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• W2128807789 abstract "In the past decade, type 2 diabetes mellitus has become an increasingly more common occurrence in children, a trend that parallels the increase in childhood obesity (1). Obesity is strongly associated with insulin resistance (2) and type 2 diabetes mellitus (T2DM), and currently .20% of all children and adolescents in the United States are overweight (3). Childhood obesity is also a strong predictor of adult obesity and other aspects of the metabolic syndrome, including insulin resistance and abnormal lipids (4). However, the distribution of adiposity rather than body mass index (BMI) alone is a better predictor of insulin resistance. Waist circumference is more associated with visceral fat (5), whereas BMI is more associated with subcutaneous fat, and in most reports it is visceral fat rather than BMI that is associated with fasting insulin and triglycerides, rather than BMI alone. This makes visceral adipose tissue (VAT) an independent predictor of metabolic disease (6), which supports the following American Heart Association statement: ‘‘Given the significant increase in waist circumference among US children and adolescents over the past 2 decades, a marker of abdominal obesity should be considered as an important component of the pediatric metabolic syndrome definition’’ (1). It therefore becomes important to understand the effect of diet not just on overall BMI but on the distribution of adiposity. The study by Davis et al (7) in this issue of the Journal is thus significant. On the basis of considerable previous research from their laboratory showing that high intakes of total and added sugar were the only dietary components associated with total body fat and poor b cell function in overweight Latino children (8), and a 16-wk nutrition and exercise trial that showed decreased added sugar intake had a 33% improvement in insulin secretion and increased fiber intake had a 10% reduction in VAT (9), Davis et al (7) hypothesized that a decrease in fiber over time and/or an increase in added sugar would negatively affect indicators of T2DM. With the use of cohort data from the University of Southern California SOLAR (Study of Latino Adolescents at Risk), which began in 2000, the authors addressed changes in diet and T2DM risk factors over time (at the beginning and end of an ’2-y time period). Interestingly, they found no effect of added sugar on any indicator, but they did find an effect of decreased fiber intake on VAT. At issue are the following questions: Why was no effect of added sugar observed, and how significant is the effect of fiber in decreasing visceral adiposity? The authors suggest that the lack of effect of added sugar intake on BMI, total fat, visceral adiposity, or blood glucose or insulin concentrations could be attributed to the lack of variability in ‘‘added sugar’’ intake, which was relatively high at baseline and follow-up (7), and this is probably the explanation that is most plausible. However, it should be noted that the strength of the effect of added sugar intake on BMI and T2DM is actually quite controversial, and many other studies have failed to report such a relation. When the Dietary Reference Intake Committee for the Macronutrients reviewed the data on added sugar intake and BMI, they found it inconclusive (10). In fact, when it comes to interpreting cross-sectional studies on added sugar and calories or added sugar and weight gain, results are often counterintuitive. For example, in the literature review on added sugars and BMI in the Dietary Reference Intake Macronutrient Report (10) (pp 307–313; Tables 6–11), there is a consistent negative correlation between total sugar intake and BMI both for children and adults (10). This may be due to underreporting of food intake in general (11) and of sugar intake specifically (12), which is more prevalent in obese than in lean individuals. It may also help to explain why individuals in the current study (7) who reported sugar intake in 2 sets of 2-d dietary recalls also did not show an effect of sugar on any tested variable, particularly because the subjects were overweight and the dietary recall data were selfreported. The 2005 Dietary Guidelines Advisory Committee also reviewed the data on added sugar and weight gain and BMI (13) and benefited from additional longitudinal studies that were published subsequent to the Dietary Reference Intake Macronutrient Report. They concluded, in part, that ‘‘Although more research is needed, available prospective studies suggest a positive association between the consumption of sugar-sweetened beverages and weight gain’’ (13) (section 4, Carbohydrates). It will be of interest to see the conclusions of the 2010 Dietary Guidelines Advisory Committee on the overall significance to health of added sugars in the diet. It appears from previous studies mentioned in the Davis et al (7) article and others that weight gain due to added sugar consumption causes a more generalized increase in BMI, when it occurs, that affects subcutaneous fat rather than causing a specific effect on VAT as seen with dietary fiber. Fiber, on the other hand, showed a protective effect against excess adiposity, and there is a developing literature to support this. There are a number of potential mechanisms by which fiber" @default.
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• W2128807789 date "2009-11-01" @default.
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• W2128807789 title "Sugar and fiber intake and type of adiposity: are they related?" @default.
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• W2128807789 doi "https://doi.org/10.3945/ajcn.2009.28724" @default.
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