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New Markers of Cardiovascular
Health
Michael Lam, MD, MPH
www.DrLam.com
(READING TIPS: For
fast reading, scan through the topic headings in BOLD BLACK, important conclusions
in BOLD BLUE, and " Must Know " in BOLD
RED. To jump to specific sections in this article, click on the
respective LINKS in the Contents.)
Before You Begin
Information presented here is for general
educational purposes only. Each one of us is biochemically and metabolically
different. If you have a specific health concern and wish my personalized
nutritional recommendation, write to me by clicking
here. |
Contents
Introduction
1. Lipoprotein(a) Connection
 2.
The Mitochondrial Connection
3. The Homocysteine Connection
4. The Oxidative Stress Connection
5. Normalization of Traditional
Risk Factors
Discussion
Introduction
Everyone is at risk for cardiovascular
disease, the leading cause
of death worldwide. The established risk factors for heart disease, such as
serum cholesterol level, smoking, and family history, account for only one-half
to three-fourths of the cases. The remainder are a result of other factors that
promote atherosclerosis (the buildup of fatty deposits in blood vessels) such
as infections. C. pneumoniae, a bacterium that causes respiratory infection,
has been found in 70-80% of plaques taken from a heart disease patient. The
jury is still out as far as the exact mechanism of injury is concerned. However,
it has been postulated that the infection triggers the immune system's response
and inflammation within the blood vessel wall. Large-scale research to determine
mechanism is currently underway.
Efforts to determine more ways of preventing heart disease have led to the
unearthing of about 300 predictors. One of these new markers for heart disease
is male baldness. Hair loss to the crown area has been linked to a three-fold
greater risk of heart disease in men, according to a study at Harvard Medical
School by Joanne Manson, chief of the Division of Preventive Medicine at Brigham
and Women's Hospital in Boston, and her colleagues. The connection may be elevated
male hormone levels. These findings will pave the way in the coming years to
new therapies.
Four new markers will be studied
- lipoprotein(a), mitochondrial function, homocysteine, and oxidative stress
and their ramifications for the promotion of optimum cardiovascular health.
1.
Lipoprotein(a) Connection
Fifty percent of Americans
have elevated serum cholesterol levels. And the increase occurs naturally
as we age. In men, most of the increase occurs after about age 45. In women,
most of the increase occurs after age 55, and especially after menopause. The
goal for cholesterol management is to lower the blood level of bad (low-density
lipoprotein, or LDL)- cholesterol and increase the level of good (high-density
lipoprotein, or HDL-) cholesterol as its job is to mop up LDL-cholesterol. There is no question that lowering dietary intake of cholesterol and saturated
fats prevent heart disease because it lowers blood LDL-cholesterol levels.
Cholesterol
levels alone
cannot explain many heart attack deaths. Autopsy studies of heart
attack victims, however, show that a good percentage of heart attack victims
have clean vessels and ideal lipoprotein levels. It is obvious that there are
other causes for heart disease than the traditional. Indeed, researchers with
the Framingham Heart Study (the decades-long study that brought us the term
"risk factor") identified a relative of LDL-cholesterol called lipoprotein(a)
[Lp(a)], which is now recognized as MAJOR
independent risk factor for heart disease. Lp(a) fosters the deposition of
cholesterol on artery walls as well as interferes with the body's means of dissolving
clots. Lp(a) fosters cholesterol deposition by enhancing oxidation of LDL-cholesterol.
It is the oxidized form of cholesterol that penetrates the endothelium, leading
to the build up of plaque and vascular disease.
Cardiovascular Disease and Supplementation
Some researchers believe that cardiovascular
disease is primarily caused by chronic deficiencies of vitamins and other essential
nutrients with defined biochemical properties, such as coenzymes, cellular energy
carriers, and antioxidants. Chronic depletion of these essential nutrients in
endothelial and vascular smooth muscle cells impairs their ability to function
properly.
Take the effects of Vitamin
C (ascorbic acid) deficiency as an example. Humans are one of a few animals
that cannot produce ascorbate. Humans must get Vitamin C from external sources.
Deficiency of Vitamin C leads to a disease called scurvy, the symptoms of which
are caused the reduced ability of the body to make collagen, an essential component
of wound healing, bones and joints, and blood vessels. Chronic ascorbate
deficiency leads to impairment in the structure of the blood vessel walls and
tiny lesions in its inner wall. These changes are the hallmarks of early atherosclerosis.
Atherosclerotic plaques can develop as the result of an overcompensating repair
mechanism consisting of deposition of systemic plasma and local cellular response
which includes extra cellular accumulation of Lp(a) and fibrinogen/fibrin at
the site of injury. This repair mechanism is exacerbated primarily at sites
of hemodynamic stress. This explains why the most frequent clinical manifestation
of cardiovascular disease such as myocardial infarction, is the local development
of atherosclerotic plaques in coronary arteries.
As a result of confirmation in animal studies, ascorbate with other essential
nutrients is now being recommended for the prevention and treatment of cardiovascular
diseases.
Mathias Rath and colleague conducted a yearlong study to determine the effect
of a defined nutritional supplementation program on the natural progression
of coronary artery disease. He gave 55 patients with various stages of coronary
artery disease, aged 44-67, a daily nutritional supplementation program including
2,700 mg of Vitamin C, vitamin B complex, 600 IU of Vitamin E (d-alpha-tocopherol),
450 mg of L-proline, 450 mg of L-lysine, 390 mcg of folic acid, 30 mg of coenzyme
Q-10, and 450 mg of citrus bioflavinoids. Changes in the progression of coronary
artery calcification before and during the program were determined by Ultrafast
Computerized Tomography. Before the intervention, the natural progression rate
of the coronary artery calcification averaged 44% per year. However, during
the year of treatment, the progression of coronary artery calcification decreased
by an average of 15%. In a subgroup of patients with early stages of coronary
artery disease, treatment resulted in a statistically significant decrease,
with no further progression of coronary calcification. In individual cases,
reversal and complete disappearance of previously existing coronary calcification
were documented. This landmark study, published in the Journal of Applied Nutrition
(1996, 48:3), showed that coronary
artery disease could be effectively prevented and treated by natural means.
In patients with early coronary calcification, progression was halted. In individual
cases with small-calcified deposits, nutritional supplement intervention led
to the complete disappearance of the deposits.
It is postulated that the nutrients
used by Rath initiate the reconstitution of the vascular wall. Ascorbate is
essential for the synthesis and hydroxylation of collagen. L-lysine and
L-proline are important substrates for the biosynthesis of matrix protein and
competitively inhibit the binding of lipoprotein(a) to the vascular matrix.
Maintaining the integrity and physiological function of the vascular wall
is the key therapeutic target in controlling cardiovascular disease.
 It
is worth noting that Vitamin C, being water-soluble, is cleared through the
body very quickly, giving it a very short half-life. To
maintain continuous
optimum levels of Vitamin C in the body, ascorbate should be taken in divided
dosages throughout the day. To overcome this problem, a fat-soluble form of
Vitamin C, ascorbyl palmitate, has been developed. It
is readily absorbed from the gastrointestinal track and finds its way to the
micro-capillaries where it stays to exerts its health enhancing properties mentioned
above.
The amount of each nutrient required to prevent the onset of disease states
is outlined in the Recommended Dietary Allowances (RDAs).
As of July 2000, the RDA for Vitamin
C is 60 mg per day. This is about the amount present in one RED and will
prevent scurvy. The amount
for optimum health however, is less well defined.
Humans, other primates, and
guinea pigs do not produce ascorbate endogenously. Guinea-pigs
fed a diet low in ascorbate, an amount equivalent to the usual human intake,
rapidly developed atherosclerotic plaques, similar to those found in humans.
When large amounts of supplementary ascorbate were given to these guinea pigs,
there was a regression in plaque formation.
Linus Pauling, two-time Nobel Laureate, postulated that Lp(a) may be the surrogate
for ascorbate in the human. Low dietary intake of ascorbate leads to weakened
blood vessels because ascorbate is required for the synthesis of collagen and
elastin, which strengthen the blood vessel wall. In the absence of sufficient
ascorbate, Lp(a) is mobilized to repair these structural defects in arterial
walls by being deposited to strengthen the tissue. However, if the plasma concentration
of Lp(a) is too high, the process goes too far. Too much Lp(a) gets deposited
in the arterial wall, and plaque formation is initiated. Dr. Pauling concluded
that the optimum intake of Vitamin C is perhaps 100 times more than the RDA.
During the last 25 years of his life (he died at age 93 from cancer), Dr Pauling
increased his own intake of Vitamin C from 50 time to 300 times the RDA, taking
3,000 mg to 18,000 mg per day. This amount is consistent with the amount of
ascorbate in animals that are capable of producing their own on a daily basis.
It is fair to say that Dr. Pauling believed that cardiovascular disease is the
general result of ascorbate deficiency.
Preventive Nutritional Supplement
Consideration:
Ascorbyl Palmitate: 200 - 400 mg
L-Lysine: 200 - 400 mg
L-Proline: 200 - 00 mg
Ascorbate: 1,000 - 3,000 mg
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