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Background: Low-calorie sweeteners (LCSs) provide sweetness with little or no energy. However, each LCS's unique chemical structure has potential to elicit different sensory, physiological, and behavioral responses that affect body weight., Objective: The purpose of this trial was to compare the effects of consumption of 4 LCSs and sucrose on body weight, ingestive behaviors, and glucose tolerance over a 12-wk intervention in adults (18-60 y old) with overweight or obesity (body mass index 25-40 kg/m2)., Methods: In a parallel-arm design, 154 participants were randomly assigned to consume 1.25-1.75 L of beverage sweetened with sucrose (n = 39), aspartame (n = 30), saccharin (n = 29), sucralose (n = 28), or rebaudioside A (rebA) (n = 28) daily for 12 wk. The beverages contained 400-560 kcal/d (sucrose treatments) or <5 kcal/d (LCS treatments). Anthropometric indexes, energy intake, energy expenditure, appetite, and glucose tolerance were measured at baseline. Body weight was measured every 2 wk with energy intake, expenditure, and appetite assessed every 4 wk. Twenty-four-hour urine collections were completed every 4 wk to determine study compliance via para-aminobenzoic acid excretion., Results: Of the participants enrolled in the trial, 123 completed the 12-wk intervention. Sucrose and saccharin consumption led to increased body weight across the 12-wk intervention (Δweight = +1.85 ± 0.36 kg and +1.18 ± 0.36 kg, respectively; P ≤ 0.02) and did not differ from each other. There was no significant change in body weight with consumption of the other LCS treatments compared with baseline, but change in body weight for sucralose was negative and significantly lower compared with all other LCSs at week 12 (weight difference ≥ 1.37 ± 0.52 kg, P ≤ 0.008). Energy intake decreased with sucralose consumption (P = 0.02) and ingestive frequency was lower for sucralose than for saccharin (P = 0.045). Glucose tolerance was not significantly affected by any of the sweetener treatments., Conclusions: Sucrose and saccharin consumption significantly increase body weight compared with aspartame, rebA, and sucralose, whereas weight change was directionally negative and lower for sucralose compared with saccharin, aspartame, and rebA consumption. LCSs should be categorized as distinct entities because of their differing effects on body weight. This trial was registered at clinicaltrials.gov as NCT02928653., (Copyright © American Society for Nutrition 2019.)

Background: Sugar-sweetened beverages (SSBs) have been associated with an increased risk of diabetes mellitus (DM), whereas the association with artificially sweetened beverages (ASBs) is unclear. Objective: We aimed to evaluate the associations of ASB and SSB consumption with the risk of developing DM and the potential benefit of replacing SSBs with ASBs or water. Design: The national Women's Health Initiative recruited a large prospective cohort of postmenopausal women between 1993 and 1998. ASB, SSB, and water consumption was measured by lifestyle questionnaires, and DM was self-reported. Results: Of 64,850 women, 4675 developed diabetes over an average of 8.4 y of follow-up. ASBs and SSBs were both associated with an increased risk of DM with an HR of 1.21 (95% CI: 1.08, 1.36) comparing ASB consumption of ≥2 serving/d to never or <3 serving/mo, and an HR of 1.43 (95% CI: 1.17, 1.75) comparing SSB consumption of ≥2 serving/d to <1 serving/wk (1 serving = one 12-ounce can or 355 mL). Subgroup analysis found an increased risk of DM associated with ASBs only in the obese group. Modeling the substitution of SSBs with an equal amount of ASBs did not significantly reduce the risk of developing DM. However, statistically substituting 1 serving of ASBs with water was associated with a significant risk reduction of 5% (HR: 0.95; 95% CI: 0.91, 0.99), whereas substituting 1 serving of SSBs with water was associated with a risk reduction of 10% (HR: 0.90; 95% CI: 0.85, 0.95). Conclusions: ASBs were associated with a 21% increased risk of developing DM, approximately half the magnitude of SSBs (associated with a 43% increased risk). Replacing ASBs and SSBs with water could potentially reduce the risk. However, caution should be taken in interpreting these results as causal because both residual confounding and reverse causation could explain these results., (© 2017 American Society for Nutrition.)

Background: Current obesity theories suggest that the repeated intake of highly palatable high-sugar foods causes adaptions in the striatum, parietal lobe, and prefrontal and visual cortices in the brain that may serve to perpetuate consumption in a feed-forward manner. However, the data for humans are cross-sectional and observational, leaving little ability to determine the temporal precedence of repeated consumption on brain response. Objective: We tested the impact of regular sugar-sweetened beverage intake on brain and behavioral responses to beverage stimuli. Design: We performed an experiment with 20 healthy-weight individuals who were randomly assigned to consume 1 of 2 sugar-sweetened beverages daily for 21 d, underwent 2 functional MRI sessions, and completed behavioral and explicit hedonic assessments. Results: Consistent with preclinical experiments, daily beverage consumption resulted in decreases in dorsal striatal response during receipt of the consumed beverage ( r = -0.46) and decreased ventromedial prefrontal response during logo-elicited anticipation ( r = -0.44). This decrease in the prefrontal response correlated with increases in behavioral disinhibition toward the logo of the consumed beverage ( r = 0.54; P = 0.02). Daily beverage consumption also increased precuneus response to both juice logos compared with a tasteless control ( r = 0.45), suggesting a more generalized effect toward beverage cues. Last, the repeated consumption of 1 beverage resulted in an explicit hedonic devaluation of a similar nonconsumed beverage ( P < 0.001). Conclusions: Analogous to previous reports, these initial results provide convergent data for a role of regular sugar-sweetened beverage intake in altering neurobehavioral responses to the regularly consumed beverage that may also extend to other beverage stimuli. Future research is required to provide evidence of replication in a larger sample and to establish whether the neurobehavioral adaptations observed herein are specific to high-sugar and/or nonnutritive-sweetened beverages or more generally related to the repeated consumption of any type of food. This trial was registered at clinicaltrials.gov as NCT02624206., (© 2017 American Society for Nutrition.)

Background: Sugar has been suggested as a central risk factor in the development of noncommunicable diseases., Objective: We assessed the evidence of the effects of free sugars compared with complex carbohydrates on selected cardiovascular disease risk factors., Design: We conducted a systematic review and meta-analysis of intervention trials to compare diets that provide a given amount of energy from free sugars with a control diet that provides the same amount of energy from complex carbohydrates. The primary outcomes were: blood pressure, total cholesterol, low-density lipoprotein (LDL) cholesterol, high-density lipoprotein (HDL) cholesterol, triacylglycerols, apolipoproteins A-I and B, or very low-density lipoprotein cholesterol. Body weight was also recorded but was not a primary outcome of the studies., Results: In all, 28 studies involving 510 volunteers were included. When free sugars were substituted for complex carbohydrates, no significant increases were detected in systolic or diastolic blood pressure, and no heterogeneity was observed. There were significant increases in HDL cholesterol, LDL cholesterol, and triacylglycerols, although for LDL cholesterol and triacylglycerols there was significant heterogeneity between studies and evidence of publication bias. After adjustment for missing studies, these increases lost significance. Subgroup analyses showed that diets providing the largest total energy intake and energy exchange enhanced the effect of free sugars on total and LDL cholesterol and triacylglycerols. The increase of triacylglycerols was no longer significant when studies with the highest risk of bias were excluded or when only randomized trials were considered. Free sugars had no effect on body weight., Conclusions: In short- or moderate-term isoenergetic intervention trials, the substitution of free sugars for complex carbohydrates had no effect on blood pressure or body weight and an unclear effect on blood lipid profile. Further independent trials are required to assess whether the reduction of free sugars improves cardiovascular disease risk factors. This review was registered at http://www.crd.york.ac.uk/prospero as CRD42016042930., (© 2017 American Society for Nutrition.)

Background: Telomere length (TL) is a marker of cellular aging, with the majority of lifetime attrition occurring during the first 4 y. Little is known about risk factors for telomere shortening in childhood., Objective: We evaluated the relation between early life feeding variables and preschool TL., Design: We assessed the relation between dietary, feeding, and weight-associated risk factors measured from birth and TL from blood samples taken at 4 y of age (n = 108) and 5 y of age (n = 92) in a cohort of urban, Latino children (n = 121 individual children). Feeding variables were evaluated in children with repeat measurements (n = 77)., Results: Mean TL (in bp) was associated with exclusive breastfeeding at 4-6 wk of age (adjusted coefficient: 353.85; 95% CI: 72.81, 634.89; P = 0.01), maternal TL (adjusted coefficient: 0.32; 95% CI: 0.11, 0.54; P < 0.01), and older paternal age (adjusted coefficient: 33.27; 95% CI: 4.10, 62.44; P = 0.03). The introduction of other foods or drinks in addition to breast-milk or replacement-milk substitutes before 4-6 wk of age was associated with mean TL at 4 and 5 y of age (adjusted coefficient: -457.01; 95% CI: -720.50, -193.51; P < 0.01). Infant obesity at 6 mo of age and soda consumption at 4 y of age mediated the relation in part between exclusive breastfeeding at 4-6 wk of age and mean TL at 4 and 5 y of age. High soda consumption at 3 y of age was associated with an accelerated attrition from 4 to 5 y of age (adjusted coefficient: -515.14; 95% CI: -986.06, -41.22; P = 0.03)., Conclusion: Exclusive breastfeeding at 4-6 wk of age may have long-term effects on child health as evidenced by longer TL at 4 and 5 y of age., (© 2016 American Society for Nutrition.)

Background: Evidence maps are a new method that systematically characterize the range of research activity in broad topic areas and are used to guide research priority setting, systematic reviews, and meta-analyses., Objective: We expanded evidence mapping methods by demonstrating their usefulness as a tool for organizing epidemiologic research on sugar-sweetened beverage (SSB) intake and health outcomes: obesity, type 2 diabetes, metabolic syndrome, and coronary heart disease/stroke., Design: We performed a search of the PubMed, Scopus, and Cochrane databases and a hand search of references. Studies selected were reviews and longitudinal studies (intervention and cohort) published between 1 January 1966 and 31 October 2012., Results: We identified and mapped 77 studies (18 review and 59 primary research articles); most of the research focused on obesity (n = 47). For all outcomes, >30% (n = 18) of the primary research studies we identified were not referenced in published reviews. We found considerable variability among primary research studies of SSBs and the 4 health outcomes in terms of designs, definitions of SSBs, and definitions of outcomes, which renders these studies difficult to interpret collectively. For example, we counted 14 different definitions of weight/obesity in 29 observational cohort studies, and ≤6 studies reported the use of the same outcome measure., Conclusions: Establishing field standards in the study of SSB intake and health outcomes would facilitate interpretation across research studies and thereby increase the utility of systematic reviews/meta-analyses and ultimately the efficiency of research efforts. Rapid publication of new data suggests the need for regular updates and caution when reading reviews.

Background: Macronutrient "preloads" can stimulate glucagon-like peptide 1 (GLP-1) and glucose-dependent insulinotropic polypeptide (GIP), slow gastric emptying, and reduce postprandial glycemic excursions. After sweet preloads, these effects may be signaled by sodium-glucose cotransporter-1 (SGLT1), sweet taste receptors, or both., Objective: We determined the effects of 4 sweet preloads on GIP and GLP-1 release, gastric emptying, and postprandial glycemia., Design: Ten healthy subjects were studied on 4 separate occasions each. A preload drink containing 40 g glucose, 40 g tagatose/isomalt mixture (TIM), 40 g 3-O-methylglucose (3OMG; a nonmetabolized substrate of SGLT1), or 60 mg sucralose was consumed 15 min before a (13)C-octanoic acid-labeled mashed potato meal. Blood glucose, plasma total GLP-1 and GIP, serum insulin, and gastric emptying were determined., Results: Both glucose and 3OMG stimulated GLP-1 and GIP release in advance of the meal (each P < 0.05), whereas TIM and sucralose did not. The overall postprandial GLP-1 response was greater after glucose, 3OMG, and TIM than after sucralose (P < 0.05), albeit later after TIM than the other preloads. The blood glucose and insulin responses in the first 30 min after the meal were greatest after glucose (each P < 0.05). Gastric emptying was slower after both 3OMG and TIM than after sucralose (each P < 0.05)., Conclusions: In healthy humans, SGLT1 substrates stimulate GLP-1 and GIP and slow gastric emptying, regardless of whether they are metabolized, whereas the artificial sweetener sucralose does not. Poorly absorbed sweet tastants (TIM), which probably expose a greater length of gut to nutrients, result in delayed GLP-1 secretion but not in delayed GIP release. These observations have the potential to optimize the use of preloads for glycemic control. This trial was registered at www.actr.org.au as ACTRN12611000775910.

Background: Both nutritional and genetic factors are involved in the pathogenesis of nonalcoholic fatty liver disease and insulin resistance., Objective: The aim was to assess the effects of fructose, a potent stimulator of hepatic de novo lipogenesis, on intrahepatocellular lipids (IHCLs) and insulin sensitivity in healthy offspring of patients with type 2 diabetes (OffT2D)--a subgroup of individuals prone to metabolic disorders., Design: Sixteen male OffT2D and 8 control subjects were studied in a crossover design after either a 7-d isocaloric diet or a hypercaloric high-fructose diet (3.5 g x kg FFM(-1) x d(-1), +35% energy intake). Hepatic and whole-body insulin sensitivity were assessed with a 2-step hyperinsulinemic euglycemic clamp (0.3 and 1.0 mU x kg(-1) x min(-1)), together with 6,6-[2H2]glucose. IHCLs and intramyocellular lipids (IMCLs) were measured by 1H-magnetic resonance spectroscopy., Results: The OffT2D group had significantly (P < 0.05) higher IHCLs (+94%), total triacylglycerols (+35%), and lower whole-body insulin sensitivity (-27%) than did the control group. The high-fructose diet significantly increased IHCLs (control: +76%; OffT2D: +79%), IMCLs (control: +47%; OffT2D: +24%), VLDL-triacylglycerols (control: +51%; OffT2D: +110%), and fasting hepatic glucose output (control: +4%; OffT2D: +5%). Furthermore, the effects of fructose on VLDL-triacylglycerols were higher in the OffT2D group (group x diet interaction: P < 0.05)., Conclusions: A 7-d high-fructose diet increased ectopic lipid deposition in liver and muscle and fasting VLDL-triacylglycerols and decreased hepatic insulin sensitivity. Fructose-induced alterations in VLDL-triacylglycerols appeared to be of greater magnitude in the OffT2D group, which suggests that these individuals may be more prone to developing dyslipidemia when challenged by high fructose intakes. This trial was registered at clinicaltrials.gov as NCT00523562.

Background: Endothelial function deteriorates after glucose ingestion. This may be attributed to hyperglycemia-induced oxidative stress. Acute endurance exercise might improve postprandial endothelial function by enhancing glucoregulation and reducing postprandial hyperglycemia., Objective: The objective was to determine whether endurance exercise performed 17 h before high-sugar-food ingestion attenuates postprandial impairment in endothelial function., Design: Healthy men and women (n = 13; age: 48 +/- 17 y) were studied on 2 occasions: after > or = 48 h with no exercise and 17 h after a 60-min bout of endurance exercise. During each trial, brachial artery flow mediated dilation (FMD) was used to assess endothelial function before and after the ingestion of a candy bar and soft drink. Glucose, insulin, and thiobarbituric acid-reactive substances (TBARS), a marker of oxidative stress, were measured in blood obtained during each FMD measurement. The insulin sensitivity index was calculated from the glucose and insulin data., Results: FMD decreased significantly after food ingestion in both trials. However, prior exercise shifted the entire FMD curve upward (main treatment effect: P = 0.0002), which resulted in a greater area under the curve for FMD (774 +/- 122%.min) than did no exercise (607 +/- 122%.min) (P = 0.01). Prior exercise shifted the glucose and insulin curves downward (main treatment effects: P = 0.05 and P = 0.0007, respectively) and resulted in a significantly greater insulin sensitivity index (10.8 +/- 0.7) than did no exercise (9.2 +/- 0.7) (P = 0.01). TBARS did not differ significantly between trials., Conclusion: Postprandial endothelial function was improved by endurance exercise performed approximately 17 h earlier. This effect was accompanied by exercise-induced improvements in insulin action and reductions in glycemia, but did not correspond with reductions in oxidative stress, as assessed by TBARS.

Background: Studies suggest cardioprotective benefits of dark chocolate containing cocoa., Objective: This study examines the acute effects of solid dark chocolate and liquid cocoa intake on endothelial function and blood pressure in overweight adults., Design: Randomized, placebo-controlled, single-blind crossover trial of 45 healthy adults [mean age: 53 y; mean body mass index (in kg/m(2)): 30]. In phase 1, subjects were randomly assigned to consume a solid dark chocolate bar (containing 22 g cocoa powder) or a cocoa-free placebo bar (containing 0 g cocoa powder). In phase 2, subjects were randomly assigned to consume sugar-free cocoa (containing 22 g cocoa powder), sugared cocoa (containing 22 g cocoa powder), or a placebo (containing 0 g cocoa powder)., Results: Solid dark chocolate and liquid cocoa ingestion improved endothelial function (measured as flow-mediated dilatation) compared with placebo (dark chocolate: 4.3 +/- 3.4% compared with -1.8 +/- 3.3%; P < 0.001; sugar-free and sugared cocoa: 5.7 +/- 2.6% and 2.0 +/- 1.8% compared with -1.5 +/- 2.8%; P < 0.001). Blood pressure decreased after the ingestion of dark chocolate and sugar-free cocoa compared with placebo (dark chocolate: systolic, -3.2 +/- 5.8 mm Hg compared with 2.7 +/- 6.6 mm Hg; P < 0.001; and diastolic, -1.4 +/- 3.9 mm Hg compared with 2.7 +/- 6.4 mm Hg; P = 0.01; sugar-free cocoa: systolic, -2.1 +/- 7.0 mm Hg compared with 3.2 +/- 5.6 mm Hg; P < 0.001; and diastolic: -1.2 +/- 8.7 mm Hg compared with 2.8 +/- 5.6 mm Hg; P = 0.014). Endothelial function improved significantly more with sugar-free than with regular cocoa (5.7 +/- 2.6% compared with 2.0 +/- 1.8%; P < 0.001)., Conclusions: The acute ingestion of both solid dark chocolate and liquid cocoa improved endothelial function and lowered blood pressure in overweight adults. Sugar content may attenuate these effects, and sugar-free preparations may augment them.

Background: A high fructose intake can lead to postprandial hypertriacylglycerolemia. The underlying mechanism is unclear., Objective: The objective of the study was to investigate the mechanisms involved in fructose-induced hypertriacylglycerolemia and the contribution of de novo lipogenesis in an acute setting., Design: In a randomized, crossover study, 14 subjects were given a fructose or glucose test meal after an overnight fast. [(2)H2]Palmitate and [U(13)C]d-fructose or [U(13)C]d-glucose were added to trace the handling of dietary fats and the fate of dietary sugars in the body. Blood samples were taken before and after the meal. Respiratory exchange ratio was measured by using indirect calorimetry, and breath samples were collected., Results: Plasma triacylglycerol and VLDL-triacylglycerol concentrations were significantly higher (P = 0.001 for both), whereas the concentrations of insulin and [(2)H2]palmitate in nonesterified fatty acids were significantly lower after fructose than after glucose (P = 0.002 and 0.03, respectively). The respiratory exchange ratio was higher after fructose (P = 0.04); significantly (P = 0.003) more carbon from sugars was recovered in breath carbon dioxide over 6 h after fructose (30.5%) than after glucose (24.5%). At 240 min, newly synthesized fatty acids from fructose made up approximately 0.4% of circulating VLDL-triacylglycerol, whereas newly synthesized triacylglycerol-glycerol made up 38%. Newly synthesized fatty acids and triacylglycerol-glycerol from glucose contributed almost none of VLDL-triacylglycerol (P = 0.002 and 0.007 for glucose and fructose, respectively)., Conclusions: The lower insulin excursion after fructose may result in less activation of adipose tissue lipoprotein lipase, which led to impaired triacylglycerol clearance. The contribution of de novo lipogenesis to fructose-induced hypertriacylglycerolemia is small, but its effect on altering the partitioning of fatty acids toward esterification may be considerable.

Background: The E4 allele of the apolipoprotein gene (APOE) is associated with a greater serum cholesterol response to dietary changes in fat and cholesterol. However, less is known about the interaction between APOE polymorphism and other macronutrients in the diet., Objective: We evaluated the interaction between APOE polymorphism and dietary fat and carbohydrate, particularly sucrose, in relation to serum lipid concentrations., Design: A total of 284 men and 130 women with coronary artery disease (mean age: 61 y; range: 33-74 y) participated in the cross-sectional EUROASPIRE study. Serum lipids and fatty acids in cholesteryl esters (CEs) were measured and APOE genotypes were determined. Dietary intake was examined by using a 4-d food record., Results: Patients were grouped by APOE genotype: E2 (E2/E2 and E2/E3; n = 21), E3 (E3/E3; n = 245), and E4 (E4/E2, E4/E3, and E4/E4; n = 148). Patients with the E2 allele had lower LDL-cholesterol concentrations and tended to have higher triacylglycerol concentrations than did patients with the E3 or E4 allele; concentrations were not significantly different between the last 2 groups. In regression analysis, significant predictors of serum triacylglycerol were the interaction between sucrose intake and the E2 allele, proportion of n-3 fatty acids in CEs, body mass index, and diabetes. A high sucrose intake was associated with high triacylglycerol concentrations only in patients with the E2 allele. Interaction between saturated fat intake and the E2 allele, proportion of linoleic acid in CEs, and fiber intake predicted serum cholesterol., Conclusion: Coronary artery disease patients with the E2 allele will likely have a greater triacylglycerol response to high dietary sucrose intakes than will patients with the E3 or E4 allele.

Background: The influence of the amount and type of carbohydrates in the diet on risk factors for obesity, diabetes, and cardiovascular disease remains unclear., Objective: We investigated the effects of 2 low-fat diets (high-sucrose and high-starch) and a high-fat diet on glycemia, lipidemia, and hormonal responses in never-obese and postobese women., Design: Eighteen normal-weight women (8 postobese and 10 never-obese) consumed 3 ad libitum diets (high-fat, high-starch, and high-sucrose) for 14 d each. On day 15, we measured fasting and postprandial glucose, lactate, insulin, triacylglycerol, nonesterified fatty acids (NEFA), glycerol, glucagon, glucose-dependent insulinotropic polypeptide, and glucagon-like peptide 1., Results: The high-sucrose diet induced significantly lower total areas under the curve (AUCs) for glucose and NEFA and a significantly higher lactate AUC than did the high-fat and high-starch diets; there were no significant differences in the insulin AUCs. The triacylglycerol AUC was greater with the high-fat and high-sucrose diets than with the high-starch diet. Gastrointestinal hormone concentrations differed between diets, but not between the 2 subject groups. Comparisons between subject groups for all diets combined showed lower relative insulin resistance and lower AUCs for glucose, insulin, and triacylglycerol in the postobese group., Conclusions: High-starch and high-sucrose diets had no adverse effects on postprandial glycemia, insulinemia, or lipidemia compared with a high-fat diet. A sucrose-rich diet may improve glucose metabolism, but may have an adverse effect on lipidemia, compared with a starch-rich diet. Postobese women seemed to be more insulin-sensitive and more efficient at storing triacylglycerol than were never-obese women, regardless of dietary composition.

Decreased insulin sensitivity is associated with diabetes mellitus, ischemic heart disease, and hypertension, both independently and in association as what is called the metabolic syndrome. Although the negative effects of obesity, sedentary lifestyles, and high-fat diets on insulin sensitivity are well established, the influence of type and quantity of dietary carbohydrate is more controversial. This study aimed to assess the acute (24 h) effects of a high-sucrose compared with a high-starch diet on insulin sensitivity and to identify changes in blood metabolites that might lead to altered insulin sensitivity. Eight healthy adults consumed high-sucrose or high-starch diets (50% of dietary energy) in a randomized, crossover trial. Insulin sensitivity was assessed by a short insulin tolerance test the following morning. No differences were detected in insulin sensitivity, either for glucose metabolism [Kitt(glucose) (the rate constant for the decline in blood glucose concentrations) for sucrose diet = 3.86%/min, for starch diet = 3.72%/min; pooled SEM = 0.23] or for lipid metabolism [Kitt(NEFA) (the rate constant for the decline in blood fatty acid concentrations) for sucrose diet = 12.9%/min, for starch diet = 11.4%/min; pooled SEM = 1.18]. Profiles for blood glucose and serum insulin concentrations revealed higher peaks and lower troughs with the high-sucrose diet whereas area under the curve for glucose was higher with the high-starch diet (6780 +/- 245 mmol x L/min) than with the high-sucrose diet (6290 +/- 283 mmol x L/min) (P < 0.001). Plasma fatty acid concentrations showed a late postprandial rise with the sucrose-rich diet relative to the starch-rich diet, which was mirrored with a fractionally later peak in triacylglycerol concentrations.

The nutritional implications of the consumption of reduced-fat and reduced-sugar foods were assessed in nonobese, free-living female consumers in a 10-wk intervention trial. Subjects in control (C; n = 13), reduced-fat (RF; n = 17), and reduced-sugar (RS; n = 19) groups, all initially nonusers of reduced-fat and reduced-sugar products, kept 4-d food-intake records to establish energy and macronutrient intakes at baseline and at 2,4,7, and 10 wk. Groups RF and RS were instructed to use reduced-fat and reduced-sugar foods, respectively, ad libitum in place of habitually consumed foods with traditional composition, whereas group C was to maintain their usual diet. All foods were purchased by subjects in normal retail outlets and consumed at home. Analyses revealed no main or interactive effect of group on reported energy intake. RF subjects reduced their reported fat intake during the study (P = 0.017) compared with RS and C subjects, and RS subjects reduced their reported sucrose intake compared with RF and C subjects (P = 0.049). Group differences in total sugar intake were not significantly different. All groups reported a small but significant increase in reported protein intake during the study, whereas there were no significant effects on percentage energy from total carbohydrate. Body weights did not change significantly in any group over the study period. These results indicate that, as a single dietary strategy, casual use of macronutrient-substituted foods by consumers under normal eating conditions can significantly influence the macronutrient composition of the diet, but has little net effect on total energy intake or body weight status.

In response to evidence linking obesity and high amounts of dietary fat, the food industry has developed numerous reduced-fat and nonfat food items. These items frequently derive a relatively large percentage of their energy from sugars and the effect of these sugars on weight regulation is not well known. We studied the comparative effects of high- and low-sucrose, low-fat, hypoenergetic diets on a variety of metabolic and behavioral indexes in a 6-wk weight-loss program. Both diets contained approximately 4606 kJ energy/d with 11% of energy as fat, 19% as protein, and 71% as carbohydrate. The high-sucrose diet contained 43% of the total daily energy intake as sucrose; the low-sucrose diet contained 4% of the total daily energy intake as sucrose. Twenty women aged 40.6 +/- 8.2 y (mean +/- SD) with a body mass index (in kg/m2) of 35.93 +/- 4.8 consumed the high-sucrose diet; 22 women aged 40.3 +/- 7.3 y with a body mass index of 34.93 +/- 4.4 consumed the low-sucrose diet. Mixed-design analysis of variance showed a main effect of time (P < 0.01), with both diet groups showing decreases in weight, blood pressure, resting energy expenditure, percentage body fat, free triiodothyronine (FT3), urinary norepinephrine, and plasma lipids. Small but significant interactions were found between group and time in total cholesterol (P = 0.009) and low-density lipoprotein (LDL) (P = 0.01). Both groups showed decreases in depression, hunger, and negative mood, and increases in vigilance and positive mood with time (P < 0.01). Results showed that a high sucrose content in a hypoenergetic, low-fat diet did not adversely affect weight loss, metabolism, plasma lipids, or emotional affect.

This paper reviews the evidence that salt sensitivity of blood pressure is related both to the anion ingested with sodium as well as to other components of the diet. In several experimental models of salt-sensitive hypertension and in humans, blood pressure is not increased by a high sodium intake provided with anions other than chloride. Salt-induced increase of blood pressure depends on the concomitant ingestion of both sodium and chloride. Both epidemiologic and clinical evidence suggest that sodium chloride-induced increases of blood pressure are augmented by diets deficient in potassium or calcium. In experimental animals, a high intake of simple carbohydrates also augments sodium chloride sensitivity of blood pressure. These observations indicate that the effect of dietary sodium on blood pressure is modulated by other components of the diet.