Iron is an essential mineral for brain health and development. It can also be a villainous mineral when the delicate balance between the amounts of iron necessary for brain function is far exceeded. Excessive iron in the brain has been implicated in many neurological diseases including Alzheimer’s Disease.
Alzheimer’s disease is now the sixth leading cause of death among Americans, affecting nearly 1 in 8 people over the age of 65. There is currently no treatment that alters the course of this disease. However, an increasing amount of evidence suggests that changes in the way the body handles iron and other metals may lead to the onset of Alzheimer’s disease symptoms. Addressing these changes as they occur may have the desired preventative effect.
It is hard to get rid of excess iron. This was discussed in new research by doctors at the The Florey Institute for Neuroscience and Mental Health at The University of Melbourne. “Excess iron is a potent source of oxidative damage through radical formation and because of the lack of a body-wide export system, a tight regulation of its uptake, transport and storage is crucial in fulfilling cellular functions while keeping its level below the toxicity threshold.”1
Chelation and Iron Toxicity
- Please see our article on Chelation therapy for a discussion of this treatment.
A new paper from December 2016, lead by researchers at the Department of Neurology and Center of Clinical Neuroscience, Charles University in Prague suggests that disturbance of brain iron regulation, as mentioned in the above study, is almost universal in neurodegenerative disorders, and, “iron chelation therapy has been investigated in many neurological disorders including rare genetic syndromes with neurodegeneration with brain iron accumulation as well as common sporadic disorders such as Parkinson’s disease, Alzheimer’s disease, and multiple sclerosis.”2 With studies suggesting that it may prevent or slow down disease progression of several neurodegeneration disorders.
- Doctors in South Korea published new research in which they found iron chelation protected neural cells and cell mitochondria (the energy centers of the cells).3
In a recent study, a group of investigators from the University of North Dakota School of Medicine and Health Sciences, fed rabbits a diet that caused them to accumulate plaques of a small protein called beta-amyloid (Aβ).
These plaques are toxic to neurons and central to the development of Alzheimer’s disease. Following treatment with a chelation agent called deferiprone (an iron chelator), the iron level in the rabbits’ blood plasma was reduced and the levels of both beta-amyloid and phosphorylated tau in the brain were returned to normal levels. 4
At the Magaziner Center in Cherry Hill, New Jersey, we begin our treatment of Alzheimer’s patients with a full analysis of a person’s mitochondrial function, including testing for heavy metal toxicity. If detected, we utilize chelating agents to rid the body of these metals, as well as other natural detoxification techniques.
We work to repair oxidative damage with Hyperbaric Oxygen therapy and the use of antioxidant nutritional supplements including Vitamins E, Vitamin B12 and folate, amino acids, and fatty acids as well as the intake of “superfoods” known for their natural healing properties.
In addition, we utilize intravenous vitamin infusions to help regulate any nutrient imbalances and vitamin and mineral deficiencies. To balance the flow of energy and help promote clearer thinking, we also utilize ONDAMED®, a high-tech biofeedback machine designed in Germany.
1 Belaidi AA, Bush AI. Iron neurochemistry in Alzheimer’s disease and Parkinson’s disease: targets for therapeutics. J Neurochem. 2016 Oct;139 Suppl 1:179-197. doi: 10.1111/jnc.13425. Epub 2016 Feb 10.
2 Dusek P, Schneider SA, Aaseth J.Iron chelation in the treatment of neurodegenerative diseases. J Trace Elem Med Biol. 2016 Dec;38:81-92. doi: 10.1016/j.jtemb.2016.03.010.
3 Lee DG, Park J, Lee HS, Lee SR, Lee DS. Iron overload-induced calcium signals modulate mitochondrial fragmentation in HT-22 hippocampal neuron cells. Toxicology. 2016 Jul 29;365:17-24. doi: 10.1016/j.tox.2016.07.022.
4 Prasanthi JRP, Schrag M, Dasari B, Marwarha G, Kirsch WM, Ghribi O. Deferiprone Reduces Amyloid-β and Tau Phosphorylation Levels but not Reactive Oxygen Species Generation in Hippocampus of Rabbits Fed a Cholesterol-Enriched Diet. Journal of Alzheimer’s disease : JAD. 2012;30(1):167-182. doi:10.3233/JAD-2012-111346.