The means for each endpoint have a common SE based on the appropriate repeated-measures ANOVA error term; to convert cholesterol to mg/dl, multiply by 38.6; to convert triglycerides to mg/dl, multiply by 88.5.
aBecause 6 paired comparisons of this endpoint were made (all data not shown), only p < 0.008 (0.05/6) should be considered significant at the 0.05 level.
Consistent with the idea that dietary fructose might increase energy intake are data from Ludwig et al.  which demonstrated an association between consumption of sugar-sweetened drinks and obesity in children. Further evidence is provided by Raben et al.  who fed overweight subjects supplements of either sucrose or artificial sweeteners for 10 weeks. The subjects who consumed sucrose demonstrated increases in energy intake, body weight, fat mass and blood pressure. However, it is important to point out that subjects in the sucrose group were 'instructed' to consume 2g sucrose/kg body weight daily (~23% of energy intake) and were provided with the necessary sucrose-sweetened beverages and foods to do so. Thus, the increased sucrose intake was not spontaneous. These two studies were the main evidence cited by the World Health Organization when implicating sugars as a cause of obesity and to justify their recommendation that free sugar consumption be less than 10% of total daily energy intake .
Fig. 2. Mean plasma triacylglycerol (triglyceride) concentrations in women (a) and men (b) during the 24-hour metabolic profiles on day 42 of the fructose (-) and glucose (------) diets. Significant difference (*) between the two points is shown, p < 0.006 (0.05/9, Bonferroni adjustment for multiple comparisons). To convert triglycerides to mg/dl, multiply by 88.5 [from 22].
Although increasing fructose consumption is temporally associated with the increasing worldwide prevalence of obesity, there is little or no evidence proving cause and effect. In the US, increasing energy intake was associated with increased restaurant and fast-food meals and increased consumption of salty snacks and pizza as well as soft drinks . Decreased physical activity is also almost certainly a factor in the increasing prevalence of obesity. To demonstrate that dietary fructose is important in causing obesity, it would be necessary to conduct a clinical trial demonstrating that fructose caused a spontaneous increase in energy intake. Given fructose's availability, low cost and pleasant taste, such a clinical trial might provide important new information.
In summary, fructose is a naturally occurring sugar with a pleasant taste. It produces a smaller postprandial rise in plasma glucose than other common carbohydrates and thus may be a useful sweetening agent in the diabetic diet. However, dietary fructose appears to have adverse effects on plasma lipids. Moreover, there is concern that dietary fructose may stimulate energy intake and promote weight gain and obesity. Thus, adding large amounts of fructose to the diet may be undesirable. Nevertheless, concern about fructose should not extend to the naturally occurring fructose in fruits and vegetables. These are healthy foods which provide only a modest amount of fructose in most diets.
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