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Objectives. We investigated whether eating behaviors were concordant among diverse sets of social ties. Methods. We analyzed the socioeconomic and demographic distribution of eating among 3418 members of the Framingham Heart Study observed from 1991 to 2001. We used a data-classification procedure to simplify choices into 7 nonoverlapping patterns that we matched with information on social network ties. We used correlation analysis to examine eating associations among 4 types of peers (spouses, friends, brothers, and sisters). Longitudinal multiple logistic regression was used to evaluate evidence for peer influences on eating. Results. Of all peer types, spouses showed the strongest concordances in eating patterns over time after adjustment for social contextual factors. Across all peers, the eating pattern most likely to be shared by socially connected individuals was “alcohol and snacks.” Models estimating one's current eating pattern on the basis of a peer's prior eating provided supportive evidence of a social influence process. Conclusions. Certain eating patterns appeared to be socially transmissible across different kinds of relationships. These findings represent an important step in specifying the relevant social environment in the study of health behaviors to include eating.

Dietary protein plays a role in counteracting age-related muscle loss. However, limited long-term data exist on protein intake and markers of cardiometabolic health, which tend to deteriorate with age. Prospective cohort study. FFQ-derived protein intake (g/d) and cardiometabolic markers were assessed up to five times across 20 years. Markers included systolic (SBP) and diastolic (DBP) blood pressures, circulating lipids (total, HDL and LDL cholesterol; TAG), estimated glomerular filtration rate (eGFR), fasting glucose (FG), weight and waist circumference (WC). Mixed models accounting for repeated measures were used to estimate adjusted mean annualized changes in outcomes per quartile category of protein. Framingham Heart Study Offspring cohort, USA. Participants (n 3066) with 12 333 unique observations, baseline (mean (sd)) age=54·0 (9·7) years, BMI=27·4 (4·9) kg/m2, 53·5 % female. In fully adjusted models, there were favourable associations (mean (se)) of total protein with annualized changes in SBP (lowest v. highest intake: 0·34 (0·06) v. 0·04 (0·06) mmHg, P trend=0·001) and eGFR (-1·03 (0·06) v. -0·87 (0·05) ml/min per 1·73 m2, P trend=0·046), unfavourable associations with changes in FG (0·013 (0·004) v. 0·028 (0·004) mmol/l, P trend=0·004) and no associations with weight, WC, DBP or lipids. Animal protein was favourably associated with SBP and unfavourably with FG and WC; plant protein was favourably associated with FG and WC. The present study provides evidence that protein intake may influence changes in cardiometabolic health independent of change in weight in healthy adults and that protein's role in cardiometabolic health may depend on the protein source.

Amino acid profiles could aid in diabetes risk assessment, as a five-amino-acid signature had highly significant associations with the development of future diabetes in two large, independent cohorts. Emerging technologies allow the high-throughput profiling of metabolic status from a blood specimen (metabolomics). We investigated whether metabolite profiles could predict the development of diabetes. Among 2,422 normoglycemic individuals followed for 12 years, 201 developed diabetes. Amino acids, amines and other polar metabolites were profiled in baseline specimens by liquid chromatography–tandem mass spectrometry (LC-MS). Cases and controls were matched for age, body mass index and fasting glucose. Five branched-chain and aromatic amino acids had highly significant associations with future diabetes: isoleucine, leucine, valine, tyrosine and phenylalanine. A combination of three amino acids predicted future diabetes (with a more than fivefold higher risk for individuals in top quartile). The results were replicated in an independent, prospective cohort. These findings underscore the potential key role of amino acid metabolism early in the pathogenesis of diabetes and suggest that amino acid profiles could aid in diabetes risk assessment.

In a recent study of older participants (age >=60 years) in the 1999-2002 National Health and Nutrition Examination Survey (NHANES), we showed that a combination of high serum folate and low vitamin B₁₂ status was associated with higher prevalence of cognitive impairment and anemia than other combinations of vitamin B₁₂ and folate status. In the present study, we sought to determine the joint influence of serum folate and vitamin B₁₂ concentrations on two functional indicators of vitamin B₁₂ status, total homocysteine (tHcy) and methylmalonic acid (MMA), among adult participants in phase 2 of the NHANES III (1991-1994) and the NHANES 1999-2002. Exclusion of subjects who were <20 years old, were pregnant, had evidence of kidney or liver dysfunction, or reported a history of alcohol abuse or recent anemia therapy left 4,940 NHANES III participants and 5,473 NHANES 1999-2002 participants for the study. Multivariate analyses controlled for demographic factors, smoking, alcohol use, body mass index, self-reported diabetes diagnosis, and serum concentrations of creatinine and alanine aminotransferase revealed significant interactions between serum folate and serum vitamin B₁₂ in relation to circulating concentrations of both metabolites. In subjects with serum vitamin B₁₂ >148 pmol/liter (L), concentrations of both metabolites decreased significantly as serum folate increased. In subjects with lower serum vitamin B₁₂, however, metabolite concentrations increased as serum folate increased starting at [almost equal to]20 nmol/L. These results suggest a worsening of vitamin B₁₂'s enzymatic functions as folate status increases in people who are vitamin B₁₂-deficient.

Adiposity, Cardiometabolic Risk, and Vitamin D Status: The Framingham Heart Study Susan Cheng 1 , 2 , 3 , 4 , Joseph M. Massaro 1 , 5 , Caroline S. Fox 1 , 6 , 7 , Martin G. Larson 1 , 5 , Michelle J. Keyes 1 , 5 , Elizabeth L. McCabe 1 , 2 , Sander J. Robins 1 , 8 , Christopher J. O'Donnell 1 , 2 , 6 , Udo Hoffmann 9 , Paul F. Jacques 10 , Sarah L. Booth 10 , Ramachandran S. Vasan 1 , 8 , 11 , Myles Wolf 12 and Thomas J. Wang 1 , 2 1 Framingham Heart Study, Framingham, Massachusetts; 2 Cardiology Division, Massachusetts General Hospital, Harvard Medical School, Boston, Massachusetts; 3 Division of Cardiovascular Medicine, Department of Medicine, Brigham and Women's Hospital, Harvard Medical School, Boston, Massachusetts; 4 Clinical Investigator Training Program, Beth Israel Deaconness Medical Center, Harvard Medical School, Boston, Massachusetts; 5 Department of Mathematics and Statistics, Boston University, Boston, Massachusetts; 6 Center for Population Studies, National Heart, Lung, and Blood Institute, Bethesda, Maryland; 7 Division of Endocrinology, Metabolism, and Diabetes, Department of Medicine, Brigham and Women's Hospital, Harvard Medical School, Boston, Massachusetts; 8 Department of Medicine, Boston University School of Medicine, Boston, Massachusetts; 9 Radiology Department, Massachusetts General Hospital, Harvard Medical School, Boston, Massachusetts; 10 Nutritional Epidemiology Program, Jean Mayer U.S. Department of Agriculture Human Nutrition Research Center on Aging, Tufts University, Boston, Massachusetts; 11 Epidemiology Department, Boston University School of Public Health, Boston, Massachusetts; 12 Division of Nephrology and Hypertension, Department of Medicine, University of Miami Miller School of Medicine, Miami, Florida. Corresponding author: Thomas J. Wang, tjwang{at}partners.org . Abstract OBJECTIVE Because vitamin D deficiency is associated with a variety of chronic diseases, understanding the characteristics that promote vitamin D deficiency in otherwise healthy adults could have important clinical implications. Few studies relating vitamin D deficiency to obesity have included direct measures of adiposity. Furthermore, the degree to which vitamin D is associated with metabolic traits after adjusting for adiposity measures is unclear. RESEARCH DESIGN AND METHODS We investigated the relations of serum 25-hydroxyvitamin D (25[OH]D) concentrations with indexes of cardiometabolic risk in 3,890 nondiabetic individuals; 1,882 had subcutaneous adipose tissue (SAT) and visceral adipose tissue (VAT) volumes measured by multidetector computed tomography (CT). RESULTS In multivariable-adjusted regression models, 25(OH)D was inversely associated with winter season, waist circumference, and serum insulin ( P < 0.005 for all). In models further adjusted for CT measures, 25(OH)D was inversely related to SAT (−1.1 ng/ml per SD increment in SAT, P = 0.016) and VAT (−2.3 ng/ml per SD, P < 0.0001). The association of 25(OH)D with insulin resistance measures became nonsignificant after adjustment for VAT. Higher adiposity volumes were correlated with lower 25(OH)D across different categories of BMI, including in lean individuals (BMI <25 kg/m 2 ). The prevalence of vitamin D deficiency (25[OH]D <20 ng/ml) was threefold higher in those with high SAT and high VAT than in those with low SAT and low VAT ( P < 0.0001). CONCLUSIONS Vitamin D status is strongly associated with variation in subcutaneous and especially visceral adiposity. The mechanisms by which adiposity promotes vitamin D deficiency warrant further study. Footnotes The costs of publication of this article were defrayed in part by the payment of page charges. This article must therefore be hereby marked “advertisement” in accordance with 18 U.S.C. Section 1734 solely to indicate this fact. Received July 10, 2009. Accepted September 22, 2009. © 2010 American Diabetes Association

Resistance training is recognised as a good strategy for retarding age-related declines in muscle mass and strength. Recent studies have also highlighted the potential value of protein intakes in excess of present recommendations. The roles that leisure-time physical activity and protein quality play in the preservation of skeletal muscle during ageing, and how such influences interact in free-living people are unclear. We sought to clarify these issues using data collected on 2425 participants aged ≥ 50 years in the US National Health and Nutrition Examination Survey (2003–2006). We estimated subjects’ usual intakes of total protein and beef from two 24 h diet recalls and computed the appendicular skeletal muscle mass index from anthropometric measures. Participants self-reported their physical activity levels. Analyses accounted for demographic factors and smoking. The association between muscle-strengthening activity and the appendicular skeletal muscle mass index varied with protein intake. Furthermore, among obese subjects with protein intakes < 70 g/d, those who performed such activities had a lower appendicular skeletal muscle mass index than those who were physically inactive. Protein intakes above the present recommendations were associated with benefits to obese subjects only. The appendicular skeletal muscle mass index of non-obese subjects who performed vigorous aerobic activities was consistently high; in obese subjects, it varied with protein intake. High-protein intake was associated with a modest increase in the appendicular skeletal muscle mass index in non-obese, physically inactive subjects. The present findings reinforce the idea that muscle-strengthening exercise preserves muscle when combined with adequate dietary protein. Vigorous aerobic activity may also help.

In an analysis from the Framingham Heart Study, 10 biomarkers were evaluated for their ability to predict clinical outcomes. The addition of biomarkers to conventional risk factors resulted in significant increases in the hazard ratios for death and major cardiovascular events but only small increases in the C statistic for each end point. The incremental value of the assessment of biomarkers to the evaluation of established risk factors appears to be modest. The addition of biomarkers to conventional risk factors resulted in significant increases in the hazard ratios for death and major cardiovascular events but only small increases in the C statistic for each end point. Established cardiovascular risk factors, including dyslipidemia, smoking, hypertension, and diabetes mellitus, have been incorporated into algorithms for risk assessment in the general population, 1 , 2 but these characteristics do not fully explain cardiovascular risk. 3 – 5 There is substantial interest in the use of newer biomarkers to identify persons who are at risk for the development of cardiovascular disease and who could be targeted for preventive measures. 6 Many individual biomarkers have been related to cardiovascular risk in ambulatory persons, including levels of C-reactive protein, 7 , 8 B-type natriuretic peptide, 9 fibrinogen, 10 d-dimer, 11 and homocysteine. 12 Measurement of several biomarkers simultaneously (the “multimarker” approach) could enhance . . .

Background While low-carbohydrate diet (LCD) patterns have been promoted to improve cardiometabolic risk factors, evidence from long-term studies on the impact of carbohydrate quality in these diets remains equivocal. We examined long-term associations among LCD patterns varying in carbohydrate quality and changes in cardiometabolic risk factors. Methods Dietary, health and lifestyle data were collected from Framingham Offspring cohort participants ( n  = 3294) every 4 years over a median 16.4-year follow-up. We assessed LCD patterns using 2 LCD scores (LCDSs) reflecting higher total fat and protein intake, and lower intake of (i) low-quality carbohydrates (high-quality LCDS, HQ-LCDS) and (ii) high-quality carbohydrates (low-quality LCDS, LQ-LCDS). Adjusted means of annualized changes in cardiometabolic risk factors across quintiles of LCDSs were estimated using repeated measures linear models. Results Baseline median age was 55 years, with 54% female participants. Waist circumference annual gains (cm/y) increased across quintiles (mean for Quintile 1, Quintile 5; P-trend) for HQ-LCDS (0.58, 0.69; 0.004), and LQ-LCDS (0.56, 0.74; <0.001). A slower annual increase in systolic blood pressure (mmHg/y) observed for HQ-LCDS (0.16, 0.00; 0.03), and LQ-LCDS (0.21, -0.05; 0.01). Higher HQ-LCDS was associated with a greater annual increase in HDL cholesterol concentrations (mg/dL/y) (0.51, 0.68; 0.005) and greater annual decline in triglyceride concentrations (mg/dL/y) (-1.24, -1.99; <0.001). Conclusions Although both high- and low-quality LCD patterns were associated with greater increases in waist circumference, our findings support recommendations to preserve high-quality carbohydrate in the context of low-carbohydrate diets and to replace low-quality carbohydrate with more healthy energy sources.

Higher carbohydrate intake, glycaemic index (GI), and glycaemic load (GL) are hypothesised to increase cancer risk through metabolic dysregulation of the glucose-insulin axis and adiposity-related mechanisms, but epidemiological evidence is inconsistent. This prospective cohort study investigates carbohydrate quantity and quality in relation to risk of adiposity-related cancers, which represent the most commonly diagnosed preventable cancers in the USA. In exploratory analyses, associations with three site-specific cancers: breast, prostate and colorectal cancers were also examined. The study sample consisted of 3184 adults from the Framingham Offspring cohort. Dietary data were collected in 1991–1995 using a FFQ along with lifestyle and medical information. From 1991 to 2013, 565 incident adiposity-related cancers, including 124 breast, 157 prostate and sixty-eight colorectal cancers, were identified. Cox proportional hazards models were used to evaluate the role of carbohydrate nutrition in cancer risk. GI and GL were not associated with risk of adiposity-related cancers or any of the site-specific cancers. Total carbohydrate intake was not associated with risk of adiposity-related cancers combined or prostate and colorectal cancers. However, carbohydrate consumption in the highest v. lowest quintile was associated with 41 % lower breast cancer risk (hazard ratio (HR) 0·59; 95 % CI 0·36, 0·97). High-, medium- and low-GI foods were not associated with risk of adiposity-related cancers or prostate and colorectal cancers. In exploratory analyses, low-GI foods, were associated with 49 % lower breast cancer risk (HR 0·51; 95 % CI 0·32, 0·83). In this cohort of Caucasian American adults, associations between carbohydrate nutrition and cancer varied by cancer site. Healthier low-GI carbohydrate foods may prevent adiposity-related cancers among women, but these findings require confirmation in a larger sample.

Evidence for cardioprotective effects of lycopene is inconsistent. Studies of circulating lycopene generally report inverse associations with CVD risk, but studies based on lycopene intake do not. The failure of dietary studies to support the findings based on biomarkers may be due in part to misclassification of lycopene intakes. To address this potential misclassification, we used repeated measures of intake obtained over 10 years to characterise the relationship between lycopene intake and the incidence of CVD ( n 314), CHD ( n 171) and stroke ( n 99) in the Framingham Offspring Study. Hazard ratios (HR) for incident outcomes were derived from Cox proportional hazards regression models using logarithmically transformed lycopene intake adjusted for CVD risk factors and correlates of lycopene intake. HR were interpreted as the increased risk for a 2·7-fold difference in lycopene intake, a difference approximately equal to its interquartile range. Using an average of three intake measures with a 9-year follow-up, lycopene intake was inversely associated with CVD incidence (HR 0·83, 95 % CI 0·70, 0·98). Using an average of two intake measures and 11 years of follow-up, lycopene intake was inversely associated with CHD incidence (HR 0·74, 95 % CI 0·58, 0·94). Lycopene intake was unrelated to stroke incidence. The present study of lycopene intake and CVD provides supporting evidence for an inverse association between lycopene and CVD risk; however, additional research is needed to determine whether lycopene or other components of tomatoes, the major dietary source of lycopene, are responsible for the observed association.