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Prostate cancer prevention by nutritional means to alleviate metabolic syndrome^1,2,3,4

¹ From the Department of Physiological Science, University of California, Los Angeles

ABSTRACT

In 1987 when Reaven introduced syndrome X (metabolic syndrome, or MS), we were studying skeletal muscle insulin resistance and found that when rodents were fed a high-fat, refined-sugar (HFS) diet, insulin resistance developed along with aspects of MS, including hyperinsulinemia, hypertension, hypertriglyceridemia, and obesity. MS was controlled in rodents by switching them to a low-fat, starch diet and was controlled in humans with a low-fat starch diet and daily exercise (Pritikin Program). Others reported inverse relations between serum insulin and sex hormone–binding globulin (SHBG). When subjects were placed on the Pritikin Program, insulin fell and SHBG rose and it was suggested that prostate cancer might also be an aspect of MS. A bioassay was developed with tumor cell lines grown in culture and stimulated with serum before and after a diet and exercise intervention. Diet and exercise altered serum factors that slowed the growth rate and induced apoptosis in androgen-dependent prostate cancer cells. Changes in serum with diet and exercise that might be important include reductions in insulin, estradiol, insulin-like growth factor-I (IGF-I), and free testosterone with increases in SHBG and IGF binding protein-1. Hyperinsulinemia stimulates liver production of IGF-I, plays a role in the promotion of prostate cancer, and thus is the cornerstone for both MS and prostate cancer. Adopting a low-fat starch diet with daily exercise controls MS and should reduce the risk of prostate cancer.

Key Words: Insulin • insulin-like growth factor-I • IGF-I • IGFBP-1 • LNCaP • p53 • exercise

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