"No actually .. malaria is .."

  The World Health Organization estimates that 80 per cent of the
global
  population may not get enough iron, resulting in low iron levels and
  iron deficiency anemia.

  The WHO's World Malaria Report 2008, which draws upon data collected
  through 2006, paints a complex picture. Some highlights:
  New methods* estimate the number of malaria cases is 247 million for
  2006.

The world's population is about 6.4 or so billion, what percent of that
is 247 million?  The 80 percent for low iron is around 5.21 billion.
Mind your "b's" and "m's".

you apparently don't know:

"Iron deficiency is defined as a decreased total iron body content. Iron
deficiency anemia occurs when iron deficiency is sufficiently severe to
diminish erythropoiesis and cause the development of anemia. Iron
deficiency is the most prevalent single deficiency state on a worldwide
basis. It is important economically because it diminishes the capability
of individuals who are affected to perform physical labor, and it
diminishes both growth and learning in children."

[Editors: Paul Schick, MD, Emeritus Professor, Department of Internal
Medicine, Thomas Jefferson University Medical College; Research
Professor, Department of Internal Medicine, Drexel University College of
Medicine; Francisco Talavera, PharmD, PhD, Senior Pharmacy Editor,
eMedicine; Ronald A Sacher, MD, Director of the Hoxworth Blood Center,
Professor, Departments of Internal Medicine and Pathology, University of
Cincinnati Medical Center; Rajalaxmi McKenna, MD, FACP, Consulting
Staff, Department of Medicine, Southwest Medical Consultants, SC, Good
Samaritan Hospital, Advocate Health Systems; Emmanuel C Besa, MD,
Professor, Department of Medicine, Division of Hematologic Malignancies,
Kimmel Cancer Center, Thomas Jefferson University]

"Iron deficiency anaemia
The challenge

Iron deficiency is the most common and widespread nutritional disorder
in the world. As well as affecting a large number of children and women
in developing countries, it is the only nutrient deficiency which is
also significantly prevalent in industralized countries. The numbers are
staggering: 2 billion people – over 30% of the world’s population – are
anaemic, many due to iron deficiency, and in resource-poor areas, this
is frequently exacerbated by infectious diseases. Malaria, HIV/AIDS,
hookworm infestation, schistosomiasis, and other infections such as
tuberculosis are particularly important factors contributing to the high
prevalence of anaemia in some areas."
http://www.who.int/nutrition/topics/ida/en/index.html

only +3/4 of a million...

"Iron deficiency affects more people than any other condition,
constituting a public health condition of epidemic proportions. More
subtle in its manifestations than, for example, protein-energy
malnutrition, iron deficiency exacts its heaviest overall toll in terms
of ill-health, premature death and lost earnings."
"Invisible yet ubiquitous in many developing countries, the true toll of
iron deficiency and anaemia lies hidden in the statistics of overall
death rates, maternal haemorrhage, reduced school performance and
lowered productivity."
http://www.who.int/nutrition/topics/ida/en/index.html

"Iron deficiency is considered to contribute to death and disability as
a risk factor for maternal and perinatal mortality, and also through its
direct contributions to cognitive impairment, decreased work
productivity, and death from severe anemia."
http://www.ncbi.nlm.nih.gov/pubmed/17016951?dopt=Abstract

"Globally, iron deficiency ranks number 9 among 26 risk factors included
in the GBD 2000, and accounts for 841,000 deaths..."
http://www.ncbi.nlm.nih.gov/pubmed/17016951?dopt=Abstract

you are undereducated:

Iron deficiency anemia/Incidence Rate: approx 1 in 24 or 4.12% or 11.2
million people in USA [about data]

Incidence extrapolations for USA for Iron deficiency anemia: 11,212,400
per year, 934,366 per month, 215,623 per week, 30,718 per day, 1,279 per
hour, 21 per minute, 0 per second.

Prevalance of Iron deficiency anemia: In the United States, 20% of all
women of childbearing age have iron-deficiency anemia, compared with
only 2% of adult men. (Source: excerpt from Anemia: NWHIC)

Hospitalizations for Iron deficiency anemia: 47,000 (NHLBI 1999)

Deaths from Iron deficiency anemia: 118 deaths (NHLBI 1999)

Death rate extrapolations for USA for Iron deficiency anemia: 117 per
year, 9 per month, 2 per week, 0 per day, 0 per hour, 0 per minute, 0
per second.

snip <<

YOU **specifically** were TOLD to stay off my threads ..
You got some problem with those orders .. ?
Stay off my threads .. fat boy ..

Stay off my threads like you've been told ..

Need some MORE insults .. fat boy .. ?

Do ya .. ?

Heed the .. words .. fat boy ..
-------------
Iron causes vitamin E deficiency AND vitamin D deficiency.
Vitamin E deficiency depletes vitamin D .

Phlebotomy / blood donation is KNOWN to increase vitamin D.

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

Vitamin D Deficiency May Cause Severe Muscle Weakness in Fibromyalgia

Endocrinologists at the University at Buffalo suggest that adults
afflicted with incapacitating muscle weakness and pain may be
suffering from an easily treatable vitamin D deficiency. A report by
Paresh Dandona, M.D. in the Archives of Internal Medicine (April 24,
2000) reported that five patients confined to wheelchairs because of
severe muscle weakness regained normal muscle strength after four to
six weeks of vitamin D supplementation.

This study was the first to describe cases of severe myopathy due to
a
lack of vitamin D in the United States.

Vitamin D is produced by the liver in the presence of sufficient
calcium and sunlight.

Dandona, a native of India and educated in the United Kingdom, said
that individuals who have limited exposure to the sun are
particularly
vulnerable to this condition. "In addition to osteomalacia (softening
of the bones), myopathy is a well-recognized feature of this
condition.”

"In the United States, vitamin D deficiency has only recently been
appreciated, especially in the northern areas bordering Canada. We
see
vitamin D deficiency in the hospital setting and in the community at
large during the winter months, but in this country, there are no
reports of incapacitating muscle weakness associated with vitamin D
deficiency."

In each of his cases, the weakness had been attributed previously to
other causes: old age, problems associated with diabetes, and general
debility. "The diagnosis in these cases was either masked by the
presence of neurological disease or had been totally unrecognized
because of its insidious onset," said Dr. Dandona. Tests revealed
vitamin D deficiency in all five patients. After vitamin D
replacement
therapy, four patients regained normal muscle strength and were able
to walk without support. The fifth -- the patient with anorexia
nervosa -- was able to stop using a wheelchair and walk with support.

Dr. Dandona listed the following situations that should raise
suspicions about a severe vitamin D deficiency:

limited sunlight exposure, due to climate or limited sun exposure
Body aches and pains, especially in the shins and ribs
Impaired absorption of nutrients

Vitamin D Deficiency Study Raises New Questions About Disease And
Supplements

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

Increased oxidative stress suggested by low serum vitamin E
concentrations in patients with chronic fatigue syndrome.
Miwa K, Fujita M
Int J Cardiol 2008 Aug 4.

Serum alpha-tocopherol concentrations were determined in 50 patients
with chronic fatigue syndrome (CFS) and 40 control subjects
(Control).
Prevalence of each or any coronary risk factor was not significantly
different between CFS and Control. CFS had significantly lower alpha-
tocopherol concentrations than Control.
The concentrations were significantly lower in the subjects with any
coronary risk factors than those without in CFS as well as Control.
Even among the subjects with any coronary risk factors and also among
those without, CFS had significantly lower alpha-tocopherol
concentrations than Control.
In conclusion, CFS had significantly lower alpha-tocopherol
concentrations irrespective of coronary risk factors than Control,
suggesting the presence of increased oxidative stress in CFS.

International journal of cardiology [Int J Cardiol]

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

ScienceDaily (Jan. 27, 2008) — Low blood levels of vitamin D have
long
been associated with disease, and the assumption has been that
vitamin
D supplements may protect against disease. However, this new research
demonstrates that ingested vitamin D is immunosuppressive and that
low
blood levels of vitamin D may be actually a result of the disease
process. Supplementation may make the disease worse.

In a new report Trevor Marshall, Ph.D., professor at Australia’s
Murdoch University School of Biological Medicine and Biotechnology,
explains how increased vitamin D intake affects much more than just
nutrition or bone health. The paper explains how the Vitamin D
Nuclear
Receptor (VDR) acts in the repression or transcription of hundreds of
genes, including genes associated with diseases ranging from cancers
to multiple sclerosis.

"The VDR is at the heart of innate immunity, being responsible for
expression of most of the antimicrobial peptides, which are the
body’s
ultimate response to infection," Marshall said.

"Molecular biology is now forcing us to re-think the idea that a low
measured value of vitamin D means we simply must add more to our
diet.
Supplemental vitamin D has been used for decades, and yet the
epidemics of chronic disease, such as heart disease and obesity, are
just getting worse."

"Our disease model has shown us why low levels of vitamin D are
observed in association with major and chronic illness," Marshall
added. "Vitamin D is a secosteroid hormone, and the body regulates
the
production of all it needs. In fact, the use of supplements can be
harmful, because they suppress the immune system so that the body
cannot fight disease and infection effectively."

Marshall's research has demonstrated how ingested vitamin D can
actually block VDR activation, the opposite effect to that of
Sunshine. Instead of a positive effect on gene expression, Marshall
reported that his own work, as well as the work of others, shows that
quite nominal doses of ingested vitamin D can suppress the proper
operation of the immune system. It is a different metabolite, a
secosteroid hormone called 1,25-dihydroxyvitamin D, which activates
the VDR to regulate the expression of the genes. Under conditions
that
exist in infection or inflammation, the body automatically regulates
its production of all the vitamin D metabolites, including 25-
hydroxyvitamin D, the metabolite which is usually measured to
indicate
vitamin D status.

Vitamin D deficiency, long interpreted as a cause of disease, is more
likely the result of the disease process, and increasing intake of
vitamin D often makes the disease worse. "Dysregulation of vitamin D
has been observed in many chronic diseases, including many thought to
be autoimmune," said J.C. Waterhouse, Ph.D., lead author of a book
chapter on vitamin D and chronic disease.

"We have found that vitamin D supplementation, even at levels many
consider desirable, interferes with recovery in these patients."

"We need to discard the notion that vitamin D affects a disease state
in a simple way," Marshall said. "Vitamin D affects the expression of
over 1,000 genes, so we should not expect a simplistic cause and
effect between vitamin D supplementation and disease. The
comprehensive studies are just not showing that supplementary vitamin
D makes people healthier."

Journal reference: Marshall TG. Vitamin D discovery outpaces FDA
decision making. Bioessays. 2008 Jan 15;30(2):173-182 [Epub ahead of
print] Online ISSN: 1521-1878 Print ISSN: 0265-9247 PMID: 18200565

Adapted from materials provided by Autoimmunity Research Foundation,
via AlphaGalileo.

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

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

"Low 25-OHD concentration is directly related to iron loading"
"Improved by venesection therapy."

"Iron may impair bone formation and aggravate osteomalacia."

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

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

Who loves ya.
Tom

Jesus Was A Vegetarian!
http://tinyurl.com/634q5a

Man Is A Herbivore!
http://tinyurl.com/4rq595

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