Intake of high-intensity sweeteners alters the ability of sweet taste to signal caloric consequences: implications for the learned control of energy and body weight regulation.

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Abstract

Recent results from both human epidemiological and experimental studies with animals suggest that intake of noncaloric sweeteners may promote, rather than protect against, weight gain and other disturbances of energy regulation. However, without a viable mechanism to explain how consumption of noncaloric sweeteners can increase energy intake and body weight, the persuasiveness of such results has been limited. Using a rat model, the present research showed that intake of noncaloric sweeteners reduces the effectiveness of learned associations between sweet tastes and postingestive caloric outcomes (Experiment 1) and that interfering with this association may impair the ability of rats to regulate their intake of sweet, but not nonsweet, high-fat and high-calorie food (Experiment 2). The results support the hypothesis that consuming noncaloric sweeteners may promote excessive intake and body weight gain by weakening a predictive relationship between sweet taste and the caloric consequences of eating.

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Sweetened beverage consumption and risk of coronary heart disease in women.

Teresa Fung, Vasanti Malik, Kathryn Rexrode … (2009)

Previous studies have linked full-calorie sugar-sweetened beverages (SSBs) with greater weight gain and an increased risk of type 2 diabetes. We prospectively examined the association between consumption of SSBs and the risk of coronary heart disease (CHD) in women. Women (n = 88,520) from the Nurses' Health Study aged 34-59 y, without previously diagnosed coronary heart disease (CHD), stroke, or diabetes in 1980, were followed from 1980 to 2004. Consumption of SSBs was derived from 7 repeated food-frequency questionnaires administered between 1980 and 2002. Relative risks (RRs) for CHD were calculated by using Cox proportional hazards models and adjusted for known cardiovascular disease risk factors. During 24 y of follow-up, we ascertained 3105 incident cases of CHD (nonfatal myocardial infarction and fatal CHD). After standard and dietary risk factors were adjusted for, the RRs (and 95% CIs) of CHD according to categories of cumulative average of SSB consumption ( or =2 servings/d) were 1.0, 0.96 (0.87, 1.06), 1.04 (0.95, 1.14), 1.23 (1.06, 1.43), and 1.35 (1.07, 1.69) (P for trend < 0.001). Additional adjustment for body mass index, energy intake, and incident diabetes attenuated the associations, but they remained significant. Artificially sweetened beverages were not associated with CHD. Regular consumption of SSBs is associated with a higher risk of CHD in women, even after other unhealthful lifestyle or dietary factors are accounted for.

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Nonnutritive sweetener consumption in humans: effects on appetite and food intake and their putative mechanisms.

Richard D Mattes, Barry M. Popkin (2008)

Nonnutritive sweeteners (NNS) are ecologically novel chemosensory signaling compounds that influence ingestive processes and behavior. Only about 15% of the US population aged >2 y ingest NNS, but the incidence is increasing. These sweeteners have the potential to moderate sugar and energy intakes while maintaining diet palatability, but their use has increased in concert with BMI in the population. This association may be coincidental or causal, and either mode of directionality is plausible. A critical review of the literature suggests that the addition of NNS to non-energy-yielding products may heighten appetite, but this is not observed under the more common condition in which NNS is ingested in conjunction with other energy sources. Substitution of NNS for a nutritive sweetener generally elicits incomplete energy compensation, but evidence of long-term efficacy for weight management is not available. The addition of NNS to diets poses no benefit for weight loss or reduced weight gain without energy restriction. There are long-standing and recent concerns that inclusion of NNS in the diet promotes energy intake and contributes to obesity. Most of the purported mechanisms by which this occurs are not supported by the available evidence, although some warrant further consideration. Resolution of this important issue will require long-term randomized controlled trials.