Alternative names: NAD, Coenzyme I, or by the older name Diphosphopyridine Nucleotide Reduced, or DPNH.
NADH (nicotinamide adenine dinucleotide hydrogen) is a natural substance found in most life forms and is necessary for energy production. NADH is synthesized by the body and thus is not an essential nutrient. It does, however, require the essential nutrient nicotinamide for its synthesis, and its role in energy production is certainly an essential one.
The action of supplemental NADH is unclear. Its fans claim that it alleviates fatigue, fights jet lag, enhances mental clarity, and lifts depression.
NADH is typically supplied in the form of 2.5mg or 5mg tablets. The most common brand name is "Enada", which is stabilized and enteric-coated, thus preventing stomach acid from destroying the NADH before it enters the bloodstream.
NADH is the body's most potent antioxidant, but any comments on the mechanism of action are speculative. NADH is a redox active substance and participates in biologic energy production. However, how the known roles of endogenous NADH relate to any possible action of supplemental NADH is not known.
Speculation on how it works: NADH is the coenzyme form of vitamin B3, and you'll find it in every cell in your body. The more active the cell, the more NADH it has. Heart cells, for example, have plenty. And they wouldn't need any additional help from you if it weren't for the fact that NADH gets depleted over time. Once a cell has less than it needs, everything slows down – the very definition of aging. And the body doesn't make additional NADH, so to replenish your supply you have to turn to an outside source.
There is preliminary evidence suggesting that NADH might be useful in Parkinson's disease, chronic fatigue syndrome, Alzheimer's disease and cardiovascular disease.
Reports that NADH may stimulate endogenous dopamine biosynthesis have led to its experimental use in Parkinson's disease. Some favorable results have been reported in case studies and open-label trials using both intravenous and oral NADH. In one study of 885 subjects with Parkinson's disease, half received oral NADH and half received parenteral NADH with similar results. Some 80% of patients were said to have benefited clinically, with 19.3% showing good improvement, 58.8% moderate improvement and 21.8% not responding. Younger patients and those with the shortest duration of disease showed the most improvement.
Only one very small double-blind study (with five Parkinson's patients) has been conducted as at the time of writing. This was a short-term study which found no benefit from NADH. More research is needed to determine the therapeutic role, if any, of NADH in Parkinson's disease.
Hope that NADH might be helpful in treating Chronic Fatigue Syndrome was raised by a double-blind, placebo-controlled cross-over study of 26 patients. In the first phase of the study, subjects were randomly assigned to receive either 10mg of NADH or a placebo for four weeks. After a four-week washout period, subjects were assigned to the alternate regimen for the final four-week trial period. Among the NADH-treated patients, 31% were judged to have notable improvement, while 8% of controls were similarly improved.
Results of a FDA-approved study conducted at Georgetown University Medical Center in Washington, DC, indicated that a nutritional supplement called NADH may be a valuable adjunctive therapy in the management of chronic fatigue and immune dysfunction syndrome (CFIDS). These research findings were presented at the November 9, 1997 meeting of the American College of Allergy, Asthma and Immunology in San Diego. The positive nature of these findings also suggests that more and larger clinical trials be performed to further establish NADH's efficacy.
In another pilot study, 17 patients with dementia associated with Alzheimer's disease were treated with NADH for eight to 12 weeks. Researchers reported improvement in cognitive function in all 17 patients in this open-label trial, but they cautioned that "a double-blind, placebo-controlled study is necessary to demonstrate the clinical efficacy of NADH."
Yet another study sought to see whether oral NADH might lower blood pressure and affect lipids in a hypertensive animal model. This was a blinded, placebo-controlled, 10-week study. Systolic blood pressure was the same in the treated and placebo groups over the first month but thereafter was significantly reduced in the NADH group. Total cholesterol and LDL cholesterol were significantly reduced in the NADH group. No significant differences were noted in blood levels of glucose, insulin, triglyceride or HDL cholesterol. More research is warranted to see whether NADH might be useful in cardiovascular disease.
Those who use NADH typically take either 5mg once daily or 5mg twice a day. Take it on an empty stomach, with at least eight ounces of water. Try this for four months, then take one month off.
There are a few reports of gastrointestinal side effects, including nausea and loss of appetite. There are no reported drug, nutritional supplement, food or herb interactions.
Because of lack of long-term safety studies, NADH should be avoided by children, pregnant women and nursing mothers.
Because of its potential to stimulate endogenous L- DOPA synthesis, 17 patients in one study with symptoms ranging from mild cognitive decline to severe dementia received oral NADH as the disodium salt 10mg in the morning 30 minutes before breakfast. All showed a significant improvement in mental function within 8-12 weeks.