Emerging research indicates that nutritional components that target specific mechanisms associated with age-associated cellular decline (AACD) hold promise for improving the health and well-being of adults.
"Cellular Nutrition and Its Influence on Age-Associated Cellular Decline," the latest issue of The Gerontological Society of America’s What's Hot newsletter with accompanying infographic, provides an overview of current research regarding evidence regarding the influence of nutritional components on health and aging.
"Declining mitochondrial health is increasingly being recognized as a common mediator of declining function and development of chronic diseases associated with aging," noted Nathan K. LeBrasseur, PT, PhD, FGSA, a member of the newsletter’s content development faculty who is professor and co-chair of research at the Department of Physical Medicine and Rehabilitation and co-director of the Paul F. Glenn Center for Biology of Aging Research at the Mayo Clinic. "This report describes contributions of mitochondria to cellular functions and homeostasis and reviews emerging evidence regarding how nutritional components can influence these functions."
Mitochondria are commonly known as the powerhouses of cells and are responsible for the production of cellular energy. They also regulate cellular metabolism, apoptosis (programmed cell death), signaling by producing reactive oxygen species (ROS). ROS are highly reactive molecules derived from oxygen that are key to many biochemical reactions; however, when present in excess, they can result in molecular damage. Mitochondria also have their own DNA (mtDNA) that encode for 13 proteins that are components of the respiratory chain and can develop mutations as a result of oxidative stress.
Declines in mitochondrial function and metabolism are among the key components of AACD. Evidence suggests that changes associated with AACD act as triggers for age-associated diseases and conditions.
"Because abnormalities in the function of mitochondria are associated with many diseases, including cancer, cardiovascular diseases, and neurodegenerative diseases, drivers of mitochondrial dysfunction are promising targets for addressing multiple age-related conditions," said Roger A. Fielding, PhD, FGSA, a member of the newsletter’s content development faculty who is associate director of the Jean Mayer USDA Human Nutrition Research Center on Aging and professor of medicine at the Tufts University School of Medicine.
Adoption of healthful eating patterns and exercise has been shown to improve markers of age-associated diseases and attenuate biological aging.
"Calorie restriction appears to improve markers of disease risk in humans, but its acceptability and feasibility particularly over the long term remains a challenge," said LeBrasseur. "Dietary supplementation with nutritional components that target specific mechanisms associated with AACD may be an alternative or complementary approach to lifestyle interventions targeting AACD."
Further, identifying AACD risk factors and intervening with cellular nutrients earlier in the aging process, before major mobility disabilities and disease-driven limitations emerge, could help improve overall healthy aging.
Emerging research indicates that some nutritional compounds can support healthy aging by influencing mitochondrial repair and preservation, quality control, and signaling. Examples of emerging compounds that have been shown to address mitochondrial damage and clinical disease states include SS peptides, coenzyme Q10 (CoQ10), MitoQ, and glycine and N-acetylcysteine (GlyNAC). Compounds that may address mitochondrial quality control include sirtuins, mitochondrial division inhibitor (mdivi), urolithin A, and epicatechin. Finally, nutritional compounds that have been shown to address mitochondrial signaling include nicotinamide riboside and nicotinamide mononucleotide. Dietary supplementation with these components may be an alternative approach to lifestyle interventions targeting AACD, although more research is needed before making definitive recommendations.
Article originally found on The Gerontological Society of America website.