Dietary and lifestyle evolutionary discordance is hypothesised to play a role in the aetiology of CVD, including CHD and stroke. We aimed to investigate associations of a previously reported, total (dietary plus lifestyle) evolutionary-concordance (EC) pattern score with incident CVD, CHD and stroke. We used multivariable Cox proportional hazards regression to investigate associations of the EC score with CVD, CHD and stroke incidence among USA Black and White men and women ≥45 years old in the prospective REasons for Geographic and Racial Differences in Stroke study (2003–2017). The EC score comprised seven equally weighted components: a previously reported dietary EC score (using Block 98 FFQ data) and six lifestyle characteristics (alcohol intake, physical activity, sedentary behaviour, waist circumference, smoking history and social network size). A higher score indicates a more evolutionary-concordant dietary/lifestyle pattern. Of the 15 467 participants in the analytic cohort without a CVD diagnosis at baseline, 1563 were diagnosed with CVD (967 with CHD and 596 with stroke) during follow-up (median 11·0 years). Among participants in the highest relative to the lowest EC score quintile, the multivariable-adjusted hazards ratios and their 95 % CI for CVD, CHD and stroke were, respectively, 0·73 (0·62, 0·86; P trend < 0·001), 0·72 (0·59, 0·89; P trend < 0·001) and 0·76 (0·59, 0·98; P trend = 0·01). The results were similar by sex and race. Our findings support that a more evolutionary-concordant diet and lifestyle pattern may be associated with lower risk of CVD, CHD and stroke.

The Southern dietary pattern, derived within the REasons for Geographic And Racial Differences in Stroke (REGARDS) cohort, is characterised by high consumption of added fats, fried food, organ meats, processed meats and sugar-sweetened beverages and is associated with increased risk of several chronic diseases. The aim of the present study was to identify characteristics of individuals with high adherence to this dietary pattern. We analysed data from REGARDS, a national cohort of 30 239 black and white adults ≥45 years of age living in the USA. Dietary data were collected using the Block 98 FFQ. Multivariable linear regression was used to calculate standardised beta coefficients across all covariates for the entire sample and stratified by race and region. We included 16 781 participants with complete dietary data. Among these, 34·6 % were black, 45·6 % male, 55·2 % resided in stroke belt region and the average age was 65 years. Black race was the factor with the largest magnitude of association with the Southern dietary pattern (Δ = 0·76 sd, P < 0·0001). Large differences in Southern dietary pattern adherence were observed between black participants and white participants in the stroke belt and non-belt (stroke belt Δ = 0·75 sd, non-belt Δ = 0·77 sd). There was a high consumption of the Southern dietary pattern in the US black population, regardless of other factors, underlying our previous findings showing the substantial contribution of this dietary pattern to racial disparities in incident hypertension and stroke.

Increased dietary Na intake and decreased dietary K intake are associated with higher blood pressure. It is not known whether the dietary Na:K ratio is associated with all-cause mortality or stroke incidence and whether this relationship varies according to race. Between 2003 and 2007, the REasons for Geographic And Racial Differences in Stroke (REGARDS) cohort enrolled 30 239 black and white Americans aged 45 years or older. Diet was assessed using the Block 98 FFQ and was available on 21 374 participants. The Na:K ratio was modelled in race- and sex-specific quintiles for all analyses, with the lowest quintile (Q1) as the reference group. Data on other covariates were collected using both an in-home assessment and telephone interviews. We identified 1779 deaths and 363 strokes over a mean of 4·9 years. We used Cox proportional hazards models to obtain multivariable-adjusted hazard ratios (HR). In the highest quintile (Q5), a high Na:K ratio was associated with all-cause mortality (Q5 v. Q1 for whites: HR 1·22; 95 % CI 1·00, 1·47, P for trend = 0·084; for blacks: HR 1·36; 95 % CI 1·04, 1·77, P for trend = 0·028). A high Na:K ratio was not significantly associated with stroke in whites (HR 1·29; 95 % CI 0·88, 1·90) or blacks (HR 1·39; 95 % CI 0·78, 2·48), partly because of the low number of stroke events. In the REGARDS study, a high Na:K ratio was associated with all-cause mortality and there was a suggestive association between the Na:K ratio and stroke. These data support the policies targeted at reduction of Na from the food supply and recommendations to increase K intake.

Although diet is thought to affect the natural history of heart failure (HF), nutrient intake in HF patients has not been well studied. Based on prior research linking high intake of Ca, Mg and K to improved cardiovascular health, we hypothesised that these nutrients would be inversely associated with mortality in people with HF. Of the 161 808 participants in the Women's Health Initiative (WHI), we studied 3340 who experienced a HF hospitalisation. These participants were followed for post-hospitalisation all-cause mortality. Intake was assessed using questionnaires on food and supplement intake. Hazard ratios (HR) and 95 % CI were calculated using Cox proportional hazards models adjusted for demographics, physical function, co-morbidities and dietary covariates. Over a median of 4·6 years of follow-up, 1433 (42·9 %) of the women died. HR across quartiles of dietary Ca intake were 1·00 (referent), 0·86 (95 % CI 0·73, 1·00), 0·88 (95 % CI 0·75, 1·04) and 0·92 (95 % CI 0·76, 1·11) (P for trend = 0·63). Corresponding HR were 1·00 (referent), 0·86 (95 % CI 0·71, 1·04), 0·88 (95 % CI 0·69, 1·11) and 0·84 (95 % CI 0·63, 1·12) (P for trend = 0·29), across quartiles of dietary Mg intake, and 1·00 (referent), 1·20 (95 % CI 1·01, 1·43), 1·06 (95 % CI 0·86, 1·32) and 1·16 (95 % CI 0·90, 1·51) (P for trend = 0·35), across quartiles of dietary K intake. Results were similar when total (dietary plus supplemental) nutrient intakes were examined. In summary, among WHI participants with incident HF hospitalisation, intakes of Ca, Mg and K were not significantly associated with subsequent mortality.

α-Linolenic acid (18 : 3n-3) intake and linoleic acid (18 : 2n-6) intake have been associated with lower rates of CHD, though results have not been consistent. The relationship of these fatty acids with incident heart failure (HF) is not well established. We examined the hypothesis that women with higher intakes of 18 : 3n-3 and 18 : 2n-6 would have lower rates of HF hospitalisation and mortality. We measured 18 : 3n-3 and 18 : 2n-6 intake in 36 234 Swedish Mammography Cohort participants aged 48–83 years using FFQ and followed participants through Swedish inpatient and cause-of-death registers from 1 January 1998 until 31 December 2006. Cox models were used to calculate incidence rate ratios (RR) and 95 % CI. Because of multicollinearity, 18 : 3n-3 and 18 : 2n-6 were examined separately. Over 9 years, 596 women were hospitalised and fifty-five died due to HF. In models accounting for age and other covariates, the RR for HF comparing the top quintile of 18 : 3n-3 (median 1·50 g/d) with the bottom quintile (median 0·88 g/d) was 0·91 (95 % CI 0·71, 1·17, Ptrend = 0·41). The RR comparing the top quintile of 18 : 2n-6 (median 7·8 g/d) with the bottom quintile (median 4·6 g/d) was 1·14 (95 % CI 0·88, 1·46, Ptrend = 0·36). We did not find evidence for the interaction of 18 : 3n-3 and 18 : 2n-6 with each other or with long-chain n-3 fatty acids. In conclusion, these data do not support our hypothesis that 18 : 3n-3 and 18 : 2n-6 are associated with HF. However, these results may not be generalisable to populations with higher intakes of 18 : 3n-3.

The association of dietary glycaemic index (GI) and glycaemic load (GL) with CVD has been examined in several populations with varying results. We tested the hypothesis that women with diets high in GI or GL would have higher rates of myocardial infarction (MI), and the associations would be stronger in overweight women. We measured dietary GI and GL in 36 234 Swedish Mammography Cohort participants aged 48–83 years using FFQ. Cox models were used to calculate incidence rate ratios (RR) and 95 % CI for hospitalisation or death due to MI assessed using the Swedish inpatient and cause-of-death registers from 1 January 1998 until 31 December 2006. Over 9 years of follow-up, 1138 women were hospitalised or died due to a first MI. In multivariable-adjusted models, the RR comparing top to bottom quartile of dietary GI were 1·12 (95 % CI 0·92, 1·35, P-trend = 0·24), and the RR comparing top to bottom quartile of dietary GL were 1·22 (95 % CI 0·90, 1·65, P-trend = 0·23). Among overweight women, the RR comparing top to bottom quartile of dietary GI were 1·20 (95 % CI 0·91, 1·58, P-trend = 0·22), and the RR comparing top to bottom quartile of dietary GL were 1·45 (95 % CI 0·93, 2·25, P-trend = 0·16). There were no statistically significant associations of dietary GI or GL with MI in this population.