The Relationship of Sugar to Population-Level Diabetes Prevalence: An Econometric Analysis of Repeated Cross-Sectional Data

Stanford Prevention Research Center, Department of Medicine, Stanford University, Palo Alto, California, United States of America.
PLoS ONE (Impact Factor: 3.23). 02/2013; 8(2):e57873. DOI: 10.1371/journal.pone.0057873
Source: PubMed


While experimental and observational studies suggest that sugar intake is associated with the development of type 2 diabetes, independent of its role in obesity, it is unclear whether alterations in sugar intake can account for differences in diabetes prevalence among overall populations. Using econometric models of repeated cross-sectional data on diabetes and nutritional components of food from 175 countries, we found that every 150 kcal/person/day increase in sugar availability (about one can of soda/day) was associated with increased diabetes prevalence by 1.1% (p <0.001) after testing for potential selection biases and controlling for other food types (including fibers, meats, fruits, oils, cereals), total calories, overweight and obesity, period-effects, and several socioeconomic variables such as aging, urbanization and income. No other food types yielded significant individual associations with diabetes prevalence after controlling for obesity and other confounders. The impact of sugar on diabetes was independent of sedentary behavior and alcohol use, and the effect was modified but not confounded by obesity or overweight. Duration and degree of sugar exposure correlated significantly with diabetes prevalence in a dose-dependent manner, while declines in sugar exposure correlated with significant subsequent declines in diabetes rates independently of other socioeconomic, dietary and obesity prevalence changes. Differences in sugar availability statistically explain variations in diabetes prevalence rates at a population level that are not explained by physical activity, overweight or obesity.

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Available from: Nancy Hills, Sep 02, 2014
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    • "Excessive consumption of high sugar foods and drinks, which are both cheap and readily available, plays a central role in development of obesity in humans. Increasing sugar consumption affects the majority of the developed and developing world (Lustig et al. 2012; Basu et al. 2013) and a major contributor to this increase is the widespread availability of relatively cheap sugar sweetened beverages or soft drinks (Guthrie and Morton 2000; Popkin and Nielsen 2003). Consumption of soft drinks has been shown to contribute to 80% of the increase in added sugar consumption during the period 1962–2000 in the USA (Popkin and Nielsen 2003) and today are the largest single source of added sugar consumption (Yang et al. 2014). "
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    ABSTRACT: In this study we sought to determine the effect of daily sucrose consumption in young rats on their subsequent performance in tasks that involve the prefrontal cortex and hippocampus. High levels of sugar consumption have been associated with the development of obesity, however less is known about how sugar consumption influences behavioral control and high-order cognitive processes. Of particular concern is the fact that sugar intake is greatest in adolescence, an important neurodevelopmental period. We provided sucrose to rats when they were progressing through puberty and adolescence. Cognitive performance was assessed in adulthood on a task related to executive function, a rodent analog of the Stroop task. We found that sucrose-exposed rats failed to show context-appropriate responding during incongruent stimulus compounds presented at test, indicative of impairments in prefrontal cortex function. Sucrose exposed rats also showed deficits in an on object-in-place recognition memory task, indicating that both prefrontal and hippocampal function was impaired. Analysis of brains showed a reduction in expression of parvalbumin-immunoreactive GABAergic interneurons in the hippocampus and prefrontal cortex, indicating that sucrose consumption during adolescence induced long-term pathology, potentially underpinning the cognitive deficits observed. These results suggest that consumption of high levels of sugar-sweetened beverages by adolescents may also impair neurocognitive functions affecting decision-making and memory, potentially rendering them at risk for developing mental health disorders. © 2015 Reichelt et al.; Published by Cold Spring Harbor Laboratory Press.
    Learning & memory (Cold Spring Harbor, N.Y.) 04/2015; 22(4):215-24. DOI:10.1101/lm.038000.114 · 3.66 Impact Factor
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    • "This is also the case in many other epidemiological research papers that have used sugar production or disappearance data as the bases for correlations with obesity, as well as papers that cite such data for building their arguments. More recently, Basu et al. ( 100 ) used food supply data from the UN FAO to capture the market availability of different food items worldwide. From this, the authors concluded that an increase in sugar availability was associated with higher diabetes prevalence after testing for potential selection biases and controlling for other food types, total energy intake, overweight and obesity, period effects, and several socio-economic variables such as ageing, urbanisation and income. "
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    ABSTRACT: A causal role of fructose intake in the aetiology of the global obesity epidemic has been proposed in recent years. This proposition, however, rests on controversial interpretations of two distinct lines of research. On one hand, in mechanistic intervention studies, detrimental metabolic effects have been observed after excessive isolated fructose intakes in animals and human subjects. On the other hand, food disappearance data indicate that fructose consumption from added sugars has increased over the past decades and paralleled the increase in obesity. Both lines of research are presently insufficient to demonstrate a causal role of fructose in metabolic diseases, however. Most mechanistic intervention studies were performed on subjects fed large amounts of pure fructose, while fructose is ordinarily ingested together with glucose. The use of food disappearance data does not accurately reflect food consumption, and hence cannot be used as evidence of a causal link between fructose intake and obesity. Based on a thorough review of the literature, we demonstrate that fructose, as commonly consumed in mixed carbohydrate sources, does not exert specific metabolic effects that can account for an increase in body weight. Consequently, public health recommendations and policies aiming at reducing fructose consumption only, without additional diet and lifestyle targets, would be disputable and impractical. Although the available evidence indicates that the consumption of sugar-sweetened beverages is associated with body-weight gain, and it may be that fructose is among the main constituents of these beverages, energy overconsumption is much more important to consider in terms of the obesity epidemic.
    Nutrition Research Reviews 03/2014; FirstView(3):2014. DOI:10.1017/S0954422414000067 · 3.91 Impact Factor
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    • "Population prevalence of diabetes from 173 countries was found to be positively related to sugar exposure [13]. Duration and degree of sugar exposure was found to correlate with diabetes prevalence in a dose-dependent manner, while declines in sugar exposure correlated with significant subsequent declines in diabetes rates independently of other socioeconomic, dietary and obesity prevalence changes [14]. "
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    ABSTRACT: Diabetes mellitus (DM) is a rampant epidemic worldwide. Causative factors and predisposition is postulated to be multi-factorial in origin and include changing life styles and diet. This paper examines the relationship between per capita sugar consumption and diabetes prevalence worldwide and with regard to territorial, economic and geographical regions. Data from 165 countries were extracted for analysis. Associations between the population prevalence of diabetes mellitus and per capita sugar consumption (PCSC) were examined using Pearson's correlation coefficient (PCC) and multivariate linear regression analysis with, infant mortality rates (IMR, as an general index maternal and child care), low birth weight (LBW, as an index of biological programming) and obesity prevalence included in the model as confounders. Despite the estimates for PCSC being relatively crude, a strong positive correlation coefficient (0.599 with p < 0.001) was observed between prevalence of diabetes mellitus and per capita sugar consumption using data from all 165 countries. Asia had the highest correlation coefficient with a PCC of 0.660 (p < 0.001) with strongest correlation noted in Central (PCC = 0.968; p < 0.001), South (PCC = 0.684; p = 0.050) and South East Asia (PCC = 0.916; p < 0.001). Per capita sugar consumption (p < 0.001; Beta = 0.360) remained significant at the last stage as associations of DM prevalence (R2 = 0.458) in the multivariate backward linear regression model. The linear regression model was repeated with the data grouped according to the continent. Sugar was noted to be an independent association with DM only with regard to Asia (p < 0.001 Beta = 0.707) and South America (p = 0.010 Beta 0.550). When countries were categorized based on income PCS and DM demonstrated significant association only for upper middle income countries (p < 0.001 Beta 0.656). These results indicate independent associations between DM prevalence rates and per capita sugar consumption both worldwide and with special regard to the Asian region. Prospective cohort studies are proposed to explore these associations further.
    BMC Public Health 02/2014; 14(1):186. DOI:10.1186/1471-2458-14-186 · 2.26 Impact Factor
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