NAD+ is a very important coenzyme in the redox reaction of organisms and plays a vital role in various biological processes including metabolism, aging, cell death, DNA repair and gene expression. However, as we age, the homeostatic balance of NAD+ is disrupted, resulting in a significant decrease in its content.
If you want to "lock time", you need to accurately control the on/off key of NAD+ decline.
On February 17, Li Xiang's team from the Institute of Brain Cognition and Brain Diseases of the Shenzhen Institutes of Advanced Technology, Chinese Academy of Sciences published an online paper titled Nicotine rebalances NAD+ homeostasis and improves aging-related symptoms in male in the journal Nature Communications. The article of mice by enhancing NAMPT activity reveals the mechanism of chronic low-dose nicotine improving energy metabolism and delaying systemic aging by activating the NAD+ rescue pathway.
With increasing age, the activity of the rate-limiting enzyme of the NAD+ salvage pathway: nicotinamide phosphoribosyltransferase NAMPT gradually decreases, and the activity of NAMPT depends on the degree of its deacetylation by SIRT1. Similarly, as age increases, the binding of SIRT1 to NAMPT weakens, and the acetylation level of NAMPT gradually increases.
In order to explore the regulatory effect of nicotine on NAD+, the research team divided 48 experimental mice into two groups and conducted a one-year controlled experiment. The mice in the experimental group drank 2 micrograms (μg)/ml of nicotine water every day, while the mice in the control group did not receive any intervention. After the 12-month experiment, the mice in the experimental group had undergone "tremendous" changes.
The team found that when the experiment reached 10 months, the difference between the two groups of mice gradually became apparent: the mice that consumed nicotine not only performed more "lively" every day, but their reaction speed was also better than that of the control group. After 12 months of feeding, the survival rate of mice in the experimental group was as high as 91.67%, while the survival rate of the control group was only 54.17%. That is, chronic low-dose nicotine intake reduced the mortality rate of mice by 40%. The experiment also found that under nicotine intervention, the surviving mice in the experimental group had better memory and reduced Alzheimer's-related indicators; the telomeres in their muscles and hearts were lengthened, which further confirmed that The anti-aging effects of nicotine.
Mouse experimental results confirmed that nicotine can promote the interaction between SIRT1 and NAMPT, reduce the acetylation level of NAMPT, enhance the activity of NAMPT, improve the energy metabolism of aging tissues, and increase the content of β-NMN and NAD+. That is, chronic low-dose nicotine can improve metabolism and delay aging.
So, is this equivalent to the fact that the human body can also achieve anti-aging purposes through nicotine intake?
Before drawing this conclusion, we must focus on marking the three key factors of "low dose", "drinking" and "non-addictive state", which are indispensable conditions for determining the success of nicotine anti-aging experiments.
First, low doses. The nicotine dose that achieved a positive anti-aging effect in mice in this study was 2 μg/ml, while the nicotine content in cigarettes was 1,000 μg, which was more than 500 times the amount consumed by the experimental mice. If directly compared with the amount converted from our experimental dose to the human body, the nicotine content in smoking would be more than 100,000 times
Secondly, drinking intake. This experiment uses drinking water, because after slow absorption in the gastrointestinal tract and rapid metabolism in the liver, the nicotine content in the blood of mice is as low as only 0.25ng/g. When humans smoke, nicotine can be quickly absorbed through small airways and alveoli, and reaches the brain in a few seconds. At this time, the concentration of nicotine in the brain plasma can reach up to 100ng/ml, which is 400 times the blood nicotine concentration of the mice in this study.
Finally, the non-addictive state. The researchers further looked at the status of nicotinic acetylcholine receptors in the mouse brains and found that the receptors were not activated at this dose of nicotine. This means that the mice's bodies enjoyed the health-improving effects of nicotine, but did not develop addiction or dependence. For smokers, nicotine, as an addictive substance, causes the brain to continuously secrete dopamine and becomes dependent on it.
From these three points, it is almost impossible to rely on smoking to consume nicotine to resist aging.
Although the anti-aging experimental results of nicotine have been verified on mice, this is only an animal experiment that remains at the basic level of research. To confirm the conclusion that low-dose nicotine can delay human aging, a series of issues and mechanisms have yet to be clinically verified.
From mice to humans, from laboratory to clinic, nicotine still has a long way to go as a "longevity drug". Of course, we have reason to believe that one day in the future it will break through the clinical boundaries of the human body and become one of the powerful tools against aging.