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      Changes in Intakes of Total and Added Sugar and their Contribution to Energy Intake in the U.S.

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          Abstract

          This study was designed to document changes in total sugar intake and intake of added sugars, in the context of total energy intake and intake of nutrient categories, between the 1970s and the 1990s, and to identify major food sources contributing to those changes in intake. Data from the NHANES I and III were analyzed to obtain nationally representative information on food consumption for the civilian, non-institutionalized population of the U.S. from 1971 to 1994. In the past three decades, in addition to the increase in mean intakes of total energy, total sugar, added sugars, significant increases in the total intake of carbohydrates and the proportion of carbohydrates to the total energy intake were observed. The contribution of sugars to total carbohydrate intake decreased in both 1–18 y and 19+ y age subgroups, and the contribution of added sugars to the total energy intake did not change. Soft drinks/fluid milk/sugars and cakes, pastries, and pies remained the major food sources for intake of total sugar, total carbohydrates, and total energy during the past three decades. Carbonated soft drinks were the most significant sugar source across the entire three decades. Changes in sugar consumption over the past three decades may be a useful specific area of investigation in examining the effect of dietary patterns on chronic diseases.

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          Diet, nutrition and the prevention of chronic diseases.

          Shifting dietary patterns, a decline in energy expenditure associated with a sedentary lifestyle, an ageing population--together with tobacco use and alcohol consumption--are major risk factors for noncommunicable diseases and pose an increasing challenge to public health. This report of a Joint WHO/FAO Expert Consultation reviews the evidence on the effects of diet and nutrition on chronic diseases and makes recommendations for public health policies and strategies that encompass societal, behavioural and ecological dimensions. Although the primary aim of the Consultation was to set targets related to diet and nutrition, the importance of physical activity was also emphasized. The Consultation considered diet in the context of the macro-economic implications of public health recommendations on agriculture and the global supply and demand for fresh and processed foodstuffs. In setting out ways to decrease the burden of chronic diseases such as obesity, type 2 diabetes, cardiovascular diseases (including hypertension and stroke), cancer, dental diseases and osteoporosis, this report proposes that nutrition should be placed at the forefront of public health policies and programmes. This report will be of interest to policy-makers and public health professionals alike, in a wide range of disciplines including nutrition, general medicine and gerontology. It shows how, at the population level, diet and exercise throughout the life course can reduce the threat of a global epidemic of chronic diseases.
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            Consumption of high-fructose corn syrup in beverages may play a role in the epidemic of obesity.

            Obesity is a major epidemic, but its causes are still unclear. In this article, we investigate the relation between the intake of high-fructose corn syrup (HFCS) and the development of obesity. We analyzed food consumption patterns by using US Department of Agriculture food consumption tables from 1967 to 2000. The consumption of HFCS increased > 1000% between 1970 and 1990, far exceeding the changes in intake of any other food or food group. HFCS now represents > 40% of caloric sweeteners added to foods and beverages and is the sole caloric sweetener in soft drinks in the United States. Our most conservative estimate of the consumption of HFCS indicates a daily average of 132 kcal for all Americans aged > or = 2 y, and the top 20% of consumers of caloric sweeteners ingest 316 kcal from HFCS/d. The increased use of HFCS in the United States mirrors the rapid increase in obesity. The digestion, absorption, and metabolism of fructose differ from those of glucose. Hepatic metabolism of fructose favors de novo lipogenesis. In addition, unlike glucose, fructose does not stimulate insulin secretion or enhance leptin production. Because insulin and leptin act as key afferent signals in the regulation of food intake and body weight, this suggests that dietary fructose may contribute to increased energy intake and weight gain. Furthermore, calorically sweetened beverages may enhance caloric overconsumption. Thus, the increase in consumption of HFCS has a temporal relation to the epidemic of obesity, and the overconsumption of HFCS in calorically sweetened beverages may play a role in the epidemic of obesity.
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              Dietary fructose reduces circulating insulin and leptin, attenuates postprandial suppression of ghrelin, and increases triglycerides in women.

              Previous studies indicate that leptin secretion is regulated by insulin-mediated glucose metabolism. Because fructose, unlike glucose, does not stimulate insulin secretion, we hypothesized that meals high in fructose would result in lower leptin concentrations than meals containing the same amount of glucose. Blood samples were collected every 30-60 min for 24 h from 12 normal-weight women on 2 randomized days during which the subjects consumed three meals containing 55, 30, and 15% of total kilocalories as carbohydrate, fat, and protein, respectively, with 30% of kilocalories as either a fructose-sweetened [high fructose (HFr)] or glucose-sweetened [high glucose (HGl)] beverage. Meals were isocaloric in the two treatments. Postprandial glycemic excursions were reduced by 66 +/- 12%, and insulin responses were 65 +/- 5% lower (both P < 0.001) during HFr consumption. The area under the curve for leptin during the first 12 h (-33 +/- 7%; P < 0.005), the entire 24 h (-21 +/- 8%; P < 0.02), and the diurnal amplitude (peak - nadir) (24 +/- 6%; P < 0.0025) were reduced on the HFr day compared with the HGl day. In addition, circulating levels of the orexigenic gastroenteric hormone, ghrelin, were suppressed by approximately 30% 1-2 h after ingestion of each HGl meal (P < 0.01), but postprandial suppression of ghrelin was significantly less pronounced after HFr meals (P < 0.05 vs. HGl). Consumption of HFr meals produced a rapid and prolonged elevation of plasma triglycerides compared with the HGl day (P < 0.005). Because insulin and leptin, and possibly ghrelin, function as key signals to the central nervous system in the long-term regulation of energy balance, decreases of circulating insulin and leptin and increased ghrelin concentrations, as demonstrated in this study, could lead to increased caloric intake and ultimately contribute to weight gain and obesity during chronic consumption of diets high in fructose.
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                Author and article information

                Journal
                Nutrients
                nutrients
                Nutrients
                MDPI
                2072-6643
                03 August 2010
                August 2010
                : 2
                : 8
                : 834-854
                Affiliations
                [1 ]Department of Nutritional Sciences, University of Connecticut, Storrs, CT 06269, USA; Email: ying.3.wang@ 123456uconn.edu
                [2 ]Food and Nutrition, Ansan College, Ansan, Korea; Email: cechung@ 123456ansan.ac.kr
                [3 ]Department of Food Science and Human Nutrition, Michigan State University, East Lansing, MI 48824, USA; Email: ajpadgitt@ 123456juno.com (A.P.); song@ 123456msu.edu (W.O.S.)
                Author notes
                [* ] Author to whom correspondence should be addressed; Email: ock.chun@ 123456uconn.edu ; Tel.: 1-860-486-6275; Fax: 1-860-486-3674.
                Article
                nutrients-02-00834
                10.3390/nu2080834
                3257707
                22254059
                af979357-8858-4b47-9376-bcbd54a6c45e
                © 2010 by the authors; licensee MDPI, Basel, Switzerland.

                This article is an open-access article distributed under the terms and conditions of the Creative Commons Attribution license ( http://creativecommons.org/licenses/by/3.0/).

                History
                : 17 June 2010
                : 28 July 2010
                : 30 July 2010
                Categories
                Article

                Nutrition & Dietetics
                energy,diet,added sugar,obesity,total sugar
                Nutrition & Dietetics
                energy, diet, added sugar, obesity, total sugar

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