FRINK Linked Data Fragments server

Matches in SemOpenAlex for { <https://semopenalex.org/work/W2043947812> ?p ?o ?g. }

• W2043947812 endingPage "1364" @default.
• W2043947812 startingPage "1356" @default.
• W2043947812 abstract "HomeCirculationVol. 121, No. 11Sugar-Sweetened Beverages, Obesity, Type 2 Diabetes Mellitus, and Cardiovascular Disease Risk Free AccessReview ArticlePDF/EPUBAboutView PDFView EPUBSections ToolsAdd to favoritesDownload citationsTrack citationsPermissions ShareShare onFacebookTwitterLinked InMendeleyReddit Jump toFree AccessReview ArticlePDF/EPUBSugar-Sweetened Beverages, Obesity, Type 2 Diabetes Mellitus, and Cardiovascular Disease Risk Vasanti S. Malik, MSc, Barry M. Popkin, PhD, George A. Bray, MD, Jean-Pierre Després, PhD and Frank B. Hu, MD, PhD Vasanti S. MalikVasanti S. Malik From the Departments of Nutrition and Epidemiology, Harvard School of Public Health (V.S.M., F.B.H.), and Channing Laboratory, Department of Medicine, Brigham and Women’s Hospital and Harvard Medical School (F.B.H.), Boston, Mass; Centre de Recherche de l’Institut Universitaire de Cardiologie et de Pneumologie de Québec, Québec City, Québec, Canada (J.P.D.); Dietary Obesity Laboratory, Pennington Biomedical Research Center, Baton Rouge, La (G.A.B.); and Department of Nutrition, Gillings School of Global Public Health, University of North Carolina, Chapel Hill (B.M.P.). Search for more papers by this author , Barry M. PopkinBarry M. Popkin From the Departments of Nutrition and Epidemiology, Harvard School of Public Health (V.S.M., F.B.H.), and Channing Laboratory, Department of Medicine, Brigham and Women’s Hospital and Harvard Medical School (F.B.H.), Boston, Mass; Centre de Recherche de l’Institut Universitaire de Cardiologie et de Pneumologie de Québec, Québec City, Québec, Canada (J.P.D.); Dietary Obesity Laboratory, Pennington Biomedical Research Center, Baton Rouge, La (G.A.B.); and Department of Nutrition, Gillings School of Global Public Health, University of North Carolina, Chapel Hill (B.M.P.). Search for more papers by this author , George A. BrayGeorge A. Bray From the Departments of Nutrition and Epidemiology, Harvard School of Public Health (V.S.M., F.B.H.), and Channing Laboratory, Department of Medicine, Brigham and Women’s Hospital and Harvard Medical School (F.B.H.), Boston, Mass; Centre de Recherche de l’Institut Universitaire de Cardiologie et de Pneumologie de Québec, Québec City, Québec, Canada (J.P.D.); Dietary Obesity Laboratory, Pennington Biomedical Research Center, Baton Rouge, La (G.A.B.); and Department of Nutrition, Gillings School of Global Public Health, University of North Carolina, Chapel Hill (B.M.P.). Search for more papers by this author , Jean-Pierre DesprésJean-Pierre Després From the Departments of Nutrition and Epidemiology, Harvard School of Public Health (V.S.M., F.B.H.), and Channing Laboratory, Department of Medicine, Brigham and Women’s Hospital and Harvard Medical School (F.B.H.), Boston, Mass; Centre de Recherche de l’Institut Universitaire de Cardiologie et de Pneumologie de Québec, Québec City, Québec, Canada (J.P.D.); Dietary Obesity Laboratory, Pennington Biomedical Research Center, Baton Rouge, La (G.A.B.); and Department of Nutrition, Gillings School of Global Public Health, University of North Carolina, Chapel Hill (B.M.P.). Search for more papers by this author and Frank B. HuFrank B. Hu From the Departments of Nutrition and Epidemiology, Harvard School of Public Health (V.S.M., F.B.H.), and Channing Laboratory, Department of Medicine, Brigham and Women’s Hospital and Harvard Medical School (F.B.H.), Boston, Mass; Centre de Recherche de l’Institut Universitaire de Cardiologie et de Pneumologie de Québec, Québec City, Québec, Canada (J.P.D.); Dietary Obesity Laboratory, Pennington Biomedical Research Center, Baton Rouge, La (G.A.B.); and Department of Nutrition, Gillings School of Global Public Health, University of North Carolina, Chapel Hill (B.M.P.). Search for more papers by this author Originally published23 Mar 2010https://doi.org/10.1161/CIRCULATIONAHA.109.876185Circulation. 2010;121:1356–1364Obesity has recently emerged as a major global health problem. According to World Health Organization estimates, ≈1.6 billion adults worldwide were overweight (body mass index [BMI] ≥25 kg/m2) and at least 400 million were obese (BMI ≥30 kg/m2) in 2005, numbers that are expected to reach 2.3 billion and 700 million, respectively, by 2015. In the United States, the percentage of overweight and obese adults increased markedly from 47% and 15% in 1976 to 1980 to >66% and 33% in 2005 to 2006, with the greatest proportion of increase seen among non-Hispanic black and Mexican American women.1,2 The implications of excess body weight are far-reaching. Epidemiological studies indicate that overweight and obesity are important risk factors for type 2 diabetes mellitus (T2DM), cardiovascular disease, cancer, and premature death.3 In the United States, healthcare expenditures attributable to overweight and obesity are estimated to be $147 billion or 9.1% of total healthcare costs per year.4 Such excess costs could have serious repercussions for resource-poor countries, which must manage the dual burdens of chronic and infectious disease.In the setting of a pandemic of obesity and related chronic diseases, the American Heart Association recently released a scientific statement recommending reductions in added-sugar intake to no more than 100 to 150 kcal/d for most Americans.5 The statement identified sugar-sweetened beverages (SSBs) as the primary source of added sugars in the American diet.6 Although it has long been suspected that SSBs contribute at least in part to the obesity epidemic, only in recent years have large epidemiological studies been able to substantiate the relationship between SSB consumption and long-term weight gain, T2DM, and cardiovascular risk. It is thought that SSBs contribute to weight gain because of their high added-sugar content, low satiety, and potential incomplete compensation for total energy, leading to increased energy intake.7,8 In addition, because of their high amounts of rapidly absorbable carbohydrates such as various forms of sugar and high-fructose corn syrup (HFCS) and the large quantities consumed, SSBs may increase T2DM and cardiovascular risk independently of obesity as a contributor to a high dietary glycemic load (GL), leading to inflammation, insulin resistance, and impaired β-cell function.9 Fructose from any sugar or HFCS may also increase blood pressure and promote the accumulation of visceral adiposity, dyslipidemia, and ectopic fat deposition because of increased hepatic de novo lipogenesis.10 Here, we review temporal patterns in SSB consumption and clinically relevant effects on obesity, T2DM, and cardiovascular disease risk, emphasizing potential underlying biological mechanisms, clinical implications, and consideration of methodological issues inherent in the literature.SSB Global PatternAlthough carbonated beverages trace their history back to the 1760s when carbonation techniques were developed to reproduce naturally occurring carbonated mineral waters believed to be healthy, these beverages did not add sugar.11 A century later, one of the most pivotal events in soft drink history occurred when Atlanta pharmacist J.S. Pemberton combined kola, a caffeinated nut from Africa, with coca, a stimulant from South America, to create Coca-Cola, which, like most other sweetened beverages developed in the 1800s, was marketed as a tonic.12 In about 1904, Asa Candler purchased legal rights to the formula from Pemberton and soon developed the first mass factory.13 During World War II, Coca-Cola worked closely with the US Department of War to provide free Cokes to army soldiers. As a result of a lobbying campaign, they were allowed to break sugar ration rules and to create Coke plants in European countries with the support of the government, ultimately becoming synonymous globally with SSBs.13During the past 30 years, there has been a marked increase in the consumption of SSBs across the globe. For instance, in the United States, intake of these beverages, which includes the full range of soft drinks, fruit drinks, energy drinks, and vitamin water drinks, increased from 3.9% of calories in the late 1970s to 9.2% in 2001, representing a 3-fold increase in intake.14 In other countries, there have been varying levels of increase in SSBs, with some countries such as Mexico reaching such magnitudes that serious government intervention to reduce intake is being undertaken.15 Nation-level food disappearance data from China, India, Vietnam, Thailand, and other South Asian countries also show rapid trajectories of an increase in SSB intake, as well as large per capita consumption across the Americas, Germany, Australia, Spain, and Great Britain.16 The most rigorous sources of nationally representative patterns in SSB intake come from the United States and Mexico, where large-scale dietary intake surveys have been repeated in the last decade.15,17 According to these data, all age groups in Mexico consume ≈10% of their total energy intake from SSBs. As shown in Figure 1A, SSB intake has increased considerably among those ≥5 years of age in Mexico. Figure 1B presents the same data for the United States. As seen in both children 2 to 18 years of age and adults >19 years of age, substantial increases across each decade have continued. Download figureDownload PowerPointFigure 1. Trends in consumption of calories from soft drinks and all caloric beverages in Mexico and the United States (weighted to be nationally representative) by age groups (1 to 4, 5 to 11, 12 to 18, and ≥19 years) in 1999 and 2006. Soft drinks include carbonated, noncarbonated beverages with sugar added, and commercially processed, bottled/formula fountain soft drinks and fruit drinks but exclude agua frescas, Mexican hand-prepared added-sugar fruit juices, and fruit drinks.SSB and Childhood ObesityChildhood obesity is known to increase risk of obesity in adulthood and can lead to serious consequences for T2DM and cardiovascular disease risk later in life. In fact, recent evidence suggests consideration of lipid screening for children with BMI beginning at the 80th percentile rather than ≥85th percentile, the point at which a child is considered overweight.18Given the preponderance of SSB consumption among children and adolescents, several epidemiological studies have examined the relationship between SSB and weight gain or obesity in this group. Recently, we conducted a meta-analysis evaluating change in BMI per increase in 1 serving of SSB per day and found a significant positive association between SSB intake and weight gain (0.08; 95% confidence interval [CI], 0.03 to 0.13 kg)19 among studies that did not adjust for total energy intake.20–24 Because the association between SSB intake and weight gain is partially mediated by total energy intake, adjusting for energy is expected to attenuate this effect. In these data, the effect was also strongest in larger studies with longer durations of follow-up that used robust dietary assessment methods such as food frequency questionnaires rather than a single 24-hour diet recall, which is not able to capture patterns in dietary intake.20,21 These results are supported by previous systematic reviews and meta-analyses,25–27 as well as more recent studies. For example, Dubois and colleagues28 found that in >2000 children 2.5 years of age followed up for 3 years, regular consumers of SSBs between meals had a 2.4-fold greater odds of being overweight compared with nonconsumers (P<0.05). Another study conducted among 5-year-old subjects in the UK with 4 years of follow-up did not find an association between SSB intake and fatness, possibly because intake levels were too low.29 Recent studies have also shown that greater SSB consumption in childhood or adolescence predicted weight gain into adulthood.30,31Findings from intervention studies, which are few in number, generally support those from well-powered prospective cohort studies and show positive associations between SSB intake and weight gain either in the overall study22 or in subgroup analyses among participants overweight at baseline.24,32 A follow-up analysis of a school-based intervention that showed that reducing SSB intake decreased overweight and obesity22 did not see an effect 2 years after the intervention had been discontinued, which supports an effect of SSB consumption on weight gain.33SSB Consumption and Weight Gain in AdultsTo date, a large number of studies have evaluated the relationship between SSB consumption and weight gain or risk of overweight and obesity among adults. However, differences in study design, methodologies, and data quality have made it difficult to observe a consistent effect. Cross-sectional studies are not optimal because of the high potential for intractable confounding and reverse causation. Experimental studies are not well suited to capture long-term patterns because compliance tends to wane with increasing duration, but they do provide important insight into potential underlying biological mechanisms. Prospective cohort studies tend to provide the most robust evidence despite a large degree of diversity between studies in terms of outcome measurements, size, and duration of follow-up. Therefore, greater emphasis should be placed on larger studies of longer duration that are better powered to detect an effect. In this literature, the longest and largest studies34,35show stronger and more consistent associations compared with smaller and shorter studies.36,37 For example, in the study by Schulze et al34 of >50 000 nurses followed up for two 4-year periods (1991 to 1995 and 1995 to 1999), a higher consumption of SSBs was associated with a greater magnitude of weight gain. After adjustment for potential confounders, women who increased their SSB consumption from 1991 to 1995 and maintained a high level of intake gained on average 8.0 kg during the 2 periods, whereas women who decreased their SSB intake between 1991 and 1995 and maintained a low level of intake gained on average 2.8 kg during the 2 periods (Figure 2). Similar results were reported by Palmer and colleagues35 in >40 000 black women followed up for 6 years. Those whose SSB intake increased from ≤1 serving per week to ≥1 serving per day gained the most weight, whereas those who decreased their intake gained the least weight (6.8 and 4.1 kg, respectively) after adjustment for potential confounders. A smaller study from Spain38 with >7000 participants followed up for ≈2 years found that a higher consumption of SSB was associated with significant weight gain among subjects who gained ≥3 kg in the 5 years before baseline. These participants had a higher absolute intake of SSB at baseline compared with participants with no previous weight gain, consistent with a positive association between SSB intake and weight gain. It is possible that the study was not long enough to evaluate weight gain in relation to SSB intake in subjects with no previous weight gain. In a large cohort from Germany (n=17 369) with a similar duration of follow-up, SSB intake was associated with weight gain in men but not women.39 In the Framingham Offspring Study40 with an average duration of 4 years and >4000 participants, compared with infrequent consumers, participants who consumed ≥1 soft drinks per day had a 37% higher risk of obesity.40 Because this analysis included both diet and regular soft drinks, it is difficult to disentangle the independent effect of SSBs because consumers of diet soft drinks may be weight conscious or trying to lose weight. In an observational analysis of the Clinical Trial of Comprehensive Lifestyle Modification for Blood Pressure Control (PREMIER) study (n=810), Chen et al41 found that a reduction in SSB intake of 1 serving per day was associated with a weight loss of 0.49 kg (95% CI, 0.11 to 0.82; P=0.006) at 6 months and of 0.65 kg (95% CI, 0.22 to 1.09; P=0.003) at 18 months. However, participants in this study were part of a trial to lower blood pressure and had higher baseline BMI than other cohorts and stage 1 hypertension, which could partly explain why such a strong effect was seen with relatively little power. At the same time, because this study adjusted for total energy, the effect of SSBs on weight gain may have been underestimated. Download figureDownload PowerPointFigure 2. Low and high intakes were defined as ≤1/week and ≥1/day. The numbers of subjects were as follows: low-high-high=323, low-high-low=461, high-low-high=110, and high-low-low=746. Groups with similar intake in 1991 and 1995 were combined for estimates for these time points. Means were adjusted for age, alcohol intake, physical activity, smoking, postmenopausal hormone use, oral contraceptive use, cereal fiber intake, and total fat intake at each time point. Adapted with permission from Schulze et al.34SSB Consumption and T2DM and the Metabolic SyndromeSimilar to the weight-gain literature, prospective cohort studies evaluating the effect of SSBs on risk of T2DM and the metabolic syndrome (MetSyn) have found the strongest and most consistent associations in large studies with long durations of follow-up. These aspects of study design are particularly important when assessing diet in relation to chronic disease origin because sufficient time is required for causal action and disease initiation and detection to occur. In >50 000 women followed up for 8 years, after adjustment for potential confounders, those consuming ≥1 SSBs per day had an 83% greater risk of developing T2DM compared with those consuming <1 SSB per month (relative risk [RR], 1.83; 95% CI, 1.42 to 2.36; P<0.001 for trend; Figure 3).34 The RR comparing extreme categories further controlling for BMI was 1.41 (95% CI, 1.09 to 1.83; P <0.001 for trend). This finding suggests that BMI accounts for about half of the excess risk. Similarly, in the Black Women’s Health Study,35 with >40 000 women followed up for 10 years, those who consumed ≥2 SSBs per day had a 24% greater risk of developing T2DM compared with those who consumed <1 SSB per month (RR, 1.24; 95% CI, 1.06 to 1.45; P=0.002 for trend). After additional adjustment for BMI, the RR was no longer statistically significant, suggesting that in this population the majority of effect was mediated by BMI. Findings from these studies were replicated in a large cohort of >70 000 women followed up for 18 years that showed that women who consumed 2 to 3 SSBs per day had a 31% greater risk of developing T2DM than women who consumed <1 SSB per month (RR, 1.31; 95% CI, 0.99 to 1.74; P<0.01 for trend).42 Because this study adjusted for BMI and total energy intake, both potential mediators of effect, the association between SSB intake and T2DM risk may actually be underestimated. In contrast to these studies, findings from the Atherosclerosis Risk in Communities Study (n=12 204) did not show a consistent association between SSB intake and incidence of T2DM after 9 years of follow-up (men: RR, 1.09; 95% CI, 0.89 to 1.33; women: RR, 1.17; 95% CI, 0.94 to 1.46).43 Compared with the study by Schulze et al,34 participants in this study were older (53.6 versus 36.1 years of age) and heavier (27.2 versus 24.6 kg/m2) at baseline. Because the effect of SSB on T2DM is mediated in part by BMI, once BMI is increased, it is possible that the additional effect of continued SSB intake is diminished; however, further research is needed to confirm this hypothesis. Download figureDownload PowerPointFigure 3. Multivariate RRs were adjusted for age, alcohol (0, 0.1 to 4.9, 5.0 to 9.9, ≥10 g/d), physical activity (quintiles), family history of diabetes mellitus, smoking (never, past, current), postmenopausal hormone use (never, ever), oral contraceptive use (never, past, current), intake (quintiles) of cereal fiber, magnesium, trans fat, polyunsaturated:saturated fat, and consumption of sugar-sweetened soft drinks, diet soft drinks, fruit juice, and fruit punch (other than the main exposure, depending on model). These data are based on data from Schulze et al.34Few studies have examined the effect of SSBs on the development of MetSyn, but they are in line with findings from studies evaluating T2DM. For example, findings from the Framingham Offspring Study (n=6154) showed that compared with nonconsumers, individuals who consumed ≥1 soft drinks per day had a 39% greater risk of developing MetSyn during the course of 4 years.40 Although this analysis combined diet and regular soft drinks, it can be assumed that the majority of this effect was due to regular soft drink consumption. Other studies of MetSyn have found marginal effects of SSBs, but because they adjusted for total energy intake, the results may have been underestimated.44,45SSB Consumption and Cardiovascular RiskThe evidence relating SSB intake to cardiovascular risk is limited, although data are starting to accumulate that suggest that greater SSB consumption may have a role in the development of hypertension, adverse lipid parameters, inflammation, and clinical coronary heart disease (CHD). The Framingham Offspring Study, which also looked at SSB intake in the context of MetSyn components in 6154 adults followed up for 4 years, found that individuals who consumed ≥1 soft drink per day had a 22% higher incidence of hypertension (≥135/85 mm Hg or on treatment) compared with nonconsumers (RR, 1.22; 95% CI, 1.05 to 1.41).40 Similarly, in the Nurses’ Health Studies I and II, women who consumed ≥4 SSBs per day had a 44% and 28% higher risk of incident hypertension, respectively, compared with infrequent consumers (RR, 1.44; 95% CI, 0.98 to 2.11; and RR, 1.28; 95% CI, 1.01 to 1.62, respectively).46 Regarding lipids, daily soft drink consumers in the Framingham Offspring Study were found to have a 22% higher incidence of hypertriglyceridemia (≥1.7 mmol/L or on treatment) and low high-density lipoprotein cholesterol (<1.03 mmol/L for men or <1.3 mmol/L for women or on treatment) compared with nonconsumers (RR, 1.22; 95% CI, 1.07 to 1.41; and RR, 1.22; 95% CI, 1.04 to 1.44, respectively).40 Results from the Multi-Ethnic Study of Atherosclerosis (MESA) study, which had fewer participants (n=3878), showed a significant effect of SSBs on hypertriglyceridemia (≥1.7 mmol/L or on treatment) and trends toward an effect on hypertension (≥130/85 mm Hg or on treatment) and low high-density lipoprotein cholesterol (<1.03 mmol/L for men or <1.3 mmol/L for women or on treatment) in daily SSB consumers compared with nonconsumers (RR, 1.28; 95% CI, 1.02 to 1.60; RR, 1.14; 95% CI, 0.91 to 1.43; and RR, 1.28; 95% CI, 0.99 to 1.64, respectively).45 These findings are supported by a recent cross-sectional analysis of National Health and Nutrition Examination Survey data that found a positive association between SSB intake and blood pressure in adolescents.47 A 10-week intervention study comparing the effects of sucrose- and artificially sweetened foods/beverages on markers of inflammation found that serum levels of haptoglobin, transferrin, and C-reactive protein increased in the sucrose group and decreased in the sweetener group (between-group differences: P=0.006, P=0.01, and P=0.1, respectively).48 Indirect evidence for an effect of SSBs on inflammation also stems from observational studies that have found positive associations between dietary patterns that are high in SSBs with markers of inflammation such as C-reactive protein and tumor necrosis factor receptor 249 and dietary GL, to which SSB intake is a large contributor with C-reactive protein.50 In addition, higher consumption of soft drinks has been associated with hyperuricemia51 and incidence of developing gout,52 a condition commonly associated with insulin resistance and MetSyn.Recently, in the Nurses Health Study, a positive association between SSB intake and risk of CHD (nonfatal myocardial infarction or fatal CHD) was observed even after accounting for other unhealthy factors.53 In >88 000 women followed up for 24 years, those who consumed ≥2 SSBs per day had a 35% greater risk of developing CHD compared with those who consumed <1 SSB per month (RR, 1.35; 95% CI, 1.1 to 1.7; P<0.001 for trend). Additional adjustment for BMI, energy intake, and incident T2DM attenuated the associations, but they remained statistically significant, suggesting that the effect of SSBs on CHD is not entirely mediated by these factors.Potential MechanismsThe prevailing mechanisms linking SSB intake to weight gain are decreased satiety and incomplete compensatory reduction in energy intake at subsequent meals after consumption of liquid calories (Figure 4).7,8 On average, SSBs contain 140 to 150 calories and 35 to 37.5 g sugar per 12-oz serving. If normal dietary intake does not decrease by an equivalent amount of calories per serving, then weight gain is expected.25,54 This has been illustrated in short-term feeding trials showing greater energy intake and weight gain after consumption of calorically sweetened beverages (sugar, sucrose, HFCS) compared with noncaloric artificially sweetened beverages.55,56 In addition, a number of studies have shown greater energy intake and weight gain after isocaloric consumption of beverages as opposed to solid food.7 These studies argue that sugar or HFCS in liquid beverages may not suppress intake of solid foods to the level needed to maintain energy balance; however, the mechanism responsible for that weaker compensatory response to fluids is unknown.57Download figureDownload PowerPointFigure 4. SSBs may lead to weight gain as a result of incomplete compensation for liquid calories at subsequent meals, resulting in positive energy balance. Independently of weight gain, SSBs may increase the risk of MetSyn, T2DM, and cardiovascular disease because of their large contribution to a high dietary GL and large fructose fraction, leading to the development of insulin resistance, β-cell dysfunction, inflammation, hypertension, visceral adiposity, and atherogenic dyslipidemia.SSBs may contribute to T2DM and cardiovascular risk in part by their ability to induce weight gain, but an independent effect may also stem from the high amounts of rapidly absorbable carbohydrates such as any form of sugar or HFCS, the primary sweeteners used in SSBs (Figure 4). Consumption of SSBs has been shown to result in rapid and dramatic increases in blood glucose and insulin concentrations,58 which, in conjunction with the large quantities that are often consumed, contribute to a high dietary GL. High-GL diets are thought to stimulate appetite and to promote weight gain and have been shown to induce glucose intolerance and insulin resistance.59 An increase in GL has also been shown to exacerbate levels of inflammatory biomarkers such as C-reactive protein linked to T2DM and cardiovascular disease risk.50 Inflammation is known to influence atherosclerosis, plaque stability, and thrombosis; therefore, SSB consumption may affect CHD risk within just a few years.53 High dietary GL has also been associated with greater risk of CHD.60 In addition, the caramel coloring used in cola-type soft drinks is high in advanced glycation end products, which may further increase insulin resistance and inflammation.61 For instance, an 8-oz serving of cola delivers 16.3 kU advanced glycation end products.62Recent evidence also suggests that consuming fructose, which is found in similar amounts in sucrose and HFCS, may have particularly adverse effects on selective deposition of visceral and ectopic fat, lipid metabolism, de novo lipogenesis, blood pressure, and insulin sensitivity compared with glucose10 (Figure 4). The different pathways for the metabolism of fructose and glucose are clearly important potential mechanisms. Fructose alone is poorly absorbed but is enhanced by glucose in the gut, thus accounting for the rapid and complete absorption of both fructose and glucose when ingested as sucrose or HFCS. Studies in humans and animals have shown that fructose is preferentially metabolized to lipid in the liver, leading to increased triglyceride levels, which have been associated with the development of insulin resistance and cardiovascular disease.63–66 A recent study in overweight adults compared the effects of consuming glucose- or fructose-sweetened beverages providing 25% of energy requirements.10 After 10 weeks, both groups showed similar weight gain; however, only the fructose group showed a significant increase in visceral adiposity, which has also been observed in a number of recent studies.67–69 Although fasting plasma triglyceride levels increased only in the glucose group, hepatic de novo lipogenesis, postprandial triglycerides, and markers of altered lipid metabolism and lipoprotein remodeling such as fasting apolipoprotein B and small low-density lipoprotein particles significantly increased in the fructose group. In addition, fasting plasma glucose and insulin levels increased and insulin sensitivity decreased in the fructose group. Of interest, Ghanim and colleagues70 did not find evidence of oxidative or inflammatory stress after intake of 300 kcal fructose or orange juice, whereas reactive oxygen species generation and nuclear factor-κB binding were significantly increased after intake of glucose. However, the quantities of fructose contained in SSBs are far greater than those contained in these preloads.70 Fructose can also increase blood uric acid concentrations.71 The production of uric acid in the liver by xanthine oxidase may reduce endothelial nitric oxide,72 which could partly mediate the association between SSBs and risk of CHD. Increases in blood pressure have also been observed when fructose is administered acutely, an effect not seen with glucose.73 In addition, an increase in blood pressure spanning 10 weeks was found when individuals drank SSBs but not aspartame-sweetened beverages.55 Fructose intake may also lead to weight gain by decreasing the production of insulin and leptin in peripheral tissues, thereby init" @default.
• W2043947812 created "2016-06-24" @default.
• W2043947812 creator A5018513549 @default.
• W2043947812 creator A5038660025 @default.
• W2043947812 creator A5047527237 @default.
• W2043947812 creator A5056459536 @default.
• W2043947812 creator A5074444224 @default.
• W2043947812 date "2010-03-23" @default.
• W2043947812 modified "2023-10-11" @default.
• W2043947812 title "Sugar-Sweetened Beverages, Obesity, Type 2 Diabetes Mellitus, and Cardiovascular Disease Risk" @default.
• W2043947812 cites W1521042725 @default.
• W2043947812 cites W1873390252 @default.
• W2043947812 cites W1903286618 @default.
• W2043947812 cites W1935669509 @default.
• W2043947812 cites W1953389641 @default.
• W2043947812 cites W1957265225 @default.
• W2043947812 cites W1963981973 @default.
• W2043947812 cites W1984538977 @default.
• W2043947812 cites W1986059252 @default.
• W2043947812 cites W1992358256 @default.
• W2043947812 cites W1994785080 @default.
• W2043947812 cites W1999556806 @default.
• W2043947812 cites W2003662371 @default.
• W2043947812 cites W2003695584 @default.
• W2043947812 cites W2004740810 @default.
• W2043947812 cites W2008352538 @default.
• W2043947812 cites W2016436332 @default.
• W2043947812 cites W2019437564 @default.
• W2043947812 cites W2019758319 @default.
• W2043947812 cites W2030062071 @default.
• W2043947812 cites W2033941910 @default.
• W2043947812 cites W2038873103 @default.
• W2043947812 cites W2044549026 @default.
• W2043947812 cites W2047111293 @default.
• W2043947812 cites W2052212087 @default.
• W2043947812 cites W2056526409 @default.
• W2043947812 cites W2061643792 @default.
• W2043947812 cites W2063161169 @default.
• W2043947812 cites W2068423669 @default.
• W2043947812 cites W2073982294 @default.
• W2043947812 cites W2074538032 @default.
• W2043947812 cites W2076601678 @default.
• W2043947812 cites W2080917116 @default.
• W2043947812 cites W2092509345 @default.
• W2043947812 cites W2096526724 @default.
• W2043947812 cites W2096546427 @default.
• W2043947812 cites W2099187882 @default.
• W2043947812 cites W2101976191 @default.
• W2043947812 cites W2104117318 @default.
• W2043947812 cites W2104822381 @default.
• W2043947812 cites W2108726171 @default.
• W2043947812 cites W2110746752 @default.
• W2043947812 cites W2110987964 @default.
• W2043947812 cites W2112566574 @default.
• W2043947812 cites W2113318243 @default.
• W2043947812 cites W2113444919 @default.
• W2043947812 cites W2117618925 @default.
• W2043947812 cites W2118772291 @default.
• W2043947812 cites W2118783525 @default.
• W2043947812 cites W2118970655 @default.
• W2043947812 cites W2119913483 @default.
• W2043947812 cites W2120678647 @default.
• W2043947812 cites W2121951329 @default.
• W2043947812 cites W2122914756 @default.
• W2043947812 cites W2124655674 @default.
• W2043947812 cites W2125745062 @default.
• W2043947812 cites W2126386728 @default.
• W2043947812 cites W2128981244 @default.
• W2043947812 cites W2133125062 @default.
• W2043947812 cites W2135266778 @default.
• W2043947812 cites W2136952779 @default.
• W2043947812 cites W2140699761 @default.
• W2043947812 cites W2145266375 @default.
• W2043947812 cites W2146966453 @default.
• W2043947812 cites W2147485883 @default.
• W2043947812 cites W2147894463 @default.
• W2043947812 cites W2149945060 @default.
• W2043947812 cites W2150685626 @default.
• W2043947812 cites W2153966472 @default.
• W2043947812 cites W2155634899 @default.
• W2043947812 cites W2156450538 @default.
• W2043947812 cites W2158496522 @default.
• W2043947812 cites W2159634370 @default.
• W2043947812 cites W2161625508 @default.
• W2043947812 cites W2163418893 @default.
• W2043947812 cites W2168407586 @default.
• W2043947812 cites W2170080893 @default.
• W2043947812 cites W2170649441 @default.
• W2043947812 cites W2171260888 @default.
• W2043947812 cites W4241296453 @default.
• W2043947812 cites W4249653516 @default.
• W2043947812 cites W4251266101 @default.
• W2043947812 cites W4252731434 @default.
• W2043947812 cites W4255196022 @default.
• W2043947812 doi "https://doi.org/10.1161/circulationaha.109.876185" @default.
• W2043947812 hasPubMedCentralId "https://www.ncbi.nlm.nih.gov/pmc/articles/2862465" @default.
• W2043947812 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/20308626" @default.
• W2043947812 hasPublicationYear "2010" @default.

• next