Modern yaşam tarzı ve yeni hastalıkları: Metabolik sendrom örneği

Modern insanın genetik yükü aynı kalmasına rağmen, çevresinde başdöndürücü bir değişim ortaya çıkmıştır. Bu değişime ayak uydurmak için zamana ihtiyacı olan genetik yük, çevre ile uyumsuzluk gösterdiği için ortaya “uygarlık hastalıkları” olarak tanımlanabilecek mortalite ve morbiditesi yüksek, tedavi maliyetleri son derece ağır rahatsızlıklar ortaya çıkmıştır. Çevresel değişimin asıl sorumlularından iki tanesi günlük yaşam tarzı ve beslenme değişiklikleridir. Bu değişim sanayi devrimi ile başlamış ve 20. yüzyıl ile hız kazanmıştır. Değişimin devam ettiği kabul edilirse “uygarlık hastalıkları”nın da bir süre daha ciddi bir toplum sağlığı sorunu olarak karşımızda duracağı açıktır. Bu sorun gelişmesini tamamlamış batı ülkeleri kadar, halen gelişmekte olan ülkemiz için de ciddiyetini korumaktadır.

Anahtar Kelimeler:

Metabolik hastalıklar, Hareketsiz yaşam tarzı, Metabolik sendrom X, Yaşam tarzı

Modern life style and new diseases: Metabolic syndrome

Although modern human genome remained relatively constant, the profound changes in its environment has been appeared. Genome are needed time to adapt these changes and at this point, the discordance leed the problem which have high mortality, morbidity, so-called “diseases of civilisation”. Some of the main changes occurred in environment are daily lifestyle conditions and dietary habits. These changes has started with industrial revolution and hastened with 20th century. If the environmental changes is accepted to continue, it is clear to understand that “diseases of civilisation” remain as a serious public health problem in front of us. This problem is not only for industrialized Western civilitasion but also for our country that continue to industrialize.

Keywords:

Metabolic Diseases, Sedentary Lifestyle, Metabolic Syndrome X, Life Style,

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1. Nesse RM, Williams GC. Why we get sick. The new science of Darwinian medicine. New York: Times Books, 1994.
2. Eaton SB, Konner MJ. Paleolithic nutrition. A consideration of its nature and current implications. N Engl J Med 1985; 312: 283–9.
3. Frassetto L, Morris RC Jr, Sellmeyer DE, Todd K, Sebastian A. Diet, evolution and aging—the pathophysiologic effects of the postagricultural inversion of the potassium-to-sodium and base-to-chloride ratios in the human diet. Eur J Nutr 2001; 40: 200 –13.
4. Gould SJ. The structure of evolutionary theory. Cambridge, MA: Harvard University Press, 2002.
5. Boaz NT. Evolving health: the origins of illness and how the modern world is making us sick. New York: Wiley & Sons, Inc, 2002.
6. Hedley AA, Ogden CL, Johnson CL, Carroll MD, Curtin LR, Flegal KN. Prevalence of overweight and obesity among US children, adolescents, and adults, 1999–2002. JAMA 2004; 291: 2847–50.
7. Allison DB, Fontaine KR, Manson JE, Stevens J, VanItallie TB. Annual deaths attributable to obesity in the United States. JAMA 1999; 282: 1530–8.
8. American Heart Association. Heart and stroke statistics—2004 update. Dallas: American Heart Association, 2003.
9. American Cancer Society. Cancer facts&figures 2004. Atlanta: American Cancer Society, 2004.
10. Cleave TL. The saccharine disease. Bristol, United Kingdom: John Wright & Sons, Ltd, 1974; 1974: 6 –27.
11. US Department of Agriculture, Economic Research Service. Food Consumption (per capita) data system, sugars/sweeteners. 2002. Internet: http: //www.ers.usda.gov/Data/foodconsumption/datasystem.asp (accessed 11 May 2004).
12. Ziegler E. Secular changes in the stature of adults and the secular trend of modern sugar consumption. Z Kinderheilkd 1967; 99: 146–66.
13. Meehan B. Shell bed to shell midden. Canberra, Australia: Australian Institute of Aboriginal Studies, 1982.
14. Hawkes K, Hill K, O’Connell JF.Whyhunters gather: optimal foraging and the Ache of eastern Paraguay. Am Ethnologist 1982; 9: 379 –98.
15. Gerrior S, Bente L. Nutrient content of the U.S. food supply, 1909-99: a summary report. Washington, DC: US Department of Agriculture, Center for Nutrition Policy and Promotion, 2002. (Home Economics report no. 55.)
16. Institute of Medicine of the National Academies. Dietary fats: total fat and fatty acids. In: Dietary reference intakes for energy, carbohydrate, fiber, fat, fatty acids, cholesterol, protein, and amino acids (macronutrients).Washington, DC: The National Academy Press, 2002: 335– 432.
17. Kris-Etherton PM, Harris WS, Appel LJ. Fish consumption, fish oil, omega-3 fatty acids, and cardiovascular disease. Circulation 2002; 106: 2747–57.
18. Simopoulos AP. Omega-3 fatty acids in inflammation and autoimmune disease. J Am Coll Nutr 2002; 21: 495–505.
19. Cordain L, Watkins BA, Florant GL, Kehler M, Rogers L, Li Y. Fatty acid analysis of wild ruminant tissues: evolutionary implications for reducing diet-related chronic disease. Eur J Clin Nutr 2002; 56: 181–91.
20. Jenkins DJ, Wolever TM, Taylor RH, et al. Glycemic index of foods: a physiological basis for carbohydrate exchange. Am J Clin Nutr 1981; 34: 362– 6.
21. Thorburn AW, Storlien LH, Jenkins AB, Khouri S, Kraegen EW. Fructose-induced in vivo insulin resistance and elevated plasma triglyceride levels in rats. Am J Clin Nutr 1989; 49: 1155– 63.
22. Taghibiglou C, Carpentier A, Van Iderstine SC, et al. Mechanism of hepatic very low density lipoprotein overproduction in insulin resistance. J Biol Chem 2000; 275: 8416 –25.
23. Reiser S, Powell AS, Scholfield DJ, Panda P, Fields M, Canary JJ. Day-long glucose, insulin, and fructose responses of hyperinsulinemic and non-hyperinsulinemic men adapted to diets containing either fructose or high-amylose cornstarch. Am J Clin Nutr 1989; 50: 1008–14.
24. Dirlewanger M, Schneiter P, Jequier E, Tappy L. Effects of fructose on hepatic glucose metabolism in humans. Am J Physiol Endocrinol Metab 2000; 279: E907–11.