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NADH
What is it?
Nicotinamide adenine dinucleotide (NADH) is a coenzyme that can be found in most living systems. It
is found in high concentrations in the mitochondria (energy producing part of all cells) and throughout
the rest of cells. It is synthesized from adenylic acid and nicotinamide and plays a role in thousands of
chemical reactions that occur in the body. NADH is essential in the creation of cellular energy through
the production of ATP, in a process known as oxidative phosphorylation. NADH is a key component in
the production of energy for the whole body.
NADH is the activated form of niacin (vitamin B3) in the body, without this key nutrient, energy
production doesn’t take place. The side effects of taking NADH are considered nonsignificant and it
has no drug interactions, making it an extremely safe supplement with the potential for great benefits.
What is good for?
Supplementing with NADH has been shown to have two key functions in the body. First, it increases
cellular energy production (ATP). This makes NADH essential in conditions where there is a lack of
energy or fatigue, or even for athletic performance.
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. Taking NADH can help in conditions where these neurotransmitters are low (such as
Parkinson’s disease or depression), but also for people who want to improve mental performance.
CHRONIC FATIGUE SYNDROME (CFS)
The cause of Chronic Fatigue Syndrome (CFS) is unknown, but the disease is marked by low energy
production (low ATP). Supplementing with NADH is known to increase the production of ATP. Two
small trials have supported the use of CFS in chronic fatigue. The first trial was conducted for 12
weeks and showed dramatic improvement in 30% in energy levels in the people taking the
supplement. The second trial followed patients for 2 years who were taking NADH. Following 3 months
of treatment, the patients showed dramatic reduction in their painful symptom scores.
PARKINSON’S DISEASE
Supplementing with NADH has been shown to increase dopamine in patients with Parkinson’s disease
in several large, well-controlled trials. Along with the increase in dopamine, as measured by urinary
homovanillic acid (a byproduct of dopamine metabolism), clinical symptoms of the disease also
improved. While the vast majority of studies have been done with using intervenous (into a vein) and
intermuscular (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 Parkinson’s patients
who are younger and those who are early in the disease.
Studies show a dramatic improvement in symptoms of Parkinson’s disease along with an increase in
dopamine production in patients supplemented with NADH. While supplementing with NADH is not a
cure for Parkinson’s disease, it does improve symptoms and prolong the deterioration of symptoms.
ALZHEIMER’S DISEASE
Two small open (non-blinded; non-randomized) and one small double-blind randomized trial have
been performed on the use of NADH in Alzheimer’s disease. The trial showed no loss of cognitive
function after 6 months and improvement over placebo in areas of verbal fluency and visual-
constructional ability using the Mattis Dementia Rating Scale (MDRS). No differences between the
groups were noted for attention, memory, or in clinician ratings of dementia severity.
The results have been mixed. Of the open trials, one demonstrated improvement in the Mini Mental
State Examination (MMSE), while the other showed no improvement in cognitive functioning at all.
DEPRESSION
One open trial has demonstrated improvement in depression with supplemental NADH in 204 patients
with clinical depression. Further double blind, randomized studies are needed in order to assess the
ability of NADH to treat depression. NADH has been shown in other trials (with Parkinson’s patients) 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 depression.
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. NADH performed well in this first small trial and its
use may well prove to be very effective. Taking NADH on arrival to the new time zone is a good
therapy to try.
How Much to Take
Most studies use 5-10 mg / day of NADH.
Side Effects / Interactions
References
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.
PARKINSON’S DISEASE
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.
ALZHEIMER’S DISEASE
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.
DEPRESSION
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.
JET LAG
1. Birkmayer GD, Kay GG, Vurre E. Stabilized NADH (ENADA) 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 (ENADA) 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 ENADA/NADH for chronic toxicity study in rats. Drugs Exp Clin Res. 2002;28(5):185-92.
What is it?
Nicotinamide adenine dinucleotide (NADH) is a coenzyme that can be found in most living systems. It
is found in high concentrations in the mitochondria (energy producing part of all cells) and throughout
the rest of cells. It is synthesized from adenylic acid and nicotinamide and plays a role in thousands of
chemical reactions that occur in the body. NADH is essential in the creation of cellular energy through
the production of ATP, in a process known as oxidative phosphorylation. NADH is a key component in
the production of energy for the whole body.
NADH is the activated form of niacin (vitamin B3) in the body, without this key nutrient, energy
production doesn’t take place. The side effects of taking NADH are considered nonsignificant and it
has no drug interactions, making it an extremely safe supplement with the potential for great benefits.
What is good for?
Supplementing with NADH has been shown to have two key functions in the body. First, it increases
cellular energy production (ATP). This makes NADH essential in conditions where there is a lack of
energy or fatigue, or even for athletic performance.
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. Taking NADH can help in conditions where these neurotransmitters are low (such as
Parkinson’s disease or depression), but also for people who want to improve mental performance.
CHRONIC FATIGUE SYNDROME (CFS)
The cause of Chronic Fatigue Syndrome (CFS) is unknown, but the disease is marked by low energy
production (low ATP). Supplementing with NADH is known to increase the production of ATP. Two
small trials have supported the use of CFS in chronic fatigue. The first trial was conducted for 12
weeks and showed dramatic improvement in 30% in energy levels in the people taking the
supplement. The second trial followed patients for 2 years who were taking NADH. Following 3 months
of treatment, the patients showed dramatic reduction in their painful symptom scores.
PARKINSON’S DISEASE
Supplementing with NADH has been shown to increase dopamine in patients with Parkinson’s disease
in several large, well-controlled trials. Along with the increase in dopamine, as measured by urinary
homovanillic acid (a byproduct of dopamine metabolism), clinical symptoms of the disease also
improved. While the vast majority of studies have been done with using intervenous (into a vein) and
intermuscular (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 Parkinson’s patients
who are younger and those who are early in the disease.
Studies show a dramatic improvement in symptoms of Parkinson’s disease along with an increase in
dopamine production in patients supplemented with NADH. While supplementing with NADH is not a
cure for Parkinson’s disease, it does improve symptoms and prolong the deterioration of symptoms.
ALZHEIMER’S DISEASE
Two small open (non-blinded; non-randomized) and one small double-blind randomized trial have
been performed on the use of NADH in Alzheimer’s disease. The trial showed no loss of cognitive
function after 6 months and improvement over placebo in areas of verbal fluency and visual-
constructional ability using the Mattis Dementia Rating Scale (MDRS). No differences between the
groups were noted for attention, memory, or in clinician ratings of dementia severity.
The results have been mixed. Of the open trials, one demonstrated improvement in the Mini Mental
State Examination (MMSE), while the other showed no improvement in cognitive functioning at all.
DEPRESSION
One open trial has demonstrated improvement in depression with supplemental NADH in 204 patients
with clinical depression. Further double blind, randomized studies are needed in order to assess the
ability of NADH to treat depression. NADH has been shown in other trials (with Parkinson’s patients) 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 depression.
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. NADH performed well in this first small trial and its
use may well prove to be very effective. Taking NADH on arrival to the new time zone is a good
therapy to try.
How Much to Take
Most studies use 5-10 mg / day of NADH.
Side Effects / Interactions
- Side Effects: Supplementing with NADH appears to be very safe with no significant reported
side effects.
- Drug Interactions: No reported drug interactions
References
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.
PARKINSON’S DISEASE
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.
ALZHEIMER’S DISEASE
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.
DEPRESSION
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.
JET LAG
1. Birkmayer GD, Kay GG, Vurre E. Stabilized NADH (ENADA) 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 (ENADA) 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 ENADA/NADH for chronic toxicity study in rats. Drugs Exp Clin Res. 2002;28(5):185-92.