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Objective: We aimed to study whether dietary fat composition (n-3 and n-6 polyunsaturated fatty acids ratio (PUFAs) and PUFAs and saturated fatty acids (SFAs) ratio) is associated with total body fat (TF) and body fat distribution and whether this association was modified by the presence of chronic disease in middle-aged and elderly women in two population-based cohorts in the Netherlands and Australia., Methods: The study was performed in the Rotterdam Study (RS), a prospective cohort study among subjects aged 55 years and older (N = 1182 women) and the Calcium Intake Fracture Outcome Study (CAIFOS), a 5-year randomized controlled trial among women age 70+ (N = 891). At baseline, diet (i.e. PUFAs and SFAs) was measured by validated food frequency questionnaires. TF was assessed using Dual-energy X-ray absorptiometry in both studies and android abdominal fat (AF), gynoid fat (GF) and the android/gynoid ratio (A/G ratio) in the RS but not the CAIFOS. Chronic disease was defined as the presence of cardiovascular disease, diabetes mellitus and cancer., Results: No association was found between dietary n-3/n-6 PUFAs ratio or SFA/PUFAs ratio with TF in both cohorts. In the RS, a high n-3/n-6 PUFAs ratio was associated with a higher AF (3rd vs. 2nd tertile (reference): β: 0.15; 95% CI: 0.05, 0.24) but not with the A/G ratio. A low SFA/PUFA ratio was associated with a lower AF (1st vs. 2nd tertile (reference): β: -0.12; 95% CI: -0.22, -0.06) but not with the A/G ratio. Presence of chronic disease was found to be a significant effect modifier in both cohorts with regard to n-3/n-6 PUFAs and TF (P < 0.05). In participants without chronic disease, a higher n-3/n-6 PUFAs ratio was associated with a higher TF in the RS cohort (3rd vs. 2nd tertile (reference): β: 0.94; 95% CI: 0.12, 1.76), but this was not replicated in CAIFOS., Conclusion: These findings do not support the hypothesis that dietary fat composition is consistently associated with TF and body fat distribution in women. Future studies should clarify to what extent these findings may be influenced by the presence of chronic disease., (Copyright © 2016 Elsevier Ltd and European Society for Clinical Nutrition and Metabolism. All rights reserved.)

It remains largely unclear whether consumption of total and individual polyunsaturated fatty acids (PUFAs) is associated with chronic systemic inflammation in healthy, free-living individuals. While available evidence (stemming principally from mechanistic studies) has indicated that greater intake of n-6 PUFAs may lead to increased levels of inflammation-for instance, by their acting as precursors to proinflammatory eicosanoids and increasing levels of oxidized linoleic acid metabolites-n-3 PUFAs are precursors to some antiinflammatory eicosanoids. New human data from a Dutch prospective study, the Rotterdam Study-as presented by Muka et al. ( Am J Epidemiol. 2015;181(11):846-856) in this issue of the Journal-now make an important contribution to the relatively scarce literature on the association of dietary n-3 and n-6 PUFAs with serum levels of C-reactive protein (CRP), a key marker of inflammation, in a general population. The study by Muka et al. benefitted from repeated CRP measurements, comprehensive correction for potential confounding, and wide-ranging sensitivity analyses. The findings show no significant trend regarding n-3 PUFAs but indicate an important inverse association between n-6 PUFAs and chronic systemic inflammation. This study provides support for existing dietary guidelines, which encourage consumption of a combination of n-3 and n-6 PUFAs in the diet., (© The Author 2015. Published by Oxford University Press on behalf of the Johns Hopkins Bloomberg School of Public Health. All rights reserved. For permissions, please e-mail: journals.permissions@oup.com.)

Background: Dietary polyunsaturated fatty acids (PUFA) are inversely related to coronary heart disease (CHD) in epidemiological studies. We examined the associations of plasma n-6 and n-3 PUFA in cholesteryl esters with fatal CHD in a nested case-control study. Additionally, we performed a dose-response meta-analysis of similar prospective studies on cholesteryl ester PUFA., Methods: We used data from two population-based cohort studies in Dutch adults aged 20-65 y. Blood and data collection took place from 1987-1997 and subjects were followed for 8-19 y. We identified 279 incident cases of fatal CHD and randomly selected 279 controls, matched on age, gender, and enrollment date. Odds ratios (OR) were calculated per standard deviation (SD) increase of cholesteryl ester PUFA., Results: After adjustment for confounders, the OR (95%CI) for fatal CHD per SD increase in plasma linoleic acid was 0.89 (0.74-1.06). Additional adjustment for plasma total cholesterol and systolic blood pressure attenuated this association (OR:0.95; 95%CI: 0.78-1.15). Arachidonic acid was not associated with fatal CHD (OR per SD:1.11; 95%CI: 0.92-1.35). The ORs (95%CI) for fatal CHD for an SD increase in n-3 PUFA were 0.92 (0.74-1.15) for alpha-linolenic acid and 1.06 (0.88-1.27) for EPA-DHA. In the meta-analysis, a 5% higher linoleic acid level was associated with a 9% lower risk (relative risk: 0.91; 95% CI: 0.84-0.98) of CHD. The other fatty acids were not associated with CHD., Conclusion: In this Dutch population, n-6 and n-3 PUFA in cholesteryl esters were not significantly related to fatal CHD. Our data, together with findings from previous prospective studies, support that linoleic acid in plasma cholesteryl is inversely associated with CHD.

Background: A reduced dietary intake of n-3 fatty acids, in association with increased n-6 fatty acid intake, has been proposed as a potential aetiological factor for chronic obstructive pulmonary disease (COPD) and asthma. However, the relative importance of individual fatty acids within the n-3 and n-6 categories on this effect has not been widely investigated. We have studied the relation between individual fatty acid intakes, lung function and self-reported respiratory symptoms and diagnoses in a representative sample of more than 13,000 Dutch adults., Methods: Intake of individual fatty acids was estimated by a food frequency questionnaire and analysed in relation to measures of forced expiratory volume in 1 s (FEV1) and to questionnaire reported wheeze, asthma and COPD symptoms., Results: After adjusting for confounding, we found no protective association between individual n-3 fatty acid intakes and FEV1. Higher intakes of some n-6 fatty acids were associated with lower FEV1, this effect being most marked for c22:4 n-6 docosatetraenoic acid (reduction in FEV1 between the highest and lowest quintile of intake 54.5 ml (95% CI -81.6 to -27.4)). Most of the n-6 fatty acid effects interacted significantly with smoking, their effects being strongest in current smokers. Individual n-3 fatty acid intakes were generally associated with a higher risk of wheeze in the past year, but otherwise there was little or no association between fatty acid intake and wheeze, doctor diagnosed asthma or other respiratory symptoms., Conclusions: A high intake of n-3 fatty acids does not appear to protect against COPD or asthma, but a high intake of several n-6 fatty acids is associated with a significant reduction in FEV1, particularly in smokers. These findings indicate that high dietary intake of n-6 fatty acids, rather than reduced n-3 intake, may have an adverse effect on lung health.