|
What Is Cholesterol?
Cholesterol is a fatty substance that is an important part of the
outer lining (membrane) of cells in the body of animals. Cholesterol is also
found in the blood circulation of humans. The cholesterol in a person's blood
originates from two major sources, dietary intake and liver production. Dietary
cholesterol comes mainly from meat, poultry, fish, and dairy products. Organ
meats, such as liver, are especially high in cholesterol content, while foods
of plant origin contain no cholesterol. After a meal, cholesterol is absorbed
by the intestines into the blood circulation and is then packaged inside a
protein coat. This cholesterol-protein coat complex is called a chylomicron.
The liver is capable of removing cholesterol from the blood circulation as well
as manufacturing cholesterol and secreting cholesterol into the blood
circulation. After a meal, the liver removes chylomicrons from the blood
circulation. In between meals, the liver manufactures and secretes cholesterol
back into the blood circulation.
LDL And HDL Cholesterol:
Cholesterol, like oil, cannot dissolve in the blood unless it is
combined with special proteins called lipoproteins. (Without combining with
lipoproteins, cholesterol in the blood will turn into a solid substance.) The
cholesterol that is secreted by the liver into the blood is combined either
with very low-density lipoproteins (VLDL) or high-density lipoproteins (HDL).
VLDL cholesterol is then metabolized in the bloodstream to produce LDL
cholesterol. The cholesterol combined with low-density lipoprotein is called
LDL cholesterol, and the cholesterol combined with high-density lipoproteins is
called HDL cholesterol.
How Does
Cholesterol Cause Heart Disease?
LDL cholesterol is called 'bad' cholesterol, because elevated LDL
cholesterol is associated with an increased risk of coronary heart disease. LDL
lipoprotein deposits cholesterol on the artery walls, causing the formation of
a hard, thick substance called cholesterol plaque. Over time, cholesterol
plaque causes thickening of the artery walls and narrowing of the arteries, a
process called atherosclerosis. Arteries that supply blood and oxygen to the
heart muscles are called coronary arteries. When coronary arteries are narrowed
by atherosclerosis, they are incapable of supplying enough blood and oxygen to
the heart muscle during exertion. Lack of oxygen (ischemia) to the heart muscle
causes chest pain, also formation of a blood clot in the artery can clause
complete blockage of the artery, leading to death of heart muscle (heart
attack). Atherosclerotic disease of coronary arteries (coronary heart disease)
is the most common cause of death.
What Determines The Level Of LDL Cholesterol In The Blood?
The liver not only manufactures and secretes LDL cholesterol into the
blood, it also removes LDL cholesterol from the blood. To remove LDL
cholesterol from the blood, the liver relies on special proteins called LDL
receptors that are normally present on the surface of liver cells. LDL
receptors snatch LDL cholesterol particles from the blood and transport them
inside the liver. A high number of active LDL receptors on the liver surfaces
is associated with the rapid removal of LDL cholesterol from the blood and low
blood LDL cholesterol levels. A deficiency of LDL receptors is associated with
high LDL cholesterol blood levels.
Both heredity and diet have a significant influence on a patient's LDL, HDL and
total cholesterol levels. For example, familial hypercholesterolemia (FH) is a
common inherited disorder whose victims have a diminished number or nonexistent
LDL receptors on the surface of liver cells. The resultant decreased activity
of the LDL receptors limits the liver's ability to remove LDL cholesterol from
blood. Thus, affected family members have abnormally high LDL cholesterol
levels in the blood. They also tend to develop atherosclerosis and heart
attacks during early adulthood.
Diets that are high in saturated fats and cholesterol
decrease the LDL receptor activity in the liver, thereby raising the levels of
LDL cholesterol in the blood. Fats are classified as saturated or unsaturated
according to their chemical structure. Saturated fats are derived primarily
from meat and dairy products and can raise blood cholesterol levels. Some
vegetable oils made from coconut, palm, and cocoa are also high in saturated
fats. On the other hand, most other vegetable oils are high in unsaturated
fats. Unlike saturated fats, unsaturated fats do not raise blood cholesterol
and can sometimes lower cholesterol. Olive and canola oil are high in
monounsaturated fats, which may have a protective effect against coronary heart
disease. Unfortunately, some vegetable oils are converted to saturated fats
during a process called 'hydrogenation' which can be required for food
processing.
Does Lowering LDL Cholesterol Prevent Atherosclerosis And Heart Attacks?
In the past 10 years, clinical trials have conclusively demonstrated
that lowering LDL cholesterol reduces heart attacks and saves lives. The
benefits of lowering LDL cholesterol include:
-
Reducing the formation of new cholesterol plaques
-
Eliminating existing plaques
-
Preventing rupture of existing plaques
-
Decreasing the risk of heart attacks
-
Lowering the chance of strokes.
How Low Should LDL Cholesterol Be?
The National Cholesterol Education Program (NCEP) has issued LDL
cholesterol treatment guidelines for adults. The NCEP target levels are
different for people who have varying risks for heart attacks. For example,
since individuals who have already suffered a heart attack have a greater
chance of experiencing another heart attack than individuals without known
coronary heart disease, their LDL cholesterol levels need to be more
aggressively lowered than people without known coronary heart diseases.
In July 2004 the NCEP (National Cholesterol Education Program) issued a new set
of guidelines for treatment of high blood cholesterol in adults. Please read
the New Cholesterol Guidelines article for more information.
Whether the NCEP LDL cholesterol treatment target levels are low enough is
controversial. An increasing number of experts in treating blood lipid
disorders believe that aggressively lowering LDL cholesterol below 80 further
decreases atherosclerosis and heart attack rates. In order to achieve these
levels, diet and exercise are insufficient and moderate to high doses of a
statin drug also will be necessary on a long-term basis. However, the safety of
moderate to high doses of statins over several decades is unknown. Thus, the
decision to aggressively reduce the patient's LDL cholesterol level below the
levels recommended by NCEP should be individualized after consultation with a
doctor familiar with the treatment of lipid disorders. Factors that must be
taken into account in making treatment decisions include the patient's age,
family history of early coronary heart diseases, other risk factors, and
cholesterol profile.
How can
LDL cholesterol levels be lowered?
In order to lower LDL cholesterol, the activity level of the LDL receptors must
be increased. LDL receptor activities can be increased by diets that are low in
cholesterol and saturated fats and by medications.
Lowering LDL cholesterol involves losing excess weight, exercising regularly,
and following a diet that is low in saturated fat and cholesterol. Medications
are prescribed when diet and exercise cannot reduce the LDL cholesterol to
acceptable levels. The most effective and widely used medications to lower LDL
cholesterol are called statins. Other medications used in lowering LDL
cholesterol and in altering cholesterol profiles include nicotinic acid
(niacin), fibrates such as gemfibrozil (Lopid), and resins such as
cholestyramine (Questran).
Is lowering LDL
cholesterol enough?
Unfortunately,
the prevention and treatment of atherosclerosis are more complicated than just
lowering LDL cholesterol levels. LDL cholesterol reduction is only half of the
battle against atherosclerosis. Individuals who have normal or only mildly
elevated LDL cholesterol levels can still develop atherosclerosis and heart
attacks even in the absence of other risk factors such as cigarette smoking,
high blood pressure, and diabetes mellitus. Additionally, successfully lowering
elevated LDL cholesterol levels cannot always prevent atherosclerosis and heart
attacks. In many clinical trials to lower LDL cholesterol, there were patients
who adhered to their assigned diets, faithfully took their cholesterol-lowering
medications, successfully lowered their LDL cholesterol to target levels, yet
still suffered progressive atherosclerosis and heart attacks. It is clear that
while lowering LDL cholesterol below NCEP target levels is an important step,
there are other factors involved.
What are the other risk factors for heart attacks?
The other risk factors include:
a. Abnormally low HDL cholesterol levels.
b. he size of the LDL cholesterol particles in the blood may be too small.
Scientists have found that the size of LDL cholesterol particles in the blood
is predominantly genetically inherited. People who have small and dense LDL
cholesterol particles have a higher risk of developing atherosclerosis and
heart attacks than those who have larger and more buoyant particles.
c. Elevated Lp(a) cholesterol levels. The level of Lp(a) cholesterol is also
predominantly genetically inherited. Individuals with elevated levels of Lp(a)
cholesterol have a higher rate of atherosclerosis and risk of heart
attacks.
d. Elevated homocysteine levels.
What are LDL cholesterol particle size patterns A and B?
The LDL patterns A and B refer to the size of LDL cholesterol particles in the
blood. Some doctors believe that small LDL cholesterol particles in the blood
may pose a greater risk for developing atherosclerosis and heart attacks than
the absolute level of LDL cholesterol in the blood. The size of LDL cholesterol
particles is primarily inherited. A special blood test called polyacrylamide
gradient gel electrophoresis can measure particle size and determine whether a
person has blood cholesterol LDL pattern A or LDL pattern B.
Persons with LDL cholesterol pattern A have large, buoyant LDL cholesterol
particles. Individuals with pattern A are more likely to have normal blood
levels of LDL cholesterol, HDL cholesterol, and triglycerides. Pattern A is
usually not associated with an increased likelihood of atherosclerosis.
Persons with LDL cholesterol pattern B have predominantly small and dense LDL
cholesterol particles. Pattern B is frequently associated with low HDL
cholesterol levels, elevated triglyceride levels, and the tendency to develop
high blood sugar levels and type II diabetes mellitus. Individuals with pattern
B are also more likely to develop high blood triglyceride levels after a fatty
meal (postprandial hyperlipidemia). Pattern B is associated with accelerated
atherosclerosis and a 3 to 5- fold increase in heart attack risk. Pattern B is
believed to be the most important cause of atherosclerosis in people with
normal or near normal total and LDL cholesterol levels.
Some scientists believe that the smaller LDL particles are more dangerous than
the larger ones because they can more easily squeeze through the tiny gaps
between the cells in the endothelium to reach inside the artery walls. The
endothelium is a thin layer of cells which covers the inner wall of the
arteries. The cells making up the endothelium have tiny gaps between them.
Others postulate that the smaller LDL cholesterol particles are more easily
oxidized. Oxidation of cholesterol is significant in the formation of
cholesterol plaques.
How can LDL cholesterol size be enlarged?
Even though LDL cholesterol particle size is mainly genetically inherited,
individuals who have small LDL particles (pattern B) can increase their
particle size through diet, exercise, and medications.
Diets that are low in saturated fat and cholesterol, regular aerobic exercise,
and loss of excess body fat have been determined to decrease the number of
small LDL particles and increase the number of large LDL particles in the
blood. In other words, lifestyle modifications can change pattern B to pattern
A.
When lifestyle changes alone are unsuccessful, medications can be used. Even
though the statin medications (discussed below) are effective in lowering the
absolute levels of LDL cholesterol, they appear to have a limited effect on LDL
cholesterol size pattern. Medications such as nicotinic acid (niacin) and
gemfibrozil (Lopid) have been found effective in many instances in increasing
the size of LDL cholesterol particles.
Why is HDL the
good cholesterol?
HDL is the good cholesterol because it protects the arteries from the
atherosclerosis process. HDL cholesterol extracts cholesterol particles from
the artery walls and transports them to the liver to be disposed through the
bile. It also interferes with the accumulation of cholesterol in the artery
walls by the LDL cholesterol particles.
The risk of atherosclerosis and heart attacks in both men and women is strongly
related to HDL cholesterol levels. Low levels of HDL cholesterol are linked to
a higher risk, whereas high HDL cholesterol levels are associated with a lower
risk.
Very low and very high HDL cholesterol levels can run in families. Families
with low HDL cholesterol levels have a higher incidence of heart attacks than
the general population, while families with high HDL cholesterol levels tend to
live longer with a lower frequency of heart attacks.
Like LDL cholesterol, life style factors and other conditions influence HDL
cholesterol levels. HDL cholesterol levels are lower in persons who smoke
cigarettes, eat a lot of sweets, are overweight and inactive, and in patients
with type II diabetes mellitus.
HDL cholesterol is higher in people who are lean, exercise regularly, and do
not smoke cigarettes. Estrogen increases a person's HDL cholesterol, which
explains why women generally have higher HDL levels than men do.
For individuals with low HDL cholesterol levels, a high total or LDL
cholesterol blood level further increases the incidence of atherosclerosis and
heart attacks. Therefore, the combination of high levels of total and LDL
cholesterol with low levels of HDL cholesterol is undesirable whereas the
combination of low levels of total and LDL cholesterol and high levels of HDL
cholesterol is favorable.
LDL/HDL and
total/HDL ratios:
The total cholesterol to HDL cholesterol ratio is a number that is helpful in
predicting atherosclerosis. The number is obtained by dividing total
cholesterol by HDL cholesterol. (High ratios indicate higher risks of heart
attacks, low ratios indicate lower risk).
High total cholesterol and low HDL cholesterol increases the ratio, and is
undesirable. Conversely, high HDL cholesterol and low total cholesterol lowers
the ratio, and is desirable. An average ratio would be about 4.5. Ideally we
want to be better than average if we can. Thus the best ratio would be 2 or 3
or less than 4.
Another ratio is LDL/HDL. The LDL/HDL ratio is actually a more pure ratio than
total cholesterol/HDL.
-
LDL is a measure of bad cholesterol
-
HDL is a measure of good cholesterol
Adding up the HDL, LDL and VLDL makes up the total cholesterol measurement.
Even though total cholesterol/HDL ratio is not as accurate or pure as the
LDL/HDL ratio, the former is more commonly obtained because the total
cholesterol is easier and cheaper to obtain than the LDL cholesterol level.
The Treatment Guidelines For Low HDL Cholesterol:
In clinical trials involving lowering LDL cholesterol, scientists also studied
the effect of HDL cholesterol on atherosclerosis and heart attack rates. They
found that even small increases in HDL cholesterol could reduce the frequency
of heart attacks. For each 1 mg/dl increase in HDL cholesterol there is a 2 to
4% reduction in the risk of coronary heart disease. Although there are no
formal guidelines, proposed treatment goals for patients with low HDL
cholesterol are:
" To increase HDL cholesterol to higher than 35 mg/dl in men and 45 mg/dl in
women with a family history of coronary heart disease and
" To increase HDL cholesterol to approach 45 mg/dl in men and 55 mg/dl in women
with known coronary heart disease (such as patients who have already suffered a
heart attack).
How
can levels of HDL cholesterol be raised?
The first step in increasing HDL cholesterol levels (and decreasing LDL/HDL
ratios) is life style modification. When life style modifications are
insufficient, medications are used. In prescribing medications or medication
combinations, doctors have to take into account medication side effects as well
as presence or absence of other abnormalities in cholesterol profiles.
Regular aerobic exercise, loss of excess weight (fat), and cessation of
cigarette smoking cigarettes will increase HDL cholesterol levels. Regular
alcohol consumption (such as one drink a day) will also raise HDL cholesterol.
However, there are different subclasses of HDL cholesterol which have varying
degrees of effectiveness in preventing atherosclerosis. Alcohol is believed to
increase the level of the less important subtype of HDL cholesterol. Because of
other adverse health consequences of excessive alcohol consumption, alcohol is
not recommended as a standard treatment for low HDL cholesterol.
Medications that are effective in increasing HDL cholesterol include nicotinic
acid (niacin), gemfibrozil (Lopid), estrogen, and to a lesser extent, the
statin drugs (discussed below).
Lipoprotein (a), Lp(a) Cholesterol
Lipoprotein (a), Lp(a), is a LDL cholesterol particle that is attached to a
special protein called apo(a). In large part, a person's level of Lp(a) in the
blood is genetically inherited. Elevated levels of Lp(a) (higher than 20 mg/dl
to 30 mg/dl) in the blood are linked to a greater likelihood of atherosclerosis
and heart attacks in both men and women. The risk is even more significant if
the Lp(a) cholesterol elevation is accompanied by high LDL/HDL ratios.
Certain diseases are associated with elevated Lp(a) levels. Patients on chronic
kidney dialysis and those with nephrotic syndromes (kidney diseases that cause
leakage of blood proteins into the urine) tend to have high levels of Lp(a).
There are many theories as to how Lp(a) causes atherosclerosis although exactly
how Lp(a) accumulates cholesterol plaques on the artery walls has not been well
defined. Clinical trials that conclusively prove that lowering Lp(a) reduces
atherosclerosis and the risk of heart attacks have not been conducted.
Currently, there is no international standard for determining Lp(a) cholesterol
levels, and commercial sources of Lp(a) testing may not have the same accuracy
as research laboratories. Therefore, specifically measuring and treating
elevated Lp(a) cholesterol levels are not widely performed in this country.
How can Lp(a) cholesterol levels be reduced?
Most lipid-lowering medications such as statins, Lopid, and cholestyramine have
a limited effect in lowering Lp(a) cholesterol levels. Estrogen has been shown
to lower Lp(a) cholesterol levels by approximately 20% in women with elevated
Lp(a) cholesterol. Estrogen can also increase HDL cholesterol levels when given
to postmenopausal women. Additionally, nicotinic acid (Niacin or Niaspan) in
high doses has been found to be effective in lowering Lp(a) cholesterol levels
by approximately 30%.
Triglycerides,
Chylomicrons and VLDL
Triglyceride is a fatty substance that is composed of three fatty acids each of
which is attached to a glycerol molecule. Like cholesterol, triglyceride in the
blood either comes from the diet or the liver. Also, like cholesterol,
triglyceride cannot dissolve and circulate in the blood without combining with
a lipoprotein. Thus, after a meal, the triglyceride and cholesterol that are
absorbed into the intestines are packaged into round particles called
chylomicrons before they are released into the blood circulation.
A chylomicron is a collection of cholesterol and triglyceride that is
surrounded by a lipoprotein outer coat. (Chylomicrons contain 90% triglyceride
and 10% cholesterol.) There are special enzymes on the blood vessels that break
up the triglyceride inside the chylomicrons, releasing fatty acids in the
process. The fatty acids can either be used by the muscles as energy, or
absorbed by fat cells where they are incorporated again into triglyceride that
can be stored in the fat cells for future energy needs. The chylomicrons are
then removed from the circulation by the liver.
The liver not only removes triglyceride and chylomicrons from the blood, it
also synthesizes and packages triglyceride into VLDL (very low-density
lipoprotein) particles and releases them back into the blood circulation.
Therefore, before breakfast after an overnight fast, most of the triglyceride
in the blood comes from the liver in the form of VLDL particles. Like
chylomicrons, VLDL particles contain mostly triglyceride. Some of the VLDL
particles lose triglyceride in the blood and become cholesterol-rich LDL
particles.
Do
high triglyceride levels
cause atherosclerosis?
Whether elevated triglyceride levels in the blood lead to atherosclerosis and
heart attacks is controversial. While most doctors now believe that an
abnormally high triglyceride level is a risk factor for atherosclerosis, it is
difficult to conclusively prove that raised triglyceride by itself can cause
atherosclerosis. However, it is increasingly recognized that elevated
triglyceride is often associated with other conditions that increase the risk
of atherosclerosis including obesity, low levels of HDL- cholesterol, insulin
resistance and poorly controlled diabetes mellitus, and small, dense LDL
cholesterol particles.
Causes of Elevated Triglyceride Levels:
In some people, abnormally high triglyceride levels (hypertriglyceridemia) are
inherited. Examples of inherited hypertriglyceridemia disorders include mixed
hypertriglyceridemia, familial hypertriglyceridemia, and familial
dysbetalipoproteinemia.
Hypertriglyceridemia can often be caused by non-genetic factors such as
obesity, excessive alcohol intake, diabetes mellitus, kidney disease, and
estrogen containing medications such as birth control pills.
How can elevated blood triglyceride levels be treated?
The first step in treating hypertriglyceridemia is a low fat diet with a limited
amount of sweets, regular aerobic exercise, loss of excess weight, reduction of
alcohol consumption, and stopping cigarette smoking. In patients with diabetes
mellitus, meticulous control of elevated blood glucose is also important.
When medications are necessary, fibrates (such as Lopid), nicotinic acid, and
statin medications can be used. Lopid not only decreases triglyceride levels
but also increases HDL cholesterol levels and LDL cholesterol particle size.
Nicotinic acid lowers triglyceride levels, increases HDL cholesterol levels and
the size of LDL cholesterol particles, as well as lowers the levels of Lp (a)
cholesterol. The statin drugs has been found effective in decreasing
triglyceride as well as LDL cholesterol levels and, to a lesser extent, in
elevating HDL cholesterol levels.
A chylomicron is a collection of cholesterol and triglyceride that is
surrounded by a lipoprotein outer coat. (Chylomicrons contain 90% triglyceride
and 10% cholesterol.) There are special enzymes on the blood vessels that break
up the triglyceride inside the chylomicrons, releasing fatty acids in the
process. The fatty acids can either be used by the muscles as energy, or
absorbed by fat cells where they are incorporated again into triglyceride that
can be stored in the fat cells for future energy needs. The chylomicrons are
then removed from the circulation by the liver.
The liver not only removes triglyceride and chylomicrons from the blood, it
also synthesizes and packages triglyceride into VLDL (very low-density
lipoprotein) particles and releases them back into the blood circulation.
Therefore, before breakfast after an overnight fast, most of the triglyceride
in the blood comes from the liver in the form of VLDL particles. Like
chylomicrons, VLDL particles contain mostly triglyceride. Some of the VLDL
particles lose triglyceride in the blood and become cholesterol-rich LDL
particles.
Do
high triglyceride levels cause atherosclerosis?
Whether elevated triglyceride levels in the blood lead to atherosclerosis and
heart attacks is controversial. While most doctors now believe that an
abnormally high triglyceride level is a risk factor for atherosclerosis, it is
difficult to conclusively prove that raised triglyceride by itself can cause
atherosclerosis. However, it is increasingly recognized that elevated
triglyceride is often associated with other conditions that increase the risk
of atherosclerosis including obesity, low levels of HDL- cholesterol, insulin
resistance and poorly controlled diabetes mellitus, and small, dense LDL
cholesterol particles.
Causes of Elevated Triglyceride Levels:
In some people, abnormally high triglyceride levels (hypertriglyceridemia) are
inherited. Examples of inherited hypertriglyceridemia disorders include mixed
hypertriglyceridemia, familial hypertriglyceridemia, and familial
dysbetalipoproteinemia.
Hypertriglyceridemia can often be caused by non-genetic factors such as
obesity, excessive alcohol intake, diabetes mellitus, kidney disease, and
estrogen containing medications such as birth control pills.
How can elevated blood triglyceride levels be treated?
The first step in treating hypertriglyceridemia is a low fat diet with a limited
amount of sweets, regular aerobic exercise, loss of excess weight, reduction of
alcohol consumption, and stopping cigarette smoking. In patients with diabetes
mellitus, meticulous control of elevated blood glucose is also important.
When medications are necessary, fibrates (such as Lopid), nicotinic acid, and
statin medications can be used. Lopid not only decreases triglyceride levels
but also increases HDL cholesterol levels and LDL cholesterol particle size.
Nicotinic acid lowers triglyceride levels, increases HDL cholesterol levels and
the size of LDL cholesterol particles, as well as lowers the levels of Lp (a)
cholesterol. The statin drugs has been found effective in decreasing
triglyceride as well as LDL cholesterol levels and, to a lesser extent, in
elevating HDL cholesterol levels.
The statins act by repressing or inhibiting an enzyme called HMG-CoA reductase.
The role of this enzyme is the promotion of a chemical reaction early in the
synthesis of cholesterol. By inhibiting HMG-CoA reductase, the statins hinder
the production (synthesis) of cholesterol by the liver. Diminished synthesis of
cholesterol in the liver in turn stimulates (increases) the activity of LDL
receptors on the surface of liver cells. Increasing LDL receptor activity
decreases LDL cholesterol levels in blood.
Studies have conclusively established that lowering LDL cholesterol with diet
and statins reduces the risk of a second heart attack. The prevention of
recurrent heart attacks in patients who have already suffered a heart attack is
called secondary prevention.
Studies have also demonstrated that reducing LDL cholesterol with diet and
statins reduces the risk of having the first heart attack. Prevention of heart
attacks in those who have never had a heart attack is called primary
prevention.
Studies have also confirmed that reducing LDL cholesterol benefits both men and
women.
Limitations of
Statins:
Statins are currently the most important class of medications in lowering LDL
cholesterol, which is now the most important first step in preventing
atherosclerosis and heart attacks. But statins are not the only answer. Other
cholesterol-altering medications can also be important in the fight against
atherosclerosis.
For example, in certain patients with familial hypercholesterolemia (FH), a
statin alone may not be enough when LDL cholesterol levels are very high. A
statin may need to be combined with another medication such as cholestyramine
or nicotinic acid in order to lower the LDL cholesterol to acceptable levels.
Statins may also not be as effective as other medications in treating elevated
Lp(a) cholesterol levels and in enlarging small LDL cholesterol particle sizes.
For example, estrogen and niacin are more effective than statins in decreasing
the blood Lp(a) cholesterol levels. Gemfibrozil and niacin are more effective
than statins in raising blood HDL levels and in increasing the size of the LDL
cholesterol particle. Diets rich in B vitamins or vitamin supplements, such as
folic acid and vitamin B6, help lower blood homocysteine levels. Elevated
homocysteine levels also aggravate atherosclerosis.
Nicotinic acid is most suited for individuals whose only problem is low HDL
cholesterol. Nicotinic acid used alone can raise HDL cholesterol levels by 30%
or more.
Nicotinic acid is not as effective as a statin in lowering LDL cholesterol
levels. Therefore, when low HDL cholesterol is accompanied by high LDL
cholesterol, most doctors use a statin to decrease the LDL cholesterol first.
Statins can also modestly increase HDL cholesterol levels. If necessary,
nicotinic acid can be added to a statin to further raise HDL cholesterol
levels.
The most common side effect of nicotinic acid is a flushing sensation of the
face and a general sense of itching, which occur about half an hour after
taking the drug. Another side effect is upset stomach. These side effects can
be partially alleviated by taking nicotinic acid with meals. Nicotinic acid
comes in regular tablets or slow and sustained release capsules. The sustained
release capsules release nicotinic acid from the stomach into the blood
circulation more gradually than the regular tablets. Therefore, the sustained
release capsules such as Niaspan produce a lower incidence of upset stomach and
skin flushing than the niacin tablets.
Another side effect is irritation of the liver with an abnormal elevation of
liver enzymes in the blood. This liver irritation is usually reversible upon
discontinuing nicotinic acid. Other side effects of nicotinic acid include
aggravating blood sugar levels in patients with diabetes mellitus and
precipitating painful arthritis attacks in patients with gout.
Cholestyramine
(Questran):
Cholestyramine (Questran) and colestipol (Colestid) are sand-like materials
which bind bile salts in the intestine and allow fat and cholesterol to be
eliminated in the stool. Cholestyramine is a resin that increases LDL receptor
activity and lowers LDL cholesterol. Cholestyramine has been used effectively
in combination with gemfibrozil to help lower LDL cholesterol levels. With
these drugs, cholesterol can be reduced by 20%, but triglyceride levels may
increase. These drugs can have the side effects of bloating, nausea,
indigestion, and constipation. They also interfere with the absorption of many
other drugs from the stomach and intestine.
Who
should undergo standard lipid profile testing?
It is recommended that every adult over 20 should have lipid panel tests (total
cholesterol, LDL cholesterol, HDL cholesterol, and triglyceride levels) every 5
years if LDL cholesterol is less than 130, and every 1-3 years if LDL
cholesterol is borderline (between 130 and 160). This is particularly important
for those with a family history of coronary artery disease. Once these
cholesterol figures are known, the chance of developing heart disease can be
determined in combination with the other risk factors that play a role in its
development.
Who should undergo testing for LDL cholesterol particle size
and Lp(a) cholesterol levels?
The scientific analysis for the determination of LDL size and Lp(a) is
relatively new and is not standardized from laboratory to laboratory. Thus,
results will vary to some degree between different laboratories. Also, because
the use of any specific laboratory test is not widespread, the cost of testing
remains expensive.
Because of the cost and the variability of testing, determination of these
cholesterol components is not for everyone. Currently, persons who have been
diagnosed with coronary artery disease whose risk factor profile would not
otherwise predict coronary artery disease at the age at which it occurred,
should be tested for these more specific cholesterol components. For example,
if heart disease occurs at a young age without high LDL levels, high blood
pressure, diabetes, or cigarette smoking, the physician and patient should then
search for another risk factor such as small LDL size or elevated Lp(a).
Among persons without coronary heart disease, those with a family history of
heart disease occurring early in life should be tested for these entities,
which are predominantly determined by genetic inheritance. As the cost and
accuracy of testing improves, the evaluation of these components should become
more widespread.
For more information, please read the Heart Attack and Atherosclerosis
Prevention article.
Cholesterol
and The Heart At A Glance
-
Cholesterol is produced in the liver and carried in the bloodstream by
lipoproteins.
-
LDL cholesterol is associated with an increased risk of coronary artery
disease.
-
Coronary heart disease is the most common cause of death in the U.S.
-
Risk factors for coronary heart disease have been identified.
-
After 20 years of age, cholesterol level testing is recommended every 5 years.
-
Treatment recommendations for elevated cholesterol are based on the levels of
total cholesterol, LDL cholesterol, HDL cholesterol, and other risk factors for
coronary heart disease.
-
Diets high in cholesterol and saturated fats can increase blood cholesterol
levels.
-
Diets high in unsaturated fats can lower blood cholesterol.
-
The most effective natural means of lowering blood cholesterol is to reduce
dietary saturated fat intake.
-
Treatment of elevated cholesterol includes diet, weight loss, regular exercise,
and occasionally medications.
|
