Thursday, March 7, 2013

Can Too Much Iron Cause Brain Deterioration?

Reposted from Life Extension

http://blog.lef.org/2012/03/excess-iron-causes-brain-deterioration.html

By Michael A. Smith, MD

Daily iron intake is important, but getting too much may be a big reason behind brain disorders like Alzheimer’s and Parkinson’s disease. This is because iron creates oxidative stress, meaning it can create a damaging micro-environment in and around your brain cells.

So the basic consensus among doctors is that the interplay between dietary iron intake and total health is more complex than most people grasp. And here’s why: Iron is not readily eliminated from the body but instead becomes “locked” or stored in an unbound state inside our cells in compartments called lysosomes.

Intracellular Iron Creates Reactive Compounds

Our bodies use iron because it’s a powerful catalyst for hundreds of chemical reactions that are necessary for life. But it’s the catalytic activity that makes excess stored iron dangerous. This stored iron inside lysosomes is unbound and free to unselectively react with water and oxygen to produce highly reactive oxygen species or free radicals.1The free radical produced from unbound iron can damage cells and tissues, especially in the brain. The result is neurodegenerative diseases like Alzheimer’s and Parkinson’s.

Iron Collects in the Brains of Alzheimer’s Patients

The department of Neuroscience and Human Behavior at UCLA has a better understanding of the role that iron plays in human brain development, function, and aging, with a particular emphasis on the link between iron and neurodegenerative disorders, like Alzheimer’s disease.

The researchers at UCLA showed that they could accurately measure iron levels in living humans’ brains by using a highly specialized MRI technique.2 Applying this technique to groups of people with and without Alzheimer’s disease, the researchers quickly discovered significantly larger amounts of stored iron in certain brain regions in those with Alzheimer’s than in control subjects.3,4What does this mean? Damaged brain cells. Now, are we saying that iron is the cause of Alzheimer’s? No. But we are saying that excess iron in the brain is probably playing a role in neurodegenerative diseases.

Natural Ways to Control Excess Iron

Here are some natural suggestions to help your body sequester and eliminate excess iron:

  • Quercetin — has strong iron-chelating capacity (chelation is the removal of iron from the body).5
  • Pomegranate — can reduce iron’s damaging oxidative reactions.6
  • Cranberry — like quercetin, cranberry antioxidants have iron-chelating properties.5
  • Curcumin — powerful iron chelator for the brain, heart, and liver.7
  • Green Tea — the powerful antioxidant EGCG protects from iron’s damaging reactions.8
  • Lipoic Acid — can chelate iron within the lysosome before any damage can occur.9
The accumulation of iron in cells is a widely overlooked and inevitable consequence of aging. Pathologic age-related iron overload damages cells and tissues and is a causative factor in numerous degenerative diseases, including liver fibrosis, cardiovascular disease, and cancer.

Few doctors even know about the dangers of excess iron, let alone test for total-body iron status. Excessive iron accumulations are found in affected brain areas of people suffering from Alzheimer’s, Parkinson’s, and other neurodegenerative diseases.

Keep in mind that a simple blood test can test for serum iron levels. We suggest getting tested at least yearly for iron levels. And why not supplement with some of our suggestions above for the best prevention of iron-induced damage?

References

  1. Free Radic Biol Med. 2011 Apr 15;50(8):934-44.
  2. AJNR Am J Neuroradiol. 1994 Jun;15(6):1129-38.
  3. Arch Gen Psychiatry. 2000 Jan;57(1):47-53.
  4. Biol Psychiatry. 1994 Apr 1;35(7):480-7.
  5. J Inorg Biochem. 2011 May;105(5):693-701.
  6. J Agric Food Chem. 2007 Feb 21;55(4):1491-500.
  7. Free Radic Biol Med. 2006 Apr 1;40(7):1152-60.
  8. Biochem Pharmacol. 1997 Nov 1;54(9):973-8.
  9. Redox Rep. 2001;6(5):327-34.