Some life extensionists have voiced concerns about the
free-radical-promoting nature of the mineral iron. The
Life Extension Foundation has raised such concerns and
does not include iron in their main formula. All I've
seen on iron since first hearing such concerns supports
such concerns, such as the following new study that finds
unusually high levels of iron in the brains of Alzheimer
patients. The study notes: "Iron can catalyze [promote]
free radical reactions and may contribute to oxidative
damage observed in AD brains." It then concludes: "The
data replicate and extend prior results and suggest that
basal ganglia ferritin iron levels are increased in AD."
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Arch Gen Psychiatry 2000 Jan;57(1):47-53
In vivo evaluation of brain iron in Alzheimer disease
using magnetic resonance imaging.
Bartzokis G, Sultzer D, Cummings J, Holt LE, Hance DB,
Henderson VW, Mintz J
Department of Psychiatry, University of Arkansas for
Medical Sciences and the Mental Health Service, Central
Arkansas Veterans Healthcare System, Little Rock, USA.
gbar@ucla.edu
BACKGROUND: The basal ganglia contain the highest levels
of iron in the brain, and postmortem studies indicate a
disruption of iron metabolism in the basal ganglia of
patients with Alzheimer disease (AD). Iron can catalyze
free radical reactions and may contribute to oxidative
damage observed in AD brains. Treatments aimed at reducing
oxidative damage have offered novel ways to delay the rate
of progression and could possibly defer the onset of AD.
Brain iron levels were quantified in vivo using a new
magnetic resonance imaging method. METHODS: Thirty-one
patients with AD and 68 control subjects participated
in this study. A magnetic resonance imaging method was
employed that quantifies the iron content of ferritin
molecules (ferritin iron) with specificity through the
combined use of high and low field-strength magnetic
resonance imaging instruments. Three basal ganglia
structures (caudate, putamen, and globus pallidus)
and one comparison region (frontal lobe white matter)
were evaluated. RESULTS: Basal ganglia ferritin iron
levels were significantly increased in the caudate
(P = .007; effect size, 0.69) and putamen (P = .008;
effect size, 0.67) of AD subjects, with a trend toward
an increase in the globus pallidus (P = .13). The
increased basal ganglia ferritin iron levels were not
a generalized phenomenon; white matter ferritin iron
levels were unchanged in patients with AD (P = .50).
CONCLUSIONS: The data replicate and extend prior
results and suggest that basal ganglia ferritin iron
levels are increased in AD. Prospective studies are
needed to evaluate whether premorbid iron levels are
increased in individuals who develop AD.
http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=10632232&form=6&db=m
&Dopt=b
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GODDARD'S JOURNAL: http://www.erols.com/igoddard/journal.htm
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