Which fats are suspected of contributing to heart disease

Asked by: Neville Eichholt asked in category: General Last Updated: 6th February, Which fats are suspected of contributing to heart disease? Saturated fats , found in high- fat dairy, meats, and fried foods, as well as trans- fats , found in processed foods such as chips and cookies, should be limited. Experts agree they raise the risk of heart disease. What are some examples of unsaturated fats? Examples of unsaturated fatty acids are palmitoleic acid, oleic acid, myristoleic acid, linoleic acid, and arachidonic acid.

Foods containing unsaturated fats include avocado, nuts, olive oils, and vegetable oils such as canola. Meat products contain both saturated and unsaturated fats. What fat is good for your heart?

Is butter bad for your heart? Butter is high in saturated fat, which can raise your bad cholesterol and make heart disease more likely. You're better off to replace butter with olive oil or vegetable oil-based spreads, which contain heart-healthy mono- and polyunsaturated fats.

Regular use can help lower your LDL cholesterol levels. What foods are high in unsaturated fat? Dietary sources of unsaturated fats include: avocados and avocado oil. What are good carbs to eat? Good Carbs: Vegetables: All of them. Whole fruits: Apples, bananas, strawberries, etc. Legumes: Lentils, kidney beans, peas, etc. Nuts: Almonds, walnuts, hazelnuts, macadamia nuts, peanuts, etc.

Seeds: Chia seeds, pumpkin seeds. Whole grains: Choose grains that are truly whole, as in pure oats, quinoa, brown rice, etc. What are fatty foods to avoid? Trans fat: Must avoid! What are saturated fats? How do saturated fats affect my health?

Replacing foods that are high in saturated fat with healthier options can lower blood cholesterol levels and improve lipid profiles What foods contain saturated fat? Examples of foods with saturated fat are: fatty beef, lamb, pork, poultry with skin, beef fat tallow , lard and cream, butter, cheese and other dairy products made from whole or reduced-fat 2 percent milk. What are alternatives to replace saturated fats in the foods I eat?

To get the nutrients you need, eat a dietary pattern that emphasizes: fruits, vegetables , whole grains , low-fat dairy products , poultry , fish and nuts, while limiting red meat and sugary foods and beverages. Should I eat them or not? First Name required First Name Required. Last Name required Last Name Required. Email required Email Required.

Zip Code required Zip Code Required. I agree to the Terms and Conditions and Privacy Policy. Furthermore, trials with substances increasing HDL-C levels failed to reduce cardiovascular events or increased them and mortality [ 43 ].

However, these trials were performed in patients at high risk of CHD, whose HDL may have lost its putative cardioprotective function [ 44 , 45 ]. These findings favored the view that HDL functions beyond cholesterol efflux may be more important for cardiovascular protection than absolute HDL levels [ 46 ].

The third commonly assessed lipid marker of CHD risk is plasma TG, chauffeured in particles of chylomicrons and their remnants, very low- and intermediate-density lipoproteins [ 46 , 47 ].

Many studies reported significant associations between fasting and nonfasting TG concentrations and risk of CHD [ 48 , 49 ], but there is disagreement whether TG-rich lipoproteins constitute an independent causal risk factor [ 49 , 50 ].

The difficulty in establishing causality relates to the close relationship between TG and remnant cholesterol, and the inverse relationship between TG and HDL-C concentrations in plasma, both of which are significantly associated with the risk of ischemic heart disease, but in opposite directions [ 51 ]. In addition, these relationships are confounded by lifestyle factors, such as physical activity, alcohol consumption, higher body mass index, diabetes, and by reverse causation [ 52 , 53 ].

Because most cells can degrade TG, but not cholesterol, it is likely that the atherogenic part of TG-rich lipoproteins is cholesterol, not the TG itself.

This implies that the plasma TG level could be a risk marker rather than a causal factor. Thus, data in individuals with specific gene variants lead either to elevated or reduced TG or TG-rich lipoprotein levels, supporting a causal association between TG, remnant cholesterol, and risk of CHD. Unfortunately, there are no large randomized clinical trials that could verify this hypothesis. A clutch of hemostatic factors and inflammatory mediators [ 58 , 59 ], as well as elevated BP [ 60 ] and disturbed endothelial cell function [ 61 ], is also associated with CHD risk.

Fibrinogen, a positive acute phase protein essential for clot formation, has a long and consistent association with CHD risk [ 62 ]. Its association with CHD might reflect its responsiveness to inflammation [ 58 , 59 ], but clot formation and the presence of fibrin in atherosclerotic plaque suggest a more direct influence on CHD risk [ 63 , 64 ]. Still, a multiethnic meta-analysis of genome-wide association studies reported no strong evidence of a causal relationship between fibrinogen and coronary artery disease, stroke, or venous thromboembolism [ 65 ].

Other hemostatic factors, such as von Willebrand factor, fibrin D-dimer, and tissue plasminogen activator antigen, appear to be modestly associated with first-ever CHD [ 59 , 68 ]. Several hemostatic factors associated with CHD are also associated with inflammatory markers, which may confound CHD risk analyses [ 69 ].

Although higher SAFA intake might increase CHD risk by increasing plasma LDL-C [ 70 ], recent meta-analyses of prospective observational studies [ 1 , 71 , 72 ] reported that when compensating nutrients were not taken into account, SAFA intake was not associated with CHD or stroke mortality, all-cause mortality, or myocardial infarction. Two large, independent, prospective cohorts of US men and women confirmed this result [ 73 ] 1.

Several experimental conditions and methodological shortcomings could have obscured a potential relationship between SAFA intake and CHD risk. These include limited range of SAFA intakes within cohorts, possible heterogeneity in the health effects of different fatty acids, and large measurement errors in estimating dietary SAFA intake, without the ability to discriminate among individual fatty acids [ 76 ].

The balance among different fatty acids within the fatty acid class may be important [ 77 ], as might the food sources of SAFA.

A recent review and meta-analysis [ 6 ] of intervention studies concluded that lowering SAFA intake significantly reduced the risk of combined cardiovascular events, but not mortality.

According to a meta-analysis of 84 controlled trials [ 6 ], isocaloric replacement of mixed carbohydrates by a common dietary SAFA mixture markedly increased plasma LDL-C and apoB concentrations, indicating an increase in LDL-P number.

Compared with carbohydrates, lauric, myristic, and palmitic acids differently increase LDL-C and HDL-C levels and decrease TG concentrations, while stearic acid does not affect these lipoproteins [ 6 ]. Myristic acid has the strongest effect, but because of its much higher intake, palmitic acid has the greatest overall effect on plasma lipoprotein levels. The different effects of individual SAFA explain why dietary fats with different fatty acid compositions vary in their potency to alter lipid and lipoprotein levels.

As reviewed some time ago [ 84 ], the consumption of dietary fat significantly increased the postprandial amounts, activation, and activity of plasma clotting factor VII, which seemed to be associated with the degree of lipemia. Interestingly, the effects of SAFA-rich fats were less pronounced than those of fats rich in MUFA, and were further reduced by fatty acid randomization.

Up-to-date comprehensive reviews covering the effects of dietary fats on platelet function and thrombosis are lacking. Systematic studies with a well-validated rat model of arterial thrombosis revealed that, compared to unsaturated fatty acids, dietary SAFA but not stearic acid promote an arterial thrombosis tendency [ 85 ].

Effects of dietary SAFA on human platelet thrombotic functions have been studied repeatedly with inconsistent results [ 86 ]. The evidence for different effects of SAFA on flow-mediated dilatation, inflammation, and insulin sensitivity was considered unconvincing.

The cardinal risk factor for stroke is elevated BP. Furthermore, high BP is strongly and progressively associated with risk of CHD, heart failure, peripheral vascular disease, and other serious health conditions [ 87 , 88 ]. The Prospective Studies Collaboration, a meta-analysis of data from 61 prospective studies in individuals aged years, reported that each 20 mm of mercury increase in systolic BP above usual was associated with a more than 2-fold difference in stroke mortality and a 2-fold difference in CHD mortality [ 89 ].

A meta-analysis of 11 clinical trials of BP-lowering drugs showed that regardless of baseline cardiovascular risk, lowering the BP reduced the risk of cardiovascular events in all risk groups [ 87 ]. Overall, these data and many other studies support a causal relationship between BP and risk of CHD and stroke.

Moreover, the results of meta-analyses are inconsistent. When replacement nutrients were not considered, dietary SAFA were not significantly associated with the risk of ischemic stroke [ 1 ] or mixed types of stroke [ 2 ]. In a recent meta-analysis, higher SAFA intakes appeared associated with lower risks of both stroke types [ 90 ]. However, significant effects were limited to males, East Asians, participants with lower body mass index, and studies of high quality and long follow-up.

A meta-analysis of 7 intervention studies concluded that SAFA reduction had no clear effect on any type of stroke [ 4 ]. As dairy products are a major source of dietary SAFA, it is notable that a study of 3 large prospective studies reported that dairy fat intake was not significantly related to the risk of stroke risk [ 91 ]. In 2 large prospective cohorts, circulating biomarkers of dairy fat intake were not significantly associated with the risk of any type of incident stroke [ 92 ].

A recent systematic review and meta-analysis of 31 prospective cohort studies of dairy intake and risk of CVD, CHD, and stroke reported significant inverse relative risks for intakes of total dairy, cheese, and calcium from dairy foods and total stroke, but dose-response associations did not hold after adjustment for within-study covariance [ 93 ].

Another meta-analysis of prospective studies reported a significant inverse association between stroke and low-fat dairy and cheese consumption [ 94 ]. The investigators noted heterogeneity and publication bias in the studies on stroke. Thus, the available evidence suggests that SAFA reduction has little, if any, direct effect on stroke risk, but that the consumption of SAFA-rich dairy foods may be associated with a lower risk of ischemic stroke.

This topic deserves more thorough investigation [ 4 ]. Dietary guidelines now focus on foods and dietary patterns to improve consumer understanding of more healthful food choices and to acknowledge food matrix and nutrient interactions. Examples include the Nordic Nutrition Recommendations [ 95 ], Dietary Guidelines for Americans [ 96 ,] and Dutch food-based dietary guidelines [ 97 ].

Identifying healthy food choices to replace specific, less healthy ones, as in several updated dietary guidelines, may facilitate dietary modifications that lower the risk of CHD. SAFA have important metabolic functions, but their consumption is not essential because they can be synthesized de novo. However, their functional properties make them virtually indispensable for the production of fat-containing foods. In prospective observational studies and randomized controlled trials, higher total SAFA intakes were not associated with higher incident CHD events or mortality, but replacement nutrients were not taken into account.

The effect of reducing dietary SAFA is most strongly affected by the macronutrients that replace them. The consumption of several dairy foods has been associated with a lower risk of CVD, but data are insufficient to justify dietary recommendations. Increasing evidence suggests that TG-rich lipoproteins may be a causal risk factor for CHD and stroke.

Consistent evidence for specific effects of SAFA on any of these markers has not been reported. Studies on SAFA intakes and risk of ischemic stroke are inconsistent. National Center for Biotechnology Information , U. Ann Nutr Metab. Published online Jan Joyce A. Brouwer , b Johanna M. Geleijnse , c and Gerard Hornstra d. Ingeborg A.

Johanna M. Author information Article notes Copyright and License information Disclaimer. Received Sep 29; Revised Dec Karger AG, Basel. This article has been cited by other articles in PMC. Abstract At a workshop to update the science linking saturated fatty acid SAFA consumption with the risk of coronary heart disease CHD and ischemic stroke, invited participants presented data on the consumption and bioavailability of SAFA and their functions in the body and food technology.

Introduction For decades, the consumption of long-chain saturated fatty acids SAFA; containing carbon atoms was thought to undermine cardiovascular health. SAFA Background SAFA intake is inevitable as these fatty acids occur in all fat-containing foods, for example, dairy products, butter, meats, and some vegetable fats and oils [ 10 ]. Dietary Guidelines for SAFA Dietary guidelines now focus on foods and dietary patterns to improve consumer understanding of more healthful food choices and to acknowledge food matrix and nutrient interactions.

Summary and Conclusions SAFA have important metabolic functions, but their consumption is not essential because they can be synthesized de novo. Footnotes 1 While this paper was in revision, re-analyses of these cohorts were unable to verify this finding. References 1. Intake of saturated and trans unsaturated fatty acids and risk of all cause mortality, cardiovascular disease, and type 2 diabetes: systematic review and meta-analysis of observational studies.

Meta-analysis of prospective cohort studies evaluating the association of saturated fat with cardiovascular disease. Am J Clin Nutr.

Major types of dietary fat and risk of coronary heart disease: a pooled analysis of 11 cohort studies. Reduction in saturated fat intake for cardiovascular disease. Cochrane Database Syst Rev. Effects on coronary heart disease of increasing polyunsaturated fat in place of saturated fat: a systematic review and meta-analysis of randomized controlled trials.

PLoS Med. Mensink RP. Geneva: World Health Organization; Ridker PM. LDL cholesterol: controversies and future therapeutic directions. DiNicolantonio JJ. Open Heart. Hoenselaar R. Saturated fat and cardiovascular disease: the discrepancy between the scientific literature and dietary advice.