Ten putative contributors to the obesity epidemic.
ABSTRACT 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.
Full-textDOI: · Available from: Douglas Ruden, Jun 29, 2015
- SourceAvailable from: Polina Panchenko[Show abstract] [Hide abstract]
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.Journal of Experimental Biology 01/2015; 218(Pt 1):50-58. DOI:10.1242/jeb.110320 · 3.00 Impact Factor
- [Show abstract] [Hide abstract]
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.Environmental Pollution 08/2014; 195C:9-15. DOI:10.1016/j.envpol.2014.08.003 · 3.90 Impact Factor
- [Show abstract] [Hide abstract]
ABSTRACT: Maternal obesity has adverse effects on oocyte quality, embryo development and it also affects the health of the offspring. To understand the underlying mechanisms responsible for these negative effects, we investigated the DNA methylation status of several imprinted genes and metabolism-related genes. A high-fat-diet (HFD)-induced mouse model was utilized to analyze the DNA methylation of several imprinted genes and of metabolism-related genes in oocytes from obese mice and in oocytes and liver from their offspring by employing combined bisulfite restriction analysis (COBRA) and bisulfite sequencing (BS). The DNA methylation of imprinted genes in oocytes was not altered in both obese mothers and their offspring, while DNA methylation of metabolism-related genes was changed. The DNA methylation level in the promoter of Leptin was significantly increased and that in the promoter of Ppar-alpha (Ppar-α) was reduced in oocytes of obese mice. The increased methylation of Leptin and decreased methylation of Ppar-α was also observed in the liver of female offspring from obese mothers (OHFD). The mRNA expressions of Leptin and Ppar-α were significantly altered in the liver of offspring from obese mothers. In OHFD oocytes, the DNA methylation level in the promoter of Ppar-α was increased. These results indicate that DNA methylation patterns of several metabolism-related genes are not only changed in oocytes of obese mice, but also in oocytes and liver of their offspring. These data may contribute to elucidating the adverse effects of maternal obesity on reproduction and the offspring's health.Environmental Health Perspectives 12/2013; 122(2). DOI:10.1289/ehp.1307047 · 7.03 Impact Factor