Let’s take a closer look at these cholesterol “fractions,” and at what makes HDLs “good” and LDLs “bad.” After you have fasted, a blood test will show three carriers of cholesterol: HDLs, LDLs, and very-low-density lipoproteins, or VLDLs. LDL cholesterol usually makes up about 65 percent of total cholesterol; about 20 percent circulates as HDL, and the remainder of total cholesterol is VLDL.
Cholesterol is a white, waxy substance that cannot dissolve in water; neither can it dissolve in blood, which is mostly water. But cholesterol has to get to the cells where it may be needed, so a fleet of special water-soluble carriers called lipoproteins – literally, molecules of fat linked with protein – are used to transport cholesterol and other water-insoluble products (like triglycerides, which are blood fats) throughout the bloodstream. Thus, although HDL and LDL are sometimes respectively thought of as “good” and “bad” cholesterol, they are, more precisely, cholesterol carriers. In fact, the actual cholesterol molecules found in HDL, LDL, and VLDL are really the same. What’s crucial to our understanding of how cholesterol is metabolized is how these lipoproteins do their carrying.
First, very-low-density lipoproteins are secreted by the liver into the bloodstream, where they carry triglycerides (which come from the diet or are produced by the liver), primarily to the fat cells. They also carry cholesterol produced in the liver or coming from the diet. The VLDLs actually contain five times more triglycerides than cholesterol, but as they travel through the bloodstream they are broken down by enzymes which release the triglycerides. As the triglyceride is removed from the VLDL particle, the particle becomes concentrated with cholesterol. Eventually some of this VLDL particle is converted to low-density (“bad”) lipoprotein, which delivers cholesterol directly to cells. If the serum level of LDL cholesterol is elevated, some of it will end up in the cells of the arterial walls, where it triggers the growth of atherosclerotic plaque. And if LDL cholesterol remains high for many years, this plaque eventually blocks blood flow and can trigger a heart attack or stroke.
By contrast, HDLs, or “good” cholesterol, appear to act as scavengers that seek out excess cellular cholesterol and usher it away from tissues and arteries and back to the liver, where it enters the liver’s cholesterol pool and can be used for bile acids.
So, while HDLs appear to play a beneficial role in partially counteracting the harmful effects of too much LDL, the public is receiving a distorted message about these “good” high-density lipoproteins. The facts are that HDL levels are determined primarily by genetic factors; that the only safe ways to increase them are to quit smoking, lose weight, and exercise; and that high-fat diets are associated with increased levels of both HDL and total cholesterol, resulting in more deaths from atherosclerosis. What’s best is to have low total cholesterol and the lowest possible level of LDLs as well. Once you achieve this, you won’t have to worry about not having enough “good” cholesterol, because when your total cholesterol is 160 mg/dl or less, and/or your LDLs are below 100 mg/dl, a somewhat lower HDL figure loses most of its risk significance. In this “cholesterol safety zone,” minimal risk is associated with lower than average HDLs. This stands to reason, because if you don’t have excess cholesterol in your bloodstream and tissues, you don’t have as much need for the scavenging efforts of HDLs.
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CHOLESTEROL: THE GOOD AND THE BADLet’s take a closer look at these cholesterol “fractions,” and at what makes HDLs “good” and LDLs “bad.” After you have fasted, a blood test will show three carriers of cholesterol: HDLs, LDLs, and very-low-density lipoproteins, or VLDLs. LDL cholesterol usually makes up about 65 percent of total cholesterol; about 20 percent circulates as HDL, and the remainder of total cholesterol is VLDL.Cholesterol is a white, waxy substance that cannot dissolve in water; neither can it dissolve in blood, which is mostly water. But cholesterol has to get to the cells where it may be needed, so a fleet of special water-soluble carriers called lipoproteins – literally, molecules of fat linked with protein – are used to transport cholesterol and other water-insoluble products (like triglycerides, which are blood fats) throughout the bloodstream. Thus, although HDL and LDL are sometimes respectively thought of as “good” and “bad” cholesterol, they are, more precisely, cholesterol carriers. In fact, the actual cholesterol molecules found in HDL, LDL, and VLDL are really the same. What’s crucial to our understanding of how cholesterol is metabolized is how these lipoproteins do their carrying.First, very-low-density lipoproteins are secreted by the liver into the bloodstream, where they carry triglycerides (which come from the diet or are produced by the liver), primarily to the fat cells. They also carry cholesterol produced in the liver or coming from the diet. The VLDLs actually contain five times more triglycerides than cholesterol, but as they travel through the bloodstream they are broken down by enzymes which release the triglycerides. As the triglyceride is removed from the VLDL particle, the particle becomes concentrated with cholesterol. Eventually some of this VLDL particle is converted to low-density (“bad”) lipoprotein, which delivers cholesterol directly to cells. If the serum level of LDL cholesterol is elevated, some of it will end up in the cells of the arterial walls, where it triggers the growth of atherosclerotic plaque. And if LDL cholesterol remains high for many years, this plaque eventually blocks blood flow and can trigger a heart attack or stroke.By contrast, HDLs, or “good” cholesterol, appear to act as scavengers that seek out excess cellular cholesterol and usher it away from tissues and arteries and back to the liver, where it enters the liver’s cholesterol pool and can be used for bile acids.So, while HDLs appear to play a beneficial role in partially counteracting the harmful effects of too much LDL, the public is receiving a distorted message about these “good” high-density lipoproteins. The facts are that HDL levels are determined primarily by genetic factors; that the only safe ways to increase them are to quit smoking, lose weight, and exercise; and that high-fat diets are associated with increased levels of both HDL and total cholesterol, resulting in more deaths from atherosclerosis. What’s best is to have low total cholesterol and the lowest possible level of LDLs as well. Once you achieve this, you won’t have to worry about not having enough “good” cholesterol, because when your total cholesterol is 160 mg/dl or less, and/or your LDLs are below 100 mg/dl, a somewhat lower HDL figure loses most of its risk significance. In this “cholesterol safety zone,” minimal risk is associated with lower than average HDLs. This stands to reason, because if you don’t have excess cholesterol in your bloodstream and tissues, you don’t have as much need for the scavenging efforts of HDLs.*9/345/5*