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Added-sugar consumption in the U.S. exceeds recommended limits. Policymakers are considering requiring restaurants to use menu warning labels to indicate items high in added sugar. We sought to determine whether icon-only and icon-plus-text added-sugar menu labels were (1) perceived as more effective at potentially reducing consumption of items high in added sugar and (2) increased knowledge of menu items' added-sugar content relative to control labels, and if effects differed by label design. A national sample of U.S. adults (n=1327) participated in an online randomized experiment. Participants viewed menu items with either a control label, 1 of 6 icon-only labels, or 1 of 18 icon-plus-text labels with 3 text variations. For their assigned label, participants provided ratings of perceived message effectiveness (a validated scale of a message's potential to change behavior). Participants were also asked to classify menu items by their added-sugar content. The icon-only and icon-plus-text labels were perceived as more effective than the control label (means: 3.7 and 3.7 vs. 3.1, respectively, on a 5-point scale; p&nbsp

Purpose of Review The mechanistic role of sugar-sweetened beverage (SSB) in the etiology of obesity is undetermined. We address whether, compared to other foods, does consumption of SSB (1) automatically lead to failure to compensate for the energy it contains? (2) fail to elicit homeostatic hormone responses? (3) promote hedonic eating through activation of the brain’s reward pathways? We followed the evidence to address: (4) Would restriction of targeted marketing of SSB and other unhealthy foods to vulnerable populations decrease their prevalence of obesity? Recent Findings The data are lacking to demonstrate that SSB consumption promotes body weight gain compared with isocaloric consumption of other beverages or foods and that this is linked to its failure to elicit adequate homeostatic hormone responses. However, more recent data have linked body weight gain to reward activation in the brain to palatable food cues and suggest that sweet tastes and SSB consumption heightens the reward response to food cues. Studies investigating the specificity of these responses have not been conducted. Nevertheless, the current data provide a biological basis to the body of evidence demonstrating that the targeted marketing (real life palatable food cues) of SSB and other unhealthy foods to vulnerable populations, including children and people of color and low socioeconomic status, is increasing their risk for obesity. Summary While the mechanisms for the association between SSB consumption and body weight gain cannot be identified, current scientific evidence strongly suggests that proactive environmental measures to reduce exposure to palatable food cues in the form of targeting marketing will decrease the risk of obesity in vulnerable populations.

Increased hepatic lipid content and decreased insulin sensitivity have critical roles in the development of cardiometabolic diseases. Therefore, our objective was to investigate the dose-response effects of consuming high fructose corn syrup (HFCS)-sweetened beverages for two weeks on hepatic lipid content and insulin sensitivity in young (18–40 years) adults (BMI 18–35 kg/m2). In a parallel, double-blinded study, participants consumed three beverages/day providing 0% (aspartame: n = 23), 10% (n = 18), 17.5% (n = 16), or 25% (n = 28) daily energy requirements from HFCS. Magnetic resonance imaging for hepatic lipid content and oral glucose tolerance tests (OGTT) were conducted during 3.5-day inpatient visits at baseline and again at the end of a 15-day intervention. During the 12 intervening outpatient days participants consumed their usual diets with their assigned beverages. Significant linear dose-response effects were observed for increases of hepatic lipid content (p = 0.015) and glucose and insulin AUCs during OGTT (both p = 0.0004), and for decreases in the Matsuda (p = 0.0087) and Predicted M (p = 0.0027) indices of insulin sensitivity. These dose-response effects strengthen the mechanistic evidence implicating consumption of HFCS-sweetened beverages as a contributor to the metabolic dysregulation that increases risk for nonalcoholic fatty liver disease and type 2 diabetes.

Background: As the only place in a store where all customers must pass through and wait, the checkout lane may be particularly influential over consumer purchases. Because most foods and beverages sold at checkout are unhealthy (e.g., candy, sweets, sugar-sweetened beverages, and salty snacks), policymakers and advocates have expressed growing interest in healthy checkout policies. To understand the extent to which such policies could improve nutrition equity, we assessed the prevalence and sociodemographic correlates of purchasing items found at (i.e., from) checkout. Methods: We assessed self-reported checkout purchasing and sociodemographic characteristics in a national convenience sample of adults (n = 10,348) completing an online survey in 2021. Results: Over one third (36%) of participants reported purchasing foods or drinks from checkout during their last grocery shopping trip. Purchasing items from checkout was more common among men; adults < 55 years of age; low-income consumers; Hispanic, non-Hispanic American Indian or Alaska Native, and non-Hispanic Black consumers; those with a graduate or professional degree; parents; and consumers diagnosed with type 2 diabetes or pre-diabetes (p-values < 0.05). Conclusions: Purchasing foods or beverages from store checkouts is common and more prevalent among low-income and Hispanic, American Indian or Alaska Native, and Black consumers. These results suggest that healthy checkout policies have the potential to improve nutrition equity.

Context Studies in rodents and humans suggest that high-fructose corn syrup (HFCS)–sweetened diets promote greater metabolic dysfunction than sucrose-sweetened diets. Objective To compare the effects of consuming sucrose-sweetened beverage (SB), HFCS-SB, or a control beverage sweetened with aspartame on metabolic outcomes in humans. Methods A parallel, double-blinded, NIH-funded study. Experimental procedures were conducted during 3.5 days of inpatient residence with controlled feeding at a research clinic before (baseline) and after a 12-day outpatient intervention period. Seventy-five adults (18-40 years) were assigned to beverage groups matched for sex, body mass index (18-35 kg/m2), and fasting triglyceride, lipoprotein and insulin concentrations. The intervention was 3 servings/day of sucrose- or HFCS-SB providing 25% of energy requirement or aspartame-SB, consumed for 16 days. Main outcome measures were %hepatic lipid, Matsuda insulin sensitivity index (ISI), and Predicted M ISI. Results Sucrose-SB increased %hepatic lipid (absolute change: 0.6 ± 0.2%) compared with aspartame-SB (-0.2 ± 0.2%, P Conclusion Consumption of both sucrose- and HFCS-SB induced detrimental changes in hepatic lipid, insulin sensitivity, and circulating lipids, lipoproteins and uric acid in 2 weeks.

Sugar-sweetened beverage (sugar-SB) consumption is associated with body weight gain. We investigated whether the changes of (&Delta, ) circulating leptin contribute to weight gain and ad libitum food intake in young adults consuming sugar-SB for two weeks. In a parallel, double-blinded, intervention study, participants (n = 131, BMI 18&ndash, 35 kg/m2, 18&ndash, 40 years) consumed three beverages/day containing aspartame or 25% energy requirement as glucose, fructose, high fructose corn syrup (HFCS) or sucrose (n = 23&ndash, 28/group). Body weight, ad libitum food intake and 24-h leptin area under the curve (AUC) were assessed at Week 0 and at the end of Week 2. The &Delta, body weight was not different among groups (p = 0.092), but the increases in subjects consuming HFCS- (p = 0.0008) and glucose-SB (p = 0.018) were significant compared with Week 0. Subjects consuming sucrose- (+14%, p &lt, 0.0015), fructose- (+9%, p = 0.015) and HFCS-SB (+8%, p = 0.017) increased energy intake during the ad libitum food intake trial compared with subjects consuming aspartame-SB (&minus, 4%, p = 0.0037, effect of SB). Fructose-SB decreased (&minus, 14 ng/mL &times, 24 h, p = 0.0006) and sucrose-SB increased (+25 ng/mL &times, 24 h, p = 0.025 vs. Week 0, p = 0.0008 vs. fructose-SB) 24-h leptin AUC. The &Delta, ad libitum food intake and &Delta, body weight were not influenced by circulating leptin in young adults consuming sugar-SB for 2 weeks. Studies are needed to determine the mechanisms mediating increased energy intake in subjects consuming sugar-SB.

BackgroundFructose consumption increases risk factors for cardiometabolic disease. It is assumed that the effects of free sugars on risk factors are less potent because they contain less fructose. We compared the effects of consuming fructose, glucose or their combination, high fructose corn syrup (HFCS), on cardiometabolic risk factors.MethodsAdults (18-40 years; BMI 18-35 kg/m2) participated in a parallel, double-blinded dietary intervention during which beverages sweetened with aspartame, glucose (25% of energy requirements (ereq)), fructose or HFCS (25% and 17.5% ereq) were consumed for two weeks. Groups were matched for sex, baseline BMI and plasma lipid/lipoprotein concentrations. 24-h serial blood samples were collected at baseline and at the end of intervention. Primary outcomes were 24-h triglyceride AUC, LDL-cholesterol (C), and apolipoprotein (apo)B. Interactions between fructose and glucose were assessed post hoc.Findings145 subjects (26.0 ± 5.8 years; body mass index 25.0 ± 3.7 kg/m2) completed the study. As expected, the increase of 24-h triglycerides compared with aspartame was highest during fructose consumption (25%: 6.66 mmol/Lx24h 95% CI [1.90 to 11.63], P = 0.0013 versus aspartame), intermediate during HFCS consumption (25%: 4.68 mmol/Lx24h 95% CI [-0.18 to 9.55], P = 0.066 versus aspartame) and lowest during glucose consumption. In contrast, the increase of LDL-C was highest during HFCS consumption (25%: 0.46 mmol/L 95% CI [0.16 to 0.77], P = 0.0002 versus aspartame) and intermediate during fructose consumption (25%: 0.33 mmol/L 95% CI [0.03 to 0.63], P = 0.023 versus aspartame), as was the increase of apoB (HFCS-25%: 0.108 g/L 95%CI [0.032 to 0.184], P = 0.001; fructose 25%: 0.072 g/L 95%CI [-0.004 to 0.148], P = 0.074 versus aspartame). The post hoc analyses showed significant interactive effects of fructose*glucose on LDL-C and apoB (both P

Rodent studies demonstrate that compared with diets sweetened with sucrose, high fructose corn syrup (HFCS) produces greater metabolic dysfunction. However, the effects of sustained consumption of HFCS and sucrose have not been adequately compared in humans. The objective of this study was to compare HFCS-, sucrose-, or aspartame- sweetened beverage (-SB) consumption on hepatic lipid content and insulin sensitivity in young adults. In a parallel, double-blinded study, adult men and women (18-40 yrs) were assigned to beverage groups matched for sex, BMI and fasting triglycerides. Inpatient magnetic resonance imaging for hepatic lipid content and oral glucose tolerance tests were performed at baseline and intervention 15 days later. For 12 outpatient days subjects consumed their usual diets with 3 servings/day of HFCS- (n=28) or sucrose-SB (n=24) providing 25% energy requirement (Ereq), or aspartame-SB (n=23). Matched standardized diets were provided during inpatient testing with the sugar in beverages replacing complex carbohydrate during intervention. Hepatic lipid content was increased by consumption of HFCS-SB (LS means of absolute Δ±SEM: 0.5%±0.2, P Consumption of SB providing 25% of Ereq as HFCS or sucrose for 2 weeks increased hepatic lipid content and reduced insulin sensitivity in young adults compared with consumption of aspartame-SB. Disclosure D. Sigala: None. B. Hieronimus: None. C. Price: None. V. Lee: None. M. Nunez: None. V. Medici: None. A.J. Chaudhari: None. J.P. McGahan: None. Y. Abdelhafez: None. N.L. Keim: None. M.I. Goran: Advisory Panel; Self; Yumi. Other Relationship; Self; Penguin Random House. G. Pacini: None. A. Tura: None. P.J. Havel: Research Support; Self; Arrowhead Pharmaceuticals, Inc., Magnamosis, Inc. Other Relationship; Self; None. K.L. Stanhope: None. Funding National Institutes of Health (R01HL091333, R01HL107256)

Calories from any food have the potential to increase risk for obesity and cardiometabolic disease because all calories can directly contribute to positive energy balance and fat gain. However, various dietary components or patterns may promote obesity and cardiometabolic disease by additional mechanisms that are not mediated solely by caloric content. Researchers explored this topic at the 2017 CrossFit Foundation Academic Conference 'Diet and Cardiometabolic Health - Beyond Calories', and this paper summarizes the presentations and follow-up discussions. Regarding the health effects of dietary fat, sugar and non-nutritive sweeteners, it is concluded that food-specific saturated fatty acids and sugar-sweetened beverages promote cardiometabolic diseases by mechanisms that are additional to their contribution of calories to positive energy balance and that aspartame does not promote weight gain. The challenges involved in conducting and interpreting clinical nutritional research, which preclude more extensive conclusions, are detailed. Emerging research is presented exploring the possibility that responses to certain dietary components/patterns are influenced by the metabolic status, developmental period or genotype of the individual; by the responsiveness of brain regions associated with reward to food cues; or by the microbiome. More research regarding these potential 'beyond calories' mechanisms may lead to new strategies for attenuating the obesity crisis.

Overconsumption of sugar-sweetened beverages increases risk factors associated with cardiometabolic disease, in part due to hepatic fructose overload. However, it is not clear whether consumption of beverages containing fructose as naturally occurring sugar produces equivalent metabolic dysregulation as beverages containing added sugars. We compared the effects of consuming naturally-sweetened orange juice (OJ) or sucrose-sweetened beverages (sucrose-SB) for two weeks on risk factors for cardiometabolic disease. Healthy, overweight women (n = 20) were assigned to consume either 3 servings of 100% orange juice or sucrose-SB/day. We conducted 16-hour serial blood collections and 3-h oral glucose tolerance tests during a 30-h inpatient visit at baseline and after the 2-week diet intervention. The 16-h area under the curve (AUC) for uric acid increased in subjects consuming sucrose-SB compared with subjects consuming OJ. Unlike sucrose-SB, OJ did not significantly increase fasting or postprandial lipoproteins. Consumption of both beverages resulted in reductions in the Matsuda insulin sensitivity index (OJ: −0.40 ± 0.18, p = 0.04 within group, sucrose-SB: −1.0 ± 0.38, p = 0.006 within group, p = 0.53 between groups). Findings from this pilot study suggest that consumption of OJ at levels above the current dietary guidelines for sugar intake does not increase plasma uric acid concentrations compared with sucrose-SB, but appears to lead to comparable decreases of insulin sensitivity.