Significant and relatively recent changes in dietary habits and other lifestyle conditions, for example, the introduction of processed foods and the sedentary nature of modern transportation, have been too rapid for the human genome to adjust, and it is believed that such unhealthy changes in nutritional, cultural, and activity patterns may underlie many of the “chronic diseases of Western civilization” (). In contrast, most chronic diseases, including coronary heart disease and type 2 diabetes, can be avoided or attenuated by healthy dietary lifestyles that are consistent with the traditional Mediterranean diet (; ; ). This diet includes high ratios of mono-unsaturated to saturated fats and omega-3 to omega-6 fatty acids, plus an ample supply of fruits, vegetables, legumes, and whole grains ()—that is, foods rich in antioxidant and anti-inflammatory nutrients.
The complex interplay of nutrition and environmental pollutants in disease risk is influenced not only by nutrients that can modulate environmental insults but also by food that can serve as a source of healthy nutrients as well as contaminants. Furthermore, recent findings indicate that obesogens, in addition to a diet-induced positive energy balance, may contribute to obesity and associated health problems (; ). Obesogens are environ-mental chemicals that might synergize with specific nutrients to accelerate metabolic dysfunctions or to interfere with mechanisms that regulate adipocyte number and energy balance, thus leading to compromised health associated with obesity ().
Although nutritional interventions (e.g., anti-oxidants) have been shown to be of benefit in animal studies, the robustness of the results is sometimes diminished in human inter-vention studies (). However, this fact does not invalidate the overall benefit of healthy nutrition; more research is needed to understand the human variability associated with such results. It is recognized that for a given individual the impact of a particular nutrient will vary with the amount consumed. Such variability is influenced by multiple factors including an individual’s genome (e.g., polymorphisms). Thus, genomics should not be overlooked in public health policy (; ). Furthermore, an important but largely unexplored issue is the combined epigenetic effects of nutrition and pollutants and their implications in risk assessment and human health. Future research in nutrigenetics and nutrigenomics is likely to yield individualized nutritional inter-vention plans that will allow risk assessments to directly incorporate such variability. Given this probability, it is important that we begin to consider the possible implications of such developments in the context of risk assessment and nutritional intervention.
Many persistent environmental pollutants, including polychlorinated biphenyls (PCBs), brominated flame retardants, and organometallic compounds, can accumulate in the body. In addition, these persistent organic pollutants can generate free radicals, which in turn can trigger proinflammatory signaling pathways and associated inflammatory diseases, including atherosclerosis, diabetes, and hypertension (; ; ). B.H.’s laboratory has conducted extensive research over the years to study the effects of PCBs on the early pathology of atherosclerosis, with a particular focus on vascular endothelial cell function. These studies have shown that an increase in cellular oxidative stress and an imbalance in antioxidant status are critical events in PCB-mediated induction of inflammatory genes and endothelial cell dysfunction (reviewed by ). The research team also found that specific dietary fats can further compromise endothelial dysfunction induced by selected PCBs by further adding to a cellular oxidative and inflammatory insult. Importantly, study data suggest that antioxidant nutrients, such as vitamin E and dietary flavonoids, as well as a high ratio of omega-3 to omega-6 fatty acids, can protect against endothelial cell damage mediated by these persistent organic pollutants (; ; ). Recent data further suggest that membrane lipid rafts such as caveolae may play a major role in the regulation of PCB-induced inflammatory signaling in endothelial cells, as well as in protective mechanisms of dietary-derived polyphenols such as quercetin and the green tea catechin epigallocatechin-gallate (; ). These studies provide strong evidence that healthy nutrition can protect against proinflammatory environmental stressors. However, human studies are needed to confirm such therapeutic effects of protective nutrients. In the same context, it is important to be mindful that long-term effects of excessive antioxidant intake in the form of supplements have been questioned (; ). In addition, a multitude of bioactive food components occur in the food supply, and some of these bioactive constituents likely share the same molecular targets. Thus, continued research and a greater understanding of nutrition science will be needed to optimize any dietary intervention in order to reduce health risks associated with exposure to environmental pollutants. Evolving studies suggest that the interaction of toxicants and nutrients occurs throughout the body, and that the consequences of tissue damage by environmental pollutants can be significant. For example, a review of the National Health and Nutrition Examination Survey (NHANES) found that PCB, lead, and mercury exposures were associated with elevated blood levels of alanine aminotransferase (ALT), a marker for nonalcoholic fatty liver disease (). Interestingly, high-fructose diets also can induce non-alcoholic fatty livers or steatohepatitis, which was accompanied by a multi-fold increase in blood ALT levels (). Nonalcoholic steatohepatitis is usually associated with obesity, but it also has been reported in lean individuals exposed to industrial chemicals, such as vinyl chloride (). Taken together, these studies suggest that the involvement of similar and possibly additive liver pathologies can be induced by both environmental pollutants and certain dietary components.
Fenech M, El-Sohemy A, Cahill L, Ferguson LR, French TA, Tai ES, et al. 2011. Nutrigenetics and nutrigenomics: viewpoints on the current status and applications in nutrition research and practice. J Nutrigenet Nutrigenom 4(2):69–89.
Group Therapy Options : A 75 page in-depth research paper providing an overview of the current literature concerning breast cancer treatment and mental health.
To explore further the paradigm that nutrition can modulate toxicological insults, and to identify the potential implications of this paradigm for risk assessment of environmental pollutants and human health, the University of Kentucky Superfund Research Center invited experts from the fields of nutritional sciences, medicine, public health, and environmental toxicology, as well as scientists from the U.S. EPA National Center for Environmental Assessment, to participate in a workshop titled “Nutrition and Chemical Toxicity: Implications in Risk Assessment.” In a previous commentary (), we stated how nutrition can be used to modulate toxicological events associated with exposure to hazardous substances. Here we expand on this reasoning, and on a growing body of evidence supporting its validity, to explore new ways of incorporating nutrition within the paradigm of risk assessment. Thus, this recent meeting focused on nutrition as a modulator of environ-mental toxicity and on the need to consider nutrition (diet) as a component of risk assessment methodologies. Presentations highlighted studies that suggest that nutrition can be a potential modulator of diseases associated with exposure to environ-mental stressors. However, critical questions remain. For example, to what extent can health risks associated with exposure to environ-mental pollutants be reduced or improved through healthy nutrition? Can nutrition be a critical component in redefining methodologies used in risk assessment? That is, can nutrition (or dietary practices) be considered either a stressor or a buffer of cumulative risk from exposure to environmental pollutants?
We recruited men and postmenopausal women with a body-mass index (BMI, the weight in kilograms divided by the square of the height in meters) between 27 and 40 by means of newspaper advertisement. Smokers, persons with clinically significant illness, including diabetes, and those taking medications known to affect body weight were excluded. The study was approved by the Austin Health Human Research Ethics Committee, and all participants provided written informed consent.
This advanced-level,14 page research paper examines the conflicting views in the literature on the effects of prenatal exposure to drugs and reports on an early intervention project in a specific inner-city agency.
Conclusion: We recommend that nutrition and dietary practices be incorporated into future environmental research and the development of risk assessment paradigms. Healthful nutrition interventions might be a powerful approach to reduce disease risks associated with many environmental toxic insults and should be considered a variable within the context of cumulative risk assessment and, where appropriate, a potential tool for subsequent risk reduction.
Discussion: A convincing body of research indicates that nutrition is a modulator of vulnerability to environmental insults; thus, it is timely to consider nutrition as a vital component of human risk assessment. Nutrition may serve as either an agonist or an antagonist (e.g., high-fat foods or foods rich in antioxidants, respectively) of the health impacts associated with exposure to environmental pollutants. Dietary practices and food choices may help explain the large variability observed in human risk assessment.