Supplementing with NADH is known to improve cellular energy safely by increasing production of the cellular fuel ATP. NADH also plays a vital role in creation of the neurotransmitters (brain chemicals) serotonin, dopamine, and norepinephrine – important for mood, memory, alertness, and concentration.
But what is NADH? How does it deliver benefits to the cells? And how does this compare with the actions of chemical stimulants such as caffeine? Naturopathic Doctor Scott Olson outlines the science, and offers a Q&A with Professor Jorg Birkmayer, MD, PhD, director of the Institute for Parkinson's Therapy in Vienna, and a leader in NADH research for nearly 30 years.
What is NADH?
Beta-nicotinamide adenine dinucleotide (NADH) has long been the most popular non-drug regimen for Chronic Fatigue Syndrome (CFS) and is also highly favored by Fibromyalgia Syndrome (FMS) patients. Its use in CFS is supported by two randomized, placebo-controlled clinical studies suggesting that NADH supplementation may be helpful in some patients to enhance energy (see for example http://www.immunesupport.com/library/showarticle.cfm/id/192), and many patients are convinced that NADH enhances their quality of life.
NADH is a naturally occurring coenzyme that is necessary for the production of energy in each of our 100 trillion cells. Found in the highest concentrations in the cell’s mitochondria, this essential nutrient and potent antioxidant facilitates the production of cellular energy in the form of adenosine triphosphate (ATP) – and plays a role in thousands of chemical reactions that occur in the body. Without NADH, energy production is severely impaired.
NADH is considered an extremely safe supplement with "insignificant" side effects and no known drug interactions. Technically, it is the activated form of niacin (vitamin B3) in the body, synthesized from adenylic acid and nicotinamide.
What is NADH Good For?
Supplementing with NADH has been shown to have two key functions in the body.
First, it improves cellular energy by increasing the production of the cellular fuel, ATP. This makes it beneficial in conditions where there is a lack of energy or fatigue, such as CFS and FMS, and even for athletic performance. The benefits of supplemental NADH are also supported by anecdotal experiences of individuals with Parkinson’s disease, Alzheimer’s disease, and jet lag.
Second, NADH also plays a vital role in the creation of neurotransmitters (brain chemicals), such as serotonin, dopamine, and norepinephrine. These brain chemicals are important for mood, memory, alertness and concentration – and users claim that supplementing with NADH helps to elevate mental clarity and improve alertness and concentration.
The use of NADH in various conditions – and related studies to date – are summarized in the following table, and detailed below. (See also Resources* for research citations.)
|n Dopamine Production||The nutrient has been well-studied for both effectiveness and safety issues and can be recommended for these conditions on the basis of scientific support.|
| n Low Energy or Fatigue|
n Mood Support
n Jet Lag
|The nutrient has at least some good clinical studies in humans to support its use, and/or a long history of traditional use. It can be recommended for these conditions on the basis of its traditional use and its relative safety.|
|n Cognitive Function||The nutrient lacks the support of good clinical studies in humans, but has been used traditionally, and a few studies suggest it might be effective. It can be recommended for use for these conditions with the caution that it is not well-supported by research.|
NADH and Low Energy or Recurring Fatigue
The cause of recurring fatigue is unknown, but is marked by low cellular energy production (low cellular ATP). Supplementing with NADH is known to increase the production of ATP. Two trials have supported the use of NADH as a dietary supplement for lifestyle support in recurring fatigue.
n The first trial was conducted for 12 weeks and showed a dramatic improvement of 30 percent in the energy levels of people taking the supplement.
n The second trial followed patients who were taking NADH for 2 years. Following 3 months of supplementation, the patients showed dramatic improvement in their lifestyle comfort scores.
NADH and Dopamine Production
Supplementing with NADH has been shown to increase dopamine in several large, well-controlled trials. The increase in dopamine was measured by urinary homovanillic acid (a byproduct of dopamine metabolism).
While the vast majority of these studies have been conducted using intravenous (into a vein) and intramuscular (into a muscle) injections of NADH, a few studies have been done with oral NADH, and have shown the oral form to be just as effective. NADH seems to work better in individuals who are younger and those who have nearly-normal dopamine levels.
NADH and Cognitive Function
Two small open (non-blinded; non-randomized) and one small double-blind randomized trial have been performed on the use of NADH as a dietary supplement to support cognitive function.
n The double-blind randomized trial showed no loss of cognitive function after 6 months and improvement over placebo in areas of verbal fluency and visual-constructional ability. No differences between the groups were noted for attention or memory.
n The other trial results have been mixed. Of the open trials, one demonstrated improvement, while the other showed no improvement in cognitive functioning at all.
NADH and Mood Support
One open trial has demonstrated improvement in mood support with supplemental NADH in 204 patients. Further double blind, randomized studies are needed in order to assess the ability of NADH to promote normal mood. NADH has been shown in other trials to increase dopamine and it is logical to conclude that NADH increases other brain neurotransmitters (such as serotonin, norepinephrine) that are thought to play a role in promoting normal mood.
NADH and Jet Lag
One small randomized, double blind study demonstrated improvement in cognitive symptoms of jet lag and sleepiness in patients taking supplemental NADH.
Further, larger, studies are needed to demonstrate the effectiveness of NADH in jet lag. But NADH performed well in this first small trial, and its use may well prove to be very effective. Taking NADH on arrival in the new time zone is a good strategy to try.
How Much to Take?
Most studies use 5 to 10 mg per day of NADH.
Side Effects or Interactions?
Side Effects: Supplementing with NADH appears to be very safe with no significant reported side effects.
Drug Interactions: There are no reported drug interactions.
How Does NADH Escape Destruction by Stomach Acid?
Importantly, supplemental NADH may be unstable, and can be rendered ineffective if it dissolves in the stomach, where stomach acid destroys it. It must be absorbed in the intestinal tract to be effective. Therefore, to be bioavailable, NADH must be formulated for stability and delivered via a coated tablet so that it will not dissolve in the stomach, but rather stay intact until it reaches the intestine where it quickly dissolves.
Following are Professor Birkmayer’s explanations of NADH deficiency and the action of supplemental NADH, based on his own studies and a review of the literature.
Q&A With NADH Expert Jorg Birkmayer
Professor Birkmayer: All we need is energy. Every living cell needs energy to stay alive. But exactly how is this energy for life produced? Hydrogen and oxygen react to form water and energy. The biological form of hydrogen is NADH.
Q: How does a deficiency in NADH cause problems with energy levels?
Professor Birkmayer: NADH is the fuel for cellular energy production. All living cells require energy to stay alive. Without energy a cell dies because energy production represents the essential prerequisite for every living cell.
NADH reacts with oxygen, present in every living cell, to produce in a cascade of reactions both water (H2O) and energy. This energy is stored in the form of the chemical compound adenosine triphosphate, abbreviated ATP. Scientific studies have shown that a loss of NADH leads to an ATP depletion, which in turn leads to cell death.
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Simply put, the more NADH a cell has available, the more energy it can produce. Most recent scientific studies have discovered that the energy level in a cell can actually be increased by NADH.
Q: How does NADH help enhance mental clarity? What is the process through which NADH affects cognitive function?
Professor Birkmayer: 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.
This has been demonstrated in a study performed at Cornell University in New York. When you suffer from sleep deprivation your cognitive performance goes down. Nearly a third of the U.S. adults manage less than seven hours of sleep each night according to the National Sleep Foundation, and 69 percent complain of frequent sleep problems.
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.
Q: How is NADH different from chemical stimulants (like caffeine) and how is it better?
Professor Birkmayer: NADH is by all means much better than caffeine or other stimulants for various reasons. Caffeine and the other stimulants release adrenaline (also called epinephrine) from the nerve cells. This triggers a quick boost in adrenaline. You are less tired and more alert.
However, it is only for a very short time. The next coffee will not give you the same boost as the first one because your adrenaline pool in the nerve cells has been emptied.
NADH on the other hand stimulates the biosynthesis of adrenaline and due to this fills the pool of adrenaline in the central nervous system. This is the essential prerequisite for caffeine to become active.
In addition, NADH increases the real ATP energy in the cells. With more energy the nerve cells produce not only more adrenaline, dopamine, and serotonin, but also other components necessary for good performance.
NADH is the only substance which has been shown to improve cellular energy. Coffee, and all of the so-called ‘energy drinks’, do not increase cellular energy. In fact they do nothing but release adrenaline from nerve cells and are therefore mere stimulants. Too much and too high stimulation can cause considerable side effects or adverse reactions such as irregular heart beat.
Q: How is NADH different from Coenzyme Q10?
Professor Birkmayer: Both support cellular energy production. Coenzyme Q10 is involved in cellular energy production; however, at a much lower level than NADH. Coenzyme Q10 needs NADH to be transformed into its reduced form. Only in its reduced form is CoQ10 active and can transport electrons from NADH to oxygen which then leads to energy production in the form of ATP.
NADH, however, has many more functions in the body in addition to producing energy. It does repair cell and DNA damage, it stimulates the immune system, it stimulates the biosynthesis of the neurotransmitters adrenaline, dopamine and serotonin. It stimulates the production of NO (Nitric Oxide), which induces relaxation of blood vessels in many organs such as the heart, lungs, brain, and kidneys.
Supplemental NADH holds great promise for those seeking support for their energy needs, including individuals with CFS and FMS. When effectively delivered to the cells, research indicates NADH may enhance energy naturally, improve cellular energy, elevate mental clarity, and improve alertness and concentration optimally.
Chronic Fatigue Syndrome (CFS)
1. Forsyth LM, Preuss HG, MacDowell AL, Chiazze L Jr, Birkmayer GD, Bellanti JA. “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.
1. 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.
2. Birkmayer JG, Vrecko C, Volc D, Birkmayer W. “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.
3. Birkmayer W, Birkmayer GJ, Vrecko K, Mlekusch W, Paletta B, Ott E. “The coenzyme nicotinamide adenine dinucleotide (NADH) improves the disability of parkinsonian patients.” J Neural Transm Park Dis Dement Sect. 1989;1(4):297-302.
4. 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.
5. Birkmayer W, Birkmayer JG, Vrecko K, Paletta B. “The clinical benefit of NADH as stimulator of endogenous L-dopa biosynthesis in parkinsonian patients.” Adv Neurol. 1990;53:545-9. No abstract available.
6. Dizdar N, Kagedal B, Lindvall B. “Treatment of Parkinson's disease with NADH.” Acta Neurol Scand. 1994 Nov;90(5):345-7.
7. Kuhn W, Muller T, Winkel R, Danielczik S, Gerstner A, Hacker R, Mattern C, Przuntek H. “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.
8. Swerdlow RH. “Is NADH effective in the treatment of Parkinson's disease?” Drugs Aging. 1998 Oct;13(4):263-8. Review.
1. Birkmayer JG. “Coenzyme nicotinamide adenine dinucleotide: New therapeutic approach for improving dementia of the Alzheimer type.” Ann Clin Lab Sci. 1996 Jan-Feb;26(1):1-9.
2. 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.
3. Rainer M, Kraxberger E, Haushofer M, Mucke HA, Jellinger KA. “No evidence for cognitive improvement from oral nicotinamide adenine dinucleotide (NADH) in dementia.” J Neural Transm. 2000;107(12):1475-81.
1. Birkmayer JGD, Birkmayer W. “The coenzyme nicotinamide adenine dinucleotide (NADH) as biological antidepressive agent: Experience with 205 patients.” New Trends Clin Neuropharmacol. 1991;5:19–25.
1. Birkmayer GD, Kay GG, Vurre E. “Stabilized NADH improves jet lag-induced cognitive performance deficit.” Wien Med Wochenschr. 2002;152(17-18):450-4.
Interactions and Side Effects
1. Birkmayer GD, Kay GG, Vurre E. [Stabilized NADH improves jet lag-induced cognitive performance deficit] Wien Med Wochenschr. 2002;152(17-18):450-4. German.
2. Birkmayer JG, Nadlinger KF, Hallstrom S. “On the safety of reduced nicotinamide adenine dinucleotide (NADH).” J Environ Pathol Toxicol Oncol. 2004;23(3):179-94.
3. Birkmayer JG, Nadlinger K. “Safety of stabilized, orally absorbable, reduced nicotinamide adenine dinucleotide (NADH): A 26-week oral tablet administration of NADH for chronic toxicity study in rats.” Drugs Exp Clin Res. 2002;28(5):185-92.
Note: This information has not been evaluated by the FDA. It is not meant to prevent, diagnose, treat, or cure any condition, illness, or disease. It is very important that you make no change in your healthcare plan or regimen without researching and discussing it in collaboration with your professional healthcare team.