Fructose consumption and body weight

Fructose is a monosaccharide (simple sugar), which the body can use for energy. Because it does not cause blood sugar rise tremendously, it was once thought that fructose was a good substitute for sucrose (table sugar). However, nutritional experts have changed their minds about this. A small amount of fructose, such as the amount found in most vegetables and fruits, is not a bad thing. In fact, there is evidence that a little bit may help your body process glucose properly. However, consuming too much fructose at once seems to overwhelm the body's capacity to process it and it causes overweight. Is that true?

Acute studies in humans: fructose, food intake and satiety
In an acute-term study (short-term studies with exposure periods usually lasting 48 to 96 hours), 12 normal -weight women consumed meals containing 55, 30 or 15% of total calories as carbohydrate, fat and proteins with 30% of Kcal as either fructose sweetened or glucose sweetened beverages. As expected, glucose excursions and insulin secretion were lower after fructose meals than after glucose ones. This was associated to a decrease in leptin levels (leptin hormones signal your brain that you are full; decrease in leptin levels meaning, less appetite), which is an expected consequence of lowering insulin levels. It is important to notice that the reduction in leptin levels remained within physiological normal levels. Fructose meals might increase caloric intake and ultimately contribute to weight gain and obesity.



Chronic studies in humans
Although acute fructose consumption could not stimulate leptin secretion, an increase in fasting leptin levels was detected after chronic high fructose intake (1 to 4 weeks) in healthy individuals, which may suggest that high fructose feeding may suppress food intake in the long term. Another long term study in overweight/obese humans showed no change in body weight after 10 week-supplementation with glucose or fructose, indicating that the effect of fructose or glucose on food intake might not differ on long term bases.



Cross-sectional studies
In a cross-sectional study, BMI had a statistically positive relationship with diet carbonated soft drink consumption for 1749 of children (6-11 years) and adolescents (12-19 years). Other cross-sectional studies in American children demonstrated a positive correlation between soft drinks and BMI. The obese children consumed more of all types of food with no difference between obese and non obese children's consumption patterns. However, most of the cross-sectional studies included no controls for sedentary behaviors, physical activity, and energy intake from other sources other than beverages in the model. Moreover, in these studies BMI and beverage consumption were self-reported and hence subject to measurements errors. Causal relationship cannot be made from cross-sectional study design.



Longitudinal epidemiologic studies
In a cohort of more than 10,000 males and females (9-14 years in 1996), authors did not find a correlation between BMI and snack food consumption, including sugar-sweetened beverages when controlling for total energy. Even in another study among 30 children aged 6-13 years who was attending a summer camp in 1997, excessive sweetened drink consumption (>370g/day) did not correlate with weight gain. Again results of these longitudinal studies are not conclusive. Most of the positive correlations presented disappeared when corrected by total energy.


Conclusion
The relation between fructose and obesity has been derived mainly from epidemiological studies trying to relate the increase in consumption of dietary fructose on one hand and to the increase in obesity. In the epidemiological, cross -sectional and longitudinal studies, the overall evidence for a positive correlation between consumption of soft drinks and overweight is limited. Causal inferences cannot be made from cross-sectional study designs with values subjected to measurement error. Clearly fructose itself is not driving the obesity epidemic, but there is evidence supporting the possibility that refined carbohydrates in general could have a contributory role, if not a major one. Very recently, this problem has been attributed to all added sugars and not only added fructose. Whatever the cause of obesity, based on the currently available evidence, an expert panel formed by the Centre of Food Nutrition and Agriculture Policy concluded that fructose does not appear to contribute to overweight and obesity any differently than other energy sources (Rizkalla, 2010).


Reference
Rizkalla, S. (2010). Health implications of fructose consumption: A review of recent data. Nutrition & Metabolism. doi:10.1186/1743-7075-7-82. Retrieved from http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2991323/?tool=pubmed