Kombuchas from green and black teas reduce oxidative stress, liver steatosis and inflammation, and improve glucose metabolism in Wistar rats fed a high-fat high-fructose diet.

The aim of this study was to evaluate the effect of green and black tea kombuchas consumption on adiposity, lipid and glucose metabolism, liver steatosis, oxidative stress, and inflammation in Wistar rats fed a high-fat high-fructose (HFHF) diet. Wistar rats, after 8 weeks to induce metabolic alterations, were divided into an AIN-93M control group, HFHF control group, green tea kombucha + HFHF diet (GTK group), and black tea kombucha + HFHF diet (BTK group), for 10 weeks. The kombuchas improved glucose metabolism, plasma total antioxidant capacity, superoxide dismutase activity, and decreased nitric oxide concentration. Moreover, both kombuchas reduced systemic inflammation by decreasing the neutrophil/lymphocyte ratio (NLR), reduced the total adipose tissue and blood triglyceride, and reverted liver steatosis (from grade 2 to 1), besides the modulation of genes related to adipogenesis and ß-oxidation. Therefore, kombuchas from green and black teas have bioactive properties that can help control metabolic alterations induced by the HFHF diet.

Isorhamnetin attenuates high-fat and high-fructose diet induced cognitive impairments and neuroinflammation by mediating MAPK and NFκB signaling pathways.

Isorhamnetin (ISO), a flavonoid compound isolated from sea-buckthorn (Hippophae rhamnoides L.) fruit, has anti-inflammatory effects. However, the effects of ISO on neuroinflammation and cognitive function are still unclear. The purpose of this study was to evaluate the protective effect of ISO on cognitive impairment in obese mice induced by a high-fat and high fructose diet (HFFD). It has been found that oral administration of ISO (0.03% w/w and 0.06% w/w) for 14 weeks significantly reduced the body weight, food intake, liver weight, liver lipid level, and serum lipid level of HFFD-fed mice. ISO can also significantly prevent HFFD-induced neuronal working, spatial, and long-term memory impairment. Notably, the ISO treatment activated the CREB/BDNF pathway and increased neurotrophic factors in the brains of mice. Furthermore, ISO inhibited HFFD-induced microglial overactivation and down-regulated inflammatory cytokines in both serum and the brain. It can also inhibit the expression of p-JNK, p-p38, and p-NFκB protein in the mouse brain. In conclusion, these results indicated that ISO mitigated HFFD-induced cognitive impairments by inhibiting the MAPK and NFκB signaling pathways, suggesting that ISO might be a plausible nutritional intervention for metabolic syndrome-related cognitive complications.

Component changes of mulberry leaf tea processed with honey and its application to in vitro and in vivo models of diabetes.

Honey is a traditional food additive that can be used to preserve food, increase the flavour of food, and enhance the effect of some functional foods. Mulberry leaf is a popular tea, and it is also an anti-diabetic medicinal material. In the traditional processing of mulberry leaf tea, honey is a commonly used additive. This study used ultra-high performance liquid chromatography-tandem mass spectrometry (UPLC-MS/MS) to measure the changes in the contents of 11 components of mulberry leaves before and after processing using honey as an additive. We analysed the absorption and elimination characteristics of mulberry leaves before and after processing in diabetes in vivo models, and then compared the effect of mulberry leaves before and after processing in resisting hyperglycaemia and hyperlipidaemia damage in in vitro models. The results showed that honey, as an additive, not only improves the dissolution of mulberry leaves, but in diabetes models also increases the utilisation of some components. In an in vitro model, honey mulberry leaves could significantly reduce the apoptosis of vascular endothelial cells. This demonstrated that the traditional processing method using honey as an additive could promote the anti-diabetic effect of mulberry tea. So far, this is the first research report on the quality and role of honey as an additive in mulberry leaf processing.Abbreviations: ML: mulberry leaves; HML: honey mulberry leaves; QC: quality control; HQC: high quality control sample; LLOQ: lower limit of quantification; LQC: low-quality control sample; MQC: medium-quality control sample; MRM: multiple reaction monitoring; STZ: streptozotocin.

AMPK in the gut-liver-brain axis and its influence on OP rats in an HSHF intake and WTD rat model.

Obesogenic diets (ODs) can affect AMPK activation in several sites as the colon, liver, and hypothalamus. OD intake can impair the hypothalamic AMPK regulation of energy homeostasis. Despite consuming ODs, not all subjects have the propensity to develop or progress to obesity. The obesity propensity is more associated with energy intake than expenditure dysregulations and may have a link with AMPK activity. While the effects of ODs are studied widely, few evaluate the short-term effects of terminating OD intake. Withdrawing from OD (WTD) is thought to improve or reverse the damages caused by the intake. Therefore, here we applied an OD intake and WTD protocol aiming to evaluate AMPK protein content and phosphorylation in the colon, liver, and hypothalamus and their relationship with obesity propensity. To this end, male Wistar rats (60 days) received control or high-sugar/high-fat (HSHF) OD for 30 days. Half of the animals were OD-withdrawn and fed the control diet for 48 h. After intake, we found a reduction in AMPK phosphorylation in the hypothalamus and colon, and after WTD, we found an increase in its hepatic and hypothalamic phosphorylation. The decrease in colon pAMPK/AMPK could be linked with hypothalamic pAMPK/AMPK after HSHF intake, while the increase in hepatic pAMPK/AMPK could have prevented the increase in hypothalamic pAMPK/AMPK. In the obesity-prone rats, we found higher levels of hypothalamic and colon pAMPK/AMPK despite the higher body mass gain. Our results highlight the relevance in multi-organ investigations and animal phenotype evaluation when studying the energy metabolism regulations.

Network Pharmacology-Based Strategy Reveals the Effects of Hedysarum multijugum Maxim.-Radix Salviae Compound on Oxidative Capacity and Cardiomyocyte Apoptosis in Rats with Diabetic Cardiomyopathy.

OBJECTIVE: To explore the effects of the Hedysarum multijugum Maxim.-Radix Salviae compound (Huangqi-Danshen Compound (HDC)) on oxidative capacity and cardiomyocyte apoptosis in rats with diabetic cardiomyopathy by a network pharmacology-based strategy. METHODS: Traditional Chinese Medicine (TCM)@Taiwan, TCM Systems Pharmacology Database and Analysis Platform (TCMSP), TCM Integrated Database (TCMID), and High-Performance Liquid Chromatography (HPLC) technology were used to obtain and screen HDC's active components, and the PharmMapper database was used to predict HDC human target protein targets. The DCM genes were collected from the GeneCards and OMIM databases, and the network was constructed and analyzed by Cytoscape 3.7.1 and the Database for Annotation, Visualization, and Integrated Discovery (DAVID). Finally, HDC was used to intervene in diabetic cardiomyopathy (DCM) model rats, and important biological processes and signaling pathways were verified using techniques such as immunohistochemistry. RESULTS: A total of 176 of HDC's active components and 442 potential targets were obtained. The results of network analysis show that HDC can regulate DCM-related biological processes (such as negative regulation of the apoptotic process, response to hypoxia, the steroid hormone-mediated signaling pathway, cellular iron ion homeostasis, and positive regulation of phosphatidylinositol 3-kinase signaling) and signaling pathways (such as the HIF-1 signaling pathway, the estrogen signaling pathway, insulin resistance, the PPAR signaling pathway, the VEGF signaling pathway, and the PI3K-Akt signaling pathway). Animal experiments show that HDC can reduce fasting plasma glucose (FPG), HbA1c, and malondialdehyde (MDA) and increase superoxide dismutase (SOD) and glutathione peroxidase (GSH-Px) (P < 0.05). The results of immunohistochemistry showed that HDC can regulate the protein expression of apoptosis-related signaling pathways in DCM rats (P < 0.05). CONCLUSION: It was initially revealed that HDC improves DCM through its antiapoptotic and anti-inflammatory effects. HDC may play a therapeutic role by improving cardiomyocyte apoptosis in DCM rats.

Designing an Effective Front-of-Package Warning Label for Food and Drinks High in Added Sugar, Sodium, or Saturated Fat in Colombia: An Online Experiment.

Policies to require warnings on the front of food and drinks high in nutrients of concern (e.g., added sugar, sodium, or saturated fat) are becoming increasingly common as an obesity prevention strategy. Colombia, a country with growing prevalence of obesity, is considering implementing a similar policy. The objective of this study was to assess perceptions and reactions to different warning designs. We conducted a randomized experiment in an online panel of adults age > 18y (n = 1997). Participants were randomized to view one of four labels: a control label (barcode), an octagon warning, a circle warning, and a triangle warning. Participants viewed their randomly assigned label on a series of products and answered questions (continuous outcomes ranged from 1-4). Compared to the control, all warnings led to higher perceived message effectiveness (increase in mean from 1.79 in the control to 2.59-2.65 in the warning conditions, p < 0.001), a higher percentage of participants who correctly identified products high in nutrients of concern (from 48% in the control condition to 84-89% in the warning conditions, p < 0.001), and reduced intentions to purchases these products (decrease in mean from 2.59 to 1.99-2.01 in the warning conditions, p < 0.001). Relative to the control, warnings performed similarly across education levels, suggesting this policy would be equitable in Colombia. Looking at differences by warning type, the pattern of results suggested that the octagon warnings performed best. After viewing all label types, 49% of participants selected the octagon warning as the one that most discouraged them from consuming products high in nutrients of concern, while 21% and 27% selected the circle and triangle warning. Colombian policymakers should consider the octagon warning as part of a front-of-package labeling policy to help consumers identify and reduce consumption of foods and drinks high in nutrients of concern.

High-Sugar Diet Disrupts Hypothalamic but Not Cerebral Cortex Redox Homeostasis.

Despite several reports on the relationship between metabolic and neurodegenerative diseases, the effect of a high-sugar diet (HSD) on brain function is still unknown. Given the crucial role of oxidative stress in the pathogenesis of these disorders, this study was the first to compare the effect of an HSD on the activity of prooxidative enzymes, enzymatic and non-enzymatic antioxidants, and protein oxidative damage in the brain structures regulating energy metabolism (hypothalamus) and cognitive functions (cerebral cortex). Male Wistar rats were randomly divided into two groups (n = 10)-control diet (CD) and high-sugar diet (HSD)-for 8 weeks. We showed a decrease in glutathione peroxidase and superoxide dismutase activity and an increase in catalase activity in the hypothalamus of HSD rats compared to controls. The activity of xanthine oxidase and NADPH oxidase and the contents of oxidation (protein carbonyls), glycoxidation (dityrosine, kynurenine and N-formylkynurenine) and protein glycation products (advanced glycation end products and Amadori products) were significantly higher only in the hypothalamus of the study group. The HSD was also responsible for the disruption of antioxidant systems and oxidative damage to blood proteins, but we did not show any correlation between systemic redox homeostasis and the brain levels. In summary, HSD is responsible for disorders of enzymatic antioxidant defenses only at the central (plasma/serum) and hypothalamic levels but does not affect the cerebral cortex. The hypothalamus is much more sensitive to oxidative damage caused by an HSD than the cerebral cortex.

Sugar consumption, sugar sweetened beverages and Attention Deficit Hyperactivity Disorder: A systematic review and meta-analysis.

BACKGROUND: Attention-deficit/hyperactivity disorder (ADHD) is a significant neurobehavioral disorder in children and adolescence which may be affected by diet. OBJECTIVE: To evaluate the possible relationship between sugar consumption and the development of symptoms of ADHD. METHODS: In March 2020, an exhaustive systematic literature search was conducted using Google Scholar, PubMed, and Scopus. In this meta-analysis of observational studies, odds ratios, relative risks, hazard ratios, and their 95% confidence intervals, which was reported for ADHD regarding SSBS, soft drink consumption, and dietary sugars, were used to calculate ORs and standard errors. At first, a fixed-effects model was used to drive the overall effect sizes using log ORs and SEs. If there was any significant between-studies heterogeneity, the random-effects model was conducted. Cochran's Q test and I2 were used to measure potential sources of heterogeneity across studies. The Newcastle-Ottawa scale was used to assess the quality of the included articles. RESULTS: Seven studies, two cross-sectional, two case-control, and three prospective with a total of 25,945 individuals were eligible to include in the current meta-analysis. The association between sugar and soft drink consumption and the risk of ADHD symptoms were provided based on the random-effects model (pooled effect size: 1.22, 95%CI: 1.04-1.42, P = 0.01) (I² = 81.9%, P heterogeneity< 0.0001). CONCLUSION: This meta-analysis indicated a positive relationship between overall sugar and sugar-sweetened beverages consumption and symptoms of ADHD; however, there was heterogeneity among included studies. Future well-designed studies that can account for confounds are necessary to confirm the effect of sugar on ADHD.

Effect of Added Sugar on the Consumption of A Lipid-Based Nutrient Supplement Among 7-24-Month-Old Children.

Small-quantity lipid-based nutrient supplements (SQ-LNS) could help prevent malnutrition. Our primary objective was to examine the acceptability and consumption of sweetened and unsweetened versions of SQ-LNS before and after 14-days of repeated exposure. A total of 78 mother-infant dyads recruited from health centers in Morelos, Mexico, were randomized to two groups of SQ-LNS (sweetened, LNS-S; unsweetened, LNS-U). During the study, infants were fed SQ-LNS (20 g) mixed with 30 g of complementary food of the caregiver's choice. The amount of supplement-food mixture consumed was measured before, during and after a 14-day home exposure period. We defined acceptability as consumption of at least 50% of the offered food mixture. At initial exposure, LNS-U consumption was on average 44.0% (95% CI: 31.4, 58.5) and LNS-S 34.8% (25.3, 44.0); at final exposure, LNS-U and LNS-S consumption were 38.5% (27.8, 54.0) and 31.5% (21.6, 43.0). The average change in consumption did not differ between the groups (2.2 p.p. (-17.2, 24.4)). We conclude that the acceptability of sweetened and unsweetened SQ-LNS was low in this study population. Since consumption did not differ between supplement versions, we encourage the use of the unsweetened version given the potential effects that added sugar may have on weight gain especially in regions facing the double burden of malnutrition.

Prolonged overnutrition with fructose or fat induces metabolic derangements in rats by disrupting the crosstalk between the hypothalamus and periphery: Possible amelioration with fenofibrate.

Metabolic Syndrome (MetS) increases the risk of developing type 2 diabetes mellitus and cardiovascular complications. The crosstalk between the hypothalamus and periphery is vital for regulating food intake and energy homeostasis. However, it is impaired during MetS. The present study aimed to compare the distinct central and peripheral metabolic derangements induced by a high-fructose drink or high-fat diet, as well as the possible intervention by fenofibrate. Rats were divided into five groups: standard chow diet (SCD) group, high-fructose group (FR), high-fat group (HF), FR plus fenofibrate group (FR-F), and HF plus fenofibrate group (HF-F). FR and HF groups showed hyperglycemia, hyperinsulinemia, hypertriglyceridemia, hyperleptinemia, steatosis, and adipocyte hypertrophy. This was associated with elevated circulating levels of proinflammatory cytokines and free fatty acids (FFAs). The latter mediators are involved in the hypothalamic inflammation and dysregulation of signaling cascades that control food intake and glucose homeostasis. The effects were more pronounced in the HF group than FR group, which were matched with the observed higher levels of plasma FFAs and cytokines. Fenofibrate administration improved not only the peripheral metabolic disturbances, but also the central disturbances associated with insulin resistance induced by FR or HF diet. This study sheds light on the pivotal role of the hypothalamus in diet-induced MetS. Furthermore, the study suggests the utmost importance of developing a standardized model of metabolic syndrome in place of the great diversity between available models, which can induce different effects and negatively impact the validity of prospective studies.

Dietary Melatonin Protects Against Behavioural, Metabolic, Oxidative, and Organ Morphological Changes in Mice that are Fed High-Fat, High- Sugar Diet.

BACKGROUND: Metabolic syndrome is a complex pattern of disorders that occur jointly and is associated with an increased risk of cardiovascular and cerebrovascular disease. Therefore the need for more-efficient options of treatment has become imperative. OBJECTIVE: This study examined the effect of dietary-melatonin in the management of behavioural, metabolic, antioxidant, and organ changes due to high-fat/high-sugar (HFHS) diet-induced metabolic syndrome in mice. METHODS: Mice were randomly assigned into five groups of ten animals each. Groups were normal control [fed standard diet (SD)], HFHS control, and 3 groups of melatonin incorporated into HFHS at 2.5, 5, and 10 mg/kg of feed. Mice were fed for seven weeks, and body weight was assessed weekly. Open-field behaviours, radial-arm, and Y-maze spatial memory were scored at the end of the experimental period. Twenty-four hours after the last behavioural test, blood was taken for estimation of blood glucose levels after an overnight fast. Animals were then euthanised, and blood was taken for estimation of plasma insulin, leptin, and adiponectin levels, and serum lipid profile. The liver, kidneys, and brain were excised and processed for general histology, while homogenates of the liver and whole brain were used to assess oxidative stress parameters. RESULTS: Results showed that dietary melatonin (compared to HFHS diet) was associated with a decrease in body weight, food intake, and novelty-induced behaviours; and an increase in spatial-working memory scores. A decrease in glucose, insulin, leptin, and malondialdehyde levels; and an increase in adiponectin levels and superoxide dismutase activity were also observed. Histomorphological/ histomorphometric examination revealed evidence of organ injury with HFHS diet, and varying degrees of amelioration with melatonin-supplemented diet. CONCLUSION: In conclusion, dietary melatonin supplementation may have beneficial effects in the management of the metabolic syndrome.

The Color Nutrition Information Paradox: Effects of Suggested Sugar Content on Food Cue Reactivity in Healthy Young Women.

Color nutrition information (CNI) based on a traffic light system conveys information about food quality with a glance. The color red typically indicates detrimental food characteristics (e.g., very high sugar content) and aims at inhibiting food shopping and consumption. Red may, however, also elicit cross-modal associations with sweet taste, which is a preferable food characteristic. We conducted two experiments. An eye-tracking study investigated whether CNI has an effect on cue reactivity (dwell time, saccadic latency, wanting/liking) for sweet foods. The participants were presented with images depicting sweets (e.g., cake). Each image was preceded by a colored circle that informed about the sugar content of the food (red = high, green = low, gray = unknown). It was tested whether the red circle would help the participants to direct their gaze away from the 'high sugar' item. A second experiment investigated whether colored prime circles (red, green, gray) without nutrition information would influence the assumed sweetness of a food. In Experiment 1, CNI had the opposite of the intended effect. Dwell time and saccadic latency were higher for food items preceded by a red compared to a green circle. This unintended response was positively associated with participants' liking of sweet foods. CNI did not change the wanting/liking of the displayed foods. In Experiment 2, we found no evidence for color priming on the assumed sweetness of food. Our results question whether CNI is helpful to influence initial cue reactivity toward sweet foods.

Dietary Sugars Alter Hepatic Fatty Acid Oxidation via Transcriptional and Post-translational Modifications of Mitochondrial Proteins.

Dietary sugars, fructose and glucose, promote hepatic de novo lipogenesis and modify the effects of a high-fat diet (HFD) on the development of insulin resistance. Here, we show that fructose and glucose supplementation of an HFD exert divergent effects on hepatic mitochondrial function and fatty acid oxidation. This is mediated via three different nodes of regulation, including differential effects on malonyl-CoA levels, effects on mitochondrial size/protein abundance, and acetylation of mitochondrial proteins. HFD- and HFD plus fructose-fed mice have decreased CTP1a activity, the rate-limiting enzyme of fatty acid oxidation, whereas knockdown of fructose metabolism increases CPT1a and its acylcarnitine products. Furthermore, fructose-supplemented HFD leads to increased acetylation of ACADL and CPT1a, which is associated with decreased fat metabolism. In summary, dietary fructose, but not glucose, supplementation of HFD impairs mitochondrial size, function, and protein acetylation, resulting in decreased fatty acid oxidation and development of metabolic dysregulation.

Ginsenoside Rg1 attenuates hepatic insulin resistance induced by high-fat and high-sugar by inhibiting inflammation.

Ginsenoside Rg1 is the active ingredient of Chinese herbal medicine ginseng and sanqi, which has remarkable effects on anti-inflammation and anti-diabetes. In this study, we explored the molecular mechanism of ginsenoside Rg1 against diabetes in rat subjected to insulin resistance induced by high-fat and high-sugar (HFHS). Biochemical analysis revealed that ginsenoside Rg1 significantly decreased the serum levels of alanine transaminase, aspartate transaminase, alkaline phosphatase, total cholesterol, triglyceride, low-density lipoprotein and increased the serum levels of high-density lipoprotein, which indicated ginsenoside Rg1 improved the extent of hepatic steatosis. Furthermore, ginsenoside Rg1 suppressed the expression of IL-1ß, IL-6,TNF-α,NF-κB and G6Pase, however, p-Akt was up-regulated. These results suggested that ginsenosideRg1 improved insulin resistance through suppressing inflammatory response and glucose output, which may be a potential therapeutic strategy in protecting hepatic steatosis.

Aspalathin-Enriched Green Rooibos Extract Reduces Hepatic Insulin Resistance by Modulating PI3K/AKT and AMPK Pathways.

We previously demonstrated that an aspalathin-enriched green rooibos extract (GRE) reversed palmitate-induced insulin resistance in C2C12 skeletal muscle and 3T3-L1 fat cells by modulating key effectors of insulin signalling such as phosphatidylinositol-4,5-bisphosphate 3-kinase/protein kinase B (PI3K/AKT) and AMP-activated protein kinase (AMPK). However, the effect of GRE on hepatic insulin resistance is unknown. The effects of GRE on lipid-induced hepatic insulin resistance using palmitate-exposed C3A liver cells and obese insulin resistant (OBIR) rats were explored. GRE attenuated the palmitate-induced impairment of glucose and lipid metabolism in treated C3A cells and improved insulin sensitivity in OBIR rats. Mechanistically, GRE treatment significantly increased PI3K/AKT and AMPK phosphorylation while concurrently enhancing glucose transporter 2 expression. These findings were further supported by marked stimulation of genes involved in glucose metabolism, such as insulin receptor (Insr) and insulin receptor substrate 1 and 2 (Irs1 and Irs2), as well as those involved in lipid metabolism, including Forkhead box protein O1 (FOXO1) and carnitine palmitoyl transferase 1 (CPT1) following GRE treatment. GRE showed a strong potential to ameliorate hepatic insulin resistance by improving insulin sensitivity through the regulation of PI3K/AKT, FOXO1 and AMPK-mediated pathways.

Treatment with myo-inositol attenuates binding of the carbohydrate-responsive element-binding protein to the ChREBP-ß and FASN genes in rat nonalcoholic fatty liver induced by high-fructose diet.

Dietary supplementation with the major lipotrope myo-inositol (MI) potently reduces triglyceride (TG) content and expression levels of the fatty acid synthesis genes, for example, fatty acid synthase (FASN), in rat nonalcoholic fatty liver induced by high-fructose diet. Fatty acid synthesis genes are regulated by the carbohydrate-responsive element-binding protein (ChREBP) that exists in 2 isoforms: ChREBP-α and ChREBP-ß. The gene encoding the latter isoform is more responsive to fructose. Because MI repressed the induction of fatty acid synthesis gene expression by high-fructose diet, we hypothesized that MI may reduce binding of ChREBP to the carbohydrate response elements (ChoREs) in the ChREBP-ß gene as well as in fatty acid synthesis genes in the liver. Rats were fed high-glucose, high-fructose, or high-fructose diets supplemented with MI (0.05% and 0.25%) for 2 weeks. Hepatic TG content and expression levels of the glucose-6-phosphate dehydrogenase, malic enzyme 1, FASN, acetyl-CoA carboxylase alpha, S14, and ChREBP-ß were remarkably elevated in rats fed with high fructose compared with the corresponding levels in high-glucose group. Notably, elevated values of these parameters in high-fructose group were reduced by MI. Similarly, high-fructose-induced ChREBP binding to the ChoREs of the ChREBP-ß and FASN genes was nominally decreased by MI. This study showed that treatment with MI reduced elevated TG content and expression of genes related to fatty acid synthesis, such as FASN and ChREBP-ß, in rat nonalcoholic fatty liver induced by high-fructose diet. Furthermore, MI treatment nominally decreased increased binding of ChREBP to the ChoREs of ChREBP-ß and FASN genes.

Gaps in the Evidence on Population Interventions to Reduce Consumption of Sugars: A Review of Reviews.

There is currently considerable attention directed to identifying promising interventions to reduce consumption of sugars among populations around the world. A review of systematic reviews was conducted to identify gaps in the evidence on such interventions. Medline, EMBASE CINAHL, and the Cochrane Database of Systematic Reviews were searched to identify systematic reviews published in English from January 2005 to May 2017 and considering research on interventions to reduce sugar intake. Twelve systematic reviews that considered price changes, interventions to alter the food available within specific environments, and health promotion and education programs were examined. Each of the identified reviews focused on sugar-sweetened beverages (SSBs). The existing literature provides some promising indications in terms of the potential of interventions to reduce SSB consumption among populations. However, a common thread is the limited scope of available evidence, combined with the heterogeneity of methods and measures used in existing studies, which limits conclusions that can be reached regarding the effectiveness of interventions. Reviewed studies typically had limited follow-up periods, making it difficult to assess the sustainability of effects. Further, there is a lack of studies that address the complex context within which interventions are implemented and evaluated, and little is known about the cost-effectiveness of interventions. Identified gaps speak to the need for a more holistic approach to sources of sugars beyond SSBs, consensus on measures and methods, attention to the implementation of interventions in relation to context, and careful monitoring to identify intended and unintended consequences.

A Clinician's Guide for Trending Cardiovascular Nutrition Controversies: Part II.

The potential cardiovascular (CV) benefits of many trending foods and dietary patterns are still incompletely understood, and scientific inquiry continues to evolve. In the meantime, however, a number of controversial dietary patterns, foods, and nutrients have received significant media attention and are mired by "hype." This second review addresses some of the more recent popular foods and dietary patterns that are recommended for CV health to provide clinicians with current information for patient discussions in the clinical setting. Specifically, this paper delves into dairy products, added sugars, legumes, coffee, tea, alcoholic beverages, energy drinks, mushrooms, fermented foods, seaweed, plant and marine-derived omega-3-fatty acids, and vitamin B12.

Antihyperlipidemic and anti-hyperglycemic effects of Cymbopogon jwarancusa in high-fat high-sugar diet model.

Hyperlipidemia is the root cause for development of atherosclerosis, coronary heart disease, diabetes mellitus, obesity, hypertension and cerebral palsy. Cymbopogon jwarancusa is an aromatic grass (Rusha grass, khavi grass) belonging to family Poaceaea. C. jwarancusa essential oil is famous for its use in perfumery, soaps cosmetics, detergents, medicine and pharmaceuticals. The anti-pyretic, anti-fungal, antibacterial, anti-oxidant and cytotoxic activities of C. jwarancusa have been reported in literature. In the present study different doses of C. jwarancusa extract have been investigated for anti-hyperlipidemic and anti-hyperglycemic activities in high-fat high sugar diet model in rats. Hyperlipidemia and hyperglycemia were assessed by measuring body weight, serum lipid profile and fasting blood glucose levels. Administration of ethanol leaves extract of C. jwarancusa exhibited significant dose-dependent reduction in body weight, lipid parameters and blood sugar levels. Hence it may be concluded that C. jwarancusa aids in ameliorating hyperlipidemic, hyperglycemic conditions and has potential to reduce the risk of cardiovascular problems.