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.
References
Dalton, J.T., and T.C. Leung. (2011). Why is Polygyny More Prevalent in Western Africa?
An African Slave Trade Perspective,
http://www.wfu.edu/~daltonjt/PolygynySlaveTrade.pdf
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
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
https://www.frontiersin.org/articles/10.3389/fgene.2014.00290/full
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
http://via.library.depaul.edu/etd/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.
9 comments:
According to a recent study, 28% of young men (18-30) have not had sex in the past year compared to 18% of young women, whereas a decade earlier -- in 2008 -- the percentages were 10% and 8%, respectively. (https://www.fastcompany.com/90327099/gen-z-men-arent-having-sex-and-the-internet-of-course-may-be-to-blame) And it's not just the young men: men of all ages are now on the receiving end of #MeToo, a female "sex strike" of sorts, where women have declared war on sex, men, flirtatious behavior. The result is that the world is now in a deep freeze with respect to reproduction, and the brakes are being applied by the women. The US birth rate has been in free fall since 2007. My question is: what kind of "pathogen" could be behind women's sudden exit from mating that we're observing now? Is the planet overpopulated, especially given recent declines in mortality, which makes less sex less necessary? Is childlessness, frigidity, or lesbianism also a pathogen of some kind?
Anon,
The causes are largely cultural. In the past, young men and women were brought together by the local church, by the community, or simply by mutual friends. All three factors are much weaker today. There has been an atomization of social life, and this trend is supported by a broad Left-Right "consensus."
There is also the widening gap in sexual activity between young men and young women. A growing proportion of young men are being squeezed out of the marriage market. This is largely due to four factors:
- decline in male mortality (the male-biased sex ratio at birth now persists into the sixth decade of life)
- a steady increase in polygyny (or "polyamory").
- growing numbers of single mothers who drop out of the mate market
- disproportionate numbers of single males among immigrants
Fungi cause brain infection and impair memory in mice Fungal infections causing airway allergic diseases and sepsis have been associated with increased risk for dementia later. In mouse experiments the fungus that commonly kills Aids patients was found to have been cleared by the time of greatest mortality, and it seems to be a case of provoking over inflammation:
https://labblog.uofmhealth.org/lab-report/fungal-brain-infection-results-from-hosts-own-immune-response.'“Scientists have thought the disease is caused by the immune system being too weak to control the fungus,” Olszewski says. The team notes that a major immune cell subset appeared to accumulate in the mice: Th1-polarized IFN-y-producing CD4+ T cells.
“After examining those cells, we found that the development of those deadly central nervous system symptoms could be prevented by depleting CD4+ T cells, even though the fungus was persistently growing and increasing within the central nervous system,” Olszewski says. “This demonstrated that Th1 cells are a central mediator of central nervous system pathology, and central nervous system injury and mortality are mediated by the host’s own immune response.”'
Sean,
I don't want to seem negative, but I don't see the relevance of your examples. Fungal infections of the nervous system are common when the immune system is weakened. Data from AIDS victims becomes interesting when we find that restoration of the immune system causes some pathogens to disappear while having little or no effect on fungal infections in the brain. Even in that situation it's possible to come up with alternate explanations.
Peter, but regardless of what you wrote about sex squeezes, what kind of pathogen would make women publicly accuse men of sexual harassment after largely consensual encounters? This is happening on a mass scale now. Just today there was a vicious article in the media about some guy's attempted seduction of women who all had given him signals of sexual consent by coming to his apartment late at night and making out with him, and then publicly accused him of sexual assault: https://www.nytimes.com/2019/11/01/dining/drinks/anthony-cailan-sexual-assault.html What is going with women nowadays, are they trying to curb all sexual activity, or destroy men out of spite? What is the biological or evolutionary origin of MeToo?
Young women are in a sellers' market. Unfortunately, this is the kind of behavior you see when supply is limited and demand is strong.
@Anonymous
1. Movements like #MeToo are nothing new (and are mostly effecting White Westerners, not everyone living in the West), and are largely cultural. Not driven by any pathogen. Its nothing more than attempt by women to gain more sexual power over men since the aftermath of the Sexual Revolution and the easy availability of internet porn.
2. Declining birth rates don't necessarily mean decline in sexual activity. There's no universal link between fertility rates and rates of sexual intercourse.
3. The decline in sexual activity in the US is mostly effecting White America, with no changes in Blacks and Latinos compared to past eras:https://www.ncbi.nlm.nih.gov/pubmed/27480753
https://www.ncbi.nlm.nih.gov/pubmed/25940736
https://www.nytimes.com/2016/08/05/science/millennials-sex.html
http://gssq.blogspot.com/2017/07/the-male-sexual-deficit-social-fact-of.html
''[...] 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)''
Just so stories... like the misunderstood ''hybrid vigor'' but reverse.
Environmentalism strikes again...
I thought humans were more stable, that's what ''unideological'' hbd taught us one decade ago.
Are you aware about the consequences if these ideas become popular* Or not*
Even if it's was the case.
Natural selection is not ''all traits must be selected or in-selection and have a collaborative purpose within organism''.
Natural selection is also about keep open the diversity to possible or new adaptive challenges. Without diversity specially with increased endogamy is the dead end for any species.
If you think selective processes are all about select only-useful traits [i mean, collaborative
Autism as well homossexuality [i mean, masculine.. i thought it was ''exclusive'' male homossexuality] are both part of human diversity. We have virtually any evidence that both are less common in the longer conservative past because practically absolute absence of data about it.
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