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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