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Background: Noncommunicable diseases (NCDs) predominantly affect adults, but pathophysiological changes begin decades earlier, as a continuum, with initial events apparent in adolescence. Hence, early identification and intervention are crucial for the prevention and management of NCDs. We investigated the complex network of socioeconomic, behavioral, and metabolic factors associated with the presence of NCD in Brazilian adolescents. Methods: We conducted a cross-sectional study nested within the São Luís segment of the Ribeirão Preto, Pelotas, and São Luís (RPS) cohort's consortium, focusing on 18–19-year-olds (n = 2515). Data were collected prospectively, from which we constructed a complex network with NCD-related factors/indicators as nodes and their co-occurrences as edges. General and sex-based models analyzed: socioeconomic status, behavioral (smoking, alcohol, and other drugs use, unhealthy diet, poor sleep, physical inactivity), and metabolic factors (overweight/obesity, elevated blood pressure, poor lipid profile). We also looked for NCDs in adolescence like asthma, abnormal spirometry, depression, suicide risk, and poor oral health. The network was characterized by degree, betweenness, eigenvector, local transitivity, Shannon entropy, and cluster coefficient. Results: The adolescents had an average age of 18.3 years, 52.3% were female and 47.7% male. 99.8% of them have a diet rich in free sugars, 15% are overweight/obese and 72.3% had an elevated TyG index. High free sugar emerged as the central hub, followed by high TyG index (an early marker of insulin resistance) and low socioeconomic class. In males, low fiber intake and a high triglycerides/HDL ratio highlighted cardiometabolic concerns; in females, sedentary behavior and poor sleep marked metabolic and psychological challenges, along with caries in both sexes. Conclusions: Our findings provide insights into central health challenges during adolescence, such as high free sugars, insulin resistance, and low socioeconomic indicators, suggesting that interventions targeted at these central hubs could have a significant impact on their NCD network. [ABSTRACT FROM AUTHOR]

Abstract Background Noncommunicable diseases (NCDs) predominantly affect adults, but pathophysiological changes begin decades earlier, as a continuum, with initial events apparent in adolescence. Hence, early identification and intervention are crucial for the prevention and management of NCDs. We investigated the complex network of socioeconomic, behavioral, and metabolic factors associated with the presence of NCD in Brazilian adolescents. Methods We conducted a cross-sectional study nested within the São Luís segment of the Ribeirão Preto, Pelotas, and São Luís (RPS) cohort’s consortium, focusing on 18–19-year-olds (n = 2515). Data were collected prospectively, from which we constructed a complex network with NCD-related factors/indicators as nodes and their co-occurrences as edges. General and sex-based models analyzed: socioeconomic status, behavioral (smoking, alcohol, and other drugs use, unhealthy diet, poor sleep, physical inactivity), and metabolic factors (overweight/obesity, elevated blood pressure, poor lipid profile). We also looked for NCDs in adolescence like asthma, abnormal spirometry, depression, suicide risk, and poor oral health. The network was characterized by degree, betweenness, eigenvector, local transitivity, Shannon entropy, and cluster coefficient. Results The adolescents had an average age of 18.3 years, 52.3% were female and 47.7% male. 99.8% of them have a diet rich in free sugars, 15% are overweight/obese and 72.3% had an elevated TyG index. High free sugar emerged as the central hub, followed by high TyG index (an early marker of insulin resistance) and low socioeconomic class. In males, low fiber intake and a high triglycerides/HDL ratio highlighted cardiometabolic concerns; in females, sedentary behavior and poor sleep marked metabolic and psychological challenges, along with caries in both sexes. Conclusions Our findings provide insights into central health challenges during adolescence, such as high free sugars, insulin resistance, and low socioeconomic indicators, suggesting that interventions targeted at these central hubs could have a significant impact on their NCD network.

Introduction: Single-nucleotide polymorphism (SNP) rs9939609 in the FTO gene has been associated with dietary intake and appetite traits, mainly in participants with obesity; however, it remains widely unexplored in normal weight participants. Thus, the aims of this study were (1) to compare the changes in subjective appetite sensations, ghrelin, and insulin concentrations according to the SNP rs9939609 T>A in FTO and (2) to compare dietary intake between rs9939609 genotype groups in normal weight young participants. Methods: We conducted a quasi-experimental study involving 88 normal weight participants to analyze subjective perception of appetite, hormonal response for hunger and satiety, and dietary intake according to the rs9939609 SNP. Participants received a standardized single breakfast. Visual analogue scales (VAS) were utilized for assessing the subjective perception of appetite at fasting and immediately after breakfast and at 30, 60, 90, and 120 min postprandially. Glucose, lipid profile, ghrelin, and insulin were measured at fasting and at 120 min after breakfast. Dietary intake was assessed with a 3-day food record. The SNP was determined by allelic discrimination with TaqMan probes. To compare dietetic, biochemical, and the subjective appetite sensations, Student t test, ANCOVA test, and the repeated measures ANOVA were used. The linear regression model and the linear mixed model were used for the association analysis. Pearson correlation was used to test the correlation between two quantitative variables. Results: A total of 88 people participated, 81.8% were female, with a mean body mass index of 21.8 ± 2.0 kg/m2 and a mean age of 20.6 ± 2.0. Genotype frequencies of the rs9939609 SNP were 52% for the TT allele and 48% for the TA/AA. The subjective perception of appetite named hunger, fullness, satiety, desire to eat, and prospective food consumption were similar between genotypes of the rs9939609. Participants with the TA/AA genotype showed a higher intake of added sugar (p = 0.039) than TT participants. No differences were found in ghrelin, insulin, glucose, or lipid parameters between genotypes. Conclusion: Carriers of the A allele from FTO gene SNP rs9939609 may have an increased preference for foods, specifically for added sugars.

ABSTRACTThe mammalian gut microbiota is a critical human health determinant with therapeutic potential for remediation of many diseases. The host diet is a key factor governing the gut microbiota composition by altering nutrient availability and supporting the expansion of distinct microbial populations. Diets rich in simple sugars modify the abundance of microbial subsets, enriching for microbiotas that elicit pathogenic outcomes. We previously demonstrated that diets rich in fructose and glucose can reduce the fitness and abundance of a human gut symbiont, Bacteroides thetaiotaomicron, by silencing the production of a critical intestinal colonization protein, called Roc, via its mRNA leader through an unknown mechanism. We have now determined that dietary sugars silence Roc by reducing the activity of BT4338, a master regulator of carbohydrate utilization. Here, we demonstrate that BT4338 is required for Roc synthesis, and that BT4338 activity is silenced by glucose or fructose. We show that the consequences of glucose and fructose on orthologous transcription factors are conserved across human intestinal Bacteroides species. This work identifies a molecular pathway by which a common dietary additive alters microbial gene expression in the gut that could be harnessed to modulate targeted microbial populations for future therapeutic interventions.

Background: It is well established that unrefined sugarcane products have antioxidant activity due to phytochemicals, polyphenols, and total antioxidant capacity, which may decrease inflammation and oxidative stress. Therefore, we conducted a systematic review to evaluate the association of unrefined sugar consumption with inflammatory biomarkers. Methods: Google Scholar, ScienceDirect, Scopus, Cochrane Library, and ProQuest databases were searched up to December 2021 for studies that report the effect of unrefined sugar on inflammation according to inflammatory cytokines, chemokine, and adhesion molecules as outcome measures. Results: Thirty-six studies were evaluated. Across all research, five studies (two in vitro and three animal studies) reported the effect of unrefined sugar on levels of cytokines, including IL-6, TNF-α, IL-10, IL-1β, and IFN-γ. Additionally, the quality of the studies was assessed for risk of bias. Conclusions: it is possible to affirm that unrefined sugarcane products, including jaggery, may have a protective effect on inflammation via regulating some of the inflammatory pathways and a favorable impact on cytokines secretion according to the results of in vitro and animal model studies. However, since the findings are still insufficient, more scientific research, especially well-designed human trials, is highly recommended to conclude the outcomes confidently. Human data may encourage industries and the public to replace purified sugar with unrefined sugarcane in sugar-based food and for further health-care policy decisions. [ABSTRACT FROM AUTHOR]

The influence of sugar consumption on the risk of colorectal cancer (CRC) remains controversial. Prospective cohort studies focusing on total and specific types of sugar intake among the Asian population who have different patterns of sugar intake sources than American and European populations are scarce. We intended to examine the association of sugar intake with CRC risk among middle‐aged adults in a Japanese large‐scale population‐based cohort study. The participants (42,405 men and 48,600 women) who were 45–74 years old and answered the questionnaire in 1995–1999 in the Japan Public Health Center‐based Prospective Study were followed up until December 2013. Total sugars, total fructose, and specific types of sugar intake were estimated using a validated 147‐item food frequency questionnaire and divided into quintiles (Q1–Q5). We used Cox proportional hazard regression models adjusted for potential confounders to estimate hazard ratios (HRs) and 95% confidence intervals (CIs). During the follow‐up, 2118 CRC cases (1226 men and 892 women) were identified. We did not observe any clear association between all types of sugar intake and an increased risk of CRC. Analyses by tumor sites yielded a positive association of total sugar consumption with rectal cancer in women (1.75 [1.07–2.87] for Q1 vs. Q5; plinear trend = 0.03), but no statistically significant trend was detected among men. Sugar intake was not associated with CRC risk in middle‐aged Japanese adults. However, for rectal cancer, the probability of an increased risk among women with a higher total sugar intake cannot be excluded. [ABSTRACT FROM AUTHOR]

Background: Dietary sugars are often linked to the development of overweight and type 2 diabetes (T2D) but inconsistencies remain. Objective: We investigated associations of added, free, and total sugars, and glycaemic index (GI) with indices of glucose metabolism (IGM) and indices of body fatness (IBF) during a 3-year weight loss maintenance intervention. Design: The PREVIEW (PREVention of diabetes through lifestyle Intervention and population studies in Europe and around the World) study was a randomised controlled trial designed to test the effects of four diet and physical activity interventions, after an 8-week weight-loss period, on the incidence of T2D. This secondary observational analysis included pooled data assessed at baseline (8), 26, 52, 104 and 156 weeks from 514 participants with overweight/obesity (age 25–70 year; BMI ≥ 25 kg⋅m−2) and with/without prediabetes in centres that provided data on added sugars (Sydney and Helsinki) or free sugars (Nottingham). Linear mixed models with repeated measures were applied for IBF (total body fat, BMI, waist circumference) and for IGM (fasting insulin, HbA1c, fasting glucose, C-peptide). Model A was adjusted for age and intervention centre and Model B additionally adjusted for energy, protein, fibre, and saturated fat. Results: Total sugars were inversely associated with fasting insulin and C-peptide in all centres, and free sugars were inversely associated with fasting glucose and HbA1c (Model B: all p < 0.05). Positive associations were observed between GI and IGM (Model B: fasting insulin, HbA1c, and C-peptide: (all p < 0.01), but not for added sugars. Added sugar was positively associated with body fat percentage and BMI, and GI was associated with waist circumference (Model B: all p < 0.01), while free sugars showed no associations (Model B: p > 0.05). Conclusions: Our findings suggest that added sugars and GI were independently associated with 3-y weight regain, but only GI was associated with 3-y changes in glucose metabolism in individuals at high risk of T2D. [ABSTRACT FROM AUTHOR]

Diet-induced obesity contributes to the development of type 2 diabetes, insulin resistance, metabolic inflammation, oxidative and endoplasmic reticulum (ER) stress. Overall, obesity is associated with deviations in the composition and functionality of the gut microbiota. There are many divergent findings regarding the link between the excessive intake of certain dietary components (i.e., fat and sugar) and obesity development. We therefore investigated the effect of specific diets, with a different content of sugar and fat, in promoting obesity and related comorbidities as well as their impact on microbial load and gut microbiota composition/diversity. C57BL/6J mice were fed either a low-sugar, low-fat control diet (CT), a high-sugar diet (HS), a high-fat, high-sugar diet (HF/HS), or a high-fat diet (HF) for 8 wk. The impact of the different diets on obesity, glucose metabolism, inflammation, and oxidative and ER stress was determined. Diet-induced changes in the gut microbiota composition and density were also analyzed. HF diet-fed mice showed the highest body weight and fat mass gains and displayed the most impaired glucose and insulin profiles. HS, HF/HS, and HF diets differently affected hepatic cholesterol content and mRNA expression of several markers associated with immune cells, inflammation, oxidative and ER stress in several organs/tissues. In addition, HF diet feeding resulted in a decreased microbial load at the end of the experiment. When analyzing the gut microbiota composition, we found that HS, HF/HS, and HF diets induced specific changes in the abundance of certain bacterial taxa. This was not associated with a specific change in systemic inflammatory markers, but HS mice exhibited higher FGF21 plasma levels compared with HF diet-fed mice. Taken together, our results highlight that dietary intake of different macronutrients distinctively impacts the development of an obese/diabetic state and the regulation of metabolic inflammation in specific organs. We propose that these differences are not only obesity-driven but that changes in the gut microbiota composition may play a key role in this context. [ABSTRACT FROM AUTHOR]

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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.

Purpose of Review: This review aims to assess how nutrition can be addressed in the integrative oncology setting, taking into account cancer patients' unmet needs as they relate to nutrition in cancer care and the evidence-based information that is available on this topic. Recent Findings: During and after cancer treatment, nutrition is an important component of supportive care, for patients and their family members. Current scientific data consistently show that poor nutrition can reduce survival and decrease adherence to cancer treatments. Unfortunately, the limited availability of dietitians makes access to individualized nutrition counseling challenging, and many cancer patients still do not receive adequate nutritional support. As a result, one of the main unmet needs of patients and their families through the whole cancer trajectory is accessible and up-to-date evidence-based nutritional counseling that emphasizes basic healthy nutrition. The popularity of complementary and integrative medicine among patients with cancer makes the integrative oncology setting an excellent avenue for providing such support. A suggested simple approach that utilizes World Cancer Research Fund/American Institute for Cancer Research and American Cancer Society basic information is described. This approach can be easily incorporated into integrative oncology settings, while reserving the role for the registered dietician to address underweight patients, patients with malnutrition, and patients with more complicated dietary situations. Summary: The integrative oncology setting is in a unique place in oncology that can be utilized for enhancing dissemination of healthy nutrition information and addressing the unmet needs expressed by patients and families. [ABSTRACT FROM AUTHOR]

Excessive dietary intake of fats and sugars ("Western diet", WD) is one of the leading causes of obesity. The consumption of the microalga Arthrospira platensis (spirulina, Sp) is increasing due to its presumed health benefits. Both WD and Sp are also consumed by pregnant and breastfeeding women. This study investigated if gestating and lactating domestic pigs are an appropriate model for WD-induced metabolic disturbances similar to those observed in humans and if Sp supplementation may attenuate any of these adverse effects. Pigs were fed a WD high in fat, sugars, and cholesterol or a control diet. Half of the animals per diet group were supplemented with 20 g Sp per day. The WD did not increase body weight or adipose tissue accumulation but led to metabolic impairments such as higher cholesterol concentration in plasma, lower IGF1 plasma levels, and signs of hepatic damage compared to the control group. Spirulina supplementation could not reduce all the metabolic impairments observed in WD-fed animals. These findings indicate limited suitability of gestating and lactating domestic pigs as a model for WD but a certain potential of low-dose Sp supplementation to partially attenuate negative WD effects. [ABSTRACT FROM AUTHOR]

Purpose: Our understanding of the influence of sugar intake on anthropometrics among young children is limited. Most existing research is cross-sectional and has focused on sugar-sweetened beverages. The study objective was to investigate longitudinal associations between young children's total, free, and added sugar intake from all food sources at baseline with anthropometric measures at baseline and 18 months. Methods: The Guelph Family Health Study (GFHS) is an ongoing randomized controlled trial and a family-based health promotion study. Food records and anthropometric data were collected at baseline (n = 109, 55 males; 3.7 ± 1.1 y, mean ± SD) and 18 months (n = 109, 55 males; 5.1 ± 1.1 y) of the GFHS pilots. Associations between sugar intakes and anthropometrics were estimated using linear regression models with generalized estimating equations adjusted for age, sex, household income, and intervention status. Results: Total sugar intake was inversely associated with body weight at 18 months ( P  = 0.01). There was no effect of time on any other associations between total, free, and added sugar intakes and anthropometrics. Conclusions: Early life dietary sugar intakes may not relate to anthropometric measures in the short term. Further investigation into potential associations between dietary sugar intakes and anthropometric variables over longer time periods is warranted.

Appalachian youth are highconsumers of added dietary sugar and are very sedentary. Mentoring to be Active trains teens to deliver atheoretically based program to promote home-based physical activity (PA) and reduce dietary sugar among rural Appalachian youth. For this pre-test/post-test pilot study, 52 seventh graders from two Appalachian schools participated as mentees. Twenty-two 10th grade students served as peer mentors. The study estimated sedentary activity,and physical activity by accelerometers and dietary sugars (snacks, beverages) during 'out of school' time. Descriptive statistics and effect sizes (ES) were calculated. When the pre-post standard deviations differed, Hedge's g were reported. Sedentary activity decreased 36.7% (ES =.798). Moderate activity levels increased 16.5% (ES =.359). Vigorous activity increased 88% (ES =.359). Sugary- beverages declined over 4 ½ servings. Sugary snacks declined 2 ¼ servings. Peer mentoring is a strategy to promote social support for healthier behaviors among youth at risk for obesity and co-morbidities. Accelerometers rigorously assessed physical activity during 'out of school' time in rural youth. [ABSTRACT FROM AUTHOR]

Background: It is well established that unrefined sugarcane products have antioxidant activity due to phytochemicals, polyphenols, and total antioxidant capacity, which may decrease inflammation and oxidative stress. Therefore, we conducted a systematic review to evaluate the association of unrefined sugar consumption with inflammatory biomarkers. Methods: Google Scholar, ScienceDirect, Scopus, Cochrane Library, and ProQuest databases were searched up to December 2021 for studies that report the effect of unrefined sugar on inflammation according to inflammatory cytokines, chemokine, and adhesion molecules as outcome measures. Results: Thirty-six studies were evaluated. Across all research, five studies (two in vitro and three animal studies) reported the effect of unrefined sugar on levels of cytokines, including IL-6, TNF-α, IL-10, IL-1β, and IFN-γ. Additionally, the quality of the studies was assessed for risk of bias. Conclusions: it is possible to affirm that unrefined sugarcane products, including jaggery, may have a protective effect on inflammation via regulating some of the inflammatory pathways and a favorable impact on cytokines secretion according to the results of in vitro and animal model studies. However, since the findings are still insufficient, more scientific research, especially well-designed human trials, is highly recommended to conclude the outcomes confidently. Human data may encourage industries and the public to replace purified sugar with unrefined sugarcane in sugar-based food and for further health-care policy decisions.

Background: The influence of sugar intake on the risk of colorectal cancer (CRC) remains controversial, and there is a need to investigate the heterogeneity of effects among racial and ethnic groups., Objectives: To examine the association of intake of simple sugars and their food sources with CRC risk according to race/ethnicity in a multiethnic cohort study., Methods: We analyzed data from 192,651 participants who participated in the Multiethnic Cohort Study comprising African American, Japanese American, Latino, Native Hawaiian, and White older adults living in Hawaii and California with an average follow-up of 19 y. Intakes of total and specific types of sugars and sugary foods were estimated from a quantitative food frequency questionnaire completed by the participants in 1993-1996. We estimated hazard ratios (HRs) and 95% confidence intervals (CIs) for CRC risk according to quintiles (Q) of sugar and food intakes using Cox models adjusted for potential confounders., Results: As of December 2017, 4403 incident CRC cases were identified. Among all participants, multivariable-adjusted CRC HRs for Q2, Q3, Q4, and Q5 compared with Q1 for total sugars were 1.03 (95% CI: 0.94, 1.13), 1.05 (95% CI: 0.96, 1.16), 1.12 (95% CI: 1.01, 1.24), and 1.13 (95% CI: 1.01, 1.27), respectively. A similar positive association was observed for total fructose, glucose, fructose, and maltose but not for added sugars and sugary foods. The increased risk appeared to be limited to colon cancer and to be strongest among younger participants (i.e., 45-54 y at baseline); an association with CRC was observed for sugar-sweetened beverages in the latter group. Among racial and ethnic groups, increased risk of CRC was most apparent in Latinos., Conclusions: In this diverse cohort, intakes of total sugar, total fructose, glucose, fructose, and maltose were associated with an increased risk of CRC, and the association was strongest for colon cancer, younger participants, and Latinos., (Copyright © 2024 The Authors. Published by Elsevier Inc. All rights reserved.)

To examine associations between intake of simple sugars and cancer incidence, cancer mortality, and total mortality in a prospective cohort study based on the PREDIMED trial conducted from 2003 to 2010. Participants were older individuals at high cardiovascular risk. Exposures were total sugar, glucose and fructose from solid or liquid sources, and fructose from fruit and 100% fruit juice. Cancer incidence was the primary outcome; cancer mortality and all-cause mortality were secondary outcomes. Multivariable-adjusted, time-dependent Cox proportional hazard models were used. Of 7447 individuals enrolled, 7056 (94.7%) were included (57.6% women, aged 67.0 ± 6.2 years). 534 incident cancers with 152 cancer deaths and 409 all-cause deaths were recorded after a median follow-up of 6 years. Intake of simple sugars in solid form was unrelated to outcomes. Higher cancer incidence was found per 5 g/day increase in intake of liquid sugars, with multivariable-adjusted HR of 1.08 (95% CI, 1.03–1.13) for total liquid sugar, 1.19 (95% CI, 1.07–1.31) for liquid glucose, 1.14 (95% CI, 1.05–1.23) for liquid fructose, and 1.39 (95% CI, 1.10–1.74) for fructose from fruit juice. Cancer and all-cause mortality increased to a similar extent with intake of all sugars in liquid form. In categorical models, cancer risk was dose-related for all liquid sugars. Simple sugar intake in drinks and fruit juice was associated with an increased risk of overall cancer incidence and mortality and all-cause mortality. This suggests that sugary beverages are a modifiable risk factor for cancer and all-cause mortality. [ABSTRACT FROM AUTHOR]

Dental plaque is a complex colorless film of bacteria that develops on the surfaces of teeth. Different mechanisms of microbial adhesion to tooth surfaces exist. Both non-specific and specific types of adherence have been anticipated. The present review evaluated the effect of sugar-rich diet and salivary proteins on oral hygiene and dental plaque development. The oral microbiota is essential for maintaining and reestablishing a healthy oral cavity. Different types of sugars have different effects on the inhibition and formation of dental plaque. The peptides, proteins, and amino acids secreted by parotid glands in the oral cavity facilitate neutralizing the acidity in dental plaque and preventing dental caries. A properly balanced diet is crucial for both a healthy oral cavity and the oral microbiome. [ABSTRACT FROM AUTHOR]

Summary Introduction This report presents a synopsis of a three‐part, cross‐sector, seminar series held at the George Washington University (GWU) in Washington, DC from February–April, 2018. The overarching goal of the seminar series was to provide a neutral forum for diverse stakeholders to discuss and critically evaluate approaches to address added sugar intake, with a key focus on the role of low‐calorie sweeteners (LCS). Methods During three seminars, twelve speakers from academic institutions, federal agencies, non‐profit organizations, and the food and beverage industries participated in six interactive panel discussions to address: 1) Do Farm Bill Policies Impact Population Sugar Intake? 2) What is the Impact of Sugar‐sweetened Beverage (SSB) Taxes on Health and Business? 3) Is Sugar Addictive? 4) Product Reformulation Efforts: Progress, Challenges, and Concerns? 5) Low‐calorie Sweeteners: Helpful or Harmful, and 6) Are Novel Sweeteners a Plausible Solution? Discussion of each topic involved brief 15‐minute presentations from the speakers, which were followed by a 25‐minute panel discussion moderated by GWU faculty members and addressed questions generated by the audience. Sessions were designed to represent opposing views and stimulate meaningful debate. Given the provocative nature of the seminar series, attendee questions were gathered anonymously using Pigeonhole™, an interactive, online, question and answer platform. Results This report summarizes each presentation and recapitulates key perspectives offered by the speakers and moderators. Conclusions The seminar series set the foundation for robust cross‐sector dialogue necessary to inform meaningful future research, and ultimately, effective policies for lowering added sugar intakes.

It has been hypothesized that the incretin hormone, glucagon-like peptide-1 (GLP-1), decreases overeating by influencing mesolimbic brain regions that process food-cues, including the dorsal striatum. We previously showed that habitual added sugar intake was associated with lower glucose-induced circulating GLP-1 and a greater striatal response to high calorie food cues in lean individuals. Less is known about how dietary added sugar and obesity may interact to affect postprandial GLP-1 and its relationship to striatal responses to food cues and feeding behavior. The current study aimed to expand upon previous research by assessing how circulating GLP-1 and striatal food cue reactivity are affected by acute glucose consumption in participants with varied BMIs and amounts of habitual consumption of added sugar. This analysis included 72 participants from the Brain Response to Sugar Study who completed two study visits where they consumed either plain water or 75g glucose dissolved in water (order randomized; both drinks were flavored with non-caloric cherry flavoring) and underwent repeated blood sampling, a functional magnetic resonance imaging (fMRI) based food-cue task, and an ad-libitum buffet meal. Correlations between circulating GLP-1 levels, striatal food-cue reactivity, and food intake were assessed, and interactions between obesity and added sugar on GLP-1 and striatal responses were examined. An interaction between BMI and dietary added sugar was associated with reduced post-glucose GLP-1 secretion. Participants who were obese and consumed high levels of added sugar had the smallest increase in plasma GLP-1 levels. Glucose-induced GLP-1 secretion was correlated with lower dorsal striatal reactivity to high-calorie versus low-calorie food-cues, driven by an increase in reactivity to low calorie food-cues. The increase in dorsal striatal reactivity to low calorie food-cues was negatively correlated with sugar consumed at the buffet. These findings suggest that an interaction between obesity and dietary added sugar intake is associated with additive reductions in postprandial GLP-1 secretion. Additionally, the results suggest that changes to dorsal striatal food cue reactivity through a combination of dietary added sugar and obesity may affect food consumption.

It has been hypothesized that the incretin hormone, glucagon-like peptide-1 (GLP-1), decreases overeating by influencing mesolimbic brain regions that process food-cues, including the dorsal striatum. We previously showed that habitual added sugar intake was associated with lower glucose-induced circulating GLP-1 and a greater striatal response to high calorie food cues in lean individuals. Less is known about how dietary added sugar and obesity may interact to affect postprandial GLP-1 and its relationship to striatal responses to food cues and feeding behavior. The current study aimed to expand upon previous research by assessing how circulating GLP-1 and striatal food cue reactivity are affected by acute glucose consumption in participants with varied BMIs and amounts of habitual consumption of added sugar. This analysis included 72 participants from the Brain Response to Sugar Study who completed two study visits where they consumed either plain water or 75g glucose dissolved in water (order randomized; both drinks were flavored with non-caloric cherry flavoring) and underwent repeated blood sampling, a functional magnetic resonance imaging (fMRI) based food-cue task, and an ad-libitum buffet meal. Correlations between circulating GLP-1 levels, striatal food-cue reactivity, and food intake were assessed, and interactions between obesity and added sugar on GLP-1 and striatal responses were examined. An interaction between BMI and dietary added sugar was associated with reduced post-glucose GLP-1 secretion. Participants who were obese and consumed high levels of added sugar had the smallest increase in plasma GLP-1 levels. Glucose-induced GLP-1 secretion was correlated with lower dorsal striatal reactivity to high-calorie versus low-calorie food-cues, driven by an increase in reactivity to low calorie food-cues. The increase in dorsal striatal reactivity to low calorie food-cues was negatively correlated with sugar consumed at the buffet. These findings suggest that an interaction between obesity and dietary added sugar intake is associated with additive reductions in postprandial GLP-1 secretion. Additionally, the results suggest that changes to dorsal striatal food cue reactivity through a combination of dietary added sugar and obesity may affect food consumption. [ABSTRACT FROM AUTHOR]

There is an increasing public awareness about the danger of dietary sugars with respect to their caloric contribution to the diet and the rise of overweight throughout the world. Therefore, low-calorie sugar substitutes are of high interest to replace sugar in foods and beverages. A promising alternative to natural sugars and artificial sweeteners is the fructose derivative 5-keto-D-fructose (5-KF), which is produced by several Gluconobacter species. A prerequisite before 5-KF can be used as a sweetener is to test whether the compound is degradable by microorganisms and whether it is metabolized by the human microbiota. We identified different environmental bacteria (Tatumella morbirosei, Gluconobacter japonicus LMG 26773, Gluconobacter japonicus LMG 1281, and Clostridium pasteurianum) that were able to grow with 5-KF as a substrate. Furthermore, Gluconobacter oxydans 621H could use 5-KF as a carbon and energy source in the stationary growth phase. The enzymes involved in the utilization of 5-KF were heterologously overproduced in Escherichia coli, purified and characterized. The enzymes were referred to as 5-KF reductases and belong to three unrelated enzymatic classes with highly different amino acid sequences, activities, and structural properties. Furthermore, we could show that 15 members of the most common and abundant intestinal bacteria cannot degrade 5-KF, indicating that this sugar derivative is not a suitable growth substrate for prokaryotes in the human intestine. Key points: • Some environmental bacteria are able to use 5-KF as an energy and carbon source. • Four 5-KF reductases were identified, belonging to three different protein families. • Many gut bacteria cannot degrade 5-KF. [ABSTRACT FROM AUTHOR]

Objective To provide a systematic overview of world dietary sugar and sugar-sweetened beverage (SSB) intake trends in children and adolescents. Data Sources Medline, Embase, and the Cochrane Central Register of Controlled Trials in the Cochrane Library were searched through January 2019 to identify longitudinal follow-up studies with time-trend data and repeated cross-sectional studies. Data Extraction Data from studies reporting ≥ 2 measurements (sugars, SSB, or sweets/candy) over ≥ 2 years and included ≥ 20 healthy, normal- or overweight children or adolescents aged 1–19 years. Data Analysis Data from 43 articles (n = 4 prospective cohort studies; n = 39 repeated cross-sectional studies) from 15 countries (n = 8 European countries plus Australia, Canada, China, South Korea, Mexico, Russia, and the United States) are presented narratively. According to the risk of bias in nonrandomized studies of interventions tool, 34 studies were judged to have a moderate risk of bias, and 5 to have a serious risk of bias. Conclusions Consumption among US children and adolescents increased substantially in the decades preceding 2000, followed by a faster and continued decline. As a whole, other international intake trends did not reveal drastic increases and decreases in SSB and dietary sugars; they tended to change only slightly across 3 decades. [ABSTRACT FROM AUTHOR]

Purpose: To examine the prospective relevance of dietary sugar intake (based on dietary data as well as urinary excretion data) in adolescent years for insulin sensitivity and biomarkers of inflammation in young adulthood.Methods: Overall 254 participants of the DONALD study who had at least two 3-day weighed dietary records for calculating intakes of fructose, glucose, sucrose, total, free, added sugars, total sugars from sugar-sweetened beverages (SSB), juice, and sweets/sugar or at least two complete 24 h urine samples (n = 221) for calculating sugar excretion (urinary fructose and urinary fructose + sucrose) in adolescence (females: 9–15 years, males: 10–16 years) and a fasting blood sample in adulthood (18–36 years), were included in multivariable linear regression analyses assessing their prospective associations with adult homeostasis model assessment insulin sensitivity (HOMA2-%S) and a pro-inflammatory score (based on CRP, IL-6, IL-18, leptin, chemerin, adiponectin).Results: On the dietary intake level, no prospective associations were observed between adolescent fructose, sucrose, glucose, added, free, total sugar, or total sugar from SSB, juice or sweets/sugar intake and adult HOMA2-%S (p > 0.01). On the urinary level, however, higher excreted fructose levels were associated with improved adult HOMA2-%S (p = 0.008) among females only. No associations were observed between dietary or urinary sugars and the adult pro-inflammatory score (p > 0.01).Conclusion: The present study did not provide support that dietary sugar consumed in adolescence is associated with adult insulin sensitivity. The one potential exception was the moderate dietary consumption of fructose, which showed a beneficial association with adult fasting insulin and insulin sensitivity.

Aims: Although diet is one of the main modifiable risk factors of cardiovascular disease, few studies have investigated the association between added sugar intake and cardiovascular disease risk. This study aims to investigate the associations between intake of total added sugar, different sugar-sweetened foods and beverages, and the risks of stroke, coronary events, atrial fibrillation and aortic stenosis.Methods: The study population consists of 25,877 individuals from the Malmö Diet and Cancer Study, a Swedish population-based prospective cohort. Dietary data were collected using a modified diet history method. National registers were used for outcome ascertainment.Results: During the mean follow-up of 19.5 years, there were 2,580 stroke cases, 2,840 coronary events, 4,241 atrial fibrillation cases, and 669 aortic stenosis cases. Added sugar intakes above 20 energy percentage were associated with increased risk of coronary events compared to the lowest intake category (HR: 1.39; 95% CI: 1.09–1.78), and increased stroke risk compared to intakes between 7.5 and 10 energy percentage (HR: 1.31; 95% CI: 1.03 and 1.66). Subjects in the lowest intake group for added sugar had the highest risk of atrial fibrillation and aortic stenosis. More than 8 servings/week of sugar-sweetened beverages were associated with increased stroke risk, while ≤2 servings/week of treats were associated with the highest risks of stroke, coronary events and atrial fibrillation.Conclusion: The results indicate that the associations between different added sugar sources and cardiovascular diseases vary. These findings emphasize the complexity of the studied associations and the importance of considering different added sugar sources when investigating health outcomes.

Summary: Pancreatic cancer is a rare but fatal form of cancer, the fourth highest in absolute mortality. Known risk factors include obesity, diet, and type 2 diabetes; however, the low incidence rate and interconnection of these factors confound the isolation of individual effects. Here, we use epidemiological analysis of prospective human cohorts and parallel tracking of pancreatic cancer in mice to dissect the effects of obesity, diet, and diabetes on pancreatic cancer. Through longitudinal monitoring and multi-omics analysis in mice, we found distinct effects of protein, sugar, and fat dietary components, with dietary sugars increasing Mad2l1 expression and tumor proliferation. Using epidemiological approaches in humans, we find that dietary sugars give a MAD2L1 genotype-dependent increased susceptibility to pancreatic cancer. The translation of these results to a clinical setting could aid in the identification of the at-risk population for screening and potentially harness dietary modification as a therapeutic measure.

Background Obesity prevalence remains high in the United States, and there is an increased risk among women who do not lose their gestational weight gain during the postpartum period. Indicators of dietary carbohydrate quality including added sugar consumption, glycemic load, and glycemic index have been linked with weight gain, whereas fiber may protect against obesity. However, these dietary factors have not been examined during the postpartum period. Objectives The aim of this study was to determine whether dietary sugars and fiber intake were associated with changes in postpartum weight. Methods We examined Hispanic women from the longitudinal Southern California Mother's Milk Study (n  = 99) at 1 and 6 mo postpartum. Maternal assessments included height, weight, and dietary intake based on 24-h diet recalls. We used multivariable linear regression to examine the relation between maternal diet and change in postpartum weight after adjusting for maternal age, height, and energy intake. Results Higher intake of added sugar was associated with postpartum weight gain (β: 0.05; 95% CI: 0.004, 0.10; P  = 0.05). In addition, a half 8-ounce (8 fluid ounces = 236.6 mL) serving per day increase in soft drinks was associated with a 1.52-kg increase in weight (95% CI: 0.70, 2.34 kg; P  < 0.001). A high glycemic index (β: 0.25; 95% CI: 0.07, 0.42; P  = 0.006) and glycemic load (β: 0.04; 95% CI: 0.002, 0.08; P  = 0.04) were associated with postpartum weight gain. Higher soluble fiber was associated with a decrease in postpartum weight (β: −0.82 kg; 95% CI: −1.35, −0.29 kg; P  = 0.003) and the negative effects of added sugar, sugary beverages, and high-glycemic-index and -load diets were partially attenuated after adjusting for soluble fiber intake. Conclusions Increased consumption of added sugar, sugar-sweetened beverages, and high-glycemic diets were associated with greater weight gain in the first 6 mo postpartum. In addition, increased consumption of soluble fiber was associated with postpartum weight loss, which may partially offset the obesogenic effects of some dietary sugars. [ABSTRACT FROM AUTHOR]

Purpose of Review: High-sugar diets have been hypothesized to promote colorectal cancer development and progression by contributing to hyperinsulinemia and insulin resistance or through other mechanisms. This review summarizes the available evidence for sugar intake related to colorectal cancer (CRC) risk and survival and discusses future research directions. Recent Findings: Most of the prospective studies report a null association between sugar intake and CRC risk; the evidence based on ten publications, including a pooling project of 13 studies, is reasonably robust. In contrast, a relatively small number of studies examining sugar intake and CRC survival suggest that consumption of sugars, particularly sugar-sweetened beverages, may negatively impact survival outcomes among CRC patients. Summary: Excessive sugar intake may contribute to worse CRC survival. To date, studies do not show a clear association between total sugar intake and CRC risk, but further work is required to isolate effects of added sugar, define risk for potentially susceptible subgroups, and explore interactions with other dietary and lifestyle factors. [ABSTRACT FROM AUTHOR]

Background There is controversy on the relevance of dietary sugar intake for cardiometabolic health. Objective The aim of this network meta-analysis (NMA) was to assess how isocaloric substitutions of dietary sugar with other carbohydrates affect cardiometabolic risk factors, comparing different intervention studies. Methods We included randomized controlled trials (RCTs) investigating the isocaloric effect of substituting dietary sugars (fructose, glucose, sucrose) with other sugars or starch on cardiometabolic risk markers, including LDL cholesterol, triacylglycerol (TG), fasting glucose (FG), glycated hemoglobin (HbA1c), insulin resistance (HOMA-IR), uric acid, C-reactive protein (CRP), alanine transaminase (ALT), aspartate transaminase (AST), and liver fat content. To identify the most beneficial intervention for each outcome, random-effects NMA was conducted by calculating pooled mean differences (MDs) with 95% CIs, and by ranking the surface under the cumulative ranking curves (SUCRAs). The certainty of evidence was evaluated using the Confidence In Network Meta-Analysis tool. Results Thirty-eight RCTs, including 1383 participants, were identified. A reduction in LDL-cholesterol concentrations was shown for the exchange of sucrose with starch (MD: −0.23 mmol/L; 95% CI: −0.38, −0.07 mmol/L) or fructose with starch (MD: −0.22 mmol/L; 95% CI: −0.39, −0.05 mmol/L; SUCRAstarch: 98%). FG concentrations were also lower for the exchange of sucrose with starch (MD: −0.14 mmol/L; 95% CI: −0.29, 0.01 mmol/L; SUCRAstarch: 91%). Replacing fructose with an equivalent energy amount of glucose reduced HOMA-IR (MD: −0.36; 95% CI: −0.71, −0.02; SUCRAglucose: 74%) and uric acid (MD: −23.77 µmol/L; 95% CI: −44.21, −3.32 µmol/L; SUCRAglucose: 93%). The certainty of evidence was rated very low to moderate. No significant effects were observed for TG, HbA1c, CRP, ALT, and AST. Conclusions Our findings indicate that substitution of sucrose and fructose with starch yielded lower LDL cholesterol. Insulin resistance and uric acid concentrations were beneficially affected by replacement of fructose with glucose. Our findings are limited by the very low to moderate certainty of evidence. This review was registered at www.crd.york.ac.uk/prospero as CRD42018080297. [ABSTRACT FROM AUTHOR]

Objective: School meals comprise a significant amount of children's overall dietary intake. The Healthy Hunger-Free Kids Act made substantial improvements to the nutritional quality of meals served within the School Breakfast Program (SBP); yet, there are limited guidelines regarding sugar. In this study, we carried out a systematic evaluation of the sugar content of breakfast items offered within the SBP in Virginia elementary schools with free meals. Methods: We obtained menus and nutritional information from 32 districts, and examined one week of breakfasts. We categorized entrées based on standard deviations (SD) from the grand mean total sugar available: higher-sugar (>+1 SD), average-sugar (within 1SD), or lower-sugar (>-1 SD). Total sugar (g), energy (kcal), and % energy from sugar were examined for entrées and milk. Results: Across districts, entrées varied in total sugar (0-39g; mean+SD = 10.4±4.5g) and energy (60-530kcal; mean+SD = 205±47.8kcal). Most (96.9%) offered 100% fruit juice; of those that specified, 50.0% offered sugar-sweetened milk. Highly processed foods were prevalent. Conclusion: Findings suggest that meals offered might contribute to excessive overall sugar availability for children. Continued enhancements to the SBP are needed to optimize the nutritional content of meals served to low-income children. [ABSTRACT FROM AUTHOR]

Summary: Introduction: This report presents a synopsis of a three‐part, cross‐sector, seminar series held at the George Washington University (GWU) in Washington, DC from February–April, 2018. The overarching goal of the seminar series was to provide a neutral forum for diverse stakeholders to discuss and critically evaluate approaches to address added sugar intake, with a key focus on the role of low‐calorie sweeteners (LCS). Methods: During three seminars, twelve speakers from academic institutions, federal agencies, non‐profit organizations, and the food and beverage industries participated in six interactive panel discussions to address: 1) Do Farm Bill Policies Impact Population Sugar Intake? 2) What is the Impact of Sugar‐sweetened Beverage (SSB) Taxes on Health and Business? 3) Is Sugar Addictive? 4) Product Reformulation Efforts: Progress, Challenges, and Concerns? 5) Low‐calorie Sweeteners: Helpful or Harmful, and 6) Are Novel Sweeteners a Plausible Solution? Discussion of each topic involved brief 15‐minute presentations from the speakers, which were followed by a 25‐minute panel discussion moderated by GWU faculty members and addressed questions generated by the audience. Sessions were designed to represent opposing views and stimulate meaningful debate. Given the provocative nature of the seminar series, attendee questions were gathered anonymously using Pigeonhole™, an interactive, online, question and answer platform. Results: This report summarizes each presentation and recapitulates key perspectives offered by the speakers and moderators. Conclusions: The seminar series set the foundation for robust cross‐sector dialogue necessary to inform meaningful future research, and ultimately, effective policies for lowering added sugar intakes. [ABSTRACT FROM AUTHOR]

Purpose: Excessive consumption of free sugar increases the risk for non-communicable diseases where a proper assessment of this intake is necessary to correctly estimate its association with certain diseases. Urinary sugars have been suggested as objective biomarkers for total and free sugar intake in adults but less is known about this marker in children and adolescents. Therefore, the aim of this exploratory study is to evaluate the relative validity of self-reported intake using urinary sugars in children and adolescents. Methods: The study was conducted in a convenience subsample of 228 participants aged 5–18 years of the I.Family study that investigates the determinants of food choices, lifestyle and health in European families. Total, free and intrinsic sugar intake (g/day) and sugar density (g/1000 kcal) were assessed using 24-h dietary recalls (24HDRs). Urinary sucrose (USUC) and urinary fructose (UFRU) were measured in morning urine samples and corrected for creatinine excretion (USUC/Cr, UFRU/Cr). Correlation coefficients, the method of triads and linear regression models were used to investigate the relationship between intake of different types of sugar and urinary sugars. Results: The correlation between usual sugar density calculated from multiple 24HDRs and the sum of USUC/Cr and UFRU/Cr (USUC/Cr + UFRU/Cr) was 0.38 (p < 0.001). The method of triads revealed validity coefficients for the 24HDR from 0.64 to 0.87. Linear regression models showed statistically significant positive associations between USUC/Cr + UFRU/Cr and the intake of total and free sugar. Conclusions: These findings support the relative validity of total and free sugar intake assessed by self-reported 24HDRs in children and adolescents. [ABSTRACT FROM AUTHOR]

Background: Excess dietary fat and sugar are linked to obesity and metabolic syndrome. Polyamines such as spermidine are implicated in fat accumulation and may support activity-induced weight loss.Objective: This study tested interventional spermidine supplementation and voluntary activity against fat- and sucrose-induced systemic and gut microbiota changes.Methods: A 3-factorial study design (3 × 2 × 2) was used to test the factors diet, activity, and spermidine. Male 6-wk-old C57BL/6N mice were fed a control diet (CD; carbohydrate:protein:fat, 70%:20%:10% of energy; 7% sucrose), a high-fat diet (HFD; carbohydrate:protein:fat, 20%:20%:60% of energy; 7% sucrose), or a high-sucrose diet (HSD; carbohydrate:protein:fat, 70%:20%:10% of energy; 35% sucrose). Diet groups were left untreated (+0) or had unlimited access to running wheels (+A) or were supplemented with 3 mM spermidine via drinking water (+S) or a combination of both (+A+S) for 30 wk (n = 7-10).Results: In comparison to the CD, the HFD enhanced body weights (by 36%, P < 0.001), plasma lipids (cholesterol by 24%, P < 0.001; triglycerides by 27%, P = 0.004), and glucose concentrations (by 18%, P < 0.001), whereas the HSD increased weight by 13% (P < 0.001) and fasting glucose by 17% (P < 0.001) but did not increase plasma lipids. Microbiota taxonomic composition changed upon the HFD and HSD (both P < 0.001); however, only the HSD increased microbial diversity (P < 0.001) compared with the CD. Activity influenced microbiota composition (P < 0.01) and reduced glucose concentrations in HSD-fed (P = 0.021) and HFD-fed (P < 0.001) mice compared with nonactive mice. The combination of activity and spermidine affected energy intake (P-interaction = 0.037) and reduced body weights of HSD+A+S mice compared with HSD+0 mice (P = 0.024).Conclusions: In male C57BL/6N mice, dietary sucrose and fat caused diverse metabolic and microbiota changes that were differentially susceptible to physical exercise. Spermidine has the potential to augment activity-induced beneficial effects, particularly for sucrose-induced obesity. [ABSTRACT FROM AUTHOR]

Sugar consumption in the United States exceeds recommendations from the American Heart Association. Overconsumption of sugar is linked to risk for obesity and metabolic disease. Animal studies suggest that high-sugar diets alter functions in brain regions associated with reward processing, including the dorsal and ventral striatum. Human neuroimaging studies have shown that these regions are responsive to food cues, and that the gut-derived satiety hormones, glucagon-like peptide-1 (GLP-1), and peptide YY (PYY), suppress striatal food-cue responsivity. We aimed to determine the associations between dietary added sugar intake, striatal responsivity to food cues, and postprandial GLP-1 and PYY levels. Twenty-two lean volunteers underwent a functional magnetic resonance imaging (fMRI) scan during which they viewed pictures of food and non-food items after a 12-h fast. Before scanning, participants consumed a glucose drink. A subset of 19 participants underwent an additional fMRI session in which they consumed water as a control condition. Blood was sampled for GLP-1, and PYY levels and hunger ratings were assessed before and ~75 min after drink consumption. In-person 24-h dietary recalls were collected from each participant on three to six separate occasions over a 2-month period. Average percent calories from added sugar were calculated using information from 24-h dietary recalls. A region-of-interest analysis was performed to compare the blood oxygen level-dependent (BOLD) response to food vs. non-food cues in the bilateral dorsal striatum (caudate/putamen) and ventral striatum (nucleus accumbens). The relationships between added sugar, striatal responses, and hormone changes after drink consumption were assessed using Spearman’s correlations. We observed a positive correlation between added sugar intake and BOLD response to food cues in the dorsal striatum and a similar trend in the nucleus accumbens after glucose, but not water, consumption. Added sugar intake was negatively associated with GLP-1 response to glucose. Post hoc analysis revealed a negative correlation between GLP-1 response to glucose and BOLD response to food cues in the dorsal striatum. Our findings suggest that habitual added sugar intake is related to increased striatal response to food cues and decreased GLP-1 release following glucose intake, which could contribute to susceptibility to overeating.

Efforts to reduce sugar intake levels have been primarily limited to increasing knowledge and changing attitudes. We conducted a systematic review to (1) identify factors influencing adults' knowledge and attitudes about sugar, and (2) determine if there is an association between knowledge and attitudes about sugar and sugar intake. We searched 15 electronic databases from inception to December 2016 for English language publications including adults with relevant exposure and outcome measures. Findings were summarised meta-narratively. Of 3287 studies, 22 studies (14 for objective one and 8 for objective two) were included. Individual (liking of sugary food), interpersonal (attitudes of peers) and environmental factors (media, health professionals and food labelling) influenced adults' knowledge and attitudes about sugar, at least to some extent. Overall, quality of the studies included in our review was weak, and evidence for the application of the Knowledge-Attitude-Behavior model for understanding sugar intake is limited. Protocol registered in the PROSPERO International prospective register of systematic reviews (registration number CRD42015027540). [ABSTRACT FROM AUTHOR]

Sugar consumption in the United States exceeds recommendations from the American Heart Association. Overconsumption of sugar is linked to risk for obesity and metabolic disease. Animal studies suggest that high-sugar diets alter functions in brain regions associated with reward processing, including the dorsal and ventral striatum. Human neuroimaging studies have shown that these regions are responsive to food cues, and that the gut-derived satiety hormones, glucagon-like peptide-1 (GLP-1), and peptide YY (PYY), suppress striatal food-cue responsivity. We aimed to determine the associations between dietary added sugar intake, striatal responsivity to food cues, and postprandial GLP-1 and PYY levels. Twenty-two lean volunteers underwent a functional magnetic resonance imaging (fMRI) scan during which they viewed pictures of food and nonfood items after a 12-h fast. Before scanning, participants consumed a glucose drink. A subset of 19 participants underwent an additional fMRI session in which they consumed water as a control condition. Blood was sampled for GLP-1, and PYY levels and hunger ratings were assessed before and ~75 min after drink consumption. In-person 24-h dietary recalls were collected from each participant on three to six separate occasions over a 2-month period. Average percent calories from added sugar were calculated using information from 24-h dietary recalls. A region-of-interest analysis was performed to compare the blood oxygen level-dependent (BOLD) response to food vs. non-food cues in the bilateral dorsal striatum (caudate/putamen) and ventral striatum (nucleus accumbens). The relationships between added sugar, striatal responses, and hormone changes after drink consumption were assessed using Spearman's correlations. We observed a positive correlation between added sugar intake and BOLD response to food cues in the dorsal striatum and a similar trend in the nucleus accumbens after glucose, but not water, consumption. Added sugar intake was negatively associated with GLP-1 response to glucose. Post hoc analysis revealed a negative correlation between GLP-1 response to glucose and BOLD response to food cues in the dorsal striatum. Our findings suggest that habitual added sugar intake is related to increased striatal response to food cues and decreased GLP-1 release following glucose intake, which could contribute to susceptibility to overeating. [ABSTRACT FROM AUTHOR]

The oral cavity houses a diverse consortium of microorganisms, heavily influenced by host diet, that can mediate dental health and disease. While the impact of dietary carbohydrates to the dental microbiome has been well-documented, the effect of fiber as a mechanical influence on the dental microbiome is unexplored. We performed 16S rRNA gene analysis to investigate the response of the dental microbiome to the presence of increased fiber in terms of microbial taxonomic abundance and diversity. Dental microbial community structure was significantly different in mice fed a diet supplemented with increased fiber and/or sugar. Fiber significantly affected measures of beta diversity at the phylum and genus levels, and a strong interactive effect on alpha diversity was observed between sugar and fiber at the phylum level. The addition of fiber also induced significant variation in relative taxonomic abundance. This study demonstrates that fiber can promote significant variations in the mouse dental microbiome.

Sugars are important energy sources, but high sugar intake poses a metabolic challenge and leads to diseases. Drosophila melanogaster is a generalist fruit breeder that encounters high levels of dietary sugars in its natural habitat. Consequently, Drosophila displays adaptive responses to dietary sugars, including highly conserved and unique metabolic adaptations not described in mammals. Carbohydrate homeostasis is maintained by a network comprising intracellular energy sensors, transcriptional regulators, and hormonal and neuronal mechanisms that together coordinate animal behavior, gut function, and metabolic flux. Here we give an overview of the physiological responses associated with sugar intake and discuss some of the emerging themes and applications of the Drosophila model in understanding sugar sensing and carbohydrate metabolism. [ABSTRACT FROM AUTHOR]