Reduction in saturated fat intake for cardiovascular disease.
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ABSTRACT:
SUBMITTER: Hooper L
PROVIDER: S-EPMC8092457 | biostudies-literature |
REPOSITORIES: biostudies-literature
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Project description: Not available
| S-EPMC7388853 | biostudies-literature
Project description:BackgroundAlthough dietary recommendations have focused on restricting saturated fat (SF) consumption to reduce cardiovascular disease (CVD) risk, evidence from prospective studies has not supported a strong link between total SF intake and CVD events. An understanding of whether food sources of SF influence these relations may provide new insights.ObjectiveWe investigated the association of SF consumption from different food sources and the incidence of CVD events in a multiethnic population.DesignParticipants who were 45-84 y old at baseline (n = 5209) were followed from 2000 to 2010. Diet was assessed by using a 120-item food-frequency questionnaire. CVD incidence (316 cases) was assessed during follow-up visits.ResultsAfter adjustment for demographics, lifestyle, and dietary confounders, a higher intake of dairy SF was associated with lower CVD risk [HR (95% CI) for +5 g/d and +5% of energy from dairy SF: 0.79 (0.68, 0.92) and 0.62 (0.47, 0.82), respectively]. In contrast, a higher intake of meat SF was associated with greater CVD risk [HR (95% CI) for +5 g/d and a +5% of energy from meat SF: 1.26 (1.02, 1.54) and 1.48 (0.98, 2.23), respectively]. The substitution of 2% of energy from meat SF with energy from dairy SF was associated with a 25% lower CVD risk [HR (95% CI): 0.75 (0.63, 0.91)]. No associations were observed between plant or butter SF and CVD risk, but ranges of intakes were narrow.ConclusionAssociations of SF with health may depend on food-specific fatty acids or other nutrient constituents in foods that contain SF, in addition to SF.
| S-EPMC3396447 | biostudies-literature
Project description:BACKGROUND: The aim of the study was to examine associations between intake of macronutrients and dietary fiber and incident ischemic cardiovascular disease (iCVD) in men and women. METHODS: We used data from 8,139 male and 12,535 female participants (aged 44-73 y) of the Swedish population-based Malmö Diet and Cancer cohort. The participants were without history of CVD and diabetes mellitus, and had reported stable dietary habits in the study questionnaire. Diet was assessed by a validated modified diet history method, combining a 7-d registration of cooked meals and cold beverages, a 168-item food questionnaire (covering other foods and meal patterns), and a 1-hour diet interview. Sociodemographic and lifestyle data were collected by questionnaire. iCVD cases, which included coronary events (myocardial infarctions or deaths from chronic ischemic heart disease) and ischemic strokes, were ascertained via national and local registries. Nutrient-disease associations were examined by multivariate Cox regressions. RESULTS: During a mean follow-up of 13.5 years, we identified 1,089 male and 687 female iCVD cases. High fiber intakes were associated with lower incidence rates of iCVD in women and of ischemic stroke in men. In post-hoc analysis, we discovered statistically significant interactions between intake of fiber and saturated fat; these interactions also differed between men and women (p<0.001). CONCLUSIONS: In this well-defined population, a high fiber intake was associated with lower risk of iCVD, but there were no robust associations between other macronutrients and iCVD risk. Judging from this study, gender-specific nutrient analysis may be preferable in epidemiology.
| S-EPMC3288044 | biostudies-other
Project description:OBJECTIVE:To assess the effect of reduction or modification of dietary fat intake on total and cardiovascular mortality and cardiovascular morbidity. DESIGN:Systematic review. DATA SOURCES:Cochrane Library, Medline, Embase, CAB abstracts, SIGLE, CVRCT registry, and biographies were searched; trials known to experts were included. INCLUDED STUDIES:Randomised controlled trials stating intention to reduce or modify fat or cholesterol intake in healthy adult participants over at least six months. Inclusion decisions, validity, and data extraction were duplicated. Meta-analysis (random effects methodology), meta-regression, and funnel plots were performed. RESULTS:27 studies (30 902 person years of observation) were included. Alteration of dietary fat intake had small effects on total mortality (rate ratio 0.98; 95% confidence interval 0.86 to 1.12). Cardiovascular mortality was reduced by 9% (0.91; 0.77 to 1.07) and cardiovascular events by 16% (0.84; 0.72 to 0.99), which was attenuated (0.86; 0.72 to 1.03) in a sensitivity analysis that excluded a trial using oily fish. Trials with at least two years' follow up provided stronger evidence of protection from cardiovascular events (0.76; 0.65 to 0.90). CONCLUSIONS:There is a small but potentially important reduction in cardiovascular risk with reduction or modification of dietary fat intake, seen particularly in trials of longer duration.
| S-EPMC30550 | biostudies-literature
Project description:BackgroundA reduction in dietary saturated fat has generally been thought to improve cardiovascular health.ObjectiveThe objective of this meta-analysis was to summarize the evidence related to the association of dietary saturated fat with risk of coronary heart disease (CHD), stroke, and cardiovascular disease (CVD; CHD inclusive of stroke) in prospective epidemiologic studies.DesignTwenty-one studies identified by searching MEDLINE and EMBASE databases and secondary referencing qualified for inclusion in this study. A random-effects model was used to derive composite relative risk estimates for CHD, stroke, and CVD.ResultsDuring 5-23 y of follow-up of 347,747 subjects, 11,006 developed CHD or stroke. Intake of saturated fat was not associated with an increased risk of CHD, stroke, or CVD. The pooled relative risk estimates that compared extreme quantiles of saturated fat intake were 1.07 (95% CI: 0.96, 1.19; P = 0.22) for CHD, 0.81 (95% CI: 0.62, 1.05; P = 0.11) for stroke, and 1.00 (95% CI: 0.89, 1.11; P = 0.95) for CVD. Consideration of age, sex, and study quality did not change the results.ConclusionsA meta-analysis of prospective epidemiologic studies showed that there is no significant evidence for concluding that dietary saturated fat is associated with an increased risk of CHD or CVD. More data are needed to elucidate whether CVD risks are likely to be influenced by the specific nutrients used to replace saturated fat.
| S-EPMC2824152 | biostudies-literature
Project description:BackgroundThe putative functional variant -265T>C (rs5082) within the APOA2 promoter has shown consistent interactions with saturated fatty acid (SFA) intake to influence the risk of obesity.ObjectiveThe aim of this study was to implement an integrative approach to characterize the molecular basis of this interaction.DesignWe conducted an epigenome-wide scan on 80 participants carrying either the rs5082 CC or TT genotypes and consuming either a low-SFA (<22 g/d) or high-SFA diet (≥22 g/d), matched for age, sex, BMI, and diabetes status in the Boston Puerto Rican Health Study (BPRHS). We then validated the findings in selected participants in the Genetics of Lipid Lowering Drugs and Diet Network (GOLDN) Study (n = 379) and the Framingham Heart Study (FHS) (n = 243). Transcription and metabolomics analyses were conducted to determine the relation between epigenetic status, APOA2 mRNA expression, and blood metabolites.ResultsIn the BPRHS, we identified methylation site cg04436964 as exhibiting significant differences between CC and TT participants consuming a high-SFA diet, but not among those consuming low-SFA. Similar results were observed in the GOLDN Study and the FHS. Additionally, in the FHS, cg04436964 methylation was negatively correlated with APOA2 expression in the blood of participants consuming a high-SFA diet. Furthermore, when consuming a high-SFA diet, CC carriers had lower APOA2 expression than those with the TT genotype. Lastly, metabolomic analysis identified 4 pathways as overrepresented by metabolite differences between CC and TT genotypes with high-SFA intake, including tryptophan and branched-chain amino acid (BCAA) pathways. Interestingly, these pathways were linked to rs5082-specific cg04436964 methylation differences in high-SFA consumers.ConclusionsThe epigenetic status of the APOA2 regulatory region is associated with SFA intake and APOA2 -265T>C genotype, promoting an APOA2 expression difference between APOA2 genotypes on a high-SFA diet, and modulating BCAA and tryptophan metabolic pathways. These findings identify potential mechanisms by which this highly reproducible gene-diet interaction influences obesity risk, and contribute new insights to ongoing investigations of the relation between SFA and human health. This study was registered at clinicaltrials.gov as NCT03452787.
| S-EPMC6454512 | biostudies-literature
Project description: Not available
| S-EPMC8174346 | biostudies-literature
Project description:OBJECTIVE: The aim of dietary modification, as a cornerstone of type 2 diabetes (T2DM) management, is to optimise metabolic control and overall health. This study describes food and nutrient intake in a sample of adults with T2DM, and compares this to recommendations, and to intake in age, sex, body mass index (BMI) and social-class matched adults without T2DM. DESIGN: A cross-sectional analysis of food and nutrient intake in 124 T2DM individuals (64% male; age 57.4±5.6 years, BMI 32.5±5.8?kg?m(-2)) and 124 adults (age 57.4±7.0 years, BMI 31.2±5.0?kg?m(-2)) with no diabetes (ND) was undertaken using a 4-day semiweighed food diary. Biochemical and anthropometric variables were also measured. RESULTS: While reported energy intake was similar in T2DM vs ND (1954 vs 2004?kcal per day, P=0.99), T2DM subjects consumed more total-fat (38.8% vs 35%, P?0.001), monounsaturated-fat (13.3% vs 12.2%; P=0.004), polyunsaturated-fat (6.7% vs 5.9%; P<0.001) and protein (18.6% vs 17.5%, P?0.01). Both groups exceeded saturated-fat recommendations (14.0% vs 13.8%). T2DM intakes of carbohydrate (39.5% vs 42.9%), non-milk sugar (10.4% vs 15.0%) and fibre (14.4 vs 18.9?g) were significantly lower (P<0.001). Dietary glycaemic load (GL) was also lower in T2DM (120.8 vs 129.2; P=0.02), despite a similar glycaemic index (59.7 vs 60.1; P=0.48). T2DM individuals reported consuming significantly more wholemeal/brown/wholegrain breads, eggs, oils, vegetables, meat/meat products, savoury snacks and soups/sauces and less white breads, breakfast cereals, cakes/buns, full-fat dairy, chocolate, fruit juices, oily fish and alcohol than ND controls. CONCLUSION: Adults with T2DM made different food choices to ND adults. This resulted in a high saturated-fat diet, with a higher total-fat, monounsaturated-fat, polyunsaturated-fat and protein content and a lower GL, carbohydrate, fibre and non-milk sugar content. Dietary education should emphasise and reinforce the importance of higher fibre, fruit, vegetable and wholegrain intake and the substitution of monounsaturated for saturated-fat sources, in energy balanced conditions.
| S-EPMC3940826 | biostudies-other
Project description:Current dietary recommendations advise reducing the intake of saturated fatty acids (SFAs) to reduce coronary heart disease (CHD) risk, but recent findings question the role of SFAs. This expert panel reviewed the evidence and reached the following conclusions: the evidence from epidemiologic, clinical, and mechanistic studies is consistent in finding that the risk of CHD is reduced when SFAs are replaced with polyunsaturated fatty acids (PUFAs). In populations who consume a Western diet, the replacement of 1% of energy from SFAs with PUFAs lowers LDL cholesterol and is likely to produce a reduction in CHD incidence of ?2-3%. No clear benefit of substituting carbohydrates for SFAs has been shown, although there might be a benefit if the carbohydrate is unrefined and has a low glycemic index. Insufficient evidence exists to judge the effect on CHD risk of replacing SFAs with MUFAs. No clear association between SFA intake relative to refined carbohydrates and the risk of insulin resistance and diabetes has been shown. The effect of diet on a single biomarker is insufficient evidence to assess CHD risk. The combination of multiple biomarkers and the use of clinical endpoints could help substantiate the effects on CHD. Furthermore, the effect of particular foods on CHD cannot be predicted solely by their content of total SFAs because individual SFAs may have different cardiovascular effects and major SFA food sources contain other constituents that could influence CHD risk. Research is needed to clarify the role of SFAs compared with specific forms of carbohydrates in CHD risk and to compare specific foods with appropriate alternatives.
| S-EPMC3138219 | biostudies-literature
Project description:Triphenylphosphine reduction of saturated endoperoxides derived from 6,6-dimethylfulvene and spiro[2.4]hepta-4,6-diene in the presence of nucleophiles results in the formation of products that mainly stem from deoxygenation followed by carbocation formation. Nucleophilic attack by solvent proceeds by an S(N)1 like mechanism; allyl shifts and cyclopropylcarbinyl-cyclobutyl rearrangements also occur. With the systems lacking carbocation-stabilizing groups, the deoxygenation step is preceded by attack of H(2)O at the phosphorus.
| S-EPMC2760492 | biostudies-literature