Since they have found free floating iron in those with diabetes ..
then the finding of low vitamin D really comes as no surprise ..
because .. iron destroys vitamin D ..

**Specifically** ..

What significance is the fact 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.

---------------------------------------------------------------------------­----------------

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]

---------------------------------------------------------------------------­-----

http://health.enotes.com/genetic-disorders-encyclopedia/major-histoco...

Major histocompatibility complex

HLA disease associations
Disease  MHC allele  Approximate relative risk

Ankylosing spondylitis  B27  77?90
Patients with ankylosing spondylitis may have extremely low levels of
25(OH)D.
http://tinyurl.com/8tonv
Celiac disease  DR3 + DR7  5?10
A low 25-(OH)D vitamin concentration was a typical biochemical
abnormality in our patients (64% of men and 71% of women).
http://tinyurl.com/b7b9d
Diabetes, Type 1  DR3  5
decreased zinc and 25OHD serum levels in poorly controlled
insulin-dependent (Type I) diabetic patients
http://tinyurl.com/73fsu
Diabetes, Type 1  DR4  5?7
Diabetes, Type 1  DR3 + DR4  20?40
Graves disease  DR3  5
[High prevalence of secondary hyperparathyroidism due to vitamin D
insufficiency in Graves' disease]
http://www.hubmed.org/search.cgi?q=25-hydroxyvitamin+D+and+graves
Hemochromatosis  A3  6?20
Lupus  DR3  1?3
There was a high prevalence of hypovitaminosis D (65.2%),
http://tinyurl.com/8wfws
Multiple sclerosis  DR2  2?4
Vitamin D Defends Against MS
http://www.hon.ch/News/HSN/516850.html
Myasthenia gravis  B8  2.5?4
Psoriasis vulgaris  Cw6  8
These data suggest that exogenous active forms of vitamin D3 are
effective for treatment of psoriasis and that the endogenous
1,25-dihydroxyvitamin D level also may be involved in the development
of this skin disease.
http://tinyurl.com/9c88e
Rheumatoid arthritis  DR4  3?6
We suggest that there is a disturbance in vitamin D metabolism in RA.
http://tinyurl.com/df6zv
---------------------------------------------------------------------------­------------------

Prabhala, A., R. Garg, and P. Dandona,
Severe myopathy associated with vitamin D deficiency in western New
York.
Arch Intern Med, 2000. 160(8): p. 1199-203.
Five cases of severe myopathy associated with vitamin D deficiency
are
described. Each patient was confined to a wheelchair because of
weakness and immobility. Two were elderly, 1 was a 37-year-old
African
American with type 1 diabetes mellitus, 1 was being treated for
carcinoid syndrome, and 1 was severely malnourished due to poor oral
intake. In each, weakness had previously been attributed to other
causes, including old age, concomitant diabetic neuropathy, or
general
debility. Correct diagnosis was made initially by a high index of
suspicion, following the demonstration of clinical proximal myopathy;
confirmation was made by the demonstration of low 25-hydroxyvitamin D
and elevated parathyroid hormone concentrations. Treatment with
vitamin
D caused a resolution of body aches and pains and a restoration of
normal muscle strength in 4 to 6 weeks. Four patients became fully
mobile and had normal 25-hydroxyvitamin D concentrations, and the
fifth
also became mobile. In the 4 fully recovered cases, parathyroid
hormone
levels on follow-up were lower but still elevated. This finding
suggests a degree of autonomy of parathyroid secretion known to occur
in cases of long-standing vitamin D deficiency. Myopathy, due to
chronic vitamin D deficiency, probably contributes to immobility and
ill health in a significant number of patients in the northern United
States. An awareness of this condition may significantly improve
mobility and quality of life in patient populations vulnerable to
vitamin D deficiency.

Who loves ya.
Tom

Jesus Was A Vegetarian!
http://jesuswasavegetarian.7h.com

Man Is A Herbivore!
http://tinyurl.com/a3cc3

DEAD PEOPLE WALKING
http://tinyurl.com/zk9fk

Here some additional interesting references about vitamin D and type
diabetes:

Borissova AM, Tankova T, Kirilov G, Dakovska L, Kovacheva R.
The effect of vitamin D3 on insulin secretion and peripheral insulin
sensitivity in type 2 diabetic patients.
Int J Clin Pract. 2003;57(4):258-261. (PubMed)
<http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=1
2800453&dopt=Abstract>

   "Our results suggest that vitamin D3 supplementation could be an
   element in the complex treatment of type 2 diabetes mellitus
   during the winter.

Inomata S, Kadowaki S, Yamatani T, Fukase M, Fujita T.
Effect of 1 alpha (OH)-vitamin D3 on insulin secretion in diabetes
mellitus.
Bone Miner. 1986;1(3):187-192
<http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=3
334207&dopt=Abstract>

   "The findings that 1 alpha (OH)D3 enhances insulin secretion
   and reduces the levels of serum free fatty acid in non-
   insulin-dependent diabetics provide us with the possibility
   that vitamin D may play some role in the regulation of
   insulin secretion."