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"An avalanche of new studies suggest than an amino acid called homocysteine
plays a critical role in destroying our arteries."
Newsweek, August 11, 1997
"Homocysteine appears to respond to nothing more
demanding than...taking a few vitamins."
Time, August 4, 1997
Homocysteine? I never heard of it - it's new to most doctors as well - until the Cooper Clinic's Dr. Arno Jensen told me mine is normal, but higher than he'd like to see it.
Homocysteine (pronounced Ho-mo-SIS-teen) is an amino acid that attacks the lining of our arteries, setting off a chain of events that often leads to heart attack or stroke. The startling fact is that people with none of the commonly known risk factors (sedentary lifestyle, smoking, obesity, high blood pressure, high cholesterol) often have high levels of homocysteine in their blood. What's more, about a fourth of all heart attacks occur in people with normal cholesterol and none of the other health hazards. That's why homocysteine has been called the "silent killer."
As long ago as the late '60s, Dr. Kilmer McCully began to suspect a link between homocysteine and arterial disease; but until recently most doctors were too focused on cholesterol to pay much attention. McCully discovered the connection while studying a rare genetic disorder called homocystinuria. Children born with this condition lack proper levels of an enzyme required to process homocysteine, so it reaches extremely high levels in their blood. If untreated, they often die of heart attack or stroke before reaching adulthood.
McCully observed during autopsy that the victim's arteries were scarred and thickened like those of elderly heart patients. If high levels of homocysteine can destroy young arteries, he reasoned, then lower levels over a long period of time might cause vascular disease in adults. As I'll explain shortly, subsequent research strongly suggests that McCully's hunch was correct.
Like cholesterol, homocysteine performs a desirable function. It is derived from the essential amino acid methionine and is used to build and maintain tissue. During normal conditions excess homocysteine - with the help of some B-complex vitamins - is converted back to methionine or broken down for excretion. The problem arises when the conversion process fails. Understanding what happens helps clarify the harmful role of cholesterol. Dr. McCully believes homocysteine buildup is "the underlying cause of heart disease."
Initial Injury Starts Long Process
Arterial disease usually develops over a long period of time: the process, if not the root cause, is well known. It begins when something injures the lining of the artery and the body tries to repair the damage. In simplified terms, scar tissue builds up, like it would on other parts of the body, inhibiting blood flow and promoting the formation of clots.
Many people probably assume that cholesterol in the blood somehow causes the initial injury to the arterial wall. Dr. McCully says that's not so, that the first injury is caused by excessive homocysteine. The injury makes the blood vessels vulnerable to cholesterol buildup; the scarring and thickening on the arterial wall gives the cholesterol a place to stick and grow.
Significantly, smoking tends to raise homocysteine levels. Homocysteine levels also increase in old age. And when arterial disease runs in families there is often a minor genetically based flaw in homocysteine metabolism; roughly one person in eight inherits a gene that slows disposal of excess homocysteine. (That may be my problem. My father had arterial disease. I don't know about his homocysteine, but he battled high cholesterol for years. He died from a stroke.)
Dr. McCully's hypothesis is still based on circumstantial evidence. But vindicating his long-held belief, Newsweek reported in its August 11, 1997 cover story: "An avalanche of new studies suggest that ... homocysteine plays a critical role in destroying our arteries."
Evidence Is Strong
As is usually the case, the evidence starts outside the human body. In test-tube studies, homocysteine not only injures blood-vessel linings but accelerates the buildup of scar tissue and promotes the formation of blood clots. Moreover, researchers have long known that homocysteine injections produce arterial plaques in animals.
People studies also provide convincing evidence. Harvard researchers followed 14,000 male physicians for five years and found those with homocysteine levels in the highest 5% had three times the heart attack risk of those in the bottom 90%. Likewise, researchers involved in the famous Framingham Heart Study found that people with high homocysteine levels are the most likely to suffer from dangerous narrowing of the carotid artery, the main vessel feeding blood to the brain. And Norwegian scientists, in a study involving 21,000 men and women, showed that heart patients with elevated homocysteine are the most likely to die.
So how can homocysteine be controlled? Surprisingly, and unlike cholesterol, the solution appears to be simple and inexpensive. Time magazine, in the August 4, 1997, issue, reported: "Homocysteine appears to respond to nothing more demanding than eating more vegetables and taking a few vitamins."
Recall that B-complex vitamins help breakdown homocysteine. It stands to reason, therefore, that a lack of key B vitamins would "freeze" homocysteine metabolism, allowing the substance to accumulate in the bloodstream and damage blood vessels. It also seems logical that supplying more B vitamins would help the body to reduce homocysteine to safe levels. That seems to be how it works. Simply consuming more vitamin B6, B12 and folic acid could be all that's required to disarm homocysteine.
Two large new studies directly correlate folic acid and B6 with vascular disease. The first study, reported in the February 4, 1998 Journal of the American Medical Association, was part of the ongoing Nurses' Health Study. Researchers followed more than 80,000 women without heart disease for 14 years. Those least likely to have a heart attack consumed more than 400 micrograms (mcg, or one thousandth of a milligram) of folic acid a day from food or supplements. Likewise, those who consumed more than 4 milligrams (mg) of Vitamin B6 a day had the lowest heart disease rates.
The February 10, 1998 issue of Circulation published the second study. Researchers measured levels of folate and vitamin B6 in the blood of 800 healthy volunteers and 750 people with vascular disease. They also measured homocysteine. Patients with vascular disease had high homocysteine levels compared with the healthy volunteers. In men - but not women - with vascular disease, high homocysteine went hand-in-hand with low folate levels. People with vascular disease also had low B6 levels, even though many did not have high homocysteine.
That's pretty strong evidence. Even though we are still waiting for a controlled study, where some people are given vitamins and others a dummy pill, showing that supplements reduce the incidents of heart attack and stroke, many physicians now recommend that everyone get at least 400 mcg of folate a day. That amount was found to be most protective against heart disease in the latest results from the Nurses' Health Study. (Those with a flawed homocysteine metabolism may require more than 400 mcg. I'll discuss Dr. Jensen's advice to me in a moment)
Why the emphasis on folic acid? Unless you're a strict vegetarian, chances are you're getting plenty of B12. Vitamin B6 is also easy to come by, since it's added to many processed foods. But folic acid is another story. Folate is found mostly in beans, grains and greens, which are hardly abundant in the normal American diet. Nearly half of Americans get less than 200 mcg., the current FDA for men, and only a small minority get 400 mcg.
Blood drawn in the course of my latest exam at the Cooper Clinic showed my homocysteine to be 11.2 umol/L, at the upper end of the 8-12 normal range. (Between 12 and 15 is borderline, and over 15 is considered high risk.)
My result sounds OK. Dr. Jensen says it's not a reason for major concern. Still, there's a hooker: The risk for vascular disease increases progressively with homocysteine concentrations above 9. Ideally, Dr. Jensen says he'd like to see mine below 9. (That may be especially important in view of my family history of vascular disease.)
My diet is already excellent. Unlike most Americans, I eat plenty of grains and greens, and some beans. Computer analysis (excluding supplements) shows that my intake of all the B vitamins is well above recommended levels. For example, my folic acid intake is 912 mcg., more than 4 times the RDA. In addition, I take a multi vitamin/mineral packet containing all the B complex vitamins. I am already meeting the Cooper Clinic recommendations for heavy exercisers over 50 (men and women): folic acid 800 mcg., B6 50 mg. and B12 400 mcg. What should I do?
As indicated earlier, it's possible that I am among the one in eight people who have inherited a flawed gene that slows the disposal of homocysteine. To test that possibility doctors often recommend a daily multivitamin containing 400 mcg of folic acid plus an additional 800 mcg. If that doesn't bring the homocysteine level down in 8 weeks, the dosage may be increase to 2 mg./day for another 8 weeks. Folic acid supplements are considered safe up to 5 mg/day.
I have upped my intake of folic acid, B6 and B12, and I'll have my homocysteine checked again in the next few weeks. Hopefully, it will be under 9, as Dr. Jensen recommends. If not, I'll consider increasing the dosage again.
Kudos to the Cooper Clinic
Needless to say, I'm grateful that Dr. Jensen and the Cooper Clinic alerted me to this newly prominent risk factor, the big one that may be the underlying cause of vascular disease. Thanks Arnie.
What's your homocysteine level?
I had another blood test on May 6, eight weeks after the test referred to above. My homocysteine came down to 10 from 11.2. That's an improvement of almost 11%, but still above the ideal of 9, which Dr. Jensen would prefer it to be.
After consulting with Dr. Jensen, I've decided to increase my folic acid intake by 50%, to a little over 3 mg./day. I'll have my blood tested again in about two months.
Good news! My blood test on July 22 showed that my homocysteine dropped to 7.9, which is at the bottom of the 8.0-12.0 normal range, and well below the 9.0 level Dr. Jensen wanted to see. As indicated in the last update, I upped my folic acid intake to a little over 3 mg./day. Apparently that did the trick. I'll keep my folic acid intake at the present level and have my blood tested again in a few months.
It's certainly gratifying to see that we can help ourselves in matters of this kind. As Dr. Jensen often says, our health is largely in our own hands.
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