Do you ever feel like a car that has run out of gas? If so, it may be time to add some NADH to your cellular tank. NADH is the fuel our cells need to produce energy and function properly.
NADH, a reduced form of nicotinamide adenine dinucleotide, is a naturally occurring coenzyme formed from Niacin (vitamin B3) that plays an essential role in the energy production of every human cell – all 100 trillion of them.
Studies suggest NADH may help:
• Increase energy and reduce fatigue.
• Support the immune system with powerful antioxidants and free-radical scavengers.
• Improve memory, focus and mental clarity.
• Support the creation of neurotransmitters, like serotonin, dopamine, and norepinephrine.
• Enhance mood and emotional balance.
How NADH Works
In order to understand how NADH works, it is first necessary to understand mitochondria. Picture the mitochondria as little engines – or energy producers – within each cell of your body. It’s the job of your mitochondria to supply energy to your cells in the form of adenosine triphosphate (ATP). But exactly how does that happen?
This is where NADH comes in. NADH sets off a chemical chain reaction by transforming Coenzyme Q10 into its reduced form. Then, in its reduced form, Co-Q10 becomes active and serves as the catalyst that makes it possible for the mitochondria to produce ATP. Every molecule of NADH results in the production of three molecules of ATP energy.
NADH is a critical component of your body’s ability to function. Without NADH, the mitochondria cannot produce energy and the cells will die.
ME/CFS and Fibromyalgia
Fatigue is a key symptom of ME/CFS, fibromyalgia and Lyme disease. Since recurring fatigue is marked by low cellular ATP, which results in low cellular energy production, researchers have studied the use of NADH to increase energy.
• A pilot study at Georgetown University gave 26 ME/CFS patients either 10 mg of NADH or a placebo daily for four weeks. After a four-week washout period, participants switched to the alternate regimen for four weeks. At the end of the study 31% had a favorable response to the NADH. The scientists concluded that “NADH may be a valuable adjunctive therapy in the management of the chronic fatigue syndrome.”(1)
• In a 2004 study, 31 ME/CFS patients were randomly assigned to receive either NADH or nutritional supplements and psychological therapy for two years. The patients who received NADH had a dramatic and statistically significant reduction of the mean symptom score in the first eight months and they tended to continue improving through the rest of the trial.(2)
Another major complaint of ME/CFS, fibromyalgia and Lyme disease patients is cognitive functioning problems, such as memory loss, difficulty concentrating and mental fogginess.
George Birkmayer, MD, PhD, director of the Institute for Parkinson’s Therapy in Vienna, and a leader in NADH research for nearly 30 years, explains how NADH can help improve mental clarity.
“One third of all the energy we produce in our body is used up by our brain. Due to this, an energy deficiency is first realized in the brain with symptoms such as lack of concentration and alertness, or mental fog. With more NADH the brain cells function better…
“A further mechanism by which NADH affects cognitive function is by stimulating the production of adrenaline and dopamine. Both of these substances are essential for our cognitive performance and our memory.”(3)
NADH is frequently recommended for ME/CFS and fibromyalgia patients by well-known specialists like Drs. Charles Lapp, Jacob Teitelbaum, Dale Guyer, Michael Rosenbaum, and Mark Pellegrino.
Because NADH is known to help increase levels of the important neurotransmitter dopamine, there have been several studies of NADH as a possible adjunctive treatment for Parkinson’s disease (which involves a slow destruction of the nerve cells in the brain that make dopamine).
• Between 1989 and 1993, Austrian scientists, led by Dr. Birkmayer, conducted a series of open label trials of NADH on more than 2,000 Parkinson’s patients. Through these studies, Dr. Birkmayer found that NADH not only alleviated the impairment in motor skills caused by Parkinson’s but also effectively treated their cognitive dysfunction.
Below is a summary of the results from three of those studies. More than a 30% improvement was considered to be a very good response and up to 30% was rated as a moderate response.
The researchers found a dose of 25 to 50 mg of NADH per day to be the most effective. They also discovered that younger patients and patients with a shorter duration of disease have a better chance to gain a marked improvement than older patients and patients with a longer duration of the disease.(4-7)
• In a German study, 15 Parkinson’s patients received intravenous infusions of 10 mg NADH for seven days in addition to conventional Parkinsonian pharmacotherapy. The patients all showed a significantly positive response and the scientists found that the application of NADH significantly increased the bioavailability of their plasma levodopa. They concluded that NADH “may be a potent stimulator of endogenous levodopa biosynthesis with clinical benefit for Parkinsonian patients.”(8)
Although several of the Parkinson’s studies have used intravenous or intramuscular injections of NADH, trials using oral NADH have shown it to be equally effective.(4)
In 2004, a randomized, placebo-controlled, matched-pairs, double-blind, clinical study was conducted testing NADH as a treatment for Alzheimer’s disease. Twenty-four patients with probable Alzheimer’s disease received either 10 mg of oral NADH or a placebo.
After six months, participants treated with NADH showed no evidence of progressive cognitive deterioration. They also showed significantly higher performance scores than the placebo group in the areas of verbal fluency and visual-constructional ability as well as a trend to better performance in abstract verbal reasoning. The researchers concluded, “Consistent with earlier studies, the present findings support NADH as a treatment for AD.”(9)
Food Sources – NADH can be found naturally in the muscle tissue of fish, poultry and cattle, and in food products made with yeast. However, it is not known whether the NADH from these food sources is efficiently absorbed or utilized by the body.
Absorption – NADH must be absorbed in the intestinal tract to be effective. Therefore, oral NADH must be formulated for stability and delivered via a coated tablet so it does not dissolve in the stomach, but rather stays intact until it reaches the intestine. ProHealth’s Energy NADH is an exclusive formulation that provides improved stability for 100% guaranteed potency. And its unique cellulose matrix coating enhances absorption by ensuring that the NADH reaches the intestine where it is quickly dissolved.
Dosage -The recommended dosage is generally 5 to 10 mg per day taken in the morning on an empty stomach, 30 minutes before a meal. However, studies with Parkinson’s disease patients found that 25 to 50 mg per day was the most effective dose.
Side Effects – No significant side effects have been reported. Supplementing with NADH appears to be very safe.
Drug Interactions – There are no reported drug interactions.
NADH is a powerful cellular energy producer. Research has demonstrated the ability of supplemental NADH to promote fatigue reduction, enhanced mental clarity, and increased levels of important neurotransmitters like dopamine.
1. Forsyth LM, et al. “Therapeutic effects of oral NADH on the symptoms of patients with chronic fatigue syndrome.” Ann Allergy Asthma Immunol. 1999 Feb;82(2):185-91.
2. Santaella ML, Font I, Disdier OM. “Comparison of oral nicotinamide adenine dinucleotide (NADH) versus conventional therapy for chronic fatigue syndrome.” P R Health Sci J. 2004 Jun;23(2):89-93.
3. “Interview: Dr. George Birkmayer on NADH for Energy, Healthy Immune Function and More.” ProHealth. January 30, 2006.
4. Birkmayer GJ, Birkmayer W. “Stimulation of endogenous L-dopa biosynthesis – a new principle for the therapy of Parkinson’s disease. The clinical effect of nicotinamide adenine dinucleotide (NADH) and nicotinamide adenine dinucleotidephosphate (NADPH).” Acta Neurol Scand Suppl. 1989;126:183-7.
5. Birkmayer JG, et al. “Nicotinamide adenine dinucleotide (NADH) – a new therapeutic approach to Parkinson’s disease. Comparison of oral and parenteral application.” Acta Neurol Scand Suppl. 1993;146:32-5.
6. Birkmayer W, et al. “The coenzyme nicotinamide adenine dinucleotide (NADH) improves the disability of parkinsonian patients.” J Neural Transm Park Dis Dement Sect. 1989;1(4):297-302.
7. Birkmayer W, Birkmayer GJ. “Nicotinamidadenindinucleotide (NADH): the new approach in the therapy of Parkinson’s disease.” Ann Clin Lab Sci. 1989 Jan-Feb;19(1):38-43. .
8. Kuhn W, et al. “Parenteral application of NADH in Parkinson’s disease: clinical improvement partially due to stimulation of endogenous levodopa biosynthesis.” J Neural Transm. 1996;103(10):1187-93.
9. Demarin V, Podobnik SS, Storga-Tomic D, Kay G. “Treatment of Alzheimer’s disease with stabilized oral nicotinamide adenine dinucleotide: A randomized, double-blind study.” Drugs Exp Clin Res. 2004;30(1):27-33.
* Supplement research writer Karen Lee Richards is the Lead Expert specializing in Fibromyalgia and ME/CFS, for HealthCentral’s ChronicPainConnection. Karen is co-founder of the National Fibromyalgia Association (NFA) and was Executive Editor of Fibromyalgia AWARE magazine for four years.
Note: This information has not been evaluated by the FDA. It is general information and is not intended to diagnose, prevent, treat or cure any illness, condition or disease. It is very important that you make no change in your healthcare plan or health support regimen without researching and discussing it in collaboration with your professional healthcare team.