*Under certain circumstances and in some individuals, diet can be a serious risk factor for a number of diseases.
*Common nutrients can act on the human genome, either directly or indirectly, to alter gene expression or structure.
*The degree to which diet influences the balance between healthy and disease states may depend on an individual’s genetic makeup.
*Some diet-regulated genes (and their normal, common variants) are likely to play a role in the onset, incidence, progression, and/or severity of chronic diseases.
*Dietary intervention based on knowledge of nutritional requirement, nutritional status, and genotype (i.e personalized nutrition) can be used to prevent, ameliorate or cure chronic disease.
Nutrigenomics as a branch of Nutrition
The promise of nutritional genomics is personalized medicine and health based upon an understanding of our nutritional needs, nutritional and health status, and our genotype. Nutrigenomics will also have impacts on society from medicine to agricultural and dietary practices to social and public policies and its applications are likely to exceed that of even the human genome project. Chronic diseases (and some types of cancer) may be preventable, or at least delayed, by balanced, sensible diets. Knowledge gained from comparing diet/gene interactions in different populations may provide information needed to address the larger problem of epidemics and malnutrition.
Nutrition and genes:
Personalised nutrition hinges on a two-way relationship between nutrients and genes. On the one hand, the nutrients we consume can affect the way our genes are expressed; on the other, our genes are able to influence how our bodies respond and utilize to nutrients.
The goal for nutrigenomic scientists is to unravel this complex interaction so that tailored diets can be developed which complement a person’s unique genetic profile. Not only will this optimise the health of the individual, but it may also work on a larger scale to help prevent society-wide diseases such as obesity, Type 2 diabetes, cardiovascular disease, cancer, and malnutrition.
A perfect example of genetically predisposed disease is inflammatory bowel disease (or IBM). Inflammatory bowel disease refers to both ulcerative colitis and Crohn’s disease, two inflammatory disorders of the gastrointestinal tract. Inflammatory bowel disease has a complex aetiology; a genetically determined susceptibility interacting with environmental factors, including nutrients and gut microbiota.
Diet and Exercise:
Exercise modulates genes involved in energy metabolism, insulin response and inflammation. Dietary nutrients modulate the same genes. Both can stimulate BDNF (Brain-derived Neurotrophic Factor). Together, they bring energy provision to the brain, improving neuronal function and brain plasticity. It’s a synergistic relationship — they work in tandem, not alone. For instance, combining exercise with a DHA-enriched diet enhances cognitive function; coupled with a flavonoid-rich diet, it protects the brain from inflammation and cell death. Even with a diet rich in saturated fats, exercise can reduce the decline in brain plasticity induced by a poor diet.
While there’s on-going research on food, cooking and diets, our bodies remain hard-wired to environmental changes that once predicted our survival or extinction. Poor dietary and exercise lifestyle affects us deeply. And this “gene” gets passed down from generation to generation. So that old saying “you are what you eat” may need rephrasing. Perhaps, “You are what your father’s ate” is more fitting. The better informed we are about our food choices, the better we can preserve not only our own health, but that of future generations.
A large number of different dietary approaches have been studied in an attempt to achieve healthy, sustainable weight loss among individuals with overweight and obesity. Restriction of energy intake is the primary method of producing a negative energy balance leading to weight loss. However, owing to the different metabolic roles of proteins, carbohydrates and lipids in energy homeostasis, diets of similar overall energy content but with different macronutrient distribution can differentially affect metabolism, appetite and thermogenesis. Evidence increasingly suggests that the fuel values of calories provided by distinct macronutrients should be considered separately, as metabolism of specific molecular components generates differences in energy yield. The causes of variation in individual responses to various diets are currently under debate, and some evidence suggests that differences are associated with specific genotypes. Recent research suggests there are roles played by the macronutrient composition of food on weight management. There are indications that personalized nutrition is a wholesome package consisting of interactions of macronutrient intake and genetic background and its potential influence on dietary intervention strategies.
Martinez, J. A. Body-weight regulation: causes of obesity. Proc. Nutr. Soc. 59, 337–345 (2000).
Galgani, J. & Ravussin, E. Energy metabolism, fuel selection and body weight regulation. Int. J. Obes. (Lond.) 32, S109–S119 (2008).
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