Where Does Obesity Begin?

Where Does Obesity Begin?
by Majid Ali, MD

This article was provided by:
Aging Healthfully Magazine

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It is not a substitute for the advice of a qualified professional.

My clinical work and research with patients with immune disorders, chronic fatigue, chemical sensitivity and obesity have led me to the conclusion that the primary site of catabolic maladaptation, and the obesity that it causes, is in the mitochondria. Injury to the mitochondria is primarily inflicted by increased oxidative stress on their structure and function. There is considerable clinical and experimental evidence to support this viewpoint.

    Patients with immune disorders, chronic fatigue, chemical sensitivity and obesity almost always show electrophysiologic, biochemical and microscopic profiles indicative of mitochondrial dysfunction. These patients in general show excellent response to nondrug treatment protocols of molecular medicine (environmental medicine, nutritional medicine, medicine of self-regulation and medicine of fitness). With rare exceptions, the most important change my patients observe within 6-12 weeks of initiating treatment with these protocols is higher levels of energy.

    The increased level of energy brought about by the treatment protocols of molecular medicine is by far the most telling evidence for improvement in mitochondrial health.

    I know many of my physician-colleagues will jump at this statement in anger. They will decry it as subjective and will challenge its validity. I am amazed at how my physician friends are offended by any reference to the subject of energy when treatment protocols used do not include drugs. When my patients feel more energetic, they also show me clear and unequivocal objective laboratory evidence of molecular and immunologic changes. More importantly, my patients begin to reduce the dose of drugs they were taking previously for a variety of diseases previously until they can stop all drugs in most cases.

    Now for my scientist-physician colleagues. Many years ago, Peng and co-researchers discovered that mitochondria from the heart muscle which have been deprived of its blood supply are defective in energy (electron) transport and in energy-dependent calcium uptake (J Mol Chem Cardiol 9:897; 1961). This defect in mitochondrial function slows the rate of production of ATP, the principal energy molecule, and, quite literally, causes fatigue. They also made a crucial observation: The mitochondrial dysfunction - fatigue for the person afflicted by it - can be partially or completely reversed with EDTA chelation therapy.

    Investigations of how mitochondria age in health and disease performed by Gallagher several years earlier had suggested the same, i.e., that EDTA carries the potential for slowing the aging process of mitochondria (Nature 187:162; 1960). EDTA was thought to exert its beneficial effects by chelating (removing) toxic heavy metals as well as excess calcium within the mitochondria. Several subsequent studies clearly showed that mitochondrial health is essential for converting the chemical bond energy of foods into other forms of energy (electrical, osmotic, chemical and mechanical) for the various life processes (The Mitochondria, Chapter 13, John Wiley & Sons 1975).

    Japanese researchers were the first to report the increased incidence of DNA deletion in mitochondria of aging cells, sparking intense interest in the role of mitochondria in many other disorders. At present, many of my colleagues at Columbia University are engaged in active mitochondria research looking for a molecular basis of some primary muscle disorders (myopathies) and other muscle disorders such as Parkinson's disease. These and other studies are likely to provide direct experimental evidence for mitochondrial dysfunction in obesity.

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