Cardiovascular disease (CVD) is the leading global cause of death, accounting for 17.3 million deaths per year. Preventive treatment that reduces CVD by even a small percentage can substantially reduce, nationally and globally, the number of people who develop CVD and the costs of caring for them. This American Heart Association presidential advisory on dietary fats and CVD reviews and discusses the scientific evidence, including the most recent studies, on the effects of dietary saturated fat intake and its replacement by other types of fats and carbohydrates on CVD. In summary, randomized controlled trials that lowered intake of dietary saturated fat and replaced it with polyunsaturated vegetable oil reduced CVD by ≈30%, similar to the reduction achieved by statin treatment. Prospective observational studies in many populations showed that lower intake of saturated fat coupled with higher intake of polyunsaturated and monounsaturated fat is associated with lower rates of CVD and of other major causes of death and all-cause mortality. In contrast, replacement of saturated fat with mostly refined carbohydrates and sugars is not associated with lower rates of CVD and did not reduce CVD in clinical trials. Replacement of saturated with unsaturated fats lowers low-density lipoprotein cholesterol, a cause of atherosclerosis, linking biological evidence with incidence of CVD in populations and in clinical trials. Taking into consideration the totality of the scientific evidence, satisfying rigorous criteria for causality, we conclude strongly that lowering intake of saturated fat and replacing it with unsaturated fats, especially polyunsaturated fats, will lower the incidence of CVD. States died of heart disease, stroke, and other CVDs in 2014, translating to about 1 of every 3 deaths. The annual direct and indirect costs of these deaths total more than $316.1 billion, including health expenditures and lost productivity.1 Preventive treatment that reduces CVD by even a small percentage can substantially reduce, nationally and globally, the number of people who develop CVD and the costs of caring for them.Since 1961, the American Heart Association (AHA) has recommended reduction in dietary saturated fat to reduce the risk of CVD.2,3 The purpose of this AHA presidential advisory on dietary fats and CVD is to review and discuss the scientific evidence, including the most recent studies, on the effects on CVD of dietary saturated fat and its replacement by other types of fats and carbohydrates. A presidential advisory is initiated by the AHA president to address a topic of special current importance. This report discusses the major classes of dietary fatty acids, except for the verylong-chain n-3 fatty acids in fish, which are covered by other AHA reports.The scientific rationale for decreasing saturated fat in the diet has been and remains based on wellestablished effects of saturated fat to raise low-density lipoprotein (LDL) cholesterol, a leading cause of atherosclerosis 4 ; to cause atherosclerosis in seve...
These results confirm that long-term heavy cannabis users show impairments in memory and attention that endure beyond the period of intoxication and worsen with increasing years of regular cannabis use.
Apolipoprotein C-III (apoC-III) inhibits triglyceride hydrolysis and has been implicated in coronary artery disease. Through a genome-wide association study, we have found that about 5% of the Lancaster Amish are heterozygous carriers of a null mutation (R19X) in the gene encoding apoC-III (APOC3) and, as a result, express half the amount of apoC-III present in noncarriers. Mutation carriers compared to noncarriers had lower fasting and postprandial serum triglycerides, higher levels of HDL-cholesterol and lower levels of LDL-cholesterol. Subclinical atherosclerosis, as measured by coronary artery calcification, was less common in carriers than noncarriers, suggesting that lifelong deficiency of apoC-III has a cardioprotective effect.Elevated plasma levels of low density lipoprotein cholesterol (LDL-C) and triglycerides (TG) are important contributors to premature coronary heart disease (CHD) (1-3), and genetic variants causing low LDL-C are associated with reduced risk of CHD (4). Recently, nonfasting TG was found to be an independent CHD risk factor (5,6), in one study showing higher predictive power than fasting TG (FTG), the traditional measure, likely because of the atherogenic remnant lipoproteins generated during absorption and clearance of dietary fat (5).To identify genetic factors contributing to FTG and post-prandial TG (ppTG) dietary response, we performed a single high fat feeding intervention and genome-wide association study (GWAS) in 809 Old Order Amish individuals as part of the Heredity and Phenotype Intervention (HAPI) Heart Study (7). Characteristics of these participants are shown in Table S1. These individuals were fed a milkshake containing 782 kcal/m 2 body surface area with 77.6% of these calories from fat and had blood drawn for lipid levels 0, 1, 2, 3, 4 and 6 hours after the intervention. The Affymetrix GeneChip® Human Mapping 500K Array Set was used for genotyping leukocyte DNA from these 809 participants. Traits were normalized and * This manuscript has been accepted for publication in Science. This version has not undergone final editing. Please refer to the complete version of record at http://www.sciencemag.org/cgi/content/full/322/5908/1702. Their manuscript may not be reproduced or used in any manner that does not fall within the fair use provisions of the Copyright Act without the prior, written permission of AAAS. analyses accounting for sex and sex-specific age and age 2 , body mass index (BMI) and relatedness among participants were performed as described in the Methods (8).Results of the GWAS of FTG and ppTG (as estimated by the incremental area under the curve, iAUCTG (8)), transformed by their natural logarithm (ln), are shown in Table S2 and Figure S1. The strongest evidence for association with both ln-FTG (p = 3.8 × 10 −14 ) and ln-iAUCTG (p = 2.8 × 10 −10 ) occurred on chromosome 11q23 at single nucleotide polymorphism (SNP) rs10892151, which had a minor allele frequency (MAF) of 0.028 (A allele; Table S2). SNP rs10892151 is located within an intron of th...
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