Cholesterol

Cholesterol (chol from the greek = bile and stereos = solid) is a steroid for the living animal. In fact:
Cholesterol is an essential ingredient of cell membranes of all animal cells
Together with protein molecules cholesterol regulates the exchange of messenger substances via the cell membrane.
Growth and cell division is not possible, without cholesterol.
Cholesterol is the basic substance for the synthesis of steroidal hormones such as aldosterone, cortisone, testosterone, estradiol, etc.. (See the adrenal glands and vitamin D).
Cholesterol is essential for embryonic development: malformations of the newborn after administration of Contergan mothers were caused by a disturbance in the biosynthesis of cholesterol.
Cholesterol produced in the liver is used largely for the production of bile, a substance secreted into the duodenum, which serves to emulsify dietary lipids to make absorbable d intestino tenuous.

The man produces for biosynthesis independently most of the needed cholesterol (endogenous cholesterol), and only a small part (exogenous cholesterol) is taken with food.

All human cells are capable of synthesizing cholesterol as d acetilcoenzima A, but most is produced in the peroxisome of liver cells that move to the blood for transport throughout the body.
Cholesterol, like all fats, is not soluble in water, so its transport in the blood is carried by proteins, called apolipoprotein (APO). The complex formed by the apolipoprotein from cholesterol, and triglycerides from phospholipids is the lipoprotein particles relatively large circulating in the blood in order to transport fats to all tissues.

Cholesterol food (exogenous cholesterol) is absorbed d intestino and is incorporated, along with triglycerides, phospholipids and apolipoprotein (APOB mostly 48) in chilomicroni formed by the epithelial cells of the intestinal mucosa, the enterocytes. The maximum daily amount absorbed is about 500 mg / day. After the chilomicroni issued their triglycerides to adipose tissue, by the action of endothelial lipoproteinlipasi, the remaining particles dissociate from the endothelial surface and transport the exogenous cholesterol to the liver.

In the liver a part of exogenous cholesterol is eliminated in bile, either as bile acid or as free cholesterol. The amount of cholesterol converted to bile salts (usually around 200-400 mg / day) is regulated by the amount of bile salts which are overcome d intestino and return to the liver: entero-hepatic circulation of bile acids.
A major part of exogenous cholesterol is incorporated, along with the cholesterol synthesized in the liver (endogenous cholesterol) in VLDL (very low density lipoproteins-density lipoprotein or very low). The VLDL also contain endogenous synthesis of triglycerides, and apolipoprotein fosfolipi (mainly APOB 100).
Once secreted by the liver, VLDL catabolism suffer the same chilomicroni of: triglycerides are hydrolyzed by endothelial lipoproteinlipasi are released and the remaining particles or intermediate-density lipoprotein (IDL). Part of the IDL is removed from the hepatocytes to be catabolizzata, while 50-90% is converted to LDL (low density lipoproteins), by the action of hepatic lipase.
LDL transport cholesterol from the liver to the tissues, where it is used for a variety of processes, however, when LDL are present in excessive concentrations, their accumulation in the arterial wall promotes the development of atherosclerosis. Consequently, the cholesterol from LDL is a major risk factor for cardiovascular disease *.
The HDL (high density lipoproteins) are responsible for "reverse transport of cholesterol from tissues to the liver, and thus removes excess cholesterol from tissues and the liver trasportanoo, which is eliminated in the intestinal lumen as part of bile salts and partly as free cholesterol. The HDL thus play a protective role on the development of cardiovascular disease. An excess of HDL cholesterol is therefore a favorable factor.

Hypercholesterolemia

The hypercholesterolemia is an excess of cholesterol in the blood and, more specifically, is given by an increase in cholesterol carried by low density lipoprotein (LDL).

The increase in plasma values of LDL may occur through two mechanisms physiopathological:
increased production of hepatic VLDL. Because VLDL are the precursors of LDL, excessive production of VLDL necessarily lead to increased plasma LDL. In this case  ipecolesterolemia is associated with hypertriglyceridemia (type IIb iperlipoproteinemia) as the carrying mainly VLDL triglycerides endogenous
insufficient removal of LDL from the circulation deficit specific LDL receptor-R (or rarely on abnormalities APOB 100, which bind these receptors). In this case, the triglycerides are normal (iperlipoproteinemia type IIa)

Based on the causes, high cholesterol can be distinguished in primitive or secondary. The first are not associated with other diseases that may alter lipid metabolism, while the latter is caused by other diseases that can affect the metabolism of lipoprotein (primary biliary cirrhosis, liver disease with biliary stasis, diabetes mellitus, hypothyroidism, nephrotic syndrome, using Prolonged medication such as cortisone and oral contraceptives).

The hypercholesterolaemia of two primitive forms of hypercholesterolemia:
Polygenic: polygenic hypercholesterolemia is the most frequent (> 85% of hypercholesterolemia). It's a disease caused by environmental factors (diet high in saturated fat and physical inactivity) that act in the presence of genetic predisposing factors, the deficit likely to affect the genetic mechanisms of feedback, which was mentioned, thereby compromising the ability adequately compensate for the excess fat in the diet. Moreover, when an excess of cholesterol food reaches the liver (through the remaining particles of chilomicroni), high levels of intracellular cholest suppress the synthesis of hepatic LDL receptors and consequent reduction in the uptake of circulating LDL cause increased cholesterolaemia. The concentration of total cholesterol is usually between 240 and 350 mg / dl. Saturated fats are especially abundant in meat, milk and dairy products, eggs. In comparison, polyunsaturated fat-rich double bonds, contained in vegetable oils and fish play a protective role against of ipercolesterolemia; exception of olive oil as the oleic acid contains one double bond.
Family: Less common is a disease associated with a mutation in the gene encoding the LDL receptor.

The identification of ipercolesterolemia as cardiovascular risk factor (ie, a factor which increases the likelihood of developing a cardiovascular event) is the result of a long series of epidemiological studies that have highlighted the correlation between cholesterolaemia (values of plasma cholesterol ) and ischemic cardiovascular events, primarily myocardial infarction and cardiovascular mortality, which the myocardial infarction and stroke are the most frequent causes.

Some longitudinal studies (ie studies that were kept under observation the same individuals for several years)) have shown that the risk of death from ischemic heart disease is closely proportional to the levels of cholesterolaemia: the higher the cholesterol values higher cardiovascular mortality.
Also from these studies showed clearly that the various risk factors examined (mainly hypertension, smoking, diabetes, obesity, family history ischemic heart disease and low HDL) reinforce each other, so the more numerous are the risk factors in an individual, the greater the probability of death from cardiovascular causes.

The treatment involves the use of several means:
Diet: A diet low in saturated fat (less than 7% of total calories) and cholesterol in particular (less than 200 mg daily). Only when the diet proves ineffective in obtaining a satisfactory reduction cholesterolaemia (as unfortunately happens very often) is the simultaneous intake of drugs, which must be matched to the diet.
Lifestyle: The diet should be complemented an appropriate lifestyle, which, under the guidance of adults Panel ** Treatment must include regular physical activity, stopping smoking and reducing weight.
Drugs: The Adult Treatment Panel (ATP) has developed a scheme of preventive therapy for ischemic heart disease, based on the values of LDL cholesterolaemia associated with overall risk of developing ischemic heart disease. The current ATP III guidelines (2001, updated in 2004) set the threshold values for LDL cholesterol, over and above what is appropriate to start pharmacological treatment with statins, fibrates, ion exchange resins, Ezetimibe, probucol or nicotinic acid.
Nutritional Supplements: artichoke, bitter melon, boldo, velvet bean, Chanca piedra, guava, carqueja, yerba mate, suma, sarsaparilla, vassourinha, maca, cat's claw, annatto, Acerola, andiroba, graviola

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