Increased dietary potassium intake is thought to be associated with low blood pressure (BP). Whether potassium supplementation may be used as an antihypertensive agent is a question that should be answered. To assess the effect of oral potassium supplementation on blood pressure in patients with primary hypertension. We searched Medline, Web of Science, Scopus, Cochrane Central Register of Controlled Trials until October 2016. We also screened reference lists of articles and previous reviews. We applied no language restrictions. We included randomized placebo-controlled clinical trials addressing the effect of potassium supplementation on primary hypertension for a minimum of 4 weeks. We extracted data on systolic and diastolic BP (SBP and DBP) at the final follow-up. We explored the heterogeneity across studies using Cochran's test and I² statistic and assessed the probability of publication bias using Begg's and Egger's tests. We reported the mean difference (MD) of SBP and DBP in a random-effects model. We found a total of 9059 articles and included 23 trials with 1213 participants. Compared to placebo, potassium supplementation resulted in modest but significant reductions in both SBP (MD -4.25 mmHg; 95% CI: -5.96 to -2.53; I² = 41%) and DBP (MD -2.53 mmHg; 95% CI: -4.05 to -1.02; I² = 65%). According to the change-score analysis, based on 8 out of 23 trials, compared to baseline, the mean changes in SBP (MD -8.89 mmHg; 95% CI: -13.67 to -4.11) and DBP (MD -6.42 mmHg; 95% CI: -10.99 to -1.84) was significantly higher in the intervention group than the control group. Our findings indicated that potassium supplementation is a safe medication with no important adverse effects that has a modest but significant impact BP and may be recommended as an adjuvant antihypertensive agent for patients with essential hypertension.

Background Despite our awareness of the significant effect of smoking on multiple sclerosis (MS), there was a serious lack of information about the effect of different types of smoking habit on MS as well as the dose–response relationship between smoking and MS, but this gap was addressed by this meta-analysis. Methods Major electronic databases, including PubMed, Web of Science and Scopus were searched until July 2015. Epidemiological studies addressing the association between smoking and MS were enrolled. The heterogeneity across studies was investigated by Q-test and I2 statistic. The probability of publication bias was explored using Begg's and Egger's tests. The results were expressed as odds ratio (OR) with 95% confidence intervals (CI) using a random effects model. Results We identified a total of 10 687 references and included 34 studies involving 623 852 participants. Compared with nonsmokers, the OR estimate of MS was 1.46 (1.33, 1.59) among ever smokers, 1.57 (1.34, 1.80) among current smokers, 1.36 (1.27, 1.46) among ex-smokers and 1.12 (0.87, 1.36) among passive smokers. In addition, analyzing the effect of cigarette pack-year on MS indicated that the OR estimate of MS was 1.34 (1.06, 1.61) for 1–5 cigarette pack-years, 1.56 (1.15, 1.97) for 6–10 cigarette pack-years, 1.74 (1.16, 2.33) for 11–15 cigarette pack-years and 1.46 (0.49, 2.43) for more than 15 cigarette pack-years. Conclusions Smoking habits are significantly associated with MS, although the association is not very strong. However, there is a dose–response relationship between the smoking habits and MS.

Background A 25% relative reduction in the prevalence of hypertension is a global target. This meta-analysis estimated the effect of excess weight loss on hypertension. Methods We searched PubMed, Web of Science and Scopus until January 2016. We included prospective cohort studies addressing the association between overweight/obesity and hypertension. We expressed the strength of association using risk ratio and the excess risk using attributable risk fraction with 95% CI based on the random-effects model. Results We found 7617 references and included 10 studies with 173 828 participants. Compared with normal weight, the risk ratio of hypertension was 1.52 (1.37, 1.67; 9 studies, I² = 82.4%) for overweight and 2.17 (1.84, 2.50; 9 studies, I² = 88.9%) for obesity. The excess risk of hypertension attributable to overweight was 32% (24%, 40%; 8 studies, I² = 85.5%) and that attributable to obesity was 47% (40%, 54%; 8 studies, I² = 88.2%). That means, excess weight loss may reduce the risk of hypertension by between 24% and 40% in people who are overweight and by between 40% and 54% in people who are obese. Conclusions Excess weight loss is a vital strategy for controlling hypertension and is sufficient for achieving the global target, particularly if it is accompanied with other preventive measures.