Dr. Lam Author of
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Lipoprotein(a)
Some of the natural cholesterol produced by the liver in response to free
radical damage is converted into LDL cholesterol and its relative lipoprotein
(a) (Lp (a)). While LDL cholesterol maybe known as the "bad" cholesterol,
Lp (a) is even worse. Lp(a) is a plasma lipoprotein that structurally
resembles LDL, but with an additional adhesive protein. Lp(a) is also made
in the liver and transported to the cell. Studies have shown that Lp(a)
holds fast to damaged blood vessel, attracting other Lp(a) molecules, and
finally constituting the atherosclerotic plaques. In fact, a high Lp (a) level (more than 30 mg/dl) has been revealed
to carry a 10 times greater risks for heart disease than LDL cholesterol
level. Lp(a) level should be part of a routine blood screening
test for cardiovascular disease risk.
Lp(a), according to Drs. Pauling and Rath, is the body's way of repairing
its damaged vessel wall that has micro leakages caused at least in part
by free radical damage and vitamin deficiencies (more specifically vitamin
C) Humans do not make any endogenous vitamin
C and have no self-repair mechanism of the vascular system. Lp(a)
is used by the body as a surrogate vitamin C, so to say. Lp(a), unfortunately,
has a sticky characteristic and adheres to each other, forming an atherosclerotic
plaque over time. The body, at the interim, is unaware. As long as the damage
persists due to free radical presence (either from improper diet, aging,
pollution, lack of vitamins, or toxins), the body responds by making more
cholesterol endogenously in the liver, feeding a viscous cycle of ever increasing
Lp(a).
Cholesterol and Cardiovascular
Disease
The notion that total blood cholesterol level alone is the key determinant
of cardiovascular heath should be dispelled. Polar
bears, for example, maintain total blood cholesterol of over 400 mg/dl and
they seldom develop heart attacks. There is obviously a lot more
to learn about cholesterol and its link to cardiovascular disease that we
currently know.
It is proven that single focused dietary strategy
of lowering dietary cholesterol does not reduce coronary heart disease risks.
To make matters worse, "low-fat, high carbohydrate" diets are often high in
the wrong type of carbohydrate. Instead of taking in complex, paleo
type carbohydrates such as green leafy vegetables of low glycemic index,
the ignorant consumer often ends up consuming carbohydrates of high glycemic
index such as pasta, soda, processed foods, and fast foods. These types
of food are rich in sugar and starch (carbohydrate). They actually lower
the important "good" HDL cholesterol. A low HDL cholesterol level is inversely
proportional to the cardiovascular disease risk. It should be remembered
that cholesterol and fat are concentrated sources of calories and can lead
to obesity if too much is consumed.
In the Framingham study for example, men and women consumed an average cholesterol
intake of 700 mg and 500 mg per day respectively were studied (one egg provides
200 mg). The average serum concentration of cholesterol for men and women
with higher than average cholesterol intake were found to be 237 and 245
mg/dl respectively. Subjects with lower than average intakes were found
to be 237 and 241 mg/dl. The difference is statistically insignificant.
Statistically, studies have shown that people who consume 4 eggs per week (one egg provides 200mg cholesterol)
actually have average serum cholesterol (193 mg/dl) same than those who
reported consuming only 1 egg per week (197 mg/dl). Clearly dietary
cholesterol in and of itself is not the critical link to heart disease risks
as we once thought.
What is "Normal"
Cholesterol Level?
A low total serum cholesterol level (under 150 mg/dl) is undesirable
for the healthy person. It is very difficult to lower cholesterol only without
other types of fats because they are often found intermingled with each
other in food. While saturated fatty acid (SFA) from animal and dairy products
is not subject to lipid peroxidation, all animal fats contain some PUFA
and cholesterol, both of which undergo auto-oxidation. Those who are serious
in reducing total serum cholesterol level should refrain from intake of
lipid peroxide-containing fats (trans fat such as margarine) with resulting
reduction of free radical pathology. Like trans fat, oxidized cholesterol
should be limited as much as possible.
A low fat diet may actually bring harm to health. The
correct way is to discern the right type of fat and cholesterol to take
and those to avoid. The overall fat intake as a percentage of dietary
calories should not fall below 25-30%. One should have plenty of "good" mono-unsaturated
fatty acids (MUFA) like olive oil, seeds, nuts, and cold-water fish
that have high omega-3 fatty acid
(N3) content.
Saturated fat is
necessary for good health. It should come from free-range poultry or beef,
and organic eggs. It is very important to avoid "bad" trans fat, like margarine
and fried foods. Moreover, the use of processed PUFA such as corn, safflower
or sunflower oil should be restricted.
The optimum level of blood cholesterol should
be at the upper end of normal around 200 mg/dl.
Cholesterol Lowering Drugs
A class of drugs used to aggressively treat elevated LDL levels is the synthetically
derived HMG-CoA reductase inhibitors such as Iovastatin, pravastatin, and
simvastatin. They are collectively called "statin" drugs. By inhibiting the production of HMG-CoA reductase,
cholesterol production in the liver is reduced. These are among the most
potent lipid-lowering agents available. To compensate for the resulting
reduction of cholesterol production, the liver increases absorption of LDL
cholesterol, further contributing to an overall reduction of LDL cholesterol
levels.
While statin drugs are effective in lowering
LDL cholesterol, they have serious side effects. For years, the
public was led to believe that the wonders of statin drugs not only in lowered
cholesterol but possessed other health benefits as well. Millions of statin
prescriptions are written yearly in the United States alone. In
August 2001, however, German Pharmaceutical giant Bayer AG withdrew the
cholesterol-lowering statin drug Baycol from the market because it was linked
to 31 deaths. Moreover, deaths occurred at the manufacturer's recommended
initial dose (0.4 mg/day) as well as at the highest dose (0.8 mg/day). The
majority of deaths occurred in elderly patients and more often in women.
There are other statin drugs on the market, such as Lipitor (the best seller).
Like Baycol, these drugs are linked to the same rare muscle weakness, known
as myositis, which occurs in about 1 in 1,000 statin users. Myositis
occasionally progresses to rhabdomyolysis -- a complete breakdown of muscle
cells that can lead to kidney failure and death. Some experts believe
that pravastatin (Pravachol) and fluvastatin (Lescol) may have less potential
for this deadly drug interactions. The data at this time are not sufficient
to declare one statin drug safer or more dangerous than the others.
Statin drugs also inhibits the intrinsic biosynthesis
of Coenzyme Q10 (CoQ10), a central compound in the mitochondrial
respiratory chain. CoQ10 is indispensable for optimum cardiac function.
Reduction of CoQ10 constitutes new risk of cardiac disease, especially for
those whose cardiac function is compromised, such as those with congestive
heart failure or cardiomyopathy.
Furthermore, statin drugs have been linked to various forms of cancer in laboratory animals. It will be years before we know the full side effects
of statin drugs.
Using statin drugs on a short-term basis to normalize
blood cholesterol is a reasonable alternative if a drug-free approach fails.
Anyone on long term statin type cholesterol lowering drug would be wise
to get regular checkups, especially on liver function.
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