Slowing the effects of the aging process is always a popular topic of conversation in health and scientific arenas. Recent research regarding aspects of the aging process shows a connection to cellular function. This research also delineates the importance of certain nutritional elements in association with cellular degeneration (AACD) due to aging and mitochondrial malfunctions.
Mitochondrial Function and Aging
Research-based evidence shows that AACD and abnormal cellular functions are catalysts for ailments and illnesses linked to aging. Along with this, declining mitochondrial processes and metabolism are among the main features of AACD.
The mitochondria are responsible for producing cellular fuel in the form of energy. This tiny organ also regulates metabolism at a cellular level, carries out cellular cessation (called apoptosis), and assembles reactive oxygen species (ROS). ROS molecules are essential to many internal biochemical processes and reactions. Yet when they are in overabundance, they can contribute to molecular impairment. Additionally, oxidative stress can lead to mutations in mitochondrial DNA or mtDNA, thus resulting in the miscoding of 13 essential proteins.
“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,” explains Roger A. Fielding, Ph.D., FGSA in a statement. Fielding is the associate director of Jean Mayer USDA Human Nutrition Research Center on Aging, and a professor of medicine at the Tufts University School of Medicine.
Study Results and Remedies for the Future
The report also explains how the effects of regular exercise and physical activity coupled with wholesome eating habits slow the biological aging process and contribute to less age-induced cellular decline. In addition, identifying AACD risk factors and intervening in cellular malfunctions early on improves overall health and prevents the onset of many age-related diseases.
“Calorie restriction appears to improve markers of disease risk in humans, but its acceptability and feasibility particularly over the long term remains a challenge,” says Nathan K. LeBrasseur, 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. “Dietary supplementation with nutritional components that target specific mechanisms associated with AACD may be an alternative or complementary approach to lifestyle interventions targeting AACD.”
Studies also find that certain supplements may aid in slowing cellular degeneration and AACD. Additional research and trials are needed before these supplements can be implemented as medical recommendations and treatments. However, the initial trial tests show that SS peptides, coenzyme Q10 (CoQ10), MitoQ, glycine, and N-acetylcysteine (GlyNAC) managed mitochondrial damage. Sirtuins, mitochondrial division inhibitor (MDiv), urolithin A, and epicatechin improve mitochondrial quality control. Lastly, nutritional compounds such as nicotinamide riboside and nicotinamide mononucleotide enhance mitochondrial signaling.
The hope is that the mixture of scientific evidence, manageable lifestyle adaptations, and possible nutritional compounds as supplementation will lessen the effects of cellular degeneration that comes with the aging process. This nourishing combination of therapies and preventions may allow more people to live longer, happier, and healthier lives.
This report is published in The Gerontological Society of America.