The difficulty in defining and diagnosing this
illness suggests a potential multifactorial etiology. (7)
Regardless of the cause, a common etiology in this disease
may be one or more metabolic blocks that prevent
optimal ATP production in cells. CFS patients exhibit
elevated blood lactate levels which could reflect such a
deficit. (5) Recent organic acid profiles on CFS patients
in a post-exercise condition reveal significant
abnormalities in levels of the citric acid cycle intermediates
indicating derangements in this critical ATP production
cycle. (8) Red blood cell magnesium was also found to be
deficient and intravenous administration of magnesium
improved symptoms in CFS patients. (9) Magnesium is an
essential element in ATP utilization. The considerable
energy requirements of the brain would make this organ
particularly susceptible to a deficit in ATP production and
utilization. Amino acids directly impact the TCA cycle and
could ATP production. <br><br>Adenosine monophosphate
(AMP) has been used successfully to treat other viral
infections perhaps by stimulating increased ATP production.
(10) If CFS has a viral origin, an increase in ATP
production may be a factor in recovery. <br><br>The two most
commonly deficient amino acids seen in CFS subjects are
phenylalanine and tryptophan. These serve as precursors to
catecholamines and serotonin, neurotransmitters that are
intimately involved in depressive disorders. Depression is a
common symptom in CFS patients. Significant improvement
was seen in fibromyalgia patients (a disease similar
to CFS) with administration of 5-hydroxytryptophan.
(11) Yet electrophysiological evidence can apparently
differentiate CFS type patients from patients with clinical
depression,suggesting an additional metabolic impairment in CFS
patients.(12) <br><br>Determination of deficient metabolic
factors, such as amino acids, that can be reintroduced
into the system to correct potential metabolic blocks
by mass action may represent a new, effective
approach to treatment of CFS patients in whom a final
common defect is an inability to generate optimal
amounts of cellular energy or other critical metabolites.
Additional double- blind/placebo controlled clinical trials
are needed to confirm the efficacy of amino acid
therapy for CFS as well as research into underlying
mechanisms regarding the metabolic fate of these substances
and their mode of action.
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