Description

NAD+ (Nicotinamide Adenine Dinucleotide) – Product Information

What is NAD+?

Nicotinamide adenine dinucleotide (NAD) is a coenzyme that regulates several metabolic pathways, including glycolysis, -oxidation, and oxidative phosphorylation.

NAD also functions as a substrate for poly(ADP-ribose) polymerase (PARP), sirtuin, and NAD glycohydrolase, as well as regulating DNA repair, gene expression, energy metabolism, and stress responses. Many studies have shown that NAD metabolism plays an important role in aging and aging-related diseases.[R]

There is no good scientific evidence to support the use of NADH for chronic fatigue syndrome (CFS), high blood pressure, high cholesterol, athletic performance, depression, Parkinson’s disease, and many other conditions. [R]

NAD+
CAS Number	53-84-9
Molar Mass	663.43 g/mol
Chemical Formula	C21H27N7O14P2
IUPAC Name	[[(2R,3S,4R,5R)-5-(6-aminopurin-9-yl)-3,4-dihydroxyoxolan-2-yl]methoxy-oxidophosphoryl] [(2R,3S,4R,5R)-5-(3-carbamoylpyridin-1-ium-1-yl)-3,4-dihydroxyoxolan-2-yl]methyl phosphate

 

How does NAD+ work?

In the human body, there are two major NAD+ synthesis pathways: de novo synthesis and salvage from precursors. The kynurenine pathway is used in the de novo synthesis of NAD+, which converts tryptophan to quinolinic acid (QA). The recovery of nicotinamide mononucleotide (NMN), nicotinamide riboside (NR), nicotinamide (NAM), and nicotinic acid is the main salvage pathway (NA).

To maintain a certain level of NAD+ in the body, the salvage pathways produce the majority of NAD+, rather than de novo synthesis.[R]

Nicotinamide adenine dinucleotide (NAD+) is a coenzyme for redox processes, making it crucial to energy metabolism. The non-redox NAD+-dependent enzymes sirtuins, CD38, and poly(ADP-ribose) polymerases all require NAD+ as a cofactor. NAD+ can, directly and indirectly, regulate several essential biological activities.

NAD+ Research

Numerous animal and human studies have been conducted on the potential application of NAD+. Following are some of the relevant findings:

NAD+ on Anti-aging

As many people search for an anti-aging tip, a study found that Niacinamide adenine dinucleotide (NAD+) levels fall as we age, and this can cause cell damage and potentially shorten life spans. In numerous crucial biological pathways, NAD+ functions as an enzyme cofactor and as a substrate for a number of regulatory proteins.

Numerous studies have revealed that increasing the levels of NAD+ in tissues or cells can slow the aging process. Clinical studies on the security and effectiveness of NAD+ have been done.[R]

There is evidence that NAD+ precursor supplementation or NAD+ degradation inhibition may enhance metabolic activity. Supplementation with NAD+ precursors has been shown to slow down the aging process in mice. To date, NAD+’s anti-aging properties have not yet been proven in humans.[R]

NAD+ on Neurodegenerative Conditions

Several articles mentioned that NAD+ depletion has been observed in both normal and accelerated aging. Neurodegeneration is seen in several accelerated aging diseases, including ataxia telangiectasia (AT), xeroderma pigmentosum group A (XPA), and Cockayne syndrome (CS).

Given the significance of NAD+ depletion in neurodegeneration, several NAD+ augmentation strategies (including treatment with NAD+ precursors NR or NMN, or both with a PARP1 inhibitor or a SIRT1 activator) increased life expectancy and longevity in accelerated aging animal models [R]

NAD+ precursors have been used to protect severed axons from degeneration [R].

Further studies are needed to evaluate the long-term safety and efficacy of NAD+ on neurodegenerative conditions.

NAD+ on Hearing Loss

Noise causes a decrease in cochlear NAD+ levels, and NAD+ augmentation restores noise-induced neurite retraction from inner hair cells, implying that NAD+ levels are critical for proper cochlear function. Indeed, in a premature aging disease model associated with dramatic hearing loss, NAD+ supplementation improves synaptic connectivity in the cochlea and prevents the progression of hearing loss.

The effect of long-term NAD+ supplementation on age-related hearing loss has, however,  not been tested using a direct NAD+ precursor. [R]

Further study in the future is therefore recommended.

NAD+ on Muscle Wasting

The authors believe that NAD+ repletion could be a successful treatment for a variety of muscle-wasting diseases. NAD+ levels were restored in mice or worms with disease-like degenerating muscles, which improved muscle function as a result of more mitochondria, more muscle structural proteins, and a decrease in inflammation. [R]

NAD+ on Cancer

Inhibiting the NAD+ salvage pathway has been shown to be very effective in killing cancer cells both in vitro and in vivo. Reduced NAD+ levels in cancer cells impair energy metabolism and production, as well as increase Reactive Oxygen Species production.

Energy depletion and increased Reactive Oxygen Species cause changes in cell signals, resulting in decreased proliferation and an increase in autophagy and apoptosis, which leads to cell death. [R]

The knowledge of using NAD+ for human use needs further study since the articles focused on animal models and a few clinical trials. The critical role NAD+ has in metabolism and cellular health has opened up the possibility of targeting it to kill off cancerous cells.

NAD+ on Chronic Fatigue Syndrome

Chronic fatigue syndrome (CFS) is a disorder of unknown etiology, consisting of prolonged, debilitating fatigue, and a multitude of symptoms including neurocognitive dysfunction, flu-like symptoms, myalgia, weakness, arthralgia, low-grade fever, sore throat, headache, sleep disturbances, and swelling and tenderness of lymph nodes.

No effective treatment for CFS is known. The study included 26 eligible patients who met the Centers for Disease Control and Prevention’s criteria for CFS.

The findings of this pilot study suggest that NADH may be a turntable for finding adjunctive therapy in the management of chronic fatigue syndrome and that additional clinical trials be conducted to establish its efficacy in this clinically perplexing disorder.[R]

NAD+ on Opioid and Alcohol Withdrawal

Some speakers at a summit connected the use of NAD+ in patient treatment with substance use disorders. An IV Nicotinamide Adenine Dinucleotide (NAD) was done for acute withdrawal symptoms caused by chronic opioid use and alcohol consumption. According to the data, it significantly reduces the symptoms of acute withdrawal. Studies are being conducted to validate this data in order to standardize and validate the protocol.[R]

NAD+ on Antidepressant-like effect

NAD+ cosubstrate for energy transfer in oxidative phosphorylation, is said to be beneficial in CNS-related diseases. In the forced swim test (FST), Wistar rats were tested to assess the acute effects of NADH and its precursor nicotinamide in comparison to controls and the antidepressants desipramine and fluoxetine. With a minimal effective dose of 5 mg/kg, NADH, but not nicotinamide, promoted swimming behavior in the FST. [R]

NAD+ on Covid-19

Numerous lines of epidemiological and mechanistic data suggest a connection between NAD+ metabolism and infections with SARS-CoV-2 and other viruses. To better comprehend its mechanical function and value as a target of intervention, more research is necessary.[R]

NAD+ Side Effects

There were no reports of common NAD+ side effects in research subjects. [R]

FAQs

Is NAD+ safe?

In addition to a lack of consistent evidence of direct benefits, the potential long-term effects of NAD+ are also unknown. Purerawz sells NAD+ for research purposes only.

NAD+ amplifiers – How do subjects acquire more NAD+? [R]

• Pharmacologically boosting NAD+
• Supplementation of its precursors, NR and NMN, or inhibition of its subjects by the use of CD38 and PARPs inhibitors.

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