Walking speed and the risk of type 2 diabetes: a systematic review and meta-analysis.

OBJECTIVE: To investigate the association between walking speed and the risk of type 2 diabetes. DESIGN: Systematic review and meta-analysis. DATA SOURCES: PubMed, Scopus, CENTRAL and Web of Science to 30 May 2023. ELIGIBILITY CRITERIA FOR SELECTING STUDIES: We included cohort studies that explored the association between walking speed and the risk of type 2 diabetes in adults. We used random-effects meta-analyses to calculate relative risk (RR) and risk difference (RD). We rated the credibility of subgroup differences and the certainty of evidence using the Instrument to assess the Credibility of Effect Modification ANalyses (ICEMAN) and Grading of Recommendations Assessment, Development and Evaluation (GRADE) tools, respectively. RESULTS: Ten cohort studies were included. Compared with easy/casual walking (<3.2 km/hour), the RR of type 2 diabetes was 0.85 (95% CI 0.70 to 1.00); RD=0.86 (95% CI 1.72 to 0) fewer cases per 100 patients; n=4, GRADE=low) for average/normal walking (3.2-4.8 km/hour), 0.76 (95% CI 0.65 to 0.87); RD=1.38 (95% CI 2.01 to 0.75) fewer cases per 100 patients; n=10, GRADE=low) for fairly brisk walking (4.8-6.4 km/hour) and 0.61 (95% CI 0.49 to 0.73; RD=2.24 (95% CI 2.93 to 1.55) fewer cases per 100 patients; n=6, GRADE=moderate) for brisk/striding walking (>6.4 km/hour). There was no significant or credible difference across subgroups based on adjustment for the total volume of physical activity and time spent walking per day. Dose-response analysis suggested that the risk of type 2 diabetes decreased significantly at a walking speed of 4 km/h and above. CONCLUSIONS: Low to moderate certainty evidence, mainly from studies with a high risk of bias, suggests that walking at faster speeds is associated with a graded decrease in the risk of type 2 diabetes. PROSPERO REGISTRATION NUMBER: CRD42023432795.

Central fatness and risk of all cause mortality: systematic review and dose-response meta-analysis of 72 prospective cohort studies.

OBJECTIVE: To quantify the association of indices of central obesity, including waist circumference, hip circumference, thigh circumference, waist-to-hip ratio, waist-to-height ratio, waist-to-thigh ratio, body adiposity index, and A body shape index, with the risk of all cause mortality in the general population, and to clarify the shape of the dose-response relations. DESIGN: Systematic review and meta-analysis. DATA SOURCES: PubMed and Scopus from inception to July 2019, and the reference lists of all related articles and reviews. ELIGIBILITY CRITERIA FOR SELECTING STUDIES: Prospective cohort studies reporting the risk estimates of all cause mortality across at least three categories of indices of central fatness. Studies that reported continuous estimation of the associations were also included. DATA SYNTHESIS: A random effects dose-response meta-analysis was conducted to assess linear trend estimations. A one stage linear mixed effects meta-analysis was used for estimating dose-response curves. RESULTS: Of 98 745 studies screened, 1950 full texts were fully reviewed for eligibility. The final analyses consisted of 72 prospective cohort studies with 2 528 297 participants. The summary hazard ratios were as follows: waist circumference (10 cm, 3.94 inch increase): 1.11 (95% confidence interval 1.08 to 1.13, I2=88%, n=50); hip circumference (10 cm, 3.94 inch increase): 0.90 (0.81 to 0.99, I2=95%, n=9); thigh circumference (5 cm, 1.97 inch increase): 0.82 (0.75 to 0.89, I2=54%, n=3); waist-to-hip ratio (0.1 unit increase): 1.20 (1.15 to 1.25, I2=90%, n=31); waist-to-height ratio (0.1 unit increase): 1.24 (1.12 to 1.36, I2=94%, n=11); waist-to-thigh ratio (0.1 unit increase): 1.21 (1.03 to 1.39, I2=97%, n=2); body adiposity index (10% increase): 1.17 (1.00 to 1.33, I2=75%, n=4); and A body shape index (0.005 unit increase): 1.15 (1.10 to 1.20, I2=87%, n=9). Positive associations persisted after accounting for body mass index. A nearly J shaped association was found between waist circumference and waist-to-height ratio and the risk of all cause mortality in men and women. A positive monotonic association was observed for waist-to-hip ratio and A body shape index. The association was U shaped for body adiposity index. CONCLUSIONS: Indices of central fatness including waist circumference, waist-to-hip ratio, waist-to-height ratio, waist-to-thigh ratio, body adiposity index, and A body shape index, independent of overall adiposity, were positively and significantly associated with a higher all cause mortality risk. Larger hip circumference and thigh circumference were associated with a lower risk. The results suggest that measures of central adiposity could be used with body mass index as a supplementary approach to determine the risk of premature death.

Adult weight gain and the risk of cardiovascular disease: a systematic review and dose-response meta-analysis of prospective cohort studies.

We aimed to examine the association of weight gain during adulthood with the risk of cardiovascular disease (CVD) in the general population. We performed a systematic search of PubMed and Scopus, from inception to June 2019. Prospective cohort studies investigating the association of weight gain during adulthood with the risk of CVD were included. The relative risks (RRs) were calculated by using random-effect models. Twenty-three prospective cohort studies with 1,093,337 participants were included. The RRs for a 5-kg increment in body weight were 1.11 (95% CI: 1.04, 1.19; I2 = 80%, n = 11) for CVD mortality, 1.18 (95% CI: 1.04, 1.32; I2 = 90%, n = 8) for coronary heart disease (CHD), 1.08 (95% CI: 1.04, 1.12; I2 = 0%, n = 3) for stroke, 1.18 (95% CI: 1.12, 1.25; I2 = 0%, n = 2) for myocardial infarction and 1.05 (95% CI: 0.86, 1.23; I2 = 80%, n = 2) for heart failure. A dose-response analysis demonstrated that the risk of CVD mortality was unchanged with weight gain of 0-5 kg, and then increased sharply and linearly (P for nonlinearity < 0.001). The analysis of CHD indicated a sharp increase in risk from baseline up to weight gain equal to 25 kg (P for nonlinearity = 0.12). Adult weight gain may be associated with a higher risk of CVD. Measuring weight gain during adulthood may be better than static, cross-sectional assessment of weight because it considers trend over time, and thus, can be used as a supplementary approach to predict CVD.

Dietary approaches to stop hypertension, mediterranean dietary pattern, and diabetic nephropathy in women with type 2 diabetes: A case-control study.

BACKGROUND AND AIMS: The association between dietary habits and kidney function in patients with type 2 diabetes (T2D) has been poorly investigated. We aimed to test the relationship between adherences to the Dietary Approaches to Stop Hypertension (DASH) diet and the Mediterranean dietary pattern (Med diet) and likelihood of diabetic nephropathy (DN) in women with T2D. METHODS: In a case-control study, 105 women with T2D and DN (albumin-creatinine ratio ≥ 30 mg/g, mean age: 55.3 ± 7.0 years; diabetes duration: 7.6 ± 2.2 years), and 105 controls with T2D and without DN (mean age: 55.4 ± 7.1 years; diabetes duration: 7.6 ± 2.1 years) who attended at Kowsar diabetes clinic in Semnan, Iran were matched for age and diabetes duration. Dietary intakes were assessed using a validated 147-item semiquantitative food frequency questionnaire. The DASH and Med diet scores were calculated using the methods developed by Fung and Trichopoulou, respectively. A generalized estimating equation model was used to examine the relationship between dietary scores and odds of DN across tertiles of dietary patterns scores. RESULTS: Type 2 diabetic women with moderate and high Med diet scores had 62% and 86% lower odds of DN in comparison with low adherent (ORs: 0.38, 95%CI: 0.20, 0.73; and 0.14, 95%CI: 0.06, 0.33; respectively). A moderate adherence to the DASH diet was not associated with risk of DN, but a significant inverse relationship was found in those with high adherence (OR: 0.71, 95%CI: 0.57, 0.90). CONCLUSIONS: Adherence to the DASH and Med diets was inversely and dose-dependently associated with risk of DN. Further observational studies are needed to confirm the present results.

Fish consumption and risk of myocardial infarction: a systematic review and dose-response meta-analysis suggests a regional difference.

Limited evidence suggests that the association between fish consumption and risk of cardiovascular disease may be confounded by some regional-related factors. We aimed to quantify the association of fish consumption with risk of myocardial infarction (MI) and to clarify the shape of the dose-response relation in Western and Asian countries. A systematic literature review was performed in PubMed and Scopus from inception to January 2018. Prospective observational studies reporting risk estimates of MI for 3 or more quantitative categories of fish intake were included. A random-effects dose-response meta-analysis was conducted. Eleven prospective cohort studies, comprising a total of 398,221 participants and 8468 cases of MI, were analyzed. A significant inverse association was found for the highest compared with the lowest category of fish intake (relative risk: 0.73, 95% confidence interval: 0.59-0.87; I2 = 72%) and for a 15-g/d (105 g/wk, approximately equal to a 1 serving/wk) increment in fish consumption (relative risk: 0.96, 95% confidence interval: 0.94-0.99; I2 = 65%). A subgroup analysis showed a significant inverse association only in the subgroup of Asian studies as compared to Western studies. A nonlinear dose-response analysis suggested a linear decrement in the risk with the increase in fish consumption in the analysis of Asian studies. A modest U-shaped association was observed in the analysis of Western studies. In conclusion, higher fish consumption was associated with a lower risk of MI. However, considering the observed regional difference in this association, further observational studies are needed to provide more detailed explanations about this difference.

Inflammation markers and risk of developing hypertension: a meta-analysis of cohort studies.

OBJECTIVE: To systematically assess the association of circulating inflammation markers with the future risk of hypertension. METHODS: We did a systematic literature search of PubMed and Scopus, from database inception to July 10, 2018. Prospective and retrospective cohort studies evaluating the association of circulating C reactive protein (CRP), high-sensitive CRP (hs-CRP), interleukin 6 (IL-6) and IL-1ß to the risk of developing hypertension in the general population were included. The relative risks (RRs) for the top versus bottom tertiles of circulating biomarkers were calculated using a fixed-effects/random-effects model. A potential non-linear dose-response association was tested. RESULTS: Fourteen prospective cohort studies, two retrospective cohort studies and five nested case-control studies involving 142 640 participants and 20 676 cases were identified. The RR for the third versus first tertiles of circulating CRP was 1.23 (95% CI 1.11 to 1.35; I2=59%, n=12). The association remained unchanged after adjustment for body mass index. The RRs for other biomarkers were as follows: hs-CRP (RR 1.20, 95% CI 1.02 to 1.37; I2=74%, n=7), IL-6 (RR 1.51, 95% CI 1.30 to 1.71; I2=0%, n=5), and IL-1ß (RR 1.22, 95% CI 0.92 to 1.51; I2=0%, n=3). A non-linear dose-response meta-analysis demonstrated that the risk of hypertension increased linearly with increasing circulating inflammation markers, even within the low-risk and intermediate-risk categories. CONCLUSIONS: Higher levels of circulating CRP, hs-CRP and IL-6, but not IL-1ß, were associated with the risk of developing hypertension. The association persisted in subgroups of studies defined by major sources of heterogeneity.

Dietary and circulating vitamin C, vitamin E, ß-carotene and risk of total cardiovascular mortality: a systematic review and dose-response meta-analysis of prospective observational studies.

OBJECTIVE: The present review aimed to quantify the association of dietary intake and circulating concentration of major dietary antioxidants with risk of total CVD mortality. DESIGN: Systematic review and meta-analysis. SETTING: Systematic search in PubMed and Scopus, up to October 2017.ParticipantsProspective observational studies reporting risk estimates of CVD mortality across three or more categories of dietary intakes and/or circulating concentrations of vitamin C, vitamin E and ß-carotene were included. A random-effects meta-analysis was conducted. RESULTS: A total of fifteen prospective cohort studies and three prospective evaluations within interventional studies (320 548 participants and 16 974 cases) were analysed. The relative risks of CVD mortality for the highest v. the lowest category of antioxidant intakes were as follows: vitamin C, 0·79 (95 % CI 0·68, 0·89; I 2=46 %, n 10); vitamin E, 0·91 (95 % CI 0·79, 1·03; I 2=51 %, n 8); ß-carotene, 0·89 (95 % CI 0·73, 1·05; I 2=34 %, n 4). The relative risks for circulating concentrations were: vitamin C, 0·60 (95 % CI 0·42, 0·78; I 2=65 %, n 6); α-tocopherol, 0·82 (95 % CI 0·76, 0·88; I 2=0 %, n 5); ß-carotene, 0·68 (95 % CI 0·52, 0·83; I 2=50 %, n 6). Dose-response meta-analyses demonstrated that the circulating biomarkers of antioxidants were more strongly associated with risk of CVD mortality than dietary intakes. CONCLUSIONS: The present meta-analysis demonstrates that higher vitamin C intake and higher circulating concentrations of vitamin C, vitamin E and ß-carotene are associated with a lower risk of CVD mortality.

Dietary sodium, sodium-to-potassium ratio, and risk of stroke: A systematic review and nonlinear dose-response meta-analysis.

BACKGROUND & AIMS: The association of high sodium intake with risk of stroke has been accepted. But considering the proposed J/U-shaped association between sodium intake and risk of all-cause mortality, the shape of the dose-response relationship has not been determined yet. This study aimed to test the dose-response association of dietary sodium and sodium-to-potassium ratio with risk of stroke in adults aged 18 years or older. METHODS: We performed a systematic search using PubMed and Scopus, from database inception up to October 2017. Prospective and retrospective observational studies reporting risk estimates of stroke for three or more quantitative categories of dietary sodium or sodium-to-potassium ratio were included. Studies that reported results as continuous were also included. Two independent authors extracted the information and assessed the quality of included studies. Pooled relative risk (RR) was calculated using a random-effects model. Publication bias was tested. Sensitivity and subgroup analyses were done. RESULTS: Of initial 20,412 studies identified, 14 prospective cohort studies, one case-cohort study, and one case-control study (total n = 261,732) with 10,150 cases of stroke were included. The Pooled RRs of stroke were 1.06 (95%CI: 1.02, 1.10; I2 = 60%, n = 14 studies) for a 1 gr/d increment in dietary sodium intake, and 1.22 (95%CI: 1.04, 1.41; I2 = 60%, n = 5 studies) for a one-unit increment in dietary sodium-to-potassium ratio (mmol/mmol). The risk of stroke increased linearly with increasing dietary sodium intake, and also along with the increase in dietary sodium-to-potassium ratio. No evidence of a J/U-shaped association was found in the analyses of total stroke, stroke incidence, and stroke mortality. High sodium intake was associated with a somewhat worse prognosis among Asian countries as compared to westerns. CONCLUSION: Higher sodium intake and higher dietary sodium-to-potassium ratio were associated with a higher risk of stroke. Reducing dietary sodium-to-potassium ratio can be considered as a supplementary approach in parallel with the decrease in sodium intake in order to decrease stroke risk. The interpretation of the results is limited by observational nature of studies examined.

Dietary calcium intake and hypertension risk: a dose-response meta-analysis of prospective cohort studies.

The association of calcium intake with risk of developing hypertension in the general population has not been established yet. We systematically searched PubMed and Scopus databases up to February 2018 to find prospective observational studies investigating the association of calcium intake with risk of developing hypertension. The reported risk estimates were pooled using a random-effects model. Eight prospective cohort studies (248,398 participants and 30,838 cases) were included. Seven studies measured dietary calcium intake, but one study measured total calcium intake (calcium from food and supplements). A significant inverse association was found for the highest versus lowest category of calcium intake (relative risk: 0.89, 95%CI: 0.86, 0.93; I2 = 0%, n = 8), and for each 500 mg/d increment (relative risk: 0.93, 95%CI: 0.90, 0.97; I2 = 64%, n = 7). Summary results were the same with the main analyses when the analyses were restricted only to dietary calcium intake. A nonlinear dose-response meta-analysis exhibited a linear inverse association, with a somewhat steeper trend within the low and moderate intakes. In conclusion, higher dietary calcium intake, independent of adiposity and intake of other blood pressure-related minerals, is slightly associated with a lower risk of developing hypertension.

Intake of vitamin B6, folate, and vitamin B12 and risk of coronary heart disease: a systematic review and dose-response meta-analysis of prospective cohort studies.

The objective of this study was to quantify the association of B-vitamins intake with the future risk of coronary heart disease (CHD). A systematic search was performed with the use of PubMed and Scopus from inception to April 30, 2018. Prospective cohort studies evaluating the association of intake of folate, vitamin B6, and vitamin B12 with risk of CHD in the general population were included. A random-effects meta-analysis was performed. Eleven prospective cohort studies (total n = 369,746) with 5133 cases of CHD were included in the analyses. The relative risks were: 0.79 (95%CI: 0.69, 0.89; I2 = 67%) for a 250 µg/d increment in folate intake; 0.87 (95%CI: 0.78, 0.96; I2 = 80%) for a 0.5 mg/d increment in vitamin B6 intake; and 0.97 (95%CI: 0.80, 1.14: I2 = 67%) for a 3 µg/d increment in vitamin B12 intake. The results did not change materially when the analyses were restricted only to dietary vitamins intake. A nonlinear dose-response meta-analysis demonstrated a linear inverse association between folate and vitamin B6 intake and risk of CHD. In conclusion, higher intake of folate and vitamin B6 is associated with a lower risk of CHD in the general population.

Dietary Antioxidants, Circulating Antioxidant Concentrations, Total Antioxidant Capacity, and Risk of All-Cause Mortality: A Systematic Review and Dose-Response Meta-Analysis of Prospective Observational Studies.

The associations of various dietary or circulating antioxidants with the risk of all-cause mortality in the general population have not been established yet. A systematic search was performed in PubMed and Scopus, from their inception up to October 2017. Prospective observational studies reporting risk estimates of all-cause mortality in relation to dietary intake and/or circulating concentrations of antioxidants were included. Random-effects meta-analyses were conducted. Forty-one prospective observational studies (total n = 507,251) involving 73,965 cases of all-cause mortality were included. The RRs of all-cause mortality for the highest compared with the lowest category of circulating antioxidant concentrations were as follows: total carotenes, 0.60 (95% CI: 0.46, 0.74); vitamin C, 0.61 (95% CI: 0.53, 0.69); selenium, 0.62 (95% CI: 0.45, 0.79); ß-carotene, 0.63 (95% CI: 0.57, 0.70); α-carotene, 0.68 (95% CI: 0.58, 0.78); total carotenoids, 0.68 (95% CI: 0.56, 0.80); lycopene, 0.75 (95% CI: 0.54, 0.97); and α-tocopherol, 0.84 (95% CI: 0.77, 0.91). The RRs for dietary intakes were: total carotenoids, 0.76 (95% CI: 0.66, 0.85); total antioxidant capacity, 0.77 (95% CI: 0.73, 0.81); selenium, 0.79 (95% CI: 0.73, 0.85); α-carotene, 0.79 (95% CI: 0.63, 0.94); ß-carotene, 0.82 (95% CI: 0.77, 0.86); vitamin C, 0.88 (95% CI: 0.83, 0.94); and total carotenes, 0.89 (95% CI: 0.81, 0.97). A nonsignificant inverse association was found for dietary zinc, zeaxanthin, lutein, and vitamin E. The nonlinear dose-response meta-analyses demonstrated a linear inverse association in the analyses of dietary ß-carotene and total antioxidant capacity, as well as in the analyses of circulating α-carotene, ß-carotene, selenium, vitamin C, and total carotenoids. The association appeared to be U-shaped in the analyses of serum lycopene and dietary vitamin C. The present study indicates that adherence to a diet with high antioxidant properties may reduce the risk of all-cause mortality. Our results confirm current recommendations that promote higher intake of antioxidant-rich foods such as fruit and vegetables.