NAD+ (Nicotinamide adenine dinucleotide) is a coenzyme found in all living cells and is involved in various metabolic processes, including energy production, DNA repair, and gene expression regulation. When NAD+ levels are low in the body, it can have several potential signs and symptoms, including:

❌ Fatigue: NAD+ plays a crucial role in cellular energy production, so low levels may lead to feelings of fatigue and low energy.

❌ Decreased cognitive function: NAD+ is involved in maintaining brain health and cognitive function. Low levels may contribute to problems with memory, concentration, and mental clarity.

❌ Muscle weakness: NAD+ is essential for muscle function and repair. Low levels may result in muscle weakness, decreased exercise performance, and slower recovery after physical activity.

❌ Accelerated aging: NAD+ is involved in DNA repair mechanisms and plays a role in protecting cells from oxidative stress and damage. Low levels may contribute to accelerated aging processes, including wrinkles, reduced skin elasticity, and age-related diseases.

❌ Metabolic dysfunction: NAD+ is involved in regulating various metabolic processes, including glucose and lipid metabolism. Low levels may contribute to metabolic disorders such as insulin resistance, diabetes, and obesity.

❌ Mood disturbances: NAD+ has been linked to neurotransmitter regulation and mood stabilization. Low levels may contribute to mood swings, anxiety, and depression.

It's essential to note that these signs and symptoms can be indicative of various health conditions, and low NAD+ levels may not always be the primary cause. If you suspect you have low NAD+ levels or are experiencing any of these symptoms, it's important to consult with a healthcare professional for proper evaluation and diagnosis.

In numerous mouse models of disease and aging, NMN has demonstrated a wide array of remarkable effects, benefitting conditions ranging from diabetes to Alzheimer’s disease to ischemia.

Orally administered NMN is quickly synthesized into NAD+ in tissues in mice. NMN has been able to suppress age-associated weight gain, enhance energy metabolism and physical activity, improve insulin sensitivity, improve eye function, improve mitochondrial metabolism and prevent age-linked changes in gene expression. In mice bred to be diabetic or obese, NMN improved both the action and secretion of insulin.

NMN also protected the mouse heart from ischemia and/or reperfusion injury. It has restored skeletal muscle in aged mice, and slowed cognitive decline in a mouse model of Alzheimer’s disease, by improving the survival of neurons, improving energy metabolism, and reducing reactive oxygen species. It may help maintain the integrity of the blood brain barrier. NMN is likely a good candidate to suppress inflammaging—the increase in inflammation associated with aging—since studies show it lowers adipose tissue inflammation associated with age. In fact, older mice appear to be more responsive to NMN, in comparison with young mice.

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7238909/

To investigate the impact of NMN on weight, Bhasin and colleagues administered two daily doses of 1,000 mg of NMN to middle-aged and older overweight or obese adults for 28 days. This led to more than a 6 lb. decrease in body weight when compared to participants who did not receive NMN for 28 days. This finding suggests that NMN supplementation promotes metabolic benefits, as evidenced by a substantial indicator of metabolic health, namely body weight.

To investigate the impact of NMN on weight, Bhasin and colleagues administered two daily doses of 1,000 mg of NMN to middle-aged and older overweight or obese adults for 28 days. This led to more than a 6 lb. decrease in body weight when compared to participants who did not receive NMN for 28 days. This finding suggests that NMN supplementation promotes metabolic benefits, as evidenced by a substantial indicator of metabolic health, namely body weight.

https://academic.oup.com/jcem/advance-article-abstract/doi/10.1210/clinem/dgad027/7027634?redirectedFrom=fulltext&login=false