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Fructose And Diabetes Term Paper

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Fructose and Diabetes Does Fructose Consumption Cause Diabetes?

The availability of unlimited amounts of simple sugars is a modern phenomenon, having emerged with the onset of world trade in cane sugar during the 18th century (Tappy and Le, 2010). During the last half of the 20th century the development of high fructose corn syrup (HFCS), consisting of an equal mixture of glucose and fructose, has captured approximately 50% of the sweetener market because of lower cost, sweeter taste, improved shelf-life, and better moisture retention. Concern over its use as a sweetener in a variety of popular foods and drinks is growing though, because it coincides with a worldwide epidemic increases in obesity, diabetes, and metabolic syndrome (Yki-Jarvinen, 2010). This essay examines the evidence supporting or not supporting a causative role for fructose in type 2 diabetes.

Evidence for Fructose Causing Type 2 Diabetes

The prevalence of obesity and type 2 diabetes is significantly higher among African-American women than among Caucasian-American women, a difference that may be a function of diet. To determine whether consuming fructose in the form of sugar-sweetened soft drinks or fruit drinks is associated with type 2 diabetes in African-American women, a large prospective cohort study of approximately 59,000 subjects was examined (Palmer, Boggs, Krishnan, Hu, Singer, and Rosenberg,...

After excluding women with diabetes, cancer, heart disease, or who were pregnant or younger than 30 years of age, a cohort of 43,960 women was left. During the 10-year follow-up period, 2713 women developed type 2 diabetes. The relative risk ratios for developing diabetes was 1.11 and 1.24 for drinking one, or two or more, sweetened soft drinks per day, respectively (p = 0.002). Sweetened fruit juice produced a similar effect, with relative risk factors of 1.17 and 1.31 for one, or two or more, drinks per day, respectively (p = 0.001). By comparison, drinking equivalent amounts of orange or grapefruit juice did not increase the risk of developing type 2 diabetes (p = 0.28).
The above findings have been replicated using study subjects with different ethnic backgrounds. A cohort study (N = 4304) using a northern European sample of both men and women found an increased risk with fructose and glucose consumption (RR = 1.87, p = 0.003), regardless of whether it was in the form of food or drink (Montonen, Jarvinen, Knekt, Heliovaara, and Reunanen, 2007). Sucrose, lactose, or maltose was not associated with an increased risk for diabetes. The relative risk was greater in northern Europeans, when compared to African-American women, because the baseline levels of diabetes and obesity are generally elevated in African-American women independently of fructose or glucose consumption (Palmer, Boggs,…

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Studies using laboratory rodents have consistently shown that dietary fructose supplementation causes diabetes (reviewed in Rizkalla, 2010). For example, rats with free access to 10% fructose water developed glucose intolerance, hypertriglyceridemia, hyperinsulinemia, and ?-cell apoptosis (Maiztegui, Borelli, Raschia, Zotto, and Gagliardino, 2009). In agreement with these results, feeding six healthy, non-obese, young males a high-fructose diet for one week caused a significant reduction in plasma nonesterified fatty acid (NEFA) and increased triacylglyceride levels (Abdel-Sayed, Binnert, Le, Bortolotti, Schneiter, and Tappy, 2008). This finding suggests a fructose-rich diet suppresses lipid oxidation and thereby contributes to ectopic fat deposition in organs such as the liver. When 20 healthy subjects were fed a diet supplemented with either glucose or fructose, only the glucose diet resulted in weight gain (Silbernagel, Machann, Unmuth, Schick, Norbert, Haring, et al., 2011). However, the high fructose diet significantly increased fasting glucose levels, insulin insensitivity (also glucose), and serum triglyceride levels, which are all metabolic changes consistent with increased diabetes risk.

Evidence against Fructose Causing Type 2 Diabetes

A prospective cohort study of 15,792 men and women, with either Caucasian or African-American ethnicities and between the ages of 45 and 64, revealed no significant association between sweetened beverage consumption and diabetes onset during a nine-year follow-up period (Paynter, Yeh, Voutilainen, Schmidt, Heiss, Folsom, et al., 2006). Even the authors were surprised by this finding, in light of the results from studies. The authors suggested that age might be a factor, but the epidemiological studies presented here included
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