Meta-analysis supports α-Linolenic acid Intake and Reduced Coronary Heart Disease

Flaxseed provides a unique mix of fatty acids. It is low in saturates (less than 9% of total fatty acids) and contains the essential polyunsaturated fatty acids omega-3 α-linolenic acid (ALA; 18:3n-3) and omega-6 linoleic acid (LA; 18:2n-6). Essential fatty acids are required in the diet as they cannot be made by humans. Most notably, ALA comprises on average 53 to 57% of the fatty acids in flaxseed oil, making it the richest plant source.

Higher dietary ALA intake has been associated with a reduced risk of coronary heart disease which is the worldwide leading cause of mortality over the past decade (1). Dietary strategies are an important component to preventing CHD. The American Heart Association recommends eating sources of ALA, including flaxseed and its oil, due to large epidemiologic studies suggesting that people at risk for coronary heart disease benefit from consuming both plant and marine sources of omega-3 fatty acids (2).

A recent meta-analysis examined an aggregate association between ALA intake and risk of CHD, and assessed any dose-response relationships (3). The investigators searched the PubMed, EMBASE and Web of Science databases over a 50-year period (from January 1966 to August 2017) that investigated the associations between dietary ALA intake and CHD. They included original full-text studies that were: cohort studies, included adult participants free from CHD history with assessments of dietary intake of ALA, assessed primary outcomes including fatal and/or non-fatal CHD and had a comparison between the highest and the lowest level of dietary ALA intake. They excluded studies that: included only assessed ALA level in plasma or serum as biomarkers, and included composite outcomes that combined different cardiovascular events and CHD could not be distinguished.

Data were pooled using random-effects meta-analysis models, comparing the highest category of ALA intake with the lowest across studies. Subgroup analysis was conducted based on study design, geographic region, age and sex. In all, fourteen studies of thirteen cohorts were identified and included in the meta-analysis. The pooled results showed that higher ALA intake was associated with modest reduced risk of composite CHD (risk ratios (RR)=0·91; 95 % CI 0·85, 0·97) and fatal CHD (RR=0·85; 95 % CI 0·75, 0·96). The analysis showed a J-shaped relationship between ALA intake and relative risk of composite CHD (χ 2=21·95, P<0·001). Compared with people without ALA intake, only people with ALA intake <1·4 g/d showed reduced risk of composite CHD. 

ALA intake was linearly associated with fatal CHD. Every 1 g/d increase in ALA intake was associated with a 12 % decrease in fatal CHD risk (95 % CI -0·21, -0·04).

This meta-analysis supports several large population studies that have demonstrated an inverse relationship between ALA levels and cardiovascular events (4). An earlier meta-analysis reported that each 1 g/day increment of ALA intake was associated with a 10% lower risk of death from coronary heart disease (5). Risk of non-fatal myocardial infarction was shown to decrease by 57% with a median ALA intake of 1.79 g/day (0.65% energy) compared to 1.11 g/day (0.42% energy) (6). Individuals with low initial ALA intakes may experience the greatest cardiovascular benefits with increased intakes (6). This evidence has led to the recommendation that ALA intake be increased to 2–3 g/d to reduce the risk of CVD (7).

According to the authors, this is the largest meta-analysis of dietary ALA intake and CHD risk based on prospective studies. However, the investigators indicate that with the heterogeneity among studies, the results should be interpreted with caution.

References

  1. World Health Organization. 2013. The top 10 causes of death. http://www.who.int/mediacentre/factsheets/fs310/en/
  2. American Heart Association. 2014. Fish 101. http://www.heart.org/HEARTORG/GettingHealthy/NutritionCenter/Fish-101_UCM_305986_Article.jsp
  3. Wei J, Hou R, Xi Y, Kowalski A, et al. Br J Nutr. 2018 Jan;119(1):83-89. doi: 10.1017/S0007114517003294.
  4. Rodriguez-Leyva D, et al. Can J Cardiol 2010;26:489-496.
  5. Pan A, et al. Am J Clin Nutr 2012;96:1262-1273.
  6. Campos H, et al. Circulation 2008;118:339-345.
  7. Fleming JA, et al. Adv Nutr 2014;5:863s-876s.