Ten Putative Contributors to the Obesity Epidemic

Department of Infections and Obesity, Pennington Biomedical Research Center, Louisiana State University System, Baton Rouge, LA, USA.
Critical reviews in food science and nutrition (Impact Factor: 5.18). 11/2009; 49(10):868-913. DOI: 10.1080/10408390903372599
Source: PubMed


The obesity epidemic is a global issue and shows no signs of abating, while the cause of this epidemic remains unclear. Marketing practices of energy-dense foods and institutionally-driven declines in physical activity are the alleged perpetrators for the epidemic, despite a lack of solid evidence to demonstrate their causal role. While both may contribute to obesity, we call attention to their unquestioned dominance in program funding and public efforts to reduce obesity, and propose several alternative putative contributors that would benefit from equal consideration and attention. Evidence for microorganisms, epigenetics, increasing maternal age, greater fecundity among people with higher adiposity, assortative mating, sleep debt, endocrine disruptors, pharmaceutical iatrogenesis, reduction in variability of ambient temperatures, and intrauterine and intergenerational effects as contributing factors to the obesity epidemic are reviewed herein. While the evidence is strong for some contributors such as pharmaceutical-induced weight gain, it is still emerging for other reviewed factors. Considering the role of such putative etiological factors of obesity may lead to comprehensive, cause specific, and effective strategies for prevention and treatment of this global epidemic.

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    • "Worryingly, the number of children classified as overweight or obese has increased 150% worldwide in this timeframe (Ng et al., 2014) and the rate of obesity in women of child-bearing age is still rising (Fisher et al., 2013). Whilst genetic factors that predispose to obesity in an obesogenic environment, have likely contributed to the current global obesity epidemic, the short timescale of this increase implicates non-genetic factors including the impact of the intrauterine and neonatal environment on adult health and disease (McAllister et al., 2009). It is vital that we understand the mechanisms underlying such developmental programming of disease by maternal obesity in order to develop effective interventions to help mitigate the current rise in obesity, cardiovascular and metabolic diseases as well as mental health disorders. "
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    ABSTRACT: Obesity in women of child-bearing age is a growing problem in developed and developing countries. Evidence from human studies indicates that maternal BMI correlates with offspring adiposity from an early age and predisposes to metabolic disease in later life. Thus the early life environment is an attractive target for intervention to improve public health. Animal models have been used to investigate the specific physiological outcomes and mechanisms of developmental programming that result from exposure to maternal obesity in utero. From this research, targeted intervention strategies can be designed. In this review we summarise recent progress in this field, with a focus on cardiometabolic disease and central control of appetite and behaviour. We highlight key factors that may mediate programming by maternal obesity, including leptin, insulin and ghrelin. Finally, we explore potential lifestyle and pharmacological interventions in humans and the current state of evidence from animal models. Copyright © 2015. Published by Elsevier Inc.
    No preview · Article · Jul 2015 · Hormones and Behavior
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    • "The recent and rapid worldwide increase in non-communicable diseases (NCDs) challenges the assumption that genetic factors are the primary contributors to such diseases (McAllister et al., 2009). The 'developmental origins of health and disease' (DOHaD) paradigm states that the environment during the periconception, gestation and lactation periods shapes the developing individuals, leading, in the case of a deleterious environment, to a predisposition to adult-onset diseases. "
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    ABSTRACT: The recent and rapid worldwide increase in non-communicable diseases challenges the assumption that genetic factors are the primary contributors to such diseases. A new concept of the 'developmental origins of health and disease' (DOHaD) is at stake and therefore requires a paradigm shift. Maternal obesity and malnutrition predispose offspring to develop metabolic syndrome, a vicious cycle leading to transmission to subsequent generation(s), with differences in response and susceptibility according to the sex of the individual. The placenta is a programming agent of adult health and disease. Adaptations of placental phenotype in response to maternal diet and metabolic status alter fetal nutrient supply. This implies important epigenetic changes that are, however, still poorly documented in DOHaD studies, particularly concerning overnutrition. The aim of this review is to discuss the emerging knowledge on the relationships between the effect of maternal nutrition or metabolic status on placental function and the risk of diseases later in life, with a specific focus on epigenetic mechanisms and sexual dimorphism. Explaining the sex-specific causal variables and how males versus females respond and adapt to environmental perturbations should help physicians and patients to anticipate disease susceptibility. © 2015. Published by The Company of Biologists Ltd.
    Full-text · Article · Jan 2015 · Journal of Experimental Biology
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    • "Obesity is usually recognized as the result of increased calorie intake and decreased energy expenditure, with a genetic contribution that has been estimated as 20e84% (Sharpe and Drake, 2013). However, there is increasing evidence that environmental factors play a major role in this condition (McAllister et al., 2009). It is well documented that adipose tissue is an endocrine organ that actively participates in the regulation of metabolism (Kershaw and Flier, 2004), and that the accumulation and mobilization of lipids in adipose tissue is highly influenced by hormonal signaling (Grun and Blumberg, 2009b). "
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    ABSTRACT: The aim of this research was to study the association of the accumulated human exposure to persistent organic pollutants with serum lipid levels and obesity, in a cohort of 298 adults. In the multivariable analyses, HCB concentrations evidenced a significant quadratic association with levels of total cholesterol, HDL, LDL, and total serum lipids. Likewise, PCBs 138 and 180 were associated with triglycerides and total serum lipids, and PCB 153 with LDL. HCB, p,p'-DDE, and β-HCH showed quadratic associations with BMI. All quadratic models showed a positive trend at low exposure levels, while the slope decreased or even became negative at higher exposure levels. Additionally, PCB 138 was positively associated with BMI but in a linear manner. Our results suggest a potential relationship between historical POP exposure and serum lipids/obesity, which followed a non-linear pattern in most cases.
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