After 13.3 years of follow-up in this cohort of approximately 14,000 white and African-American men and women, greater intake of eggs and of high-fat dairy foods were both associated with greater risk of incident HF, whereas greater intake of whole-grain foods was associated with lower risk of incident HF. These associations were independent of demographic characteristics, lifestyle factors, prevalent CVD, diabetes, hypertension, and other food groups.
Consistent with the findings of the present investigation, whole-grain intake has been associated with lower risk of overt CVD (15
) and hypertension (20
), improvements in glycemic control (21
), and lower levels of inflammatory biomarkers (23
), all factors related to HF risk (24
). Also consistent with the data presented here are the results of a recent report from the Physicians’ Health Study, which showed that greater cereal intake—particularly whole-grain cereal—was associated with a significantly lower risk of HF (5
). However, that study, like the current study, relied on a relatively simple FFQ to quantify intake (5
), and the previous study did not evaluate the association between HF risk and total whole-grain intake.
The Physicians’ Health Study also reported a positive association between egg consumption and HF risk (6
), which was corroborated in the current analysis. Furthermore, the risk estimates presented here were of similar magnitude to those observed in the Physician’s Health Study: ie, if analyses were modeled in categories similar to those used in the previous study, risk of HF was approximately 30% in individuals who regularly consumed eggs (at least daily) vs those who did not consume eggs or who consumed eggs less than once per week. Although the association was independent of the intake of other foods, egg consumption may simply be a marker for a larger dietary pattern that, in total, influences HF risk. Given the long history of debate regarding egg consumption and CVD in general (27
), it is important that these observations be disentangled in studies of varying design to determine whether to recommend omitting eggs from the diet.
A positive association between high-fat dairy intake and HF risk also existed in the ARIC cohort. The positive association between CVD risk and intake of saturated fat, which is found in high-fat dairy foods, is fairly well established (28
). Although few studies have reported specifically on associations between intake of high-fat dairy foods and CVD, existing studies suggest the fat content of dairy foods (high-fat vs low-fat) is important. Low-fat dairy generally shows more favorable associations with CVD and risk factors than high-fat dairy, suggesting that the fat component of high-fat dairy foods may be partly responsible for these associations.
The hypothesis that fish consumption would be related to lower risk of incident HF was not supported by the ARIC data, but the contrasting effects of fried vs baked or broiled fish may partly explain the absence of association in this cohort. Mozaffarian and colleagues (4
) observed a 20% to 30% lower incidence of HF in those who consumed baked/broiled fish at least weekly vs those who consumed baked/broiled fish less than once per month. In contrast, fried fish was associated with greater HF risk. Unfortunately, unlike the Mozaffarian study, the current study was unable to differentiate fried fish from fish prepared in other ways. Given the frequency of total fried food consumption in the ARIC study (approximately 70% consumed fried food weekly and approximately 17% consumed fried food daily), it seems likely that a large proportion of the fish consumed was fried.
In the current study, neither consumption of fruits and vegetables nor consumption of low-fat dairy was associated with HF risk, despite prior evidence suggesting these food groups would be inversely associated with risk (12
). At the time dietary intake was assessed in this study, foods low in fat and cholesterol, such as fruits and vegetables and low-fat dairy, were recommended for health maintenance and for specific CVD conditions (32
). Thus, it is possible that awareness of these diet-disease relationships among those at greater risk for HF may have prevented us from detecting true associations. That is, intake reflective of lifelong habits (which may be most relevant to the development of HF), may not have been accurately measured. However, this limitation is not unique to the ARIC study but is a well-known limitation of any analysis relying on a proxy measure of food intake.
There are limitations to this study. First, because the ARIC study relied on hospital discharge records and death certificates to ascertain cases of HF, outpatient HF was not included (therefore, less severe cases were likely not included) (35
). Although this compromises sensitivity and generalizability, it results in high specificity of the HF definition. It is also likely that subjects with less-severe HF in early years of follow-up were eventually hospitalized by the end of the 13.3 years of follow-up.
Second, although the ARIC study used a fairly short FFQ to quantify dietary intake, the questionnaire has been validated (11
) and criterion validity with respect to cardiovascular outcomes in the ARIC cohort has been demonstrated (13
Third, some questions assessing intake of grains included a combination of whole- and refined-grain foods (eg, rice included white rice, brown rice, and wild rice) (13
). However, this type of measurement error would likely attenuate risk estimates, suggesting estimates of HF risk associated with whole-grain intake may actually be greater than presented here.
Fourth, although confounding was carefully assessed and several variables known to confound diet–CVD associations were included in the multivariable model, the possibility of residual confounding cannot be excluded. Because these data were based on HF hospitalizations and death only, it is equally possible that dietary changes may have occurred secondary to HF symptoms, resulting in attenuated risk estimates. However, sensitivity analyses excluding participants with prevalent conditions known to influence HF risk largely addressed this possibility. Although there was less power in the smaller subset, whole-grain and egg intake remained associated with HF risk. Furthermore, when CVD, diabetes, and BMI were modeled as time-varying covariates (status updated throughout follow-up), again, there was no substantial attenuation in risk estimates.
Lastly, these data indicate only association. Randomized interventions are necessary to demonstrate causality and begin to better understand potential mechanisms.