The Impact of Maternal Nutrition and its Effects on Offspring Obesity
Obesity is a global epidemic which is associated with many life threatening diseases. Obesity is having a major impact on human morbidity, mortality, quality of life and is placing a large strain on healthcare. In recent years, there has been growing evidence from epidemiological studies and animal models that suggest that the origins of obesity are not solely from the interaction between genes and traditional adult risk factors (diet and inactivity), but also the effects of maternal nutrition. Maternal nutrition prior to conception, during pregnancy, and lactation affects the subsequent risk of obesity through the alterations of mechanisms mediating the development of obesity (such as adipocyte metabolism, appetite control, physical activity and food preference).
There has been a growing body of evidence that has illustrated that the origins of obesity may lie in prenatal development. Exposure to an inappropriately high or low level of nutrition in prenatal development may lead to obesity later in life due to alterations in the mechanisms that regulate body weight and energy intake. One of the landmark studies on early life under nutrition (including prenatal life) and the subsequent risk of obesity came from victims of the 1944-45 Dutch famine. 50 year old women who were exposed to the Dutch famine in early gestation had higher BMI’s and were more likely to be obese (BMI + waist circumference) than non-exposed women (Ravelli et. al). The majority of studies on the effects of maternal nutrition on later life look at animal models. Experimental studies in animals (Budge et al. 2005 as reviewed by Taylor et. al 2007) support the notion that during specific stages of gestation, maternal under nutrition may programme adipocyte metabolism and fat mass which may give rise to obesity when coupled with a hypernutritional diet postnatally. (Bispham et al. 2005; Budge et al. 2005 as reviewed by Taylor et. al 2007). Maternal overnutrition has also been suggested to result in programming effects on the offspring which increase the risk of obesity in later life. Overfeeding in the pre-weaning period of baboons increases adiposity in females in adulthood (Lewis et al. 1986 as reviewed by Drake et al. 2010). Not only does maternal nutrition during pregnancy and lactation influence the risk of obesity in later life, recent evidence suggest that maternal nutrition during preconception may also play a role. Studies on lab rats suggest that maternal preconceptional nutrition can have important influences on offspring body composition and digestive system, which increase the risk of obesity (Mortensen et. al as reviewed by PubMed). The macronutrient composition of the maternal diet also indicated programmed effects on the offspring which increases their predisposition to an obese phenotype. Rats who’s maternal nutritional histories consisted of a high fat diet were consistently larger and had greater fat mass then control groups (measured at post weaning), independent of their diet postnatally. (Howie et. al 2009).
The brain is the central component regulating appetite and food preferences. Recent research suggests that the brain structures and associated neurotransmitters involved in the regulation of appetite and food preference are acutely sensitive to the intrauterine environment (along with the food environment immediately after birth). The fetus does not have the same opportunity to respond to alterations in nutrient supply by altering nutrient intake as it receives its nutrition from the maternal circulation (Hay et. al 2004 as reviewed by Mühlhäusler et. al 2008). The system which regulates appetite in postnatal life is responsive to the signals of nutritional status (glucose and insulin) prenatally. Plagemann and his colleagues (1999) have convincingly demonstrated that there are substantial changes in the development of the hypothalamic architecture (which regulates hunger among other things) in rodents exposed to prenatal or postnatal overnutrition (as reviewed by Mühlhäusler et. al 2008). Leptin is a protein that acts as a hormone on the hypothalamus to increase energy expenditure and decrease appetite (regulate energy balance). There is considerable evidence that leptin may play an important role in energy balance regulation before birth as well and that leptin may be important in the structural development of appetitive structures (Bouret et. al as reviewed by Mühlhäusler et. al 2008). Not only are the neural structures associated with appetite altered by maternal nutrition, but there also appears to be altered physical activity due to maternal nutrition. Vickers and colleagues (2000, 2003) illustrated in animal studies that severe maternal undernutrition in pregnancy followed by a richer nutritional environment postnatally results in offspring with programmed overeating (hyperphagia), as well as reduced locomotor activity and profound obesity (as reviewed by Taylor et. al 2007). Another factor which appears to be influenced by maternal nutrition is the programming of food preferences. Highly palatable foods (high fat and/or sugar) may lead to overeating and rapid weight gain to a greater extent then other foods. In a study of rats, the offspring of dams fed a junk food (highly palatable foods including donuts, cakes and potato chips) diet during pregnancy and lactation consumed significantly more junk food than the control offspring. This suggest that maternal consumption of junk food during pregnancy programs a preference for junk food in the offspring (Bayol et. al 2007 as reviewed by Mühlhäusler et. al 2008).
The effects of preconception maternal nutrition as seen in the study above by Mortensen and colleagues may be explained by possible epigenetic changes that occur over the mother’s lifetime which have altered the expression of certain genes for mechanisms that regulate energy balance. An explanation proposed by Hales and Barker in 1992 helps explain the link between the fetal intra-uterine environment and the susceptibility to chronic diseases later in life. If a malnourished fetus is born into an environment of adequate or overnutrition, the offspring becomes more susceptible to chronic diseases such as diabetes and obesity due to the permanent fetal adaptations made in relation to the malnourished environment in-utero. This is known as the thrifty phenotype hypothesis (Hales and Barker 1992 as reviewed by Martin-Gronert and Ozanne 2006). Gluckman and Hanson proposed the “predictive adaptive response” hypothesis which asserts that the developing fetus predicts the postnatal nutritional environment that it will encounter by assessing its current nutritional environment and tries to adapt to give itself the best chance of survival (Gluckman and Hanson 2004 as reviewed by Martin-Gronert et. al 2006).
Maternal undernutrion and overnutrition, and the macronutrient make-up of maternal diets (preconception, during pregnancy, and lactation) have been shown to increase the risk of obesity in later life. This is due to the underlying mechanism which regulate energy balance which include the hypothalamus, insulin and leptin among others, which result in increased appetite and hyperphasia, and reduced locomotive activity. Possible explanations for the changes in these mechanisms are the thrifty phenotype hypothesis, the predictive adaptive response hypothesis and epigenetic changes. Through research evidence it is apparent that early life nutritional environment plays an important role in later life metabolic health. This Research has profound implications due to the social and economic burden of the obesity epidemic.
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