A Cutting Edge Reply

A recent article 1 emphasized the increasing obesity within the American population, and the author criticized the Food and Drug Administration for not allowing wider use of olestra to reduce fat/caloric intake. This article crystallizes what is wrong with much health-related research today. It is a classic example of looking for a 'magic bullet' approach to a serious problem rather than making the comprehensive lifestyle changes required. I have been conducting a text-mining study on the discipline of caloric restriction, focusing on the eclectic laboratory and clinical nonpathological experiences with controlled caloric restriction for health improvement, applied to all living species. Excluded are starvation, disease-caused caloric restriction, surgically-driven caloric restriction, and psychologically-driven caloric restriction (bulimia, anorexia). Preliminary results offer the following conclusions: Caloric restriction in species with short life spans, mainly rodents, increases mean and maximal life-span substantially. 2-6 In parallel, some of these studies show how the degenerative diseases that contribute to reduced longevity are eliminated or ameliorated. 2, 4, 7, 8, 9 Highly controlled laboratory studies are under way to see whether similar benefits of caloric restriction apply to larger and longer-lived species, such as nonhuman primates.10-12 While more than a decade will be required to observe changes in maximal life span, preliminary results show that the median life span of one group of restricted monkeys is already exceeding that of ad libitum-fed monkeys.11 In addition, emerging data from primate studies strongly support that physiological responses to caloric restriction in monkeys parallel the extensive findings reported in rodents.10 Parallel long-term controlled studies on humans have not been done, and even if started today, would take many decades to obtain definitive quantitative results. Short-term studies on humans have been performed, using very-low-calorie/hypocaloric diets, and fasting. Positive changes in biomarkers for a number of physical problems, such as cardiovascular, hypertension, and diabetes (and obesity itself), have been observed.13-15 Thus, the hard laboratory and clinical evidence shows that caloric restriction can provide longevity and good health for small species, may provide such benefits to nonhuman primates, and may offer the potential to provide such benefits to humans. As far as I have been able to determine, controlled caloric restriction is the only regimen that has been demonstrated in the laboratory to increase life span, and therefore may be the foundational requirement for proper diet. In particular for humans, how can we make optimal use of these findings before all the conclusive laboratory and clinical data have been obtained? Controlled laboratory and clinical studies on caloric restriction are not the only source of useful information. Another completely ignored source of information is examining the food available to humans, and deducing its intrinsic impact on human structure. From an engineering perspective, human beings were designed to be lean, to minimize loads on the body's weight-bearing structures and joints and to minimize circulation restrictions. The fundamental fuel available for humans is designed to ensure that humans remain lean. Unprocessed human food is mainly high bulk and low calorie. In addition, it has high ratios of fiber, vitamins, and minerals to calories, thereby satisfying nutritional as well as leanness requirements. The human body has built-in governors to limit the amount of unprocessed food that can be ingested. All food processing has the effect of artificially stimulating the appetite, allowing more food to be ingested than the body's natural governors would allow, and thereby increasing caloric consumption beyond functional requirements. Most low-calorie and low-volume processed food diets don't work in the long-term, because low amounts of processed food lead to stimulated appetite along with unnatural feelings of food deprivation. The 'magic bullet' approach adds yet another artificial substance to the dietary armamentarium. It modifies a few biomarkers, has a few negative side effects, but mainly serves as a vehicle to allow highly processed and low nutritive value food items. Obesity is the prime result of poor dietary practices today, and is a biomarker for myriad serious diseases. To seriously reduce obesity over the long term, substances and processes that artificially stimulate appetite need to be eliminated from the diet. The whole idea of 'tasty' food needs to be modified. The terminology needs to be changed: Caloric Restriction is nature's design for all species; there is nothing restrictive about it. Ronald N. Kostoff, Ph. D. Alexandria, VA 22304 References 1. H.I. Miller, "The cutting edge of cutting calories," The Scientist, 15[4]:39, Feb. 19, 2001. 2. E.J. Masoro, "Caloric restriction and aging: an update," Experimental Gerontology, 35:299-305, 2000. 3. A.S. Nicolas et al., "Caloric Restriction and Aging," Journal of Nutrition, Health, and Aging, 3[2]: 77-83, 1999. 4. K. Yoshida et al., "Caloric restriction and spontaneous hepatic tumors in CH3H/He mice," Journal of Nutrition, Health, and Aging, 3:121-6, 1999. 5. H. Sogawa, C. Kubo, "Influence of short-term repeated fasting on the longevity of female (NZB x NZW)F1 mice," Mechanisms of Aging and Development, 115[1-2]:61-71, 2000. 6. A. Mittal et al., "Reduced food consumption increases water intake and modulates renal aquaporin-1 and -2 expression in autoimmune prone mice," Life Sciences, 66:1471-9, 2000. 7. K. Eckles-Smith et al., "Caloric restriction prevents age-related deficits in LTP and in NMDA receptor expression," Molecular Brain Research, 78[1-2]:154-62, 2000. 8. W.T. Cefalu et al., "Chronic caloric restriction alters muscle membrane fatty acid content," Experimental Gerontology, 35:331-41, 2000. 9. W. Hart et al., "Adaptive role of caloric intake on the degenerative disease processes," Toxicological Sciences, 52[2 Suppl]:3-12, 1999. 10. M.A. Lane, "Nutritional modulation of aging in nonhuman primates," Journal of Nutrition, Health, and Aging, 3[2]:69-76, 1999. 11. B.C. Hansen et al., "Caloric restriction in nonhuman primates: mechanisms of reduced morbidity and mortality," Toxicological Sciences, 52[2 Suppl]: 56-60, 1999. 12. J. Wanagat et al., "Caloric intake and aging: mechanisms in rodents and a study in nonhuman primates," Toxicological Sciences, 52[2 Suppl]:35-40, 1999. 13. T. Pekkarinen et al., "Weight loss with very-low-calorie diet and cardiovascular risk factors in moderately obese women: one-year follow-up study including ambulatory blood pressure monitoring," International Journal of Obesity & Related Metabolic Disorders, 22:661-6, 1998. 14. F. Capstick et al., "Very low calorie diet (VLCD): a useful alternative in the treatment of the obese NIDDM patient," Diabetes Research & Clinical Practice, 36[2]:105-11, 1997. 15. C.M. Rotella et al., "Short cycles of very low calorie diet in the therapy of obese type II diabetes mellitus," Journal of Endocrinological Investigation, 17:171-179, 1994.

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