Re: International traffic in CONTRABAND blood and blood products

> [snippage]
>
>> Iron is a
>> powerful catalyst of one electron oxidation and so reduction of iron
>> load will lead to life extension in all other subgroups. This should
>> be self evident to all doctors.
>
> Maybe. From:
> http://www.springerlink.com/content/b5157486m8q1348l/
>
> Role of antioxidant nutrients in aging: Overview
[more snippage]

Sorry for doubting your wisdom. The article below gives greater confirmation
of your point of view for _one_ specific disorder.

From:
http://www.ncbi.nlm.nih.gov/pubmed/18469261?ordinalpos=1&itool=EntrezSystem2.PEntrez.P
ubmed.Pubmed_ResultsPanel.Pubmed_RVDocSum

Am J Clin Nutr. 2008 May;87(5):1374-83.

Pathways underlying iron accumulation in human nonalcoholic fatty liver
disease.
Aigner E, Theurl I, Theurl M, Lederer D, Haufe H, Dietze O, Strasser M, Datz
C, Weiss G.

Department of Internal Medicine, General Hospital Oberndorf, Oberndorf,
Austria.

BACKGROUND:

Mild iron overload is frequently observed in nonalcoholic fatty liver
disease (NAFLD).

OBJECTIVE:

We aimed to study putative pathways underlying iron accumulation in NAFLD.

DESIGN:

Hepatic and duodenal expression of critical iron molecules in NAFLD patients
with (n = 32) and without (n = 29) iron overload, hereditary hemochromatosis
(n = 10), and controls (n = 20) were investigated. Phlebotomy treatment was
performed in 14 NAFLD patients.

RESULTS:

The hepatic expressions of the iron-export protein ferroportin-1 (FP-1) and
of the iron-sensing molecule hemojuvelin (HJV) were significantly lower in
NAFLD patients. The mRNA expression of the iron-regulatory peptide hepcidin
was increased in NAFLD patients with iron overload, which was paralleled by
low duodenal FP-1 expression. Hepatic mRNA and serum protein concentrations
of tumor necrosis factor-alpha (TNF-alpha) were increased in NAFLD patients
and were inversely correlated with both liver FP-1 and HJV mRNA and
positively associated with body mass index and hepatic hepcidin mRNA.
Accordingly, TNF-alpha inhibited the FP-1 and HJV mRNA formation in HepG2
cells. Phlebotomy treatment of NALFD patients reduced serum ferritin,
transferrin saturation, and TNF-alpha concentrations and improved liver
function tests.

CONCLUSIONS:

Iron accumulation in NAFLD may result from an impaired iron export due to
down-regulation of FP1 and ineffective hepatic iron sensing, as indicated by
low HJV expression. TNF-alpha appears to play a role in exerting these
regulatory changes. Increased hepcidin formation in iron-overloaded NAFLD
patients, however, results in decreased duodenal FP-1 expression, whereas a
reduction in liver FP-1 may perpetuate hepatic iron retention. Phlebotomy
offers a safe and efficient therapy for these metabolic disturbances.
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