NAD+ Helps Restore Age-Related Muscle Deterioration by Dr. Joseph Mercola for Mercola
The tendency is to lose muscle as you age, a condition known as sarcopenia. If you don’t do anything to stop it you can expect to lose about 15% of your muscle mass between your 30s and your 80s.1 An estimated 10% to 25% of seniors under the age of 70 have sarcopenia and as many as half those over the age of 80 are impaired with it.2
Enforced bedrest, due to hospitalization, for example, can also have a dramatic impact on your muscle mass, even if you’re younger. According to a 2015 review3 in Extreme Physiology & Medicine, you can lose 5.2% of your muscle mass in the first two weeks of bedrest. By Day 23, you can have lost up to 10% of your quadriceps muscle mass.
Not only are strong muscles a requirement for mobility, balance and the ability to live independently, but having reserve muscle mass will also increase your chances of survival4 when sick or hospitalized. Since muscle is lost far more easily and quicker than it’s built, finding ways to continuously promote and maintain your muscle mass is of utmost importance.
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The Crucial Role of NAD+
As reported by Science Daily,5 scientists recently discovered that Alzheimer’s-like protein aggregates underlie the muscle deterioration commonly seen in aging, and that nicotinamide adenine dinucleotide (NAD+) is essential for combating this condition.
Their study,6 published in the journal Cell Reports, showed that protein aggregates (amyloid) could be blocked by boosting the levels of NAD+, a biomolecule that is also essential for maintaining mitochondrial function.
Higher levels of NAD+ were found to turn on the defense systems of the mitochondria and restore muscle function. Aggregated proteins have long been thought to be a contributor to brain aging, and this study proves aggregated proteins also contribute to muscle aging.
“The most prominent component of these protein aggregates is beta-amyloid, just like in the amyloid plaques in the brains of patients with Alzheimer’s disease,” said Johan Auwerx at EPFL’s School of Life Sciences. “These abnormal proteotoxic aggregates could serve as novel biomarkers for the aging process, beyond the brain and muscle.”
The study points out that NAD+ homeostasis is required to maintain proteostasis, i.e., the regulation of protein creation, folding, trafficking and degradation. It turns out that boosting NAD+ in later life will reduce amyloidosis (the buildup of amyloid) and mitochondrial dysfunction.
The importance of NAD+ for healthy muscle function is also reviewed in “Sarcopenia and Muscle Aging: A Brief Overview,”7 published in the journal Endocrinology and Metabolism. The paper highlights:
“… recent findings that describe key pathophysiological phenotypes of this condition, including alterations in muscle fiber types, mitochondrial function, nicotinamide adenine dinucleotide (NAD+) metabolism, myokines, and gut microbiota, in aged muscle compared to young muscle or healthy aged muscle.”
As indicated by the Cell Report study, this Endocrinology and Metabolism paper highlights the connection between sarcopenia and mitochondrial dysfunction in both skeletal muscle and motor neurons.
People with sarcopenia have been found to have both reduced mitochondrial oxidative capacity and inhibited NAD+ biosynthesis, and several studies have proposed that mitochondrial dysfunction in your neurons actually drive the development of sarcopenia.8
