When homocysteine is not
completely broken down by the body, it becomes a very dangerous
substance, causing clotting, oxidization, atherosclerosis and
blocked blood flow. Increased blood levels of homocysteine
usually indicate faulty methionine metabolism. If this
biochemical pathway is defective high homocysteine levels can
cause clotting, increased oxidation, and can injure the blood
vessel wall, allowing cholesterol and other fats to infiltrate
into the wall and create what is called a foam cell; thereby
blocking the blood flow and creating blood wall plaque.
When homocysteine is broken
down properly, it can supply the body with many necessary
substances that in turn aid other normal chemical reactions. For
example, processes such as cartilage rebuilding, bone
regeneration, liver detoxification, and adrenal gland support
come from substances supplied when the normally functioning body
breaks down homocysteine. The supplementation required to
correct homocysteine levels in a person's blood are the B
vitamins folate, B3, B6, and B12. Other substances involved in
this critical problem are an extract of red beets called betaine,
and the minerals molybendum and magnesium.
A major study involving 80,000
nurses over 14 years showed that, for example, for every 200 mcg
of folate consumed on a daily basis, heart disease fell by 11%.
For every 2 mg of B6, heart disease fell by 17%. An increased
blood homocysteine level has been implicated in the cause of
osteoporosis. It has been suggested by the major medical
journal, Metabolism, that folic acid could be a useful
supplement to prevent osteoporosis. Perhaps it is the
effectiveness of folic acid in helping to deal with elevated
homocysteine levels that is the link this journal has observed.
A recent large European
research project demonstrated that low B6 consumption increased
heart disease and stroke by 200%. Stress, excessive exercise,
and overcooked food can decrease B vitamins in your body.
Vitamin B12 is especially vulnerable to overcooking even in a
microwave oven. I would urge readers to
investigate homocysteine further by consulting with a
knowledgeable health care professional. Homocysteine metabolism
is best dealt with by a well-formulated nutritional supplement
designed to combat this problem.
homo-SIS-teen) is an amino acid and is found normally in the
body. Its metabolism is linked to that of several vitamins,
especially folic acid, B6, and B12. Deficiencies of those
vitamins may cause elevated levels of homocysteine.
In recent years, studies have
accumulated suggesting that a high level of homocysteine
increases a person's chance of developing heart disease, stroke,
and peripheral vascular disease (a reduced blood flow to the
hands and feet). In September 1995, the National Heart, Lung,
and Blood Institute (NHLBI) convened a special panel to review
the scientific evidence about homocysteine's possible link to
heart disease. The information that follows is based on the
Briefly, the panel said that an
elevated homocysteine level appears to increase the risk of
heart disease, stroke, and peripheral vascular disease.
However, no studies have been done to show that lowering the
homocysteine level reduces the risk of heart disease. The panel
stressed that more research, especially a clinical trial, must
be done to understand the possible association between the level
of homocysteine and heart and related diseases.
HOMOCYSTEINE AND HEART DISEASE
Various studies have found that
persons with elevated levels of homocysteine in their blood are
at an increased risk of heart and vessel disease. These studies
include the Physicians' Health Study, the Tromso Study from
Norway, the Framingham Heart Study, and a meta-analysis of
nearly 40 studies. Some studies indicate that persons with
elevated homocysteine levels tend to also have other risk
factors for heart disease: high blood
pressure, and high blood cholesterol.
Much more basic research must
be done before scientists understand how an elevated
homocysteine level affects the development and progression of
heart disease. However, scientists have several theories:
First, a high level of homocysteine may be involved with the
process called atherosclerosis, the gradual buildup of fatty
substances in arteries. Homocysteine also may make blood more
likely to clot by increasing the stickiness of blood platelets.
Clots can block blood flow, causing a heart attack or stroke.
Increased homocysteine may affect other substances involved in
clotting too. Finally, higher homocysteine levels may make
blood vessels less flexible--and so less able to widen to
increase blood flow.
WHAT DETERMINES HOMOCYSTEINE
Individuals differ in their
levels of homocysteine. Two key factors affect a person's
homocysteine level--genetics and environment.
Genetics: Genetic factors help regulate the level
of homocysteine in the blood. For instance, genetic flaws
(mutations) can affect homocysteine's metabolism. The NHLBI
Family Heart Study found families with genetic mutations in
the enzymes involved in homocysteine metabolism. The NHLBI
Framingham Heart Study and other investigations have found a
relationship between elevated homocysteine levels and families
with early heart disease.
Environment: The level of homocysteine in the blood
also is affected by the consumption of vitamins, especially
folic acid, B6, and B12. Data from the Framingham Heart Study
show that only 30-40 percent of the population was getting 200
or more micrograms of folic acid in their diet. The data
indicated that for many persons an intake of at least 400
micrograms was needed to keep homocysteine levels from
becoming elevated. Data also indicate that homocysteine levels
are higher in older persons than younger ones, and in women
after menopause than in those before. But more research is
needed to confirm and explain these differences.
WHAT LIES AHEAD?
The September NHLBI panel
called for more research to help answer the many questions about
homocysteine's possible role in the development and progression
of heart disease and stroke. These questions include:
Does homocysteine damage
blood vessel walls?
What regulates the level of
homocysteine in the blood and how?
What happens to heart disease
when homocysteine levels drop?
What are the differences in
homocysteine levels among men and pre-and post-menopausal
women? If significant differences exist, why?
Can keeping homocysteine
levels low prevent heart disease and stroke?
Can reducing homocysteine
levels prevent repeat heart attacks?
What is the best amount and
of which vitamins to prevent heart attack and stroke?
Does the homocysteine level
interact with known modifiable risk factors for heart disease?
HOMOCYSTEINE AND HEART ATTACKS
SuperNutrients Can Protect You,
By Paul Frankel, Ph.D. and Terri
Heart disease is the No. 1
killer in the U.S., killing more people than cancer, infectious
diseases, and homocides combined. Nearly a third of all victims
will not survive their first symptom. Half of all victims won't
reach the hospital alive. For the past few decades, cholesterol
has been the demon of heart disease. Fat consciousness has
become America's favorite dietary preoccupation, with entire
industries growing up around the idea of reducing dietary fat
and cholesterol. While cholesterol is associated with heart
disease in some studies, and Americans do eat too much fat, it
appears that cholesterol may have less to do with heart disease
than most people think. A much stronger case has emerged for a
toxic amino acid called homocysteine. Homocysteine is a
naturally synthesized by-product of methionine metabolism. If
the right cofactors are present, it will eventually convert to
cysteine and other beneficial compounds. If the cofactors are
lacking, it will build up to toxic levels.
Data from a study on healthy
U.S. physicians with no prior history of heart disease shows
that highly elevated homocysteine levels are associated with a
more than three-fold increase in the risk of heart attack over a
five-year period. This finding was published in 1992 in JAMA as
part of the Physicians' Health Study. The study included 14,916
male physicians; it is the same one that showed the benefits of
aspirin. The Framingham Heart Study and other studies have
confirmed that elevated homocysteine is an independent risk
factor for heart disease. It is especially imperative for people
with a family history of cardiovascular disease to control their
homocysteine levels. In one study, 37 men and women with early
familial heart disease had 29% higher levels of homocysteine
than controls. Dr. Rene Malinow of the Oregon Health Sciences
Center concluded that some cases of elevated homocysteine could
be the result of an inherited abnormality. This would be one
explanation for premature coronary artery disease that runs in
families. Mostly, however, elevated homocysteine levels can be
traced to inadequate or improper nutrition.
Different Forms Of Heart Disease
manifests as peripheral artery disease, coronary artery disease,
myocardial infarction (heart attack), stroke, aneurysm,
thromboembolism, extracranial carotid artery and stenosis. As an
artery (or vein) becomes diseased, the inner arterial wall
becomes thick - a condition known as arteriosclerosis. Cells
lining the artery proliferate and combine with protein and
lipids in a mass called an atherosclerotic plaque. Plaques are
commonly the first indication of cardiovascular disease. Plaques
change with time, gathering cholesterol and fat, finally
becoming atheromas. Atheromas distort the artery wall, allowing
calcification. Eventually, the inside of arteries become so
rough that if you run your fingers over them, they feel like
bits of broken glass. When an atheroma blocks blood to the
heart, it is referred to as a heart attack. When it blocks blood
to the brain, it is a stroke. If the penile artery is damaged or
occluded, impotence results. Partial blockage in the chest
(which causes pain) is referred to as angina, and weaknesses or
rupturing of the arteries or veins are referred to as aneurysms.
Homocysteine is thought to
initiate these events by irritating the inner lining of arteries
and veins. In addition, it was recently reported in the journal
Circulation that hyper-homocysteinemia (high homocysteine) impairs
blood vessels' ability to dilate, or expand. Millions of dollars
are spent annually on drugs designed to lower blood pressure by
dilating blood vessels. It is likely that in some people, this
life-threatening problem could be reversed by the supernutrients
that lower homocysteine.
Stroke and Homocysteine
According to a study in the
European Journal of Clinical Investigation, 40% of stroke
victims have elevated homocysteine compared to only 6% of
controls. The study found increased homocysteine in lacunar,
hemorrhagic and embolic strokes. A study published in Lancet in
1996 showed that even after adjustment for other risk factors,
homocysteine was an independent risk factor for stroke and
arterial thrombosis in patients with the autoimmune disease
Another study published in
Lancet came to the same conclusion after studying 107
middle-aged British men who participated in a 2-year
investigation. The authors concluded that "these findings
suggest that homocysteine is a strong and independent risk
factor for stroke." It has even been reported that the level of
homocysteine in blood correlates with the thickness of arteries.
And it was reported in the Journal of Nutrition that men with
levels of homocysteine above 14 mmol/L had a greater than 50%
chance of stenosis in an extracranial carotid artery, whereas
men with levels below 9.1 mmol/L only had a 27% incidence of
stenosis. (The data for women were slightly different. Women
with levels of homocysteine greater than 14.3 mmol/L had a 39%
chance of having carotid artery stenosis: below 9.1 mmol/L,
their chances were about even with men).
Known for Over Two Decades
In 1982, Edward Gruber and
Stephen Raymond of MIT wrote in their book, Beyond Cholesterol:
B6, Arteriosclerosis and Your Heart: "Homocysteine rapidly
induces the initial states of arteriosclerosis and cholesterol's
effects are not apparent." A comparison of the data on
homocysteine with the data on cholesterol illustrates the
strength of the homocysteine theory. There are many problems
with the theory that dietary cholesterol causes heart disease.
For one thing, non-oxidized cholesterol is not atherogenic in
animals. Further, dietary cholesterol doesn't cause vascular
disease in animals except under extreme conditions. Heart and
vascular disease can be observed in the complete absence of
added dietary cholesterol in animals. The cholesterol hypothesis
preaches that a multitude of things increase the risk of heart
attack. The list includes triglycerides, lipoprotein(a),
fibrinogen, smoking, blood pressure, inactivity and poor
genetics. Such a multiple risk factor approach should raise a
red flag. Dr. Lewis Thomas (former president of Memorial
Sloan-Kettering Cancer Center) has stated that every disease
turns out to have one central mechanism of action.
Cholesterol has too many ifs,
ands and buts to be the cause of heart disease.
Levels of cholesterol in blood
do correlate with heart disease. However, cholesterol is no
longer thought to be the cause of heart disease. Also, a recent
study by Dr. Franziska Loehrer and co-workers at University
Hospital in Switzerland showed that cholesterol and
triglycerides failed to demonstrate a statistically significant
correlation with coronary artery disease. Elevated homocysteine,
low S-adenosylmethionine (SAM), age, and body mass index did.
According to Dr. Loehrer: "...high levels of homocysteine occur
before the disease. The finding of similar homocysteine values
in patients after an interval (of approximately) one year
supports the idea that this parameter [homocysteine] plays a
role in the disease process and is not just altered by the
disease itself. Homocysteine is a clearly-established risk
factor for heart disease - a better predictor of heart attacks than
As We See
It: Inflammation and Heart Disease
by William Faloon
A growing consensus amongst
scientists is that common disorders such as atherosclerosis,
colon cancer and Alzheimer's disease are all caused in part by a
chronic inflammatory syndrome. The New England Journal of
Medicine recently published three articles showing that the
presence of blood indicators of inflammation are strong
predictive factors for determining who will develop coronary
artery disease and suffer cardiac-related death. The good news
is many supplements appear to suppress these dangerous
inflammatory components of blood.
One of the inflammatory markers
The NEJ of Medicine identified is a protein
called fibrinogen. High fibrinogen levels can induce a heart
attack via several mechanisms, including increased platelet
aggregation, hyper-coagulation and excessive blood thickening.
The NEJ of Medicine studies showed that those
with high levels of fibrinogen were more than twice as likely to
die of a heart attack. Another inflammatory marker reported on
was C-reactive protein. This marker indicates an increased risk
for destabilized atherosclerotic plaque and abnormal arterial
clotting. When arterial plaque becomes destabilized, it can
burst open and block the flow of blood through a coronary
artery, resulting in an acute heart attack. One of the NEJ of Medicine studies showed that people with high
levels of C-reactive protein were almost three times as likely
to die from a heart attack.
Why are cardiologists so slow
to react? It was back in 1996 that there appeared published
article showing that high levels of fibrinogen represented a
significant risk factor for heart attack and ischemic stroke,
based on studies dating back to the 1980's showing that people
with elevated fibrinogen levels were more likely to die from a
cardiovascular-related disease. Despite numerous studies linking
elevated fibrinogen to increased heart attack risk, few doctors
bother to check their patients blood levels of fibrinogen or
other correctable risk factors such as homocysteine and
C-reactive protein. When physicians are challenged to incorporate these published findings
into their clinical practice, a common response from doctors who
appreciate the importance of these tests is that managed care
(HMOs and PPOs) refuse to pay for them. Other doctors demand a
higher standard of proof before they test their patient's blood
for what they consider to be "newly identified" cardiac risk
The sad fact is that the
majority of practicing physicians are not even aware of these
documented methods of measuring cardiovascular risk factors such
as C-reactive protein, fibrinogen and homocysteine in the blood.
Sad to say, many physicians are educated by their pharmaceutical
sales reps who have no interest in alerting physicians to
nutritionally-related testing. As a result of physician ignorance
combined with pharmaceutical industry influence, many Americans suffer progressive debilitating
congestive heart failure or cerebral circulatory impairment when
the underlying causes could be corrected if the physician
ordered and properly interpreted these blood tests.
Sources of Inflammatory Markers and
New England Journal of Medicine, October 19,
inflammatory risk factors
Cardiovascular risk factors
such as fibrinogen and C-reactive protein are produced in the
liver by pro-inflammatory cytokines called interleukin-1B,
interleukin-6 and tumor necrosis factor alpha. Supplements such as DHEA
can suppress excess production of some of these dangerous
cytokines. One recent study showed that interleukin-6 by itself
increased the risk of heart attack, even after adjustment for
the elevation in C-reactive protein induced by interleukin-6.
Both vitamin K and DHEA suppress interleukin-6, which helps
explain why these supplements have been shown to protect against
such a wide range of age-related diseases.
As far as suppressing the
dangerous tumor necrosis factor alpha and interleukin-1B
cytokines, nettle leaf extract appears to be the most effective
dietary supplement. Nettle leaf extract is found in many popular
formulas. To protect against
fibrinogen-induced heart attack, agents that inhibit platelet
aggregation reduce the risk that fibrinogen will cause an
abnormal arterial blood clot. Popular platelet aggregation inhibitors
include aspirin, green tea, ginkgo, garlic and vitamin E.
For optimal protection against the formation of arterial blood
clots, it makes sense to utilize therapies that directly lower
elevated fibrinogen levels - (read up on Nattokinase).
Diet-wise, high doses of fish or olive oil
have been shown to lower fibrinogen in humans with elevated
fibrinogen levels.(30-31) Excessive homocysteine blocks the
natural breakdown of fibrinogen by inhibiting the production of
tissue plasminogen activator (tPA).(32) Folic acid , TMG,
vitamin B12 and vitamin B6 reduce elevated homocysteine levels.
Vitamin C, in pharmacological doses, has been shown to break
down excess fibrinogen. In one study, heart disease patients
were given either 1000 mg or 2000 mg a day of vitamin C to
measure the fibrinogen breakdown effect. At 1000 mg a day, there
was no detectable change in fibrinolytic activity or
cholesterol. At 2000 mg a day of vitamin C, there was a 27%
decrease in the platelet aggregation index, a 12% reduction in
total cholesterol and a 45% increase in fibrinolysis (fibrinogen
An additional marker of heart
attack risk Troponin T is a blood marker of heart muscle damage.
A recent study showed this marker is the most powerful long-term
predictor of cardiac death in those suffering from underlying
heart disease. Compared to patients with the
lowest levels of troponin T, those with the highest troponin T
blood levels were almost 13 times more likely to die over a
37-month period. Why is troponin T such a powerful predictor?
It turns out that even those with a minor elevation of troponin
T have a larger number of tiny coronary artery blood clots,
complex atherosclerotic coronary artery lesions and impaired
coronary artery blood flow. Those with elevated troponin T
levels, therefore, are the heart attack patients most likely to
benefit from antiplatelet and antithrombotic therapies. The type
of "troponin" blood test preferred by most clinical laboratories
is called Troponin I." (Repeat: check out Nattokinase)
Taking charge of your own
It has become increasingly
apparent that people will have to take a more active role in
protecting their health. That means those who are concerned
about optimal health are going to have to stand up to their
doctors and demand that certain blood and other diagnostic tests
be performed, whether their physician agrees with them or not!
It is high time that humans stop sacrificing their lives because
of the inability of doctors and insurance companies to recognize
diagnostic approaches that are substantiated in respected
Managed care, physician apathy
and FDA over-regulation is a lethal combination that is causing
over one million Americans to needlessly die every single year.
In the meantime, those with chronic degenerative disease should
take a pro-active role in their health care. If your physician
does not appear to care about keeping you in an optimal state of
health, find another doctor! Don't become a victim of the
current broken-down healthcare system that fails to incorporate
scientific findings into the clinical practice of medicine.
Don't let complacent doctors
put you at risk for heart disease and stroke. The following
chart shows the most common blood tests that can help reveal
underlying cardiovascular disease risk factors. As can be seen
on the chart below, blood test results that conventional doctors
accept as being "normal" can be lethal to you. In other words,
what the "Standard Reference Range" allows is not always a
practical indicator for where your "optimal" level should be.
In many cases, a "Standard
Reference Range" reflects what is expected to be seen in the
average population. Since cardiovascular disease remains the
number one killer of Americans, you don't ever want to be part
of the "average" range when it comes to cardiovascular disease
risk factors. By keeping your blood levels in the "Optimal
Range," rather than the average "Standard Reference Range," you
take advantage of the increasing volume of evidence showing that
most heart attacks and strokes are preventable.
As you can see, the "Standard
Reference Range" often dangerously differs from what the
published research indicates is protective against
"Standard Reference Range"
Up to 460
(Some studies indicate
C-reactive protein levels should be below 1.3 mg/L)
Up to 4.9
Under 2 mg/L
Up to 15
Up to 109
Up to 180
Up to 199
Up to 129
than 35 mg/dL
Over 50 mg/dL
Up to 199
than 80 mcg/dL
than 35 mcg/dL
There are numerous published
studies indicating that cholesterol levels should ideally be
under 200. Many researchers believe it is more
important to concentrate on suppressing dangerous LDL
cholesterol and increasing beneficial HDL levels. If other risk
factors such as homocysteine, fibrinogen, C-reactive protein,
etc. are individually adjusted to reflect "optimal" ranges, then
a slightly higher total cholesterol of up to 220 might be
Please note that cholesterol
levels below 180 present increased risk of hemorrhagic stroke
and other diseases, so it is important that people maintain a
minimal amount of cholesterol, i.e. 180 milligrams per deciliter
of blood. It is important to note that in the past, cholesterol
levels well above 200 were considered within the "normal"
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