High-sugar intake is a risk factor for chronic diseases such as cardiovascular disease and type 2 diabetes, but less is known about its role in anxiety disorders. This systematic review aimed to systematically synthesise and assess the existing evidence regarding the association between dietary sugars intake and anxiety disorders. Following PRISMA guidelines, a systematic search of PubMed, MEDLINE, Embase, APA PsycArticles and APA PsycINFO was conducted up to 19th August 2022. Study quality was assessed by the Newcastle-Ottawa scale (NOS) and the Cochrane risk of bias tool. Eleven studies (10 cross-sectional and 1 randomised controlled trial [RCT]) were included. Seven cross-sectional studies had very good quality or good quality, and the quality of the RCT was at low risk of bias. These studies examined sugar-sweetened beverages (n = 7), sugar-sweetened foods (n = 4) and/or added sugar (n = 5). The findings suggest a possible positive relationship of added sugar consumption with anxiety disorders, with age as a potential moderator in such association. No conclusions can be drawn on the associations between sugar-sweetened beverages, sugar-sweetened foods consumption and anxiety disorders. Due to the included studies being mostly cross-sectional, the conclusions drawn from the existing evidence should be interpreted with caution. The longitudinal design is warranted to investigate any causal relationship and the potential mechanisms underlying these heterogeneous results. The potential difference in effect at different ages observed in this review should be further examined.

The 2020-2025 Dietary Guidelines for Americans recommend limiting intakes of saturated fat and added sugars (SF/AS) to <10% total energy. Data-driven approaches to identify sources of SF/AS are needed to meet these goals. We propose using a population-based approach to identify the leading food and beverage sources of SF/AS consumed by US adults. Foods and beverages reported as consumed were assessed from two, 24 h dietary recalls (24HRDR) from 36,378 adults aged 19 years and older from the 2005-2018 National Health and Nutrition Examination Survey. Intakes of SF/AS were aggregated across both 24HRDR to identify What We Eat in America food categories accounting for ≥90% of SF/AS, respectively, by the total population and within population subgroups. Data were weighted to estimate a nationally representative sample. Ninety-five discrete food categories accounted for ≥90% of the total SF/AS intakes for >88% of the representative sample of U.S. adults. The top sources of SF were cheese, pizza, ice cream, and eggs. The leading sources of AS were soft drinks, tea, fruit drinks, and cakes and pies. This analysis reflects a parsimonious approach to reliably identify foods and beverages that contribute to SF/AS intakes in U.S. adults.

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UNASSIGNED: Nutritive compounds play critical roles in DNA replication, maintenance, and repair, and also serve as antioxidant and anti-inflammatory agents. Sufficient dietary intakes support genomic stability and preserve health.
UNASSIGNED: To investigate the associations of dietary patterns, including intakes of essential nutrients and added sugar, and diet quality scores of established and new nutrient indices with epigenetic age in a diverse cohort of Black and White women at midlife.
UNASSIGNED: This cross-sectional study included analyses (2021-2023) of past women participants of the 1987-1997 National Heart, Lung, and Blood Institute Growth and Health Study (NGHS), which examined cardiovascular health in a community cohort of Black and White females aged between 9 and 19 years. Of these participants who were recruited between 2015 and 2019 from NGHS\'s California site, 342 females had valid completed diet and epigenetic assessments. The data were analyzed from October 2021 to November 2023.
UNASSIGNED: Diet quality scores of established nutrient indices (Alternate Mediterranean Diet [aMED], Alternate Healthy Eating Index [AHEI]-2010); scores for a novel, a priori-developed Epigenetic Nutrient Index [ENI]; and mean added sugar intake amounts were derived from 3-day food records.
UNASSIGNED: GrimAge2, a second-generation epigenetic clock marker, was calculated from salivary DNA. Hypotheses were formulated after data collection. Healthier diet indicators were hypothesized to be associated with younger epigenetic age.
UNASSIGNED: A total of 342 women composed the analytic sample (mean [SD] age, 39.2 [1.1] years; 171 [50.0%] Black and 171 [50.0%] White participants). In fully adjusted models, aMED (β, -0.41; 95% CI, -0.69 to -0.13), AHEI-2010 (β, -0.05; 95% CI, -0.08 to -0.01), and ENI (β, -0.17; 95% CI, -0.29 to -0.06) scores, and added sugar intake (β, 0.02; 95% CI, 0.01-0.04) were each significantly associated with GrimAge2 in expected directions. In combined analyses, the aforementioned results with GrimAge2 were preserved with the association estimates for aMED and added sugar intake retaining their statistical significance.
UNASSIGNED: In this cross-sectional study, independent associations were observed for both healthy diet and added sugar intake with epigenetic age. To our knowledge, these are among the first findings to demonstrate associations between added sugar intake and epigenetic aging using second-generation epigenetic clocks and one of the first to extend analyses to a diverse population of Black and White women at midlife. Promoting diets aligned with chronic disease prevention recommendations and replete with antioxidant or anti-inflammatory and pro-epigenetic health nutrients while emphasizing low added sugar consumption may support slower cellular aging relative to chronological age, although longitudinal analyses are needed.

It was previously shown in striatal slices obtained from male rats that insulin excites cholinergic interneurons and increases dopamine (DA) release via α4β2 nicotinic receptors on DA terminals. The effect of insulin on DA release was blocked either by maintaining rats on a high sugar-high fat (HS-HF) diet that induced hyperinsulinemia and nucleus accumbens (NAc) insulin receptor insensitivity, or applying the α4β2 antagonist DHβE. In vivo, NAc shell insulin inactivation decreased a glucose lick microstructure parameter indicative of hedonic impact in male and female rats, and prevented flavor-nutrient learning, tested only in males. The HS-HF diet decreased hedonic impact in males but not females, and prevented flavor-nutrient learning, tested only in males. The present study extends testing to more fully assess the translation of brain slice results to the behaving rat. Insulin inactivation by antibody microinjection in NAc shell was found to decrease the number of lick bursts emitted and average lick burst size, measures of incentive motivation and hedonic impact respectively, for a wide range of glucose concentrations in male and female rats. In contrast, the HS-HF diet decreased these lick parameters in males but not females. Follow-up two-bottle choice tests for 10 % versus 40 % glucose showed decreased intake of both concentrations by males but increased intake of 40 % glucose by females. In a further set of experiments, it was predicted that α4β2 receptor blockade would induce the same behavioral effects as insulin inactivation. In females, DHβE microinjection in NAc shell decreased both lick parameters for glucose as predicted, but in males only the number of lick bursts emitted was decreased. DHβE also decreased the number of lick bursts emitted for saccharin by females but not males. Finally, DHβE microinjection in NAc shell decreased flavor-nutrient learning in both sexes. The few discrepancies seen with regard to the hypothesized insulin-nicotinic-dopaminergic regulation of behavioral responses to nutritive sweetener, and its inhibition by HS-HF diet, are discussed with reference to sex differences in DA dynamics, female resistance to diet-induced metabolic morbidities, and extra-striatal cholinergic inputs to NAc.

BACKGROUND: In MASLD (formerly called NAFLD) mouse models, oversupply of dietary fat and sugar is more lipogenic than either nutrient alone. Fatty acids suppress de novo lipogenesis (DNL) from sugars, while DNL inhibits fatty acid oxidation. How such factors interact to impact hepatic triglyceride levels are incompletely understood.
METHODS: Using deuterated water, we measured DNL in mice fed 18-weeks with standard chow (SC), SC supplemented with 55/45-fructose/glucose in the drinking water at 30% (w/v) (HS), high-fat chow (HF), and HF with HS supplementation (HFHS). Liver glycogen levels and its sources were also measured. For HS and HFHS mice, pentose phosphate (PP) fluxes and fructose contributions to DNL and glycogen were measured using [U-13C]fructose.
RESULTS: The lipogenic diets caused significantly higher liver triglyceride levels compared to SC. DNL rates were suppressed in HF compared to SC and were partially restored in HFHS but supplied a minority of the additional triglyceride in HFHS compared to HF. Fructose contributed a significantly greater fraction of newly synthesized saturated fatty acids compared to oleic acid in both HS and HFHS. Glycogen levels were not different between diets, but significant differences in Direct and Indirect pathway contributions to glycogen synthesis were found. PP fluxes were similar in HS and HFHS mice and were insufficient to account for DNL reducing equivalents.
CONCLUSIONS: Despite amplifying the lipogenic effects of fat, the fact that sugar-activated DNL per se barely contributes suggests that its role is likely more relevant in the inhibition of fatty acid oxidation. Fructose promotes lipogenesis of saturated over unsaturated fatty acids and contributes to maintenance of glycogen levels. PP fluxes associated with sugar conversion to fat account for a minor fraction of DNL reducing equivalents.

BACKGROUND: Limited evidence demonstrated the potential relationship between dietary sugar intake and dementia. This association demands further clarification in a large-scale population.
METHODS: A total of 210,832 participants from the UK Biobank cohort were included in this prospective cohort study. Absolute and relative sugar intake and high-sugar dietary scores were utilized to reflect dietary sugar intake. Absolute sugar intake was identified by the Oxford WebQ in the UK Biobank. Relative sugar intake was calculated by dividing the absolute sugar intake by total diet energy. High-sugar dietary pattern was identified using the method of reduced rank regression. Cox proportional hazards regression analyses and restricted cubic splines were performed to examine the longitudinal associations between dietary sugar intake and all-cause dementia and its main subtype, Alzheimer\'s disease. Explorative mediation analyses were conducted to explore underlying mechanisms.
RESULTS: Increased absolute sugar intake (g/day) was significantly associated with a higher risk of all-cause dementia (HR = 1.003, [95%CI: 1.002-1.004], p < 0.001) and Alzheimer\'s disease (1.002, [1.001-1.004], 0.005). Relative sugar intake (%g/kJ/day) also demonstrated significant associations with all-cause dementia (1.317, [1.173-1.480], p < 0.001) and Alzheimer\'s disease (1.249, [1.041-1.500], 0.017), while the high-sugar dietary score was only significantly associated with a higher risk of all-cause dementia (1.090, [1.045-1.136], p < 0.001). In addition, both sugar intake and high-sugar dietary score demonstrated significant non-linear relationships with all-cause dementia and Alzheimer\'s disease (all p values for non-linearity < 0.05).
CONCLUSIONS: Our study provided evidence that excessive sugar intake was associated with dementia. Controlling the excess consumption of dietary sugar may be of great public health implications for preventing dementia.

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BACKGROUND: The UK soft drinks industry levy (SDIL) was announced in March 2016 and implemented in April 2018, encouraging manufacturers to reduce the sugar content of soft drinks. This is the first study to investigate changes in individual-level consumption of free sugars in relation to the SDIL.
METHODS: We used controlled interrupted time series (2011-2019) to explore changes in the consumption of free sugars in the whole diet and from soft drinks alone 11 months after SDIL implementation in a nationally representative sample of adults (>18 years; n=7999) and children (1.5-19 years; n=7656) drawn from the UK National Diet and Nutrition Survey. Estimates were based on differences between observed data and a counterfactual scenario of no SDIL announcement/implementation. Models included protein consumption (control) and accounted for autocorrelation.
RESULTS: Accounting for trends prior to the SDIL announcement, there were absolute reductions in the daily consumption of free sugars from the whole diet in children and adults of 4.8 g (95% CI 0.6 to 9.1) and 10.9 g (95% CI 7.8 to 13.9), respectively. Comparable reductions in free sugar consumption from drinks alone were 3.0 g (95% CI 0.1 to 5.8) and 5.2 g (95% CI 4.2 to 6.1). The percentage of total dietary energy from free sugars declined over the study period but was not significantly different from the counterfactual.
CONCLUSIONS: The SDIL led to significant reductions in dietary free sugar consumption in children and adults. Energy from free sugar as a percentage of total energy did not change relative to the counterfactual, which could be due to simultaneous reductions in total energy intake associated with reductions in dietary free sugar.

As a way of modeling healthier eating habits for their children, parents may intentionally avoid consuming sugary foods and drinks (SFDs) in their presence but consume these on other occasions (later referred to as parental secretive eating). This study aimed to 1) explore the prevalence of parental secretive eating, 2) investigate the associations between parental secretive eating and SFD consumption in parents and children, and 3) qualitatively explore the reasons for parental secretive eating. Participants were Finnish mothers (n = 362), fathers (n = 123), and their 3-6-year-old children (n = 403); this data was collected in 2017 as part of the baseline assessment of the DAGIS intervention. Parents reported how often they avoided eating SFDs in the presence of their child, completed food frequency questionnaires for themselves and their child, and responded to an open-ended question of explaining reasons for secretive eating. The overall prevalence of parental secretive eating was 68%. It was more common among mothers than fathers (p < 0.001) and most prevalent in chocolate (61%) and sweets (59%). Parental secretive eating was positively associated with SFD consumption both among mothers (ꞵ = 0.274, p < 0.001) and fathers (ꞵ = 0.210, p = 0.028) in linear regression models adjusted for parents\' and child\'s age, child\'s gender, parental education level, and number of household members. Mothers\' or fathers\' secretive eating and child\'s SFD consumption were not associated (ꞵ = 0.031, p = 0.562; ꞵ = -0.143; p = 0.167). Three themes describing reasons for parental secretive eating were found: family food rules, avoiding child\'s requests, and aspiration for healthy modeling. In conclusion, parental secretive eating may play an important role in determining SFD consumption in families with preschoolers. Additional research is needed to determine whether parents can prevent their own eating habits from influencing their child through secretive eating.