the supervitamin body and mind energizer
by James South MA
NADH is the abbreviation used for Nicotinamide Adenine Dinucleotide, one of
the most important coenzymes in the human brain and body.
A coenzyme is the active, or working form
of a vitamin. NADH is the reduced (electron- energy rich) coenzyme form of
vitamin B3, while NAD is the oxidized (burned) coenzyme form of B3.
NAD and NADH are converted
into each other in numerous different metabolic activities. In some metabolic
reactions it is NAD which is the needed catalyst, with NADH a useful by-product,
in other reactions the situation is reversed.
NAD and NADH also serve to
activate various enzymes, NAD for example, activates alcohol dehydrogenase and
acetaldehyde dehydrogenase that are the two enzymes needed to detoxify the
alcohol we drink into carbon dioxide and water.
NADH is the first of five
enzyme complexes of the electron transport chain, where much of the ATP
bioenergy that runs every biological process of our lives is formed.
NADH its vital chemical
As already noted, NAD(H) is the coenzyme or active form of vitamin B3. The
chemistry of NAD(H) is some of the most complex in the human body. NAD(H) is
necessary to oxidize (burn) all foodstuffs (fats, sugars, amino-acids) into ATP
bioenergy. There are three interlinked energy production cycles: the glycolytic
(sugar burning) and Krebs citric acid cycles (aminos and fats are
"burned" through the Krebs cycle), and the electron transport side
A glycolytic cycle
"waste" end product- pyruvic acid- helps power the Krebs cycle,
while electron "sparks" released from the step by step slow
"burning" that occurs in the Krebs cycle provide the fuel used by
the electron transport side
chain to generate much of the ATP bioenergy that literally powers our life.
NAD(H) is involved in all of these different cycles, as well as in the
conversion of the pyruvate end product of the glycolytic cycle into the
beginning fuel of the Krebs citric acid cycle. It is NADH, which captures the
electron "sparks" thrown off during Krebs cycle oxidation and
shuttles them to the electron transport side
chain energy production cycle.
Each unit of NADH is
capable of generating three units of ATP energy. In a very real sense, NADH is
the "energy of life" coenzyme.
NAD(H) is a relatively
large and complex molecule, as coenzymes go. It is vitamin B3 (niacinamide)
combined with a ribose (5-carbon sugar), a phosphate group and an adenine
nucleotide (a DNA component). NAD(H) can be made in the liver and other cells
from vitamin B3.
It can also be made from
the amino acid L-Tryptophan at the "expensive" ratio of 60mg
tryptophan for 1mg B3. Taking in exogenous (from outside the body) B3 or NAD(H)
may spare the scarce amino acid tryptophan, which is the least plentiful amino
in any normal diet. Tryptophan is the precursor of one of the most important
antidepressant neurotransmitters, serotonin.
NADHs role in
J.D. and W. Birkmayer of the Birkmayer Institute have pioneered the clinical use
of NADH only in the last decade for Parkinson Therapy, Vienna, Austria.
The Birkmayers are the
first to develop a stable and absorbable oral tablet form of NADH. They have
also conducted groundbreaking research on the use of NADH in Parkinsons
disease, depression, Alzheimers dementia and fatigue.
In a series of scientific
papers published between 1989 and 1993 the Birkmayers have related their
clinical success with NADH in Parkinsons, as well as provided supporting
biochemical experiments and rationale for their success with NADH.
Parkinsons disease, one
of the most common neurological diseases of aging, involves the gradual and even
more severe destruction of the dopamine using neurons, in a brain region called
the substantia nigra. Parkinsons involves movement disorders, speech
difficulties, depression and cognitive dysfunction.
The traditional medical
therapy for Parkinsons is L-dopa, the amino acid precursor of dopamine.
However, this therapy has serious drawbacks. After a period of use, even higher
L-dopa doses are required, and these eventually cause severe side effects. In
addition the dopamine formed through L-dopa therapy is prone to auto-oxidation
to free radical forms that eventually "burn out" what few dopaminergic
neurons are left.
begins when the substantia nigra neuron population has dropped to 20-30% of
brain formula Raise your IQ
Dopamine is usually made
inside the neurons that use it through a two step process. The amino acid
tyrosine is first converted to L-dopa through an enzyme called tyrosine
hydroxylase. L-dopa is then converted to dopamine. Research has
shown that it is the activity of tyrosine
hydroxylase, which is the rate-limiting controller of
dopamine synthesis, and tyrosine
hydroxylase activity is considerably lower in Parkinsons
patients than healthy people.
Research has also shown
that giving Parkinsons disease patients L-dopa diminishes their already weak
hydroxylase activity, thus further limiting their own L-dopa production and increasing
the need for L-dopa supplements in an ever worsening vicious spiral.
The Birkmayers discovered
that the coenzyme that activates tyrosine
hydroxylase- tetrahydrobiopterin (H4BP) is reduced 50%
in the brains of Parkinsons patients compared to age matched healthy
controls. They further discovered that NADH activates the enzyme, which helps
Cell culture studies
showed that NADH could elevate H4BP production, tyrosine
hydroxylase activity and dopamine
The Birkmayers thus
decided to try a therapy that might increase the brains own production of
dopamine, rather than suppress it as L-dopa therapy eventually does.
The Birkmayers treated
a group of 885 patients with NADH, 415 with intravenous (IV) NADH and 470 with
oral NADH (Acta Neurol Scanda, 1993, PP 32-35).
Both groups showed overall
good response to treatment, especially in motor improvements, walking, pushing,
posture and speech. They also noted cognitive and emotional improvements in some
patients, and surprisingly, the improvement figures for both IV and oral NADH
were almost identical, and the maximum total improvement was actually shown by
oral NADH users.
The Birkmayers also found
increased urinary excretion of dopamine metabolites in the patients, indicating
there was an actual NADH induced increase in dopamine production. They also were
able to reduce and even eliminate other anti-Parkinson medications in some
NADH and its
Based on their success with NADH treatment of Parkinsons patients, the
Birkmayers decided to try NADH as an antidepressant in 205 depressed patients.
There are multiple theoretical rationales for such use.
NADH increases brain
dopamine and noradrenaline using brain cells use dopamine to make noradrenaline.
It is generally accepted
that dopamine and/ or noradrenaline are frequently diminished in the brains of
depressed patients, and drugs that raise brain dopamine/ noradrenaline levels
will frequently end depression. In addition, through NADHs sparing of
tryptophan (discussed earlier in this article), more tryptophan would be left to
end up as brain serotonin, another neuro-transmitter frequently reduced in
depressives, and when drugs or tryptophan supplements raise brain serotonin,
this frequently halts depression.
Lastly, it should be noted
that the human brain must produce and use 20% of the bodys total ATP
bioenergy, and PET scans of the brains of depressed and demented people
frequently show reduced brain energy production. Thus, through its multiple
roles in producing ATP energy, NADH might be expected to literally energize the
brain, and depression may be in part the mental/ emotional direct experience of
the brains lowered energy status.
therefore, the Birkmayers reported in their 1992 paper in New Trends in
Clinical Pharmacology, a beneficial effect in 93% of the NADH treated
As with their
Parkinsons patients, the Birkmayers found that NADH tended to induce serious
improvement more in younger (less than 65 years old) than older patients. Their
Parkinsons studies also showed shorter duration illness patients to benefit
more than longer duration patients.
NADH and Alzheimers
Because many Parkinsons patients exhibit dementia as well as neurotransmitter
problems, while many Alzheimers patients exhibit neuromotor dysfunction as
well as dementia, the Birkmayers next tried oral NADH on 17 Alzheimers
dementia (AD) patients (unpublished paper). These patients ranged from mildly to
severely demented. The results were nothing short of astounding! Not only did
NADH halt the progression of Alzheimers disease, it significantly reversed
the cognitive and behavioral problems, even in the worst cases.
The NADH therapy was even
able to restore some patients from being virtual "vegetables" to a
semblance of normalcy. The Birkmayers also did before and after urinary analyses
of dopamine and noradrenaline metabolites and found evidence indicating
significantly improved brain dopamine/ noradrenaline activity. While deficits in
the function of acetylcholine neurons is the more well known pathology of
Alzheimers dementia, studies have also shown seriously diminished dopamine/
noradrenaline nerve activity in Alzheimers dementia.
In several patients NADH
was halted briefly to determine if the improvements would last without it. After
several weeks absence of NADH (after a years NADH treatment), deterioration
began. Once again, NADH was started, and the previous improvements were
NADH a possible fatigue
In June 1997 W. Birkmayer was to announce the details of a successful trial
using NADH to combat fatigue at a Las Vegas health convention. I was unable to
get the details at the time of writing this article.
However, given the
multi-dimensional roles of NADH in all aspects of human cellular ATP production,
favorable results with NADH in fatigue situations is hardly surprising.
NADH doses and uses
The standard dosage of NADH has been 10mg, taken with water 30 minutes before
Animal studies suggest
1000mg per kilogram of body weight (70,000mg for a 154 pound human!) to be a
tolerable dosage, so aside from the expense, there is no reason not to
experiment with higher doses should 10mg not suffice to bring a hoped for
Those wishing to use NADH
in Parkinsons cases might do well to accompany it with tyrosine and
Those wishing to try NADH
for depression might add DLPA, tyrosine and/ or tryptophan or 5-hydroxy
Those wishing to try NADH
for Alzheimers dementia might include acetyl L-carnitine and
centrophenoxine (Lucidril) with NADH.
In serious fatigue
situations, B-complex vitamins, alpha-lipoic
acid, CoQ10 or Idebenone and
magnesium would be synergistic with NADH.
In situations involving
chronic alcoholism, however the cellular NAD/ NADH ratio is already
detrimentally skewed in favor of NADH, so NADH would not be appropriate.
Given the routine interconversions in all
cells between niacin, niacinamide (2 forms of vitamin B3), NAD and NADH, as well
as B3s sparing effect on tryptophan, it may be useful to add small (50-100mg)
doses of vitamin B3 to any NADH regimen.