We found that 3 measures of low SES, household income, education level, and occupation, were associated with low RBC levels of 2 (n-3) fatty acids in 987 outpatients with CHD. After multivariable adjustment, participants with less than a high school education had mean DHA+EPA levels that were 24% lower than those with a college degree, participants with a household income <$20,000 had DHA+EPA levels that were 14% lower than those with a household income >$50,000, and laborers had DHA+EPA levels that were 18% lower than participants with professional or technical occupations. These results raise the possibility that low (n-3) fatty acid levels, an easily modifiable risk factor, may contribute to the increased risk of CVD in patients with low SES. Our study extends the existing literature by examining 4 different measures of SES, measuring RBC levels of fatty acids rather than using dietary questionnaires, and providing comprehensive assessment of potential confounding variables.
Prior studies examining the association between SES and (n-3) fatty acids have relied on self-reported dietary intake questionnaires to estimate (n-3) levels (15
). Such questionnaires may not capture hidden dietary fats and are susceptible to reporting errors (16
). Computer simulations or published correlation coefficients were often used to convert dietary data to fatty acid levels. One prior study reported an association between occupation and measured serum levels of fatty acids in Nigerian civil servants (17
). Another study, the only one known to address this question in patients with established CHD who are at highest risk for cardiovascular events, reported no association between education and serum levels of EPA or DHA (18
). However, >85% of surveyed CHD patients in this study had <12 y of education (in contrast to <15% in our study) and >60% had <9 y of education, potentially limiting the ability to capture the true benefits of higher education.
Because (n-3) fatty acids cannot be synthesized in the body de novo, they must be obtained through dietary sources. The best sources for DHA and EPA are oily, coldwater fish (such as salmon, sardines, mackerel, and albacore tuna) and fish oils (10
), as well as nonhydrogenated vegetable oils. However, the quantity of (n-3) fatty acids present varies greatly, depending on fish size and species, season, geography, and preparation methods (29
). Vegetable oils, especially canola or soybean, contain 7–10% α
-linolenic acid, a short-chain (n-3) fatty acid that can be converted to EPA and DHA in the body but with very limited efficiency (31
). The extent to which the differences in RBC EPA and DHA levels in the present study were the result of differences in the intake of fish or fish oil supplements is not known, because these data were not collected. There is, however, a clear dose-response relationship between fish intake (21
) or fish oil supplementation (32
) and EPA and DHA levels. Because lower levels of (n-3) fatty acids are associated with increased CHD risk (6
) and increased intake reduces this risk (14
), it seems reasonable to hypothesize that increased fish oil intake could reduce risk for CHD in lower SES populations.
Previous epidemiological studies have found significant differences in the diets and nutrient intakes of different socioeconomic classes (18
). Specifically, reduced fish consumption has been associated with lower education levels and less-skilled, lower-paying occupations (15
). Several explanations have been suggested to explain such dietary disparities, including the increased cost of healthy foods (39
) and decreased health knowledge in lower SES individuals (40
). However, such explanations are not yet conclusive. It has also been suggested that poorer social support and limited availability of affordable healthy foods in socioeconomically disadvantaged neighborhoods negatively influence diet (41
Our study results raise the possibility that (n-3) fatty acids may be an important mediating factor in the association between low SES and CVD. Although a Cochrane meta-analysis has challenged the view that (n-3) fatty acids reduce adverse cardiac outcomes (12
), the review has been criticized due to the controversial inclusion of the DART-2 trial (42
), the use of composite endpoints, the wide range of intakes included, and the questionable exclusion of many potential cohorts (43
). Despite such challenges, major cardiac societies and national health agencies continue to endorse the intake of (n-3) fatty acid for CVD prevention and treatment. The AHA currently recommends all adults eat fish at least twice a week and that all patients with CAD take 1 g/d of DHA and EPA through dietary and/or supplemental sources (45
). It is not clear what levels of RBC DHA+EPA would represent an increased risk for CVD, but prior studies may provide some guidance. In a nested case-control analysis among men followed for up to 17 y in the Physicians’ Health Study, baseline levels of EPA+DHA were significantly lower in 94 men who had sudden cardiac death than in 184 controls matched for age and smoking status (median EPA+DHA 3.84% vs. 4.22%) (46
). The median level of EPA+DHA in our participants with known CHD was 3.6%, which is even lower than the cases from the Physician’s Health Study and consistent with the high risk of our study population.
Current dietary recommendations to increase (n-3) fatty acid intake, a modifiable risk factor, are especially relevant to our cohort of patients with diagnosed CHD. In comparison to the general public, CHD patients would likely have more encounters with the healthcare system and should be more knowledgeable about their health condition and the cardioprotective role of (n-3) fatty acids. Our results demonstrate that significant socioeconomic disparities in (n-3) fatty acid levels still exist in this high-risk population, suggesting even stronger disparities may be affecting the general population. Current cardiovascular prevention strategies need to more adequately address the socioeconomic barriers to (n-3) consumption, especially in patients with CHD. More effective methods should be devised to uniformly disseminate knowledge regarding the benefits of (n-3) fatty acids. The RBC (n-3) fatty acid level has been proposed as a new risk factor for CHD (47
) and a growing body of literature has been exploring the value and cost-effectiveness of using supplements, fortified foods, or bioengineered plant foods to increase (n-3) consumption (48
). These dietary alternatives may help address economic, geographic, social, and cultural barriers to consuming foods rich in (n-3) fatty acids.
Several limitations must be considered in interpreting our results. First, the lack of data on dietary intake or use of dietary supplements limited our ability to confirm that dietary intake was responsible for the low RBC DHA and EPA levels found in patients with low SES. However, given that (n-3) fatty acids must be obtained through dietary sources and cannot be synthesized de novo in humans, it follows that RBC (n-3) fatty acid levels should be an accurate reflection of dietary intake. Second, the cross-sectional nature of our study precludes any definitive conclusions of causality in the association between SES and RBC (n-3) fatty acids. In this study, reverse causality is unlikely given that it is less plausible that adult (n-3) fatty acid consumption could significantly affect SES. Third, the study participants were mostly urban men and are thus not completely reflective of the general population. Finally, we cannot eliminate the possibility of residual confounding by factors correlated with both SES and RBC (n-3) levels. Although many factors can affect SES, it is unlikely these same factors alter RBC (n-3) levels, which are primarily a function of diet.
In summary, we found that 3 indicators of low SES, household income, education level, and occupation, were strongly associated with low RBC levels of 2 (n-3) fatty acids, EPA and DHA, among patients with CHD. These observations provide evidence that (n-3) fatty acids may be an important mediating factor in the association between lower SES and CVD. Future prevention efforts to raise awareness about and increase the dietary intake of (n-3) fatty acids in patients with CHD may help reduce existing socioeconomic disparities.