Monday, December 23, 2019

Not what you think

Preparing for a test (Wikicommons - Excelz)

Why do West African immigrants outperform native-born whites in UK schools? This is the question posed by Chanda Chisala using data from the GCSE, the General Certificate of Secondary Education. 

To be sure, the GCSE is not the same as an IQ test. For most subjects it includes things like coursework and attendance. The test-taker is also motivated by self-interest: a high GCSE score can be a ticket to a good university and a good job. Nonetheless, Thompson (2013) has argued that the GCSE has a correlation of 0.81 with IQ. So perhaps the two are roughly equivalent.

Let's look at the GCSE results from England for 2012. They are indeed astounding for immigrant children from English-speaking Africa. Just look at the percentage difference from the mean by country of origin:

Nigerians -     +21.8
Ghanaians -     +5.5
Sierra Leone - +1.4

Source: Chisala (2019)

This academic excellence seems to be unusually concentrated among Nigerian immigrants. Are we looking at our friends from the Niger delta? Often known as the "Jews of West Africa," the Igbo have a long record of academic and economic success. This has been attributed to their openness to Western learning and the commercial opportunities it creates, although the Igbo were, in fact, a trading nation long before the colonial era (Frost 2015). They became receptive to Western learning because they had long been receptive to learning in general, much like the Japanese during the Meiji era.

Chisala (2015) provides an ethnic breakdown of GCSE results for the years 2009 to 2011:

2009: Igbo - 100%, Yoruba - 39%
2010: Igbo - 80%, Yoruba - 68%
2011: Igbo - 76%, Yoruba - 75%

The Igbo started off as top achievers, but their lead evaporated over the next two years as the Yoruba made remarkable gains. There were 90 Yoruba kids, so sampling error could hardly explain their increase from 39% to 75%. Because the Igbo kids numbered only 16, the decrease from 100% to 76% might not be significant.

Perhaps the Yoruba kids got better coaching and tutoring. Whatever the explanation, GCSE cannot be used as a proxy for IQ, at least not for Nigerians. Yes, IQ can change over the course of a lifespan, but not that fast and not that much—unless you suffer a serious accident.

Exam malpractice

There are less innocent explanations for the rapid rise in Yoruba scores. A study of students in Nigeria found that test-retest reliability ranged from 77 to 85% (Petters and Okon 2014). The authors blame the low test reliability on cheating, calling it "a plague":

Examination malpractice in Nigeria has attained a frightening proportion and it is becoming more sophisticated as years pass by. Efforts by government and stakeholders to curtail this trend have not yielded much success. If this trend is not given an urgent attention, it may utterly destroy the quality of education in Nigeria.

Bisong et al. (2009) come to similar conclusions:

The implication of this study is that the cheating tendency is becoming endemic in Nigerian society. A situation where one in every four students tends to cheat in every examination calls for a significant moral questioning of our society. Even with a high level of supervision, as the results show, students are still prone to indulge in cheating behaviour.

In their review of the literature, Bisong et al. (2009) note that "in 1980, out of the 190,000 candidates who sat the West African Examination Certificate in May and June, 46,000 candidates from Nigeria had their results nullified." Cheating is partly due to Nigerian parents, who understand the value of academic success and push their children to get good grades "by all means":

Parents expect nothing less than passing in examination from their children. There must not be failure. That is to say that he who fails is not entertained in any way. Where there is weakness or a psychological measure that one is not prepared to pass the examination, then fear begins to disturb the minds of students as to how to make it. This leads to serious reading throughout the night, pressing lectures for areas of concentration and arranging to enter the examination hall with every possible means to cheat during the examination. (Halima 2003, p. 17)

Halima (2003, p. 19) notes the harshness of penalties for cheating: "in 1983 the punishment for cheating was increased to a jail term of 21 years without the option for fine. In spite of this cheating in examination increased."

Nigeria's cognitive elite?

It has been argued, notably by Greg Cochran, that Nigerian immigrants are skimmed from the top of their country's IQ distribution (Cochran 2019). They are the best that Nigeria has to offer—la crème de la crème. To make that argument work, however, Nigerian immigrants to the UK would have to be much smarter than the average Nigerian, with an IQ more than one standard deviation higher and probably two.

There is only a rough consensus on the mean IQ of sub-Saharan Africa. In their review of the literature, Wicherts et al. (2010) argue for a mean of 82, whereas Lynn (2010) puts it at 66. Rindermann (2013) favors a "best guess" of 75. Even if we take the high estimate of 82, we must still assume extreme selection to get a mean IQ above 100. Is that a reasonable assumption?  Elite individuals exist among immigrants from Nigeria, but they are not the majority: 

Socially, the Nigerian diaspora is by no means homogenous. There are those who struggle for basic means of survival such as car park attendants, cleaners and other menial workers working long hours to make ends meet. But some professionals have distinguished themselves and moved on to become members of the Black middle class. (Akinrinade and Ogen 2011)

Furthermore, some doubt may be cast on the credentials of middle-class Nigerians: "they have acquired a notorious reputation for arrogance and fraud" (Akinrinade and Ogen 2011). Finally, the cognitive elite argument fails to explain why immigrants from Nigeria do so much better than those from Ghana and Sierra Leone.

Math scores

On many GCSE components, there is much room for cheating, particularly on coursework. But what about the mathematics component? GCSE math has not had coursework since 2009. It is simply a timed test. How can one cheat on a timed test?

By impersonation. A "ghost" who knows the subject takes the exam by impersonating the student, and the actual student never takes the exam (Azuka 2014). This method requires a photo ID that combines the ghost's photo with the test-taker's name. In most cases, the fake ID is sufficient to dispel any suspicions.


For whatever reason, the GCSE is too volatile to be used as a proxy for IQ, particularly in the case of Nigerian students. The volatility seems to be due to cheating, as well as to the grey area of coaching and tutoring services. Cheating is rife among Nigerians in Nigeria, and it would be naïve to suppose that such behavior disappears once they relocate to another country, especially if their new country imposes none of the harsh penalties that are regularly imposed in Nigeria.

Nigerian academic achievement may be genuine in some cases. This is particularly so with respect to the Igbo, who have a longstanding record of achievement within and outside school. Unfortunately, genuine ability can be cofounded with fake ability. Smart people are better at gaming the system and making themselves look smarter than they really are.

Indeed, I can't help wondering when I look at the GCSE results for Igbo students in 2009. Every single Igbo got a perfect score—that's unusual even for a smart population and even with a sample size that small. Chanda suggests that year-to-year fluctuations might have made the sample even smaller in that year. Well, perhaps.

It would be easy to say that we need more data. Additional GCSE results, however, will be just as distorted by academic fraud. We need data from real IQ tests that provide no incentive for cheating.


Akinrinade, S., and O. Ogen. (2011). Historicising the Nigerian Diaspora: Nigerian Migrants and Homeland Relations. Turkish Journal of Politics 2(2): 71-85.

Azuka, E.B. (2014). Academic Fraud among Students in Higher Education in Nigeria: Reasons, Methods Adopted and Strategies to curb it. Journal of Educational and Social Research 4(3): 289-296. 

Bisong, N.N., F. Akpama, and P.B. Edet. (2009). Cheating Tendency in Examinations among Secondary School Students in Nigeria:  a case study of schools in the Odukpani Local Government Area, Cross River State. Policy Futures in Education 7(4): 410-415  
Chisala, C. (2019). Why Do Blacks Outperform Whites in UK Schools? The Unz Review, November 29 

Chisala, C. (2015). UK: Igbo Nigeria Academic performance destroys the myth of Black Low IQ. Afripol November 28

Cochran, G. (2019). Selective immigration. West Hunter, March 13

Frost, P. (2015). The Jews of West Africa? The Unz Review, July 4 

Halima, D. (2003). A study of some socio-psychological factors of cheating in examination among students of Kaduna Polytechnic. Post Graduate School Ahmadu Bello University Zaria. 

Lynn, R. (2010). The average IQ of sub-Saharan Africans assessed by the Progressive Matrices: A reply to Wicherts, Dolan, Carlson & van der Maas. Learning and Individual Differences 20(3): 152-154.

Petters, J.S., and M.O. Okon. (2014). Students' Perception of Causes and Effects of Examination Malpractice in the Nigerian Educational System: The Way Forward for Quality Education. Procedia - Social and Behavioral Sciences 114: 125-129

Rindermann, H. (2013). African cognitive ability: Research, results, divergences and recommendations. Personality and Individual Differences 55: 229-233.

Thompson, J. (2013). IQ and GCSE Results in England R=0.81. The Unz Review, November 5 

Wicherts, J.M., C.V. Dolan, and H.L.J. van der Maas. (2010). A systematic literature review of the average IQ of sub-Saharan Africans. Intelligence 38: 1-20.

Monday, December 16, 2019

Weird people

Weird people. Northwest Europeans are more individualistic, less loyal to kin, and more trusting of strangers. (Wikicommons)

Northwest Europeans are WEIRD ... as in Western, Educated, Industrialized, Rich, and Democratic. These traits are in turn associated with certain behavioral and psychological characteristics: "People from these societies tend to be more individualistic, independent, and impersonally prosocial (e.g., trusting of strangers) while revealing less conformity and in-group loyalty" (Schulz et al. 2019).

In a recent study, Schulz et al. (2019) argue that WEIRDness is a heritage of Western Christianity: the branch of the Christian faith that gradually evolved into Roman Catholicism and, later, Protestantism: "we propose that the Western Church's transformation of European kinship, by promoting small, nuclear households, weak family ties, and residential mobility, fostered greater individualism, less conformity, and more impersonal prosociality."

Social relations are indeed different north and west of a line running approximately from Trieste to St. Petersburg, Everyone is single for at least part of adulthood, and many stay single their entire lives. In addition, households often have non-kin members, and children usually leave the nuclear family to form new households (Hajnal, 1965; ICA, 2013; Laslett, 1977). This is the Western European Marriage Pattern (WEMP), and there is an extensive literature on it going back to work by John Hajnal.

Was the Western Church a cause or an effect?

Schulz et al. (2019) stress the role of the Western Church in creating the WEMP, particularly by banning consanguineous marriages. The ban came about because "the Church had become obsessed with incest."

That isn't the whole story. Even before Christianity, Roman Civil Law forbade marriages within four degrees of consanguinity. The number was increased from four to seven in 732 by Pope Gregory III, but in this he was following similar bans among the newly converted Germanic peoples. The mid-seventh century Visigothic Code proclaimed that "it shall not be lawful to defile the blood of such as are related even to the sixth degree, either by marriage or otherwise" (McCann 2010, p. 57). In the early ninth century, the Church changed its way of calculating degrees of kinship by adopting the Germanic system. Under the old Roman system, first cousins were considered fourth degree; the Germanic system made them second degree. This change had the effect of doubling the number of ineligible marriage partners (McCann 2010, pp. 57-58).

Schulz et al. (2019, p. 2) assume that the WEMP postdates these prohibitions against cousin marriage: "by 1500 CE (and centuries earlier in some regions), much of Europe was characterized by a virtually unique configuration of weak (nonintensive) kinship marked by monogamous nuclear households, bilateral descent, late marriage, and neolocal residence." 

Actually, no one really knows when this pattern arose. As we go farther back in time, we have less demographic data to work with, but the same pattern still appears in the little we do have. In thirteenth-century Lincolnshire before the Black Death, households were already nuclear and a late age of first marriage was the norm, being 24 for the woman and 32 for the man (Hallam 1985, p. 66). In ninth-century France, two surveys show that households were small and nuclear among married people and that 12 to 16% of the adult population were unmarried (Hallam 1985, p. 56). A third survey shows that both men and women were marrying in their mid to late twenties; (Seccombe 1992, p. 94). Admittedly, the earliest data are limited to France, hence the authors' caveat "centuries earlier in some regions," but France was hardly an outlier in the demographic evolution of northwest Europe.

Earlier demographic data are too fragmentary to produce firm conclusions. Furthermore, the data usually concern elite males who typically took much younger brides. Nonetheless, in the general population we see some evidence of first marriages at late ages. The first-century Roman historian Tacitus wrote about the Germanic tribes: "Late comes love to the young men, and their first manhood is not enfeebled; nor for the girls is there any hot-house forcing; they pass their youth in the same way as the boys" (Tacitus Germania 20). Julius Caesar made the same observation: 

Those who have remained chaste for the longest time, receive the greatest commendation among their people: they think that by this the growth is promoted, by this the physical powers are increased and the sinews are strengthened. And to have had knowledge of a woman before the twentieth year they reckon among the most disgraceful acts; of which matter there is no concealment, because they bathe promiscuously in the rivers and [only] use skins or small cloaks of deers' hides, a large portion of the body being in consequence naked. (Caesar De Bello Gallico 6: 21)

The direction of causality may thus run in the other direction. The WEMP does not exist because the Western Church diverged from the Eastern Church on the issue of consanguineous marriage. Rather, this divergence arose because the Western Church was assimilating the behavioral norms of its newly converted peoples, including the WEMP. By the eighth century, those peoples were dominant within the Western Church and able to push Christian practice in certain directions, particularly postponement of marriage and marriage outside the kin group (Frost 2017). The tail began to wag the dog.

Sources of inspiration?

Schulz et al. (2019) seem to have been inspired by earlier work by Steven Heine and Joseph Henrich (who is one of the co-authors). Curiously, no references are made to the literature on the WEMP, not even to the work by John Hajnal. Less curiously, they pass over the more speculative work by myself, hbd chick, and Kevin MacDonald (Frost 2011; Frost 2017; hbd chick 2011; hbd chick 2012; hbd chick 2014; MacDonald 1990; MacDonald 2011). To the best of my knowledge, Kevin was the first to notice an apparent relationship between northwest Europeans, Western Christianity, and certain psychological and behavioral characteristics. This is evident in his 1990 article and even more so in his 2011 one:

The nuclear family, freed from extended kinship obligations, is the basis of Western social organization. It is unique relative to other culture areas. This pattern is particularly noticeable in the Northwest of Europe rather than the Pontic steppe region. As one goes from the Northwest of Europe to the Southeast, there is an increase in joint family structure, with brothers living together with parents, grandparents and children. Family historian John Hajnal discovered the "Hajnal line" that separates Western Europe from Eastern Europe, the former characterized by nuclear family structure, relatively late marriage and large numbers of unmarried in economically difficult times, the latter by joint family structure and relatively early and universal marriage.

I suspect Schulz et al. (2019) had read material by all three of us. I base my suspicion partly on their use of certain terms and expressions and partly on their references, particularly the curious reference to Claude Lévi-Strauss as an authority on kinship. An American anthropologist would normally cite Lewis Henry Morgan or Robin Fox. I like to cite Lévi-Strauss partly because I was trained at a French-language university and partly because he was, in a sense, my academic grandfather, being the dissertation supervisor of my dissertation supervisor.  He was also the first to come up with the concept of gene-culture coevolution, but that fact is poorly known even among francophone anthropologists.

Anyway, does it matter? The important thing is to put new ideas into circulation.


Frost, P. (2017). The Hajnal line and gene-culture coevolution in northwest Europe. Advances in Anthropology 7: 154-174. 

Frost, P. (2011). The Western European Marriage Pattern. Evo and Proud. November 12 

Hajnal, J. (1965). European marriage patterns in perspective: essays in historical demography. In D.V. Glass and D.E. Eversley (eds). Population in History. Chicago: Aldine Publishing, pp. 101-143.

Hallam, H.E. (1985). Age at first marriage and age at death in the Lincolnshire Fenland, 1252-1478. Population Studies 39(1): 55-69.

hbd chick (2014). Big summary post on the Hajnal Line. October 3

hbd chick (2012). Behind the Hajnal Line. January 16  

hbd chick (2011). The Hajnal Line. June 30  

ICA (2013). Research Themes - Marriage Patterns, Institutions for Collective Action

Laslett, P. (1977). Characteristics of the Western family considered over time. Journal of Family History 2(2): 89-115.

MacDonald, K. (2011). Going against the Tide: Ricardo Duchesne's Intellectual Defence of the West. The Occidental Quarterly 11(3): 1-22. 

MacDonald, K. (1990). Mechanisms of sexual egalitarianism in Western Europe. Ethology and Sociobiology 11: 195-238.

McCann, C.A. (2010). Transgressing the Boundaries of Holiness: Sexual Deviance in the Early Medieval Penitential Handbooks of Ireland, England and France 500-1000. Theses. 76.  Seton Hall University 

Schulz, J.F., D. Bahrami-Rad, J.P. Beauchamp, and J. Henrich. (2019). The Church, intensive kinship, and global psychological variation. Science 366(707): 1-12.

Seccombe, W. (1992). A Millennium of Family Change. Feudalism to Capitalism in Northwestern Europe. London: Verso.

Sunday, November 3, 2019

Candida and autism

Shamanic ritual (Wikipedia - Idries Shah). There is a correlation between autism and antibodies for Candida albicans. Does a pathogenic strain of this yeast promote the development of autism? Cui bono?

In my previous posts I've argued that certain pathogens have acquired the capacity to manipulate human behavior. Humans are an interesting target for several reasons:

1. The human mind oversees an extensive range of complex behaviors

2. Humans are long-lived, thus providing a useful vehicle for spreading to other potential hosts.

3. Humans have particularly long generation times and are thus less able to develop resistance to short-generation pathogens, which can more easily “outmanoeuvre” the evolution of human resistance.

Among animal hosts in general, behavior can be manipulated by many pathogens, including fungi. Fungi seem to be better able than viruses and bacteria at producing and coordinating the array of chemicals needed for the targeted neural tissue. One of them may be Candida, a genus of yeasts that most often live in the gut but can be found elsewhere in the body. In particular, there seems to be a connection between their presence and the development of autism spectrum disorders (ASD):

We aimed to determine if children with ASD exhibit elevations in antibodies that target C. albicans, indicating current or previous overgrowth of this fungal species. [...] Plasma anti-C. albicans antibody positivity was found in 36.5% (19/52) of children with ASD. Anti-C. albicans antibodies in typically developing controls was (14.3%; 4/28). Overall, ASD children had a higher rate of high-positive values compared to typically developed children with an unadjusted odds ratio of 3.45 (95% confidence interval, 1.0409 to 11.4650; p = 0.041, two-tailed). (Hughes and Ashwood 2018)

The above study takes the line that Candida albicans is a "passive commensal" that "under certain conditions [...] is capable of transitioning to its pathogenic and invasive fungal form" (Hughes and Ashwood 2018). In reality, C. albicans encompasses a variety of strains, some of which live more as a commensal and others more as a pathogen: 

Here, intra-species analyses of C. albicans isolates revealed extensive variation between strains, both at the genotypic and phenotypic level. Substantial genomic differences were observed between the set of 21 clinical strains and included single nucleotide polymorphisms, inversions, copy number changes, LOH events, and whole or partial chromosomal aneuploidies.

[...] The phenotypic plasticity of this species has long been recognized, and our studies reveal the genetic differences underlying phenotypic differences are due to a variety of mechanisms, of which LOH and aneuploidy are major contributors. Furthermore, we uncover a genetic polymorphism responsible for altered phenotypic behavior, including a change in the balance between commensalism and pathogenesis. (Hirakawa et al. 2015)

Some strains of C. albicans have evolved the capacity to adhere to neural tissue:

An ex vivo adhesion assay was used to examine adhesion of Candida albicans yeast cells to brain tissue of the primate Macaca mulata. Tissues from frontal lobes and striatum (caudate, putamen, and portions of the globus pallidus) were used in the assay. Yeast cells adhered to gray matter at about six times the level of adhesion to white matter. The fungus was able to bind to different cell types within the cortex, basal ganglia, and white matter. Binding to neurons, small neurons or glia, endothelial cells, and neuropil was observed. (Denaro et al. 1995)

What's in it for the pathogen?

This is the weakest link in the argument for behavioral manipulation. How does autism benefit the pathogen? Does it help Candida spread to another host? If not, where is the benefit? People have speculated about the evolutionary advantage of autism, but only from the standpoint of the affected person. Perhaps a low dose makes one more inventive and creative (Pickard et al. 2011). Perhaps it gives rise to the "autonomous imagination" of shamans:

[…] “autonomous imagination” [is] a framework for cross-cultural interpretations of inner experience such as dreams, waking visions, trance, spirit possession and mediumship, and shamanistic and meditative states.

[…] Autonomous imagination is characterized by: a) being more freely and richly inventive than ordinary thought; b) emerging into conscious awareness in the form of vivid hallucinatory imagery which is experienced as an external reality; c) possessing a more extensive access to memory; d) exhibiting a special sensitivity to external cues and direction which enables communication to and from deeper levels of the mind, while bypassing conscious awareness, and; e) possessing a capacity to influence somatic and intrapsychic processes usually beyond conscious control (Stephen and Suryani 2000)

Shamans, through their prestige and reproductive success, may have favored a predisposition to autism in the gene pool. This hypothesis assumes that autism is mainly due to a genetic predisposition, i.e., that autism is highly heritable. In fact, heritability is "moderate": 37% for autism and 38% for autism spectrum disorder (Hallmayer et al. 2011). As with male homosexuality, it looks like something in the environment is interacting with a genetic predisposition.

If we take the pathogen's standpoint, we must ask how an autistic person might become an interesting means to spread from one host to another. One possibility is the shaman's role as a community healer. Certain healing practices involve intimate contact. In particular, a shaman's phlegm may be thought to contain the essence of his power. 

A shaman also has a magical phlegm called yachay, lodged in his stomach, which gives him the ability to blow away evil and to such out the sorcery objects (virote) that cause certain forms of illness. (Gow 1996, p. 93)

By targeting people who are likely to fill the position of community healer, a pathogen could greatly increase its opportunities for transmission. 

Parting thought

This example suggests that the evolution of behavioral manipulation can involve more than a pathogen and a host. It may also require a genetic predisposition and a cultural context that create opportunities for behavioral manipulation.


Denaro, F.J., J.L. Lopez-Ribot, and W.L. Chaffin. (1995). Adhesion of Candida albicans to brain tissue of Macaca mulata in an ex vivo assay. Infection and Immunity 63(9): 3438-3441.

Gow, P. (1996). River People: Shamanism and History in Western Amazonia. In Thomas, N., and C. Humphrey (eds). Shamanism, History, and the State (pp. 90-113). Ann Arbor: The University of Michigan Press.

Hallmayer, J., S. Cleveland, A. Torres, et al. (2011). Genetic Heritability and Shared Environmental Factors Among Twin Pairs With Autism. Archives of General Psychiatry 68(11): 1095-1102. 

Hirakawa, M.P., D.A. Martinez, S. Sakthikurmar, M.Z. Anderson, A. Berlin, S. Gujja; et al. (2015). Genetic and phenotypic intra-species variation in Candida albicans. Genome Research 25: 413-425.

Hughes, H.K., and P. Ashwood. (2018). Anti-Candida albicans IgG antibodies in children with autism spectrum disorders. Psychiatry 26 November

Pickard, C., B. Pickard, and C. Bonsall. (2011). Autistic spectrum disorder in prehistory. Cambridge Archaeological Journal 21(3): 357-364.

Stephen, M. and L.K. Suryani. (2000). Shamanism, psychosis and autonomous imagination. Culture, Medicine and Psychiatry 24: 5-40.

Sunday, October 27, 2019

Behavioral manipulation: population differences in virulence

Helicobacter pylori (Wikicommons – NIH). Some human populations have become resistant to this bacterium; others have not. Could the same be true for pathogens that manipulate human behavior?

Humans are behavioral creatures par excellence. Our brains oversee a large repertoire of behaviors, each of which is vulnerable to manipulation. We can be manipulated by psychological means, like the parasite who lives off the altruism of others.  There's also ideological manipulation. 

And then there's hardwired manipulation—an organism enters your mind and rewires some of its circuitry. That kind of manipulation is poorly known. We know a lot about short-term infections that make you sick. We know much less about long-term infections where the pathogen hangs around in your body without triggering an immune response. There’s no fever, no rash, no abscess. Yet it may be doing something to the most important organ of your body, perhaps to increase its chances of spreading to another host. Not surprisingly, the adverse effects become worse when you're no longer of much help. It no longer has anything to lose from trashing its host.

So if a pathogen is screwing with your mind, the symptoms will be especially severe in two cases: 

- You’re approaching the end of your life. The pathogen has less incentive to keep you healthy. You’re also less active socially and sexually, and thus less useful as a vehicle for transmission to other hosts.

- The pathogen is spreading out of its original host population and into new hosts that have not had time to develop resistance to its worse effects

This post is about the second case. You pay a cost when a pathogen monkeys around with your mental circuitry. Over time, there will be selection for humans who better resist such manipulation. Eventually, an equilibrium is reached: the pathogen still screws around with your mind, but the negative consequences are kept to a minimum. In most cases. And until it spreads to people who have no resistance.

The latter situation has been covered by a recent review article:

[...] the effects of susceptibility and virulence alleles in the respective gene pools of humans and pathogens are often contingent upon each other. The evolution of virulence is a dynamic process, easily perturbed by extrinsic variables over space and time, and therefore unlikely to follow the same trajectory in every population. [...] Whether the result is a steady-state equilibrium due to a perpetual "arms race" or a commensal detente, the same genes and pathways are unlikely to be involved in every population. As a consequence, when humans and pathogens migrate to new environments or admix, the ensuing disruption of co-evolutionary equilibria and loss of complementarity between host and pathogen genotypes may yield unpredictable and potentially deleterious biomedical consequences. (Kodaman et al. 2014)

The authors cite the example of Helicobacter pylori, a bacterium that lives in the stomach lining. It is a risk factor for gastric cancer, but the level of risk varies according to the population it infects:

Studies of human or H. pylori genetics in isolation have generally failed to explain why populations with similar rates of H. pylori infection exhibit strikingly different susceptibilities to gastric cancer. For example, in many African and South Asian countries, the low incidences of gastric cancer in the presence of almost universal rates of H. pylori infection remain a source of much speculation, and have been referred to collectively as the "African enigma" and the "Asian enigma" [...] In Latin America, where H. pylori strains native to Amerindian populations have been largely displaced by European strains [...], the predominantly Amerindian populations living at high altitudes suffer disproportionately from gastric cancer relative to other populations with similar infection rates [...]. These and other points of evidence raise the possibility that the pathogenicity of a given H. pylori strain may vary with human genomic variation, and that some individuals may be better adapted to their infecting strains than others. (Kodaman et al. 2014)

Manipulating sexual behavior

Pathogens thus differ in their virulence from one human population to another. The same should be true for those pathogens that manipulate human behavior to improve their chances of spreading from one human to another. For them, our most interesting behavior is sex, and the most interesting human populations are "leaky" polygynous ones with high rates of infidelity. In that kind of context they can spread rapidly from one household to another.

Polygyny rates are highest among the tropical farming peoples of sub-Saharan Africa (Dalton and Leung 2011; Pebley and Mbugua 1989). Traditionally, 20 to 40% of all marriages are polygynous, and most women live in polygynous households. Not surprisingly, many men, particularly young men, are single. Their opportunities for sex are limited to rape, affairs with the wives of other men, or abduction of women during times of war:

Typically, the more men are polygynous in a given society, the greater the age difference between husbands and wives. [...] The temporary celibacy of young men in polygynous societies is rarely absolute, however. While it often postpones the establishment of a stable pair-bond and the procreation of children, it often does not preclude dalliance with unmarried girls, adultery with younger wives of older men, or the rape or seduction of women conquered in warfare. Thus, what sometimes looks like temporary celibacy is, in fact, temporary promiscuity. (van den Berghe 1979, pp. 50-51)

Cuckold envy: a case of behavioral manipulation?

This is the environment in which a sexually transmitted pathogen can leapfrog from one polygynous household to another. The main obstacle is male jealousy and male "guarding behavior." The pathogen can increase its chances of transmission by disabling mate guarding or, better yet, reversing it. This kind of host manipulation has been shown in a non-human species: male isopods no longer guard their mates when they get infected by a certain parasite (Mormann, 2010).

In a human context, a pathogen may reverse male jealousy and make its host want to be cuckolded, as a means to gain access to more hosts (Frost 2013). Many sexual fetishes are mentioned in ancient writings: pedophilia, cunnilingus, fellatio, and bestiality, but not cuckold envy. The oldest mentions go back to seventeenth-century England (Kuchar, 2011, pp. 18-19).

Perhaps a sexually transmitted pathogen came to England from West Africa during the early days of the slave trade. Such a pathogen would have evolved in a context where most women were in polygynous marriages and where cuckoldry was the main route for invading one set of wives after another. Meanwhile, the human hosts may have evolved some kind of resistance, perhaps through “overwiring.” Or perhaps a certain level of cuckoldry became socially accepted. No such resistance, however, had evolved in England or elsewhere in the Western world.

As time goes on, we will discover that many STDs have evolved a capacity for behavioral manipulation, specifically by making the host either more promiscuous or less jealous.


Dalton, J.T., and T.C. Leung. (2011). Why is Polygyny More Prevalent in Western Africa?
An African Slave Trade Perspective,

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

Kodaman, N., R.S. Sobota, R. Mera, B.G. Schneider, and S.M. Williams. (2014). Disrupted human-pathogen co-evolution: a model for disease. Frontiers in Genetics 25 August

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.

Mormann, K. (2010). Factors influencing parasite-related suppression of mating behavior in the isopod Caecidotea intermedius, Theses and Dissertations, paper 48  

Pebley, A. R., and W. Mbugua. (1989). Polygyny and Fertility in Sub-Saharan Africa. In R. J. Lesthaeghe (ed.), Reproduction and Social Organization in Sub-Saharan Africa, Berkeley: University of California Press, pp. 338-364.

van den Berghe, P.L. (1979). Human Family Systems. An Evolutionary View. New York: Elsevier.

Friday, October 18, 2019

I was really something

I was really something (2016), by Judith Carlin. A fungus may live in your brain for years while meddling only as much as necessary with your neurons. Beyond a certain age it gets less benefit and has less incentive to keep you mentally healthy. One result may be Alzheimer's.

Behavior manipulation has been perfected by many organisms: viruses, bacteria, worms, and insects. Fungi, however, seem to be the champions:

Fungi probably represent a special case study in this general field because of several unique factors peculiar to this Kingdom. The first and most prominent is the range and complexity of behavioral manipulation by fungi of arthropods. [...] It is difficult and perhaps futile to rank manipulation across different kingdoms of life and argue that fungal manipulation is more complex than that observed when the manipulator is in the Kingdom Animalia (eg, trematodes). However, what is clear is that the diversity of strategies is greater than that observed in other groups. In addition, it is evident that behavioral manipulation has arisen multiple times independently. (Hughes et al. 2016)

You've probably heard about "zombie ants." A fungus invades an ant's brain and makes it leave its nest, climb up a plant, and fix itself in place with its mandibles. The fungus then kills the ant, and a fruiting body sprouts from behind the ant's head and showers spores onto the forest floor below.

There are other examples. A fungus invades the body of a flying insect and causes a hole to form on the side of the abdomen. It then releases spores through that hole while its host is flying. The infected body gradually falls apart, except for its nervous system and its wings. Is the insect still alive? Not really. The bits and pieces that remain have become extensions of the fungus (Hughes et al. 2016).

Other fungi imitate the smell or visual appearance of a sexually receptive female to lure male insects, who then become infected (Hughes et al. 2016).

In the above cases, the fungus mutilates and kills its host in ways that are not only ghastly but also easy to observe and study. But what about the more subtle cases where the host's behavior is simply altered? Those are the ones we know much less about. Our knowledge is biased toward the most obvious cases of infection. As Greg Cochran observed:

The most conspicuous transmission chains occur when disease manifestations are externally apparent in a high proportion of infected individuals, when they occur soon after the onset of infection, and when contact between infected and susceptible individuals is easy to observe. Under these circumstances chains of transmission are apparent through everyday experience. (Cochran et al. 2000)

Even when we can detect the presence of a pathogen, the causal link with certain effects is far from obvious because the effects are either subtle or long-term:

Pathogens are often classified as relatively harmless or even commensal without sufficient long-term study to warrant such a classification. The historical record illustrates the consequences of this error. Epstein-Barr viruses and human papillomaviruses were once thought of as relatively harmless on the basis of their linkage to relatively benign diseases that occur soon after infection (infectious mononucleosis and warts respectively). But each virus can cause lethal cancers. Bacteroides was once thought to be a harmless commensal, but recent evidence indicates that it may be linked to ulcerative colitis. (Cochran et al. 2000)

Many slowly developing diseases are probably of pathogenic origin. This seems especially the case with various forms of senile dementia. The pathogen targets your brain and gains some benefit while you’re still socially and sexually active. At that stage, it’s living in a commensal relationship with you and confines its neuronal meddling to the minimum necessary. Beyond a certain age, however, it gets less benefit from you and has less incentive to keep you mentally healthy. One result may be Alzheimer's:

The possibility that Alzheimer's disease (AD) has a microbial aetiology has been proposed by several researchers. Here, we provide evidence that tissue from the central nervous system (CNS) of AD patients contain fungal cells and hyphae. Fungal material can be detected both intra- and extracellularly using specific antibodies against several fungi. Different brain regions including external frontal cortex, cerebellar hemisphere, entorhinal cortex/hippocampus and choroid plexus contain fungal material, which is absent in brain tissue from control individuals. Analysis of brain sections from ten additional AD patients reveals that all are infected with fungi. Fungal infection is also observed in blood vessels, which may explain the vascular pathology frequently detected in AD patients. Sequencing of fungal DNA extracted from frozen CNS samples identifies several fungal species. Collectively, our findings provide compelling evidence for the existence of fungal infection in the CNS from AD patients, but not in control individuals. (Pisa et al. 2015)

Alzheimer's is a late onset disease. What is the fungus doing to your brain during the long time when you’re not mentally impaired? 

Another example may be multiple sclerosis:

Many biomarkers of MS are consistent with fungal infections, such as IL-17, chitotriosidase, and antibodies against fungi. Dimethyl fumarate (DMF), first used as an industrial fungicide, was recently repurposed to reduce MS symptoms. Its mechanisms of action in MS have not been firmly established. The low risk of MS during childhood and its moderate association with herpes simplex virus type 2 suggest genital exposure to microbes (including fungi) should be investigated as a possible trigger. (Benito-Leon and Laurence 2017)


Benito-Leon, J. and M. Laurence. (2017). The Role of Fungi in the Etiology of Multiple Sclerosis. Frontiers in Neurology 16 October

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

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.

Pisa, D., R. Alonso, A. Rabano, and I. Rodal. (2015). Different Brain Regions are Infected with Fungi in Alzheimer's Disease. Scientific Reports 5(15015) 

Thursday, October 10, 2019

Is this the Gay Germ? Part II

Courtyard with Lunatics, Francisco Goya (1746-1828). Why is HIV much more likely to cause cognitive impairment in the body of a gay man than in the body of an intravenous drug user? Has an unknown pathogen been caught in the dragnet of AIDS studies?

My last post focused on certain discrepancies in data on AIDS victims: as antiretroviral therapy becomes more widespread, there has been a decline in opportunistic infections, but the decline hasn't been the same for all pathogens. In particular, some brain infections have shown modest declines or no change at all. 

Has an unknown pathogen been caught in the dragnet of AIDS studies? This pathogen would coexist with HIV only because it, too, is associated with the gay lifestyle. It would not be a "cofactor" that makes the HIV infection worse. In fact, it probably precedes the HIV infection by many years. This unknown pathogen may target certain sites in the brain of its host early in life in order to change his sexual orientation and thereby increase its chances of transmission to another host. It thereafter remains in the background until its host has reached an age when he ceases to be useful. The pathogen is then no longer penalized if it causes damage to surrounding neural tissues. Various neurocognitive disorders could therefore develop in its host from late middle age onward.

AIDS in gay men and intravenous drug users

This post will focus on discrepancies in data from two other papers. The first one is a study of AIDS victims in the Italian city of Bologna. Some of them contracted AIDS via homosexual/bisexual behavior, and some via intravenous drug use. One finding strikes me as unusual: "Compared with injecting drug users, homosexual/bisexual and heterosexual participants had ORs of 9.6 (95% CI, 2.2-42.7) and 6.3 (95% CI, 2.2-18.3), respectively, for cognitive impairment" (De Ronchi et al. 2002).

In other words, when the researchers looked at AIDS victims, they found that cognitive impairment was ten times more strongly associated with homosexuality/bisexuality than with intravenous drug use. That finding is curious because the ratio of ten to one doesn't correspond at all to the ratio of homosexuals/bisexuals to intravenous drug users among Italian AIDS cases. In fact, intravenous drug users made up about 60% of those cases in 1997 (Wikipedia 2019). The Bologna study took place between 1994 and 1997.

Why is HIV much more likely to cause cognitive impairment in the body of a gay man than in the body of an intravenous drug user? Do druggies take better care of their mental health? The evidence actually suggests the reverse: HIV-associated dementia seems to progress more rapidly in intravenous drug users (Bouwman et al. 1998). The latter finding also points to a qualitative difference between the two groups: dementia seems to develop more slowly in gay men.


The second paper is a review of studies on HAND [HIV-associated neurocognitive disorders]. It notes that HAND can develop even in individuals on HAART [Highly active antiretroviral therapy] with no detectable traces of HIV:

Furthermore, 21% [of individuals in the CHARTER study] developed HAND despite effective HAART (although the precise number who were aviremic is unclear). Similarly, in a cohort of individuals with AIDS, 21% of aviremic individuals (who also had undetectable CSF HIV RNA) progressed to HAD [HIV-associated dementia]. A third prospective study also identified HAND in 8-34% (depending on the time point of the assessment) of aviremic patients without comorbidities and with a nadir CD4 cell count less than 200 cells/µl (McArthur and Brew 2010)

The authors suggest that HIV can produce irreversible neural damage that becomes noticeable only much later in life. Well, perhaps. Nonetheless, it seems to me more parsimonious to postulate a second pathogen.

Parting thoughts

Clearly, HIV does cause cognitive impairment. The Bologna study showed a strong association between HAND and low white cell counts. But it looks like a certain proportion of HANDs are due to a cause that exists independently of HIV infection.

Please note: I'm not arguing that HIV is interacting with an unknown pathogen to cause cognitive impairment. I am arguing that these two pathogens impair cognition independently of each other and in different ways. They share only one thing in common: they have a much higher incidence among gay men than in the general population.

Finally, I'm not arguing that this unknown pathogen is the only cause of male homosexuality. There are likely multiple causes. In a nutshell, male homosexuality seems to be due to a genetic predisposition interacting with something in the environment. The genetic predisposition is a smaller-than-average neuronal population that promotes a heterosexual orientation. Normally, natural selection keeps it from falling below the threshold needed to sustain attraction to women. Certain environmental agents, however, can cause this neuronal population to fall below the threshold: fraternal birth order effects, stressful events during pregnancy, exposure to environmental estrogens during childhood, and, yes, a pathogen.

I don't know whether my views on the "gay germ theory" are consistent with Greg Cochran's. I hope he will deign to provide his comments.


Bouwman, F., R. Skolasky, D. Hes, O. Selnes, J. Glass, T. Nance-Sproson, W. Royal, G. Dal Pan,  and J. McArthur. (1998). Variable progression of HIV-associated dementia. Neurology 50(6): 1814-1820. 

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

De Ronchi, D., I. Faranca, D. Berardi, et al. (2002). Risk Factors for Cognitive Impairment in HIV-1-Infected Persons with Different Risk Behaviors. Archives of Neurology 59(5): 812-818.

McArthur, J.C., and B.J. Brew. (2010). HIV-associated neurocognitive disorders: is there a hidden epidemic? AIDS 24(9): 1367-1370|aidsonline:2010:06010:00017|| 

Wikipedia (2019). HIV/AIDS Public Health Campaigns in Italy

Wednesday, October 2, 2019

Is this the Gay Germ?

Poster for 1997 World AIDS Day (Wikicommons - Neil Curtis, Christian Michelides). Antiretroviral therapy has reduced infections in AIDS victims, but the decline hasn't been the same for all pathogens. Some infections have shown modest declines or no change at all. Could they be due to the "gay germ"?

Male homosexuality has low to moderate heritability (30 to 45%). A recent study in the UK Biobank and 23andMe has identified a number of genetic variants associated with same-sex sexual behavior. Together, they account for 8 to 25% of variation in male and female same-sex behavior (Ganna et al. 2019). There is thus a genetic predisposition, but it's weak and may simply reflect a smaller population of neurons for heterosexual orientation.

So this genetic predisposition seems to be interacting with something in the environment. But what?

There may be different environmental factors. One possibility would be a pathogen that alters its host's sexual orientation in order to enhance its chances of spreading to other hosts. This is Greg Cochran's "gay germ" theory (Cochran et al. 2000).

With the introduction of antiretroviral therapy for AIDS, we may have a chance to identify candidates for the "gay germ." Over time this therapy should reduce the incidence of infections in AIDS victims. Indeed it has, but the decline has been uneven.  A retrospective study of AIDS autopsies in Vienna between 1984 and 1999 found a lower rate of decline for infections due to fungi and most bacteria than for infections due to protozoa, viruses, and mycobacteria:

Extracerebral protozoal (Pneumocystis carinii, toxoplasmosis), Mycobacterium avium complex, viral [e.g., cytomegalovirus (CMV)], multiple opportunistic organ and CNS infections, and Kaposi sarcoma significantly decreased over time. There was less decrease in fungal infections, while bacterial organ and CNS infections (except for mycobacteriosis), lymphomas, HIV-associated CNS lesions (around 30%), non HIV-associated changes (vascular, metabolic, etc.) and negative CNS findings (10-11%) remained unchanged. (Jellinger et al. 2000)

These findings are in line with those of a retrospective study of AIDS autopsies in San Diego between 1982 and 1998:

Pneumocystis carinii pneumonia and Mycobacterium avium complex decreased, whereas bacterial infections increased and the frequency of fungal infection remained unchanged over time. (Eliezer et al. 2000)

After the lungs, such pathogens most often target the brain:

This study suggests that despite the beneficial effects of antiretroviral and anti-opportunistic infection therapy, involvement of the brain by HIV continues to be a frequent autopsy finding. (Eliezer et al. 2000).

Similar to a recent autopsy study from San Diego, these data suggest that despite the beneficial effects of modern antiretroviral combination therapy, involvement of the brain in AIDS subjects continues to be a frequent autopsy finding. (Jellinger et al. 2000)

Subjects with brain alterations at an early stage otherwise seemed almost normal:

Of the cases with early brain alterations, systemic opportunistic infections were present in only 5.9% of the cases, neoplasms in 0.5%, and neoplasms and opportunistic infections in 1.7%. (Eliezer et al. 2000)

A few caveats

The change in incidence over time partly reflects differences between fast-developing infections and slow-developing ones. By definition, people succumb more quickly to the former than to the latter. When antiretroviral therapy was still unavailable those infections were the ones that generally killed people with AIDS. Better control of aggressive infections may have also created a better environment for the growth of less aggressive infections.

But ...

It is harder to explain why the brain should remain a major pathogenic target. It is especially hard to explain why subjects with brain alterations at an early stage otherwise seemed almost normal.

Eggers et al. (2017) pointed out another apparent contradiction: HIV-associated neurocognitive disorders (HAND) are continuing to develop in people whose HIV infection is under control.

Despite the brain infection taking place in the days after primary infection, the development of HAND takes years. As an explanation for this ostensible contradiction, it has been suggested that initially, the brain infection is relatively well controlled, while later, there is a quantitative and qualitative breakdown of immune control in the CNS (Eggers et al. 2017)

Some authors have suggested co-infection by the Hepatitis C virus, but Eggers et al. (2017) ruled this out:

While some authors implicated HCV co-infection in the pathogenesis of HAND, a recent large and well-controlled study found no evidence for worse cognitive function in HCV co-infected patients, at least in the absence of liver dysfunction. (Eggers et al. 2017)

Pathogen "X"

Could we be looking at an unknown pathogen that exists independently of HIV? Over the years some have suggested that HIV is not the only pathogen involved in AIDS. In this case, pathogen "X" may cause adverse effects that get blamed on HIV, but its relationship with HIV is incidental, the only common denominator being the gay lifestyle.

I would propose the following scenario. Pathogen "X" enters its host early in life, just in time to alter that person's psychosexual development. From then on it remains in the background and reaps whatever benefit it gets from its behavior manipulation. Past the age of 40 the host becomes less useful, and the pathogen begins to cause more adverse effects, including neurocognitive disorders that are wrongly attributed to HIV.

Pathogen "X" is most likely a fungus. If we go back to the two retrospective studies, the fungal infections were the ones that seemed the least influenced by the introduction of antiretroviral therapy.


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

Eggers, C., G. Arendt, K. Hahn, K., I.W. Husstedt, M. Mashke, et al. (2017). HIV-1-associated neurocognitive disorder: epidemiology, pathogenesis, diagnosis, and treatment. Journal of Neurology 264: 1715-1727

Eliezer, M., R.M. DeTeresa, M.E. Mallory, and L.A. Hansen. (2000). Changes in pathological findings at autopsy in AIDS cases for the last 15 years. AIDS 14(1): 69-74.

Ganna, A., K.J.H. Verweij, M.C. Nivard, R. Maier, R. Weddow, et al. (2019). Large-scale GWAS reveals insights into the genetic architecture of same-sex sexual behavior. Science 365(6456) 

Jellinger, K.A., U. Setinek, M. Drlicek, G. Böhm, A. Steurer, and F. Lintner. (2000). Neuropathology and general autopsy findings in AIDS during the last 15 years. Acta Neuropathologica 100(2): 213-220.