Please take the term metabolic syndrome out of you vocabulary. Replace it with insulin toxicity. In this Metabolic Syndrome Course, I marshall a large body of scientific information to support my position.

How wide is the problem of the metabolic syndrome among adults now? What may be expected in the next two deacdes considering the rising incidence of the syndrome among children? Consider the following quote from the editorial in June 4, 2004 issue of Science:

It is not surprisng that the spokesperson of food industry did not wish to talk about direct toxicity of foods it serves. What surprised me in that editorial was that the editors of Science utterly failed to consider that subject as well. They went on to laud WHO's formal approval of Global Strategy on Diet, and wrote a few words on "behavioral modification," which, we all know, is code word for doing nothing, until the time of writing the next editorial on the subject a year or two later. How might the WHO modify the behavior of one billion people in the world?, one might ask.

If the energetic-molecular basis of the metabolic is cellular dysoxygenosis, one would expect that every clinical components of the syndrome will be found to be related to every. That, indeed, is the case. The support for that view can be drawn from diverse lines of evidence.^20-24

In the metabolic syndrome, oxidative-dysoxygenative insulin dysfunction (ODID) perpetuates and intensifies the derangement in signaling pathways of the syndrome.²¹ The prevalence of the syndrome increases with the degree of ODID. ²³ In severely obese adults, the risk of death from all causes is about twice that among individuals with moderate obesity.²⁵

Recent studies show that the metabolic syndrome in children and adolescents is far more common than previously reported and that its prevalence increases directly with the degree of obesity. Furthermore, the syndrome can develop rapidly with rapd weight gain, each element of the syndrome worsening with increasing obesity. Not unexpectedly, each aspect of the syndrome worsens with incremental weight, independent of age, sex, and pubertal status.²⁶ Waist circumference correlates well with visceral adiposity.²⁷ However, changes associated with puberty and variations among racial and ethnic groups may significantly change that relationship.²⁸

In an obesity-prone culture, one could predict that the pathophysiological mechanisms of the metabolic syndrome would be recognizable in childhood. That, indeed, is borne out by recent studies.³ As for racial and ethnic groups, in one study the prevalence of the metabolic syndrome was substantially lower in blacks than in white subjects when criteria for serum lipid levels were the same. But the differences disappeared when lipid criterai specific to blacks were employed.

If the energetic-molecular basis of the metabolic is cellular dysoxygenosis, one would expect that every biomarker of the syndrome will be found to be related to every other. That, indeed, is the case. The support for that view can be drawn from diverse lines of evidence. ^3,29,30

C-reactive protein and interleukin-6 levels are biomarkers of cellular inflammation, as well as of cellular dysoxygenosis. The rise in those biomakers is usually concordant. The adiponectin level, by contrast, may be seen as a marker of insulin sensitivity and integrity of insulin signaling as well as oxygen homeostasis. Again, the falling levels of adiponectin correlate wirth rising levls of CRP and interleukin-6. Furthermore, the raised blood levels of C-reactive protein in the metabolic syndrome are incrementally higher with increasing number of components of the syndrome.

Adiponectin levels are negatively correlated with C-reactive protein, and are lower in obesity individuals. When stratified according to obesity group and insulin-resistance category, the adiponectin levels are significantly associated with the obesity category, as well as with the insulin-resistance category. The lowest levels tend to be seen in persons with the highest level of insulin resistance. Interestingly, adiponectin levels in the severely obese group do not vary significantly according to the insulin-resistance category. Persons with severe insulin resistance have the lowest levels of adiponectin.

* Why Internists Should Not Ever Make the Diagnosis of the Metabolic Syndrome?

* Why Endocrinologists Should Not Ever Make the Diagnosis of the Metabolic Syndrome?

* Why Diabetes Specialists Should Not Ever Make the Diagnosis of the Metabolic Syndrome?

* Why Obesity Specialists mShould Not Ever Make the Diagnosis of the Metabolic Syndrome?

* Why Weight Loss Surgeons Should Not Ever Make the Diagnosis of the Metabolic Syndrome?

* Why Weight Loss Merchants Should Not Ever Make the Diagnosis of the Metabolic Syndrome?

Course on Metabolism

* Metabolism

*  Metabolic Syndrome Course

* Metabolic Syndrome in Adults

* Metabolic Syndrome in Children

* Why I Never Diagnose the Metabolic Syndrome? Nor Should Anyone Else

*  Enzymes: Oxygen's Workhorses

*  Vitamins - Oxygen's Special Agents

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