OBJECTIVES
Limited data suggest that a healthy diet is associated with a lower risk of frailty. We sought to assess the relationship between three measures of diet quality and frailty among male ...physicians.
DESIGN
Cross‐sectional analysis of a cohort study.
SETTING
Physicians’ Health Study.
PARTICIPANTS
A total of 9861 initially healthy US men, aged 60 years or older, who provided data on frailty status and dietary habits.
MEASUREMENTS
A cumulative deficit frailty index (FI) was calculated using 33 variables encompassing domains of comorbidity, functional status, mood, general health, social isolation, and change in weight. Diet quality was measured using the Alternative Healthy Eating Index (aHEI), Mediterranean Diet Score (MDS), and Dietary Approaches to Stop Hypertension (DASH).
RESULTS
The FI identified 38% of physicians as non‐frail, 44% as pre‐frail, and 18% as frail. Multinomial logistic regression models adjusted for age, smoking status, and energy intake showed that compared with the lowest aHEI quintiles, those in the highest quintiles had lower odds of frailty and pre‐frailty compared with non‐frailty (odds ratio OR for frailty = .47; 95% confidence interval CI = .39‐.58; for pre‐frailty: OR = .75; CI = .65‐.87). Exercise did not modify this association (P interaction >.1). Similar relationships were observed for DASH and MDS quintiles with frailty and pre‐frailty. Restricted cubic splines showed an inverse dose‐response relationship of diet quality scores with odds of frailty and pre‐frailty.
CONCLUSION
Cross‐sectional data show an inverse dose‐response relationship of diet quality with pre‐frailty and frailty. Future longitudinal studies are needed to investigate whether healthier diet is a modifiable risk factor for frailty.
ClinicalTrials.gov identifier: NCT00000500. J Am Geriatr Soc 68:770–776, 2020
The relationship between omega-3 polyunsaturated fatty acids (n-3 PUFA) from seafood sources (eicosapentaenoic acid, EPA; docosahexaenoic acid, DHA) or plant sources (alpha-linolenic acid, ALA) and ...risk of type 2 diabetes mellitus (DM) remains unclear. We systematically searched multiple literature databases through June 2011 to identify prospective studies examining relations of dietary n-3 PUFA, dietary fish and/or seafood, and circulating n-3 PUFA biomarkers with incidence of DM. Data were independently extracted in duplicate by 2 investigators, including multivariate-adjusted relative risk (RR) estimates and corresponding 95 % CI. Generalized least-squares trend estimation was used to assess dose-response relationships, with pooled summary estimates calculated by both fixed-effect and random-effect models. From 288 identified abstracts, 16 studies met inclusion criteria, including 18 separate cohorts comprising 540,184 individuals and 25,670 cases of incident DM. Consumption of fish and/or seafood was not significantly associated with DM (n = 13 studies; RR per 100 g/d = 1·12, 95 % CI = 0·94, 1·34); nor were consumption of EPA+DHA (n = 16 cohorts; RR per 250 mg/d = 1·04, 95 % CI = 0·97, 1·10) nor circulating levels of EPA+DHA biomarkers (n = 5 cohorts; RR per 3 % of total fatty acids = 0·94, 95 % CI = 0·75, 1·17). Both dietary ALA (n = 7 studies; RR per 0·5 g/d = 0·93, 95 % CI = 0·83, 1·04) and circulating ALA biomarker levels (n = 6 studies; RR per 0·1 % of total fatty acid = 0·90, 95 % CI = 0·80, 1·00, P = 0·06) were associated with non-significant trend towards lower risk of DM. Substantial heterogeneity (I²~80 %) was observed among studies of fish/seafood or EPA+DHA and DM; moderate heterogeneity ( < 55 %) was seen for dietary and biomarker ALA and DM. In unadjusted meta-regressions, study location (Asia vs. North America/Europe), mean BMI, and duration of follow-up each modified the association between fish/seafood and EPA+DHA consumption and DM risk (P-interaction ≤ 0·02 each). We had limited statistical power to determine the independent effect of these sources of heterogeneity due to their high collinearity. The overall pooled findings do not support either major harms or benefits of fish/seafood or EPA+DHA on development of DM, and suggest that ALA may be associated with modestly lower risk. Reasons for potential heterogeneity of effects, which could include true biologic heterogeneity, publication bias, or chance, deserve further investigation.
Purpose
While tree nut consumption has been shown to be cardioprotective, a few studies have examined the relationship between tree nut consumption and carotid atherosclerosis. We tested the ...hypothesis that tree nut consumption would be inversely related with carotid atherosclerosis in adults.
Methods
We cross-sectionally analyzed data from 4536 participants of the National Heart, Lung, and Blood Institute (NHLBI) Family Heart Study conducted in the United States. Dietary patterns among participants were variable, tree nut consumption was self-reported using the Food Frequency Questionnaire (FFQ), and B-mode ultrasound of the carotid arteries was used to assess for the presence of carotid artery plaques (primary outcome) and carotid intima media thickness (cIMT). Multivariable logistic regression was used to estimate odds ratio (95% confidence interval) of prevalent carotid artery plaques and linear regression was used to estimate adjusted mean cIMT across categories of nut consumption.
Results
The mean age was 52.3 years (SD = 13.6), 95.6% of the participants were white, and 54% were female. The median tree nut intake was 1–3 servings/month. Odds ratios (95% CI) for prevalent carotid artery plaques were 1.0 (reference), 1.03 0.86, 1.4, 0.89 0.70, 1.13, and 0.96 0.73, 1.26 for tree nut consumption of almost never, 1–3 times/month, 1/week, and 2+/week, respectively, adjusting for age, sex, race, field center, BMI, smoking status, alcohol consumption, creatinine, energy intake, fruit and vegetable consumption, exercise, and education. In secondary analysis, there was a suggestive inverse association of tree nut consumption with cIMT in the internal carotid artery, but not the common carotid or bifurcation.
Conclusion
Our data showed no association between tree nut consumption and prevalence of carotid artery plaques in adults.
Focused studies in younger to middle-aged populations have demonstrated a relationship between obesity and adverse cardiac mechanics. We examined whether measures of overall and central adiposity are ...associated with cardiac mechanics, assessed by speckle-tracking echocardiography, in an older population without prevalent coronary heart disease or heart failure.
Body composition was measured by anthropometry, bioelectrical impedance, and dual-energy x-ray absorptiometry among participants in the Cardiovascular Health Study, a population-based cohort of adults aged 65 years or older. Systolic and diastolic cardiac mechanics were measured with speckle-tracking analysis of echocardiograms. Multi-variable adjusted linear regression models were used to investigate associations of body composition measures and cardiac mechanics.
Mean age for the 3525 included participants was 72.6 years, 39% were male, and 10% were black. Mean body-mass index (BMI) was 26.3 ± 4.4 kg/m
, waist circumference (WC) was 93.2 ± 12.9 cm, and waist-to-hip ratio was 0.92 ± 0.09. In fully adjusted analyses, all adiposity measures were associated with worse LV longitudinal strain, LV early diastolic strain rate, and left atrial reservoir strain; however, associations were strongest for WC and BMI (p < 0.001). When both BMI and WC were included in the same model, only WC remained associated with each cardiac strain measure.
In this cross-sectional study of older adults, central obesity was most robustly associated with impaired left ventricular systolic and diastolic strain as well as left atrial strain. The adverse effects of central obesity appear to extend even into older age.
Elevated body mass index (BMI) is heritable and associated with many health conditions that impact morbidity and mortality. The study of the genetic association of BMI across a broad range of common ...disease conditions offers the opportunity to extend current knowledge regarding the breadth and depth of adiposity-related diseases. We identify 906 (364 novel) and 41 (6 novel) genome-wide significant loci for BMI among participants of European (N~1.1 million) and African (N~100,000) ancestry, respectively. Using a BMI genetic risk score including 2446 variants, 316 diagnoses are associated in the Million Veteran Program, with 96.5% showing increased risk. A co-morbidity network analysis reveals seven disease communities containing multiple interconnected diseases associated with BMI as well as extensive connections across communities. Mendelian randomization analysis confirms numerous phenotypes across a breadth of organ systems, including conditions of the circulatory (heart failure, ischemic heart disease, atrial fibrillation), genitourinary (chronic renal failure), respiratory (respiratory failure, asthma), musculoskeletal and dermatologic systems that are deeply interconnected within and across the disease communities. This work shows that the complex genetic architecture of BMI associates with a broad range of major health conditions, supporting the need for comprehensive approaches to prevent and treat obesity.
Long-chain n-3 polyunsaturated fatty acids (PUFAs) can derive from diet or from α-linolenic acid (ALA) by elongation and desaturation. We investigated the association of common genetic variation with ...plasma phospholipid levels of the four major n-3 PUFAs by performing genome-wide association studies in five population-based cohorts comprising 8,866 subjects of European ancestry. Minor alleles of SNPs in FADS1 and FADS2 (desaturases) were associated with higher levels of ALA (p = 3 x 10⁻⁶⁴) and lower levels of eicosapentaenoic acid (EPA, p = 5 x 10⁻⁵⁸) and docosapentaenoic acid (DPA, p = 4 x 10⁻¹⁵⁴). Minor alleles of SNPs in ELOVL2 (elongase) were associated with higher EPA (p = 2 x 10⁻¹²) and DPA (p = 1 x 10⁻⁴³) and lower docosahexaenoic acid (DHA, p = 1 x 10⁻¹⁵). In addition to genes in the n-3 pathway, we identified a novel association of DPA with several SNPs in GCKR (glucokinase regulator, p = 1 x 10⁻⁸). We observed a weaker association between ALA and EPA among carriers of the minor allele of a representative SNP in FADS2 (rs1535), suggesting a lower rate of ALA-to-EPA conversion in these subjects. In samples of African, Chinese, and Hispanic ancestry, associations of n-3 PUFAs were similar with a representative SNP in FADS1 but less consistent with a representative SNP in ELOVL2. Our findings show that common variation in n-3 metabolic pathway genes and in GCKR influences plasma phospholipid levels of n-3 PUFAs in populations of European ancestry and, for FADS1, in other ancestries.
Pharmacologic clinical trials for heart failure with preserved ejection fraction have been largely unsuccessful as compared to those for heart failure with reduced ejection fraction. Whether ...differences in the genetic underpinnings of these major heart failure subtypes may provide insights into the disparate outcomes of clinical trials remains unknown. We utilize a large, uniformly phenotyped, single cohort of heart failure sub-classified into heart failure with reduced and with preserved ejection fractions based on current clinical definitions, to conduct detailed genetic analyses of the two heart failure sub-types. We find different genetic architectures and distinct genetic association profiles between heart failure with reduced and with preserved ejection fraction suggesting differences in underlying pathobiology. The modest genetic discovery for heart failure with preserved ejection fraction (one locus) compared to heart failure with reduced ejection fraction (13 loci) despite comparable sample sizes indicates that clinically defined heart failure with preserved ejection fraction likely represents the amalgamation of several, distinct pathobiological entities. Development of consensus sub-phenotyping of heart failure with preserved ejection fraction is paramount to better dissect the underlying genetic signals and contributors to this highly prevalent condition.
Recent studies suggest that the type of saturated fatty acid bound to sphingolipids influences the biological activity of those sphingolipids. However, it is unknown whether associations of ...sphingolipids with diabetes may differ by the identity of bound lipid species. Here, we investigated associations of 15 ceramide (Cer) and SM species (i.e., all sphingolipids, measured with coefficient of variation less than 20%) with incident type 2 diabetes in the Cardiovascular Health Study (n = 3,645), a large cohort study of cardiovascular disease among elderly adults who were followed from 1989 to 2015. Diabetes incidence was defined as fasting glucose ≥126 mg/dl or nonfasting glucose ≥200 mg/dl; reported use of insulin or oral hypoglycemic medication; or documentation of diabetes diagnosis through the Centers for Medicare and Medicaid Services records. Associations of each sphingolipid with incident diabetes were assessed using a Cox proportional hazards regression model. We found that higher circulating levels of Cer with acylated palmitic acid (Cer-16), stearic acid containing Cer (Cer-18), arachidic acid containing Cer (Cer-20), and behenic acid containing Cer (Cer-22) were each associated with a higher risk of diabetes. The hazard ratios for incident diabetes per 1 SD higher log levels of each Cer species were as follows: 1.21 (95% CI: 1.09–1.34) for Cer-16, 1.23 (95% CI: 1.10–1.37) for Cer-18, 1.14 (95% CI: 1.02–1.26) for Cer-20, and 1.18 (95% CI: 1.06–1.32) for Cer-22. In conclusion, higher levels of Cer-16, Cer-18, Cer-20, and Cer-22 were associated with a higher risk of diabetes.
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