Fall CH. Evidence for the intra-uterine programming of adiposity in later life. Ann Hum Biol. 2011;38(4):410-28

MRC Lifecourse Epidemiology Unit, University of Southampton, Southampton General Hospital, Southampton, UK.
Annals of Human Biology (Impact Factor: 1.15). 07/2011; 38(4):410-28. DOI: 10.3109/03014460.2011.592513
Source: PubMed

ABSTRACT AIM: Research in animals has shown that altering foetal nutrition by under-nourishing or over-nourishing the mother or rendering her diabetic or foetal exposure to glucocorticoids and toxins can programme obesity in later life. The increased adiposity is mediated by permanent changes in appetite, food choices, physical activity and energy metabolism. In humans, increased adiposity has been shown in people who experienced foetal under-nutrition due to maternal famine or over-nutrition due to maternal diabetes. Lower birth weight (a proxy for foetal under-nutrition) is associated with a reduced adult lean mass and increased intra-abdominal fat. Higher birth-weight caused by maternal diabetes is associated with increased total fat mass and obesity in later life. There is growing evidence that maternal obesity, without diabetes, is also a risk factor for obesity in the child, due to foetal over-nutrition effects. Maternal smoking is associated with an increased risk of obesity in the children, although a causal link has not been proven. Other foetal exposures associated with increased adiposity in animals include glucocorticoids and endocrine disruptors. CONCLUSIONS: Reversing the current obesity epidemic will require greater attention to, and better understanding of, these inter-generational (mother-offspring) factors that programme body composition during early development.

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    • "More than 60% of all adults are classified as overweight or obese in most westernized societies, and as the prevalence of obesity increases it is responsible for an ever larger proportion of the overall burden of disease (Nguyen and El-Serag 2010; Ng et al. 2014). It has been well documented that maternal obesity predisposes offspring to obesity, independently of genetic inheritance (Fall 2011), thus providing the potential for intergenerational amplification of obesity and its comorbidities (Dunn and Bale 2009, 2011). Rodent models of diet-induced obesity with or without altered glucose homeostasis in the father have also been shown to impair the metabolic and reproductive health of both male and female offspring via nongenetic pathways (Ng et al. 2010; Fullston et al. 2012, 2013). "
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    ABSTRACT: Obesity and related comorbidities are becoming increasingly prevalent globally. In mice preconception paternal exposure to a high fat diet (HFD) impairs the metabolic and reproductive health of male offspring, despite their control diet (CD) consumption. However, offspring share lifestyle, including diet, with parents. We assessed if male offspring from HFD fathers have a heightened susceptibility to HFD-induced metabolic and reproductive derangements. This 2 × 2 design saw founder males (F0) and their offspring (F1) fed either a HFD or a nutritionally matched CD. Regardless of paternal diet, HFD fed male offspring had greater total body weight and adiposity. Offspring sired by a HFD male and fed a HFD were the heaviest, had the greatest adiposity and had the greatest concentration of serum cholesterol, triglyceride, HDL, and NEFA compared with CD sired/fed littermates. A synergistic increase in serum insulin was unmasked by both father/son HFD consumption, concomitant with increased sera glucose. Either a paternal or offspring HFD was associated with similar reductions to offspring sperm motility. Whereas sperm ROS concentrations and sperm-oocyte binding saw detrimental effects of both F0 HFD and F1 HFD with an interaction evident between both, culminating in the most impaired sperm parameters in this group. This indicates that metabolic and fertility disturbances in male offspring sired by HFD fathers are exacerbated by a "second-hit" of exposure to the same obesogenic environment postnatally. If translatable to human health, this suggests that adverse reproductive and metabolic outcomes may be amplified across generations through a shared calorie dense diet, relevant to the current worldwide obesity epidemic. © 2015 The Authors. Physiological Reports published by Wiley Periodicals, Inc. on behalf of the American Physiological Society and The Physiological Society.
    03/2015; 3(3). DOI:10.14814/phy2.12336
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    • "A J-shape relationship was observed between birthweight and adult BMI. Both undernutrition and overnutrition could be risk factors for adult obesity (Fall 2011 "
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    ABSTRACT: Concerns about the increasing rates of obesity in developing countries have led many policy makers to question the impacts of maternal and early child nutrition on risk of later obesity. The purposes of the review are to summarise the studies on the associations between nutrition during pregnancy and infant feeding practices with later obesity from childhood through adulthood and to identify potential ways for preventing obesity in developing countries. As few studies were identified in developing countries, key studies in developed countries were included in the review. Poor prenatal dietary intakes of energy, protein and micronutrients were shown to be associated with increased risk of adult obesity in offspring. Female offspring seem to be more vulnerable than male offspring when their mothers receive insufficient energy during pregnancy. By influencing birthweight, optimal prenatal nutrition might reduce the risk of obesity in adults. While normal birthweights (2500-3999 g) were associated with higher body mass index (BMI) as adults, they generally were associated with higher fat-free mass and lower fat mass compared with low birthweights (<2500 g). Low birthweight was associated with higher risk of metabolic syndrome and central obesity in adults. Breastfeeding and timely introduction of complementary foods were shown to protect against obesity later in life in observational studies. High-protein intake during early childhood however was associated with higher body fat mass and obesity in adulthood. In developed countries, increased weight gain during the first 2 years of life was associated with a higher BMI in adulthood. However, recent studies in developing countries showed that higher BMI was more related to greater lean body mass than fat mass. It appears that increased length at 2 years of age was positively associated with height, weight and fat-free mass, and was only weakly associated with fat mass. The protective associations between breastfeeding and obesity may differ in developing countries compared to developed countries because many studies in developed countries used formula feeding as a control. Future research on the relationship between breastfeeding, timely introduction of complementary feeding or rapid weight gain and obesity are warranted in developing countries. The focus of interventions to reduce risk of obesity in later life in developing countries could include: improving maternal nutritional status during pregnancy to reduce low birthweight; enhancing breastfeeding (including durations of exclusive and total breastfeeding); timely introduction of high-quality complementary foods (containing micronutrients and essential fats) but not excessive in protein; further evidence is needed to understand the extent of weight gain and length gain during early childhood are related to body composition in later life.
    Maternal and Child Nutrition 01/2013; 9 Suppl 1(Suppl 1):105-19. DOI:10.1111/mcn.12010 · 2.97 Impact Factor
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    • "In both cases, ''catch up'' weight gain in these children can be exacerbated by the high-calorie, high-fat dietary consumption patterns seen in much of contemporary U.S. society. Finally, researchers have given much attention to the role of maternal obesity as a risk factor for childhood and consequently adult obesity (Fall, 2011). Given the relatively high birthrates among immigrant Hispanic women (Pew Hispanic Center, 2011), the risk of obesity is perpetuated in each successive generation of Hispanic Americans. "
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    ABSTRACT: The prevalence of obesity and obesity-related illnesses is higher among Hispanics (Latinos) than other racial and ethnic groups, and rates increase exponentially with the number of years living in the United States. Mounting evidence suggests that the origins of many chronic illnesses among disadvantaged minority groups may lie with cumulative exposure to chronic psychological and physiological stressors through the biobehavioral process of allostatic load (AL). Among immigrant Latinos, acculturation stress may contribute to an increase in AL and thus may be an independent risk factor for the development of obesity and obesogenic illnesses. The purpose of this theoretical article is to present a proposed model of the effects of acculturation stress on AL and obesity among Latino immigrants. Such a model can be useful to guide intervention efforts to decrease obesity among immigrant Latinos by adding education, skill building, and social integration strategies to healthy eating and physical activity to reduce the deleterious impact of acculturation stress.
    Biological Research for Nursing 08/2012; 14(4):364-74. DOI:10.1177/1099800412457017 · 1.34 Impact Factor
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