Good way to get rid of iron is to give blood.
"Ian Goddard" <igoddard at erols.mom> wrote in message
news:bhfmiv867s916mglu8ioerf60ninn8b2hs at 4ax.com...
>> After mentioning potential risks associated with iron intake
> above necessary levels to some friends, some of whom seemed
> skeptical, I gathered some of the data, which, having
> collected, I thought I'd share with folks here...
>> This review from "Nutrition Today" (5/6/97) by two leading
> researchers examines risks associated with iron and concludes
> that apart from deficiencies, "There is little reason to support
> a general need for iron supplementation in the diet at any age.
> [...] don't expose your system to more iron than it needs."
> While essential at recommended levels, iron generates toxic
> oxygen radicals. It also notes that iron intake is cumulative,
> since "iron accumulates in the brain with normal aging."
>> Iron's possible supporting role in neurological degeneration:
>> Proceedings of the National Academy of Sciences (May 28, 2002):
> "Whereas a decade ago thoughts of metals and Alzheimer's disease
> (AD) conjured up thoughts of tossing out your aluminum cookware,
> more recently, zinc, copper, and iron have been implicated in
> AD pathology."
>http://www.pnas.org/cgi/content/full/99/11/7317>> Cellular and Molecular Biology (June 2000): "In several
> neurodegenerative diseases, iron accumulates at sites of
> brain pathology. Since post-mortem examination cannot
> distinguish whether iron accumulation caused the damage or
> resulted from damage, it is necessary to manipulate iron in
> animal and tissue culture models to assess its causal role(s).
> [...] iron supplementation to ID rats increased damage and
> microgliosis in the above regions. [...] In addition,
> iron+zinc supplementation dramatically increased damage to
> hippocampal CA1 whereas zinc supplementation alone had no effect."
>> Journal of Neurochemistry (July 1992): "Iron, a transition
> metal possibly involved in the pathogenesis of Parkinson's
> disease, was tested for its toxic effects toward cultures of
> dissociated rat mesencephalic cells. [...] Altogether, these
> results suggest (a) that ferrous iron is a potent neurotoxin
> for dopaminergic neurons as well as for other cell types in
> dissociated mesencephalic cultures [...]."
>> Professor James Connor (author of "Nutrition Today" review
> quoted at top of post): "Our data had led to the discovery
> that the brain's ability to mobilize iron is diminished in
> Alzheimer's Disease and in specific regions of the brain
> in Parkinson's Disease. This diminished iron mobilization
> could lead to increased susceptibility to oxidative damage
> and cell death; both of which are prominent features in
> Alzheimer's and Parkinson's diseases."
>> Current Opinion in Chemical Biology (April 4, 2000): "Data
> are now rapidly accumulating to show that metallochemical
> reactions might be the common denominator underlying
> Alzheimer's disease, amyotrophic lateral sclerosis, prion
> diseases, cataracts, mitochondrial disorders and Parkinson's
> disease. In these disorders, an abnormal reaction between a
> protein and a redox-active metal ion (copper or iron)
> promotes the formation of reactive oxygen species or radicalization."
>> Alzheimer's disease (AD) appears to be associated with
> a dysregulation of heavy metals, possibly as a result of
> impairment of metallothione (the body's natural defense
> against metal toxicity) that may be associated with the
> ApoE genetic defect that increases the risk of AD.
>> Aluminum and Alzheimer's disease:
>> Mercury and Alzheimer's disease:
>http://www.google.com/groups?selm=3af37029.2307577%40news.erols.com>>>http://IanGoddard.net/journal.htm>> "To lengthen thy life, lessen thy meals." Ben Franklin
>> Ongoing CR-monkey-study update: "In the monkeys...those on
> reduced feeding since the study started are dying at a rate
> that is about half that of the monkeys receiving a full food
> ration." Associated Press: Eating less may extend human life.
> August 1, 2002 : http://www.msnbc.com/news/788746.asp?0si=->>