Altering microRNA in colorectal cancer with histone deacetylase inhibitors

On 23rd November 2012

“Altering microRNA in colorectal cancer with histone deacetylase inhibitors”

Low sodium diet significantly increases morbidity and mortality in systolic HF

Discussed on 9th November 2012

Heart. 2012 Aug 21. [Epub ahead of print]

Low sodium versus normal sodium diets in systolic heart failure: systematic review and meta-analysis.

Dinicolantonio JJ, Pasquale PD, Taylor RS, Hackam DG.

Source

Ithaca, New York, USA.

Abstract

CONTEXT:

A low sodium diet has been proposed to reduce the risk of heart failure (HF) hospitalisations and is currently advocated in consensus guidelines, yet some evidence suggests adverse neurohumoral activation for sodium restriction in the HF setting.

OBJECTIVES:

To evaluate the effects of a restricted sodium diet in patients with systolic HF.

DATA SOURCES:

A systematic review and meta-analysis of randomised trials OVID MEDLINE, PubMed, Excerpta Medica (Embase), the Cochrane Controlled Trials Register, Scopus, Web of Science and Google Scholar were searched up to April 2012.

STUDY SELECTION:

Two independent reviewers selected studies for inclusion on the basis of a randomised controlled trial design that included adults with systolic HF receiving a restricted salt diet or control diet and reporting mortality (all-cause, sudden death or HF-related) and HF-related hospitalisations.

DATA EXTRACTION AND ANALYSIS:

Descriptive and quantitative information was extracted from included studies. A random-effects model was used to compute pooled risk ratios (RR) for mortality and morbidity outcomes.

RESULTS:

Six randomised trials comparing low sodium diets (1.8 g/day) with normal sodium diets (2.8 g/d) in 2747 patients with systolic HF were identified. Compared with a normal sodium diet, a low sodium diet significantly increased all cause mortality (RR 1.95, 95% CI 1.66 to 2.29), sudden death (RR 1.72, 95% CI 1.21 to 2.44), death due to HF (RR 2.23, 95% CI 1.77 to 2.81) and HF readmissions (RR 2.10, 95% CI 1.67 to 2.64).

CONCLUSION:

Compared with a normal sodium diet, a low sodium diet significantly increases morbidity and mortality in systolic HF.

Fish consumption, long chain omega 3 fatty acids, and risk of cerebrovascular disease

 Journal club on 2nd November 2012

 

BMJ. 2012 Oct 30;345:e6698. doi: 10.1136/bmj.e6698.

Association between fish consumption, long chain omega 3 fatty acids, and risk of cerebrovascular disease: systematic review and meta-analysis.

Chowdhury R, Stevens S, Gorman D, Pan A, Warnakula S, Chowdhury S, Ward H, Johnson L, Crowe F, Hu FB, Franco OH.

Source

Department of Public Health and Primary Care, University of Cambridge, UK.

Abstract

OBJECTIVE:

To clarify associations of fish consumption and long chain omega 3 fatty acids with risk of cerebrovascular disease for primary and secondary prevention.

DESIGN:

Systematic review and meta-analysis.

DATA SOURCES:

Studies published before September 2012 identified through electronic searches using Medline, Embase, BIOSIS, and Science Citation Index databases. ELIGIBILITY CRITERIA: Prospective cohort studies and randomised controlled trials reporting on associations of fish consumption and long chain omega 3 fatty acids (based on dietary self report), omega 3 fatty acids biomarkers, or supplementations with cerebrovascular disease (defined as any fatal or non-fatal ischaemic stroke, haemorrhagic stroke, cerebrovascular accident, or transient ischaemic attack). Both primary and secondary prevention studies (comprising participants with or without cardiovascular disease at baseline) were eligible.

RESULTS:

26 prospective cohort studies and 12 randomised controlled trials with aggregate data on 794 000 non-overlapping people and 34 817 cerebrovascular outcomes were included. In cohort studies comparing categories of fish intake the pooled relative risk for cerebrovascular disease for 2-4 servings a week versus ≤1 servings a week was 0.94 (95% confidence intervals 0.90 to 0.98) and for ≥5 servings a week versus 1 serving a week was 0.88 (0.81 to 0.96). The relative risk for cerebrovascular disease comparing the top thirds of baseline long chain omega 3 fatty acids with the bottom thirds for circulating biomarkers was 1.04 (0.90 to 1.20) and for dietary exposures was 0.90 (0.80 to 1.01). In the randomised controlled trials the relative risk for cerebrovascular disease in the long chain omega 3 supplement compared with the control group in primary prevention trials was 0.98 (0.89 to 1.08) and in secondary prevention trials was 1.17 (0.99 to 1.38). For fish or omega 3 fatty acids the estimates for ischaemic and haemorrhagic cerebrovascular events were broadly similar. Evidence was lacking of heterogeneity and publication bias across studies or within subgroups.

CONCLUSIONS:

Available observational data indicate moderate, inverse associations of fish consumption and long chain omega 3 fatty acids with cerebrovascular risk. Long chain omega 3 fatty acids measured as circulating biomarkers in observational studies or supplements in primary and secondary prevention trials were not associated with cerebrovascular disease. The beneficial effect of fish intake on cerebrovascular risk is likely to be mediated through the interplay of a wide range of nutrients abundant in fish.