Sugar-Sweetened Beverage, Sugar Intake of Individuals, and Their Blood Pressure International Study of Macro/Micronutrients and Blood Pressure

Department of Epidemiology and Biostatistics, School of Public Health, Imperial College London, London W2 1PG, United Kingdom.
Hypertension (Impact Factor: 6.48). 02/2011; 57(4):695-701. DOI: 10.1161/HYPERTENSIONAHA.110.165456
Source: PubMed


The obesity epidemic has focused attention on relationships of sugars and sugar-sweetened beverages (SSBs) to cardiovascular risk factors. Here we report cross-sectional associations of SSBs, diet beverages, and sugars with blood pressure (BP) for United Kingdom and US participants of the International Study of Macro/Micronutrients and Blood Pressure. Data collected include four 24-hour dietary recalls, two 24-hour urine collections, 8 BP readings, and questionnaire data for 2696 people ages 40 to 59 years of age from 10 US/United Kingdom population samples. Associations of SSBs, diet beverages, and sugars (fructose, glucose, and sucrose) with BP were assessed by multiple linear regression. SSB intake related directly to BP, with P values of 0.005 to <0.001 (systolic BP) and 0.14 to <0.001 (diastolic BP). SSB intake higher by 1 serving per day (355 mL/24 hours) was associated with systolic/diastolic BP differences of +1.6/+0.8 mm Hg (both P<0.001) and +1.1/+0.4 mm Hg (P<0.001/<0.05) with adjustment for weight and height. Diet beverage intake was inversely associated with BP (P 0.41 to 0.003). Fructose- and glucose-BP associations were direct, with significant sugar-sodium interactions: for individuals with above-median 24-hour urinary sodium excretion, fructose intake higher by 2 SD (5.6% kcal) was associated with systolic/diastolic BP differences of +3.4/+2.2 mm Hg (both P<0.001) and +2.5/+1.7 mm Hg (both P=0.002) with adjustment for weight and height. Observed independent, direct associations of SSB intake and BP are consistent with recent trial data. These findings, plus adverse nutrient intakes among SSB consumers, and greater sugar-BP differences for persons with higher sodium excretion lend support to recommendations that intake of SSBs, sugars, and salt be substantially reduced.

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    • "A prospective cohort study( 86 ) indicated that higher consumption of SSB was associated with a higher risk of CHD. Additionally, a cross-sectional study( 34 ) and two other cohort studies( 87 , 88 ) positively associated a reduction in SSB consumption with a reduction of disease risk factors such as elevated blood pressure or weight gain. It should be mentioned, however, that relevant intervention studies with such risk factors as end-point are lacking. "
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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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    • "During the last decade, there has been an increasing number of published epidemiological and interventional studies on human populations linking the high consumption of sugar-sweetened beverages, enriched in simple sugars such as fructose and glucose, to the high prevalence of chronic metabolic and related cardiovascular diseases [1] [2] [3] [4]. These diseases include dyslipidemia [5] [6], gout [7], hypertension [8] [9], obesity [10] [11], insulin resistance [12] and type 2 diabetes mellitus [10] [13] [14] [15]. High energy intake, lack of adequate energy compensation through a proportional decrease in the amount of energy ingested as solid foods, and the special metabolism of fructose, have been reported to contribute to this possible causal association [2] [3]. "
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    ABSTRACT: High consumption of fructose-sweetened beverages has been linked to a high prevalence of chronic metabolic diseases. We have previously shown that a short course of fructose supplementation as a liquid solution induces glucose intolerance in female rats. In the present work, we characterized the fructose-driven changes in the liver and the molecular pathways involved. To this end, female rats were supplemented or not with liquid fructose (10%, w/v) for 7 or 14 days. Glucose and pyruvate tolerance tests were performed, and the expression of genes related to insulin signaling, gluconeogenesis and nutrient sensing pathways was evaluated. Fructose-supplemented rats showed increased plasma glucose excursions in glucose and pyruvate tolerance tests and reduced hepatic expression of several genes related to insulin signaling, including insulin receptor substrate 2 (IRS-2). However, the expression of key gluconeogenic enzymes, glucose-6-phosphatase and phosphoenolpyruvate carboxykinase, was reduced. These effects were caused by an inactivation of hepatic forkhead box O1 (FoxO1) due to an increase in its acetylation state driven by a reduced expression and activity of sirtuin 1 (SIRT1). Further contributing to FoxO1 inactivation, fructose consumption elevated liver expression of the spliced form of X-box-binding-protein-1 as a consequence of an increase in the activity of the mammalian target of rapamycin 1 and protein 38-mitogen activated protein kinase (p38-MAPK). Liquid fructose affects both insulin signaling (IRS-2 and FoxO1) and nutrient sensing pathways (p38-MAPK, mTOR and SIRT1), thus disrupting hepatic insulin signaling without increasing the expression of key gluconeogenic enzymes.
    The Journal of nutritional biochemistry 02/2014; 25(2):250-8. DOI:10.1016/j.jnutbio.2013.10.014 · 3.79 Impact Factor
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    • "Jalal et al. [5] explored the association between intake of fructose, a major type of added sugar, and the prevalence of hypertension among 4,528 adults over aged 18 years who were free of medical history of hypertension in the NHANES 2003-2006 data and found a 77% higher prevalence of stage 2 hypertension among those who consumed 74 g/d or more of fructose compared to those who consumed less than 74 g/d of fructose. Brown et al. [6] analyzed the association between intake of SSBs and diet drinks and blood pressure in a cross-sectional design among 2,696 UK and US adults aged between 40-59 years who participated in the International Study of Macro/Micronutrients and Blood Pressure (INTERMAP), showing that one serving (355 mL) per day increment in intake of SSB was associated with SBP/DBP differences of +1.1/+0.4 mmHg. "
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    ABSTRACT: High sugar intake has been suggested to be related to hypertension. To examine the associations between intakes of sugar and sugar-sweetened beverages (SSBs) and the prevalence of hypertension, we used the US National Health and Nutrition Examination Survey (NHANES) 2003-2006. A total of 3,044 participants aged ≥19 years were included. We calculated odds ratios (ORs) and 95% confidence intervals (CIs) using multivariate logistic regression model. Prevalent hypertension cases were defined as systolic blood pressure (SBP) of ≥140 mmHg or diastolic blood pressure (DBP) of ≥90 mmHg. In the multivariate adjusted models, we observed no association between sugar consumption and the prevalence of hypertension. In the model where we adjusted for age, gender, NHANES period and BMI, those who consumed ≥3 times per day of sugar-sweetened beverages had an OR of 1.87 (95% confidence interval, CI = 1.06-3.26) for the prevalence of hypertension compared with those who consumed <1 time per month of these beverages. Further adjustment for other factors attenuated the association; ORs (95% CIs) were 1.21 (0.81-1.81) for 1 time per month-<3 times per week, 1.39 (0.86-2.24) for 3 times per week-<1 times per day, 1.26 (0.80-1.98) for 1-<3 times per day, and 1.50 (0.84-2.68) for ≥3 times per day of sugar-sweetened beverages compared to the <1 time per month (p for trend = 0.33). In conclusion, we found that sugar consumption was not associated with the prevalence of hypertension, however there was suggestion that high sugar-sweetened beverage consumption was associated with high prevalence of hypertension in the US.
    07/2012; 1(1):85-93. DOI:10.7762/cnr.2012.1.1.85
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