Let me posit a wild theory here: we know t. gondii targets the amygdala; beyond response to immediate danger and lengthening of reaction time, would it be fair to say it could impact our overall perception of danger? And consequently affects us with an attitude where people largely ignore evident threats made to them, even from obviously hostile groups?
Yes, it could have that effect. The amygdala stores memories of emotional events. Those events could be frightening, but they could also be profoundly erotic. To understand which emotions are being targeted, we would need a more detailed map of where the T. gondii cysts are located.
This might come off weirdly but in France we've had, as you know, terrible terrorist attacks and a pattern we notice is that some of the family of the victims will attempt to befriend the killer(s) and really give the impression they have no conception of what an enemy is, or what evil could be. It's like they're biologically neutered and unable and thus unwilling to defend themselves. So yeah there's a pattern of leftist thinking where absolutely nothing seems like a threat to them, like they can't conceive of danger, almost. The effects of T. Gondii made me think of that...
Merci ! C'est la même affaire au Canada et aux États-Unis. Je crois que c'est à cause de notre héritage chrétien : "Aimez vos ennemis, bénissez ceux qui vous maudissent, faites du bien à ceux qui vous haïssent, et priez pour ceux qui vous maltraitent et qui vous persécutent".
Cette philosophie peut bien fonctionner dans une population où tout le monde possède plus ou moins la même capacité à culpabiliser ou à compatir (sauf une petite minorité de sociopathes qui sont d'ailleurs faciles à repérer et à séquestrer). Il s'agit là de la population dans laquelle le christianisme s'est développé.
Malheureusement, la plupart des humains ne fonctionnent pas ainsi. La compassion, tout comme le pardon, c'est pour les autres membres du clan; ce n'est pas pour n'importe qui.
Effectivement vous avez raison. Après je ne sais pas si c'est un héritage chrétien mais en tout cas c'est certainement un aspect de la psychologie WEIRD, bien que cela détonne vis-à-vis des populations importés qui raisonnent selon des logiques toutes autres...
I encountered toxoplasmosis when I helped someone to publish a book about her experience in bringing up her son who had been affected by it at birth. The book is BECOMING KARL, the author is Norma Delgarno.
WRT toxoplasmosis. I gather from my Dr that I have antibodies to it. As a male, you suggest it can be sexually transmitted from other males, though I presume other means of transmission are more prevalent given my lack of such experiences. Where is the boundary currently between this being a 'just so' story and a valid hypothesis for further investigation?
A just-so story is a hypothesis. It becomes invalid only if it has been investigated and found wanting. One cannot therefore determine a priori whether a hypothesis is valid for further investigation. "Further investigation" is what validates the hypothesis.
You might be confusing "hypothesis" with "theory."
There actually is a large literature on T. gondii and its behavioral effects. Clearly, it does have behavioral effects. The main debate is whether these effects are an adaptation to human sexual relationships or a holdover from adaptation to the cat-rodent relationship.
With regard to your antibodies to T. gondii, there are two possibilities: 1) you got this microbe from a cat; or 2) you got it from an infected person through non-sexual contact.
Should I have said 'thesis' rather than 'hypothesis'? My understanding is that a 'just so' story is one that is framed to conform to selected evidence rather than to provide a framework for testing an idea.
If the predominant mode of transmission is through say cat faeces or non-sexual human contact any selective effects on the parasite during sexual transmission would usually 'wash out'. Ofc identifying the emergence of such a selected agent would be pretty important.
There is no clear distinction between a thesis and a hypothesis. Both are statements or propositions put forward for consideration. Conclusive or even "sufficient" evidence isn't necessary for either.
A thesis (or hypothesis) cannot be distinguished from a "just-so story." Both are hunches that an investigator pursues on the basis of limited evidence. The term "just-so story" is a negative way of framing a hypothesis or thesis, usually by a hostile critic.
The evidence suggests that sexual transmission is more important than intimate contact with cats. Perhaps men have more contact with cats than women, but that doesn't seem to be the case.
At this point, an interesting avenue for research would be to determine which strains of T. gondii have a predominance of infected men. Some strains seem t be more adapted to human-to-human transmission than others.
That's interesting about 'Just So Stories'. So I asked AI, as you do. I knew of Kipling's stories and the terms more recent use to describe extremely speculative or untestable explanations but not of Gould's use of it to disparage his opponents.
I'm guessing I got toxoplasmosis from gardening which I have done for many decades and have often cursed cats and their excretions.
The spread of t.gondii is oral (contaminated food/drink). Sexual spread (perhaps apart from fellatio connoisseurs) is speculative. Peter as an aspiring science-fiction writer doesn't mention this to stimulate creative thinking among readers and increase suspense.
If sexual spread were significant (assuming only male->male & male->female sexual spread), you would expect far more females to be infected, but it's mostly parity worldwide. This pretty much rules out significant sexual spread.
No, it's more common in men, although the gender disparity does vary.
In Italy, "the prevalence of recent infection was higher in men than in women. A two-fold attack rate was detected in males compared to females in the age range 25–34 years"
Pinto, B., Mattei, R., Moscato, G. A., Cristofano, M., Giraldi, M., Scarpato, R., ... & Bruschi, F. (2017). Toxoplasma infection in individuals in central Italy: does a gender-linked risk exist?. European Journal of Clinical Microbiology & Infectious Diseases, 36(4), 739-746. https://doi.org/10.1007/s10096-016-2857-8
In Germany, "Male gender, keeping cats and BMI ≥30 were independent risk factors for seropositivity"
Wilking, H., Thamm, M., Stark, K. et al. Prevalence, incidence estimations and risk factors of Toxoplasma gondii infection in Germany: a representative, cross-sectional, serological study. Sci Rep 6, 22551 (2016). https://doi.org/10.1038/srep22551
In the US, "In multivariable analysis, risk for IgG seropositivity increased with age and was higher in males"
Jones, J. L., Kruszon-Moran, D., Elder, S., Rivera, H. N., Press, C., Montoya, J. G., & McQuillan, G. M. (2017). Toxoplasma gondii infection in the United States, 2011–2014. The American Journal of Tropical Medicine and Hygiene, 98(2), 551. https://doi.org/10.4269/ajtmh.17-0677
I referenced the studies that indicate sexual transmission of T. gondii. Allow me to quote from the latest review article:
"It became evident that toxoplasmosis in men significantly increases the likelihood that their female partners will also be infected (Hlaváčová et al. 2021b). Our study suggests that this may not be reciprocal – toxoplasmosis in women did not affect the likelihood of their male partners becoming infected. This finding undermines the possibility that the correlation arises from a common source of infection. The prevalence of toxoplasmosis in various countries correlates with the incidence of sexually transmitted diseases in those countries (Flegr et al. 2014a), and the likelihood that a pregnant woman will be infected positively correlates with the amount of unprotected sex she had with her partner before conception (Flegr et al. 2014b).
Perhaps the strongest evidence for the existence of sexual transmission of toxoplasmosis in humans is the discovery that the ejaculate of infected men contains a large number of Toxoplasma tissue cysts, detectable immunohistochemically and with modern molecular biological techniques (Tong et al. 2023)."
Peter, you didn't address the substance of my comment. Let me repeat:
If sexual spread were significant (assuming only male-to-male and male-to-female sexual spread), you would expect far more females to be infected, but there is mostly parity worldwide (or, according to you, even higher rates in men!).
That's a glaring hole in the sexual spread theory, is it not? How do males get infected at parity (or a higher rate) if women can't infect them sexually?
I read what you quoted suggesting the possibility of sexual transmission even in your original Aporia article. I will postpone addressing that until we address this. Arguing about gender parity is irrelevant - you quoted some countries, I can quote others where it's the reverse. Both parity and male overrepresentation support doubt about the significance of sexual spread.
If the direction of sexual transmission is male-to-male and male-to-female, the prevalence of T. gondii should be higher among men than among women. Typically, it's twice as common in men as in women. I've already cited studies from Italy, Germany, and the US. The largest global study is a meta-analysis of 66 studies of workers occupationally exposed to animals. It found a prevalence of 63% among male workers and 37% among female workers (Mohammed et al., 2024).
The gender difference seems to be highest in countries where food contamination is less of a problem, i.e., the developed world. This is to be expected. To the extent that nonsexual routes of transmission are eliminated, the sexual routes will be proportionately larger.
I'm talking about all men who have sex with men, and not simply those who self-identify as gay. An analysis of 67 studies found that the lifetime prevalence of sex between men (regardless of orientation) was 3–5% for East Asia, 6–12% for South and South East Asia, 6–15% for Eastern Europe, and 6–20% for Latin America (Caceres et al., 2006).
Also, men who have sex with men tend much more to have multiple partners, sometimes hundreds of partners per year, so this group has a disproportionate impact on STD prevalence.
Caceres, C.; Konda, K.; Pecheny, M.; Chatterjee, A.; Lyerla, R. (2006). "Estimating the number of men who have sex with men in low and middle income countries". Sexually Transmitted Infections. 82 (Suppl. III): iii3 – iii9. doi:10.1136/sti.2005.019489
"[H]omosexual behavior could facilitate spread because of the larger numbers of partners homosexual males may have on average, relative to heterosexual males"
I apologize beforehand if the question is as unsophisticated as I suspect it of being, but: how would the parasites known of the average partner count difference?
See the comment by Torless Caraz. The parasite doesn't have a brain. It doesn't know what it should or should not do. Its behavior is determined by natural selection, and not by conscious thought.
For example, HIV doesn't know that certain groups of people will transmit it more effectively than other groups, yet it is much more prevalent in certain groups. How is that? How does it "know" that certain groups are better vectors? If I were a philosopher, I would answer by saying that "knowing" is not required for "being" and "doing."
Natural selection isn't conscious either. It is an inevitable process that happens with self-replicating organisms. If you're better at surviving and reproducing, your descendants will become more and more numerous. This is how things work out. It's not a conscious process.
Not surprising to see our Thought doing what it does BEST... Divert attention and responsibility from itself and blaming its own degeneration to an outside entity!
Good point! Many people lack the self-awareness or self-discipline to modify their behavior without outside help. This is why groups like AA have been crucial to helping people take charge of their lives.
As a side note, I'm not arguing that behavior-altering pathogens are solely or even largely responsible for the rise of sexual promiscuity.
Regarding multiple sclerosis, this interesting post (https://stephenskolnick.substack.com/p/ms) posits a different explanation that would explain some of the observations you note. He notes that despite some was in which MS appears like an STD, but that it does not seem to spread between spouses. His proposed answer is that it is a downstream consequence of antibiotic usage given for STDs as well as for other reasons. Wiping out the endemic bacteria with antibiotics can pave the way for the proliferation of another bacterium, Clostridium perfringens, which produces a toxin that causes MS-like symptoms in livestock.
There is some evidence of spread between spouses. A Sardinian survey found five cases of MS concordance between spouses (out of 659 cases), i.e., five times higher than chance. On the other hand, a Canadian survey found no concordance. It's possible that the route of transmission is oral or anal sex, and not vaginal sex.
The problem with Kolnick's explanation is the young age of the girls in the MS surveys. In the Faroese survey, some of the girls were under 16 years of age when they contracted MS from British soldiers (who were occupying the Faroes during the war). Were these girls taking antibiotics for another STD? Remember, this was the period of 1940 to 1945 in a small traditional society. A girl of that age could not have easily got a prescription without going through her parents.
It seems like the most obvious place to look for microbes manipulating our sexual behavior would not be T. gondii or C. albicans but rather the various well-known sexually transmitted infections that have been in human populations for a long time, like chlamydia, gonorrhea, syphilis, etc. Has anyone examined whether there is evidence that these cause increased promiscuity or other behaviors that increase their spread? Unfortunately it is difficult to tell the direction of causation, as an association (in these cases or with T. gondii or C. albicans) could also just indicate the pre-existing behaviors that increase the chances of contracting it. Maybe a longitudinal study could see whether changed behavior precedes or follows infection. Lab animal research of other species' STIs could be illuminating.
I ruled out the common STDs (chlamydia, gonorrhea, syphilis) because they're not discreet (i.e., they harm the host too quickly and too readily). However, Adamo (2014) has argued that these STDs suppress "sickness behavior" in order to increase their chances of infecting other individuals.
Adamo, S. A. (2014). Parasitic aphrodisiacs: manipulation of the hosts’ behavioral defenses by sexually transmitted parasites. Integrative and Comparative Biology, 54(2), 159-165. https://doi.org/10.1093/icb/icu036
To anyone who doubts that parasites can manipulate our behavior, I think the best and most famous example is rabies. The rabies virus is spread through bites, so it manipulates the host's behavior to be more aggressive (and thus more likely to bite) and to be afraid of water (to avoid washing the virus out of the mouth). While humans are a dead end for the rabies virus (as we don't tend to bite as a form of aggression), it still causes aggression and hydrophobia (see this video from Wikipedia: https://en.wikipedia.org/wiki/File:Hydrophobia_in_rabies.webm).
Glad to see a mention of the papers we discussed about the distinctive gut microbiome of gay men. For anyone else who is interested, I wrote a post about this at https://luckyhunterandcornmother.substack.com/p/evidence-for-a-microbial-cause-of. The microbiomes of gay men are so different from straight people that it is nearly diagnostic of sexual orientation, and you can see this at a glance when you graph the microbiome composition. It is a far stronger association than other factors, like genes or birth order, that have been discussed as causing homosexuality. The microbiome difference does not seem to be driven by HIV, receptive anal sex, diet, drug use, or any other known confound. While this could be caused by some other unknown confound, I think there is a good chance this is pointing to the proximate cause of homosexuality (even if it is not caused by gut bacteria directly).
The causality in your claim that "T. gondii manipulates not only behavior but also physical appearance" in making males more attractive through higher testosterone is unclear. According to the immunocompetence handicap hypothesis, highter testosterone suppresses the immune system as an honest signal of genetic fitness, so we would expect more masculine males to be more often infected with T gondii, as well as to have a higher parasite load in general.
Unfortunately, the human immune system cannot eliminate T. gondii, even in the best of circumstances.
As for testosterone, it can reduce immunity in some cases and enhance it in others:
"Testosterone can influence susceptibility to certain infections. Higher testosterone levels in males have been associated with an enhanced immune response against viral respiratory infections, tuberculosis, and sepsis. Conversely, low testosterone levels have been linked to increased susceptibility to infections and poorer immune response, including a higher risk of respiratory and urinary tract infections."
Fascinating article. I wonder what other behaviors the Romans and Greeks curiously made no reference to, which are prevalent today. Same for other civilizations with writing like China.
They seem to have done everything but that. There is no record of the cuckold fetish in Greco-Roman literature, which nonetheless attests to a wide range of alternative sexuality between men and women (fellatio and cunnilingus), between men, between women, with children, with sculptures, and with animals.
Although there are mentions of sexual humiliation, including flagellation, bondage, and other forms of torture, those sexual acts were desired only by the “active” partner, usually a freeborn male. For the “passive” partner the infliction of pain was neither consensual nor pleasurable. “Indeed, the vast majority of the recorded ancient cases of people engaging in practices that resemble those in modern BDSM are clearly cases of rape and/or abuse” (McDaniel 2021).
Thank you for the thorough response! You are right that it is puzzling that humiliation fetishes are strangely absent from extant Greco-Roman texts. I also wonder about specific behaviors beyond sexuality, like, for example, how charity was practiced.
Amazing article. Do any societies with rapidly falling rates of sexual activity among the young show signs of reversal of some of the proposed effects?
Sexual activity has declined only if we exclude porn-assisted masturbation. To reverse the decline in human-to-human sex, we should 1) reduce the costs of dating, 2) make real people more sexually interesting (i.e., no obesity, no tattoos), and 3) increase civility in human relationships.
But making people equally sexually appealing by reducing markers of negative traits, like high impulsivity or low intelligence, sounds dysgenic. For example, Ozempic might one day make everyone the same BMI, removing what was once a strong signal of poor self-control.
Yes, obesity is becoming a marker of low social class and poor impulse control. Perhaps the same thing is happening with tattooing.
In the current circumstances, the best approach might be laisser-faire: let people do whatever they want ... and suffer the consequences. Unfortunately, those consequences have huge spillover effects that can affect all of us.
I should have been clearer that I meant rates of interpersonal sexual contact, which presumably would make life difficult for any sexually transmitted organisms. Japan is probably the furthest along the path, though it is probably too early in the trend to gauge the behavioural impact.
Could this be a bi-stable kind of dynamic, namely either a universally promiscuous population where promiscuity inducing parasites are ubiquitous, or a universally restrained society where the parasites are rare?
There might even be an irony if the parasites induce greater focus on pornography as a substitute to sexual contact. Maybe future populations will be infected with more nuanced brain parasites which direct their hosts to the real deal.
In Japan, and elsewhere, the decline in sexual activity among young people is recent. This doesn't look like a behavior that has been shaped by natural selection.
One could argue that this is an adaptive behavior that has become maladaptive in the current context. In predominantly monogamous societies with high paternal investment, humans have been selected to mate only when certain culturally defined conditions have been met. Modern Western cultures have raised this threshold by 1) increasing the costs of dating, 2) maintaining the male-skewed sex ratio at birth throughout most of adulthood, and 3) reducing or eliminating the economic and ideological supports for family formation.
Wow. Great and horrifying article.
Let me posit a wild theory here: we know t. gondii targets the amygdala; beyond response to immediate danger and lengthening of reaction time, would it be fair to say it could impact our overall perception of danger? And consequently affects us with an attitude where people largely ignore evident threats made to them, even from obviously hostile groups?
Yes, it could have that effect. The amygdala stores memories of emotional events. Those events could be frightening, but they could also be profoundly erotic. To understand which emotions are being targeted, we would need a more detailed map of where the T. gondii cysts are located.
Interesting!
This might come off weirdly but in France we've had, as you know, terrible terrorist attacks and a pattern we notice is that some of the family of the victims will attempt to befriend the killer(s) and really give the impression they have no conception of what an enemy is, or what evil could be. It's like they're biologically neutered and unable and thus unwilling to defend themselves. So yeah there's a pattern of leftist thinking where absolutely nothing seems like a threat to them, like they can't conceive of danger, almost. The effects of T. Gondii made me think of that...
Thank you for the great piece!
Merci ! C'est la même affaire au Canada et aux États-Unis. Je crois que c'est à cause de notre héritage chrétien : "Aimez vos ennemis, bénissez ceux qui vous maudissent, faites du bien à ceux qui vous haïssent, et priez pour ceux qui vous maltraitent et qui vous persécutent".
Cette philosophie peut bien fonctionner dans une population où tout le monde possède plus ou moins la même capacité à culpabiliser ou à compatir (sauf une petite minorité de sociopathes qui sont d'ailleurs faciles à repérer et à séquestrer). Il s'agit là de la population dans laquelle le christianisme s'est développé.
Malheureusement, la plupart des humains ne fonctionnent pas ainsi. La compassion, tout comme le pardon, c'est pour les autres membres du clan; ce n'est pas pour n'importe qui.
Effectivement vous avez raison. Après je ne sais pas si c'est un héritage chrétien mais en tout cas c'est certainement un aspect de la psychologie WEIRD, bien que cela détonne vis-à-vis des populations importés qui raisonnent selon des logiques toutes autres...
Merci pour votre réponse.
I encountered toxoplasmosis when I helped someone to publish a book about her experience in bringing up her son who had been affected by it at birth. The book is BECOMING KARL, the author is Norma Delgarno.
Bob S.
WRT toxoplasmosis. I gather from my Dr that I have antibodies to it. As a male, you suggest it can be sexually transmitted from other males, though I presume other means of transmission are more prevalent given my lack of such experiences. Where is the boundary currently between this being a 'just so' story and a valid hypothesis for further investigation?
A just-so story is a hypothesis. It becomes invalid only if it has been investigated and found wanting. One cannot therefore determine a priori whether a hypothesis is valid for further investigation. "Further investigation" is what validates the hypothesis.
You might be confusing "hypothesis" with "theory."
There actually is a large literature on T. gondii and its behavioral effects. Clearly, it does have behavioral effects. The main debate is whether these effects are an adaptation to human sexual relationships or a holdover from adaptation to the cat-rodent relationship.
With regard to your antibodies to T. gondii, there are two possibilities: 1) you got this microbe from a cat; or 2) you got it from an infected person through non-sexual contact.
Should I have said 'thesis' rather than 'hypothesis'? My understanding is that a 'just so' story is one that is framed to conform to selected evidence rather than to provide a framework for testing an idea.
If the predominant mode of transmission is through say cat faeces or non-sexual human contact any selective effects on the parasite during sexual transmission would usually 'wash out'. Ofc identifying the emergence of such a selected agent would be pretty important.
There is no clear distinction between a thesis and a hypothesis. Both are statements or propositions put forward for consideration. Conclusive or even "sufficient" evidence isn't necessary for either.
A thesis (or hypothesis) cannot be distinguished from a "just-so story." Both are hunches that an investigator pursues on the basis of limited evidence. The term "just-so story" is a negative way of framing a hypothesis or thesis, usually by a hostile critic.
The evidence suggests that sexual transmission is more important than intimate contact with cats. Perhaps men have more contact with cats than women, but that doesn't seem to be the case.
At this point, an interesting avenue for research would be to determine which strains of T. gondii have a predominance of infected men. Some strains seem t be more adapted to human-to-human transmission than others.
That's interesting about 'Just So Stories'. So I asked AI, as you do. I knew of Kipling's stories and the terms more recent use to describe extremely speculative or untestable explanations but not of Gould's use of it to disparage his opponents.
I'm guessing I got toxoplasmosis from gardening which I have done for many decades and have often cursed cats and their excretions.
The spread of t.gondii is oral (contaminated food/drink). Sexual spread (perhaps apart from fellatio connoisseurs) is speculative. Peter as an aspiring science-fiction writer doesn't mention this to stimulate creative thinking among readers and increase suspense.
If sexual spread were significant (assuming only male->male & male->female sexual spread), you would expect far more females to be infected, but it's mostly parity worldwide. This pretty much rules out significant sexual spread.
No, it's more common in men, although the gender disparity does vary.
In Italy, "the prevalence of recent infection was higher in men than in women. A two-fold attack rate was detected in males compared to females in the age range 25–34 years"
Pinto, B., Mattei, R., Moscato, G. A., Cristofano, M., Giraldi, M., Scarpato, R., ... & Bruschi, F. (2017). Toxoplasma infection in individuals in central Italy: does a gender-linked risk exist?. European Journal of Clinical Microbiology & Infectious Diseases, 36(4), 739-746. https://doi.org/10.1007/s10096-016-2857-8
In Germany, "Male gender, keeping cats and BMI ≥30 were independent risk factors for seropositivity"
Wilking, H., Thamm, M., Stark, K. et al. Prevalence, incidence estimations and risk factors of Toxoplasma gondii infection in Germany: a representative, cross-sectional, serological study. Sci Rep 6, 22551 (2016). https://doi.org/10.1038/srep22551
In the US, "In multivariable analysis, risk for IgG seropositivity increased with age and was higher in males"
Jones, J. L., Kruszon-Moran, D., Elder, S., Rivera, H. N., Press, C., Montoya, J. G., & McQuillan, G. M. (2017). Toxoplasma gondii infection in the United States, 2011–2014. The American Journal of Tropical Medicine and Hygiene, 98(2), 551. https://doi.org/10.4269/ajtmh.17-0677
I referenced the studies that indicate sexual transmission of T. gondii. Allow me to quote from the latest review article:
"It became evident that toxoplasmosis in men significantly increases the likelihood that their female partners will also be infected (Hlaváčová et al. 2021b). Our study suggests that this may not be reciprocal – toxoplasmosis in women did not affect the likelihood of their male partners becoming infected. This finding undermines the possibility that the correlation arises from a common source of infection. The prevalence of toxoplasmosis in various countries correlates with the incidence of sexually transmitted diseases in those countries (Flegr et al. 2014a), and the likelihood that a pregnant woman will be infected positively correlates with the amount of unprotected sex she had with her partner before conception (Flegr et al. 2014b).
Perhaps the strongest evidence for the existence of sexual transmission of toxoplasmosis in humans is the discovery that the ejaculate of infected men contains a large number of Toxoplasma tissue cysts, detectable immunohistochemically and with modern molecular biological techniques (Tong et al. 2023)."
Flegr, J. (2025). Thirty years of studying latent toxoplasmosis: behavioural, physiological, and health insights. Folia Parasitologica, 72, 1-16.https://folia.paru.cas.cz/pdfs/fol/2025/01/05.pdf
Peter, you didn't address the substance of my comment. Let me repeat:
If sexual spread were significant (assuming only male-to-male and male-to-female sexual spread), you would expect far more females to be infected, but there is mostly parity worldwide (or, according to you, even higher rates in men!).
That's a glaring hole in the sexual spread theory, is it not? How do males get infected at parity (or a higher rate) if women can't infect them sexually?
I read what you quoted suggesting the possibility of sexual transmission even in your original Aporia article. I will postpone addressing that until we address this. Arguing about gender parity is irrelevant - you quoted some countries, I can quote others where it's the reverse. Both parity and male overrepresentation support doubt about the significance of sexual spread.
If the direction of sexual transmission is male-to-male and male-to-female, the prevalence of T. gondii should be higher among men than among women. Typically, it's twice as common in men as in women. I've already cited studies from Italy, Germany, and the US. The largest global study is a meta-analysis of 66 studies of workers occupationally exposed to animals. It found a prevalence of 63% among male workers and 37% among female workers (Mohammed et al., 2024).
The gender difference seems to be highest in countries where food contamination is less of a problem, i.e., the developed world. This is to be expected. To the extent that nonsexual routes of transmission are eliminated, the sexual routes will be proportionately larger.
"If the direction of sexual transmission is male-to-male and male-to-female, the prevalence of T. gondii should be higher among men than among women."
How so? I'd expect the opposite to be the case:
1. No female infects the males she has sexual interactions with. That's zero contribution to the male infection rate.
2. Each infected male infects a portion of the females he has sexual interactions with. That's a positive contribution to the female infection rate.
So what's the case for male overrepresentation?
P.S.: Homosexuals shouldn't explain it. Even in the worst-case scenario, they'd add only a few percent.
I'm talking about all men who have sex with men, and not simply those who self-identify as gay. An analysis of 67 studies found that the lifetime prevalence of sex between men (regardless of orientation) was 3–5% for East Asia, 6–12% for South and South East Asia, 6–15% for Eastern Europe, and 6–20% for Latin America (Caceres et al., 2006).
Also, men who have sex with men tend much more to have multiple partners, sometimes hundreds of partners per year, so this group has a disproportionate impact on STD prevalence.
Caceres, C.; Konda, K.; Pecheny, M.; Chatterjee, A.; Lyerla, R. (2006). "Estimating the number of men who have sex with men in low and middle income countries". Sexually Transmitted Infections. 82 (Suppl. III): iii3 – iii9. doi:10.1136/sti.2005.019489
How do you get rid of parasites? Lol
Researchers are working on a human vaccine for T. gondii. But you can't eliminate it from your body once it's in you and creating cysts.
You can treat active toxoplasmosis with certain antibiotics.
"[H]omosexual behavior could facilitate spread because of the larger numbers of partners homosexual males may have on average, relative to heterosexual males"
I apologize beforehand if the question is as unsophisticated as I suspect it of being, but: how would the parasites known of the average partner count difference?
It doesn't. It just, de facto, spread much more quickly among them. So the strain engaging in homosex ends up prevailing.
See the comment by Torless Caraz. The parasite doesn't have a brain. It doesn't know what it should or should not do. Its behavior is determined by natural selection, and not by conscious thought.
For example, HIV doesn't know that certain groups of people will transmit it more effectively than other groups, yet it is much more prevalent in certain groups. How is that? How does it "know" that certain groups are better vectors? If I were a philosopher, I would answer by saying that "knowing" is not required for "being" and "doing."
Natural selection isn't conscious either. It is an inevitable process that happens with self-replicating organisms. If you're better at surviving and reproducing, your descendants will become more and more numerous. This is how things work out. It's not a conscious process.
Not surprising to see our Thought doing what it does BEST... Divert attention and responsibility from itself and blaming its own degeneration to an outside entity!
Everything ultimately has an outside cause.
We are never to blame... After all blaming oneself requires a high degree of something we don't possess.
Good point! Many people lack the self-awareness or self-discipline to modify their behavior without outside help. This is why groups like AA have been crucial to helping people take charge of their lives.
As a side note, I'm not arguing that behavior-altering pathogens are solely or even largely responsible for the rise of sexual promiscuity.
Again, thank you for your insights!
Regarding multiple sclerosis, this interesting post (https://stephenskolnick.substack.com/p/ms) posits a different explanation that would explain some of the observations you note. He notes that despite some was in which MS appears like an STD, but that it does not seem to spread between spouses. His proposed answer is that it is a downstream consequence of antibiotic usage given for STDs as well as for other reasons. Wiping out the endemic bacteria with antibiotics can pave the way for the proliferation of another bacterium, Clostridium perfringens, which produces a toxin that causes MS-like symptoms in livestock.
There is some evidence of spread between spouses. A Sardinian survey found five cases of MS concordance between spouses (out of 659 cases), i.e., five times higher than chance. On the other hand, a Canadian survey found no concordance. It's possible that the route of transmission is oral or anal sex, and not vaginal sex.
The problem with Kolnick's explanation is the young age of the girls in the MS surveys. In the Faroese survey, some of the girls were under 16 years of age when they contracted MS from British soldiers (who were occupying the Faroes during the war). Were these girls taking antibiotics for another STD? Remember, this was the period of 1940 to 1945 in a small traditional society. A girl of that age could not have easily got a prescription without going through her parents.
It seems like the most obvious place to look for microbes manipulating our sexual behavior would not be T. gondii or C. albicans but rather the various well-known sexually transmitted infections that have been in human populations for a long time, like chlamydia, gonorrhea, syphilis, etc. Has anyone examined whether there is evidence that these cause increased promiscuity or other behaviors that increase their spread? Unfortunately it is difficult to tell the direction of causation, as an association (in these cases or with T. gondii or C. albicans) could also just indicate the pre-existing behaviors that increase the chances of contracting it. Maybe a longitudinal study could see whether changed behavior precedes or follows infection. Lab animal research of other species' STIs could be illuminating.
I ruled out the common STDs (chlamydia, gonorrhea, syphilis) because they're not discreet (i.e., they harm the host too quickly and too readily). However, Adamo (2014) has argued that these STDs suppress "sickness behavior" in order to increase their chances of infecting other individuals.
Adamo, S. A. (2014). Parasitic aphrodisiacs: manipulation of the hosts’ behavioral defenses by sexually transmitted parasites. Integrative and Comparative Biology, 54(2), 159-165. https://doi.org/10.1093/icb/icu036
To anyone who doubts that parasites can manipulate our behavior, I think the best and most famous example is rabies. The rabies virus is spread through bites, so it manipulates the host's behavior to be more aggressive (and thus more likely to bite) and to be afraid of water (to avoid washing the virus out of the mouth). While humans are a dead end for the rabies virus (as we don't tend to bite as a form of aggression), it still causes aggression and hydrophobia (see this video from Wikipedia: https://en.wikipedia.org/wiki/File:Hydrophobia_in_rabies.webm).
Glad to see a mention of the papers we discussed about the distinctive gut microbiome of gay men. For anyone else who is interested, I wrote a post about this at https://luckyhunterandcornmother.substack.com/p/evidence-for-a-microbial-cause-of. The microbiomes of gay men are so different from straight people that it is nearly diagnostic of sexual orientation, and you can see this at a glance when you graph the microbiome composition. It is a far stronger association than other factors, like genes or birth order, that have been discussed as causing homosexuality. The microbiome difference does not seem to be driven by HIV, receptive anal sex, diet, drug use, or any other known confound. While this could be caused by some other unknown confound, I think there is a good chance this is pointing to the proximate cause of homosexuality (even if it is not caused by gut bacteria directly).
The causality in your claim that "T. gondii manipulates not only behavior but also physical appearance" in making males more attractive through higher testosterone is unclear. According to the immunocompetence handicap hypothesis, highter testosterone suppresses the immune system as an honest signal of genetic fitness, so we would expect more masculine males to be more often infected with T gondii, as well as to have a higher parasite load in general.
Unfortunately, the human immune system cannot eliminate T. gondii, even in the best of circumstances.
As for testosterone, it can reduce immunity in some cases and enhance it in others:
"Testosterone can influence susceptibility to certain infections. Higher testosterone levels in males have been associated with an enhanced immune response against viral respiratory infections, tuberculosis, and sepsis. Conversely, low testosterone levels have been linked to increased susceptibility to infections and poorer immune response, including a higher risk of respiratory and urinary tract infections."
https://www.icliniq.com/articles/immune-disorders/relationship-between-testosterone-and-immunity
Fascinating article. I wonder what other behaviors the Romans and Greeks curiously made no reference to, which are prevalent today. Same for other civilizations with writing like China.
They seem to have done everything but that. There is no record of the cuckold fetish in Greco-Roman literature, which nonetheless attests to a wide range of alternative sexuality between men and women (fellatio and cunnilingus), between men, between women, with children, with sculptures, and with animals.
Although there are mentions of sexual humiliation, including flagellation, bondage, and other forms of torture, those sexual acts were desired only by the “active” partner, usually a freeborn male. For the “passive” partner the infliction of pain was neither consensual nor pleasurable. “Indeed, the vast majority of the recorded ancient cases of people engaging in practices that resemble those in modern BDSM are clearly cases of rape and/or abuse” (McDaniel 2021).
McDaniel, S. (2021). Did the Ancient Greeks and Romans Practice BDSM? Tales of Times Forgotten. September 19. https://talesoftimesforgotten.com/2021/09/19/did-the-ancient-greeks-and-romans-practice-bdsm/
Thank you for the thorough response! You are right that it is puzzling that humiliation fetishes are strangely absent from extant Greco-Roman texts. I also wonder about specific behaviors beyond sexuality, like, for example, how charity was practiced.
Amazing article. Do any societies with rapidly falling rates of sexual activity among the young show signs of reversal of some of the proposed effects?
Sexual activity has declined only if we exclude porn-assisted masturbation. To reverse the decline in human-to-human sex, we should 1) reduce the costs of dating, 2) make real people more sexually interesting (i.e., no obesity, no tattoos), and 3) increase civility in human relationships.
But making people equally sexually appealing by reducing markers of negative traits, like high impulsivity or low intelligence, sounds dysgenic. For example, Ozempic might one day make everyone the same BMI, removing what was once a strong signal of poor self-control.
Yes, obesity is becoming a marker of low social class and poor impulse control. Perhaps the same thing is happening with tattooing.
In the current circumstances, the best approach might be laisser-faire: let people do whatever they want ... and suffer the consequences. Unfortunately, those consequences have huge spillover effects that can affect all of us.
I should have been clearer that I meant rates of interpersonal sexual contact, which presumably would make life difficult for any sexually transmitted organisms. Japan is probably the furthest along the path, though it is probably too early in the trend to gauge the behavioural impact.
Could this be a bi-stable kind of dynamic, namely either a universally promiscuous population where promiscuity inducing parasites are ubiquitous, or a universally restrained society where the parasites are rare?
There might even be an irony if the parasites induce greater focus on pornography as a substitute to sexual contact. Maybe future populations will be infected with more nuanced brain parasites which direct their hosts to the real deal.
In Japan, and elsewhere, the decline in sexual activity among young people is recent. This doesn't look like a behavior that has been shaped by natural selection.
One could argue that this is an adaptive behavior that has become maladaptive in the current context. In predominantly monogamous societies with high paternal investment, humans have been selected to mate only when certain culturally defined conditions have been met. Modern Western cultures have raised this threshold by 1) increasing the costs of dating, 2) maintaining the male-skewed sex ratio at birth throughout most of adulthood, and 3) reducing or eliminating the economic and ideological supports for family formation.
Sounds like science fiction.
Science fiction is often a means to introduce a serious hypothesis to the general public.
We clearly need to G.E. one of these beautiful "parasites" in order to give us a Brain Free of our current Thought!