They also can be naturally found in olive oil and other healthy oils. See also how much olive oil help in lowering LDL in here! Where you can find these healthy fats? There are lots of choices you can explore. Some foods that are high in monounsaturated fats also contain polyunsaturated fats. Your email address will not be published. Please share this one! Bad cholesterol consists of low density lipoproteins, also known as LDL. These low-density lipoprotein carriers transport cholesterol from the liver to other parts of the body.
When LDL is deposited within walls of your arteries, it can cause major health problems. These cholesterol deposits form plaque which blocks blood vessels and eventually causes major damage to your arteries which can result in a heart attack or stroke. Individuals who have high levels of HDL can better reduce the cholesterol content of body tissues. Fats are in all kinds of foods we consume from meat and dairy products to nuts and oils we use for cooking.
Although we may not pay much attention to them, these fats have an effect on our overall health and take a toll on our good HDL and bad LDL cholesterol. Triglycerides are the most common type of fat found in the body.
Triglycerides come from unused calories that are stored in fat cells for later. There is an increased risk of heart disease, heart attack, and stroke in those who have high levels of triglycerides combined with low HDL cholesterol or high LDL cholesterol.
Those who have high triglyceride levels could potentially have a condition called hypertriglyceridemia which can lead to pancreatitis or further hardening of the arteries. Saturated fats contain a high number of fatty acid molecules with single bonds.
This type of fat is found in a number of foods like chicken, fatty meat, butter , and cheese. Saturated fats have a tendency to look solid at room temperature. Trans fat is another way of saying trans-fatty acid. Lipids : Scientific term referring to fat, cholesterol and other fat-like substances. Triglycerides : Scientific name for the main form of fat found in in the body and in foods.
Most of the fat in the body is stored as triglycerides, but triglycerides circulate in the blood as well. Triglycerides are made of three fatty acids and one glycerol molecule. These three fatty acids may include any combination of saturated fatty acids, monounsaturated fatty acids MUFAs , and polyunsaturated fatty acids PUFAs.
Triglycerides in the blood stream trigger the liver to make more cholesterol, so high triglyceride levels are often associated with high levels of total and LDL cholesterol. Saturated Fat Acids SFAs : Usually solid at room temperature, saturated fats have all of the hydrogen atoms they can hold saturated with hydrogen.
Saturated fats are primarily from animal products, but are also found in tropical plant oils, such as coconut and palm as well as other plant based foods, though in smaller amounts. See Table 3 for the health effects of saturated fats in the diet. Monounsaturated fats are primarily derived from plants and include olive oil, canola oil, peanut oil, and avocados. See Table 3 for the health effects of monounsaturated fats in the diet.
Polyunsaturated Fats PUFAs : Liquid at room temperature, polyunsaturated fats are missing two or more pairs of hydrogen atoms. Many common vegetable oils, such as corn, soybean, safflower and sunflower oil as well as fish are high in polyunsaturated fats.
See Table 3 for the health effects of polyunsaturated fats in the diet. Essential Fatty Acids : Fatty acids that are essential to human health but not produced in the body must be obtained through food. Only two types of fatty acids are considered essential; omega-3 fatty acids and omega-6 fatty acids, both polyunsaturated fats.
The Dietary Guidelines for Americans emphasize vegetable oils mono- and polyunsaturated fats as part of healthy eating pattern because they are the major source of essential fatty acids and vitamin E. Hydrogenated Fats : These are unsaturated fats that are processed to become solid at room temperature. Hydrogen atoms are added to unsaturated fat through a process called hydrogenation. This turns unsaturated fats into saturated fats. Hydrogenated fats can either be fully or partially hydrogenated, and are used in foods to enhance texture, extend shelf life, and prevent rancidity.
Packaged and processed foods such as cookies, crackers, and margarine most commonly contain these types of fats. Trans Fatty Acid : Trans fats occur naturally in some foods derived from cattle and sheep, but generally, this type of fat is formed during the process of hydrogenation. Only partially hydrogenated fats contain trans fats, where fully hydrogenated fats do not. Trans fatty acids mimic the properties of saturated fats in the body, and have been shown to increase LDL cholesterol and lower HDL cholesterol, which may increase the risk for heart disease.
Analysis of the Finnish, Dutch and Italian cohorts of the Seven Countries Study 14 revealed an inverse relationship between fatty fish consumption and year CAD mortality While many trials have found positive effects of n-3 PUFA supplementation and fish consumption on CVD, others have found less of a correlation.
The Health Professionals Follow-up Study 16 found no reduction in risk for CAD in men without established CVD when the number of fish meals per week was increased beyond one or two meals.
In addition, adverse effects related to fish intake and n-3 PUFA supplementation have been found. A grossly elevated intake of fish oil can cause an increased risk of bleeding 2 , 16 , Encapsulated fish oil supplements can also cause minor gastrointestinal disturbances and eructation 2. A recent study 17 also reported that fish may contain methyl mercury and other contaminants that may negatively affect CAD.
An antioxidant may need to be added to concentrated n-3 PUFA supplements to prevent the production of damaging lipid peroxides Ultimately, n-3 PUFAs may protect against CVD through several mechanisms, including acting as an antiatherogenic agent 1 , 17 ; lowering serum triglycerides 1 ; slightly lowering blood pressure 17 , 19 ; improving endothelial function 17 ; reducing inflammatory responses 17 ; inhibiting platelet aggregation and thombosis 1 , 17 ; and decreasing the incidence of arrhythmias 1 , Atherosclerosis is an inflammatory disease of the vascular system.
Dietary factors play a significant role in the development of atherosclerosis. Consumption of long-chain n-3 PUFAs demonstrated antiatherogenic effects in experimental and epidemiological studies 20 — However, this effect was not observed in the carotid arteries, suggesting that n-3 PUFAs may have different effects in different vascular beds Results from the Seven Countries Study 14 showed an inverse relationship between fish consumption and CAD, while the Health Professionals Study 16 found no relationship.
The only study to show a negative effect of fish consumption on CAD was conducted in Finland, but these results may have been influenced by mercury contamination of the fish They may exert their effect on atherogenesis by altering the circulating lipid profile; changing the physicochemical function of cell membranes, thereby affecting eicosanoid biosynthesis, cell signalling and gene expression; and modulating vascular smooth muscle cell proliferation and migration.
Many epidemiological and dietary interventions have shown that consumption of n-3 PUFAs significantly alters the serum lipid profile. A strong inverse relationship exists between n-3 PUFA consumption and circulating plasma triacylglycerol TG concentrations A negative correlation between n-3 PUFAs and plasma TG levels, and a positive relationship with high density lipoprotein HDL cholesterol levels may account for the low mortality rate due to CVD observed in this population Interestingly, an increase in low density lipoprotein LDL cholesterol and total cholesterol levels was also discovered Elevated plasma cholesterol levels have long been associated with an increased risk of atherosclerosis.
This may help to explain the cardioprotective effects of PUFAs. However, the antiatherogenic effect of n-3 PUFA supplementation is not always linked to a change in total plasma cholesterol levels 23 , 25 , Dietary intervention trials suggest that LDL cholesterol levels increase with n-3 PUFA supplementation in a dose-dependent manner 24 , 25 , 27 , HDL levels may also be altered by fish oil.
Nilsen et al 7 showed a significant decrease in total cholesterol and a significant increase in HDL cholesterol after fish oil supplementation. The concomitant increase in HDL cholesterol levels relative to increasing LDL cholesterol often leaves the total cholesterol to HDL cholesterol ratio, a common measure of atherogenic risk, unchanged 16 , 24 , The physicochemical alterations in membrane properties may directly or indirectly influence the function of membrane-bound receptors, ion channels and enzymes, and affect downstream signalling pathways that will have a direct effect on vascular endothelial and smooth muscle cell function Eicosanoid production is also affected by the FA composition of the membrane.
Alteration of the eicosanoid profile may have important effects on inflammation Eicosanoids, carbon FAs derived from n-6 and n-3 EFAs through the addition of oxygen atoms into the FA chains, confer a wide variety of potent, hormone-like actions on various tissues.
The eicosanoid families, including the prostaglandins, thromboxanes and leukotrienes, influence many biological activities, such as platelet aggregation, smooth muscle contraction and inflammatory responses. Thromboxane A 2 TxA 2 , a metabolite of arachidonic acid AA , is a potent vasoconstrictor and platelet aggregator. Fish oils inhibit TxA 2 in vitro and in vivo Increased consumption of n-3 PUFAs results in greater incorporation of n-3 PUFAs into cell membrane phospholipids, ultimately leading to the generation of more nderived eicosanoids.
The vascular endothelium is also modified by the ingestion of n-3 PUFAs. Vasoactive substances and growth factors are released by the vascular endothelium that activate immune cells, gene transcription, and functions involved in the regulation of monocyte adhesion, inflammation, vascular cell growth, cell migration and vascular tone In response to stress or injury, the endothelium can become dysfunctional and susceptible to atherogenesis.
The endothelium becomes proadhesive through cytokine-induced endothelial activation, which is important for the initiation and progression of atherosclerosis because it enables surface expression of endothelial leukocyte adhesion molecules and secretion of soluble proinflammatory products, such as interleukins-1 and -4, tumour necrosis factor, vascular cell adhesion molecule-1, platelet-derived growth factors PDGFs and monocyte chemoattractant proteins Because most adhesion molecules are not expressed under basal conditions, cytokine-induced endothelial activation requires the initiation of gene transcription.
Expression of endothelial leukocyte adhesion molecules and soluble proinflammatory proteins is inhibited when n-3 PUFAs alter the expression and production of macrophage cytokines 21 , 35 — The magnitude of the inhibitory effect of n-3 PUFAs on endothelial activation is related to the extent to which n-3 PUFAs are incorporated into cellular lipids. Nutritional supplementation can produce large enough elevations in DHA concentration to observe noticeable effects in in vitro studies 33 , The exact mechanisms of the inhibitory effects of n-3 PUFAs on endothelial activation are unknown.
However, the reduction of steady-state levels of adhesion molecule and growth factor mRNA by n-3 PUFAs persists after adhesion is activated.
Furthermore, the effects of n-3 PUFAs occur before the translation of mRNA into proteins and are independent of receptor activation 37 , NO regulates vascular relaxation and inhibits key atherosclerotic processes such as platelet aggregation, monocyte adhesion and vascular smooth muscle cell VSMC proliferation and migration. The cellular mechanisms by which n-3 PUFAs improve endothelial function remain unclear.
Migration and proliferation of VSMCs cause intimal hyperplasia, which contributes to the development of atherogenic lesions. Activated platelets aggregate at sites of endothelial dysfunction and release peptide growth factors, such as PDGF, and nonpeptide growth factors, such as serotonin 5-HT and adenosine diphosphate ADP.
The narrowing of blood vessels due to an atherosclerotic plaque can provide a setting in which a thrombus can more readily block blood flow and cause an MI. While eicosanoids derived from both parent FAs are proaggregatory, those derived from AA 2- and 4-series have fold greater activity than those derived from EPA 3- and 5-series.
Consequently, the EPA metabolites are generally considered antiaggregatory. A variety of models have been used to observe the effects of enriching the diet with n-3 PUFAs.
Experiments in which either saturated fats or PUFAs either n-3 or n-6 were added to the diet found striking results. This increased aggregation was even greater than that observed in the coconut oil group saturated fat. The same trends applied when platelet activation was initiated by collagen but not thrombin The inhibitory effects of platelet aggregation were directly related to the FA composition of platelet lipids.
It was also hypothesized that a PUFA effect on membrane viscosity could affect the activity of the proteins in the platelet membranes that are involved in aggregation as receptors or enzymes. Although beneficial in preventing the potential blocking of a blood vessel by a thrombus, extreme inhibition of clotting mechanisms could have side effects. Increases in bleeding times have been reported in humans with increased intake of fish oils 44 , 45 but not flaxseed oil There is some anecdotal evidence of individuals taking acetylsalicylic acid and n-3 supplements experiencing hematuria and spontaneous nosebleeds, likely resulting from severe effects on platelet aggregation Initial experiments performed on isolated hearts in the early s found that PUFAs antagonized the depressed ventricular arrhythmia threshold in hypoxia Animals consuming n-3 PUFAs exhibited significant reductions, or even abolition, of arrhythmias compared with control groups 49 , Direct intravenous injection of an emulsion of concentrated fish oil proved effective at preventing fatal ventricular fibrillation in dogs subjected to exercise stress tests following coronary artery ligation The antiarrhythmic effects of n-3 fish oils have also been demonstrated in nonhuman primates Some studies report a reduced incidence of cardiac arrhythmias in groups receiving n-6 PUFA supplementation 50 , 54 , whereas others have shown no protective effect The difference in findings may be due to the duration of the feeding trials because no effect was observed after four weeks of feeding compared with 10 or 12 weeks of feeding.
The sarcolemmal membrane contains a variety of ion channels, exchangers and pumps important to the conduction of action potentials and the maintenance of ion gradients. Voltage-gated sodium channels VGSCs , potassium channels and calcium channels are responsible for the initiation, duration and propagation of the action potential. Generally, in cultured neonatal cardiomyocytes, perfusion with n-3 and n-6 PUFAs raises the threshold potential required for action potential stimulation, decreases resting membrane potential and shortens action potential duration All of these effects could help the heart maintain electrical stability during ischemia and reduce the likelihood of arrhythmogenesis.
Summary of effects of omega-3 polyunsaturated fatty acids PUFAs on ion channels and transporters. This, of course, is potentially dangerous.
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