Sugars-containing beverages and post-prandial satiety and food intake (original) (raw)
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Is there an association between sweetened beverages and adiposity?
Nutrition reviews, 2006
Four mechanisms were reviewed to explain the possible association between sweetened beverages and increased overweight or obesity: excess caloric intake, glycemic index and glycemic load, lack of effect of liquid calories on satiety, and displacement of milk. The findings were inconsistent across studies. The strongest support was for the excess caloric intake hypothesis, but the findings were not conclusive. Assigning possible links between sweetened beverage consumption and adiposity requires research that compares and contrasts specific mechanisms, especially in populations at risk for obesity, while controlling for likely confounding variables.
Physiology & Behavior, 2016
For more than a decade, pioneering animal studies conducted by investigators at Purdue University have provided evidence to support a central thesis: that the uncoupling of sweet taste and caloric intake by low-calorie sweeteners (LCS) can disrupt an animal's ability to predict the metabolic consequences of sweet taste, and thereby impair the animal's ability to respond appropriately to sweet-tasting foods. These investigators' work has been replicated and extended internationally. There now exists a body of evidence, from a number of investigators, that animals chronically exposed to any of a range of LCSs-including saccharin, sucralose, acesulfame potassium, aspartame, or the combination of erythritol + aspartame-have exhibited one or more of the following conditions: increased food consumption, lower post-prandial thermogenesis, increased weight gain, greater percent body fat, decreased GLP-1 release during glucose tolerance testing, and significantly greater fasting glucose, glucose area under the curve during glucose tolerance testing, and hyperinsulinemia, compared with animals exposed to plain water or-in many caseseven to calorically-sweetened foods or liquids. Adverse impacts of LCS have appeared diminished in animals on dietary restriction, but were pronounced among males, animals genetically predisposed to obesity, and animals with diet-induced obesity. Impacts have been especially striking in animals on high-energy diets: diets high in fats and sugars, and diets which resemble a highly-processed 'Western' diet, including trans-fatty acids and monosodium glutamate. These studies have offered both support for, and biologically plausible mechanisms to explain, the results from a series of large-scale, long-term prospective observational studies conducted in humans, in which longitudinal increases in weight, abdominal adiposity, and incidence of overweight and obesity have been observed among study participants who reported using diet sodas and other LCS-sweetened beverages daily or more often at baseline. Furthermore, frequent use of diet beverages has been associated prospectively with increased long-term risk and/or hazard of a number of cardiometabolic conditions usually considered to be among the sequelae of obesity: hypertension, metabolic syndrome, diabetes, depression, kidney dysfunction, heart attack, stroke, and even cardiovascular and total mortality. Reverse causality does not appear to explain fully the increased risk observed across all of these studies, the majority of which have included key potential confounders as covariates. These have included body mass index or waist circumference at baseline; total caloric intake and specific macronutrient intake; physical activity; smoking; demographic and other relevant risk factors; and/or family history of disease. Whether non-LCS ingredients in diet beverages might have independently increased the weight gain and/or cardiometabolic risk observed among frequent consumers of LCS-sweetened beverages deserves
Nutritively Sweetened Beverage Consumption and Obesity
JAMA, 2009
The prevalence of obesity has increased substantially in the past several decades, and clinicians, policy makers, and others seek tools to abate this epidemic. One tantalizingly simple solution is to identify a single class of foods for which the elimination or radical reduction would meaningfully decrease the energy intake/expenditure ratio and obesity prevalence. Nutritively sweetened beverages (NSBs) (eg, sugar-sweetened beverages, soft drinks) seem to have become a leading contender, and the surrounding dialogue has become contentious, evoking scientific, clinical, and sociopolitical questions. The key question is whether reducing NSB consumption will help prevent the onset, reduce the prevalence, or contribute to the management of obesity. The controversy hinges on the strength of the current evidence. Clearly there are other important issues, such as potential NSB effects on overall diet quality, dental and bone health, glucose tolerance, hydration, quality of life, the economy, and the environment. In this Commentary, we address only the obesity question. Plausibility That Reducing NSB Consumption Will Reduce Obesity Some epidemiological studies support an association between NSB consumption and obesity, 1 some animal studies have shown that ad libitum NSB consumption increases body weight, 2 and some short-term food intake studies suggest that NSB consumption may be poorly compensated (compensation here refers to the adjustment of subsequent energy intake or expenditure downward or upward in response to NSB ingestion; hence, its influence on overall energy balance). 3 However, other epidemiological, 4 animal, 5 and shortterm behavioral studies 6 do not show such results. The stage for evidence that can provide clearer answers has been set. For some questions, such as whether smoking causes lung cancer, it is impractical or unethical to randomize study participants to receive or not receive the putatively influential agent and observe its effects. In such situations, consideration of the totality of evidence is
Sugary drinks in the pathogenesis of obesity and cardiovascular diseases
International journal of obesity (2005), 2008
Soft drink overconsumption is now considered to be a major public health concern with implications for cardiovascular diseases. This follows a number of studies performed in animals suggesting that chronic consumption of refined sugars can contribute to metabolic and cardiovascular dysregulation. In particular, the monosaccharide fructose has been attracting increasing attention as the more harmful sugar component in terms of weight gain and metabolic disturbances. High-fructose corn syrup is gradually replacing sucrose as the main sweetener in soft drinks and has been blamed as a potential contributor to the current high prevalence of obesity. There is also considerable evidence that fructose, rather than glucose, is the more damaging sugar component in terms of cardiovascular risk. This review focuses on the potential role of sugar drinks, particularly the fructose component, in the pathogenesis of obesity and cardiovascular diseases.
Appetite, 2020
Sensory-specific satiety (SSS) describes a reduction in the pleasantness of the taste of (momentary liking) and desire to consume a food that occurs with consumption, compared with the relative preservation of liking and desire for uneaten foods. We conducted three studies in healthy female and male participants to test whether SSS generalises from sweet drinks to sweet foods. Studies 1 (n = 40) and 2 (n = 64) used a two-condition cross-over design. Participants consumed non-carbonated, fruit squash drinks sweetened with lowcalorie sweeteners (LCS) versus water and evaluated various food and drink samples (stimuli). Generalisation of SSS was evident across all sweet stimuli, without an effect on non-sweet (savoury) stimuli. These SSS effects were present when measured shortly after consumption of the sweet drink, but not 2 hours later. There was no evidence of a 'rebound' increase above baseline in liking or desire to consume sweet foods 2 hours after the sweet drink versus water. In study 3, 51 participants consumed labelled and branded 500 ml cola and water drinks (4 conditions, cross-over design) immediately before and during ad libitum consumption of sweet and non-sweet snack foods. Compared with still water, 'diet' (LCSsweetened) cola reduced sweet food intake, but not total ad libitum intake. Carbonated water decreased hunger and increased fullness compared with still water, without differentially affecting thirst. Energy compensation from the ad libitum snacks for consumption of sugar-containing cola averaged only 20%. Together, these results demonstrate that consumption of LCS drinks acutely decreases desire for sweet foods, which supports their use in place of sugar-sweetened drinks. Further studies on the effects of carbonation of appetite are warranted.
American Journal of Clinical Nutrition, 2011
Background: Consumption of sugar-sweetened beverages has been shown to be associated with dyslipidemia, insulin resistance, fatty liver, diabetes, and cardiovascular disease. It has been proposed that adverse metabolic effects of chronic consumption of sugarsweetened beverages are a consequence of increased circulating glucose and insulin excursions, ie, dietary glycemic index (GI). Objective: We determined whether the greater adverse effects of fructose than of glucose consumption were associated with glucose and insulin exposures. Design: The subjects were studied in a metabolic facility and consumed energy-balanced diets containing 55% of energy as complex carbohydrate for 2 wk (GI = 64). The subjects then consumed 25% of energy requirements as fructose-or glucose-sweetened beverages along with their usual ad libitum diets for 8 wk at home and then as part of energy-balanced diets for 2 wk at the metabolic facility (fructose GI = 38, glucose GI = 83). The 24-h glucose and insulin profiles and fasting plasma glycated albumin and fructosamine concentrations were measured 0, 2, 8, and 10 wk after beverage consumption. Results: Consumption of fructose-sweetened beverages lowered glucose and insulin postmeal peaks and the 23-h area under the curve compared with the baseline diet and with the consumption of glucose-sweetened beverages (all P , 0.001, effect of sugar). Plasma glycated albumin concentrations were lower 10 wk after fructose than after glucose consumption (P , 0.01, effect of sugar), whereas fructosamine concentrations did not differ between groups. Conclusion: The results suggest that the specific effects of fructose, but not of glucose and insulin excursions, contribute to the adverse effects of consuming sugar-sweetened beverages on lipids and insulin sensitivity. This study is registered at clinicaltrials.gov as NCT01165853.
Journal of Clinical Investigation, 2009
Studies in animals have documented that, compared with glucose, dietary fructose induces dyslipidemia and insulin resistance. To assess the relative effects of these dietary sugars during sustained consumption in humans, overweight and obese subjects consumed glucose-or fructose-sweetened beverages providing 25% of energy requirements for 10 weeks. Although both groups exhibited similar weight gain during the intervention, visceral adipose volume was significantly increased only in subjects consuming fructose. Fasting plasma triglyceride concentrations increased by approximately 10% during 10 weeks of glucose consumption but not after fructose consumption. In contrast, hepatic de novo lipogenesis (DNL) and the 23-hour postprandial triglyceride AUC were increased specifically during fructose consumption. Similarly, markers of altered lipid metabolism and lipoprotein remodeling, including fasting apoB, LDL, small dense LDL, oxidized LDL, and postprandial concentrations of remnant-like particle-triglyceride and -cholesterol significantly increased during fructose but not glucose consumption. In addition, fasting plasma glucose and insulin levels increased and insulin sensitivity decreased in subjects consuming fructose but not in those consuming glucose. These data suggest that dietary fructose specifically increases DNL, promotes dyslipidemia, decreases insulin sensitivity, and increases visceral adiposity in overweight/obese adults.
Nutrients, 2018
Background: The effect of sugar-sweetened beverages (SSBs) on satiety and short-term food intake (FI) regulation in girls has received little attention. The objective of the present study was to compare the effect of pre-meal consumption of commercially available SSBs on subjective appetite and short-term FI in 9-14-year-old girls. The methods we used include using a randomized crossover design in which 28 girls consumed isovolumetric amounts (350 mL) of a fruit drink (154 kcal), cola (158 kcal), 1% chocolate milk (224 kcal), or water (control; 0 kcal) on four separate mornings. Subjective appetite and thirst were measured at regular intervals via visual analogue scales (VAS) and FI was assessed at 60 min post-beverage consumption. The results show that subjective appetite and thirst decreased after all beverages, but did not differ among beverages. Short-term FI was suppressed following consumption of chocolate milk (15%; p < 0.001) and cola (11%; p = 0.02) compared to the water control. However, cumulative energy intake (beverage (kcal) + test meal (kcal)) was not affected by beverage type. In conclusion, chocolate milk and cola, but not fruit drink, suppressed FI in girls while cumulative FI did not differ among treatments.