Dear Barbara:
Thank you for keeping the topic of NADH efficacy and toxicity alive.
I hope it will contine to make people aware that NADH has little biological
actvity when ingested but can cause serious toxic effects. Secondly, PDs and
their caretakers will learn more about the misinformation and selection of
results by poorly infomed or unscrupulous laboratory workers, manufacturers
and dealers use to interpretate their data more favorably than is warranted.
What called my attention to this scam were several messages in the
digest, earrly on after I joined the APDA in 1995 and read summaries of
papers presented in Germany several years ago about the treatment of PD with
NADH, DEAE and related compounds. After several hours of searching I
realized that the experimnental results in animals, tissue extracxts and
clinical testing were done in settings where the obviously prejudiced
director ran the clinic, designed the experiments to produce the deired
results, selected the data for publication and subsidized the publication of
favorable papers: trickle-down all the way, and misinterpretion of the the
results to taste. A few members of the audience pointed out deficiencies and
inconsistencies with the well establised results from a large literature.
NADH and biochemically related compounds are absolutely essential for
respiration in virually all aerobic bacteria, plants and animals. Genetic
defciencies or deficits in the intracellular utilization of NADH are likely
to be lethal. A lack of recovery of response to moderate doses of NADH was
probably due to insufficient nucleotide transport into cells. An attractive
hypothesis is that specific cell foci in the CNS utilize large amounts of
NADH for a critical step in dopamine synthesis or of a cofactor necessary
for the control of biosynthetic /biodegradative pathways. of or synthesis
of Pwhere NADH reduction is the consequence of NAD oxidation).This
oxidation is dependent on uptake of large amounts of precursors of the NAD
nulceotides. If uptake is deficient, the cells die. This is what may happen
in PD, but at such a slow rate. that the ultimate response, destrtuction of
dopaminergic cells, is detectable, but the early steps in the breakdown of
the machinery are only slowly detectible and is yet only irregularly
observed. However, the hypothesis that NADH can prevent or reduce
experimenal PD-like symptoms after adding NADH to the diet or injecting
NADH as a treatment of PD is just not supported by the results, whether from
yeast or from humans. The two chief reasons why the hypothesis has lead to
incorrect conclusions (aside from the practice of sloppy science) are: 1)
Whether small or large amounts of the nucleotides are administered, all of
the dose will be metabolically inactivated within seconds to minutes after
administration. Insufficient NADH reaches vital targets. There is no mystery
here. Membrane transport of nucleotide and nucleotide precursors is now a
very active area of research, certainly an important way to look for
candidates as anti- PD agents. Determining the relevance of results from one
kind of experiment in single cells to whole animals, requires rigorous
deductive reasoning, such as a working knowledge of the dynamics of drug
distribution and neuroelectrophysiology. Too many times is my credulity
shatterred when presumably well-trained and knowledgable scientists can be
so fooled or fool themselves.
I have been long-winded, but the kind of research that is practiced
here `needs more rigorous involvement of competent and reliable scientists
therwise the work becomes trivial and wasteful, and sometimes leads to
murder by ignorance. I therefore strongly agree with the recent
correspondence on DEAE in the PD e-mail. Parkinsonianssmust not lose hope or
give into what is popular for the moment. We will find better therapies and
sooner or later cures for PD, but phsicians and scientists must remain
critical and skeptical or we will have to deal with alot of lost hope.
With best wishes from Steven
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Steven E. Mayer, Ph.D.
