Metabolic syndrome description

The association of insulin resistance with a clustering of cardiovascular risk factors including hyperinsuhnemia, hypertension, abdominal obesity, dyslipidemia, and coagulation abnormahties has been referred to by a variety of names including the insuhn resistance syndrome, the metabolic syndrome, the dysmetabolic syndrome, and the deadly quartet, to name a few. Since the description of the insulin resistance syndrome by Reaven in 1988, the number of associated factors has continued to grow. 

This concept and the description of metabolic syndrome are used as a basis to comprehension of seaweeds against two dreadful illnesses of our times high blood pressure and cancer. 

As stated earlier, the annual cycles of species and populations divide into periods. The overall description would be the syndrome of the population, while individual metabolic characteristics would be symptoms , borrowing terms from the medical profession. Each period manifests a specific set of metabolic features which support the normal course of vital processes in the population, and the population would enter the next period of the cycle only if the preceding step had been completed. If it had not, the situation would lead to that mass mortality which is so common in nature. The change in metabolism is triggered with the help of the endocrine system, as will be described in the next section. 

Recent advances in the understanding of human purine metabolism have been stimulated by the discovery of specific inborn errors of this pathway in man. In particular, the demonstration of the deficiency of hypoxanthine-guanine phosphoribosyltransferase (HGPRT) in the Lesch-Nyhan syndrome and in some patients with gout has contributed essential information on the regulation of purine biosynthesis novo and on the critical role of this reutilization pathway in central nervous system function in man. The search for other disorders led to the description of a partial deficiency of adenine phosphoribosyltransferase (APRT) in four members in three generations of one family. Each of the subjects partially deficient in APRT exhibited a normal serum urate concentration and the propositus had a normal excretion of uric acid (Kelley, et al., 1968). We have investigated a second family partially deficient in APRT (Fox and Kelley, in press). 

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