True .. vitamin D .. in theory would be an anti-inflammatory .. and the
melanin should be .. too ..

But .. IF .. there is a .. problem between the ability to produce
ENOUGH vitamin D to OFFSET the free radicals / labile iron pool .. THAT
is the million dollar question ..

Is the iron in the body ENOUGH to skew the balance between vitamin D in
the body and the iron levels .. since iron seemingly destroys /
subverts .. vitamin D ..

Iron destroys vitamin D or more precisely
in those with iron overload .. vitamin D is decreased .. in those with
supplemental iron induced iron overload .. vitamin D is decreased.

Bleeding / venesection / bloodletting / phlebotomy .. RESTORES ..
vitamin D .

<<snip>>
The results reveal that the low serum 25-OHD concentration in patients
with hemochromatosis is directly related to the extent of iron loading
and it is improved by venesection therapy.
<<snip>>

Iron induced decreased vitamin D.

<<snip>>
when transferrin is saturated with iron, may impair bone formation and
aggravate osteomalacia.
<<snip>>

Saccharated ferric oxide (SFO)-induced osteomalacia: in vitro
inhibition by SFO of bone formation and 1,25-dihydroxy-vitamin D
production in renal tubules.
Sato K, Nohtomi K, Demura H, Takeuchi A, Kobayashi T, Kazama J, Ozawa H

Bone. 1997 Jul ; 21(1): 57-64

A 60-year-old man with portal hypertensive gastropathy due to type C
liver cirrhosis developed severe bone pains, marked hypophosphatemia
with inappropriately increased urinary excretion of phosphate (%TRP;
9.6%), and hyperalkaline phosphatasia, after intravenous administration

of saccharated ferric oxide (SFO) at a dose of 80-240 mg/week over a
period of more than 5 years. The total iron infused was estimated to be

more than 25 g. On a diagnosis of SFO-induced osteomalacia, the
infusion of iron was immediately discontinued, and phosphate and
vitamin D2 (1000 IU/day) were administered. Serum levels of 25-OHD2
increased after 1 week, whereas levels of 1,25-(OH)2D2 did not increase

until 3 months later, accompanied by improvement of renal tubular
reabsorption of phosphate and gradual improvement of the bone pains.
The patient has been doing well for the last 2 years, with normal serum

levels of phosphate, calcium, and alkaline phosphatase, without any
supplementation of phosphate, vitamin D, or iron-containing agents. In
primary culture of neonatal mouse renal tubules, in which 1,25-(OH)2D3
was produced from 25-OHD3 in response to PTH, SFO significantly
inhibited PTH-induced production of 1,25-(OH)2D3 at 30 mumol/L, which
is attainable in the urine of patients receiving a therapeutic
intravenous dose of SFO. Furthermore, SFO decreased the calcium content

and inhibited 45Ca incorporation in cultured fetal mouse parietal bones

at 3 mumol/L. Such SFO concentration may be transiently observed in the

plasma of patients receiving excessive intravenous doses of SFO for a
prolonged period. These in vitro findings together with the clinical
observations suggest that SFO, after filtration through the glomerulus
and reabsorption in the proximal renal tubules, impaired proximal renal

tubular function, such as tubular reabsorption of phosphate and 1
alpha-hydroxylase activity, leading to hypophosphatemic osteomalacia.
Furthermore, it is highly likely that SFO in the peripheral blood, when

transferrin is saturated with iron, may impair bone formation and
aggravate osteomalacia. Although SFO-induced osteomalacia is reversible

simply by discontinuation of the agent, excessive and prolonged
administration of SFO should be avoided.

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1: Gastroenterology. 1985 Apr;88(4):865-9. Related Articles, Links

Low serum 25-hydroxyvitamin D in hereditary hemochromatosis: relation
to iron status.

Chow LH, Frei JV, Hodsman AB, Valberg LS.

Under normal conditions, vitamin D absorbed from the diet or
synthesized in the skin is transported to the liver where it undergoes
hydroxylation. The purpose of this study was to determine whether
excess hepatic iron affects this process and the subsequent production
of 1,25-dihydroxyvitamin D (1,25-[OH]2D) in the kidney. Mean serum
25-hydroxyvitamin D (25-OHD) concentrations in untreated hereditary
hemochromatosis were 13 +/- 6 (SD) in 9 patients with cirrhosis, 13 +/-

6 in 5 patients with hepatic fibrosis, and 22 +/- 6 in 10 patients with

normal hepatic architecture aside from siderosis and were significantly

lower than the levels found in 24 controls matched for age, sex, and
season, p less than 0.05. The mean serum 25-OHD levels in the two
groups with hemochromatosis and hepatic damage were significantly lower

than the value in the group with normal hepatic architecture, p less
than 0.05. Serum 25-OHD levels in individual patients were inversely
related to the size of body iron stores as measured by exchangeable
body iron, r = -0.64, or serum ferritin, r = -0.47, p less than 0.05.
In 15 patients removal of excess body iron by venesection therapy
produced a significant increase in the mean serum 25-OHD from 20 ng/ml
to 30 ng/ml, p less than 0.05. In contrast, mean serum 1,25-[OH]2D
levels were similar in iron-loaded and control subjects, indicating
that the regulation of this metabolite was intact in patients with
hemochromatosis. The results reveal that the low serum 25-OHD
concentration in patients with hemochromatosis is directly related to
the extent of iron loading and it is improved by venesection therapy.

PMID: 3838288 [PubMed - indexed for MEDLINE]

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