Low to moderate sugar-sweetened beverage consumption impairs glucose and lipid metabolism and promotes inflammation in healthy young men: a randomized controlled trial
01 Aug 2011-The American Journal of Clinical Nutrition (American Society for Nutrition)-Vol. 94, Iss: 2, pp 479-485
TL;DR: The present data show potentially harmful effects of low to moderate consumption of SSBs on markers of cardiovascular risk such as LDL particles, fasting glucose, and hs-CRP within just 3 wk in healthy young men, which is of particular significance for young consumers.
About: This article is published in The American Journal of Clinical Nutrition.The article was published on 2011-08-01 and is currently open access. It has received 319 citations till now. The article focuses on the topics: Fructose & Sucrose.
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TL;DR: Among free living people involving ad libitum diets, intake of free sugars or sugar sweetened beverages is a determinant of body weight, and the change in body fatness that occurs with modifying intakes seems to be mediated via changes in energy intakes.
Abstract: Objective To summarise evidence on the association between intake of dietary sugars and body weight in adults and children. Design Systematic review and meta-analysis of randomised controlled trials and prospective cohort studies. Data sources OVID Medline, Embase, PubMed, Cumulative Index to Nursing and Allied Health Literature, Scopus, and Web of Science (up to December 2011). Review methods Eligible studies reported the intake of total sugars, intake of a component of total sugars, or intake of sugar containing foods or beverages; and at least one measure of body fatness. Minimum duration was two weeks for trials and one year for cohort studies. Trials of weight loss or confounded by additional medical or lifestyle interventions were excluded. Study selection, assessment, validity, data extraction, and analysis were undertaken as specified by the Cochrane Collaboration and the GRADE working group. For trials, we pooled data for weight change using inverse variance models with random effects. We pooled cohort study data where possible to estimate effect sizes, expressed as odds ratios for risk of obesity or β coefficients for change in adiposity per unit of intake. Results 30 of 7895 trials and 38 of 9445 cohort studies were eligible. In trials of adults with ad libitum diets (that is, with no strict control of food intake), reduced intake of dietary sugars was associated with a decrease in body weight (0.80 kg, 95% confidence interval 0.39 to 1.21; P Conclusions Among free living people involving ad libitum diets, intake of free sugars or sugar sweetened beverages is a determinant of body weight. The change in body fatness that occurs with modifying intakes seems to be mediated via changes in energy intakes, since isoenergetic exchange of sugars with other carbohydrates was not associated with weight change.
1,394 citations
TL;DR: Sensitivity analyses of RCTs in children showed more pronounced benefits in preventing weight gain in SSB substitution trials (compared with school-based educational programs) and among overweight children (comparing with normal-weight children).
1,327 citations
TL;DR: A significant relationship between added sugar consumption and increased risk for CVD mortality was observed among US adults and was largely consistent across age group, sex, race/ethnicity, educational attainment, physical activity, health eating index, and body mass index.
Abstract: RESULTS Among US adults, the adjusted mean percentage of daily calories from added sugar increased from 15.7% (95% CI, 15.0%-16.4%) in 1988-1994 to 16.8% (16.0%-17.7%; P =. 02) in 1999-2004 and decreased to 14.9% (14.2%-15.5%; P < .001) in 2005-2010. Most adults consumed 10% or more of calories from added sugar (71.4%) and approximately 10% consumed 25% or more in 2005-2010. During a median follow-up period of 14.6 years, we documented 831 CVD deaths during 163 039 person-years. Age-, sex-, and race/ethnicity– adjusted hazard ratios (HRs) of CVD mortality across quintiles of the percentage of daily calories consumed from added sugar were 1.00 (reference), 1.09 (95% CI, 1.05-1.13), 1.23 (1.12-1.34), 1.49 (1.24-1.78), and 2.43 (1.63-3.62; P < .001), respectively. After additional adjustment for sociodemographic, behavioral, and clinical characteristics, HRs were 1.00 (reference), 1.07 (1.02-1.12), 1.18 (1.06-1.31), 1.38 (1.11-1.70), and 2.03 (1.26-3.27; P = .004), respectively. Adjusted HRs were 1.30 (95% CI, 1.09-1.55) and 2.75 (1.40-5.42; P = .004), respectively, comparing participants who consumed 10.0% to 24.9% or 25.0% or more calories from added sugar with those who consumed less than 10.0% of calories from added sugar. These findings were largely consistent across age group, sex, race/ethnicity (except among non-Hispanic blacks), educational attainment, physical activity, health eating index, and body mass index.
763 citations
Cites background from "Low to moderate sugar-sweetened bev..."
...The number needed to harm at 15 years of follow-up (median follow-up) reduced from 265 (95% CI, 166-715) to 22 (13-66) (Table 2)....
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TL;DR: The evidence and lack of evidence that allows the controversy to continue are discussed, and the conclusions from several meta-analyses suggest that fructose has no specific adverse effects relative to any other carbohydrate.
Abstract: The impact of sugar consumption on health continues to be a controversial topic. The objective of this review is to discuss the evidence and lack of evidence that allows the controversy to continue, and why resolution of the controversy is important. There are plausible mechanisms and research evidence that supports the suggestion that consumption of excess sugar promotes the development of cardiovascular disease (CVD) and type 2 diabetes (T2DM) both directly and indirectly. The direct pathway involves the unregulated hepatic uptake and metabolism of fructose, leading to liver lipid accumulation, dyslipidemia, decreased insulin sensitivity and increased uric acid levels. The epidemiological data suggest that these direct effects of fructose are pertinent to the consumption of the fructose-containing sugars, sucrose and high fructose corn syrup (HFCS), which are the predominant added sugars. Consumption of added sugar is associated with development and/or prevalence of fatty liver, dyslipidemia, insulin resistance, hyperuricemia, CVD and T2DM, often independent of body weight gain or total energy intake. There are diet intervention studies in which human subjects exhibited increased circulating lipids and decreased insulin sensitivity when consuming high sugar compared with control diets. Most recently, our group has reported that supplementing the ad libitum diets of young adults with beverages containing 0%, 10%, 17.5% or 25% of daily energy requirement (Ereq) as HFCS increased lipid/lipoprotein risk factors for CVD and uric acid in a dose-response manner. However, un-confounded studies conducted in healthy humans under a controlled, energy-balanced diet protocol that enables determination of the effects of sugar with diets that do not allow for body weight gain are lacking. Furthermore, recent reports conclude that there are no adverse effects of consuming beverages containing up to 30% Ereq sucrose or HFCS, and the conclusions from several meta-analyses suggest that fructose has no specific adverse effects relative to any other carbohydrate. Consumption of excess sugar may also promote the development of CVD and T2DM indirectly by causing increased body weight and fat gain, but this is also a topic of controversy. Mechanistically, it is plausible that fructose consumption causes increased energy intake and reduced energy expenditure due to its failure to stimulate leptin production. Functional magnetic resonance imaging (fMRI) of the brain demonstrates that the brain responds differently to fructose or fructose-containing sugars compared with glucose or aspartame. Some epidemiological studies show that sugar consumption is associated with body weight gain, and there are intervention studies in which consumption of ad libitum high-sugar diets promoted increased body weight gain compared with consumption of ad libitum low- sugar diets. However, there are no studies in which energy intake and weight gain were compared in subjects consuming high or low sugar, blinded, ad libitum diets formulated to ensure both groups consumed a comparable macronutrient distribution and the same amounts of fiber. There is also little data to determine whether the form in which added sugar is consumed, as beverage or as solid food, affects its potential to promote weight gain. It will be very challenging to obtain the funding to conduct the clinical diet studies needed to address these evidence gaps, especially at the levels of added sugar that are commonly consumed. Yet, filling these evidence gaps may be necessary for supporting the policy changes that will help to turn the food environment into one that does not promote the development of obesity and metabolic disease.
484 citations
Cites background from "Low to moderate sugar-sweetened bev..."
...• A group in Switzerland reported that young, healthy men exhibited increased lowdensity lipoprotein-cholesterol (LDL-C) and small dense LDL-C levels when they consumed 80 g/d sucrose (~13%Ereq) in beverage along with their usual ad libitum diets for 3 weeks compared with when they consumed 80 g/d glucose in beverage (63, 64)....
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TL;DR: In this paper, the authors performed an analysis of the Health Professionals Follow-Up Study, a prospective cohort study including 42 883 men and found that participants in the top quartile of sugar-sweetened beverage intake had a 20% higher relative risk of coronary heart disease than those in the bottom quartile (relative risk=1.20; 95% confidence interval, 1.09-1.33; P for trend < 0.01).
Abstract: Background—Sugar-sweetened beverage consumption is associated with weight gain and risk of type 2 diabetes mellitus. Few studies have tested for a relationship with coronary heart disease (CHD) or intermediate biomarkers. The role of artificially sweetened beverages is also unclear. Methods and Results—We performed an analysis of the Health Professionals Follow-Up Study, a prospective cohort study including 42 883 men. Associations of cumulatively averaged sugar-sweetened (eg, sodas) and artificially sweetened (eg, diet sodas) beverage intake with incident fatal and nonfatal CHD (myocardial infarction) were examined with proportional hazard models. There were 3683 CHD cases over 22 years of follow-up. Participants in the top quartile of sugar-sweetened beverage intake had a 20% higher relative risk of CHD than those in the bottom quartile (relative risk=1.20; 95% confidence interval, 1.09–1.33; P for trend <0.01) after adjustment for age, smoking, physical activity, alcohol, multivitamins, family history,...
430 citations
References
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TL;DR: There has been no consensus from professional societies or governmental agencies as to how these assays of markers of inflammation should be used in clinical practice, and a workshop to address these issues was convened in Atlanta, Ga.
Abstract: In 1998, the American Heart Association convened Prevention Conference V to examine strategies for the identification of high-risk patients who need primary prevention. Among the strategies discussed was the measurement of markers of inflammation.1 The Conference concluded that “many of these markers (including inflammatory markers) are not yet considered applicable for routine risk assessment because of: (1) lack of measurement standardization, (2) lack of consistency in epidemiological findings from prospective studies with endpoints, and (3) lack of evidence that the novel marker adds to risk prediction over and above that already achievable through the use of established risk factors.” The National Cholesterol Education Program Adult Treatment Panel III Guidelines identified these markers as emerging risk factors,1a which could be used as an optional risk factor measurement to adjust estimates of absolute risk obtained using standard risk factors. Since these publications, a large number of peer-reviewed scientific reports have been published relating inflammatory markers to cardiovascular disease (CVD). Several commercial assays for inflammatory markers have become available. As a consequence of the expanding research base and availability of assays, the number of inflammatory marker tests ordered by clinicians for CVD risk prediction has grown rapidly. Despite this, there has been no consensus from professional societies or governmental agencies as to how these assays of markers of inflammation should be used in clinical practice.
On March 14 and 15, 2002, a workshop titled “CDC/AHA Workshop on Inflammatory Markers and Cardiovascular Disease: Applications to Clinical and Public Health Practice” was convened in Atlanta, Ga, to address these issues. The goals of this workshop were to determine which of the currently available tests should be used; what results should be used to define high risk; which patients should be tested; and the indications for which the tests would be most useful. These …
5,818 citations
TL;DR: The HOMA model has become a widely used clinical and epidemiological tool and, when used appropriately, it can yield valuable data, however, as with all models, the primary input data needs to be robust, and the data need to be interpreted carefully.
Abstract: Homeostatic model assessment (HOMA) is a method for assessing beta-cell function and insulin resistance (IR) from basal (fasting) glucose and insulin or C-peptide concentrations. It has been reported in >500 publications, 20 times more frequently for the estimation of IR than beta-cell function. This article summarizes the physiological basis of HOMA, a structural model of steady-state insulin and glucose domains, constructed from physiological dose responses of glucose uptake and insulin production. Hepatic and peripheral glucose efflux and uptake were modeled to be dependent on plasma glucose and insulin concentrations. Decreases in beta-cell function were modeled by changing the beta-cell response to plasma glucose concentrations. The original HOMA model was described in 1985 with a formula for approximate estimation. The computer model is available but has not been as widely used as the approximation formulae. HOMA has been validated against a variety of physiological methods. We review the use and reporting of HOMA in the literature and give guidance on its appropriate use (e.g., cohort and epidemiological studies) and inappropriate use (e.g., measuring beta-cell function in isolation). The HOMA model compares favorably with other models and has the advantage of requiring only a single plasma sample assayed for insulin and glucose. In conclusion, the HOMA model has become a widely used clinical and epidemiological tool and, when used appropriately, it can yield valuable data. However, as with all models, the primary input data need to be robust, and the data need to be interpreted carefully.
4,360 citations
3,129 citations
"Low to moderate sugar-sweetened bev..." refers background in this paper
...Subclinical inflammation has been shown to be a key factor in the development of insulin resistance and cardiovascular disease (29, 30)....
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Book•
18 Jan 1990
TL;DR: Assessment of nutrient intakes from food consumption data and the status of vitamins, A, D, and E, and niacin, and trace element status and nutritional assessment of hospital patients.
Abstract: PART 1: INTRODUCTION PART 2: FOOD CONSUMPTION AT THE NATIONAL AND HOUSEHOLD LEVELS PART 3: MEASURING FOOD CONSUMPTION OF INDIVIDUALS PART 4: ASSESSMENT OF NUTRIENT INTAKES FROM FOOD CONSUMPTION DATA PART 5: MEASUREMENT ERRORS IN DIETARY ASSESSMENT PART 6: REPRODUCIBILITY IN DIETARY ASSESSMENT PART 7: VALIDITY IN DIETARY ASSESSMENT METHODS PART 8: EVALUATION OF NUTRIENT INTAKES AND DIETS PART 9: ANTHROPOMETRIC ASSESSMENT PART 10: ANTHROPOMETRIC ASSESSMENT OF BODY SIZE PART 11: ANTHROPOMETRIC ASSESSMENT OF BODY COMPOSITION PART 12: ANTHROPOMETRIC REFERENCE DATA PART 13: EVALUATION OF ANTHROPOMETRIC INDICES PART 14: LABORATORY ASSESSMENT OF BODY COMPOSITION PART 15: LABORATORY ASSESSMENT PART 16: ASSESSMENT OF PROTEIN STATUS PART 17: ASSESSMENT OF IRON STATUS PART 18: ASSESSMENT OF THE STATUS OF VITAMINS A, D AND E PART 19: ASSESSMENT OF VITAMIN C STATUS PART 20: ASSESSMENT OF THE STATUS OF THIAMIN, RIBOFLAVIN, AND NIACIN PART 21: ASSESSMENT OF VITAMIN B6 STATUS PART 22: ASSESSMENT OF FOLATE AND VITAMIN B12 STATUS PART 23: ASSESSMENT OF CALCIUM, PHOSPHORUS AND MAGNESIUM STATUS PART 24: ASSESSMENT OF CHRONIUM, COPPER AND ZINC STATUS PART 25: ASSESSMENT OF IODINE AND SELENIUM STATUS PART 26: CLINICAL ASSESSMENT PART 27: NUTRITIONAL ASSESSMENT OF HOSPITAL PATIENTS
2,929 citations
"Low to moderate sugar-sweetened bev..." refers background in this paper
...In the week before each examination, all subjects completed a 3-d (2 weekdays and one weekend day) weighed food record (19)....
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TL;DR: The increase in consumption of HFCS has a temporal relation to the epidemic of obesity, and the overconsumption of H FCS in calorically sweetened beverages may play a role in the epidemic.
1,868 citations
"Low to moderate sugar-sweetened bev..." refers background in this paper
...The development of the obesity epidemic in the United States runs in parallel to the increase in free fructose consumption as a result of the introduction of high-fructose corn syrup as a beverage sweetener (2)....
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...These differences may be due, at least in part, to the fact that although calorically identical to glucose intake, fructose metabolism differs considerably from that of glucose (2, 34)....
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