carriership did not materially change estimated racial differences in baseline performance or cognitive decline (eTable 3).

By contrast, the association between race and AD risk varied markedly by APOE ecarriership (Pinteraction = 0.05; Table 4). Among non-carriers, blacks' AD risk was 2.32 times that of whites' (95% CI, 1.50-3.58), but this association was comparably negligible among e4 carriers (RR, 1.09; 95% CI, 0.60-1.97). (Weuve et al. 2018)

Discussion

This study offers two different explanations: why African Americans have a higher incidence of Alzheimer's and why they have a higher incidence of dementia in general. Two different explanations are needed because Alzheimer's seems to be qualitatively different from other forms of dementia.

First, African Americans have a higher incidence of Alzheimer’s because they have a higher incidence of the APOE e4 allele, a risk factor for Alzheimer's. They may also have other alleles, still unidentified, that similarly favor development of Alzheimer's. This would explain why, if we look at participants without APOE e4, Alzheimer's was still twice as common among African Americans as it was among Euro Americans. On the other hand, the two groups had virtually the same incidence of Alzheimer's if we look at participants with APOE e4.

Second, African Americans have a higher incidence of dementia in general because they have a lower cognitive reserve. When cognitive performance begins to deteriorate in old age, the ensuing decline starts from a lower level and reaches the threshold of dementia sooner. The rate of decline is nonetheless the same in both African Americans and Euro Americans. While this explanation could apply to most forms of dementia, it is hard to see how it applies to Alzheimer's. Euro Americans have a higher cognitive reserve, and yet the APOE e4 allele is just as likely to produce Alzheimer's in them as in African Americans.

Why does the APOE e4 allele exist? It must have some adaptive value, given its incidence of 37% in African Americans and 26% in Euro Americans. African Americans also seem to have other alleles, not yet identified, that likewise increase the risk of Alzheimer’s. Those alleles, too, must have some adaptive value.

This value seems to exist in sub-Saharan Africa but not in North America. When Hendrie et al. (2001) examined Yoruba living in Nigeria, they found no relationship between APOE e4 and Alzheimer’s or dementia in general:

In the Yoruba, we have found no significant association between the possession of the e4 allele and dementia or AD in either the heterozygous or homozygous states. As the frequencies of the 3 major APOE alleles are almost identical in the 2 populations, this variation in the strength of the association between e4 and AD may account for some of the differences in incidence rates between the populations, although it is not likely to explain all of it. It also raises the possibility that some other genetic or environmental factor affects the association of the e4 allele to AD and reduces incidence rates for dementia and AD in Yoruba. (Hendrie et al. 2001)

There has been speculation, notably by Greg Cochran, that Alzheimer’s is caused by apoptosis. Because of the blood-brain barrier, antibodies cannot enter the brain to fight infection, so neural tissue is more dependent on other means of defense, like apoptosis. Such a means of defense may be more important in sub-Saharan Africa because the environment carries a higher pathogen load.

If we pursue this hypothesis, APOE e4 and other alleles may enable neurons to self-destruct as a means to contain the spread of pathogens in the brain. In an environment with a lower pathogen load, like North America, this means of defense would become too inactive. The result would be autoimmune disorders where apoptosis is triggered in neural tissue for no good reason.

References

Chin, A.L., S. Negash, and R. Hamilton. (2011). Diversity and disparity in dementia: the impact of ethnoracial differences in Alzheimer disease. Alzheimer disease and associated disorders. 25(3):187-195.

https://doi.org/10.1097/WAD.0b013e318211c6c9

Cochran, G. (2018). Alzheimers or did I already say that? West Hunter, July 14

https://westhunt.wordpress.com/2018/07/14/alzheimers-or-did-i-already-say-that/

Demirovic, J., R. Prineas, D. Loewenstein, et al. (2003). Prevalence of dementia in three ethnic groups: the South Florida program on aging and health. Ann Epidemiol. 13:472-478.

https://doi.org/10.1016/S1047-2797(02)00437-4 

Hendrie, H.C., A. Ogunniyi, K.S. Hall, et al. (2001). Incidence of dementia and Alzheimer disease in 2 communities: Yoruba residing in Ibadan, Nigeria, and African Americans residing in Indianapolis, Indiana. JAMA. 285:739-47.

https://doi.org/10.1001/jama.285.6.739

Tang, M.X., P. Cross, H. Andrews, et al. (2001). Incidence of AD in African-Americans, Caribbean Hispanics, and Caucasians in northern Manhattan. Neurology 56:49-56.

https://doi.org/10.1212/WNL.56.1.49

Weuve, J., L.L. Barnes, C.F. Mendes de Leon, K. Rajan, T. Beck, N.T. Aggarwal, L.E. Hebert, D.A. Bennett, R.S. Wilson, and D.A. Evans. (2018). Cognitive Aging in Black and White Americans: Cognition, Cognitive Decline, and Incidence of Alzheimer Disease Dementia. Epidemiology 29(1): 151-159. 

https://doi.org/10.1097/EDE.0000000000000747 

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.

References

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

http://krishikosh.egranth.ac.in/bitstream/1/23082/1/IVRI%20OB%201816.pdf#page=593

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.

http://www.e-ijd.org/article.asp?issn=0019-5154;year=2002;volume=47;issue=4;spage=224;epage=226;aulast=Javanbakht;type=0

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.

https://doi.org/10.1353/pbm.2000.0016

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

https://doi.org/10.1038/sj.jidsymp.5650049 

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

https://www.morressier.com/article/5ac39997d462b8028d89a224

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

http://evoandproud.blogspot.com/2013/01/first-sexual-transmissibility-and-then.html

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.

https://doi.org/10.1016/bs.adgen.2016.01.004

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.

https://pdfs.semanticscholar.org/eaa2/e73dccf5b7cc31d8b0aa346e2d7b2db9837f.pdf

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.

https://doi.org/10.1159/000387745

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.

https://doi.org/10.1007/s11046-012-9587-y

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

https://doi.org/10.1111/j.1439-0507.2005.01091.x

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.

https://doi.org/10.1111/1523-1747.ep12261252

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

https://doi.org/10.1016/j.mehy.2003.12.050 

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.

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5043940/

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.

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3895566 

Origins of male homosexuality - Conclusion

What causes exclusive male homosexuality? This is the question I’ve addressed in the last few posts. The answer is still elusive although there seems to be consensus on some points.

One such point is the relative importance of inborn causation versus environmental causation. In men, an exclusively homosexual orientation has a heritability of 30-45%. A genetic cause must therefore be interacting with an unknown but more important environmental cause (Bailey et al., 2000). The genes in question are likewise unknown but may be located near the ones for RH factor (Ellis et al., 2008).

This raises another question. Why would natural selection create a genetic predisposition, however minor, to become exclusively gay? The answer is probably the one put forward by Ed Miller (2000). Human evolution has seen a relatively recent increase in provisioning by men of their mates and offspring, together with a corresponding decrease in polygyny. Even among present-day humans, this evolutionary trend has gone further in some populations than in others. How, then, did natural selection change male behavior over so little time? Miller’s answer: by partially feminizing the male mind (i.e., by impeding cerebral masculinization during prenatal and neonatal development). This is the fastest way with the least genetic change, the only downside being an increased risk that some boys will grow up with the wrong sexual orientation.

For several reasons, I disagree with Miller on one point: I believe that the downside of this rapid natural selection has not been a certain proportion of exclusively homosexual men but rather a larger proportion of weakly heterosexual men. First, as noted earlier, the genetic predisposition is not acting alone. It seems to be interacting with a more important cause of environmental origin. Second, I have trouble believing that a balanced polymorphism could maintain 3-5% of all men in a state of sexual indifference to women. (I incidentally feel the same way about the ‘gay uncle’ theory, where the reproductive cost of indifference to women is balanced by care given to related children—the cost seems too high to offset the presumed benefit). Third, I have trouble believing that 3-5% of all men were sexually indifferent to women before the late 19th century. Male homosexuality is attested in earlier time periods but usually in a facultative form, i.e., older heterosexual men having sex with boys or with males of servile status.

In my opinion, the likeliest scenario is one where a genetic predisposition weakens male heterosexuality but is not enough, in itself, to cause exclusive male homosexuality. Something in the environment has to push some of these heteros over the borderline. If so, there must be a large population of weakly heterosexual men, certainly much larger than the 3-5% who end up being exclusively homosexual.

Alongside this scenario would be a residual of various other causes—random genetic mutations, psychological or environmental stresses during pregnancy, chimerism, etc.—that each occur at such a low rate that natural selection cannot effectively counter any one of them. These residual causes might account for a baseline of exclusive male homosexuality that has always been with us, perhaps less than 1% of all men.

The current level of 3-5%, however, is much harder to ascribe to longstanding causes. I suspect it’s recent, essentially since the late 19th century, and due either to a pathogen that is co-evolving with its host population or to a recent environmental factor that humans have not yet overcome through natural selection.

If a pathogen is responsible, it may have become more prevalent because of the great increase in urbanization at that time or perhaps because some other factor had increased transmissibility. The main problem so far with the ‘gay germ’ theory is simply lack of evidence. Where is the smoking gun?

If a new environmental factor is responsible, it may be some kind of estrogen or estrogen-like compound in the neonatal environment. The late 19th century, however, is too early for most candidates. In fact, there seem to be only two credible ones. One is borax, which was used as a food preservative until the 1950s. The other is estrogen-rich drinking and bathing water from sources contaminated by untreated wastewater. Such effluent greatly increased in volume with the introduction of modern sewer systems in the late 19th century and decreased only with conversion to secondary and tertiary wastewater treatment during the 1970s.

How should we test these different theories? First, we should do what researchers normally do: conduct controlled studies and debate the findings in academic journals. Unfortunately, very little of either is going on. J. Michael Bailey, Lee Ellis, and the people around them, seem to account for much of the current research (and even Bailey runs into a great deal of flak). Most real debate actually seems to be happening in the blogosphere. This may or not be a bad thing, but it does say a lot about the climate surrounding this subject.


References

Bailey, J.M., M.P. Dunne, & N.G. Martin. (2000). Genetic and environmental influences on sexual orientation and its correlates in an Australian twin sample. Journal of Personality and Social Psychology, 78, 524-536.

Ellis, L, Ficek, C, Burke, D, & Das, S. (2008). Eye color, hair color, blood type, and the rhesus factor: exploring possible genetic links to sexual orientation. Archives of Sexual Behavior, 37(1), 145-9.

Miller, E.M. (2000). Homosexuality, birth order and evolution: Toward an equilibrium reproductive economics of homosexuality. Archives of Sexual Behavior, 29, 1-34.

Has male homosexuality changed over time?

One point is often raised about male homosexuality: it has always been with us. True, but has it ever changed in its nature or prevalence?

Well, more gays have been ‘coming out of the closet.’ People are practicing openly what used to be done in secret. But have there also been more fundamental changes?

Such a change has been postulated by Michel Foucault and others who argue that European societies originally had plenty of male homosexuality but few male homosexuals (Foucault, 1976; Halsall, 1988; Trumbach, 1977). In the Middle Ages, this behavior was seen as a ‘vice’ of older heterosexual men, typically with young boys or men of a servile status. In contrast, far fewer men were exclusively homosexual in the sense of being uninterested in women and resembling women in their sexual orientation (i.e., having a woman’s search image and desired self-image). This relative rarity is implied by the astonishment that European explorers felt on encountering Amerindian berdaches during the 18th and early 19th centuries (Désy, 1978).

Towards the end of the 19th century and into the early 20th century, this facultative male homosexuality seems to have been overtaken by the exclusive kind throughout northern Europe and North America. Today, at least in these regions, most male homosexuals fall into the second category, as Greg Cochran notes when comparing male and female homosexuality:

Female homosexuality is less common and women who self-label as homosexuals are a lot more likely to have children than gay men. So the overall impact on fitness is less. The distributions are different too: you find a lot more men who are Kinsey 6s, who aren't interested in women at all, than bisexual men: the distribution is J-shaped. It's the other way around in women, more bisexuals than Simon-pure lesbians. (Cochran, 2005)

Thus, around the turn of the 20th century, a shift occurred in the search image of some men, making them homosexual and exclusively so. Interestingly, a similar shift took place among heterosexual men in general, though to a lesser degree. The feminine ideal became that of a woman with long legs, a flat chest, narrow hips, large shoulders, and tanned skin, like a young boy on the brink of puberty (Bard, 1998; Marchand, 1997, 1988). This sort of woman appears in a 1925 novel, The Great Gatsby, where Miss Jordan Baker is described as "a slender, small-breasted girl with an erect carriage which she accentuated by throwing her body backward at the shoulders like a young cadet" (Fitzgerald, 1992, p. 15). Such androgyny is sometimes put down to the social impacts of World War I, either the wartime entry of women into previously male jobs or the postwar shortage of men. Yet the ‘boyish look’ was being mentioned as early as 1914, in the United States, three years before that country entered the war:

The new ideal in feminine figure, dress, and hair styles was all semi-masculine. The “1914 Girl” with her “slim hips and boy-carriage” was a “slim, boylike creature”. The “new figure is Amazonian, rather than Miloan. It is boyish rather than womanly. It is strong rather than soft.” Her dress styles, meanwhile, de-emphasized both hips and bust while they permitted the large waist. (McGovern, 1968)

It is as if something had been altering the male search image, thereby causing a preference for more boyish-looking women and, in a minority of cases, for men. But what could this ‘something’ have been?

From the perspective of Cochran’s germ theory, it may have been a pathogen that became more transmissible with the growth of towns and cities in the late 19th century. Its male hosts may have varied in their degree of susceptibility, being pushed over the threshold of male homosexuality in some cases. In most cases, the psychological change would have been less drastic.

An alternate candidate may be some kind of chemical agent, specifically an estrogen or estrogenic compound that would hinder the masculinization of male brains. There has been much talk about a long-term decline in sperm counts, allegedly because of synthetic compounds that mimic natural estrogens (e.g., contraceptive pills, DDT, PCBs). Most of these compounds, however, date back only to the 1940s. Is there reason to believe that an estrogenic agent began to enter the human environment in the late 19th century—and in large quantities?

Yes.

(to be cont’d in my next post)


References

Bard, C. (1998). Les garçonnes. Modes et fantasmes des Années folles. Paris: Flammarion.

Cochran, G.M. (2005). Cause of Homosexuality: Gene or Virus? Cochran Interview. Thrasymachus Online.

Désy, P.P. (1978). L'homme-femme. (Les berdaches en Amérique du Nord), Libre — politique, anthropologie, philosophie, 78(3), 57-102.

Fitzgerald, F. S. (1992). The Great Gatsby, New York: Collier Books.

Foucault, M. (1976) Histoire de la sexualité. Tome 1. La volonté de savoir. Paris: Gallimard.

Halsall, P. (1988). The Experience of Homosexuality in the Middle Ages. http://www.fordham.edu/halsall/pwh/gaymidages.html

Marchand, S. (1997). Rouge à lèvres et pantalon. Des pratiques esthétiques féminines controversées au Québec 1920-1939, Montréal: Éditions Hurtubise HMH.

Marchand, S. (1988). La « Garçonne », un nouveau modèle féminin (1920-1929), Cap-aux-Diamants, 4, 19-20.

McGovern, J.R. (1968). The American woman's pre-World War I freedom in manners and morals, Journal of American History, 55, 315-333.

Trumbach, R. (1977). London's sodomites: homosexual behaviour and Western culture in the eighteenth century, Journal of Social History, 11, 1-33 .

Origins of male homosexuality - The germ theory

How does male homosexuality originate? More to the point, how does it perpetuate itself? According to Ed Miller, it results from a balanced polymorphism—a delicate balancing act where too much feminization of the male brain causes attraction to one’s own sex and too little causes indifference to one’s own children. This week, I will present an alternate explanation: Greg Cochran’s germ theory.

Greg has never published his theory in a peer-reviewed journal, although it is briefly summarized in Cochran et al. (2000). In itself, this is no shortcoming. Most journals seem uninterested nowadays in real debate. But sometimes I wish he would at least pretend he was writing for a journal. He tends to be polemical, as if only political correctness—or sheer stupidity—could motivate his detractors.

His starting point is the same as Miller’s. Male homosexuality makes no sense as a reproductive strategy. It should die out for the same reason that the Shakers did (the Shakers were a Protestant sect dedicated to lifelong celibacy). This point might seem obvious. Or maybe not. The following is an exchange between a germ theory critic and Greg Cochran:

Critic: Is it not likely that human sexuality is in fact a bell curve, with "strict homosexual" on one end and "strict heterosexual" on the other end, and the majority of the people falling somewhere in between? (With the caveat that sexual preference and sexual practice are not necessarily the same thing).

Greg: No, it is not likely. Sheesh. That would make exactly as much sense as a bell curve of food preferences ranging from steak at the left to granite at the right, in which people in the middle liked steak and rocks equally well. Is an even split between a behavior that works and one that never does what you expect from biology? Do you expect half the geese to fly north for the winter? (source)

Since natural selection would tend to eliminate male homosexuality, it should be uncommon—like most genetic conditions that impair one’s ability to survive and reproduce.

First we have to say what ‘common’ means, in this context. Common means common compared to the noise in the system. So 1% is very common: no disease caused by random mutations is anywhere near that common. 1 in 10,000 is surprisingly common, but there are one or two mutation-caused diseases that are in that ballpark, like Duchenne’s muscular dystrophy. Turns out that the gene involved in muscular dystrophy is maybe 20 times longer than the typical gene — there are more opportunities for typos. So 1 in 7000 boys have Duchenne’s muscular dystrophy — that’s as common as a ‘system noise’ disease gets. (Cochran 2004?)

Since male homosexuality is not rare, it cannot have a genetic cause, at least not principally. There may be a genetic predisposition (with around 30-45% heritability, according to twin studies), but this predisposition is interacting with something in the environment. And this something cannot be a recent environmental change, since male homosexuality has been around for a long time.

The only remaining cause would be some kind of infectious agent that selectively alters certain parts of the brain while leaving the rest intact. There are precedents for this sort of thing.

Do we know of diseases in which there are very specific targets—in which certain cell types are damaged or destroyed while neighboring cells are left intact? Sure. In some cases, a pathogen targets a particular cell type and has little effect on anything else. Human parvovirus (also known as fifth disease) hits erythroid precursor cells (the cells that manufacture red cells) and temporarily inhibits red cell production. In type-I diabetes, it seems likely that Coxsackie virus infections (in people with a genetic predisposition, in which HLA type plays a major role) trigger an autoimmune disease that gradually (over a year or so) destroys the islet cells which produce insulin. Other cells are not much affected. (Cochran 2004?)

Such pathogens may be more common than we think. The ones that get our attention—that make us go and see a doctor—are the ones that cause discomfort. But those ones may be a small minority of all pathogens, with most of the others flying under the radar. After all, it is in the pathogen’s own interest to be discrete and not cause too much havoc. It needs a healthy home to live in, until it can spread to another host.

Greg also argues that male homosexuality should be less common in smaller communities than in larger ones—where pathogenic transmission is likelier.

We can deduce a few things about the hypothetical agent causing homosexuality. First, it has a small, but not incredibly small, critical community size. That is the size of the clump of people required to keep the agent going. Some agents, ones in which infection results in permanent immunity, need a _large_ number of people, big enough that there are new infected people showing up by the time it circles the community. Measles for example requires almost half a million people in close proximity. An agent that causes a persistent infection can have a very small community size: I'd guess that Epstein-Barr has a CCS under 50.

Since some communities seem to have no homosexuality at all (Bushmen, some hunter-gatherer groups in Indonesia and the Philippines, pre-contact Polynesians) we can be sure that this hypothetical agent has a critical community size larger than that of Epstein-Barr. More like chickenpox, which has a CCS of about 300 people. Not that I'm saying it _is_ chickenpox, mind you. (Cochran 2005)

Finally, this pathogen may selectively alter sexual orientation for reasons that go beyond those of not harming the host too much. There are, in fact, a number of pathogens that alter the host’s behavior in order to enhance their chances of transmission. The protozoan Toxoplasma gondii causes infected rats to lose their fear of cats, thus enabling it to enter a cat body and complete its life cycle (Wikipedia – Toxoplasmosis). The parasitic worm Euhaplorchis californiensis forms cysts in the brains of infected killifish that cause the fish to swim near the surface of the water and make tight turns that show off their glinting sides, thus enabling the worm to enter a bird’s body (Zimmer, 2008).

As a child, I remember being told that a chicken is an egg’s way of making another egg. If Greg Cochran is right, a gay man is a vehicle that a pathogen has constructed for its own survival and reproduction. Everything else is human-centered delusion.

This is an interesting argument, but it has a few holes. First, some genetic conditions do reach incidences that are comparable to that of male homosexuality (about 3-5% of all men). Abnormal hemoglobin variants can reach high incidences in sub-Saharan Africans and other populations (8% in the case of Hb AS among African Americans). These variants are typically maintained through balancing selection where the heterozygote state provides some protection against malaria. Greg acknowledges that such selection exists but sees it as being confined to malaria protection. Yet balancing selection can exist for many other reasons. For example, one in 200 Hopi is albino, apparently because cultural selection offsets the environmental disadvantages of albinism (Hedrick, 2003).

Second, male homosexuality is frequently reported in small communities, including bands of Amerindian hunter-gatherers. Known as ‘berdaches’, these male homosexuals were described by early European explorers and appear to have existed in pre-contact times, as indicated by origin myths (Desy, 1978). One witness was John Tanner, a white captive who lived among the Ottawa of Ontario and then the Ojibwa of Manitoba until 1828:

Some time in the course of this winter, there came to our lodge one of the sons of the celebrated Ojibbeway chief, called Wesh-ko-bug, (the sweet)... This man was one of those who make themselves women, and are called women by the Indians. There are several of this sort among most, if not all the Indian tribes. They are commonly called A-go-kwa, a word which is expressive of their condition. This creature, called Ozaw-wen-dib, (the yellow head), was now near fifty years old, and had lived with many husbands. I do not know whether she had seen me, or only heard of me, but she soon let me know she had come a long distance to see me, and with the hope of living with me. She often offered herself to me, but not being discouraged with one refusal, she repeated her disgusting advances until I was almost driven from the lodge. (Desy, 1978)

Of course, neither point disproves the germ theory of male homosexuality. An infectious agent may indeed be the cause or one of several causes. If we consider the developmental pathway for heterosexual orientation, there is probably a ‘default’ sequence that leads to sexual interest in men and an ‘override’ sequence that leads to sexual interest in women. The second sequence may be disrupted for many reasons: a psychological trauma, a chemical insult, or an infectious agent in combination with a pre-existing genetic predisposition for incomplete masculinization. As one comment noted:

Some of the disruptive factors implicated by empirical evidence are excess prenatal testosterone exposure (a major factor), prenatal stress, and exotic factors such as disruptive chemical agents. Infections proposed by Cochran may also disrupt development, but I do not know of any evidence that supports this assertion as of yet. (Cochran 2005)

References


Cochran, G.M. (2005). Cause of Homosexuality: Gene or Virus? Cochran Interview. Thrasymachus Online.

Cochran, G.M. (2004?). An evolutionary look at human homosexuality. World of Greg Cochran.

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

Désy, P.P. (1978). L'homme-femme. (Les berdaches en Amérique du Nord), Libre — politique, anthropologie, philosophie, 78(3), 57-102.

Hedrick, P.W. (2003). Hopi Indians, “cultural” selection, and albinism. American Journal of Physical Anthropology, 121, 151-156.

Zimmer, C. (2008). The Parasite Files. Discover. Dec. 16.