Friday, July 21, 2006

More: Why & how to avoid high homocysteine....

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In it we post health commentary & reviews of books, eBooks, & other things that improve or protect your health or which enable you to live longer, to be more prosperous, & to be more effective.

Today's post: Friday, 7-21-2006

More: Why & how to avoid high homocysteine levels:

Dr Allen Josephs is one of the best-informed of the current eNewsletter writers on supplements & nutrition.

In addition to high blood levels of homocysteine speeding aging & triggering or causing cardiovascular disease, he includes here that high blood levels of homocysteine also play a role in causing:
1. pregnancy problems;
2. “neurodegenerative disorders” – including Alzheimer’s disease;
3. depression;
4. & and “even vision problems.”

Sounds like something you’d like to stay well away from right?

In addition to recommending you get your levels tested once a year, he also includes what he recommends to his patients who find they have high or above optimum homocysteine levels.

Here’s his article from his www.vitacost.com newsletter.

(I deleted his paragraph about the history of our discovering that high homocysteine levels were damaging. And, I added some extra paragraphing to make some key points easier to read. But the words are otherwise exactly as they appeared in his article.)

How's Your Homocysteine? Get Levels Checked to Protect Heart Health

By Allen S. Josephs, M.D.
President, Vitacost.com

May 25, 2006 - Homocysteine is an amino acid naturally produced by the body as a byproduct of the digestion process. Elevated blood levels of homocysteine are believed to be linked to complications in cardiovascular, and other areas, of health. Proper nutrition, with vitamins B6, B12 and folic acid, are important for maintaining healthy homocysteine levels (and improving cellular metabolism). You should also be sure to have your levels checked by a health care provider every year.

This week's newsletter concerns the amino acid, homocysteine.

There has been a large body of medical literature in the last 15 years documenting that moderately elevated homocysteine levels appear to be an independent risk factor for not only occlusive arterial disease, but also venous thrombosis as well.

Elevations of homocysteine have also been associated with adverse pregnancy outcomes including spontaneous early abortion and birth defects.

Additionally, elevations in blood homocysteine appear to be an independent risk factor for neurodegenerative disorders, actually functioning as a neurotoxin.

It should be noted that the formation of homocysteine is part of normal cellular metabolism of the amino acid, methionine.

Homocysteine is then further metabolized, either by attaching additional methyl groups or by a process known as trans-sulphuration. The remethylation of homocysteine is directly dependent on vitamin B12 as a co-factor and folic acid as a substrate. The trans-sulphuration pathway leading to cysteine involves two reactions that both require vitamin B6 as a co-factor.

The reason homocysteine levels increase is related to several factors. It appears that as we age, homocysteine levels increase.

Other factors that can lead to elevation in homocysteine levels include: lower nutritional intake, reduced kidney function, smoking and high alcohol intake. There are certain individuals who have a predisposition toward elevations in homocysteine level.

In an article published in the May-June 2006 edition of the American Journal of Geriatric Cardiology, 172 elderly individuals underwent coronary angiography to investigate the influence of age and coronary artery disease on homocysteine levels1. The subjects were divided into three groups, those between 65 and 74 years old, 75 to 79 years old and 80 years and older. It was found that for each mmol per liter increase in homocysteine level there was a 7% increase in risk of coronary artery disease. Hyper-homocysteinemia (with levels over 14) were said to constitute an independent risk factor for coronary artery disease with a risk ratio of over 100%. There was a relative progression of homocysteine levels between the young old and the oldest old.

In the June 2006 edition of the Journal of Nutrition, Dr. Selhub, from the Vitamin Metabolism Aging Laboratory of Tufts University, discussed the many facets of hyper-homocysteinemia looking at studies from the Framingham data2. It is indicated that data from several studies suggest mild elevations of homocysteine in plasma were risk factors for occlusive vascular disease and that total plasma homocysteine concentrations were inversely related to the intake of plasma levels of folate and vitamin B6 as well as vitamin B12 plasma levels.

Almost two-thirds of the prevalence of high homocysteine was attributable to low vitamin status or intake.

In another article published in FEBS Letters from May 2006, it was noted that numerous studies in recent years investigated the role of homocysteine as a cause of brain damage3. It appears that homocysteine or folic or vitamin B12 deficiency can cause disturbed methylation and/or redox potentials, thus promoting calcium influx, amyloid and other abnormal protein accumulation leading to neuronal death.

In another study published in the journal Coronary Artery Disease June 2006, 88 patients with typical/atypical symptoms of angina underwent coronary angiography4. Half of these patients had angiographically proven coronary slow flow and 44 individuals had normal coronary flow patterns. It was found that plasma homocysteine levels and thickness of the carotid arteries in patients with coronary slow flow were found to be significantly higher to that of controls. Authors of this study suggested that the findings suggested possible disturbance in metabolism of homocysteine in patients with coronary slow flow may have a role in the pathogenesis of this phenomenon by causing generalized atherosclerosis.

Other studies have linked elevated homocysteine to depression and even vision problems.

There have been some recent studies in the medical literature questioning whether homocysteine is a true independent marker and risk factor for cardiovascular disease or something that develops after-the-fact. The debate is ongoing. There does seem to be more evidence suggesting that elevations in homocysteine do act as an independent neurotoxin to the brain.

Proper nutrition, with vitamins B6, B12 and folic acid at much higher than RDA/DV levels, will help promote healthy homocysteine levels and improve cellular metabolism. Other nutrients that have shown benefit for producing healthy homocysteine levels include trimethyl glycine (TMG) and N-acetyl cysteine (NAC).

I strongly recommend you have your doctor test your homocysteine levels on an annual basis. The ideal level is under 7 mmol/L.

I recommend folic acid at 800 mcg to 10 mg per day, B6 at 50 to 100 mg per day and B12 in the active methylcobalamin form at 500 mcg to 5 mg per day range. Contrary to popular belief, using this form and dosage of B12 in capsules will provide blood levels similar to a B12 injection without the need for a sublingual.

If this combo is not sufficient to reach your desired homocysteine level, I recommend adding 600 mg of NAC and 2,000 to 3,000 mg of TMG per day.



(Dr Josephs doesn’t mention that taking B6 of over 100 mg a day as a total from all sources produces nerve problems in some people. My suggestion is to limit B6 to 50 mg a day from all sources.

And, at www.wholhealthmd.com in their library section I found some info that suggests it may be a good idea to use higher doses of NAC only as a temporary measure.)

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