Natural Products Insider

SEP-OCT 2017

INSIDER is the leading information source for marketers, manufacturers and formulators of dietary supplements, healthy foods and cosmeceuticals. Since 1997, INSIDER has been serving the needs of the global nutrition industry.

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Page 108 of 160

100 INSIDER September/October 2017 SupplySide West In human beings, as in nature, there is a beautiful and complex array of diversity. Just like no two people are identical in physical appearance, neither are they precisely alike on a molecular level. Even the most mundane and essential processes are subject to slight individualized nuances. Your suspicion that somehow every carb you eat goes to your hips—while your best friend seemingly indulges with impunity—is not your imagination. We now know some people process carbohydrates differently than others, and these differences can be advantageous or deleterious. When it comes to DNA, a single nucleotide polymorphism (SNP) or change occurs in nearly one in 1,000 base pairs and accounts for much of an individual's uniqueness. Research on SNPs and other genetic variations such as deletions, inversions, duplications and copy number variations (CNV), which represent up to 9.5 percent of the human genome, have changed the face of human nutrition and validated that nutrition could and should be personalized. (Blood. 2007;109:1355-1362.) Our diet and genes interact. Our genes are not as intransigent—nor our diets as inert—as we once believed. It is a radical concept that a lifestyle factor like nutrition may be the primary environmental infl uencer on human health over a lifespan. Nutrigenetics, or personalized nutrition, delineates how the metabolic outcome of what we put in our mouths may be different for each person. These variations elucidate how one person might be impacted by a particular dietary intervention, while another is not. Polymorphisms explain why monitoring carbohydrates is the critical factor for some, and fat for others. It also offers an explanation for confounding data in large cohorts and other studies on vitamin use, weight loss, lipid metabolism, chronic disease development and longevity. Polymorphic populations (those with high genetic or epigenetic variability) in clinical trials may generate mixed data that doesn't necessarily mean an intervention won't work in a more targeted group. Future population selection for these studies will be based upon the nutrient-gene paradigm of each subject helping to standardize results with a higher level of reproducibility. Nutrigenomics is the umbrella encompassing epigenetics, proteomics and metabolomics. It explains how dietary factors can reprogram our genetic activity by changing which genes get turned on and off, their frequency, productivity and effi ciency of expression. New science is revealing how these changes can be imprinted over a lifetime, and even passed to future generations. Besides ameliorating gene expression, the eventual outcome of a gene can be mediated by how the resulting proteins are folded, where they are delivered, the timing of production, and with what corroborating elements they are complexed or metabolized into. Nutrient availability can modulate all of these factors. Altering how our genes are expressed can override our original genetic code. The potential exists to devise nutritional interventions for "bad" genes, just as our lifestyle choices may ruin "good" genes. The implication is nutritional choices alone can make sick people well, and healthy people sick. Certainly, prenatal and early childhood nutrition can exert a fundamental and long-lasting positive or negative impact. The development of many chronic diseases can be traced back to early epigenetic modifi cations in response to environmental stimuli during these formative life stages. Most of us make our dietary choices using less scientifi c rigor. Food is a sensory and cultural experience that is signifi cantly impacted by our genes. We are motivated to choose our food by taste, sight, smell, expense, emotion and expediency, as well as by the delicate signaling of our body denoting hunger and satiety. We eat when we are not hungry, not knowing that routinely ignoring our body's cues can cause long-term alterations in genetic expression in these metabolic pathways and modify the ability to provide "normal" signals in the future. The propensity to neglect important feedback from our body can be programmed—for better or worse— back into our genetic make-up through epigenetic adaptations, and possibly even passed to our children. Dietary choices are not the only exogenous factors that may impact genetic integrity and expression. Our genes are exposed to both deliberate and random concomitant factors, such as ultraviolet (UV) light exposure, pollution, smoking, stress, infection, drugs and exercise. The science of nutrigenetics and nutrigenomics is evolving. While initially very promising, even exciting, more randomized clinical trials are needed that demonstrate a health outcome for nutritional interventions based upon addressing a single genetic variation. The majority of SNPs and CNVs have not yet crossed the clinical standard demonstrating the link between better nutritional advice specifi c to genetic aberrations and mitigating disease. A major impediment for advancing this kind of nutritional research has been the limitations inherent in accurately assessing dietary intake. For studies that monitor what might be small, but meaningful changes, nutrigenomics needs to cultivate correspondingly sensitive biomarkers for validating food intake. The Science of Personalized Nutrition by Jennifer Cooper Learn more about the science of personalized nutrition from Jennifer Cooper during the "Making Personalized Nutrition a Reality" Panel Discussion on Thursday, Sept. 28 at 9 a.m. at SupplySide West in Las Vegas. The session is underwritten by Aker BioMarine. Scan Here Personalized Nutrition at SupplySide West

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