The burden of depression is increasing worldwide, specifically in older adults. Unhealthy dietary patterns may partly explain this phenomenon. In the Spanish PREDIMED-Plus study, we explored (1) the cross-sectional association between the adherence to the Prime Diet Quality Score (PDQS), an a priori-defined high-quality food pattern, and the prevalence of depressive symptoms at baseline (cross-sectional analysis) and (2) the prospective association of baseline PDQS with changes in depressive symptomatology after 2 years of follow-up. After exclusions, we assessed 6612 participants in the cross-sectional analysis and 5523 participants in the prospective analysis. An energy-adjusted high-quality dietary score (PDQS) was assessed using a validated FFQ. The cross-sectional association between PDQS and the prevalence of depression or presence of depressive symptoms and the prospective changes in depressive symptoms were evaluated through multivariable regression models (logistic and linear models and mixed linear-effects models). PDQS was inversely associated with depressive status in the cross-sectional analysis. Participants in the highest quintile of PDQS (Q5) showed a significantly reduced odds of depression prevalence as compared to participants in the lowest quartile of PDQS (Q1) (OR (95 %) CI = 0·82 (0·68, 0·98))). The baseline prevalence of depression decreased across PDQS quintiles (Pfor trend = 0·015). A statistically significant association between PDQS and changes in depressive symptoms after 2-years follow-up was found (β (95 %) CI = −0·67 z-score (–1·17, −0·18). A higher PDQS was cross-sectionally related to a lower depressive status. Nevertheless, the null finding in our prospective analysis raises the possibility of reverse causality. Further prospective investigation is required to ascertain the association between PDQS and changes in depressive symptoms along time.

Prospective studies assessing the association between fibre intake or fibre-rich food consumption and the risk of CVD have often been limited by baseline assessment of diet. Thus far, no study has used yearly repeated measurements of dietary changes during follow-up. Moreover, previous studies included healthy and selected participants who did not represent subjects at high cardiovascular risk. We used yearly repeated measurements of diet to investigate the association between fibre intake and CVD in a Mediterranean cohort of elderly adults at high cardiovascular risk. We followed-up 7216 men (55–80 years) and women (60–80 years) initially free of CVD for up to 7 years in the PREvención con DIeta MEDiterránea study (registered as ISRCTN35739639). A 137-item validated FFQ was repeated yearly to assess diet. The primary end point, confirmed by a blinded ad hoc Event Adjudication Committee, was a composite of cardiovascular death, myocardial infarction and stroke. Time-dependent Cox’s regression models were used to estimate the risk of CVD according to baseline dietary exposures and to their yearly updated changes. We found a significant inverse association for fibre (Pfor trend=0·020) and fruits (Pfor trend=0·024) in age-sex adjusted models, but the statistical significance was lost in fully adjusted models. However, we found a significant inverse association with CVD incidence for the sum of fruit and vegetable consumption. Participants who consumed in total nine or more servings/d of fruits plus vegetables had a hazard ratio 0·60 (95 % CI 0·40, 0·96) of CVD in comparison with those consuming <5 servings/d.

Previous studies on the association between alcohol intake and the development of the metabolic syndrome (MetS) have yielded inconsistent results. Besides, few studies have analysed the effects of red wine (RW) consumption on the prevalence of the MetS and its components. As moderate RW drinkers have a better lipid profile and lower incidence rates of diabetes, hypertension and abdominal obesity, all components of the MetS, it was hypothesised that moderate RW consumption could be associated with a lower prevalence of the MetS. In the present cross-sectional study of 5801 elderly participants at a high cardiovascular risk included in the PREDIMED (Prevención con Dieta Mediterránea) study, 3897 fulfilled the criteria of the MetS at baseline. RW intake was recorded using a validated 137-item FFQ. Multiple logistic regression analysis was carried out to estimate the association between RW intake and the prevalence of the MetS. Compared with non-drinkers, moderate RW drinkers ( ≥ 1 drink/d) were found to have a reduced risk of prevalent MetS (OR 0·56, 95 % CI 0·45, 0·68; P< 0·001), a lower risk of having an abnormal waist circumference (OR 0·59, 95 % CI 0·46, 0·77; P< 0·001), low HDL-cholesterol concentrations (OR 0·42, 95 % CI 0·32, 0·53; P< 0·001), high blood pressure (OR 0·28, 95 % CI 0·17, 0·45; P< 0·001) and high fasting plasma glucose concentrations (OR 0·67, 95 % CI 0·54, 0·82; P< 0·001) after adjusting for several confounders. This association was found to be stronger in female participants, in participants aged < 70 years and in participants who were former or current smokers. No significant association was found between RW intake ( ≥ 1 drink/d) and TAG concentrations. In conclusion, moderate RW consumption is associated with a lower prevalence of the MetS in an elderly Mediterranean population at a high cardiovascular risk.

Nutritional genomics has undergone rapid development and the concept is now very popular with the general public. Therefore, there is increasing demand for knowledge on adapting dietary composition to the genome. Our aim has been to undertake a systematic review so as to find out the level of evidence existing on whether the effects of n-3 fatty acids on health can be modulated by genetic variation. A systematic literature search was conducted on studies that jointly analyse the effect of one or more genetic variants in candidate genes and n-3 fatty acids. Both observational and experimental studies were included. Results are classified in accordance with whether the study was undertaken on intermediate phenotypes (plasma lipid concentrations, glucose, inflammation markers, anthropometric measurements) or disease phenotypes (cancer, cardiovascular diseases, metabolic syndrome, etc) and whether it was experimental or observational. A wide diversity of genetic variants and little consistency in the publication of replication studies was found. Greater consistency was observed in studies that involved the FADS1 and FADS2 locus in the determination of n-3 fatty acid concentrations in biological samples. Most of the studies were designed to measure gene-diet interactions and not diet-gene interactions. Despite the fact that multiple studies have shown statistically significant interactions between n-3 fatty acids and certain genetic variants on intermediate and disease phenotypes, the individual level of evidence is very low and recommendations cannot be made on increasing or reducing the intake of n-3 fatty acids based on each individual's genotype.

The SNP rs1260326 (P446L) and rs1799884 ( − 30G>A) for the glucokinase regulatory protein (GCKR) and glucokinase (GCK) genes, respectively, have been associated with opposing effects on TAG and glucose concentrations. However, their genetic modulation by diet (dietary patterns or foods) remains to be investigated. We studied 945 high-cardiovascular risk subjects aged 67 (sd 6) years who participated in the PREvención con DIeta MEDiterránea-Valencia Study. Demographic, clinical, biochemical and genetic data were obtained. Adherence to the Mediterranean diet (MD) and food intake were measured by validated questionnaires. Carriers of the L allele of GKCR had significantly higher TAG concentrations (PP: 1·34 (sd 0·05) mmol/l v. PL+LL: 1·54 (sd 0·03) mmol/l; P= 0·014) and LL carriers had lower glucose concentrations (PL+PP: 6·85 (sd 0·08) mmol/l v. LL: 6·40 (sd 0·16) mmol/l; P= 0·032) after multivariate adjustment. Conversely, homozygous subjects for the variant allele (A) in the GCK gene had significantly lower TAG (GG+GA: 1·48 (sd 0·03) mmol/l v. AA: 1·17 (sd 0·18) mmol/l; P= 0·033) and a higher risk of diabetes (OR 3·3, 95 % CI 1·2, 9·2). Combined effects for both SNP increased TAG concentrations by 37 % (P= 0·033). Adherence to the MD modulated the effects of GCKR polymorphism on TAG: subjects with genetic risk had lower TAG (L-allele carriers; PP: 1·48 (sd 0·14) mmol/l v. PL+LL: 1·51 (sd 0·08) mmol/l; P= 0·917) compared with those with a higher adherence. Analysis of the joint effects of the GCKR and individual food items identified significant associations (olive oil (P= 0·035), vegetables (P= 0·012), red meat (P= 0·017), butter (P= 0·039), sweetened carbonated beverages (P= 0·036) and nuts (P= 0·038)). In conclusion, we found that rs1260326 (GCKR) is significantly associated with higher TAG concentrations, but is modulated by adherence to the MD.

The aim of the present study was to assess reproducibility and relative validity of a self-administered FFQ used in the PREDIMED Study, a clinical trial for primary prevention of CVD by Mediterranean diet in a population at high cardiovascular risk. The FFQ was administered twice (FFQ1 and FFQ2) to explore reproducibility at 1 year. Four 3 d dietary records (DR) were used as reference to explore validity; participants therefore recorded their food intake over 12 d in the course of 1 year. The degree of misclassification in the FFQ was also evaluated by a contingency table of quintiles comparing the information from the FFQ2 and the DR. A total of 158 men and women (aged 55–80 years) were asked not to modify their dietary habits during the study period. Reproducibility for food groups, energy and nutrient intake, explored by the Pearson correlation coefficient (r) ranged 0·50–0·82, and the intraclass correlation coefficient (ICC) ranged from 0·63 to 0·90. The FFQ2 tended to report higher energy and nutrient intake than the DR. The validity indices of the FFQ in relation to the DR for food groups and energy and nutrient intake ranged (r) from 0·24 to 0·72, while the range of the ICC was between 0·40 and 0·84. With regard to food groups, 68–83 % of individuals were in the same or adjacent quintile in both methods, a figure which decreased to 55–75 % for energy and nutrient intake. We concluded that FFQ measurements had good reproducibility and a relative validity similar to those of FFQ used in other prospective studies.

The PPARγ gene regulates insulin sensitivity and adipogenesis. The Pro12Ala polymorphism of this gene has been related to fat accumulation. Our aim was to analyse the effects of a 2-year nutritional intervention with Mediterranean-style diets on adiposity in high-cardiovascular risk patients depending on the Pro12Ala polymorphism of the PPARγ gene. The population consisted of a substudy (774 high-risk subjects aged 55–80 years) of the Prevención con Dieta Mediterránea (PREDIMED) randomised trial aimed at assessing the effect of the Mediterranean diet for CVD prevention. There were three nutritional intervention groups: two of them of a Mediterranean-style diet and the third was a control group advised to follow a conventional low-fat diet. All the participants were genotyped by PCR-restriction fragment length polymorphism (RFLP). The results showed that carriers of the 12Ala allele allocated to the control group had a statistically significant higher change in waist circumference (adjusted difference coefficient = 2·37 cm; P = 0·014) compared with wild-type subjects after 2 years of nutritional intervention. This adverse effect was not observed among 12Ala carriers allocated to both Mediterranean diet groups. In diabetic patients a statistically significant interaction between Mediterranean diet and the 12Ala allele regarding waist circumference change was observed ( − 5·85 cm; P = 0·003). In conclusion, the Mediterranean diet seems to be able to reduce waist circumference in a high-cardiovascular risk population, reversing the negative effect that the 12Ala allele carriers of the PPARγ gene appeared to have. The beneficial effect of this dietary pattern seems to be higher among type 2 diabetic subjects.

High blood pressure (BP) has been ranked as the most important risk factor worldwide regarding attributable deaths. Dietary habits are major determinants of BP. Among them, frequent intake of low-fat dairy products may protect against hypertension. Our aim was to assess the relationship between low-fat dairy product intake and BP levels and their changes after 12-month follow-up in a cohort of asymptomatic older persons at high cardiovascular risk recruited into a large-scale trial assessing the effects of Mediterranean diets on cardiovascular outcomes. Data from 2290 participants, including 1845 with hypertension, were available for analyses. Dairy products were not a specific part of the intervention; thus, data were analysed as an observational cohort. Dietary information was collected with validated semi-quantitative FFQ and trained personnel measured BP. To assess BP changes, we undertook cross-sectional analyses at baseline and at the end of follow-up and longitudinal analyses. A statistically significant inverse association between low-fat dairy product intake and systolic BP was observed for the 12-month longitudinal analysis. In the longitudinal analysis, the adjusted systolic and diastolic BP were significantly lower in the highest quintile of low-fat dairy product intake ( − 4·2 (95% CI − 6·9, − 1·4) and − 1·8 (95% CI − 3·2, − 0·4) mmHg respectively), whereas the point estimates for the difference in diastolic BP indicated a modest non-significant inverse association. Intake of low-fat dairy products was inversely associated with BP in an older population at high cardiovascular risk, suggesting a possible protective effect against hypertension.

Nutrigenomics is the study of how constituents of the diet interact with genes, and their products, to alter phenotype and, conversely, how genes and their products metabolise these constituents into nutrients, antinutrients, and bioactive compounds. Results from molecular and genetic epidemiological studies indicate that dietary unbalance can alter gene–nutrient interactions in ways that increase the risk of developing chronic disease. The interplay of human genetic variation and environmental factors will make identifying causative genes and nutrients a formidable, but not intractable, challenge. We provide specific recommendations for how to best meet this challenge and discuss the need for new methodologies and the use of comprehensive analyses of nutrient–genotype interactions involving large and diverse populations. The objective of the present paper is to stimulate discourse and collaboration among nutrigenomic researchers and stakeholders, a process that will lead to an increase in global health and wellness by reducing health disparities in developed and developing countries.