Vitamin B12 Helps Prevent Heart Attacks

Major new risk factor for heart disease discovered
VANCOUVER, CANADA It is becoming increasingly evident
that an elevated blood level of homocysteine is a potent risk
factor for cardiovascular disease. Recent studies also suggest
that high homocysteine levels may be associated with kidney
disease, psoriasis, breast cancer, and acute lymphoblastic
leukemia. Extensive past research had shown a close link
between development of neural-tube defects in babies and the
mother's homocysteine level prior to and during pregnancy.
Researchers at the University of British Columbia have just
released a major report which summarizes the current
knowledge about homcysteine and its effect on health.
Homocysteine is formed in human tissues during the
metabolism of methionine, a sulfur-containing essential amino
acid. A normal, desirable level is 10 micromol/L or less. A level
of 12 micromol/L is considered borderline and levels of 15
micromonl/L or above are considered indicative of increased
risk for cardiovascular disease. Several factors (age, smoking,
vitamin deficiencies, and genetic abnormalities) have been
linked to increased homocysteine levels. Medications that
interact with folate such as methotrexate, carbamazepine,
phenytoin, and colestipol/niacin combinations have also been
linked to increased homocysteine levels. The researchers
reviewed 23 studies dealing with the association between
atherosclerosis and homocysteine levels and found that patients
with vascular diseases had an average level of homocysteine
that was 26 per cent higher than the level in healthy subjects.
One study found that a homocysteine level of 4 micromonl/L
above normal corresponds to a 41 per cent increase in the risk
of developing vascular disease. Another study estimates that the
lives of 56,000 Americans could be saved every year if average
homocysteine levels were lowered by 5 micromonl/L. The
researchers conclude that abnormally high homocysteine levels
are a potent risk factor for cardiovascular and several other
diseases. They point out that elevated homocysteine levels can,
in most cases, be safely and effectively lowered by
supplementation with as little as 400 micrograms per day of
folic acid. Other researchers have found that a combination of
folic acid (0.4-10 mg/day), vitamin B12 (50-1000
micrograms/day) is highly effective in lowering homocysteine
levels. (153) references. Medical doctors at the University of
Wisconsin echo the findings of the Canadian researchers in a
separate report and describe a case of a 57-year-old man who
lowered his homocysteine level from 29 micromol/L to 2
micromol/L by supplementing with 800 micrograms/day of folic
acid for two months.

Moghadasian, Mohammed H., et al. Homocysteine and
coronary artery disease. Archives of Internal Medicine. Vol.
157, November 10, 1997, pp 2299-2308
Fallest-Strohl, Patricia C., et al. Homocysteine: A new risk
factor for atherosclerosis. American Family Physician, Vol.
56, October 15, 1997, pp. 1607-12.

After being told on a forum in which I participate that B12
is dangerous and should not be taken except under careful
doctor supervision, because in Norway doctors consider it a
threat, I looked into the NORVIT study, which was the
basis of the snippet I heard.

This is the conclusion drawn from the NORVIT study,
"Lowering plasma homocysteine levels by as much as 28%
does not result in any reduction in the risk of myocardial
infarction (MI) or stroke in patients who have already had
an MI, according to the results of the Norwegian Vitamin
Trial (NORVIT). [1] The study also suggests that
administration of combination B vitamins with the aim of
reducing plasma homocysteine may actually increase the
risk of cardiovascular disease and that folic acid alone may
increase the risk of cancer."

That sounds really worrying, right?

Well, let's take a closer look at what the study, which can
be seen at www.medscape.com/viewarticle/512905 , says,
for instance, it says, "Study and Rationale"

"NORVIT was designed as a randomized, controlled,
double-blind, multicenter, secondary prevention trial, testing
the hypotheses that long-term (3.5-year) treatment with a
folate/vitamin B12 combination or vitamin B6 would lower
the incidence of MI and stroke by 20% each. A substudy
was also set up to test the hypothesis that vitamin B therapy
protects against loss of cognitive function."

That sounds good, but when it comes to listing the vitamins
actually administered, it says under, "Treatment"
Patients were randomized into 4 groups in a 2 × 2 factorial
design:

Folic acid + vitamin B6
Folic acid alone
Vitamin B6 alone
Placebo"

Do you see B12 in the list? I don't.

It goes on, in the less noticeable print, to include B12,
"Doses of drugs were folic acid 0.8 mg/day (+ vitamin B12
at a dosage of 0.4 mg/day) and vitamin B6 at a dosage of 40
mg/day; 90% of participants reported adherence to the
study medication protocol."

Okay, so the flaw that jumps out at me is that B12 was
included at the rate of 400 mcg. That's a pretty tiny amount.
Anyone having the most basic B12 replacement therapy has
1000 mcg a day.

At the same time, the amount of B6 that was administered
was relatively huge, 40 mg. (That's a hundred times more.)

Significantly, none of the tables provided even mentions
B12.

I found this at TheHeart.org, "As Bønaa reported here
today, the combination of vitamin B6 and folic acid, as well
as folic acid alone, effectively lowered homocysteine levels
by 28% but did not have the expected beneficial effect on
cardiovascular risk. At follow-up, the risk of stroke and MI
was 18% in the placebo group, roughly the same as that
seen in both the folic-acid-only group and the
vitamin-B6-only group. By contrast, in the combination
group, 23% of patients had a fatal or nonfatal stroke or MI,
a statistically significant absolute increase of 5%, compared
with the other treatment arms (p=0.029)."

Interestingly enough, the group receiving the most B12 had
the most reduction in homocysteine.

(9/19/06 was about when I added the above.)

Personally, I think the man
looks way too smug given that
his work is being broadcast as a
failure of "B vitamins" when in
fact the study included B6 and
folic acid, with a miniscule
amount of B12, so little B12
that it is not even shown on the
tables.

The American researcher, Ralph
Carmel, did an equally huge
disservice to people when he
published his opinion that raising
the level at which B12 was said
to be deficient would be useless.

I am sure, SURE, that if the
level at which B12 deficiency
was identified was higher, that I
would not have the nerve
damage I do.

To wait until the level is so low
that the person is suffering
multiple symptoms is egregious.

Especially when failure to
promptly treat can mean that the
symptoms become permanent
nerve damage.

Please read the published article
about the B12 level at which
cognitive dysfunction can begin
to be detected. Article.

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