Nutrigenomics offers a personalized medicine, using nutrient, dietary, and lifestyle interventions to mitigate adverse biochemical pathways. Here is an example of a nutrigenomic intervention that allows the practitioner to restore a muscle-building environment: Some statin medications used to treat heritably elevated cholesterol may deplete mitochondrial enzyme function and coenzyme Q10, which results in mitochondrial energy uncoupling, oxidative stress and subsequent cell death.38,39 The use of coenzyme Q10 supplements has been suggested to improve mitochondrial function in muscle and reduce myopathic pain in patients who have adverse response to statins.40-43 This intervention utilizes coenzyme Q10 as a conditionally essential nutrient to replete a critical biomolecule necessary for proper mitochondrial function. This is an example of personalizing the nutrient intake for the specific gene-environment relationship of the patient.
Another application to direct patient care is the use of strategic nutrition to enhance insulin sensitivity. The stress response prompts the adrenal glands to release glucocorticoids. Chronic stress results in chronic elevations in cortisol and eventually abdominal fat and insulin resistance.38,44 The resulting visceral obesity increases the production of inflammatory mediators such as TNF-a and IL-6. Patients caught in this cycle of inflammation and adiposity may need a clinician's help to reverse the unfavorable environment. Nutritional interventions such as improved-quality carbohydrates, vitamin D, magnesium, and chromium, each discussed in later chapters, can improve insulin sensitivity and, eventually, phenotypic expression.
Hormones that deliver anabolic messages may be repleted as part of premature aging. As Dr. Teitelbaum suggests, in the chapter on fibromyalgia, laboratory tests should be evaluated within the personalized context of the individual patient and can be used to optimal levels within age-specific parameters.
Strategic nutrition and an exercise prescription, such as those elaborated in later chapters, can measurably improve the early markers of disease and, eventually, phenotypic expression. Hackman and colleagues evaluated modestly overweight women who were placed on a medical food intervention program, along with a regular walking regimen. After following this program for several weeks, phosphorus 31 NMR spectroscopy revealed that the women had significantly improved body composition, lowered body fat and increased fat-free mass (muscle mass gain), as well as increased mitochondrial bioenergetics.45 The program resulted in preservation of muscle energy function, loss of fat mass, and preservation of lean muscle mass. A companion study used the same nutritional supplement that is high in soy protein with phytonutrients, vitamins, and minerals in another group of modestly overweight women. This program resulted in a reduction in blood cholesterol, increased muscle mass, and lowered body fat. This study compared the nutritional supplement to an over-the-counter weight-loss product. Although the two programs resulted in the same weight loss over 12 weeks, most of the weight lost using the commercially available, over-the-counter product came as muscle loss and not as fat loss. The nutrient-dense, phytonutrient-rich product, in contrast, resulted not only in the loss of weight as fat, but also in a reduction in blood cholesterol.46
Evans and his colleagues have developed an approach for managing sar-copenic obesity through regular strength and aerobic conditioning exercise. A controlled trial found that strength training improved functional capacity and muscle physiology, and reduced sarcopenia in 90-year-old men.47 Physiology research has demonstrated that properly prescribed and implemented resistance training increases the production of anabolic hormone messengers and reduces inflammatory mediators.
Sarcopenia is partly a consequence of mitochondrial uncoupling that results from oxidative stress after exposure to proinflammatory mediators, such as TNF-a, IL-6, and NFkB. Nutritional intervention using a diet augmented with nutrients that help lower the inflammatory potential and support redox function at the mitochondrial level may be important in managing these conditions. Redox-active nutrients include vitamin E, selenium, lipoic acid, coenzyme Q10,
N-acetylcysteine, and N-acetylcarnitine. Dr. Richard Weindruch, from the University of Wisconsin, proposed that interventions based on the possibility that oxidative stress contributes to sarcopenia may prove useful in managing patients with inflammation-induced muscle loss.48
Sarcopenia is related to the altered functional capacity of the individual. The symptoms in those with sarcopenic obesity are weakness, fatigue, depression, immune hypersensitivity, and inflammation. Altered aerobic capacity, altered immunological function, and altered hormone levels are commonly associated with increased inflammatory signaling associated with changes in diet, activity patterns, and lifestyle.49 Reversing dietary, activity, and lifestyle factors varies from individual to individual. Addressing them needs to be a personalized form of medicine.
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