Discussion
These results support the hypothesis that one major cause of CFS is mitochondrial failure.
Because mitochondria are a common biological unit, then it is likely that mitochondrial function
in neutrophils will reflect mitochondrial function in other cells. The
biochemical lesions result
from several possible mechanisms many of which can be tackled by appropriate nutritional
interventions. Clinical experience has demonstrated the value of the following interventions with
the following biochemical lesions:
Poor levels of ATP can be
corrected with D-ribose up to 15 grams daily.
Poor magnesium status can be corrected with oral magnesium supplements or possibly parenteral
magnesium, 50mgs daily.
Slow oxidative phosphorylation can be
tackled with supplements of co enzyme Q 10 (up to
300mgs daily),
acetyl L carnitine (2 grams daily),
vitamin B 3 (niacinamide 500mgs daily).
Translocator protein function can be improved by doing
detoxification sweating regimes to
reduce xenobiotic load. This is because translocator protein is often blocked by toxins such as
heavy metals, volatile organic compounds or pesticides. It is also sensitive to pH changes.
When mitochondrial function is impaired there is likely to be excessive production of free
radicals which cause further damage. This can be limited by attention to antioxidant status with
respect to high dose parenteral B12, correcting coenzyme Q 10 levels, correcting levels of
glutathione peroxidase, correcting levels of superoxide dismutase.
Mitochondrial function is also hormone sensitive and so there is a need to ensure optimum
hormonal environment with respect to thyroid and adrenal dysfunction and possibly others.
Indeed many of the authors of this study have started on the necessary regimes and nutritional
supplements to correct mitochondrial function and have seen clinical improvements with
improved stamina, shortened recovery time when they have over-exerted themselves beyond
their expected activity levels and reduced levels of symptoms.
It is very likely there are many ways in which mitochondria can be functionally impaired or
damaged such as immune activation in infectious disease, autoimmunity, allergic reactions (to
foods, inhalants or chemicals), poor antioxidant status, syndrome X with insulin resistance as
well as neurological damage, major organ failures and
possibly even psychological mechanisms.
These are all areas which require further research.
Conclusion
The important thing to remember about chronic fatigue syndrome is that it is not a diagnosis, but
a symptom. Obviously chronic fatigue syndrome can occur for standard medically identifiable
reasons such as major organs failures (anaemia, heart failure, respiratory failure, cancer),
lack of
sleep, hormonal failures (thyroid, adrenal, pituitary etc), starvation (which may be macronutrient
or micronutrient) or simply
“over-training syndrome”. However when these obvious problems
have been excluded,
mitochondrial failure due to functional impairment from toxic stress or
micronutrient deficiency is likely to explain a great many cases of chronic fatigue.
Therefore we now have an objective test for chronic fatigue syndrome which also indicates the
site of the biochemical lesion, its severity and most importantly gives a clear direction to
treatment.
Mr Craig Robinson, Convenor of citizens’ paper, March 2006
E mail hunterjames25@tiscali.co.uk"