A study in the current issue of Obesity Research that adds another piece to the growing pile of evidence showing fructose to be a lipogenic (fat causing) sugar.
Although this is a study of the effects of fructose consumption in mice, I think the information is valuable. I prefer human studies to rodent studies, but in many cases the data obtained from rodent (or other animal) studies could not be gathered from similar human studies. To make this study a human study, genetically similar human subjects would have to be kept under observation for a large percentage of their lives, have their food choices closely controlled, and have their livers removed at the end of the studyâ€”obviously an impossibility.
The researchers divided a genetically similar strain of mice into four groups. All groups were provided unlimited amounts of standard mice chow along with one of the following four liquids: a 15% solution of fructose in water, a soft drink made with 19% sucrose (table sugar), a diet soft drink sweetened with aspartame, or water (the control group). Food and drink intake were carefully measured.
After 73 days–a long time in mice years–the mice were analyzed for the effects of their diet. Interestingly, all the mice consumed about the same number of calories throughout the study. The mice in the fructose group consumed less food and more drink than the other groups.
The mice in the soft drink, diet soft drink, and water groups all gained about the same amount of weight. The fructose group of mice, however, had gained significantly more weight than mice in the other three groups.
In terms of body composition, the fructose fed mice had a greater percentage of body fat. The body fat percentage of the soft drink group was trending upward, but hadn’t reached statistical significance relative to the other two groups.
Finally, the mice in the fructose group had the most fat in their livers. The mice in the soft drink group had an accumulation of fat in their livers compared to the diet soft drink and water group, neither of which had significant liver fat.
The authors report:
In summary, dietary fructose consumed with beverages promotes adiposity and the risk for nonalcoholic fatty liver disease in mice. In view of the impressive rise in worldwide fructose consumption over the last two decades, fructose is, therefore, likely to represent one causal factor for the rapidly increasing number of obese patients. This may be based, in part, on the increasing per capita consumption of dietary fructose from popular carbonated soft drinks.
To our knowledge, this study shows for the first time prospectively that a causal relationship between exposure to fructose-sweetened beverages and an increase in fat mass exists. We also report that the fructose-induced increase in fat mass is mainly based not on an increased amount of ingested calories but more likely on the specific energy and sugar metabolism of dietary fructose. Studies to uncover the exact pathophysiological and biochemical mechanisms responsible for the observed adiposity-promoting effects are underway and may allow a better understanding of crucial molecular interactions between macronutrients and the regulatory mechanisms governing energy balance.
The interesting thing about fructose is that in small amounts it increases insulin sensitivity. The amount probably found in the average Paleolithic diet would make the entire insulin/glucose regulatory system work better. But more fructose than just a few grams is trouble, and that’s trouble with a T and that rhymes with P and that stands for Phat!