My primary field research is conducted in Cebu, the Philippines, where I, US and Filipino collaborators work with a large birth cohort study that enrolled more than 3,000 pregnant women in 1983 and has since followed their offspring into adulthood (now in their late 20s) [A published profile of the Cebu cohort can be found here]. We use more than 3 decades of data available for each study participant to gain a better understanding of the long-term impacts of early life environments on adult biology, function and health. A theme of much of my work is the application of principles of developmental plasticity and evolutionary biology to issues of health and human well being.

Highlights of recent research (see pubs page for a complete list):

Early environments, ecological signaling and developmental plasticity. Prenatal and early postnatal conditions can have broad, durable impacts on a wide range of biological systems. The health impacts of these responses are well documented in humans and other species. I am particularly interested in the origins of such maternal effects, and whether they might serve as a source of developmental information for offspring. Of particular interest is the fact that many biological systems have periods of heightened sensitivity which overlap with the period of direct dependence on resources or hormonal cues conveyed across the placenta or via breast milk. This opens up extensive channels allowing direct transfer of somatic information between generations.

Reproductive ecology and the evolution of the human life history. Past anthropological work on male reproductive ecology has emphasized the importance of testosterone as a regulator of energetic expenditure, which in males has little to do with pregnancy itself and more to do with building and maintaining a large and more energetically body with more muscle. Our work at Cebu explores the psychobiology of testosterone in the context of pairbonding and fatherhood, and uses developmental principles to illuminate how energetic priorities might be adjusted in response to early life nutritional cues. We are also interested in the forces that have shaped female reproductive strategy and the human lifespan.

Fetal nutrition as a cue of matrilineal nutritional history: intergenerational influences on birth outcomes. An extensive literature has documented that birth weight, as a reflection of fetal growth rate, predicts a wide range of biological and health outcomes. Understanding the functional or adaptive significance of these adjustments requires greater knowledge about what ecological information, if any, is conveyed to the fetus via fetal nutrition. A better understanding of which aspects of maternal experience fetal nutrition "tracks" could also lead to improved pregnancy supplementation strategies, which often yield only modest improvements in birth outcomes. Current NSF-funded fieldwork is following all new pregnancies in the female cohort members (the babies who were in utero when the study began) and measuring birth outcomes in their offspring (the grandoffspring of the mothers originally enrolled). We will use the lifetime of detailed information on nutrition, early life morbidity, infant feeding and growth of each young mother to gain a better understanding of the factors that predict birth weight of offspring, and at what ages in her life cycle these factors have strongest intergenerational impacts. In addition, a proposal recently funded by NIH (NICHD) will allow us to collect placentas in a subsample of these women to allow assessment of morphological and epigenetic changes that might link a woman's early life experience with fetal growth rate and birth size of her offspring. Fieldwork is ongoing for this project, but several publications in preparation use preliminary data to demonstrate the presence of maternal effects and to explore a possible mechanism for transgenerational perpetuation of birth weight:

Epigenetics, race, health disparities. That "race" categories have biological reality is made clear by the broad health disparities that are predicted by these socially defined groups, both in the US and abroad. And yet, it has long been appreciated that genes do not partition neatly according to these groupings. Processes of environment-driven developmental plasticity help explain why phenotypes tend to map onto social gradients of environmental stress and opportunity that societies organize around categories such as race. By controlling the environmental cues that developmental biology is designed to respond to, societies project their ideological biases onto the biological realm, with profound physiological and health implications. I am interested in how developmental plasticity and the new field of epigenetics can help us revise our understanding of human biological variation, including that traditionally ascribed by a subset of researchers to genetic race.

Developmental programming of adult health and immune function in the Philippines. For more than a decade, I and my collaborators have used the longitudinal data available for the participants in the Cebu cohort to gain a better understanding of the long-term impacts of early environments on adult health. In particular, we have focused on proxies of gesatational and maternal nutrition as predictors of later cardiovascular disease risk in offspring, and infancy measures of pathogen exposure as inputs that shape the development of the immune system as reflected in antibody response and cytokine profiles. A few examples of this work are listed below.

Evolutionary medicine. Public health and medicine clarify how we get sick, but they leave open the broader question of why we get sick. From an evolutionary perspective, diseases like obesity and diabetes can be viewed as a result of the body's strategy for prioritizing and allocating finite energy. I am particularly interested in the importance of the brain to the body's energy budget during infancy: not only does the brain demand most of the body's energy at this age, but it is quickly damaged if this supply line is even temporarily disrupted. The challenge of feeding the brain is compounded by the frequent nutritional disruptions that accompany weaning and childhood infectious diseases. I have argued that this confluence of factors helps explain why our highly-encephalized babies also come equipped with more body fat than any other mammalian neonate. I also believe that some of the changes in metabolism and physiology triggered in response to early life nutritional stress, such as we see in the Philippines, might be understood as a strategy to buffer the fragile and energy-hungry brain at this nutritionally-turbulent age.

The evolution of the human brain: comparative, energetic and molecular perspectives. Humans managed to pull off an interesting trick: although we evolved a large and energetically costly brain, our body's energy expenditure is the same as what is seen in other mammals of our body size. How was this achieved, and what were the dietary, energetic, metabolic and physiologic adjustments that were required? With NSF HOMINID funding, I and collaborators at Wayne State and George Washington Universities are currently investigating the energetic costs of the brain and how this changes with age, the neuronal differences between humans and other primates, the genetic changes involved with brain evolution, and age changes in neuronal gene transciption.

Human molecular variation, health and evolution. I am interested in the evolutionary origins and phenotypic impacts of modern human molecular variation. Recent collaborations have explored the extent of population variation in telomere length, tested evolutionary hypotheses for the origin of a common disease-influencing allelic variant (ApoE), and identified clinically relevant loci related to risk for cardiovascular and related diseases.

The synthesis of evolutionary and developmental biology. The melding of Mendel's laws with Darwin's principle of natural selection in the 1930s and 40s was built upon an assumption that mutation is the primary source of novel phenotypic variants, and was successful in demonstrating the plausibility of natural selection under assumptions of non-blending inheritance. The discipline that studies how genes unfold and interact with the environment to construct phenotypes - developmental biology - was not a central player in this historic synthesis. As a result, the role of developmental processes in evolutionary change was largely relegated to a black box for much of the 20th century. The currently brisk pace of research on developmental plasticity, epigenetic inheritance, life history evolution, parental effects, and the genetic architecture of developmental pathways (evo-devo) is leading to revised models of how phenotypes are generated and transmitted between generations. I have a keen interest in this emerging synthesis and the contribution that the study of humans and human biology can make to it.