Is This the Key to Managing Sarcopenia?

Sarcopenia is recognized as an issue related to the aging process and/or immobility.

From Wikipedia, here is a description of sarcopenia:

Sarcopenia is a type of muscle loss (muscle atrophy) that occurs with aging and/or immobility. It is characterized by the degenerative loss of skeletal muscle mass, quality, and strength. The rate of muscle loss is dependent on exercise level, co-morbidities, nutrition and other factors. The muscle loss is related to changes in muscle synthesis signalling pathways. It is distinct from cachexia, in which muscle is degraded through cytokine-mediated degradation, although both conditions may co-exist. Sarcopenia is considered a component of frailty syndrome.[1] Sarcopenia can lead to reduced quality of life, falls, fracture, and disability.[2][3] Obviously, remaining active as we age is a key cornerstone to optimal health however there are additional factors at play which can be modified to help to maintain muscle mass and strength/power.

In a paper published in the journal Nature Aging, it suggests that maintaining optimal NAD+ levels can be a significant factor in maintaining metabolic and physical function.

NAD+ levels decrease precipitously as we age: by the age of 50, it is down 50% and by the age of 80 it is down 90 – 96% so it is essentially gone.

One of the key functions of NAD+ is to activate the Sirtuin Longevity Genes which as the name implies are critical to healthy aging.

If these genes are not activated, it accelerates vascular aging.


If you have not yet experienced the wonders and benefits of NAD+ optimization by consuming our Pricera NAD+ precursor formulation, reach out to me.

Following is the abstract:


Healthy aging and muscle function are positively associated with NAD+ abundance in humans

Nature Aging volume 2, pages 254–263 (2022)

Abstract

Skeletal muscle is greatly affected by aging, resulting in a loss of metabolic and physical function. However, the underlying molecular processes and how (lack of) physical activity is involved in age-related metabolic decline in muscle function in humans is largely unknown.

Here, we compared, in a cross-sectional study, the muscle metabolome from young to older adults, whereby the older adults were exercise trained, had normal physical activity levels or were physically impaired. Nicotinamide adenine dinucleotide (NAD+) was one of the most prominent metabolites that was lower in older adults, in line with preclinical models.

This lower level was even more pronounced in impaired older individuals, and conversely, exercise-trained older individuals had NAD+ levels that were more similar to those found in younger individuals. NAD+ abundance positively correlated with average number of steps per day and mitochondrial and muscle functioning. Our work suggests that a clear association exists between NAD+ and health status in human aging.

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