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Background The current prospective cohort study aimed to explore the potential associations between dietary sodium (Na), potassium (K), and sodium-to-potassium (Na-to-K) ratio with an incidence risk of cardiovascular disease (CVD) among Iranian adults. Methods The participants of the Tehran Lipid and Glucose Study (men and women aged 30–84 years, n = 2050), free of CVD at baseline (2006–2008) were included. Dietary intakes were assessed using a validated food frequency questionnaire (FFQ), and incident CVD (i.e., coronary heart disease, stroke, and CVD mortality) were documented up to March 2018. Cox proportional hazard models were used to estimate hazard ratios (HRs) and 95% confidence interval (CI) regarding the association between dietary Na, K, and Na-to-K ratio with CVD events. Results During a median follow-up of 10.6 years, 10.14% of participants experienced CVD outcomes. A 41% increased risk of CVD in relation to each increase in 1000 mg/d of Na intake. In the fully-adjusted model, higher Na intake (> 4143 versus Conclusion Our study showed that the Na-to-K ratio might independently predict future risk of CVD events in adults.

Background We aimed to assess potential associations of habitual dietary pattern scores in relation to the risk of pre-diabetes (Pre-DM) progression to type 2 diabetes mellitus (T2DM) or the chance of returning to normal glycemia. Methods This cohort study included 334 Pre-DM individuals (mean age of 49.4 years, and 51.5% men) who participated in the third phase of the Tehran Lipid and Glucose Study (2006–2008) and followed up for a median of 9 years. A validated food frequency questionnaire at baseline assessed usual intakes of the participants. Major dietary patterns were identified using principal component analysis. The DASH score and Mediterranean diet score (MDS) were also calculated. Multinomial logistic regression analysis was used to estimate the odds ratios (95% confidence intervals (CIs)) of developing T2DM and returning to normal glycemia in relation to dietary pattern scores. Results During the study follow-up, 39.8% progressed to T2DM, and 39.8% returned to normal glycemia. Three following major dietary patterns, including Western-style (with a higher load of red meats, hydrogenated fats, sodium, and total fat intakes), healthy pattern (with a higher load of whole grains, vegetables, and dairy products), and processed-foods pattern (with a higher load of processed-meats, fast-foods, salty snakes, and sweets and candies) were identified. The Western-style dietary pattern increased the risk of progressing to T2DM by 38% (OR = 1.38; 95% CI = 1.00 to 1.89, P = 0.050). Other dietary pattern scores were not related to regression or progression from Pre-DM. Conclusion The Western-style dietary pattern (characterized by higher load of red meats, hydrogenated fats, sodium intake, and high-GI foods) may accelerate the progression of Pre-DM to T2DM.

Background The potential effects of dietary oxalate (Ox) intake on cardio-renal function have remained unestablished. We evaluated the effect of usual Ox intake and its interaction with dietary calcium (Ca) on incident hypertension (HTN) and chronic kidney disease (CKD). Methods Adult men and women, free of HTN and CKD at baseline (2006–2008), were recruited. Dietary intakes were assessed using a validated food frequency questionnaire, and the outcomes were documented up to 2014–2017. Multivariate Cox proportional hazard regression models were used to estimate the development of HTN and CKD in relation to Ox intakes. Repeated-measures generalized estimating equation (GEE) linear regression models were used to assess possible effect of Ox-intake on the estimated glomerular filtration rate (eGFR) and blood pressure levels over eight years. Results Dietary Ox intakes were positively associated with incident CKD (HR = 2.59, 95% CI = 1.46–4.64) and HTN (HR = 1.79, 95% CI = 1.05–3.04). Compared to high-Ca consumers, subjects who had lower Ca intakes (vs. 1580 mg/d) had a higher incidence of CKD and HTN (HR = 2.43, 95% CI = 1.06–5.55, and HR = 1.72, 95% CI = 0.76–3.78). Participants with higher intakes of Ox (> 220 vs. vs. 77.3, 95% CI = 76.6–78.1 mL/min/1.73m2, Ptime×group = 0.004) and higher SBP levels (112, 95% CI = 111–113 vs. 109, 95% CI = 108–110 mmHg, Ptime×group = 0.007) overtime. Conclusion Higher dietary Ox intake may increase the risk of HTN and CKD. The relation between dietary Ox and risk of HTN and CKD seems to be varied by Ca intake, and subjects with lower Ca intakes may be more burdened by excessive amounts of dietary Ox.

Hyperuricemia, defined as elevated serum concentrations of uric acid (UA) above 416 µmol L−1, is related to the development of cardiometabolic disorders, probably via induction of endothelial dysfunction. Hyperuricemia causes endothelial dysfunction via induction of cell apoptosis, oxidative stress, and inflammation; however, it's interfering with insulin signaling and decreased endothelial nitric oxide (NO) availability, resulting in the development of endothelial insulin resistance, which seems to be a major underlying mechanism for hyperuricemia-induced endothelial dysfunction. Here, we elaborate on how hyperuricemia induces endothelial insulin resistance through the disruption of insulin-stimulated endothelial NO synthesis. High UA concentrations decrease insulin-induced NO synthesis within the endothelial cells by interfering with insulin signaling at either the receptor or post-receptor levels (i.e., proximal and distal steps). At the proximal post-receptor level, UA impairs the function of the insulin receptor substrate (IRS) and phosphatidylinositol 3-kinase (PI3K)/protein kinase B (Akt) in the insulin signaling pathway. At the distal level, high UA concentrations impair endothelial NO synthase (eNOS)-NO system by decreasing eNOS expression and activity as well as by direct inactivation of NO. Clinically, UA-induced endothelial insulin resistance is translated into impaired endothelial function, impaired NO-dependent vasodilation, and the development of systemic insulin resistance. UA-lowering drugs may improve endothelial function in subjects with hyperuricemia.

Ramadan intermittent fasting may affect whole-body metabolism by affecting appetite-related hormones. This systematic review and meta-analysis aimed to clarify the possible effects of Ramadan intermittent fasting on the main hormones regulating appetite and satiety, including leptin and adiponectin. All English language papers in the PubMed, Scopus, and Embase databases were searched using the keywords “Ramadan fasting”, “adiponectin”, and “leptin”, up to 2020. Data extraction was conducted based on the main data of the studies; the primary outcomes of the analysis were mean changes of adiponectin and leptin levels during the holy month of Ramadan in fasted subjects. Data of 16 eligible studies, conducted between 2003 and 2020, were included in the systematic review. Of these, 10 studies with complete data on leptin and adiponectin were included in the meta-analysis. A significant decrease in leptin levels was observed after Ramadan fasting (WMD = −2.28 ng/ml, 95% CI = −3.72, −0.84). Ramadan fasting had no significant effect on adiponectin levels (WMD = 2.19 ng/ml, 95% CI = −0.29, 4.67). Sub-group analysis demonstrated a greater decrease in leptin levels among normal-weight subjects compared to those of overweight/obese subjects (WMD = −4.67 ng/ml, 95% CI = −6.03, −3.31 vs. WMD = −3.43 ng/ml, 95% CI = −5.69, −1.17). Ramadan fasting may decrease leptin levels, especially in normal-weight subjects. There was high heterogeneity, which may be explained by the differences between the wide ranges of study conditions.

Background and aim Hydrogen sulfide (H2S), a signaling gasotransmitter, is involved in carbohydrate metabolism. Here, we aimed to assess the potential association between serum H2S and dysglycemia in the framework of a population-based study. Methods Adults men and women with completed data (n = 798), who participated in the Tehran Lipid and Glucose Study (2014–2017) were included in the study. Medians of fasting serum H2S concentration were compared across the glycemic status of the participants, defined as type 2 diabetes mellitus (T2DM), isolated impaired fasting glucose (IIFG), isolated impaired glucose tolerance (IIGT), combined IFG-IGT, and normal glycemia [i.e., those with both normal fasting glucose (NFG) and normal glucose tolerance (NGT)]. Multinomial logistic regression was used to assess potential associations between serum H2S and the defined glycemic status. Results Mean age of the participants was 45.1 ± 14.0 y, and 48.1% were men. Prevalence of T2DM, IIFG, IIGT, and combined IFG-IGT was 13.9, 9.1, 8.1, and 4.8% respectively. No significant difference was observed in serum H2S concentrations between the groups. Lower serum H2S ( Conclusion Reduced serum H2S level may be associated with impaired glucose tolerance.

Background We aimed to estimate salt intake among an Iranian population using spot urine-based equations and a dietary-based method. Methods Adult men and women (n = 2069) were recruited from the Tehran Lipid and Glucose Study (2014–2017). Urinary sodium (Na), potassium (K), and creatinine (Cr) concentrations were measured in the morning spot urine samples. The 24-h urinary Na excretion and predicted salt intake was estimated using five equations, i.e., Kawasaki, Tanaka, Intersalt, Toft, and Whitton. A validated food frequency questionnaire (FFQ) was used to obtain dietary intake of salt. The agreement of each urinary- and FFQ-based salt estimation with the overall mean of the methods, considered as the gold standard, was assessed using the Bland–Altman method. Results Mean age of the participants was 45.6 ± 14.8 y, and 45.4% were men. Mean (SD) estimated salt intake, derived from the overall mean of the methods, was 9.0 ± 2.2 g/d (10.2 ± 2.1 and 7.9 ± 1.7 g/d in men and women, respectively). Mean bias of the estimations from the overall mean ranged from − 0.2.42 to 2.75 g/d, with the Tanaka equation having the least bias (mean bias = 0.13 ± 1.10, 95% CI − 2.37, 2.30 g/d). Tanaka estimated a mean salt intake of 8.9 g/d (range 2.1 to 18.7 g/d); accordingly, only 5.1% of participants adhered to the recommendation ( Conclusion The Tanaka equation could provide a more accurate mean-population estimated salt intake from casual urinary Na concentration in our population. About 95% of the Iranian population exceeded the current recommendations of salt intake.

Background Abnormal levels of liver enzymes, particularly aminotransferases, are prognostic features of non-alcoholic fatty liver disease (NAFLD). Considering the important role of dietary intakes in development of NAFLD, we aimed to determine possible association of unhealthy foods (fast foods, soft drinks, sweet and salty snacks) consumption with elevated levels of aminotransferases. Methods This cross-sectional study was conducted within the framework of sixth phase of the Tehran Lipid and Glucose Study (2014–2017), on 187 adult men and 249 adult women (19–70 y). Usual intakes of unhealthy foods (kcal/week) were measured using a validated semi-quantitative 147-items food frequency questionnaire. Serum levels of alanine aminotransferase (ALT), aspartate aminotransferase (AST) were measured. Multivariable logistic regression models were used to estimate the odds of elevated aminotransferases in each tertile of energy-dense unhealthy foods. Results Mean age of participants was 44.44 ± 15.09 years, 43% of participants were men. Higher consumption of fast foods (> 11.39% kcal/week) was associated with elevated ALT to AST ratio (OR: 3.27; 95% CI: 1.90–5.63) and elevated ALT (OR: 2.74; 95% CI: 1.57–4.76). Also, each 1 SD increased energy intakes from fast foods was related to increased chance of having elevated ALT and ALT to AST ratio by 35% (OR: 1.35; 95% CI: 1.08–1.68, OR: 1.35; 95% CI: 1.10–1.66, respectively). There was no significant association between consumption of soft drinks, sweet or salty snacks and elevated aminotransferases. Conclusions Higher intakes of energy from fast foods seems to be associated with an elevated serum levels of ALT and ALT to AST ratio, as indicators of development of NAFLD.

Our aim was to investigate the relationship between metabolic syndrome (MetS) and energy-dense nutrient-poor solid snacks intakes during 3.6 y of follow-up among children and adolescents.This population-based longitudinal study was conducted within the framework of the Tehran Lipid and Glucose Study, on 424 MetS free subjects, aged 6-18 y. Data on consumption of energy-dense nutrient-poor solid snacks, sweet and salty snacks, were collected at baseline (2006-2008). Logistic regression, adjusted for age, sex, total energy intake, physical activity, dietary fiber, family history of diabetes, and body mass index, was used to assess the relationship between snacks and incident MetS.After adjustment for confounders, compared with the lowest quartile of total energy-dense nutrient-poor solid snacks, odds ratio of incident MetS in the highest quartile was 3.04 (95% confidence interval (CI): 1.11-8.49); for sweet snacks this was 2.88 (95% CI: 1.00-8.32), and for salty ones it was 2.85 (95% CI: 1.09-7.43). The risk of incident hypertension in the highest, compared with the lowest quartile of total and salty snacks, was 2.99 (95% CI: 1.00-8.93) and 3.35 (95% CI: 1.10-10.17), respectively.Energy-dense nutrient-poor solid snacks, both salty and sweet, may have undesirable effects on the incidence of MetS, with salty snacks having the potential to increase risk of incident hypertension in children and adolescents as well.

The epidemiological association of phytochemical-rich foods with the risk of hypertension is unclear. This study aimed to determine the association of dietary phytochemical index (PI) with the occurrence of hypertension (HTN) after 3 years of follow-up in Tehranian adults.This prospective study was conducted on 1546 nonhypertensive subjects, aged 20-70 years. Dietary intake was collected by validated semiquantitative food frequency questionnaire (FFQ). Dietary PI was calculated as (dietary energy derived from phytochemical-rich foods (kcal)/total daily energy intake (kcal)) × 100. Blood pressure was measured at baseline and after 3 years of follow-up and HTN was defined by Joint National Committee on prevention, detection, evaluation and treatment of high blood pressure criteria. The odds of HTN after 3 years in each quartile category of dietary PI were estimated by logistic regression model and adjusted for potential variables.The mean age of participants was 38.0±12.0 years and 43% were male. The mean dietary PI was 29.1±11.8. After 3 years of follow-up, 265 (17.1%) new cases of HTN were identified. No significant changes were observed in the systolic and diastolic blood pressure across quartile categories of dietary PI. After adjustment for confounders, the odds (95% confidence interval) of HTN across quartiles of dietary PI were 1.00, 0.97 (0.62-1.38), 0.69 (0.45-1.07) and 0.52 (0.32-0.84) (P for trend=0.004).Consumption of phytochemical-rich foods may prevent the development of HTN. Further investigations are, however, recommended.

There are growing concern globally regarding fast food consumption and its related cardiometabolic outcomes. In this study we investigated whether fast food consumption could affect the occurrence of metabolic syndrome (MetS) after 3-years of follow-up in adults.This longitudinal study was conducted in the framework of Tehran Lipid and Glucose Study on 1476 adults, aged 19-70 y. The usual intakes of participants were measured using a validated semi-quantitative food frequency questionnaire at baseline. Biochemical and anthropometric measurements were assessed at baseline (2006-2008) and 3 years later (2009-2011). Multiple logistic regression models were used to estimate the occurrence of the MetS in each quartile of fast food consumption.The mean age of participants was 37.8±12.3 y, and mean BMI was 26.0±4.5 kg/m(2) at baseline. Participants in the highest quartile of fast food consumption were younger (33.7 vs 43.4 years, P0.01). Higher consumption of fast food was accompanied with more increase in serum triglyceride levels and triglyceride to HDL-C ratio after the 3-year follow-up. After adjustment for all potential confounding variables, the risk of metabolic syndrome, in the highest quartile of fast foods compared with the lowest, was 1.85 (95% CI=1.17-2.95). The effects of fast food consumption on the occurrence of MetS were more pronounced in younger adults (30 years), and participants who had greater wait to hip ratio, consumed less phytochemical-rich foods or had low-fiber diet (P0.05).We demonstrated that higher consumption of fast foods had undesirable effects on metabolic syndrome after 3-years of follow-up in Iranian adults.

Background We investigated the association of regular dietary intake of L-arginine and both the incidence of coronary heart disease (CHD) and changes of blood pressure. Methods Eligible adults (n = 2284) who participated in the Tehran Lipid and Glucose Study were followed for a mean of 4.7 years. Dietary intake of L-arginine was assessed at baseline (2006–2008); biochemical variables were evaluated at baseline and the follow-up examination. Multivariate Cox proportional hazard regression models adjusted for potential confounders were used to estimate the risk of CHD across tertiles of L-arginine intake. Linear regression models were also used to indicate the association of L-arginine intake with changes of serum lipids and blood pressure during the follow-up. Results Mean age of participants (42.8 % men) was 38.2 ± 13.4, at baseline. During a mean 4.7 ± 1.4 y of follow-up, 57 participants experienced CHD events. A significant negative association was observed between plant-derived L-arginine intake and changes of both systolic and diastolic blood pressure, whereas animal-derived L-arginine intake was related to increased levels of diastolic blood pressure (P

Background and aim The ability of inorganic nitrate and nitrite to convert to nitric oxide (NO), and some of its properties e.g. regulation of glucose metabolism, vascular homeostasis, and insulin signaling pathway, have recently raised the hypothesis that inorganic nitrate and nitrite could be potential therapeutic agents in type 2 diabetes. In this review, we reviewed experimental and clinical studies investigating the effect of nitrate/nitrite administration on various aspects of type 2 diabetes. Findings Studies showed that an altered metabolism of nitrate/nitrite and impaired NO pathway occurs in diabetes which could contribute to its complications. Some important beneficial properties, including regulation of glucose homeostasis and insulin signaling pathway, improvement of insulin resistance and vascular function, hypotensive, hypolipidemic as well as anti-inflammatory and anti-oxidative effects have been observed following administration of inorganic nitrate/nitrite. Conclusion It seems that dietary nitrate/nitrite could be a compensatory fuel for a disrupted nitrate/nitrite/NO pathway and related disorders in diabetes. Although some beneficial properties of nitrate/nitrite have been reported by experimental investigations, long-term clinical studies with various doses of inorganic nitrate/nitrite supplementation, are recommended to confirm these effects.