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RDA for iron skewed? / any arguments?

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ironj...@aol.com

unread,
Jan 2, 2006, 4:28:14 PM1/2/06
to
Below .. PROOF ..


The following study shows clearly .. due to previous studies which left

isotopes in the study group .. 1.46 mg/d for males and 1.15 mg/d for
females to be the loss / required intake for a growing adolescent.


This is about 5-10 times less than what is currently recommended .. ?


Recommended Dietary Allowances for Iron for Infants (7 to 12 months),
Children, and Adults
Ages Male (mg) Female (mg)
9-13 years 8mg/d 8mg/d
14-18 years 11 mg/d 15 mg/d


<<snip>>
the requirement for absorbed iron was estimated to be 1.46 mg/d for
males and 1.15 mg/d for females.
<<snip>>


Which seems even at the low of 8 to be MUCH higher than required .. ?


http://www.beefinfo.org/bh_iron.cfm


And since a growing adolescent is the SAME .. basically .. as an adult
in REQUIRED iron .. according to the same .. researchers .. then one
might .. presume .. the calculations for REQUIRED iron in an adult ..
may ALSO .. be .. skewed / wrong .. ?
---------------------------------------------------------------------------­­?-----------

Inevitable iron loss by human adolescents, with calculations of the
requirement for absorbed iron.


Fomon SJ, Drulis JM, Nelson SE, Serfass RE, Woodhead JC, Ziegler EE
Department of Pediatrics, University of Iowa, Iowa City, IA and.
Department of Preventive Medicine and Community Health, University of
Texas Medical Branch, Galveston, TX.


[Medline record in process]


In growing individuals, the requirement for absorbed iron consists of
iron needed for growth and iron needed to replace inevitable iron loss.

We were able to estimate inevitable iron loss by adolescents because
total body iron of the adolescents had been enriched with the stable
isotope, (58)Fe, as the result of earlier studies of iron absorption.
During an interval beginning at least 1.56 y after isotope
administration (a time sufficient for complete mixing of the isotope
with total body iron) and extending for no less than 3.29 y, we
determined the isotopic enrichment of circulating iron. On the basis of

several assumptions, we calculated total body (58)Fe and total body
iron at the beginning and end of the interval. Because of complete
mixing of the isotope with total body iron, fractional total (58)Fe
loss was the same as fractional loss of total iron. In males, the
fractional loss of iron was 9.70%/y and the quantitative loss was 256
mg/y or 0.70 mg/d. In females, the fractional loss of iron was 14.60%/y

and the quantitative loss was 306 mg/y or 0.84 mg/d. Using several
assumptions, we then calculated that the iron requirement for growth
during this interval was 0.76 mg/d for males and 0.31 mg/d for females.

Adding the iron loss to the iron requirement for growth, the
requirement for absorbed iron was estimated to be 1.46 mg/d for males
and 1.15 mg/d for females.


PMID: 12514285, UI: 22401955


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


Who loves ya.
Tom


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


Man Is A Herbivore!
http://pages.ivillage.com/ironjustice/manisaherbivore


DEAD PEOPLE WALKING
http://pages.ivillage.com/ironjustice/deadpeoplewalking

Erskine James

unread,
Jan 2, 2006, 9:13:09 PM1/2/06
to
This might be a troll, but there might be some data that is involved in
this as well. I have heard one cardiologist at ACC propose that the
reason women have pre-menopausal prevention against CVD is not due to
the estrogen, but due to their menses and the lower iron levels in
their blood. But this is not been confirmed in several studies, looking
at ferritin levels as markers.

Doug

unread,
Jan 3, 2006, 5:55:39 PM1/3/06
to
Just a question..... You are all over these newsgroups......What is this
iron stuff to you?


<ironj...@aol.com> wrote in message
news:1136237294.6...@z14g2000cwz.googlegroups.com...
Below .. PROOF ..


The following study shows clearly .. due to previous studies which left

isotopes in the study group .. 1.46 mg/d for males and 1.15 mg/d for
females to be the loss / required intake for a growing adolescent.


This is about 5-10 times less than what is currently recommended .. ?


Recommended Dietary Allowances for Iron for Infants (7 to 12 months),
Children, and Adults
Ages Male (mg) Female (mg)
9-13 years 8mg/d 8mg/d
14-18 years 11 mg/d 15 mg/d


<<snip>>
the requirement for absorbed iron was estimated to be 1.46 mg/d for
males and 1.15 mg/d for females.
<<snip>>


Which seems even at the low of 8 to be MUCH higher than required .. ?


http://www.beefinfo.org/bh_iron.cfm


And since a growing adolescent is the SAME .. basically .. as an adult
in REQUIRED iron .. according to the same .. researchers .. then one
might .. presume .. the calculations for REQUIRED iron in an adult ..
may ALSO .. be .. skewed / wrong .. ?

---------------------------------------------------------------------------限?-----------

sirmi...@neobee.net

unread,
Jan 5, 2006, 5:27:10 AM1/5/06
to
Dear All,
I`m writing to You, in the name of our club, hoping that You will join
us in humanitarian action "RIDE BICYCLE AGAINST DRUGS, ALCOHOL AND
VIOLENCE". After January 1., 2006. this action will become program
named "WHEEL OF ENJOYMENT". This program is supported by Ministry
of health Republic of Serbia, Ministry of labour, employment and
social policy Republic of Serbia and Ministry of education and sport
Republic of Serbia.
Program "WHEEL OF ENJOYMENT" also includes actions "Cancer is
hard, Friendship is easier" and "Diabetes has its enemy"
dedicated to people with cancer and diabetes.
Bicycling club " SIRMIUM BIKE INTERNATIONAL" from Sremska Mitrovica
is promoter and initiator of this program. Beside bicycling
promotion, this program`s goal is to build Rehabilitation center for
addiction diseases, too.
After January 1., 2006. our multiethnic bike team will ride again
across Serbia and districts of Kosovo.
In Jun 2006. we will ride trough Europe with same goal to pay
attention on existing problems of addiction diseases, cancer and
diabetes.
We invited great number of economic subjects in country and abroad, to
join us in this program giving their support.
We asking You, too, to join us and to give us your support or to
direct us to competent humanitarian, financial and medical
institutions.

Sincerely,


President of bicycling club

"SIRMIUM BIKE INTERNATIONAL"

and program`s coordinator
Mr. Kamenko Vladisavljevic

ironj...@aol.com

unread,
Jan 6, 2006, 8:56:35 PM1/6/06
to
>>Just a question..... You are all over these newsgroups......What is this
iron stuff to you?<<

I am just a joe ..
Twenty-five years ago my mother was dying of athersclerosis and the
doctors were incapable of inducing remission.

I studied health and nutrition and got pretty good.

She continued and died and I never thought a thing more about it.

Never entered the health field or anything close.

I was sitting at my doctors' one day reading a People magazine .. and
the article says .. "Is Iron A Killer?"

What is this .. ? I must of missed this ..

I go on to read about a Dr. Sullivan and how he has been for over
twenty years attempting to explain to his peers at medical conferences
he is finding large amounts of iron in the hearts of his patients.

He explains how he believes it is due to our high meat based western
diet and how the iron from meat is so easily absorbed as opposed to
iron from any other source.

He made such a good case against iron I wonder whether this is the
oxidation Linus Pauling had spoken to but couldn't find.

I decided to find the number one enemy of iron and make sure I included
that in my diet.
You know how they spell out .. don't take this supplement with this
supplement because it won't be absorbed?

Unleavened bread ..

I had been raised a Catholic .. and I was kinda stopped in my tracks ..

No eating meat on Friday .. no fish even at one time ..

In a book about a .. healer .. ?

I ran with it and found man is a herbivore .. and the gradual increase
of iron in the body .. from the blood / meat / creature he eats ..kills
..

Simple .. stuff ..

Chris Ness

unread,
Jan 7, 2006, 9:54:34 AM1/7/06
to
ironj...@aol.com wrote:

>>>Just a question..... You are all over these newsgroups......What is this

And Anemia is?

Tom Hennessy

unread,
Jan 7, 2006, 9:40:11 PM1/7/06
to

>>And Anemia is?<<

'Anemia' is NOT .. always .. 'iron deficient' anemia.

There are many types of anemia.

The 'high prevalence' of anemia which is considered to BE .. 'iron
deficient' anemia is recognized as such for a few different reasons.

Improper diagnostic .. methods .. improper .. diagnostic MARKERS ..

http://tinyurl.com/bwrxd

Nutrition
"The diagnostic criteria for iron deficiency in infants should be
reevaluated."


Acta Paediatr. 2004 Apr;93(4):436-9. Related Articles, Links


Iron deficiency and iron deficiency anaemia during infancy and
childhood.


Zetterstrom R.


The present definition of iron deficiency and iron deficiency anaemia
is under
debate. Our present figures for the prevalence of iron deficiency in
infants
and toddlers are thus disputed. CONCLUSION: Better understanding of the


regulation of iron metabolism and requirement during the critical early
period
of growth and development is needed for relevant control of iron
deficiency
anaemia.


Publication Types:
Editorial


PMID: 15188964 [PubMed - in process]


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

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

http://www.ajcn.org/cgi/content/abstract/82/2/380

Only a small proportion of anemia in northeast Thai schoolchildren is
associated with iron deficiency.

Thurlow RA, Winichagoon P, Green T, Wasantwisut E, Pongcharoen T,
Bailey KB, Gibson RS
Am J Clin Nutr. 2005 Aug ; 82(2): 380-7

CONCLUSIONS:
Hemoglobinopathies, suboptimal vitamin A status, and age were the major
predictors of hemoglobin concentration. The contribution of iron
deficiency
to anemia was low, and its detection was complicated by coexisting
suboptimal vitamin A status.

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

When .. CLOSELY .. observed .. the population .. 'considered' .. to ..
BE .. 'low' in iron / iron deficient anemia .. WERE NOT .. in fact ..
iron deficient .. at all ..


They were .. IN FACT .. not .. iron deficient ..


Extrapolate .. that .. TO .. the rest of the world .. as EVIDENCED ..
by .. medical studies .. which state the MARKER used
to diagnose iron deficiency is .. WRONG .. and voila ..


Using the wrong markers TO assess anemia
. you wind up with MANY people 'iron deficient' .. when .. IN FACT ..
very FEW .. are .. iron 'deficient' ..

http://www.vegsoc.org/info/iron.html

<<quote>>
Despite iron from plant foods being less readily absorbed research has
shown that vegetarians are no more likely to suffer from iron
deficiency than non-vegetarians. Draper & Wheeler (1989) have stated
there is no indication of increased prevalence of iron deficiency
amongst vegetarians. Anderson (1981) found the iron status of long-term
vegetarian women to be adequate, despite a high intake of fibre and
phytate.


Anderson, B. et al. (1981). The iron and zinc status of long-term
vegetarian women. American Journal of Clinical Nutrition v.34 (6)
p.1042-1048.


Draper, A. & Wheeler, E. (1989). The diet and food choice of
vegetarians in Greater London. Centre of Human Nutrition, London
----------------------------------------------------------------------
----------------------------------------------------------------------

According to the article below .. iron reduction in THIS disease ..
leads to ..
IMPROVED .. anemia ..

http://tinyurl.com/e3ztj

Clin Exp Rheumatol. 1986
Jan-Mar;4(1):25-9. Related Articles, Links


Antianemic and potential anti-inflammatory activity of desferrioxamine:
possible usefulness in rheumatoid arthritis.


Giordano N, Sancasciani S, Borghi C, Fioravanti A, Marcolongo R.

Desferrioxamine seems to be useful in the
treatment of patients suffering from RA and anemia, in order to release
iron
from synovial tissue, reduce the inflammatory process and improve
anemia,
changing an anemia which is typically resistant to the martial therapy
into an
iron-sensitive anemia.


Publication Types:
Clinical Trial


PMID: 3516495 [PubMed - indexed for MEDLINE]


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

Inflammatory disorders are known to cause anemia .. not iron deficient
anemia
. but lack of rebuilding of red blood cells.. or anemia of chronic
disease .
This anemia is commonly treated with iron when in fact the underlying
disease
is to be treated which reduces the incidence of anemia.

http://tinyurl.com/8hrp6

Oncology (Huntingt) 2002 Sep;16(9 Suppl 10):25-33


Iron and the anemia of chronic disease.


Spivak JL
Division of Hematology, Johns Hopkins University, School of Medicine,
Baltimore, Maryland, USA.

This refutes the concept that the lack of available iron is central to
the
pathogenesis of the syndrome. Indeed, it is highly likely that
abnormalities
such as reduced iron absorption and decreased erythroblast
transferrin-receptor
expression largely result from decreased erythropoietin production and
inhibition of its activity by inflammatory cytokines.


PMID: 12380952, UI: 22267988


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


Lack of tocopherol will disallow the use of iron .. as evidenced below
in
hemolytic anemia {treated in astronauts with the same .. vitamin E]

http://tinyurl.com/aqk4n

Clin Pediatr (Phila) 1994 Jan;33(1):2-7


Severe hemolytic anemia associated with vitamin E deficiency in infants
with
cystic fibrosis. Implications for neonatal screening.


Wilfond BS, Farrell PM, Laxova A, Mischler E
Department of Pediatrics, University of Wisconsin-Madison 53792-4108.

Oral administration of alpha-tocopherol resulted in rapid
correction of the in vitro hemolysis and improvement of in vivo
hematologic
indices. Investigation of these patients supports the conclusion that
the
hemolytic anemia of infancy in CF is caused by vitamin E deficiency and
should
be treated promptly with 50 IU/day of vitamin E.

PMID: 8156723, UI: 94208196

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

Who loves ya.
Tom


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


--
Sent via Health Newsgroups
http://www.healthnewsgroups.com

ironj...@aol.com

unread,
Jan 8, 2006, 8:04:17 PM1/8/06
to
>>And Anemia is?<<

You mean .. what is .. iron deficient .. anemia .. ?

That is when you have a person who is bleeding internally or externally
.. and that continues for quite some time ..

Or you have a person who is malnourished / starving for quite some time
..

Or it is when the person diagnosing anemia .. uses a marker to ..
diagnose anemia .. which is skewed ..

<<quote>>
'The diagnostic criteria for iron deficiency in infants should be
reevaluated"

Acta Paediatr. 2004 Apr;93(4):436-9. Related Articles, Links


Iron deficiency and iron deficiency anaemia during infancy and
childhood.


Zetterstrom R.


The present definition of iron deficiency and iron deficiency anaemia
is under
debate. Our present figures for the prevalence of iron deficiency in
infants
and toddlers are thus disputed. CONCLUSION: Better understanding of the

regulation of iron metabolism and requirement during the critical early

period
of growth and development is needed for relevant control of iron
deficiency
anaemia.


Publication Types:
Editorial


PMID: 15188964 [PubMed - in process]


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

------


DGReview


Inadequate Definition Of Iron Deficiency In Infancy A DGReview of :"The

diagnostic criteria for iron deficiency in infants should be
reevaluated."

Nutrition
12/20/2002
By Robert Short


The current definitions for iron deficiency and iron deficiency anaemia

in
infants are inadequate and need evaluation.


A study of 263 exclusively breast-fed infants in Honduras and Sweden
who were
randomly assigned to receive iron supplementation or placebo has led
researchers in Sweden and the United States to this conclusion.


Blood samples were taken from the children at age 4, 6 and 9 months.
Reference
ranges were determined using three different approaches for defining
iron-replete infants. The researchers evaluated various variables for
predicting the haemoglobin response to iron.


Dr M Domellof, from the Department of Clinical Sciences, Pediatrics,
Umea
University, Umea, Sweden, said, "The haemoglobin response to iron was
not a
useful definition of iron deficiency anaemia at 4 months of age.
Haemoglobin,
mean cell volume, and zinc protoporphyrin at 6 months as well as growth

variables predicted the haemoglobin response at 6-9 months, but
ferritin and
soluble transferrin receptors at 6 months did not."


The investigators concluded that there was a need for a re-evaluation
of the
definitions of iron deficiency and iron deficiency anaemia.


They had set out to establish the cut-off values for the different
variables.
They found the two standard deviation cut-off values in iron-replete
infants to
be as follows: haemoglobin <105 g/L at 4-6 months and <100 g/L at 9
months;
zinc protoporphyrin >75 micro mol/mol haem at 4.6 months and >90 micro
mol/mol
haem at 9 months; ferritin <20 micro g/L at 4 mo, <9 micro g/L at 6 mo
and <5
micro g/L at 9 mo; and soluble transferrin receptors >11 mg/L at 4-9
months.


Nutrition
"The diagnostic criteria for iron deficiency in infants should be
reevaluated."


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

There is no iron deficient anemia in a fed society ..

Anemia of chronic disease is when the body 'locks up' / sequesters iron
away FROM the invader. Part of the immune system.

<<quote>>


Iron and the anemia of chronic disease.


Spivak JL
Division of Hematology, Johns Hopkins University, School of Medicine,
Baltimore, Maryland, USA.


[Medline record in process]


The anemia of chronic disease traditionally is defined as a
hypoproliferative
anemia of no apparent cause that occurs in association with an
inflammatory,
infectious, or neoplastic disorder, and resolves when the underlying
disorder
is corrected. Disordered iron metabolism as manifested by a low serum
iron,
decreased serum transferrin, decreased transferrin saturation,
increased serum
ferritin, increased reticuloendothelial iron stores, increased
erythrocyte-free
protoporphyrin, and reduced iron absorption, is a characteristic
feature of the
anemia of chronic disease and has been thought to be a major factor
contributing to the syndrome. A mild shortening of red cell life span
also
occurs. However, we now know that impaired erythropoietin production
and
impaired responsiveness of erythroid progenitor cells to this hormone
are also
important abnormalities contributing to the anemia of chronic disease,
and
appear to be due to the effects of inflammatory cytokines. Increased
intracellular iron may also have a role in the inhibition of
erythropoietin
production, since the oxygen sensor is a hemoprotein. While the role of

inflammatory cytokines in the pathogenesis of anemia of chronic disease
appears
unequivocal, it has become apparent that disordered iron metabolism,
while
characteristic of this form of anemia, may not be central to its
pathogenesis.
It is undisputed that iron absorption is reduced, and that iron
administered
intravenously is rapidly sequestered in the reticuloendothelial system;

however, iron delivery to the bone marrow is not impaired, and
erythroid iron
utilization is not markedly depressed in anemia of chronic disease.
Importantly, recombinant erythropoietin therapy can correct the anemia
of
chronic disease, but it cannot correct the anemia due to iron
deficiency. This


refutes the concept that the lack of available iron is central to the
pathogenesis of the syndrome. Indeed, it is highly likely that
abnormalities
such as reduced iron absorption and decreased erythroblast
transferrin-receptor
expression largely result from decreased erythropoietin production and
inhibition of its activity by inflammatory cytokines.


PMID: 12380952, UI: 22267988


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

Only a small proportion of anemia in northeast Thai schoolchildren is


associated with iron deficiency.
Thurlow RA, Winichagoon P, Green T, Wasantwisut E, Pongcharoen T,
Bailey KB, Gibson RS
Am J Clin Nutr. 2005 Aug ; 82(2): 380-7


BACKGROUND: Iron deficiency is assumed to be the major cause of anemia
in northeast Thailand, but other factors may be involved. OBJECTIVE: We

determined the prevalence of anemia among schoolchildren in northeast
Thailand and the role of hemoglobinopathies, selected micronutrient
deficiencies, and other factors in hemoglobin status. DESIGN: Blood
samples were collected from 567 children aged 6-12.9 y attending 10
primary schools for the determination of a complete blood count and
hemoglobin type [Hb AA (normal hemoglobin), Hb AE (heterozygous for Hb
type E), and Hb EE (homozygous for Hb type E)] and the measurement of
serum ferritin, transferrin receptor, retinol, vitamin B-12, and plasma

and erythrocyte folate concentrations. Children with a C-reactive
protein concentration >/=10 mg/L (n = 12), which indicated infection,
were excluded. RESULTS: The prevalence of anemia was 31%. Age,
hemoglobin type, and serum retinol were the major predictors of
hemoglobin concentration. Hb AA and Hb AE children with anemia had
lower (P < 0.01) hematocrit, mean cell volume, and serum retinol values

than did their nonanemic counterparts; no significant differences in
serum ferritin were found by hemoglobin type. Only 16% (n = 22) of the
anemic Hb AA and Hb AE children were iron deficient. Hb AA and Hb AE
children with a serum retinol concentration <0.70 mumol/L (n = 14) had
a significantly higher geometric mean serum ferritin concentration than

did those with a retinol concentration >/=0.70 mumol/L (P = 0.009); no
significant difference in transferrin receptor concentrations was found

between these 2 groups. CONCLUSIONS: Hemoglobinopathies, suboptimal


vitamin A status, and age were the major predictors of hemoglobin
concentration. The contribution of iron deficiency to anemia was low,
and its detection was complicated by coexisting suboptimal vitamin A
status.

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

Iron is there and so are .. iron deficiency 'markers' ..

<<snip>>
Excessive iron depositions are found in the brain, liver, pancreas, and
other
parenchymal cells, but plasma iron concentrations are decreased
<<snip>>


Ann N Y Acad Sci. 2004 Mar;1012:267-81. Related Articles, Links


Hereditary causes of disturbed iron homeostasis in the central nervous
system.


Ponka P.


Lady Davis Institute for Medical Research, Sir Mortimer B. Davis Jewish
General
Hospital, Department of Physiology and Medicine, McGill University,
Montreal,
Quebec, Canada. prem.po...@mcgill.ca


Iron is essential for oxidation-reduction catalysis and bioenergetics;
however,
unless appropriately shielded, this metal plays a crucial role in the
formation
of toxic oxygen radicals that can attack all biological molecules.
Organisms
are equipped with specific proteins designed for iron acquisition,
export and
transport, and storage, as well as with sophisticated mechanisms that
maintain
the intracellular labile iron pool at an appropriate level. Despite
these
homeostatic mechanisms, organisms often face the threat of either iron
deficiency or iron overload. This review describes several hereditary
iron-overloading conditions that are confined to the brain. Recently, a

mutation in the L-subunit of ferritin has been described that causes
the
formation of aberrant L-ferritin with an altered C-terminus.
Individuals with
this mutation in one allele of L-ferritin have abnormal aggregates of
ferritin
and iron in the brain, primarily in the globus pallidus. Patients with
this
dominantly inherited late-onset disease present with symptoms of
extrapyramidal
dysfunction. Mice with a targeted disruption of a gene for iron
regulatory
protein 2 (IRP2), a translational repressor of ferritin, misregulate
iron
metabolism in the intestinal mucosa and the central nervous system.
Significant
amounts of ferritin and iron accumulate in white matter tracts and
nuclei, and
adult IRP2-deficient mice develop a movement disorder consisting of
ataxia,
bradykinesia, and tremor. Mutations in the frataxin gene are
responsible for
Friedreich's ataxia, the most common of the inherited ataxias. Frataxin
appears
to regulate mitochondrial iron-sulfur cluster formation, and the
neurologic and
cardiac manifestations of Friedreich's ataxia are due to iron-mediated
mitochondrial toxicity. Patients with Hallervorden-Spatz syndrome, an
autosomal
recessive, progressive neurodegenerative disorder, have mutations in a
novel
pantothenate kinase gene (PANK2). The cardinal feature of this
extrapyramidal
disease is pathologic iron accumulation in the globus pallidus. The
defect in
PANK2 is predicted to cause the accumulation of cysteine, which binds
iron and
causes oxidative stress in the iron-rich globus pallidus. Finally,
aceruloplasminemia is an autosomal recessive disorder of iron
metabolism caused
by loss-of-function mutations in ceruloplasmin gene that leads to
misregulation
of both systemic and central nervous system iron trafficking. Affected
individuals suffer from extrapyramidal signs, cerebellar ataxia,
progressive
neurodegeneration of retina, and diabetes mellitus. Excessive iron
depositions
are found in the brain, liver, pancreas, and other parenchymal cells,
but
plasma iron concentrations are decreased. These conditions are not
common, but
awareness about them is important for differential diagnosis of various

neurodegenerative disorders.


Publication Types:
Review
Review, Tutorial


PMID: 15105272 [PubMed - indexed for MEDLINE]


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

------


In those with KNOWN iron overload .. the REASON they present to the
doctor in
many cases IS .. anemia .. NOT 'iron deficient' anemia .. and the
doctor
mistakenly .. GIVES them iron .. which kills them ..


Am J Clin Pathol 1983 Nov;80(5):743-5 Serum ferritin and
sequestered
stores of body iron. Rao KR, Ray VH, Patel AR A 47-year-old
man with
sickle cell anemia, chronic cor pulmonale, and congestive heart
failure died
following a short illness. A diagnosis of iron deficiency was
established
during life by usually accepted criteria including a low serum
ferritin
concentration. Autopsy showed no stainable iron in the bone marrow,
liver,
and the heart. Marked deposits of iron were seen in the kidneys and
the
atrophic spleen. These findings suggest that the serum ferritin
concentration
may not reflect the metabolically sequestered stores of iron in the
spleen
and the kidneys. PMID: 6195914, UI: 84049241
-----------------------------------------------------------------------------------


Lack of tocopherol will disallow the use of iron .. as evidenced below
in
hemolytic anemia {treated in astronauts with the same .. vitamin E]

Clin Pediatr (Phila) 1994 Jan;33(1):2-7


Severe hemolytic anemia associated with vitamin E deficiency in infants
with
cystic fibrosis. Implications for neonatal screening.


Wilfond BS, Farrell PM, Laxova A, Mischler E

Department of Pediatrics, University of Wisconsin-Madison 53792-4108.


Three infants are described with cystic fibrosis (CF) and malnutrition
leading
to severe anemia beginning as early as 6 weeks of age. Laboratory
studies
demonstrated high reticulocyte counts, negative Coombs' tests, abnormal

peroxide hemolysis test results, and biochemical evidence of vitamin E
deficiency. Oral administration of alpha-tocopherol resulted in rapid


correction of the in vitro hemolysis and improvement of in vivo
hematologic
indices. Investigation of these patients supports the conclusion that
the
hemolytic anemia of infancy in CF is caused by vitamin E deficiency and
should

be treated promptly with 50 IU/day of vitamin E. Because two of the
three
patients were identified in a CF screening/surveillance program, we can

estimate that the frequency of clinically significant anemia in CF
infants is
4%. Our observations demonstrate a potential advantage of CF neonatal
screening
for individual patients susceptible to vitamin E-deficient hemolytic
anemia and
suggest that confirmatory follow-up diagnostic studies, such as sweat
tests,
should be performed by 4 to 6 weeks of age.


PMID: 8156723, UI: 94208196
----------------------------------------------------------------------------------

According to the article below .. iron reduction in THIS disease ..
leads to ..
IMPROVED .. anemia ..

So .. according to THIS article .. anemia .. does NOT .. necessarily ..
mean ..
iron deficiency ..


So since iron has been implicated IN the CAUSE of .. diabetes .. and
since
anemia is ONE of your .. problems .. then .. as I said before .. epogen
/
erythropoeitin is NOT .. necessarily .. your ONLY .. option ..


One might .. consider .. the effect of iron reduction .. as evidenced
.. below
..


REDUCTION .. of .. anemia ..


GuyClin Exp Rheumatol. 1986


Jan-Mar;4(1):25-9. Related Articles, Links


Antianemic and potential anti-inflammatory activity of desferrioxamine:

possible usefulness in rheumatoid arthritis.


Giordano N, Sancasciani S, Borghi C, Fioravanti A, Marcolongo R.


In order to study the role of excessive synovial iron sequestration in
the
production of anemia in rheumatoid arthritis (RA), the antianemic
efficacy and
anti-inflammatory effect of desferrioxamine administered in a
short-term
treatment (14 days), were evaluated in 10 patients suffering from
classic or
definite RA and hyposideremic anemia. Treatment with desferrioxamine
showed an
elevated urinary iron excretion, a significant increase of serum iron,
UIBC and
hemoglobin, and a marked progressive decrease of serum ferritin. A
moderate
improvement of the pain intensity, morning stiffness and Ritchie's
index was
also observed. The results obtained suggest that excessive
reticuloendothelial
iron deposits occur in RA and that the iron uptake can be an important
factor
in the production of anemia. Desferrioxamine seems to be useful in the


treatment of patients suffering from RA and anemia, in order to release
iron
from synovial tissue, reduce the inflammatory process and improve
anemia,
changing an anemia which is typically resistant to the martial therapy
into an
iron-sensitive anemia.


Publication Types:
Clinical Trial


PMID: 3516495 [PubMed - indexed for MEDLINE]


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