Risk factors for heart disease, health

Risk factors for cardiovascular disease were classified by the American Heart Association (AHA), as follows:
The main risk factors that can not be changed (age, male sex, and heredity)
The main risk factors that can be changed (hypercholesterolemia, hypertension, smoking and physical inactivity
Other contributing factors (obesity, diabetes and stress).
Key risk factors that can not be changed
Age
About 55% of all heart attacks occur in people 65 years or more. This age group represents over 80% of fatal heart attacks.
The male
Until recently, the incidence of coronary heart disease in women has been largely unexplored. Men were the main topics of coronary artery disease and studies of risk factors due to the high incidence of both men. However, coronary heart disease is the leading cause of death and disability among women, accounting for nearly 250,000 deaths per year. Women have less heart disease than men, especially before menopause. The reasons for the difference are:
Estrogen protects the coronary arteries, atherosclerosis
Women have higher levels of circulating high density lipoprotein (HDL), which also protects the arteries.
After menopause, however, the rate of heart attacks in women increases significantly until the mid-60s, when the risk of women equal to men the same age. An alarming trend in recent years is the increased incidence of heart attacks in postmenopausal women who smoked cigarettes long enough to harm their health, especially when combined with the use of oral contraceptives.
Legacy
According to the AHA, "a tendency toward heart disease or atherosclerosis appears to be hereditary, so that children of parents with heart disease are more likely to develop it." A story of men first-degree relatives (father , grandfather and brothers) who died of coronary heart disease before age 55 years or female first-degree relatives (mother, grandmother and sisters) who died of heart disease before age 65 indicates strong familial tendency. If family history is positive, the modifiable risk factors must be controlled.
Key risk factors that can be modified
Cholesterol
Cholesterol is a steroid that is an essential structure of nerve tissue and is used in building cell walls and making hormones and bile (for digestion and absorption of fats). A certain amount of cholesterol is necessary for good health, but high levels in the blood are associated with heart attacks and strokes.
The AHA suggests that Americans reduce cholesterol intake below 300 milligrams per day (300 mg / day), fat intake is reduced to a maximum of 30% of total calories and saturated fat is reduced to no more than 10% of total calories. Many authorities are convinced that the limitation of total fat and saturated fat is more important than being too restrictive cholesterol.
The Americans have made substantial progress in reducing cholesterol intake. The average cholesterol consumed by men and women, respectively, in 1960 was 704 mg / day and 493 mg / day. In 1994,
How LDL cholesterol contributes to coronary artery disease is not completely understood, but the "theory of lipid oxidation," appears to have the support of the scientific community. According to this theory, the LDL cling to artery walls, deposition of cholesterol in the time the plate. In contrast, high levels of circulating LDL cholesterol in the blood stimulates the cells in the layer of the arteries for the transport of LDL in the arterial wall. This process is facilitated when the linings of the arteries are damaged by one or a combination of the following: smoking, hypertension, diabetes mellitus, viruses and other toxic substances.
After infiltration of the arterial wall, oxidized LDL, or become harmful forms that are toxic to endothelial cells and smooth muscle and cause further damage to the arterial wall. This process activates the body's immune system, which responds by sending white blood cells called monocytes, which also penetrate the inner layer of the artery. Monocytes into macrophages, which engulf oxidized LDL in an effort to protect the artery damage. Macrophages engulf LDL swell, and in this state will eventually become foam cells. Foam cells in turn stimulate smooth muscle cells of affected arteries to grow in size and number. This adds to the thickness of the walls of arteries. At the same time, the platelets gather at the headquarters of the disease, adding to the thickening process. The outcome of these results, events in the development of fatty streaks in the arteries. This is an early sign of coronary artery disease. Some of these bands are the plates, which are lesions that define the diseased coronary arteries.
In some cases, the cells lining the artery scales or retract, exposing the foam cells located below. Again, the body tries to repair the damage, but the recovery process causes the artery to heal the wounds as a fibrous plaque. This represents an injury at an advanced stage in the development of atherosclerotic plaque.
The lesions grow over time through the accumulation of fibrous tissue, cholesterol and other wastes from the blood. At the same time, a severe narrowing of the channel, decreasing blood flow to the myocardium. At this point, the lesion has progressed to a mature plaque. Finally, further damage to the artery wall can cause a blood clot to develop or bleeding that occurs at the center of the plate, or the artery may go into spasm. Any of these events can abruptly interrupt or block the flow of blood to a portion of heart muscle, causing a heart attack.
Heart attacks are rare when the concentrations of LDL cholesterol below 100 mg / dl. A national group of experts has developed guidelines for safe levels of security and LDL. A high level of circulating LDL cholesterol is positively related to cardiovascular disease. Weight loss, diets low in saturated fat, total fat, exercise and medication (if necessary) will reduce LDL levels in the blood.
HDL are involved in the reverse transport, ie, accept cholesterol from the blood and tissues and transfer to LDL and VLDL for transport to the liver where it can be damaged, destroyed or recycled. HDL protects the arteries from atherosclerosis by clearing cholesterol from the blood. Cardiovascular health is highly dependent on low levels of total cholesterol and LDL cholesterol and HDL high. HDL smoking, diabetes, high triglycerides, low anabolic steroids, while physical exercise, weight loss and moderate alcohol consumption occur.
Moderate drinking (two drinks or less per day) increases HDL cholesterol. A drink is defined as a 5 oz glass of wine or beer 12 ounces, or 11 / 2 ounces of 80 proof spirits. However, alcohol is a depressant which causes about 50,000 deaths each year in traffic and contributes to one third of all drowning and boating deaths. It damages the trial and alcohol removes inhibitions so that people under its influence behave in ways that are not normally sober. Alcohol is not an acceptable way to increase HDL cholesterol.
The higher your HDL, the greater the protection against cardiovascular disease. The average for men is 45 mg / dl, and for women is 55 mg / dl. This biological difference in HDL levels between the sexes partly explains the low incidence of heart disease in premenopausal women compared to men. After menopause, HDL levels in women begin to decline, and the protection provided by this sub-fraction of cholesterol. The relationship between total cholesterol (TC) and HDL (TC / HDL) should also be considered when the risk is interpreted. This ratio is calculated by dividing the TC by HDL. Another blood fat, triglycerides in serum, is involved in the development and progression of atherosclerosis. Average serum triglycerides, by age and sex, about 50 mg / dl to 200 mg / dl.
High triglycerides may not directly cause atherosclerosis, but that often accompany and add to the severity of other abnormalities of blood lipids. For example, high levels of triglycerides are often accompanied by low HDL, high LDL and total cholesterol. This profile is predictive of the development of atherosclerosis and coronary heart disease.
A number of studies have shown that hypertriglyceridemia sedentary people can reduce serum triglycerides up to 45% when you regularly participate in moderate intensity exercise. People fitness metabolize serum triglycerides more efficiently than sedentary people and are able to remove the blood more quickly after a heavy meal.
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