Posted by: Chris Maloney | November 5, 2012

Which Is Better For Preventing Heart Failure? Statins or Fish Oil?

Rafael Statin [6685Crop]

My kind of Statin: Rafael Statin [6685Crop] (Photo credit: Juan N Only)

A recent study came out discussing the benefits of adding fish oil to the diet.  Not surprisingly, more fish oil lowered the risk of heart failure.  But it wasn’t a situation of more is better.  Just eating a little fish (more than once a month) gave benefit.  The drop was a 30% reduction in heart failure risk, which is a lot of bang for a little fish.

I wanted to compare the result to the effect of taking statins every day for the rest of your life.  Anyone over fifty is familiar with the idea that the conventional doctors view statins as the next best thing to sliced bread.  We all should bathe in the stuff.  Unfortunately between 6-8% of the population develops muscle cramping on the statins.  So the following is for you.

In a huge review of the effect of statins, the authors concluded that the benefit of statins on heart failure was significant, about 30%.  So it equaled the effect of having fish twice a month.  But only for those who had already had heart attacks.  To quote the study primary (before your heart attack): “prevention with statins provides only small and clinically hardly relevant improvement of cardiovascular morbidity/mortality.”

So if you’ve had a heart attack, have your statins.  But if you are trying to prevent a heart attack, start with fish regularly before you sign up for the statin-a-day for life program.

Here are the studies:

Plasma and dietary omega-3 fatty acids, fish intake, and heart failure risk in the Physicians’ Health Study

American Journal of Clinical Nutrition, 09/23/2012  Clinical Article

Wilk JB et al. – The data are consistent with an inverse and nonlinear relation of plasma phospholipid α–linolenic acid (ALA) and docosapentaenoic acid (DPA), but not EPA or DHA, with heart failure (HF) risk. Fish consumption greater than once per month was associated with a lower HF risk.

Methods

•The authors used nested case–control (n = 1572) and prospective cohort study designs (n = 19,097).

• Plasma phospholipid n–3 FAs were measured by using gas chromatography, and food–frequency questionnaires were used to assess dietary n–3 FAs and fish intake.

•Incident HF was ascertained via annual follow–up questionnaires and validated in a subsample.

Results

• The mean age was 58.7 y at blood collection.

• In a multivariable model, plasma α–linolenic acid (ALA) was associated with a lower risk of HF in a nonlinear fashion (P–quadratic trend = 0.02), and the lowest OR was observed in quintile 4 (0.66; 95% CI: 0.47, 0.94).

• Plasma EPA and DHA were not associated with HF, whereas plasma docosapentaenoic acid (DPA) showed a nonlinear inverse relation with HF for quintile 2 (OR: 0.55; 95% CI: 0.39, 0.79).

• Dietary marine n–3 FAs showed a trend toward a lower risk of HF in quintile 4 (HR: 0.81; 95% CI: 0.64, 1.02) and a nonlinear pattern across quintiles.

• Fish intake was associated with a lower risk of HF, with RRs of 0.70 for all categories of fish consumption greater than one serving per month.

Int J Clin Pharmacol Ther. 2003 Dec;41(12):567-77.

Use of statins in primary and secondary prevention of coronary heart disease and ischemic stroke. Meta-analysis of randomized trials.

Vrecer M, Turk S, Drinovec J, Mrhar A.

Source

Krka, Novo mesto, University of Ljubljana, Ljubljana, Slovenia.

Abstract

OBJECTIVE:

To estimate the relative risk reduction of the clinical outcomes (coronary events, strokes, cardiovascular, non-cardiovascular and all-cause mortality) associated with statin therapy in primary and secondary prevention.

DATA SOURCES:

A literature search of the Medline and Cohrane databases for articles published from 1985 to July 2002 was performed. The data on systematic reviews and preliminary reports were also included in this study. Primary and secondary prevention trials and regression trials were eligible. DATA EXTRACTION AND STATISTICAL METHOD: Data were extracted by 2 authors according to the defined inclusion criteria. Disagreements were resolved by consensus or by a third reviewer. Testing for heterogeneity was applied and on the basis of these results a fixed effect model or a random effect model was used for calculation of relative risk values (RR) and 95% confidence intervals (95% CI). Sensitivity analysis tested the impact of the individual study–duration of study, type of statin therapy and study size. The number of patients needed to treat was calculated as an absolute measure of clinical effectiveness of statin therapy when appropriate.

RESULTS:

Data from 15 trials with 63,410 participants and mean duration of treatment of 3.6 years, were included in this overview. Tests for heterogeneity showed that the variability between study estimates is sufficiently small to assume that they are estimating the same underlying treatment effect. Statin therapy was associated with a 22% reduction in total cholesterol, 29% reduction in LDL cholesterol, 12% reduction in triglycerides and 6% increase in HDL cholesterol. Overall (primary and secondary studies) statin therapy significantly reduces relative risk of coronary events (RR, 0.73, 95% CI, 0.68, 0.77, *p < 0.0001), relative risk of cardiovascular disease mortality (RR, 0.78, 95% CI, 0.73, 0.84, *p < 0.0001), relative risk of non-fatal stroke (RR, 0.74, 95% CI, 0.67, 0.82, *p < 0.0001), relative risk of total (fatal and non-fatal) stroke (RR, 0.77, 95% CI, 0.70, 0.84, *p < 0.001) and relative risk of all-cause death (RR, 0.85, 95% CI, 0.81, 0.89, *p < 0.0001). There was a slight and insignificant reduction of relative risk in non-cardiovascular mortality (RR, 0.94, 95% CI, 0.86, 1.03, p = 0.1677) and fatal strokes (RR, 0.86, 95% CI, 0.70, 1.07, p = 0.1912). Sensitivity analysis showed the robustness of our results for all outcomes. The results were not altered if an individual study was removed from meta-analysis.

CONCLUSIONS:

This overview indicates that statin treatment reduces the relative risk of occurrence of coronary events, cardiovascular disease mortality, non-fatal strokes and all-cause mortality. While secondary prevention with statins provides considerable improvement of cardiovascular morbidity/mortality, primary prevention with statins provides only small and clinically hardly relevant improvement of cardiovascular morbidity/mortality.

PMID: 14692706

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