How fats affect of food on our body fats
Once we know what kind of fats can be found in foods (fats from food) and how these are transformed and converted by our body moving in different lipid fractions foods (fats in our body), we interact as a with others and how this affects the development of cardiovascular disease.
Cholesterol
Despite the fear that made us have him, cholesterol in food is not as dangerous as it flows through our veins. In numerous experiments with different animal species found that dietary cholesterol was found to be highly atherogenic (forming atherosclerotic plaques in arteries), so it was thought that humans would be the same. However, humans in general are not as sensitive to dietary cholesterol as other animal species, and today we have evidence that cholesterol ingestion significantly less impact on increasing blood cholesterol (which is really dangerous ) that consumption of saturated fats.
This is because the absorption of cholesterol in the human intestine is limited to 40 or 50% of ingesta, with wide differences among individuals identified by genetic factors. This variability also depends on many factors. For example, the triglycerides in the intestine (fatty food) favor the absorption of cholesterol, while plant sterols (foods rich in vegetable fiber) and marine (seafood) to compete with the reduced absorption.
The cholesterol content of the typical Western diet is about 400 mg / day. When intake exceeds 500 mg / day percentage absorption decreases. However, official recommendations say about the cholesterol content of the diet should never exceed 300 mg / day.
Saturated fatty acids
As seen above, the saturated fatty acids have no double bonds and costs them combined with other molecules. For this reason, most saturated fats remain solid at room temperature. All are highly saturated animal fats, except fish and shellfish, which are highly polyunsaturated. Some vegetable fats like coconut oil and palm, are very rich in saturated fatty acids.
In numerous epidemiological studies have shown that intake of saturated fat increases blood cholesterol levels, especially LDL fraction. Although the mechanism by which this increase is not entirely clarified, it appears that the saturated fatty acids enriched phospholipids in the cell membrane, interfering with the normal function of LDL receptors and thus reducing the absorption of LDL by cells. By reducing the elimination of LDL, its concentration in the blood is higher.
Different saturated fatty acids have different behaviors on the levels of LDL-cholesterol:
Palmitic acid (C16: 0) is the major saturated fatty acid in foods of animal origin. Different research has shown that increased levels of total and LDL cholesterol, when substituted into the diet to carbohydrates or other fats.
Myristic Acid (C14: 0), although to a lesser extent than palmitic, also increases the concentration of total cholesterol. The usual mixed diet contains small amounts of myristic acid, present mainly in the butter.
Stearic acid (C18: 0) does not raise plasma total cholesterol levels, according to various studies in animals and humans, in contrast to other saturated acids. This acid is metabolized more rapidly toward oleic acid than other saturated fats.
The influence of lauric acid (C12: 0) on blood cholesterol levels is still unclear, but it has shown that coconut oil (rich in lauric) increases cholesterol levels more than fat from lamb.
Saturated fatty acids short chain (C10 and less) hardly change cholesterolemia.
Monounsaturated fatty acids
The main representative of monounsaturated fatty acids in our food is oleic acid (C18: 1). It has one double bond and is present in all animal fats and vegetable oils, especially olive oil.
For many years the interest on dietary fatty acids has focused on the proportions of saturated and polyunsaturated fatty acids. Monounsaturated fatty acids of the studies were forgotten for many years. In the Seven Countries Study showed that a high intake of monounsaturated fat in olive oil derivatives brought with low cholesterol levels and reduced incidence of cardiovascular disease.
Both acids and the monounsaturated fatty acids can reduce total and LDL cholesterol when they replace dietary saturated fats. But it is not gold that glitters, diets rich in polyunsaturates can lower HDL cholesterol, which has clearly demonstrated a protective role in cardiovascular disease. However, quite recent studies have shown that replacing saturated fats with monounsaturated not only reduces HDL cholesterol, but actually increases it. It was also found that the concentration of apolipoprotein AI, which is given an important antiatherogenic role.
In summary, diets rich in monounsaturated fatty acids are those that produce more favorable lipid profile for CVD prevention.
Polyunsaturated fatty acids
These fatty acids can not be synthesized by the human body yet are essential and therefore must be supplied by diet. They are classified into fatty acids w -3 w -6 depending on the position of the double bond.
W -6 fatty acids
The key is w -6 fatty acid linoleic (C18: 2), which is mainly found in vegetable seed oils (corn, soybean, sunflower, etc.)..
Polyunsaturated fatty acids reduce total and LDL cholesterol when they replace dietary saturated fats. They also reduce HDL cholesterol, which is not desirable for maximum protection against cardiovascular disease.
W -3 fatty acids
W -3 fatty acids are found in small amounts in some vegetable oils, but their main source are marine animals (fish and seafood). The main ones are linoleic acid (C18: 3), eicosapentaenoic (EPA, C20: 5) and docosahexaenoic acid (DHA, C22: 6).
Studies of populations consuming large amounts of w -3 fatty fish and marine animals have always shown a low incidence in CVD.
The effects of w -3 fatty acids on the various lipoproteins in the human body are not yet fully defined. The most striking effect and clearly demonstrated the decreased levels of triglycerides and VLDL in all kinds of subjects. This reduction is due to decreased liver synthesis of triglycerides and VLDL. However, the effects of w -3 fatty acids on levels of LDL and HDL depends on the patient and his lipid profile. Thus, in patients with elevated total cholesterol, the LDL-lowering w -3 at once if you reduce the intake of saturated fat. The effect on HDL varies from a slight decrease, which is the most common, a slight increase in patients with high triglycerides.
In addition to modifying the lipid profile, use of w -3 fatty acids results in an inhibition of platelet aggregation, mainly by decreasing the formation of thromboxane A2. This is an impediment to the formation of plaques inside blood vessels and its adherence to the endothelium, which is an important protective factor against CVD.
As if this were not enough, there is evidence also that this type of fat lowers blood pressure and decreases blood viscosity.
These are the reasons why it is always recommended to increase consumption of fish versus meat and other animal foods to reduce the risk of cardiovascular disease.
Trans fatty acids
Trans fatty acids are the latest actors who have appeared on stage at the debate anticholesterol. They are used by the food industry for the production of solid fats, especially margarine.
Most natural fats and oils contain only cis double bonds (oriented in a particular way on one side of the molecule). Commercial production of solid vegetable fats imply its hydrogenation, a process that leads to the formation of trans fatty acids (with the double bonds oriented on different sides of the molecule) from the cis addition of fatty acid saturation variable unsaturated. Most margarines contain up to 30% of trans fatty acids. The most common is elaidic acid, trans isomer of oleic acid.
The effect of trans fatty acids on lipids and lipoproteins in the human body is similar to saturated fats. Despite advertising campaigns for many products containing this type of trans fats, you can never recommend its use against vegetable fats without manipulation when it comes to preventing cardiovascular disease.
Antioxidant vitamins
Oxidation of high density lipoprotein LDL plays an important role in the initiation and development of atherosclerosis. Oxygen is essential for our cells to breathe, but if not well controlled during transport has lethal effects for the constituents of our body. During cellular respiration oxygen free radicals that can damage proteins, disrupt cell membranes. They also act on blood-borne lipoproteins. Biological systems are protected against oxidative damage caused by oxygen radicals by natural antioxidants that work both inside and outside of cells.
Oxidized LDL lipoproteins behave completely differently from normal. When a cell of the arterial wall captures an oxidized LDL becomes a fat cell that captures foaming up to several times their normal size. This gives rise to fatty streaks in arterial walls. They also act on macrophages inhibits their mobility, reduce the production of nitric oxide (endothelium relaxing factor), stimulate the proliferation of smooth muscle cells and increasing platelet aggregation. All these processes are crucial for the formation of atherosclerotic plaques.
Certain nutrients such as vitamins E and C and beta carotene behave as antioxidants, and numerous studies of all types have shown that when consumed enough of these vitamins and cardiovascular disease mortality decreases.
We must ensure that our diet contains sufficient antioxidant elements. Olive oil has high amounts of vitamin E, but refining industrial processes at high temperatures destroy this vitamin. However, virgin olive oil cold pressed and vitamins remained intact, so that its antioxidant capacity is higher than any refined oil.
It was also found that diets rich in polyunsaturated fatty acids produced a LDL more susceptible to oxidized LDL that produced from monounsaturated fatty acids such as oleic acid. This is important because it means that monounsaturated fats have antiatherogenic effects independent of derivatives that produce improvements in lipid profile.
Incoming search terms for the article:
Tags: abtioxidant vitamins, cholesterol, fats, fatty acids
