Written by Greg Arnold, DC, CSCS.

Cardiovascular diseases, including heart disease and stroke, which are the first and third leading causes of death for both men and women in the United States, account for 1 in 3 of all U.S. deaths.  Heart disease and stroke are expected to cost our healthcare system $473 billion in 2009. If all major types of cardiovascular disease were eliminated, U.S. life expectancy would increase by nearly 7 years (1).

The early stage of cardiovascular disease is marked by the damage of cholesterol by free radicals which are taken up by white blood cells called macrophages. These accumulate in the walls of blood vessel and form the “foam cells” that are the beginnings of atherosclerosis and cardiovascular disease (2).  A new study (3) has suggested that maintaining proper blood levels of iron may also help even when no inflammation is present.

In the study, 124 patients with at least 2 heart disease plaques were compared to 124 patients with less than 2 heart disease plaques and participating in the MONICA survey in Southwest France (4).  Specifically, they provided blood samples to measure for Inflammation including a protein called alpha-1 acid glycoprotein (5) and high sensitivity C-reactive protein (6).  They also measured blood levels of iron (called “serum ferritin”) to see if they was any relationship between inflammation and iron.

In adults with normal alpha-1 acid glycoprotein (less than 1 gram/Liter), iron blood levels were significantly greater (28% higher) in atherosclerotic cases than in adults in the control group (204.4 vs 146.9 micrograms/Liter).  They also found that for every 10-microgram/L increase in serum ferritin, the risk for atherosclerosis increased by 3% in those with normal alpha-1 acid glycoprotein.  No significant associations were seen between high-sensitivity c-reactive protein and iron and plaques.

The researchers suggest the association between iron and blood vessel plaques is due to iron’s ability to generate highly active free radicals, damage fats, and increase clotting lipoproteins, and activate clotting (7,8,9).  Reason has also shown that ferritin, the iron storage protein, has been found in blood vessel plaques in humans and in diseased coronary arteries from patients with coronary artery disease (10).

For the researchers, “carotid atherosclerosis was positively associated with serum ferritin in individuals free from subclinical inflammation based on AGP” and that “Further…studies are needed to corroborate the observed association of iron status with atherosclerosis.”

Source: Ahluwalia, Namanjeet, et al. “Iron status is associated with carotid atherosclerotic plaques in middle-aged adults.” The Journal of nutrition 140.4 (2010): 812-816.

© 2010 American Society for Nutrition

Posted May 4, 2010.

References:

  1. “Cardiovascular Disease at a Glance” posted on the Centers for Disease Control website.
  2. Oh J.  1,25 (OH) vitamin D inhibits foam cell formation and suppresses
    macrophage cholesterol uptake in patients with type 2 diabetes mellitus.  Circulation 2009; 120(8):687-698.
  3. Ahluwalia N.  Iron Status Is Associated with Carotid Atherosclerotic Plaques in Middle-Aged Adults.  J. Nutr. 2010 140: 812-816. First published online April 1, 2010; doi:10.3945/jn.109.110353
  4. http://www.ktl.fi/monica/public/objectives.html
  5. http://www.ncbi.nlm.nih.gov/pubmed/11058758
  6. http//www.labtestsonline.org
  7. Lamb DJ, Leake DS. Iron released from transferrin at acidic pH can catalyse the oxidation of low density lipoprotein. FEBS Lett. 1994;352:15–8.
  8. Pratico D. Iron-dependent human platelet activation and hydroxyl radical formation: involvement of protein kinase C. Circulation. 1999;99:3118–24.
  9. Yuan XM, Brunk UT, Olsson AG. Effects of iron- and hemoglobin-loaded human monocyte-derived macrophages on oxidation and uptake of LDL. Arterioscler Thromb Vasc Biol. 1995;15:1345–51
  10. You SA, Wang Q. Ferritin in atherosclerosis. Clin Chim Acta. 2005;357:1–16