OBJECTIVEDietary interventions in patients with type 2 diabetes (T2D) are important for preventing long-term complications. Although a healthy diet is crucial, there is still uncertainty about the optimal macronutrient composition. We performed a meta-analysis comparing diets high in cis-monounsaturated fatty acids (MUFA) to diets high in carbohydrates (CHO) or in polyunsaturated fatty acids (PUFA) on metabolic risk factors in patients with T2D.RESEARCH DESIGN AND METHODSWe systematically reviewed PubMed, MEDLINE, and Cochrane databases and prior systematic reviews and meta-analyses to identify interventions assessing HbA1c, fasting plasma glucose and insulin, LDL and HDL cholesterol, triglycerides, body weight, or systolic/diastolic blood pressure. Meta-analyses were conducted using both fixed- and random-effects models to calculate the weighted mean difference (WMD) and 95% CI.RESULTSWe identified 24 studies totaling 1,460 participants comparing high-MUFA to high-CHO diets and 4 studies totaling 44 participants comparing high-MUFA to high-PUFA diets. When comparing high-MUFA to high-CHO diets, there were significant reductions in fasting plasma glucose (WMD −0.57 mmol/L [95% CI −0.76, −0.39]), triglycerides (−0.31 mmol/L [−0.44, −0.18]), body weight (−1.56 kg [−2.89, −0.23]), and systolic blood pressure (−2.31 mmHg [−4.13, −0.49]) along with significant increases in HDL cholesterol (0.06 mmol/L [0.02, 0.10]). When high-MUFA diets were compared with high-PUFA diets, there was a significant reduction in fasting plasma glucose (−0.87 mmol/L [−1.67, −0.07]). All of the outcomes had low to medium levels of heterogeneity, ranging from 0.0 to 69.5% for diastolic blood pressure (Phet = 0.011).CONCLUSIONSOur meta-analysis provides evidence that consuming diets high in MUFA can improve metabolic risk factors among patients with T2D.
Objectives To assess prospective association between circulating biomarkers of individual trans fatty acids (TFAs) and incident type 2 diabetes (T2D) in diverse populations. Methods A harmonized analysis of individual level data was conducted for TFA biomarkers and incident T2D by pooling ten prospective cohort or nested-case-control studies from five countries (Australia, Germany, Iceland, UK, and USA). Fatty acids (FAs) were measured in plasma phospholipid, red blood cell membrane phospholipid, or total plasma collected between 1990–2008 from 22,711 participants aged ≥18 years without prevalent diabetes. Evaluated TFAs included trans-16:1n-9, sum of trans-18:1 isomers (trans-18:1n6 to trans-18:1n12), sum of trans-18:2 isomers (cis/trans-18:2, trans/cis-18:2, trans/trans-18:2), and individual trans-18:2 isomers. The multivariable-adjusted relative risk or odds ratio was estimated in each cohort by lipid compartments using a pre-specified protocol for definitions of exposures, covariates, and outcomes for statistical analysis. Association estimates were pooled using fixed-effects inverse-variance weighted meta-analysis. Results During an average maximum of 14 years of follow-up, 2244 cases of incident T2D were identified. Median levels of TFAs across cohorts were 0.05–0.18% total FAs for trans-16:1n-9, 0.09–2.05% for total trans-18:1, 0.10–0.73% for total trans-18:2, and 0.01–0.36% for individual trans-18:2 isomers. In overall pooled analysis, TFAs evaluated per inter-quintile range were not significantly associated with risk of T2D (Figure 1). Findings were consistent when TFAs were assessed categorically in study specific-quintiles, and when associations were pooled within lipid compartment (i.e., phospholipids vs. total plasma). Conclusions Overall, biomarker levels of TFAs were not significantly associated with risk of incident T2D in this international pooling project. Findings may be due to mixed TFA sources (industrial vs. ruminant), a general decline in TFA exposure during this period, or no effect of circulating TFA on diabetes. Associations of TFA biomarkers with T2D at higher exposures should be investigated. Funding Sources See Table 1. Supporting Tables, Images and/or Graphs
Introduction: Dietary recommendations promote low-fat rather than full fat dairy consumption. Emerging evidence, however, has raised doubts if avoidance of dairy fat will lower CVD risk. Traditionally, self-reported estimates of dairy fat intake were used to study its relationship with CVD, which are subject to recall biases and measurement error. Here, we employed circulating levels of pentadecanoic acid [15:0] as a biomarker of dairy fat intake to examine its association with CVD incidence and all-cause mortality in a Swedish population-based cohort. We also conducted a systematic review of prospective studies that assessed 15:0, and other dairy fat biomarkers (heptadecanoic acid [17:0] and trans -palmitoleic acid [ t 16n-7]) and their associations with CVD and all-cause mortality. Hypothesis: We assessed the hypothesis that higher levels of dairy fat biomarkers 15:0, 17:0 and t 16n-7 would be associated with lower risk of incident CVD events and all-cause mortality. Methods: In a cohort of 60-year old Swedish women (n=2133) and men (n=2017), we measured 15:0 in serum cholesterol esters at baseline in 1997-99. Cox proportional hazard models were used to assess the associations between serum 15:0 with CVD outcomes and all-cause mortality, after adjusting for demographics and CVD risk factors. In the meta-analysis, five databases were searched to include prospective observational studies that examined the associations between circulating or adipose tissues levels of 15:0, 17:0 and t 16n-7 and CVD and mortality risks. Pooled associations of each dairy fat biomarker with incidence of CVD and all-cause mortality were estimated using a random-effects model. Results: During a median follow-up of 16.6 years, 578 incident CVD events and 676 deaths were identified using national registers. In multivariable-adjusted models, higher serum 15:0 was associated with lower incidence of CVD in a linear dose-response manner [HR: 0.75 per interquintile range; 95% CI: 0.61, 0.93), but in a non-linear relationship with all-cause mortality (P nonlinearity = 0.03); with a nadir of mortality risk around the median level of 15:0. In the meta-analysis including our Swedish cohort and 17 other studies, the relative risk of total CVD comparing the highest versus the lowest tertile was 0.88 (0.78, 0.99) for 15:0 (n=17), 0.86 (0.79, 0.93) for 17:0 (n=12), and 1.01 (0.91, 1.12) for t16n-7 (n=6). In meta-analyses of ≤3 studies, there was little evidence that dairy fat biomarkers were associated with all-cause mortality. Conclusion: In conclusion, our de novo Swedish cohort study and an updated systematic review including 18 studies suggests that higher levels of dairy fat biomarkers (15:0 and 17:0) were associated with a lower risk of CVD incidence. These results justify further investigation in interventional and experimental studies to elucidate the potential causality of these relationships and relevant mechanisms.
Background: The few established risk factors for non-Hodgkin lymphoma (NHL) exhibit considerable heterogeneity by NHL subtype and suggest an etiologic role for factors with immune- or inflammation-modulating properties, or which otherwise influence lymphocyte proliferation and survival. Epidemiologic evidence supports a potential inverse association for fruit and vegetable intake and NHL risk, but with limited subtype-specific evidence. Glucosinates and indole-3-carbinol, both found in cruciferous vegetables, may mediate tumor suppressive effects, including anti-inflammatory and anti-proliferation effects or restoration of phosphatase and tensin homolog (PTEN), a known tumor suppressor frequently down-regulated in cancer cells. We conducted a prospective study to further elucidate the etiologic role of fruit and vegetable consumption for NHL and its most common histologic subtypes. Methods: We followed 47,971 men in the Health Professionals Follow-Up Study (HPFS; 1986-2012) and 77,115 women in the Nurses' Health Study (NHS; 1984-2012) with baseline information on diet and no baseline history of cancer. We queried diet every four years using validated food-frequency questionnaires. We calculated fruit and vegetable consumption, in broad categories and for specific food groups, by summing the intake of individual foods excluding fruit juices, potatoes and legumes. Incident NHL diagnoses were first self-reported in study questionnaires then confirmed by review of medical records. We classified histologic subtypes according to the World Health Organization (WHO) and International Lymphoma Epidemiology (InterLymph) Consortium guidelines. We analyzed all NHL (in aggregate) and separate endpoints of chronic lymphocytic leukemia/small lymphocytic lymphoma (CLL/SLL), diffuse large B-cell lymphoma (DLBCL), follicular lymphoma, other B-cell NHL and T-cell NHL. We used multivariate Cox proportional hazards regression adjusting for potential confounding variables to estimate hazard ratios (HR) and 95% confidence intervals (CI) for the association of various fruit and vegetable intake variables with risk of each NHL endpoint. Those intake variables were based on the pre-diagnosis questionnaire returned most recent to NHL diagnosis and modeled as continuous variables in increments of one serving/day. Results: During 2,747,939 person-years of follow-up, we confirmed 1,732 incident NHL cases (986 women, 746 men). In preliminary multivariable-adjusted analyses, no fruit and vegetable intake variable was significantly associated with risk of all NHL (Table 1). Each additional serving/day of all, green leafy, beta carotene rich and lycopene rich vegetables was significantly associated with a 15%-45% lower risk of DLBCL per serving/day but not with other NHL subtypes; cruciferous and lutein rich vegetable intakes had a suggestive but statistically non-significant inverse association with several B-cell NHL subtypes (Table 1). Other associations were only weakly suggestive or null. Conclusions: In this prospective investigation, preliminary findings suggest a modest reduction of risk of several individual B-cell NHL subtypes, including statistically significantly lower risks of DLBCL, with increasing intake of green and antioxidant rich vegetables. These findings warrant further exploration and confirmation in other study populations. We note that this abstract reports preliminary findings; ongoing analyses will extend the follow-up period, add a third large cohort (NHS II) and assess potential reverse causation, explore sex- and subtype-related heterogeneity and test for non-linearity of observed associations. If confirmed, these results will contribute to evidence-based prevention strategies for NHL and further support general health recommendations concerning benefits of fruit and vegetable intake. Disclosures No relevant conflicts of interest to declare.
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