Usual intake of dairy products and the chance of pre-diabetes regression to normal glycemia or progression to type 2 diabetes: a 9-year follow-up.

BACKGROUND: We assessed the possible effect of usual dairy consumption on pre-diabetes (Pre-DM) remission or progression to type 2 diabetes (T2D). METHODS: Pre-DM adults (n = 334, mean age of 49.4 years, and 51.5% men) were assessed for dairy intakes (2006-2008) and followed up to 9 years for incidence of T2D or normal glycemia (NG). All biochemical measurements were done at baseline and all subsequent examinations with 3-y follow-up intervals. Multinomial regression models with adjustment of confounding variables were used to estimate odds ratios (OR) and 95% confidence intervals (CIs) of incident T2D and NG for each serving/d dairy consumption. RESULTS: The odds of NG was significantly elevated by 69% (OR = 1.69, 95% CI = 1.00-2.86, P = 0.05) per 200 g/d increased high-fat dairy intake, while the amount of total dairy or low-fat dairy was not related to the outcomes. Higher intakes of yogurt were more likely to be associated with an increased odds of NG (OR = 1.82, 95% CI = 1.20-2.74, P = 0.01). Usual intakes of milk, cheese, or cream-butter were not associated to Pre-DM remission or progression to T2D. CONCLUSION: Regular dairy consumption may increase the chance of Pre-DM regression to NG.

Higher ultra-processed food intake is associated with an increased incidence risk of cardiovascular disease: the Tehran lipid and glucose study.

BACKGROUND: Cardiovascular disease (CVD) is a major cause of death worldwide, although limited data are currently available regarding the impact of consuming ultra-processed food (UPF) on its incidence. Given the increased consumption of UPF in Iran, we aimed to investigate the association between UPF intake and CVD risk. METHODS: Individuals without CVD (n = 2050) aged ≥ 30 years old were recruited from the Tehran Lipid and Glucose Study (TLGS). Dietary data were collected using a validated food frequency questionnaire (FFQ) and UPF intakes were assessed based on the Nova food classification. Multivariable Cox proportional hazard models adjusted for potential confounders were used to estimate the hazard ratio (HR) and 95% confidence intervals (95% CI) for the risk of CVD across tertiles of UPF intake. RESULTS: A 10.1% incidence of CVD occurred over a median follow-up of 10.6 years, with a 22% increase in CVD risk per each 50 g/day UPF intake. Participants with the highest intake of UPF had a 68% greater incidence of CVD compared to those with the lowest intake (HR = 1.68, 95% CI=1.14-2.48) after controlling for potential confounders. Regarding sub-groups of UPF, participants in the 3rd tertile compared to the reference had a significantly increased risk of CVD (HR = 1.56, 95% CI=1.04-2.34). Nevertheless, intake of bread, fast food, sweetened beverages, sweets and desserts, high-fat dairy products, and other UPFs were not associated with greater CVD risk. CONCLUSION: Our findings support the hypothesis that the incidence of CVD is enhanced with the higher consumption of UPF in a representative sample of the Iranian population.

Adipose organ dysfunction and type 2 diabetes: Role of nitric oxide.

Adipose organ, historically known as specialized lipid-handling tissue serving as the long-term fat depot, is now appreciated as the largest endocrine organ composed of two main compartments, i.e., subcutaneous and visceral adipose tissue (AT), madding up white and beige/brown adipocytes. Adipose organ dysfunction manifested as maldistribution of the compartments, hypertrophic, hypoxic, inflamed, and insulin-resistant AT, contributes to the development of type 2 diabetes (T2D). Here, we highlight the role of nitric oxide (NO·) in AT (dys)function in relation to developing T2D. The key aspects determining lipid and glucose homeostasis in AT depend on the physiological levels of the NO· produced via endothelial NO· synthases (eNOS). In addition to decreased NO· bioavailability (via decreased expression/activity of eNOS or scavenging NO·), excessive NO· produced by inducible NOS (iNOS) in response to hypoxia and AT inflammation may be a critical interfering factor diverting NO· signaling to the formation of reactive oxygen and nitrogen species, resulting in AT and whole-body metabolic dysfunction. Pharmacological approaches boosting AT-NO· availability at physiological levels (by increasing NO· production and its stability), as well as suppression of iNOS-NO· synthesis, are potential candidates for developing NO·-based therapeutics in T2D.

Severity of adipose tissue dysfunction is associated with progression of pre-diabetes to type 2 diabetes: the Tehran Lipid and Glucose Study.

BACKGROUND: The association of prediabetes (Pre-DM) regression and progression with visceral adiposity index (VAI) and adipose tissue dysfunction (ATD) remains to be investigated. METHODS: The present cohort study was conducted within the framework of the Tehran Lipid and Glucose Study (TLGS) on 1458 Pre-DM cases (aged ≥ 21 years) who were followed for nine years. VAI was estimated based on waist circumference, body mass index, triglycerides, and high-density lipoprotein cholesterol. ATD status (i.e., absent, mild-moderate, and severe) was defined based on the age-stratified cutoff values of VAI. Multinomial logistic regression models with adjustment of potential confounders were used to estimate the chance of Pre-DM regression to normoglycemia or progression to T2D across ATD status. RESULTS: During the study follow-up, 39.0% of the participants developed T2D, and 37.7% returned to normoglycemia. Compared to mild-moderate ATD, Pre-DM subjects with severe ATD had a higher risk of developing T2D by 45% (OR = 1.45, 95% CI = 11.08-1.93). Severe ATD was also associated with a decreased chance of returning to normoglycemia by 26% (OR = 0.74, 95% CI = 0.55-0.99). Participants with severe ATD had significantly higher fasting (overall mean = 111, 95% CI = 109-112 vs. 106, 95% CI = 105-108 mg/dL) and 2h-serum glucose (overall mean = 165, 95% CI = 161-168 vs. 153, 95% CI = 149-156 mg/dL) concentrations over time. CONCLUSION: Severe ATD was associated with an elevated risk of developing T2D and longitudinal poor-glycemic controls in Pre-DM subjects. ATD may be a simple and useful index for detecting subjects at a higher risk of Pre-DM progression to T2D, allowing for timely intervention strategies.

Vascular nitric oxide resistance in type 2 diabetes.

Vascular nitric oxide (NO•) resistance, manifested by an impaired vasodilator function of NO• in both the macro- and microvessels, is a common state in type 2 diabetes (T2D) associated with developing cardiovascular events and death. Here, we summarize experimental and human evidence of vascular NO• resistance in T2D and discuss its underlying mechanisms. Human studies indicate a ~ 13-94% decrease in the endothelium (ET)-dependent vascular smooth muscle (VSM) relaxation and a 6-42% reduced response to NO• donors, i.e., sodium nitroprusside (SNP) and glyceryl trinitrate (GTN), in patients with T2D. A decreased vascular NO• production, NO• inactivation, and impaired responsiveness of VSM to NO• [occurred due to quenching NO• activity, desensitization of its receptor soluble guanylate cyclase (sGC), and/or impairment of its downstream pathway, cyclic guanosine monophosphate (cGMP)-protein kinase G (PKG)] are the known mechanisms underlying the vascular NO• resistance in T2D. Hyperglycemia-induced overproduction of reactive oxygen species (ROS) and vascular insulin resistance are key players in this state. Therefore, upregulating vascular NO• availability, re-sensitizing or bypassing the non-responsive pathways to NO•, and targeting key vascular sources of ROS production may be clinically relevant pharmacological approaches to circumvent T2D-induced vascular NO• resistance.

Higher daily physical activity levels may facilitate pre-diabetes regression to normoglycemia: A longitudinal study among an Iranian population.

The possible association of habitual physical activity (PA) and the risk of pre-diabetes (Pre-DM) progression to type 2 diabetes (T2D) or the chance of returning to normoglycemia was investigated. This cohort study included 1167 Pre-DM individuals (mean age of 53.5 years, and 45.3% men) who participated in the third phase of the Tehran Lipid and Glucose Study (2006-2008) and followed up to a median of 9 years. PA, including leisure time and job activities, was measured using a reliable and validated Iranian version of the Modifiable Activity Questionnaire and reported as metabolic equivalent (MET)-minutes per week. The odds ratios (ORs) and 95% confidence intervals (CIs) of incident T2D and returning to normoglycemia were estimated in relation to PA levels (i.e., per every 500 MET-minutes/week, or across categories of PA levels < 600 as a reference, 600-1500 and > 1500 MET-minutes/week). During the study follow-up, 39.0 % progressed to T2D, and 37.8% returned to normoglycemia. Compared to subjects with a PA < 600 MET-minutes/week, the chance of regression to normoglycemia increased by 58% [OR = 1.58, 95% CI = 1.03-2.40 âˆ¼ relative risk (RR) = 1.32, 95% CI = 1.02-1.63] among the participants who had a PA > 1500 MET-minutes/week. We further noted that each 500 MET-min/week activity corresponded to an elevated chance of returning to normoglycemia by 5% (OR = 1.05, 95% CI = 1.01-1.11). The study's findings provided evidence that higher daily PA levels may facilitate Pre-DM regression to normoglycemia. The beneficial effect of PA in Pre-DM subjects needs to exceed the recommended levels (i.e., 600 MET-minutes/week).

Dietary sodium to potassium ratio is an independent predictor of cardiovascular events: a longitudinal follow-up study.

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 < 3049 mg/d) was significantly related to the increased risk of CVD (HR = 1.99, 95% CI = 1.06-3.74). Independent of the well-known risk factors, a 56% reduced risk of CVD was observed in the participants with a higher dietary K intake (HR = 0.44, 95% CI = 0.20-0.94). A Higher Na-to-K ratio was associated with an increased risk of CVD (HR = 1.99, 95% CI = 1.13-3.52). CONCLUSION: Our study showed that the Na-to-K ratio might independently predict future risk of CVD events in adults.

Scientific Publishing in Biomedicine: A Brief History of Scientific Journals.

Scientific publishing, with about 350-year historical background, has played a central role in advancing science by disseminating new findings, generalizing accepted theories, and sharing novel ideas. The number of scientific journals has exponentially grown from 10 at the end of the 17th century to 100,000 at the end of the 20th century. The publishing landscape has dramatically changed over time from printed journals to online publishing. Although scientific publishing was initially non-commercial, it has become a profitable industry with a significant global financial turnover, reaching $28 billion in annual revenue before the COVID-19 pandemic. However, scientific publishing has encountered several challenges and is suffering from unethical practices and some negative phenomena, like publish-or-perish, driven by the need to survive or get a promotion in academia. Developing a global landscape with collaborative non-commercial journals and platforms is a primary proposed model for the future of scientific publishing. Here, we provide a brief history of the foundation and development of scientific journals and their evolution over time. Furthermore, current challenges and future perspectives of scientific publishing are discussed.

Dietary pattern scores in relation to pre-diabetes regression to normal glycemia or progression to type 2 diabetes: a 9-year follow-up.

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.

High-Fat Dairy Products May Decrease the Risk of Chronic Kidney Disease Incidence: A Long-Term Prospective Cohort Study.

OBJECTIVE: The association between consumption of dairy products and risk of chronic kidney disease (CKD) is under debate. We aimed to determine the potential effects of total and subtypes of dairy intake on the occurrence of CKD. METHODS: This study was conducted within the Tehran Lipid and Glucose Study (TLGS) on 2416 CKD-free adults. At baseline, consumption of dairy products was estimated using a validated 168-items semiquantitative food frequency questionnaire. Adjusted hazard ratios (HRs) and 95% confidence intervals (CIs) of CKD were calculated in tertile categories of dairy products. Also, the CKD risk was estimated with multivariable Cox regression to substitute total dairy with other dietary protein sources. RESULTS: During 8.4 years of follow-up, the incidence rate of CKD was 21%. The participants' mean (±SD) age was 38 (±13) years and 46% were men. Dietary intakes of total dairy, low-fat dairy, and fermented dairy were not associated with CKD risk. There were significant lower risks of CKD in the highest compared to the lowest tertiles of high-fat dairy (HR = 0.76, 95% CI = 0.60-0.95) and high-fat milk (HR = 0.75, 95% CI = 0.59-0.96). However, no significant associations were found between other categories of dairy products and CKD incidence. Substitutions of total dairy with other dietary protein sources were not associated with CKD risk. CONCLUSIONS: In this study, higher intakes of high-fat dairy and high-fat milk were associated with lower risks of CKD. No significant associations were found between other dairy products and CKD. More prospective and clinical trials are needed to clarify the issue.

Dietary oxalate-calcium balance and the incidence of hypertension and chronic kidney disease: a prospective study among an Asian population.

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 (< 990 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. < 150 mg/d) had lower eGFR values (75.3, 95% CI = 75.0-76.5 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.

Scientific Publishing in Biomedicine: Information Literacy.

The literature review is an integral part of the research process, from developing research ideas to disseminating findings. It involves explaining, interpreting, and summarizing published materials around a topic to elaborate a research hypothesis/question, synthesize new concepts, identify knowledge gaps, develop new theories, and identify new research directions. Effective reading and processing of the literature (i.e., analyzing and synthesizing) and actual writing of the literature (verbal or non-verbal output, e.g., tables and figures) are essential stages of an effective literature review. This article provides a practical guide to conducting an effective literature review. In addition, literature search and evaluation are also briefly discussed.

Saturated Fatty Acid Intake and Risk of Type 2 Diabetes: An Updated Systematic Review and Dose-Response Meta-Analysis of Cohort Studies.

This systematic review and meta-analysis was conducted to pool findings of cohort studies that investigated hazards of type 2 diabetes mellitus (T2DM) in relation to intakes of SFAs. A systematic search was conducted in the PubMed, Scopus, and Embase databases up to June 2021 to find eligible studies. Review articles or commentaries, clinical trials, cross-sectional studies, studies on gestational or type 1 diabetes patients, animal studies, articles with no access to full-texts, articles published in non-English languages, and articles with missing critical data needed for the systematic review were excluded from the meta-analysis. A random-effects model was used to combine study-specific results. Thirteen cohort studies with 361,686 participants and 11,865 T2DM events were included. Dietary total SFA intake, as well as dietary palmitic acid (PA) or stearic acid (SA) were not associated with risk of T2DM when the highest was compared with the lowest intake category (HR = 0.99; 95% CI: 0.91, 1.09; n = 13 for total SFAs; HR = 0.96; 95% CI: 0.79, 1.15; n = 4 for PA; and HR = 1.08; 95% CI: 0.79, 1.49; n = 4 for SA). However, the risk of T2DM decreased by 11% in the highest compared with the lowest category of dietary lauric acid (HR = 0.89; 95% CI: 0.82, 0.97; n = 2), and by 17% in the highest compared with lowest category of dietary myristic acid (MA) (HR = 0.83; 95% CI: 0.74, 0.92; n = 3). There was evidence of publication bias among studies on dietary total SFAs and T2DM. Our results indicated no significant association between dietary total SFA and risk of T2DM. However, dietary intake of MA was negatively associated with developing T2DM.

Inulin intake and the incidence of cardiometabolic diseases: a prospective cohort study.

Inulin is a prebiotic and has beneficial effects on health, such as improving the immune function, lipid profile, and gut microbiota. Some previous studies have assessed the effects of inulin supplementation on cardiometabolic diseases, but the relationship between dietary inulin and these diseases has not been investigated yet. Thus, this survey was designed to assess the potential association between the dietary intake of inulin and the incidence of cardiometabolic diseases, including cardiovascular disease (CVD), hypertension (HTN), chronic kidney disease (CKD), and type 2 diabetes (T2D) among adults. The present prospective cohort study was conducted on participants in the third wave of the Tehran Lipid and Glucose Study (2006-2008) and was followed up until March 2018. The dietary intake of inulin was estimated using a special database that reports values of inulin and oligofructose in grams per 100 g of each food. Cox proportional hazards regression showed that higher consumption of inulin was associated with a lower risk of HTN (HR: 0.79, 95% CI: 0.63 to 0.99) and T2D (HR: 0.94, 95% CI: 0.89 to 1.00). We found no relationship between higher consumption of dietary inulin and the incidence of CKD and CVD in our population. According to our results, it seems inulin from foods had a preventive effect against HTN and T2D, which are major risk factors for cardiovascular and renal events. However, more investigations are warranted.

Carbon monoxide and ß-cell function: Implications for type 2 diabetes mellitus.

Carbon monoxide (CO), a member of the multifunctional gasotransmitters family produced by heme oxygenases (i.e., HO-1 and HO-2), has received significant attention because of its involvement in carbohydrate metabolism. Experimental evidence indicates that both HO-2- and HO-1-derived CO stimulate insulin secretion, but the latter mainly acts as a compensatory response in pre-diabetes conditions. CO protects pancreatic ß-cell against cytokine- and hypoxia-induced apoptosis and promotes ß-cell regeneration. CO cross-talks with nitric oxide (NO) and hydrogen sulfide (H2S), other important gasotransmitters in carbohydrate metabolism, in regulating ß-cell function and insulin secretion. These data speak in favor of the potential therapeutic application of CO in type 2 diabetes mellitus (T2DM) and preventing the progression of pre-diabetes to diabetes. Either CO (as both gaseous form and CO-releasing molecule) or pharmacological formulations made of natural HO inducers (i.e., bioactive components originating from plant-based foods) are potential candidates for developing CO-based therapeutics in T2DM. Future studies are needed to assess the safety/efficacy and potential therapeutic applications of CO in T2DM.

Scientific Publishing in Biomedicine: Revising a Peer-reviewed Manuscript.

Getting feedback from the journals' editorial office upon the peer-review process, revising the manuscript, and responding to reviewers' comments are the essential parts of scientific publishing. The process of revising seems cumbersome and time-consuming as authors must be engaged probably with many comments and requested changes. Authors are advised to approach the reviewer as a consultant rather than an adversary. They should carefully read and understand comments and then decide how to proceed with each requested change/suggestion. In the case of serious disagreement with reviewer comments or misunderstanding, authors can defer the issue to the editor. Preparing a scientific and well-organized "response to reviews" and the revised version of the manuscript can increase the chance of acceptance. Here, we provide a practical guide on dealing with different types of comments (i.e., minor or major revisions, conflicting comments, or those that authors disagree with or cannot adhere to) and how to craft a response to reviews. We also provide the dos and don'ts for making a successful revision.

Association between serum hydrogen sulfide concentrations and dysglycemia: a population-based study.

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 (< 39.6 µmol/L) was associated with an increased chance of having IIGT (OR = 1.96, 95% CI = 1.15-3.34) in the adjusted model. CONCLUSION: Reduced serum H2S level may be associated with impaired glucose tolerance.

Dietary oxalate to calcium ratio and incident cardiovascular events: a 10-year follow-up among an Asian population.

BACKGROUND AND AIM: The potential cardiovascular impact of usual intakes of oxalate (Ox) is uninvestigated. We evaluated the effect of dietary Ox and its interaction with dietary calcium (Ca) on incident cardiovascular disease (CVD). METHODS: We included 2966 adult men and women aged 19-84 y without known CVD during baseline enrollment (2006-2008) of the Tehran Lipid and Glucose Study. Dietary intakes were assessed using a validated FFQ, and incident CVD (i.e., coronary heart disease, stroke, and CVD mortality) were documented through March 2018. RESULTS: A 7.1% incident of CVD occurred during a median follow-up of 10.6 y. After multivariable adjustment for traditional risk factors and key dietary nutrients, including total fat and fiber, Ox intakes ≥220 mg/d increased incident CVD (HR T3 vs. T1 = 1.47, 95% CI = 1.02-2.12). This association was potentiated (HR T3 vs. T1 = 2.42, 95% CI = 1.19-4.89) in subjects who had a lower intake of Ca (< 981 mg/d); in a low-Ca diet, an even lower amount of dietary Ox (second tertile, 148-220 mg/d) was related to increased CVD events by 92% (HR = 1.92, 95% CI = 1.00-3.70). No association was observed between dietary Ox and CVD events in the presence of medium- and high levels of Ca intakes. The critical cut-off point of Ox-to-Ca for predicting CVD events was 0.14, which was related to an increased risk of CVD by 37% (HR = 1.37, 95% CI = 1.02-1.84). CONCLUSION: Higher dietary Ox intake appeared to be associated with a modestly elevated risk of incident CVD, especially in a diet with a lower amount of Ca.

Monitoring population salt intake using casual urinary sodium: Tehran Lipid and Glucose Study.

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 (< 5 g/d salt intake), whereas 26.8% and 2.4% exceeded the recommendation by 2- and threefold. 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.

Spot urinary microalbumin concentration, metabolic syndrome and type 2 diabetes: Tehran lipid and glucose study.

AIM: This study aimed to determine the association of urinary microalbumin concentrations with type 2 diabetes mellitus (T2DM), metabolic syndrome (MetS), and its phenotypes. The optimum cut-off values of urinary microalbumin and microalbumin-to-creatinine ratio (MCR) for predicting the chance of having T2DM and MetS were also defined. METHODS: Adult men and women (n = 1192) participated in the sixth phase (2014-2017) of the Tehran Lipid and Glucose Study (TLGS), with completed data, were included in the analyses. Odds ratios (ORs) (and 95% confidence intervals (CIs)) of T2DM, MetS, and its components across tertile categories of urinary microalbumin concentrations were estimated using multivariable logistic regressions. The optimal cut-off points of urinary microalbumin and MCR were determined using the receiver operator characteristic (ROC) curve analysis. RESULTS: Participants' mean (±SD) age was 44.9 (±14.0) years, and 44.6% of the participants were men. The prevalence of microalbuminuria was 14.4%. Chance of having T2DM was significantly higher in the highest tertile of urinary microalbumin concentration (OR = 2.29, 95% CI = 1.43-3.67) and MCR (OR = 1.82, 95% CI = 1.15-2.89). Subjects with the highest urinary microalbumin concentration were more likely to have MetS (OR = 1.66, 95% CI = 1.17-2.35), hypertension (OR = 1.63, 95% CI = 1.16-2.30) and hyperglycemia (OR = 1.78, 95% CI = 1.24-2.56). No significant association was observed between urinary microalbumin concentrations and other components of MetS. The optimal cut-off points of urinary microalbumin for predicting the chance of having T2DM and MetS were 14.0 and 13.6 mg/L, respectively. CONCLUSIONS: Elevated spot urinary microalbumin, below the values defined as microalbuminuria, was associated with the chance of having T2DM and MetS.