Primary Disease Name: Cholesterol
Cholesterol Information - What is Cholesterol?
Cholesterol is a waxy, fat-like substance that occurs naturally in all parts of
the body and that your body needs to function normally. It is present in cell
walls or membranes everywhere in the body, including the brain, nerves, muscle,
skin, liver, intestines, and heart. Your body uses cholesterol to produce many
hormones (e.g. testosterone), vitamin D, and the bile acids that help to digest
fat. It takes only a small amount of cholesterol in the blood to meet these
needs. If you have too much cholesterol in your bloodstream, the excess is
deposited in arteries, including the coronary arteries, where it contributes to
the narrowing and blockages that cause the signs and symptoms of heart disease.
A number of factors contribute to higher cholesterol including heredity, what
you eat, weight, physical activity/exercise, age and sex, alcohol and stress.
Heart disease is caused by narrowing of the coronary arteries that feed the
heart. When the coronary arteries become narrowed or clogged by cholesterol and
fat deposits--a process called atherosclerosis--and cannot supply enough blood
to the heart, the result is coronary heart disease (CHD). If not enough
oxygen-carrying blood reaches the heart, you may experience chest pain called
angina. If the blood supply to a portion of the heart is completely cut off by
total blockage of a coronary artery, the result is a heart attack. This is
usually due to a sudden closure from a blood clot forming on top of a previous
narrowing.
Determining a patient's absolute risk requires refined risk assessment.
Particularly in patients with severe risk factors, additional tests may be
ordered to assess levels of lipoprotein(a) (Lp(a)) and apoproteins such as
apolipoprotein (apo) B-100 or, less commonly, apo A-I. Low-density lipoprotein
(LDL) particle size may be measured to assess for the presence of small, dense
LDL, which is more atherogenic than normal LDL, but apo B-100 level may be a
better marker because it provides the number of particles. Apo E genotype may
identify a genetic dyslipidemia and may also predict response to lipid-lowering
therapy.
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Cholesterol Risk Factors
Cholesterol Risk Factors: Many factors determine whether your
blood cholesterol level is high or low. The following are the most important:
Cholesterol and Heredity -- Your genes partly determine the
amount of cholesterol your body makes, and high blood cholesterol can run in
families.
Cholesterol and Weight -- Excess weight tends to increase blood
cholesterol levels. If you are overweight and have high blood cholesterol,
losing weight may help you lower it.
Cholesterol and Diet -- There are two nutrients in the foods
you eat that can increase your blood cholesterol level: saturated fat and
cholesterol. Saturated fat is a type of fat found mostly in foods that come
from animals. Cholesterol comes only from animal products. Saturated fat raises
your cholesterol level more than anything else in the diet. Reducing the
amounts of saturated fat and cholesterol you eat is an important step in
reducing your blood cholesterol levels.
Cholesterol and Exercise -- Regular physical activity may help
to lower LDL-cholesterol and raise desirable HDL-cholesterol levels.
Cholesterol and Age and Gender -- Before menopause, women have
total cholesterol levels that are lower than those of men the same age.
Pregnancy raises blood cholesterol levels in many women, but blood cholesterol
levels should return to normal about 20 weeks after delivery. As women and men
get older, their blood cholesterol levels rise. In women, menopause often
causes an increase in their LDL-cholesterol levels. Some women may benefit from
taking estrogen after menopause, because estrogen lowers LDLs and raises HDLs.
Cholesterol and Alcohol -- Intake increases HDL-cholesterol. It
is not known whether it also reduces the risk of heart disease. Drinking too
much alcohol can certainly damage and liver and heart muscle and cause other
health problems. Because of these risks, you should not drink alcoholic
beverages to prevent heart disease.
Cholesterol andStress -- Over the long term, stress has not
been shown to raise blood cholesterol levels. The real problem with stress may
be how it affects your habits. For example, when some people are under stress
they console themselves by eating fatty foods. The saturated fat and
cholesterol in these foods probably cause higher blood cholesterol, not the
stress itself. Whilst high blood cholesterol (high total cholesterol and high
LDL-cholesterol) and low HDL cholesterol are significant risk factors for heart
disease, there are also a number of other contributing factors, many of which
can be controlled: Cigarette Smoking , High Blood Pressure, Diabetes, Obesity,
and Physical Inactivity.
Types of Cholesterol
There are several different types of cholesterol in our blood some from the
food we eat, others manufactured by the liver:
LDL, HDL, Triglyceride, Lp(a), Apo B, Homocysteine, and VLDL
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Why is LDL Cholesterol "Bad"?
When too much LDL cholesterol circulates in the blood, it can slowly build up in
the inner walls of the arteries that feed the heart and brain. Together with
other substances it can form plaque, a thick, hard deposit that can clog those
arteries. This condition is known as atherosclerosis. If a clot forms and
blocks a narrowed artery, it can cause a heart attack or stroke. The levels of
HDL cholesterol and LDL cholesterol in the blood are measured to evaluate the
risk of having a heart attack. LDL cholesterol of less than 100 mg/dL (or total
cholesterol levels of 4.7 millimoles per litre (mmol/L) is the optimal level.
Less than 130 mg/dL (total cholesterol of 5.2 millimoles per litre (mmol/L) is
near optimal for most people. A high LDL level (more than 160 mg/dL (6mmol/L)
or 130 mg/dL (>5.2m/mol) or above if you have two or more risk factors for
cardiovascular disease) reflects an increased risk of heart disease. That's why
LDL cholesterol is often called "bad" cholesterol. Prescription drugs such as
Lipitor (atorvastatin), Zocor (simvastatin), Pravachol (pravastatin), and
Lescol (fluvastatin) have been shown to interfere in the synthesis of LDL by
blocking an enzyme that helps produce cholesterol in the body.
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LDL Cholesterol Particles
The LDL cholesterol 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 researchers 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.
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
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Why is HDL Cholesterol "Good"?
About one-third of blood cholesterol is carried by high-density lipoprotein
(HDL). HDL cholesterol is known as the "good" cholesterol because a high level
of it seems to protect against heart attack. (Low HDL cholesterol levels [less
than 40 mg/dL] increase the risk for heart disease.) Medical experts think that
HDL tends to carry cholesterol away from the arteries and back to the liver,
where it's passed from the body. Some experts believe that HDL removes excess
cholesterol from plaque in arteries, thus slowing the buildup.
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What is Lipoprotein-A?
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Lipoprotein A is a genetic variation of plasma LDL, except that it has an extra
protein that is thought to interfere with an important clot-buster in the body.
A high level of Lp(a) is an important risk factor for developing fatty deposits
in arteries prematurely. The way an increased Lp(a) contributes to disease is
not fully understood. The lesions in artery walls contain substances that may
interact with Lp(a), leading to the buildup of fatty deposits. When elevated
levels of Lp(a) are deposited in the walls of the arteries, it may cause
blockages to become larger, blood to thicken, artery walls to stiffen. Genetics
-- rather than diet or other lifestyle choices -- determines Lp(a) levels.
People with a high Lp(a) level are at greater risk for cerebrovascular
(involving the brain and the blood vessels supplying it) and cardiovascular
disease, especially if they have a family history of stroke or early-onset
coronary artery disease.
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. (Lp(a) measurements cost approximately $100 and LDL size
measurements about $200 - $300). 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).
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What are Triglycerides?
Triglyceride is a type of fat. It comes from food and is also made in your body.
People with high triglyceride levels often have high total cholesterol, high
LDL cholesterol and low HDL cholesterol levels. Many people with heart disease
also have high triglyceride levels. People with diabetes or who are obese are
also likely to have high triglycerides.
Triglyceride levels of less than 150 mg/dL are normal; levels from 150-199 are
borderline high. Levels that are borderline high or high (200 mg/dL to 499
mg/dL) may need treatment in some people. Triglyceride levels of 500 mg/dL or
above are very high. Doctors need to treat high triglycerides in people who
also have high LDL 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.
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What is ApoB (Apolipoprotein)?
Cholesterol is a condition in which the bones grow porous and more likely to
break. Several prescription drugs can help treat it.
Estrogen replacement therapy (ERT) can prevent the large loss of bone mass that
women experience soon after menopause. Examples of drugs used in ERT include
conjugated estrogen (brand name Premarin) and estradiol (Estrace). Such drugs
can increase bone density by 5 percent, lower the risk of a broken wrist or hip
from 1 in 15 to 1 in 50 over a five year period. Like all medications, ERT has
positive and negative effects. It's very important for you and your doctor to
discuss the risks and benefits of ERT.
For women who can't take estrogen, other medicines are available. Medications
like raloxifene (brand name Evista), alendronate (Fosamax), and calcitonin
(Miacalcin nasal spray) have been shown to slow bone loss. Evista increases
bone density by 2.5 percent and lowers the risk of spine fractures from 1 in 25
people to 1 in 50 people. Fosamax increases bone density by 5 to 10 percent and
reduce the risk of hip fractures from 1 in 50 women to 1 in 100 women Actonel
increases bone density by 1.6 to 5 percent and reduces the risk of fractures
from 1 in 12 people to 1 in 20 people. Actonel reduces the risk of hip fracture
among women with Cholesterol. Miacalcin reduces the risk of spine fractures
from 1 in 8 people to 1 in 13 people.
Another promising alternative is a class of drugs called HMG-CoA reductase
inhibitors or "statins". Doctors prescribe statins such as pravastatin
(Pravachol), simvastatin (Zocor), lovastatin (Mevacor), and fluvastatin
(Lescol) to lower cholesterol levels in the blood and to reduce the risk of
heart disease. Researchers have found a link between the use of statins and a
lower risk of fractures. Early information suggests that statins may reduce
fractures by increasing bone density. Scientists will have to conduct more
studies to determine the role and benefits of statins in reducing fractures.
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What is Homocysteine?
Increased levels of homocysteine (an essential amino acid found in the blood)
can harm the lining of the arteries (endothelium). A homocysteine level higher
than 12 milligrams per deciliter is a risk factor for coronary artery disease.
Many health care professionals believe that using folic acid to lower
homocysteine levels may help reduce the risk of heart disease. Homocysteine is
metabolized (chemically transformed) into methionine and cysteine with the help
of the B vitamins; folic acid, B12, and B6 (pyridoxine). Therefore,
insufficient amounts of these B vitamins in the body can theoretically hamper
the metabolic breakdown of homocysteine, and hence increase its blood levels.
High levels of homocysteine in the blood (hyperhomocysteinemia) can damage the
inner surface of blood vessels, promote blood clotting, and accelerate
atherosclerosis.
The current state of knowledge regarding folic acid, homocysteine, and heart
attacks is as follows:
The level of blood folate is an important determinant of the blood homocysteine
level. Low blood folate levels are associated with high blood levels of
homocysteine.
Low blood folate is common among individuals who do not take multivitamins, but
unusual among those who do.
Taking folic acid supplements or eating folic acid fortified cereals can
increase blood folate levels and decrease blood homocysteine levels.
In a large population study involving women, those who had the highest
consumption of folic acid (usually in the form of multivitamins) had fewer
heart attacks than those who consumed the least amount of folic acid.
Even though current scientific evidence suggests that taking folic acid and
vitamin B supplements to lower homocysteine levels should help prevent
atherosclerosis and heart attacks, conclusive proof is still lacking because:
There are no conclusive studies (a prospective, randomized, placebo-controlled
trial) demonstrating that increasing folic acid intake actually prevents
atherosclerosis and heart attacks. (In this type of study, patients are
evaluated over time and are randomly assigned to either a group taking the
medication under study or a placebo. The results of this type of study are
considered determinative.)
There is no clinical study
that demonstrates lowering blood levels of homocysteine actually prevents
atherosclerosis and heart attacks.
There is also no official recommendation as to who should be tested for
hyperhomocysteinemia. The optimal doses of the B vitamins, folic acid, B12, and
B6, required to prevent and treat hyperhomocysteinemia are also uncertain. For
folic acid, a daily dose of 0.8-1.0 mg is probably adequate.
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What is VLDL?
Very low-density lipoproteins (VLDL) carry cholesterol and triglycerides from
the liver. After the liver removes triglycerides from it, VLDL becomes LDL.
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Cholesterol Levels
1. TOTAL CHOLESTEROL (mg/dl):
Total cholesterol is defined by the total level LDL and HDL cholesterol in the
blood. However, this number does not give us the exact breakdown of good versus
bad cholesterol. Hence, it simply provides us with a general guideline to
follow:
Desirable: Below 200mg/dl
Borderline: 200-239mg/dl
Undesirable: 240mg/dl and above
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2. LDL CHOLESTEROL (mg/dl)
LDL Cholesterol levels are currently the clearest signal that doctors have that
require a patient to be put on a prescription drug. LDL Levels should be as
follows:
Desirable: Below 130mg/dl
Borderline: 130-159mg/dl
Undesirable: 160mg/dl and above
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3. HDL CHOLESTEROL (mg/dl)
There is also a minimum level of HDL Cholesterol that doctors would like to see
there patients to have. If the desirable level is not present, a prescription
drug such as Zetia (Ezetrol/Ezetimibe) or Tricor (Lipidil/Fenofibrate) may be
initiated to raise those levels.
Desirable: Above 45mg/dl
Borderline: 40-45mg/dl
Undesirable: Below 40mg/dl
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4. Triglycerides mg/dl
Triglycerides are a form of fat that is carried through the bloodstream. Most
of your body's fat tissue is in the form of triglycerides. High blood
triglyceride levels alone usually do not raise your risk of heart disease. But
many people have a high triglyceride level along with high LDL- and low
HDL-cholesterol levels. In these cases, the three are often treated together.
Here's how to judge your triglyceride level:
Normal -- Triglyceride level less 200 mg/dL.
Borderline-High -- Triglyceride level between 200 and 400 mg/dL.
High -- Triglyceride level between 400 and 1000 mg/dL.
Very High -- Triglyceride level greater than 1,000 mg/dL.
Borderline-high and high triglyceride levels are first treated with the same
diet and lifestyle changes used for high blood cholesterol levels. These
changes include losing weight if you are overweight; following a diet low in
saturated fat and cholesterol; being physically active; and not smoking.
Usually, high triglyceride levels are due to heredity, and levels may need to
be lowered with medicines (e.g. Zetia, Lipidil Supra/Tricor)
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5. Lipoprotein A Levels
Lipoprotein A is a relatively newer diagnostic tool for doctors. The Advicor
Versus Other Cholesterol-modulating Agents Trial Evaluation (ADVOCATE) study
was designed to compare the efficacy of Advicor (a niacin extended-release
(ER)/lovastatin preparation) with that of 2 common monotherapies, Lipitor
(atorvastatin) and Zocor (simvastatin). After 8 weeks administration at their
starting doses, both Advicor 1,000/40 mg and Lipitor 10 mg lowered LDL
cholesterol levels by 38%. After 12 weeks, Advicor 1,000/40 mg lowered LDL-C
levels by 42%, while Zocor 20mg lowered LDL cholesterol levels by 35%.
Additionally, Advicor increased HDL cholesterol levels significantly more than
either Lipitor or Zocor at all compared doses and provided significant
improvements in other lipid parameters such as triglyceride, lipoprotein(a),
apo A-I, and apo B levels. The effect on Lipoprotein A levels was a 16%
reduction at week 8 and 20% reduction at week 12 compared to Lipitor (5%
increase) and Zocor (1% decrease). (Reference
http://www.lipidsonline.org/slides/slide01.cfm?q=apo%2Bb&dpg=8&x=168&43311).
6. APO B Levels
Because the statins (eg Lipitor/ Zocor) primarily affect LDL-C and the fibrates
primarily affect HDL-C and triglyceride, combination therapy may provide
greater benefit on the entire lipid profile. Combining Lopid (gemfibrozil) 1200
mg/d with either Pravachol (pravastatin) 20 mg/d or Zocor (simvastatin) 20 mg/d
and combining ciprofibrate 100 mg/d with simvastatin 20 mg/d produced marked
improvement of LDL-C, triglyceride, and HDL-C in patients with familial
combined hyperlipidemia; apo B, a component of atherogenic lipoproteins, was
also reduced. In addition, fibrinogen level was decreased; fibrinogen has been
shown to be a risk factor for CHD, potentially contributing to a prothrombotic
state. Fibrates are the only lipid-lowering drugs shown to decrease fibrinogen
level. Another important LDL-C-lowering drug is nicotinic acid, or niacin.
Niacin appears to exert its effects by inhibiting lipoprotein synthesis and
decreasing the production of VLDL particles by the liver. It inhibits the
peripheral mobilization of free fatty acids, thus reducing hepatic synthesis of
triglycerides and the secretion of VLDL. It also reduces apo B. The net result
is a reduction in VLDL particles secreted by the liver and thus less substrate
to make LDL particles. It increases the production of apo A-I and thereby HDL
through mechanisms that are not clear.
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Manifestations of High Cholesterol
Heart disease is the leading killer of North Americans, striking down about
600,000 people each year, primarily by heart attack (ATP III). The majority of
these deaths are caused by coronary artery disease. More than 20% of Americans
have some form of coronary artery disease.
Many people with heart disease experience symptoms, but others don't. If a
person who has heart disease doesn't have symptoms, he or she may not be aware
a problem exists. This lack of knowledge can be dangerous, because a third of
all first heart attacks are fatal. Common symptoms include chest pain, pain
that radiates from the chest up into the jaw or down the arms frequently
associated with shortness of breath, sweating, nausea/vomiting, and feelings of
pending doom.
High cholesterol can increase your risk of developing heart disease, but the
good news is that you can take steps to lower your cholesterol.
Atherosclerosis is a gradual process whereby hard cholesterol substances
(plaques) are deposited in the walls of the arteries. Cholesterol plaques cause
hardening of the artery walls and narrowing of the inner channel (lumen) of the
artery. Arteries carry blood that is enriched with oxygen and nutrients to the
vital organs such as the brain, heart, kidneys, and liver. Arteries also
transport blood to other tissues such as the fingers, toes, nerves, bones,
skin, and muscles. Healthy arteries can deliver an ample supply of blood to the
organs and tissues. In contrast, arteries that are narrowed by atherosclerosis
have difficulty delivering blood to the parts of the body they supply. For
example, atherosclerosis of the arteries in the legs causes poor circulation in
the lower extremities. Poor circulation in the lower extremities can lead to
pain while walking or exercising, deficient wound healing, and/or leg ulcers.
Atherosclerosis can also cause the complete blockage of an artery from a blood
clot. Complete blockage of an artery interrupts oxygen supply, resulting in
tissue injury or death. Thus, the blockage of an artery that furnishes blood to
the brain can lead to stroke (death of brain tissue), and the blockage of the
arteries to the heart can result in a heart attack (death of heart muscle),
also called myocardial infarction, or MI. Coronary atherosclerosis refers to
the hardening and narrowing of the coronary arteries. Coronary arteries supply
the blood that carries oxygen and nutrients to the heart muscle. When coronary
arteries are narrowed or blocked by atherosclerosis, they cannot deliver an
adequate amount of blood to the heart muscle. Disease caused by the lack of
blood supply to heart muscle is called coronary artery disease. Coronary artery
disease (CAD) includes heart attacks, sudden unexpected death, chest pain
(angina), abnormal heart rhythms, and heart failure due to weakening of the
heart muscle.
A heart attack (myocardial infarction) is the death of heart muscle due to the
sudden and complete blockage of a coronary artery by a clot. A coronary artery
blockage usually occurs in arteries that contain cholesterol plaques. A plaque
can rupture and initiate the formation of a blood clot next to it. A blood clot
can completely block blood flow through a coronary artery and deprive the heart
muscle of needed nutrients and oxygen. The heart muscle then dies, which
produces a heart attack
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Alleviating Angina
Chronic angina, or attacks of cardiac pain that can lead to heart attacks,
affects more than six million Americans. The attacks occur when the heart does
not receive all of the oxygen it needs to function effectively. These attacks
are typically triggered by physical exertion or emotional stress. A new class
of medicines called pFOX (partial fatty acid oxidation) inhibitors may be able
to reduce episodes of pain and allow patients with angina to be more active.
The medicines work by shifting the heart's metabolism to a fuel source that
requires less oxygen to generate the same amount of energy. The heart uses two
energy fuels: fatty acids and glucose. A healthy heart uses fatty acids during
times of stress. But a heart that is not receiving enough oxygen-rich blood,
due to obstructions in the arteries, can produce more energy per unit of oxygen
when using glucose instead of fatty acids. By shifting the metabolism of the
heart to use more glucose than fatty acids during periods of stress, pFOX
inhibitors can help prevent angina attacks. In clinical trials, a pFOX
inhibitor bolstered the exercise capacity of angina patients and reduced
episodes of cardiac pain.
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Bypassing Surgery
A medicine in development may enable patients to grow their own bypasses,
potentially reducing the need for coronary bypass surgery and providing
effective treatment for a debilitating cardiovascular disease. The medicine,
which is injected into the patient, contains a gene that promotes new blood
vessel growth. Clinical trials of the medicines are being conducted in patients
with peripheral vascular disease, a progressive narrowing of the blood vessels
in the legs that affects more than 10 million Americans, and in patients with
advanced coronary artery disease.
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Heart Failure Patients
Smoking is bad for your bones as well as for your heart and lungs. Women who
smoke have lower levels of estrogen compared to nonsmokers and frequently go
through menopause earlier. Postmenopausal women who smoke may require higher
doses of hormone replacement therapy and may have more side effects. Smokers
also may absorb less calcium from their diets.
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