Saturday, March 9, 2013

Why Your Homocysteine Level Matters To Your Health

Reposted from Life Extension

http://blog.lef.org/2011/11/homocysteine-level-heart-health.html

By Michael A. Smith, MD
Homocysteine is an amino acid that can inflict damage to your inner arterial lining (endothelium) and other cells of your body. In 1968, a Harvard researcher observed that children with a genetic defect that caused them to have sharply elevated homocysteine levels suffered severe atherosclerotic occlusion and vascular disorders similar to what is seen in middle-aged patients with arterial disease.

This was the first indication that excess homocysteine could be an independent risk factor for heart disease. Despite traditional doctors failing to recognize it, Life Extension has identified elevated homocysteine as one of 17 independent risk factors for cardiovascular disease.

How is Homocysteine Produced?

All homocysteine in the body is biosynthesized from methionine, an essential amino acid found abundantly in meats, seafood, dairy products, and eggs. Vegetables, with few exceptions (e.g., sesame seeds and Brazil nuts), are pretty low in methionine; even protein-rich legumes like beans, peas, and lentils contain relatively small amounts of methionine compared to animal-derived foods.

An important reaction occurs in the body when the amino acid methionine is converted by a series of chemical reactions into homocysteine. Once it’s formed, homocysteine can do two things:



  1. Convert back to methionine via vitamin B12 and folic acid — part of a process called the methylation cycle.
  2. Convert into cysteine with the help of vitamin B6 — called transsulfuration process.
This cycle between methionine, homocysteine and cysteine is known as the methylation cycle and is important to your body for the following reasons:

  1. It produces glutathione, a very important cellular antioxidant.1
  2. It helps to bind minerals like copper and zinc in order to be utilized by the body.2
  3. The methylation cycle plays a role in reactions that aid in DNA and RNA metabolism.
  4. The methylation cycle is critical for the proper synthesis of neurotransmitters that play an important role in mood regulation.
If your vitamin B12, B6 or folic acid are deficient, your homocysteine levels can increase. Now, as far as normal physiology goes, homocysteine is not biologically active. However, if you look at it from a pathological point of view — homocysteine is really active … in a bad way.

How Does Homocysteine Damage the Arteries?

If unhealthy levels of homocysteine accumulate in your blood, the delicate lining of your arteries (endothelium) can be damaged. Damage to the endothelial lining is the first step in arterial plaque development and can lead to an increased risk of heart attack and stroke.3

Several studies have shown that homocysteine can inflict damage to the arterial wall via multiple destructive molecular mechanisms. One hypothesis is that homocysteine elicits a powerful immune response within the wall of the artery, causing damage to the endothelium.

There’s another theory I came across while working at the University of Texas. The researchers hypothesized that homocysteine can damage adhesion molecules — molecules in between endothelial cells. When these adhesion points are destroyed, the endothelium can separate and lead to arterial plaque development.

Homocysteine: How High is too High?

Clinical testing laboratories consider a homocysteine blood level between 5 to 15 µmol/L as healthy. However, we believe that their upper limit of 15 is still too high for optimal health.

Studies indicate that adults with homocysteine values ≥ 8 µmol/L are at increased risk of atherosclerosis, heart attack and stroke, according to the Homocysteine Studies Collaboration. 4
As a result, we recommend doing everything you can to keep your homocysteine level less than 7-8 µmol/L.

How Can You Lower Homocysteine?

Here’s a brief rundown on the nutrients that have been shown to help people maintain healthy homocysteine blood levels. For details of each nutrient, check out our protocol on high homocysteine levels.

  1. Vitamin B6 – specifically pyridoxal-5-phosphate
  2. B12 – specifically methylcobalamin
  3. Folic acid (see note below)
  4. SAMe (S-adenosylmethionine)
  5. NAC (N-acetyl-cysteine)
  6. Omega-3 fats
  7. Taurine
  8. TMG (trimethylglycine)
Folic acid note: Many people carry a genetic variation that is linked with elevated homocysteine. People carrying this gene variant suffer from an impaired ability to metabolize folic acid to its active form. If you take folic acid and your homocysteine remains high, you might consider taking an active folate called 5-MTHF.

What Else Increases Homocysteine in your Blood?

Elevated blood levels of homocysteine have been linked with a wide range of health problems including heart disease, stroke and brain disorders. There are numerous factors that can increase homocysteine in your blood. They include:

  1. Vitamin B6, B12 and folic acid deficiencies.
  2. A high protein diet, especially a diet that includes red meat and dairy products, as these are high in methionine.
  3. Prescription drugs.
  4. Smoking.
  5. Advancing age.
In summary, knowing your homocysteine blood level is really important — get your own levels tested sooner than later. Again, we believe that an optimal level is less than 7 - 8.

Lastly, your doctor might tell you that it’s “normal” for homocysteine to increase with age, which is true. However, a high level, regardless of age, places you at risk for heart disease. For this reason, we strongly recommend working to get yours within the target level no matter how old you are.



Have you had your homocysteine level checked lately? You can request a homocysteine test from your doctor, call Life Extension at 1-800-208-3444 or order a homocysteine test from us online here.

References

  1. Anal Biochem. 2003 Jul 15;318(2):175-80.
  2. Lippard, Stephen J.; Berg, Jeremy M. (1994), Principles of Bioinorganic Chemistry, Mill Valley, CA: University Science Books,ISBN 0-935702-73-3.
  3. Annu Rev Med. 1998;49:31-62.
  4. Stroke. 2001 Mar;32(3):714-8.