and cellular processes underlying human disease. Studying these animals in a variety of psychosocial paradigms, based on variables identified through survey, epidemiological, and human experimental research, can test hypothesized causal relations derived from correlational data in humans.
It is essential to study animals as evolved biological systems in which surviving and reproducing in particular social and physical environments have selected a constellation of interactions between social, behavioral, physiological systems, and gene function. Doing so reveals insights and principles that also underlie human health and disease but that are not salient in the modern world or in a typical biomedical approach. Moreover, ethology and evolutionary biology recognize that individual differences are not necessarily just “noise,” but represent different evolved strategies for survival in different contexts. Taking an ethological approach to variation in strategies reveals the range of gene-environment interactions that occur within species as they have evolved in their natural ethological and ecological contexts.
Studies of deer mice (Peromyscus maniculatus), who live in highly seasonal environments, reveal that function of the immune system requires significant energy, so much so that during winter an animal trades off entering puberty and becoming reproductive in order to sustain the energetic requirements of fighting infectious disease (Prendergast and Nelson, 2001; Nelson, 2004). It is not the demands of the cold weather itself that signals this trade-off, but rather the shortened days that precede seasonal temperature change, allowing the animal to modulate relative balance of immune function and reproduction in anticipation of the energetic demands of winter.
In house sparrows, immune activity increases energy expenditure, illustrating the energetic costs of immune function that could otherwise be deployed to growth (Martin et al., 2003). Such animal research, set in an ecological context, provides a powerful animal model for such trade-offs in humans. When social structure restricts resources and results in a population living in an environment with a high pathogen load, slower growth can result, as is the case of children in the lowlands of Bolivia. This presumably happens because the allocation of energetic resources to immune function has been diverted from growth (McDade, 2005). This dynamic interaction between social access to energy stores, pathogen interaction, fat deposition, and growth likely involves leptin, a pleiotropic molecule with cytokine properties that is produced by fat cells during an inflammatory response (Faggioni et al., 2001; Fantuzzi, 2005).