A couple of weeks ago, I covered a study on aging that gave us a glimpse into one possible reason energy production in our cells tends to decrease as we get older. The answer was found in our mitochondria, the power supply of our cells. As a particular protein level declines, it may be leading to mitochondrial burnout and, therefore, the effects of aging.
Now, a new study out just this past week, suggests another contributor to the effects of aging may be the decrease of a molecule that occurs naturally in our cells called nicotinamide mononucleotide (NMN) due to chronic inflammation as we age. The obvious question is, is this process inevitable, or are there things we can do to combat chronic inflammation?
NMN is a precursor of nicotinamide adenine dinucleotide (NAD). As we age, NAD levels decline, causing lowered energy levels, slowed metabolism, and many other issues. NMN boosts the production of NAD, and this not only keeps our mitochondria healthy but other physiological processes, such as eye function, immune function, body weight, and much more, benefit from it. NMN is found naturally in many foods, such as broccoli, avocado, and tomatoes, though it would be difficult to eat enough of these to fully replenish the declining NMN levels seen in the aging body.
In the new study, researchers looked at three groups of mice over a period of one year. The first group was given NMN in high doses. The second group was given NMN in small doses. And the third group was the control group, meaning it was not given NMN. They quickly discovered that the NMN entered the bloodstream within minutes of consumption (supplemented via the drinking water) where it converted to NAD. The researchers looked at many different physiologic functions of each mouse every three months. The findings in the older mice were remarkable as shown below:
The study states, “Remarkably, NMN effectively mitigates the age-associated physiological decline in mice…These effects of NMN highlight the preventive and therapeutic potential of NAD+ intermediates [referring to the NMN in this case] as effective anti-aging interventions in humans.” So in all of these physiologic functions, which are associated with aging, the older mice in the NMN group remained healthier and physiologically younger than their control-group counterparts. And the researchers believe there is the potential for a similar impact on humans, so human studies are sure to follow.
So what causes this decrease in NMN and, therefore, NAD? Is it a hardwired effect of aging? One of the scientists involved in the study thinks that the increase in inflammation that happens with aging reduces the body’s ability to make NMN and, by extension, NAD. Inflammation seems to be the common denominator in so many health-related issues today. And now we’re seeing signs that chronic inflammation may be affecting our bodies all the way down to the mitochondrial level in our cells and, therefore, speeding up the effects of aging.
Listed below are ways to combat chronic inflammation, and keeping inflammation at bay may help us continue to produce higher and healthier levels of NMN as we age.
The upshot? We continue to see studies on aging that lead back to the health of the mitochondria in our cells. Whether it’s a decline in a protein, such as carbonic anhydrase, or a molecule, such as NMN, our mitochondria can’t be the energy powerhouses they are designed to be when they are losing fuel. One way we may be able to conserve this mitochondria fuel and stop intentionally contributing to the effects of our aging is to combat chronic inflammation. So clean up your lifestyle to prevent running out of cell fuel!
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About the Author
Christopher J. Centeno, M.D. is an international expert and specialist in regenerative medicine and the clinical use of mesenchymal stem cells in orthopedics. He is board certified in physical medicine as well as rehabilitation and in pain management through The American Board of Physical Medicine and Rehabilitation.…