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 the nearly 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 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.
Kuzawa CW, Thayer Z (2011), "The timescales of human adaptation: The role of epigenetic processes" Epigenomics. 3(2) 3(2)221-234
Kuzawa CW, Quinn EA (2009), “Developmental origins of adult function and health: Evolutionary hypotheses”, Annual Review of Anthropology, 38: 131-47.
Kuzawa, CW (2007), “Developmental
origins of life history strategy: growth, productivity and reproduction”
Amer J Hum Biol 19(5):654-61.
Kuzawa CW and IL Pike (2005), “The fetal origins of developmental plasticity. Introduction to the special issue.” Amer J Hum Biol 17(1) 1-4.
Kuzawa CW (2005), “The fetal origins of developmental plasticity. Are maternal cues reliable predictors of future nutritional environments?” Amer J Hum Biol 17(1) 5-21.
Male reproductive ecology and 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.
Gettler LT, McDade TW, Feranil AB, Kuzawa CW (2011), "Longitudinal evidence that fatherhood decreases testosterone in human males" Proc Nat Acad of Sciences. 108(39):16194-16199, Supporting information.
Gettler LT, McDade TW, Agustin SB, Kuzawa CW (2011), "Short-term changes in fathers' hormones during father-child play: Impacts of paternal attitudes and experience" Hormones and Behavior, Nov;60(5):599-606.
Gettler LT, McDade TW, Kuzawa CW (2011), "Cortisol and testosterone in Filipino young adult men: Evidence for co-regulation of both hormones by fatherhood and relationship status" Amer J Hum Biol. 23(5):609-20
Kuzawa CW, Adair LS, Lee N, McDade TW (2010), Rapid weight gain after birth predicts life history and reproductive strategy in Filipino males, Proceedings of the National Academy of Sciences 107(39):16800-5. Supplemental material.
Kuzawa CW, Muller M, Gettler L, McDade TW, Feranil A (2009), “Fatherhood, pairbonding and testosterone in the Philippines”, Hormones and Behavior, 56: 429-35.
Kuzawa CW, Gettler LT, Huang Y-Y, McDade TW (2010), “Mothers have lower testosterone than non-mothers: Evidence from the Philippines”, Hormones and Behavior. 57(4-5): 441-7.
Gettler LT, Agustin S, Kuzawa CW (2010), “Testosterone, physical activity and somatic outcomes among Filipino males,” Amer J Phys Anthropol, 142(4):590-9.
Kuzawa, CW (2007), “Developmental origins of life history strategy: growth, productivity and reproduction” Amer J Hum Biol 19(5):654-61.
Lee Gettler, a PhD candidate in our program, is a collaborator on many of these studies and is helping take the lead on the next generation of psychobiological work at Cebu.
Fetal nutrition as a cue of matrilineal nutritional history: transgenerational 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:
On a related and exciting note, Elizabeth Quinn, a PhD candidate in our program, recently finished her dissertation focusing on the determinants of breast milk composition in this cohort and will be joining Washington University, St Louis as an Assistant Professor in the Fall.
Epigenetics and the race concept. 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.
Kuzawa CW, Sweet E (2009), “Epigenetics and the embodiment of race: developmental origins of US racial disparities in cardiovascular health”. Amer J Hum Biol. 21(1): 2-15.
Kuzawa CW, Thayer, Z, "Toppling typologies: Developmental plasticity and the environmental origins of human biological variation" (For School for Advanced Research volume on Race and Biology)
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.
McDade TW, Rutherford J, Adair LS, Kuzawa CW (2010),“Early origins of inflammation: Infectious exposures in infancy predict lower levels of C-reactive protein in adulthood” Proceedings of the Royal Society B 277(1684): 1129-37.
Duazo P, Avila J, Kuzawa CW (2010), “Breastfeeding and later psychosocial development in the Philippines”. Am J Hum Biol. 22(6):725-30.
Kuzawa, CW, and LS Adair (2003), “Lipid profiles in an adolescent Filipino population: relationship to birth weight and maternal energy status during pregnancy”, Amer J Clin Nutr, 77: 960-66.
Adair, LS, CW Kuzawa and J Borja
energy stores and diet composition during pregnancy program adolescent blood
pressure” Circulation, 104(9)1034-9.
Dan Eisenberg, a PhD candidate in our program, is using the lifetime of data in the Cebu cohort to gain insights into developmental influences on leukocyte telomere lengths at Cebu.
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.
Kuzawa CW (2010), “Beyond feast-famine: brain evolution, human life history and the metabolic syndrome”, In Evolutionary Anthropology, M Muehlenbein (ed), Cambridge University Press. pp. 518-527.
Kuzawa CW, Gluckman PD, Hanson MA, Beedle A (2008), “Evolution, developmental plasticity, and metabolic disease”, In Evolution in Health and Disease (2nd Edition), SC Stearns and JC Koella (eds). Oxford University Press. pp. 253-264.
Kuzawa CW (2008), “The developmental origins of adult health: intergenerational inertia in adaptation and disease” In Evolution and Health, W Trevathan, EO Smith and JJ McKenna (eds). Oxford University Press. pp. 325-349.
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.
Sterner KN, Chugani, HT, Tarca AL, Sherwood CC, Hof PR, Kuzawa CW, Boddy AM, Raaum RL, Weckle A, Gregoire L, Lipovich L, Grossman LI, Uddin M, Goodman M, Wildman DE. "Ontogenetic transcriptome changes in human brain energetics and adaptive plasticity" (in review)
Kuzawa CW (2010), “Beyond feast-famine: brain evolution, human life history and the metabolic syndrome”, In Evolutionary Anthropology, M Muehlenbein (ed), Cambridge University Press. Pp. 518-527.
Leonard WR, Robertson ML, Snodgrass JJ, Kuzawa CW (2003). “Metabolic correlates of hominid brain evolution.” Comp Biochem Physiol A Mol Integr Physiol. 136(1):5-15.
Kuzawa, CW (1998), “Adipose tissue in human infancy and childhood: an evolutionary perspective.” Yearbook of Physical Anthropology, 41: 177-209.
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.
Eisenberg DTA, Salpea KD, Kuzawa CW, Hayes MG, Humphries SE (2011), "Substantial variation in qPCR measured mean blood telomere lengths in young men from eleven European countries". Amer J Hum Biol. 23(2):228-31.
Eisenberg DT, Kuzawa CW, Hayes MG (2010), “Worldwide allele frequencies of the human apolipoprotein E (APOE) gene: climate, local adaptations and evolutionary history”, American Journal of Physical Anthropology. 143(1):100-11.
Teslovich TM, Musunuru K, Smith AV...Kuzawa CW...Kathiresan K (2010). “Biological, clinical, and population relevance of 95 loci mapped for serum lipid concentrations”, Nature, 466, 707-713.
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.