Life-history theory predicts that exposure to conditions typical of low socioeconomic status (SES) during childhood will calibrate development in ways that promote survival in harsh and unpredictable ecologies. Guided by this insight, the current research tested the hypothesis that low childhood SES will predict eating in the absence of energy need. Across three studies, we measured (Study 1) or manipulated (Studies 2 and 3) participants' energy need and gave them the opportunity to eat provided snacks. Participants also reported their SES during childhood and their current SES. Results revealed that people who grew up in high-SES environments regulated their food intake on the basis of their immediate energy need; they ate more when their need was high than when their need was low. This relationship was not observed among people who grew up in low-SES environments. These individuals consumed comparably high amounts of food when their current energy need was high and when it was low. Childhood SES may have a lasting impact on food regulation.

Researchers in the evolutionary sciences have long understood men's desire to mate with a variety of women. Because men's obligatory investment in offspring production is relatively small, men can directly increase their number of descendants by mating with multiple partners. Relatively less is known, however, about the conditions that favor sexual variety seeking in women. Drawing on insights from evolutionary biology and behavioral ecology, we examined the relationship between the perceived pathogen load in an environment and women's desire for sexual variety. Across 5 experiments, we primed women with cues indicating that the rate of disease is increasing in their environment. We then measured their desire for novel sexual and dating partners. Results revealed that women with a history of vulnerability to illness respond to these cues by desiring a greater number of novel partners. This shift was not found in men and did not predict variety seeking in a nonsexual domain. In addition to providing evidence of a novel conceptual link between the pathogen load and patterns of human mating behavior, this research also provides new insights into women's mating psychology and the conditions that favor sexual variety seeking in the greater investing sex.

Here we review research suggesting that vulnerability to disease plays a significant role in modulating life history strategies. In particular, we highlight the role of immunocompetence in life history tradeoffs, predicting that individuals whose immune systems leave them more vulnerable to disease should exhibit a range of psychological and behavioral outcomes that are associated with faster life history strategies. Further, we propose that these differences should occur even after controlling for the effects of early life stress, which themselves calibrate faster life history strategies and alter immune function. We close by highlighting important issues and challenges in this emerging area of inquiry, and illuminate potentially promising avenues of future research.

Here, we present a mechanistically grounded theory detailing a novel function of the behavioral immune system (BIS), the psychological system that prompts pathogen avoidance behaviors. We propose that BIS activity allows the body to downregulate basal inflammation, preventing resultant oxidative damage to DNA and promoting longevity. Study 1 investigated the relationship between a trait measure of pathogen avoidance motivation and in vitro and in vivo proinflammatory cytokine production. Study 2 examined the relationship between this same predictor and DNA damage often associated with prolonged inflammation. Results revealed that greater trait pathogen avoidance motivation predicts a) lower levels of spontaneous (but not stimulated) proinflammatory cytokine release by peripheral blood mononuclear cells (PBMCs), b) lower plasma levels of the proinflammatory cytokine interleukin-6 (IL-6), and c) lower levels of oxidative DNA damage. Thus, the BIS may promote health by protecting the body from the deleterious effects of inflammation and oxidative stress.

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Here, we propose a novel theoretical model linking present-focused decision-making to the activities of the immune system. We tested our model by examining the relationship between inflammatory activity – in vivo and in vitro – and decision-making characterized by impulsivity, present focus, and an inability to delay gratification. Results support our model, revealing that inflammation predicts these outcomes even after controlling for factors that may contribute to a spurious linkage between them. Moreover, subsequent analyses revealed that our model was a better fit for the data than alternative models using present-focused decision-making and its health-harming behavioural sequelae (e.g., smoking, risky sexual behaviour) to predict inflammation, lending support for the proposed directionality of this relationship. Together, these results suggest that inflammation may contribute to decision-making patterns that can result in undesirable personal and societal outcomes.

Although infectious disease has posed a significant and persistent threat to human survival and welfare throughout history, only recently have the psychological and behavioral implications of disease threat become a topic of research within the behavioral sciences. This growing body of work has revealed a suite of affective and cognitive processes that motivate the avoidance of disease-causing objects and situations—a cascade of processes loosely conceptualized as a “behavioral immune system (BIS).” Recent BIS research has linked disease threat to a surprisingly broad set of psychological and behavioral phenomena. However, research examining how the BIS is nested within our broader physiology is only beginning to emerge. Here, we review research that has begun to elucidate the physiological foundations of the BIS—at the levels of sensory modalities, cells, and genes. We also discuss the future of this work.

Although frequently characterized as undesirable, risk-taking is an integral part of human social life. Research into the factors that influence risk-taking therefore represents an important area of study in the evolutionary sciences. The current research draws from research on humans' pathogen avoidance psychology, life history theory, and sickness behavior to examine the role that pathogen threat plays in modulating risk tolerance. Across 4 studies, we measured or manipulated pathogen threat cues and examined their effect on risk tolerance. Results revealed a consistent pattern whereby people preferred less risk when the threat of illness was high. This pattern was observed using both self-report measures and behavioral assays but was eliminated when the threat was experimentally minimized. The current research provides evidence of a conceptual link between pathogen threats and global tolerance for risk, demonstrating a tendency to play it safe when the threat of illness is high. Public Significance StatementThe current research examined how pathogen threats influence the psychology governing risk-taking. Four experimental studies found that when pathogen threats are made salient, people exhibit decreased willingness to take risks across domains (e.g., financial, social, health) and take fewer risks during a behavioral task. Results provide preliminary evidence that humans' pathogen management psychology may play an important role in modulating risk preferences in a variety of domains.