Fincher & Thornhill (F&T) present a compelling model of in-group assortative sociality and religiosity as adaptations to high levels of parasite-stress in local environments. Humans have acquired approximately 300 species of parasitic worms and 70 species of protozoan parasites that they have interacted and coevolved with over the last million years or so (Cox Reference Cox2002). It would seem to make evolutionary sense that humans would have developed psychological as well as biological adaptations to counter parasitic threat. F&T attempt to incorporate parasite-stress into evolutionary models of sociality. However, although they present a strong case, there are four major issues I have with their arguments.
The first issue is that their model does not address the evolutionary benefits from mutualistic associations – that is, associations between two individuals of the same or different species that confers a fitness benefit to both. Humans have received mutualistic fitness benefits from parasitic microorganisms, phylogenetically and ontogenetically. For example, it is believed that the evolutionary precursor of mitochondria, the primary energy producing organelle in our cells, originated as an invasive, parasitic bacterium (Searcy Reference Searcy2003). The microflora that inhabit our intestines are essential to many aspects of healthy human functioning, including preventing growth of pathogenic bacteria, and are transmitted horizontally from the mother to infant during the first birth year (Dethlefsen et al. Reference Dethlefsen, McFall-Ngai and Relman2007; Goodacre Reference Goodacre2007). If humans possessed adaptations for parasite stress, it would seem that they would be only for the parasites that were potentially lethal or immediately hazardous. For a parasite-stress adaptation to be considered an evolutionary success it would have to accurately identify legitimate threats from potentially beneficial microorganisms and non-communicable diseases. Additionally, false positives could occur from individual differences due to biological development, injury, or age. Without the ability to correctly sort out legitimate parasite threats from harmless non-communicable symptoms, we run the risk of avoiding anyone who does not fit an idealized healthy appearance.
The second issue stems from the first and it involves the level of analysis. The primary function of F&T's study is to examine sociological measures of large geographic areas such as states and countries comprising large populations or groups; however, it is difficult to draw conclusions about individual behavior from such domains. What I am most curious about is how the in-group pressure, or assortative sociality, would work at an individual level. F&T postulate that in-group assortative sociality results, in part, from the avoidance of out-group parasitic threats; however, individuals may also be exposed to parasites from in-group members. This issue is mentioned in section 6.3.1 in terms of a “life-history theory” in regions of high parasite-stress. Yet F&T have not addressed how collective attitudes can override the social exclusion of those group members who may be differentially likely to carry disease in areas of less-than-extreme levels of parasite-stress: At what point does an individual participating in a religious event come to regard a nearby person with a sign of parasite infection as no longer a member of the in-group? Considering that, historically, individuals with infections or illness were seen to be suffering from something they did to themselves or resulting from divine wrath (de Avila-Pires Reference de Avila-Pires1998), the drive towards collectivism seems to be a unique human trait compared to other primates; and, although this was not the primary focus of F&T's study, it nonetheless begs the question.
The third issue is regarding F&T's argument about the causal effects of parasite stress on the formation of human sociality: specifically, that parasite stress was one of the primary driving forces that shaped social, religious, and family life. The proposition that parasite stress is directly responsible for the development of animal social structure is rather overreaching for a correlational human social study. The development of any trait, including parasite avoidance, involves a complex mixture of many elements and often follows a nonlinear path. For example, the development of any disease is the direct result of the history of and interaction between biology (i.e., genetic predispositions, timing of exposure), ecology (i.e., local flora and fauna, nutritional sources, latitude), and social factors (i.e., population density, access to quality health care, group size), as opposed to a single identifiable outside threat. The concept that maintaining in-group allegiances serves to protect “coadapted gene complexes” (target article, sect. 2.1., para. 4) from outside parasitic threat does not hold up to medical evidence. For example, genetic research is finding that genes are secondary causes of health disparities in the United States, compared with social and environmental factors (i.e., racial discrimination, poverty) (Dressler et al. Reference Dressler, Oths and Gravely2005; Sankar et al. Reference Sankar, Cho, Condit, Hunt, Koenig, Marshall, Lee and Spicer2004). I believe that the patterns found on a large scale in the F&T's study will break down on an individual psychological level.
The last issue I would like to address is F&T's argument that religiosity and religious practices are derived from parasite-stress. If parasite-stress drives the development of religious beliefs and practices, this suggests that those beliefs and practices would reflect some kind of avoidance or prevention measures for parasite-stress – and in many cases this does seem to be the case, such as avoiding pork in the Jewish tradition. However, there are also many cases where religious and/or cultural practices have actually increased the spread of disease: for example, the well-known spread of the CJD-like disease among the Fore tribe in Papua New Guinea due to cannibalistic rituals. The rapid spread of HIV in Africa is connected to cultural practices that increase the risk of transmission, such as circumcision, medicinal bloodletting, and blood rituals, as well as sharing instruments during ritual sacrificing, tattooing, and piercing (Hrdy Reference Hrdy1987).
F&T present a solid model for parasite-stress factors shaping large-scale patterns of human family, cultural, and religious systems. I believe, however, that they cast a net too large to reveal the causal relationships between parasite threat and specific human behavior. Immune responses to parasite threat as well as human social systems are amazingly complex and dynamic, involving many interactions over time. F&T address the legitimate threat that parasites have posed, but the precise manner in which parasite-stress and human psychological, cultural, and religious beliefs and practices have coevolved is somewhat overlooked in their current model.
Fincher & Thornhill (F&T) present a compelling model of in-group assortative sociality and religiosity as adaptations to high levels of parasite-stress in local environments. Humans have acquired approximately 300 species of parasitic worms and 70 species of protozoan parasites that they have interacted and coevolved with over the last million years or so (Cox Reference Cox2002). It would seem to make evolutionary sense that humans would have developed psychological as well as biological adaptations to counter parasitic threat. F&T attempt to incorporate parasite-stress into evolutionary models of sociality. However, although they present a strong case, there are four major issues I have with their arguments.
The first issue is that their model does not address the evolutionary benefits from mutualistic associations – that is, associations between two individuals of the same or different species that confers a fitness benefit to both. Humans have received mutualistic fitness benefits from parasitic microorganisms, phylogenetically and ontogenetically. For example, it is believed that the evolutionary precursor of mitochondria, the primary energy producing organelle in our cells, originated as an invasive, parasitic bacterium (Searcy Reference Searcy2003). The microflora that inhabit our intestines are essential to many aspects of healthy human functioning, including preventing growth of pathogenic bacteria, and are transmitted horizontally from the mother to infant during the first birth year (Dethlefsen et al. Reference Dethlefsen, McFall-Ngai and Relman2007; Goodacre Reference Goodacre2007). If humans possessed adaptations for parasite stress, it would seem that they would be only for the parasites that were potentially lethal or immediately hazardous. For a parasite-stress adaptation to be considered an evolutionary success it would have to accurately identify legitimate threats from potentially beneficial microorganisms and non-communicable diseases. Additionally, false positives could occur from individual differences due to biological development, injury, or age. Without the ability to correctly sort out legitimate parasite threats from harmless non-communicable symptoms, we run the risk of avoiding anyone who does not fit an idealized healthy appearance.
The second issue stems from the first and it involves the level of analysis. The primary function of F&T's study is to examine sociological measures of large geographic areas such as states and countries comprising large populations or groups; however, it is difficult to draw conclusions about individual behavior from such domains. What I am most curious about is how the in-group pressure, or assortative sociality, would work at an individual level. F&T postulate that in-group assortative sociality results, in part, from the avoidance of out-group parasitic threats; however, individuals may also be exposed to parasites from in-group members. This issue is mentioned in section 6.3.1 in terms of a “life-history theory” in regions of high parasite-stress. Yet F&T have not addressed how collective attitudes can override the social exclusion of those group members who may be differentially likely to carry disease in areas of less-than-extreme levels of parasite-stress: At what point does an individual participating in a religious event come to regard a nearby person with a sign of parasite infection as no longer a member of the in-group? Considering that, historically, individuals with infections or illness were seen to be suffering from something they did to themselves or resulting from divine wrath (de Avila-Pires Reference de Avila-Pires1998), the drive towards collectivism seems to be a unique human trait compared to other primates; and, although this was not the primary focus of F&T's study, it nonetheless begs the question.
The third issue is regarding F&T's argument about the causal effects of parasite stress on the formation of human sociality: specifically, that parasite stress was one of the primary driving forces that shaped social, religious, and family life. The proposition that parasite stress is directly responsible for the development of animal social structure is rather overreaching for a correlational human social study. The development of any trait, including parasite avoidance, involves a complex mixture of many elements and often follows a nonlinear path. For example, the development of any disease is the direct result of the history of and interaction between biology (i.e., genetic predispositions, timing of exposure), ecology (i.e., local flora and fauna, nutritional sources, latitude), and social factors (i.e., population density, access to quality health care, group size), as opposed to a single identifiable outside threat. The concept that maintaining in-group allegiances serves to protect “coadapted gene complexes” (target article, sect. 2.1., para. 4) from outside parasitic threat does not hold up to medical evidence. For example, genetic research is finding that genes are secondary causes of health disparities in the United States, compared with social and environmental factors (i.e., racial discrimination, poverty) (Dressler et al. Reference Dressler, Oths and Gravely2005; Sankar et al. Reference Sankar, Cho, Condit, Hunt, Koenig, Marshall, Lee and Spicer2004). I believe that the patterns found on a large scale in the F&T's study will break down on an individual psychological level.
The last issue I would like to address is F&T's argument that religiosity and religious practices are derived from parasite-stress. If parasite-stress drives the development of religious beliefs and practices, this suggests that those beliefs and practices would reflect some kind of avoidance or prevention measures for parasite-stress – and in many cases this does seem to be the case, such as avoiding pork in the Jewish tradition. However, there are also many cases where religious and/or cultural practices have actually increased the spread of disease: for example, the well-known spread of the CJD-like disease among the Fore tribe in Papua New Guinea due to cannibalistic rituals. The rapid spread of HIV in Africa is connected to cultural practices that increase the risk of transmission, such as circumcision, medicinal bloodletting, and blood rituals, as well as sharing instruments during ritual sacrificing, tattooing, and piercing (Hrdy Reference Hrdy1987).
F&T present a solid model for parasite-stress factors shaping large-scale patterns of human family, cultural, and religious systems. I believe, however, that they cast a net too large to reveal the causal relationships between parasite threat and specific human behavior. Immune responses to parasite threat as well as human social systems are amazingly complex and dynamic, involving many interactions over time. F&T address the legitimate threat that parasites have posed, but the precise manner in which parasite-stress and human psychological, cultural, and religious beliefs and practices have coevolved is somewhat overlooked in their current model.