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Low-fat dietary pattern and breast cancer mortality by metabolic syndrome components: a secondary analysis of the Women's Health Initiative (WHI) randomised trial.
Pan, K, Aragaki, AK, Neuhouser, ML, Simon, MS, Luo, J, Caan, B, Snetselaar, L, Mortimer, JE, Manson, JE, Kroenke, C, et al
British journal of cancer. 2021;(3):372-379
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Abstract
BACKGROUND In the Women's Health Initiative (WHI) dietary modification (DM) randomised trial, the low-fat dietary intervention reduced deaths from breast cancer (P = 0.02). Extending these findings, secondary analysis examined dietary intervention influence on breast cancer mortality by metabolic syndrome (MS) components. METHODS In total, 48,835 postmenopausal women with no prior breast cancer were randomised to a low-fat dietary intervention or comparison groups. Four MS components were determined at entry in 45,833 participants: (1) high waist circumference, (2) high blood pressure, (3) high cholesterol and (4) diabetes history. Forest plots of hazard ratios (HRs) were generated with P-values for interaction between randomisation groups and MS component score. Primary outcome was death from breast cancer by metabolic syndrome score. RESULTS HRs and 95% confidence intervals (CI) for dietary intervention influence on death from breast cancer were with no MS components (n = 10,639), HR 1.09, 95% CI 0.63-1.87; with 1-2 MS components (n = 30,948), HR 0.80, 95% CI 0.62-1.02; with 3-4 MS components (n = 4,246), HR 0.31, 95% CI 0.14-0.69 (interaction P = 0.01). CONCLUSIONS While postmenopausal women with 3-4 MS components were at higher risk of death from breast cancer, those randomised to a low-fat dietary intervention more likely had reduction in this risk. REGISTRY ClinicalTrials.gov (NCT00000611).
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Carbohydrate and fat intake associated with risk of metabolic diseases through epigenetics of CPT1A.
Lai, CQ, Parnell, LD, Smith, CE, Guo, T, Sayols-Baixeras, S, Aslibekyan, S, Tiwari, HK, Irvin, MR, Bender, C, Fei, D, et al
The American journal of clinical nutrition. 2020;(5):1200-1211
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Abstract
BACKGROUND Epigenome-wide association studies identified the cg00574958 DNA methylation site at the carnitine palmitoyltransferase-1A (CPT1A) gene to be associated with reduced risk of metabolic diseases (hypertriglyceridemia, obesity, type 2 diabetes, hypertension, metabolic syndrome), but the mechanism underlying these associations is unknown. OBJECTIVES We aimed to elucidate whether carbohydrate and fat intakes modulate cg00574958 methylation and the risk of metabolic diseases. METHODS We examined associations between carbohydrate (CHO) and fat (FAT) intake, as percentages of total diet energy, and the CHO/FAT ratio with CPT1A-cg00574958, and the risk of metabolic diseases in 3 populations (Genetics of Lipid Lowering Drugs and Diet Network, n = 978; Framingham Heart Study, n = 2331; and REgistre GIroní del COR study, n = 645) while adjusting for confounding factors. To understand possible causal effects of dietary intake on the risk of metabolic diseases, we performed meta-analysis, CPT1A transcription analysis, and mediation analysis with CHO and FAT intakes as exposures and cg00574958 methylation as the mediator. RESULTS We confirmed strong associations of cg00574958 methylation with metabolic phenotypes (BMI, triglyceride, glucose) and diseases in all 3 populations. Our results showed that CHO intake and CHO/FAT ratio were positively associated with cg00574958 methylation, whereas FAT intake was negatively correlated with cg00574958 methylation. Meta-analysis further confirmed this strong correlation, with β = 58.4 ± 7.27, P = 8.98 x 10-16 for CHO intake; β = -36.4 ± 5.95, P = 9.96 x 10-10 for FAT intake; and β = 3.30 ± 0.49, P = 1.48 x 10-11 for the CHO/FAT ratio. Furthermore, CPT1A mRNA expression was negatively associated with CHO intake, and positively associated with FAT intake, and metabolic phenotypes. Mediation analysis supports the hypothesis that CHO intake induces CPT1A methylation, hence reducing the risk of metabolic diseases, whereas FAT intake inhibits CPT1A methylation, thereby increasing the risk of metabolic diseases. CONCLUSIONS Our results suggest that the proportion of total energy supplied by CHO and FAT can have a causal effect on the risk of metabolic diseases via the epigenetic status of CPT1A.Study registration at https://www.clinicaltrials.gov/: the Genetics of Lipid Lowering Drugs and Diet Network (GOLDN)-NCT01023750; and the Framingham Heart Study (FHS)-NCT00005121.
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Diet Quality, Saturated Fat and Metabolic Syndrome.
Harrison, S, Couture, P, Lamarche, B
Nutrients. 2020;(11)
Abstract
Indices reflecting overall diet quality are used globally in research to predict the risk of various diseases and metabolic disorders such as metabolic syndrome (MetS). Such indices are built to measure adherence to current dietary guidelines or to best assess the diet-disease relationship. Although mostly food-based, dietary guidelines often include recommendations to limit saturated fatty acid (SFA) intake in order to prevent cardiovascular diseases. However, not all diet quality indices consider SFA in their definition of diet quality. Additionally, the relationship between SFA consumption and the development of MetS remains unclear. The purpose of this short review was to explore the association between MetS and various diet quality indices and dietary patterns, with a focus on how SFA contributes to these associations.
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The Effects of High-Protein and High-Monounsaturated Fat Meals on Postprandial Lipids, Lipoprotein Particle Numbers, Cytokines, and Leptin Responses in Overweight/Obese Subjects.
Shah, M, Adams-Huet, B, Franklin, B, Phillips, M, Mitchell, J
Metabolic syndrome and related disorders. 2018;(3):150-158
Abstract
BACKGROUND Obesity is linked to dyslipidemia, proinflammatory state, and hyperleptinemia. The influence of high-protein (HP) versus high-monounsaturated fat (HMF) meals on postprandial lipids, lipoprotein particle numbers, cytokines, and leptin responses in overweight/obese (OW/O) subjects is unknown. METHODS Twenty-four OW/O participants consumed an HP (31.9% energy from protein) and HMF (35.2% fat and 20.7% monounsaturated fat) meal, of similar energy/carbohydrate content, in a random order. The outcome variables were assessed from blood samples collected in fasted and postprandial (3 hr) states. RESULTS Repeated measures analysis found significant (P < 0.05) meal condition by time interactions for triglycerides (TGs), very low-density lipoprotein particles (VLDLP), total high-density lipoprotein particles (T-HDLP), and the ratio of large-buoyant high-density lipoprotein 2b (LB-HDL2b) to T-HDLP, and meal effect on small-dense HDLP (SD-HDLP). Comparison of HP versus HMF condition showed significantly lower TG at 120 min [geometric mean (95% confidence interval, CI): 148 (125-175) vs. 194 (164-230) mg/dL] and 180 min [167 (138-203) vs. 230 (189-278) mg/dL] and VLDLP at 180 min [70.0 (58.2-84.3) vs. 88.0 (73.1-106) nmol/L]. HP versus HMF condition showed significantly lower LB-HDL2b/T-HDLP at 180 min [mean difference (95% CI): 0.021 (0.004-0.038)], and higher T-HDLP [671 (263-1079) nmol/L] and SD-HDLP [606 (292-920) nmol/L] at 120 min. Area under the curve was significantly lower for TG and higher for T-HDLP, SD-HDLP, and small-dense LDL III (SD-LDL III) in the HP condition. Cytokines and leptin were not different between conditions. CONCLUSION OW/O subjects had lower TG and VLDLP, but less favorable SD-LDL III, SD-HDLP, and LB-HDL2b/T-HDLP ratio responses to the HP versus HMF meals.
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Short communication: Daily intake of 125 g of cheese for 2 weeks did not alter amount or distribution of serum lipids or desaturase indexes in healthy adults in an exploratory pilot study.
Høstmark, AT, Lunde, MSH, Hjellset, VT
Journal of dairy science. 2018;(11):9625-9629
Abstract
Regular cheese contains saturated fat, consumption of which may negatively influence the amount of serum lipids. The American Dietary Guidelines (https://health.gov/dietaryguidelines/2015/guidelines/) recommend consumption of low-fat food. However, we observed a negative association between cheese intake and serum triglycerides and a positive association with high-density lipoprotein cholesterol. Cheese intake was also inversely related to metabolic syndrome and blunted the harmful association of intake of soft drinks with serum lipids. Cheese contains calcium and factors that may inhibit desaturases, thereby partly explaining why cheese might not have negative effects on serum lipids. Thus, opposing forces seem to govern the cheese effect but will any of these prevail? In an exploratory pilot study, 17 healthy subjects participated in a 4-wk crossover trial without washout. During the first 2 wk, 9 subjects were randomly assigned to add 125 g/d of regular cheese to their habitual diet. After 2 wk, cheese intake was discontinued and the subjects were instructed to return to their habitual diet. The other 8 subjects followed their habitual diet during the first 2 wk, and then added 125 g/d of cheese for the next 2 wk. Mean values (mmol/L) before and after 2 wk on habitual (cheese) diet were as follows: serum triglycerides: 0.91 (0.89) and 0.95 (0.91); total cholesterol: 5.25 (5.16) and 5.08 (5.24); low-density lipoprotein cholesterol: 3.18 (3.17) and 3.09 (3.22); and high-density lipoprotein cholesterol: 1.71 (1.64) and 1.61 (1.66). The fatty acid pattern in total serum lipids and desaturase indexes did not change significantly in response to high cheese intake. Thus, an appreciable increase in daily cheese intake for 2 wk may not alter concentrations of serum lipids, estimates of desaturases, or the distribution of serum fatty acids.
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Effects of a hypoenergetic diet rich in α-linolenic acid on fatty acid composition of serum phospholipids in overweight and obese patients with metabolic syndrome.
Egert, S, Baxheinrich, A, Lee-Barkey, YH, Tschoepe, D, Stehle, P, Stratmann, B, Wahrburg, U
Nutrition (Burbank, Los Angeles County, Calif.). 2018;:74-80
Abstract
OBJECTIVES Plant-derived α-linolenic acid (ALA) may exert cardioprotective effects. Dietary ALA can undergo desaturation and elongation to form long-chain ω-3 polyunsaturated fatty acids, but the extent to which this occurs in humans is unclear. The aim of the study was to examine the effects of an energy-restricted diet enriched with ALA on fatty acid composition of serum phospholipids in patients with metabolic syndrome. METHODS The present analysis compared the effects of a hypoenergetic diet high in ALA (3.4 g/d) with a control diet low in ALA (0.9 g/d) on fatty acid composition of serum phospholipids in 81 overweight or obese patients with features of metabolic syndrome. RESULTS After a 26-wk intervention, concentration of ALA in serum phospholipids remained constant in both diet groups. The control group had a significant decrease in serum phospholipid eicosapentaenoic acid concentration, although no significant intergroup difference was observed. Serum phospholipid docosahexaenoic acid concentration significantly decreased to a similar extent with both interventions. Additionally, both interventions significantly decreased serum phospholipid concentrations of palmitic acid, stearic acid, total saturated fatty acids, linoleic acid, total ω-6 and ω-3 polyunsaturated fatty acids, with no effect of diet group on these changes. Compared with the ALA diet, the control diet led to a significant increase in serum phospholipid oleic acid concentration. CONCLUSION Daily intake of 3.4 g of ALA during a 26-wk energy-restricted diet did not lead to an enrichment of serum phospholipids with ALA and did not increase eicosapentaenoic acid due to conversion. Additionally, dietary ALA was unable to compensate for a decrease in serum phospholipid docosahexaenoic acid.
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Nutritional factors and metabolic variables in relation to the risk of coronary heart disease: A case control study in Armenian adults.
Fazeli Moghadam, E, Tadevosyan, A, Fallahi, E, Goodarzi, R
Diabetes & metabolic syndrome. 2017;(1):7-11
Abstract
INTRODUCTION Dietary factors can affect the coronary heart disease (CHD). Results of previous studies on the association between the diet and CHD are not consistent in different countries. There were no data on this association in Armenia. OBJECTIVE Aims of this case-control study were to evaluate the association between nutritional factors and CHD among Armenians in Yerevan. METHODS During 2010 and 2011, we randomly selected 320 CHD patients with a diagnosis of CHD less than 6 months and 320 subjects without CHD (≥30years old) from the hospitals and polyclinics in Yerevan. Dietary intakes with 135 food items over the previous 12 months were evaluated using a semi-quantitative food frequency questionnaire. RESULTS After adjusting for some CHD risk factors higher intakes of polyunsaturated fatty acids (PUFA) and monounsaturated fatty acids (MUFA) were associated with a reduced risk of CHD, while this association was not witnessed for saturated fatty acids (SFA). In addition, findings indicated an inverse relation between vitamins (E, B6 and B12, folic acid) and fiber with CHD. In this population, smoking, hypertension, and metabolic syndrome (MetS) were significantly more common among patients with CHD. CONCLUSION The intake of vitamins E, B6 and B12, folic acid, PUFA, MUFA and fiber appeared to be predictors of CHD, independently of other risk factors.
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Dietary fat may modulate adipose tissue homeostasis through the processes of autophagy and apoptosis.
Camargo, A, Rangel-Zúñiga, OA, Alcalá-Díaz, J, Gomez-Delgado, F, Delgado-Lista, J, García-Carpintero, S, Marín, C, Almadén, Y, Yubero-Serrano, EM, López-Moreno, J, et al
European journal of nutrition. 2017;(4):1621-1628
Abstract
PURPOSE Obesity increases the risk of cardiovascular disease, type 2 diabetes mellitus and cancer development. Autophagy and apoptosis are critical processes for development and homeostasis in multicellular organisms and have been linked to a variety of disorders. We aimed to investigate whether the quantity and quality of dietary fat can influence these processes in the adipose tissue of obese people. METHODS A randomized, controlled trial within the LIPGENE study assigned 39 obese people with metabolic syndrome to 1 of 4 diets: (a) a high-saturated fatty acid diet, (b) a high-monounsaturated fatty acid (HMUFA) diet, and (c, d) two low-fat, high-complex carbohydrate diets supplemented with long-chain n-3 polyunsaturated fatty acids (LFHCC n-3) or placebo (LFHCC), for 12 weeks each. RESULTS We found an increase in the expression of autophagy-related BECN1 and ATG7 genes after the long-term consumption of the HMUFA diet (p = 0.001 and p = 0.004, respectively) and an increase in the expression of the apoptosis-related CASP3 gene after the long-term consumption of the LFHCC and LFHCC n-3 diets (p = 0.001 and p = 0.029, respectively). CASP3 and CASP7 gene expression changes correlated with HOMA index. CONCLUSION Our results suggest that the processes of autophagy and apoptosis in adipose tissue may be modified by diet and that the consumption of a diet rich in monounsaturated fat may contribute to adipose tissue homeostasis by increasing autophagy. They also reinforce the notion that apoptosis in adipose tissue is linked to insulin resistance. CLINICAL TRIAL REGISTRATION NUMBER ClinicalTrials.gov NCT00429195.
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Effect of a single bout of aerobic exercise on high-fat meal-induced inflammation.
Fuller, KNZ, Summers, CM, Valentine, RJ
Metabolism: clinical and experimental. 2017;:144-152
Abstract
BACKGROUND AND AIMS Chronic low-grade inflammation is involved in the development of metabolic disorders including atherosclerosis, type 2 diabetes (T2D) and metabolic syndrome. Aerobic exercise has been shown to be anti-inflammatory and attenuate postprandial blood lipids, however, the effect of exercise on postprandial inflammation remains unclear. The aim of this study was to determine the protective effect of a single bout of aerobic exercise against postprandial lipemia and peripheral blood mononuclear cell (PBMC) inflammation and to evaluate associations with changes in the energy-sensing enzyme, AMP-activated protein kinase (AMPK). MATERIALS AND METHODS Healthy male subjects (n=12, age=23±2, %Fat=19±2) reported to the laboratory following an overnight fast (12-14h) on two separate occasions for consumption of a high-fat meal (HFM). Participants completed an acute bout of aerobic exercise the afternoon prior to one of the HFM visits. RESULTS AND CONCLUSION Results indicate that the single bout of moderate aerobic exercise increased AMPK signaling in PBMCs, as shown by increased phosphorylated acetyl-CoA carboxylase (p-ACC). This may be due to decreases in the AMPK inhibitory kinases PKD and GSK3β. Additionally, prior moderate intensity exercise decreased postprandial lipemia (PPL) and some mediators of the inflammatory pathway, such as p-NF-κB. These findings that acute aerobic exercise improves AMPK and NF-κB signaling in human PBMCs contribute support to the anti-inflammatory roles of exercise.
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Proteome from patients with metabolic syndrome is regulated by quantity and quality of dietary lipids.
Rangel-Zúñiga, OA, Camargo, A, Marin, C, Peña-Orihuela, P, Pérez-Martínez, P, Delgado-Lista, J, González-Guardia, L, Yubero-Serrano, EM, Tinahones, FJ, Malagón, MM, et al
BMC genomics. 2015;(1):509
Abstract
BACKGROUND Metabolic syndrome is a multi-component disorder associated to a high risk of cardiovascular disease. Its etiology is the result of a complex interaction between genetic and environmental factors, including dietary habits. We aimed to identify the target proteins modulated by the long-term consumption of four diets differing in the quality and quantity of lipids in the whole proteome of peripheral blood mononuclear cells (PBMC). RESULTS A randomized, controlled trial conducted within the LIPGENE study assigned 24 MetS patients for 12 weeks each to 1 of 4 diets: a) high-saturated fatty acid (HSFA), b) high-monounsaturated fatty acid (HMUFA), c) low-fat, high-complex carbohydrate diets supplemented with placebo (LFHCC) and d) low-fat, high-complex carbohydrate diets supplemented with long chain (LC) n-3 polyunsaturated fatty acids (PUFA) (LFHCC n-3). We analyzed the changes induced in the proteome of both nuclear and cytoplasmic fractions of PBMC using 2-D proteomic analysis. Sixty-seven proteins were differentially expressed after the long-term consumption of the four diets. The HSFA diet induced the expression of proteins responding to oxidative stress, degradation of ubiquitinated proteins and DNA repair. However, HMUFA, LFHCC and LFHCC n-3 diets down-regulated pro-inflammatory and oxidative stress-related proteins and DNA repairing proteins. CONCLUSION The long-term consumption of HSFA, compared to HMUFA, LFHCC and LFHCC n-3, seems to increase the cardiovascular disease (CVD) risk factors associated with metabolic syndrome, such as inflammation and oxidative stress, and seem lead to DNA damage as a consequence of high oxidative stress.