arbohydrates are increasingly being seen as the cause of weight gain and obesity. More specifically, overconsumption of sugar and refined carbohydrates are now considered to be a direct cause of insulin resistance, which subsequently causes development of the metabolic syndrome and abdominal obesity. Sugar is particularly implicated in the development of obesity because the fructose moiety of the sucrose molecule, if over consumed, causes liver overload and the accumulation of lipids within hepatic tissue. This can then lead to the development of non-alcoholic fatty liver disease and modifications to normal metabolic pathways including detrimental changes to lipoprotein metabolism. Refined carbohydrates exacerbate the problem of sugar because they cause detrimental postabsorptive glycaemic effect. Animal and humans studies show that fructose is the cause of mammalian insulin resistance, and overfeeding studies confirm that this is a direct cause of non-alcoholic fatty liver disease.
For example, in one study published in the American Journal of Clinical Nutrition1, researchers placed 16 subjects on a hypercaloric diet that was comprised of their normal diet with an additional 1000 kcal of 98% refined carbohydrates, including fructose containing sugars. Following 3 weeks of overfeeding the subject consumed a hypocaloric diet for 6 months. The carbohydrate overfeeding period increased total body weight by just 2 % but at the same time increased liver fat by 27 % suggesting that lipid accumulation in hepatic tissue had occurred. This was confirmed by measurements of de novo lipogenesis, which the researchers showed were associated with increased liver fat and increases in fasting triglycerides in subjects with the PNPLA3-14811 gene variant, but not the PNPLA3-148MM gene variant. During the hypocaloric phase the subjects lost 4 % of total body weight and 25 % of their liver fat.
The researchers assumed that hypocaloric intake in the weight loss phase of this trial was the cause of the fat loss from the liver and weight loss from both the subcutaneous and abdominal fat compartments of the subjects. However, it is not possible to conclude that weight loss was caused by the forced calorie restriction, because the hypocaloric phase also removed the high intakes of sugar and refined carbohydrates from the diets of the subjects. If the researchers had included an additional group in the weight loss phase of the trial that followed an ad libitum high quality diet devoid of sugar, they would probably have found that this group also lost weight and liver fat without the need for a hypocaloric diet. This is because it was likely the addition of sugar and refined carbohydrate to the diet that caused the metabolic changes which lead to weight gain, and their withdrawal that corrected the problem.
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