Birth Size and Maternal Nutrition During Pregnancy Predict Blood Pressure in Filipino Adults

An adverse uterine environment is thought to program blood pressure (BP) later in life, most likely due to fetal under-nutrition. This study examines the relationships between adult systolic blood pressure (SBP) and diastolic blood pressure (DBP), birth weight, and maternal nutritional status and dietary intake during pregnancy. This study draws on a large sample (n=1632) of Filipino young adults aged 20-22 using data from the Cebu Longitudinal Health and Nutrition Survey (CLHNS), a community-based birth cohort study in Cebu City, Philippines begun in 1983. The baseline maternal survey was given at 30 ± 4 weeks gestation and the children were surveyed at birth and through childhood into adulthood. A series of linear regression models was used to examine the relationship between SBP and DBP to birth outcomes, maternal nutritional status during pregnancy as measured by triceps skin fold thickness, and dietary intake during pregnancy while controlling for socioeconomic status, age, height, BMI of the young adults, and other confounders. Birth weight was inversely related to SBP in males, and birth weight and length were inversely related to DBP in males. Maternal triceps skin fold thickness was inversely related to SBP and DBP in males and to DBP in females. Components of the mother’s diet during pregnancy had varying relationships with the young adult BP of male and female offspring. Maternal nutritional status and dietary intake during pregnancy have implications for offspring’s BP regulation later in life. 1 Journal of Undergraduate anthropology Introduction Cardiovascular disease (CVD) is the leading cause of morbidity and mortality worldwide. In the Philippines, CVD caused 27% of all deaths in 2002 (WHO 2005). The risk factors for CVD in adulthood have been widely studied. They include high blood pressure, smoking, lack of physical activity, age, and stress (National Heart Lung and Blood Institute, 2009). More recently, studies have been examining causes of CVD that emerge during early development. These studies attempt to explain whether an individual’s susceptibility to chronic disease later in life can be “programmed” by early life experiences, specifically those in utero. It is hypothesized that the intrauterine nutritional environment affects fetal growth, which influences the expression of cardiovascular disease later in life. Thus far, study results have been inconsistent in that they have found direct, inverse, or no relationship between birth weight or birth length and CVD. Studies examining the relationships between maternal nutrition status during pregnancy, maternal dietary intake during pregnancy, and CVD in adulthood have not gathered consistent results either. Therefore, the programming of CVD is still debatable. In this study, we use data from the Cebu Longitudinal Health and Nutrition Survey (CLHNS). We aim to examine the relationship between size at birth and systolic blood pressure (SBP) and diastolic blood pressure (DBP) in Filipino young adults, before and after taking into account maternal nutritional status and dietary intake during pregnancy, using BP as a measure of risk for CVD. This comprehensive, longitudinal data allows us to examine the long-term effects and relationships between health, culture, and behavior. Few studies have examined human maternal dietary intake during pregnancy and its effects on long-term health. Lastly, very few longitudinal studies have taken place in countries undergoing the nutrition transition, where changing dietary intake is changing the development of chronic disease. Using the CLHNS data, 2 Journal of Undergraduate anthropology we will test the hypothesis that birth weight, maternal dietary intake, and maternal nutritional status during pregnancy predict adult offspring blood pressure. DOHaD Developmental Origins of Health and Disease (DOHaD) is a model that explains how CVD and early life experiences, such as birth outcomes, maternal dietary intake and nutritional status during pregnancy, could be related. Much research has shown that early life events that determine susceptibility to disease in adulthood do not occur specifically in untero during the period of fetal development, but can also occur throughout the period of developmental plasticity. The word “developmental” rather than “fetal” encompasses both the fetal period and the period of infancy. Secondly, DOHaD incorporates ideas about disease, and also about health (Gluckman and Hanson, 2006). DOHaD can be used in public health and health education programs and presents a new way of thinking about how early life events affect adult health and disease. Programming can be defined as the “permanent or long-term change to the physiology, morphology, or metabolism of a fetus in response to a specific insult or stimulus at a critical period in development” (Langley-Evans et al. 1998). Thus, events early in life, such as nutritional deficiency in utero, play a strong role in impacting susceptibility to the metabolic syndrome which leads to chronic, non-communicable diseases later in life including non insulindependent diabetes mellitus, coronary heart disease, and hypertension (Harding, 2001; Philips 1998; Barker and Martyn, 1992; Kuzawa 2004). For example, cardiovascular disease could be the outcome of short-term fetal physiological adjustments to under-nutrition that are crucial to survival, but have harmful effects in life post-reproduction (Godfrey and Barker 2001). 3 Journal of Undergraduate anthropology Programming of tissues and organs occurs during a “critical period” during development when physiological changes can become fixed. During this time, fetuses are “plastic” and are subject to environmental influences (Godfrey and Barker 2001). The critical period occurs at various stages throughout embryonic and fetal development with different organs and tissues developing during different critical periods (Symonds et al. 2006). Several ideas in relation to life history theory can explain the relationship between early life events and the development of disease in adulthood. These include the thrifty phenotype, predictive adaptive response, environmental mismatch, or developmental programming. All of these theories claim that fetuses receive signals from their environment, and adapt to their environment, which will help them better cope with environmental stressors later in life (Silveira et al. 2007). In particular, adapted fetuses will be better prepared to cope with the stressors that the mother encountered during her pregnancy about which the “signal” is conveyed to the fetus. However, if the postnatal environment differs from the predicted environment, the adaptation can actually be harmful and there is increased risk of disease. For example, low birth weight babies who are born into an affluent environment are at a higher risk for coronary heart disease, hypertension, and type 2 diabetes (Bateson et al. 2004). This possibly occurs because their bodies have been programmed metabolically for a low resource environment but they experience nutritional abundance. Much animal model data and human epidemiological data support DOHaD, however, the exact biological mechanisms are not yet fully understood. Recently, epigenetic mechanisms to explain DOHaD have come into view. Epigenetics is the study of heritable changes in DNA caused by reasons other than alterations in the DNA sequence. These changes include histone modification, DNA methylation, and DNA-binding proteins. The epigenetic hypothesis for the 4 Journal of Undergraduate anthropology development of disease states that early environmental stressors and influences trigger epigenetic changes, which affect chronic disease risk. For example, DNA hypoand hypermethylation has been implicated early in atherogenesis, the formation of plaques that leads to CVD (Waterland and Michels 2007). Birth Weight and Maternal Nutrition and Diet During Pregnancy Nutrition is a major programming stimulus and the mechanisms by which maternal underor over-nutrition lead to low birth weight may contribute to understandings of DOHaD. Maternal under-nutrition could result from low intake of nutrients due to restricted food access or famine. Inadequate or improper maternal nutrition leads to intrauterine growth retardation (IUGR), which manifests as thinness and decreased birth length and weight, which lead to increased BP later in life. However, a distinction must be made between maternal nutrition and fetal nutrition, which is the total supply of metabolic substrates to the fetus (Harding 2001). According to Harding, fetal growth is at the end of a chain of events including maternal diet, maternal metabolic and endocrine status, placenta transport, umbilical blood flow, and finally fetal uptake. If the chain of events has a large margin of error, changes in maternal diet may not influence fetal growth strongly (Harding 2001). Hence, the fetus may be buffered from maternal environment. Few studies have been conducted in humans using measures of maternal nutrition or maternal dietary intake to test the idea that nutrition is a programming stimulus. Animal studies have shown that decreasing protein intake during pregnancy leads to reduced birth weight and increased blood pressure later in life (Langley-Evans et al. 1998). Laura et al. used maternal anthropometric variables (pre-pregnancy weight and BMI) and weight at the end of the pregnancy as a measure of maternal nutrition to show that these variables have positive 5 Journal of Undergraduate anthropology associations with SBP and DBP in male and female adolescents in a developing country (Laura et al. 2010). Adair et al. found that higher SBP and DBP in adolescent boys are associated with low maternal fat stores at around 30 weeks gestation. Further, SBP in adolescent boys was inversely related to the percent of the mother’s energy intake from protein during late gestation and SBP and DBP were inversely relate