Various Topics on Alternative Medicine

..onjusti.. ..l.c..

http://www.findarticles.com/p/articl...07/ai_n9001606

http://tinyurl.com/787m4

Chronic iron overload and toxicity: Clinical chemistry perspective
Clinical Laboratory Science, Summer 2001 by Kang, Jae O


FOCUS: IRON OVERLOAD

The content of body iron is regulated primarily by absorption since
humans have no physiological mechanism by which excess iron is
excreted. This regulation, however, is not absolute. Many factors such
as the content of diets, iron doses, life styles, etc. influence iron
absorption. In the past, nutrition programs for iron fortification and
the ingestion of iron preparations have been widely practiced because
of the seriousness of worldwide iron deficiency. Also, we now know that
a significant number of asymptomatic people carry the hemochromatosis
gene, HFE, indicating that these people have the potential to
ac***ulate excess body iron in their lifetime. Excess body iron can be
highly toxic. This toxicity involves many organs leading to a variety
of serious diseases such as liver disease, heart disease, diabetes
mellitus, hormonal abnormalities, dysfunctional immune system, etc. The
tissue damage ***ociated with iron overload is believed to result
primarily from free radical reactions mediated by iron. Iron is an
effective catalyst in free radical reactions. The diseases ***ociated
with iron overload can be managed effectively or prevented. Therefore,
early diagnosis of iron overload and appropriate therapy are critical.
By providing the necessary laboratory data, clinical chemistry
laboratories can play the pivotal role in the management of these
health problems.

INDEX TERMS: clinical chemistry laboratories; diagnosis; free radical
reactions; hemochromatosis; iron overload; iron toxicity.

Clin Lab Sci 2001; 14(3):209

LEARNING OBJECTIVES

1 . Describe the regulation of iron absorption.

2. List the three primary causes of iron overload.

3. Describe various chronic diseases ***ociated with secondary iron
overload and the mechanisms involved.

4. Contrast the absorption process for heme iron with that for non-heme
iron.

5. List compounds in the diet that inhibit iron absorption and those
that enhance iron absorption.

6. List the organs most frequently damaged by hemachromatosis.

7. Identify the clinical chemistry laboratory procedures that would
detect damage to each of the organs most frequently damaged by
hemachromatosis.

8. Discuss the biochemical theories most often proposed to explain the
mechanisms that cause tissue damage due to excess iron.

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

..

Iron overload, is that kinda like the cartoons when a character has an
anvil fall on his head or when someone gets impaled on a metal fence or
a pipe? Stepping on a nail? Too many nose rings or piercings? Smashing
ones thumb with a hammer? I can see how that might be a health problem.

TC

ironjustice@aol.com wrote:
>
http://www.findarticles.com/p/articl...07/ai_n9001606
>
> http://tinyurl.com/787m4
>
> Chronic iron overload and toxicity: Clinical chemistry perspective
> Clinical Laboratory Science, Summer 2001 by Kang, Jae O
>
>
> FOCUS: IRON OVERLOAD
>
> The content of body iron is regulated primarily by absorption since
> humans have no physiological mechanism by which excess iron is
> excreted. This regulation, however, is not absolute. Many factors
such
> as the content of diets, iron doses, life styles, etc. influence iron
> absorption. In the past, nutrition programs for iron fortification
and
> the ingestion of iron preparations have been widely practiced because
> of the seriousness of worldwide iron deficiency. Also, we now know
that
> a significant number of asymptomatic people carry the hemochromatosis
> gene, HFE, indicating that these people have the potential to
> ac***ulate excess body iron in their lifetime. Excess body iron can
be
> highly toxic. This toxicity involves many organs leading to a variety
> of serious diseases such as liver disease, heart disease, diabetes
> mellitus, hormonal abnormalities, dysfunctional immune system, etc.
The
> tissue damage ***ociated with iron overload is believed to result
> primarily from free radical reactions mediated by iron. Iron is an
> effective catalyst in free radical reactions. The diseases ***ociated
> with iron overload can be managed effectively or prevented.
Therefore,
> early diagnosis of iron overload and appropriate therapy are
critical.
> By providing the necessary laboratory data, clinical chemistry
> laboratories can play the pivotal role in the management of these
> health problems.
>
> INDEX TERMS: clinical chemistry laboratories; diagnosis; free radical
> reactions; hemochromatosis; iron overload; iron toxicity.
>
> Clin Lab Sci 2001; 14(3):209
>
> LEARNING OBJECTIVES
>
> 1 . Describe the regulation of iron absorption.
>
> 2. List the three primary causes of iron overload.
>
> 3. Describe various chronic diseases ***ociated with secondary iron
> overload and the mechanisms involved.
>
> 4. Contrast the absorption process for heme iron with that for
non-heme
> iron.
>
> 5. List compounds in the diet that inhibit iron absorption and those
> that enhance iron absorption.
>
> 6. List the organs most frequently damaged by hemachromatosis.
>
> 7. Identify the clinical chemistry laboratory procedures that would
> detect damage to each of the organs most frequently damaged by
> hemachromatosis.
>
> 8. Discuss the biochemical theories most often proposed to explain
the
> mechanisms that cause tissue damage due to excess iron.
>
> 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

..m ..nnes.. ..a ..dKB.c..

The gist of the article .. pertaining TO .. those without the ability TO ..
understand .. the article .. TC .. included .. IS .. iron absorption is
CONTROLLED .. and .. blood iron / heme iron is .. NOT .. controlled ..
therefore leading to PROGRESSIVELY .. higher and higher and higher iron ..
stores .. until one gets .. iron .. poisoning ..

Pretty .. simple .. stuff ..

For .. some ..

Heh .. heh ..

<<snip>>
The content of body iron is regulated primarily by absorption since
humans have no physiological mechanism by which excess iron is
excreted.
<<snip>>

ADAPTATION IN IRON ABSORPTION: DAILY IRON SUPPLEMENTATION DECREASES
ABSORPTION EFFICIENCY OF NONHEME, BUT NOT HEME IRON, FROM FOOD AND
SLIGHTLY INCREASES SERUM FERRITIN IN NORMAL VOLUNTEERS

Author(s):
ROUGHEAD ZAMZAM K
HUNT JANET R


Interpretive Summary:
There are two types of iron in our diet (heme and nonheme). Although we
know
that the body can adapt the absorption of iron depending on its
needs and how much iron is in the food, it is not clear if it handles
these
two types of iron differently. This iron supplementation study was designed
to test for differences in adaptation of heme and nonheme iron
absorption and
to evaluate if iron stores change with supplementation with iron and if
these changes persist once supplementation is stopped. Healthy men and
women
took either a daily supplement of 50 mg of iron or placebo for 12
weeks. Heme and nonheme Fe absorption from a meal of hamburger, french
fries,
and milk shake were measured before and after 12 weeks of
supplementation. Also, serum ferritin which indicates iron stores, was
measured with supplementation and 6 months after supplementation was
stopped. We found that with daily iron supplementation, healthy
individuals

*****
ADAPTED to DECREASE their nonheme, but NOT heme iron absorption from
food. ******

This indicates that the body handles heme and nonheme iron differently
and that there may be more control over the absorption of nonheme
iron than heme iron. Also, we found a small increase in iron stores
with
supplementation and those who had lower iron stores tended to show more
increase than those with higher iron stores. This increase in iron
stores
tended to persist 6 months after iron supplementation was stopped.

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

--
Message posted via http://www.medkb.com

..te..

tom hennessy via MedKB.com wrote:
> The gist of the article .. pertaining TO .. those without the ability
TO ..
> understand .. the article .. TC .. included .. IS .. iron absorption
is
> CONTROLLED .. and .. blood iron / heme iron is .. NOT .. controlled
...
> therefore leading to PROGRESSIVELY .. higher and higher and higher
iron ..
> stores .. until one gets .. iron .. poisoning ..
>
> Pretty .. simple .. stuff ..

The study shows, as expected, that non-heme (plant-based) iron
contributes primarily to free-iron, but does *not* show that
plant-based iron does not store. Obviously, it does both. I agree
with your view that plant-based iron is more safely handled per unit of
m*** than animal iron. This is why people should not eat large amounts
of meat. 5-8oz once a day is probably safe.

That heme iron has been shown to be the main potentiator of excess iron
storage was predictable. However, the study does not support the idea
that meat-eaters universally experience excess iron. In fact, the
study does not evaluate whether meat eaters in general are likely to
experience iron toxicity; only a long-term study could show this. What
it *does* show is that heme iron is more easily stored than plant-based
iron, and that over-consumption of meat is not a good idea.

On the other hand, doctors who prescribe non-heme iron (plant-based or
chelated) to anaemic patients are making a big mistake. Only heme iron
should be prescribed to anaemic individuals in order to correct
depressed iron stores. If one is vegan, one will not take heme-iron
because it is an animal product. That's unfortunate, because depressed
iron stores present a health risk to non meat-eaters. It works both
ways.

PeterB

..onjusti.. ..l.c..

>>(plant based iron) contributes primarily to free-iron<<

SHOW .. where .. it says .. that ..

Says no such thing ..

Says the body downregulates the absorption of plant iron but NOT ..
meat iron / blood iron / heme iron ..

*****
ADAPTED to DECREASE their nonheme, but NOT heme iron absorption from
food. ******

>>depressed iron stores<<

That would be the 'take' of the SAME PEOPLE .. who said there was no
problem with .. iron ..

That would be the same people who are now FACED with iron overload of
epidemic proportions ..

Eh ..

I would tend to believe iron researchers who say iron STORES are not ..
required ..

If you have red blood cells of a .. safe .. level .. which according to
RECENT research should not be interfered with .. UNLESS .. they are
below .. 9 for hemoglobin .. which is much lower than the level at
which doctors .. YOUR .. doctors believe should NEVER ..be .. 'allowed'
...

So in effect .. by refusing to allow the iron stores to get below a
certain level 'they' .. ARE .. in fact .. interfering .. WITH .. the ..
patient / normal human process ..

>>doctors who prescribe non-heme iron<<

So in effect you are saying a vegetarian diet will allow one to die of
... lack .. of .. iron ..

If you present an 'iron deficient' .. person .. a TRULY .. iron
DEFICIENT .. person WITH a plant based iron .. he is capable of
absorbing up to 80% .. of .. the iron .. and you seem to disagree with
the evidence ..

You seem to think one HAS to have blood in order to induce the
absorption of ENOUGH iron to continue .. good .. health ..

The studies don't support .. it ..

THAT is WHY .. you .. don't .. include .. studies ..

Eh ..

Heh .. heh ..

Who loves ya.
Tom

..te..

ironjustice@aol.com wrote:
> >>(plant based iron) contributes primarily to free-iron<<
>
> SHOW .. where .. it says .. that ..
>
> Says no such thing ..

Tom, the following link will give you foundational knowledge about iron
metabolization. I hope you'll study it and see if it doesn't broaden
your understanding.
http://www-medlib.med.utah.edu/WebPa...IRON/IRON.html.

> Says the body downregulates the absorption of plant iron but NOT ..
> meat iron / blood iron / heme iron ..
>
> *****
> ADAPTED to DECREASE their nonheme, but NOT heme iron absorption from
> food. ******
>
> >>depressed iron stores<<
>
> That would be the 'take' of the SAME PEOPLE .. who said there was no
> problem with .. iron ..
>
> That would be the same people who are now FACED with iron overload of
> epidemic proportions ..
>
> Eh ..
>
> I would tend to believe iron researchers who say iron STORES are not
...
> required ..

A small amount of stored iron is required in human biology. In fact,
it's impossible NOT to have stored iron, even as a vegan. Researchers
have not said otherwise.
>
> If you have red blood cells of a .. safe .. level .. which according
to
> RECENT research should not be interfered with .. UNLESS .. they are
> below .. 9 for hemoglobin .. which is much lower than the level at
> which doctors .. YOUR .. doctors believe should NEVER ..be ..
'allowed'
> ..
>
> So in effect .. by refusing to allow the iron stores to get below a
> certain level 'they' .. ARE .. in fact .. interfering .. WITH .. the
...
> patient / normal human process ..

I agree that reducing meat consumption is wise. I don't agree, though,
that man in an herbivore by nature. At any rate, the optimal level of
stored iron is highly individual, a factor of genetics and even
environment.

> >>doctors who prescribe non-heme iron<<
>
> So in effect you are saying a vegetarian diet will allow one to die
of
> .. lack .. of .. iron ..

No. There *may be* evidence that vegans don't store quite enough iron
to satisfy all their metabolic demands, but it doesn't effect their
lifespan. If optimal health is lacking in vegetarians, my view is that
it's due to depletion of nutrients in the agriculture, not their
aversion to meat. Of course, that means meat-eaters are in exactly the
same boat. The difference is that vegans are vulnerable to both b12
and iron deficiencies, whereas meat-eaters are not. I would never say,
though, that meat-eaters are healthier. I observe that heme iron
intake makes one more robust. To say that such robustness comes at a
price is probably defensible. The oxidation properties of iron almost
certainly contribute to an increase in glycation. But that doesn't
mean we can live without stored iron. So, what is the optimal balance
of iron intake considering a variable rate of absorption, storage, and
consumption in myriad metabolic processes over time? No one knows.
All we know is that supplements can help us compensate for our
declining agriculture. For vegetarians, that means supplemental b12,
and perhaps iron, perferrably heme.

> If you present an 'iron deficient' .. person .. a TRULY .. iron
> DEFICIENT .. person WITH a plant based iron .. he is capable of
> absorbing up to 80% .. of .. the iron .. and you seem to disagree
with
> the evidence ..

The medical literature suggests far less.

> You seem to think one HAS to have blood in order to induce the
> absorption of ENOUGH iron to continue .. good .. health ..

No, my position is that modern agriculture (even most organic) doesn't
provide adequate mineral content. It's for THAT we have to compensate.


> The studies don't support .. it ..
>
> THAT is WHY .. you .. don't .. include .. studies ..

I could find you a study to prove anything, Tom. I would rather invite
you to think.

Peter

..onjusti.. ..l.c..

>>At any rate, the optimal level of
stored iron is highly individual, a factor of genetics and even
environment. <<

The article below seems to disagree .. with .. you ..

It states .. IN .. normal people .. the soluble transferrin receptor ..
APPEARS .. at 25% transferrin saturation .. NOT .. "whatever" ..

The ONLY people it is NOT .. 25% .. are those with GENETIC iron
overload ..



Haematologica. 2005 Jan;90(1):31-7. Related Articles, Links


The soluble transferrin receptor as a marker of iron homeostasis in
normal subjects and in HFE-related hemochromatosis.

Brandao M, Oliveira JC, Bravo F, Reis J, Garrido I, Porto G.

ICBAS, Abel Salazar Institute for the Biomedical Sciences, Porto,
Portugal.

BACKGROUND AND OBJECTIVES: The soluble transferrin receptor (sTfR) is a
clinical marker of erythropoietic activity, also used in the diagnosis
of iron deficiency. In the present paper we explore the meaning of this
parameter in normal physiological conditions of iron homeostasis and in
the setting of iron overload due to hereditary hemochromatosis (HH).
DESIGN AND METHODS: Reference values for sTfR were established in a
population of 42 apparently healthy subjects, analyzed in relation to
other hematologic parameters, namely, hemoglobin (Hb), mean corpuscular
volume (MCV), transferrin saturation (TfSat) and serum ferritin. The
same analysis was done in a group of 45 patients with HH who were
homozygous for the C282Y mutation of HFE and had a wide range of TfSat
values. In addition, individual serial profiles were analyzed in three
patients. RESULTS: In normal subjects circulating sTfR correlated
significantly with the TfSat level, reflecting the systemic effect of
iron availability on the erythropoietic activity in a normal
physiological steady state. A TfSat of 25% appeared as a threshold
value, below which there was a progressive increase in sTfR; this
increase in sTfR occurred concomitantly with a decrease in Hb, MCV and
serum ferritin. In HH patients the up-regulation of sTfR started at
TfSat values as high as 50%. INTERPRETATION AND CONCLUSIONS: The fact
that sTfR up-regulation started at higher TfSat values in HH patients
suggests that the recognition of systemic iron available for
erythropoiesis is altered in this condition. Based on these results, a
new hypothesis is advanced, proposing that the HFE protein in involved
as a sensor of systemic iron availability, via the soluble transferrin
receptor.

PMID: 15642666 [PubMed - in process]

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

>>So, what is the optimal balance
of iron intake considering a variable rate of absorption, storage, and
consumption in myriad metabolic processes over time? <<

See above ..

WHEN the soluble transferrin receptors are .. UPREGULATED .. you NOW ..
know .. iron is being ACTIVELY SOUGHT ..

Contrary to what YOU seem to think of 'variable rate of absorption' ..

It seems EVERYONE who is NOT .. genetically .. predisposed .. TO ..
iron overload begins to actively seek out iron .. WHEN the transferrin
saturation .. is 25%.

Who loves ya.
Tom

..te..

ironjustice@aol.com wrote:
> >>At any rate, the optimal level of
> stored iron is highly individual, a factor of genetics and even
> environment. <<
>
> The article below seems to disagree .. with .. you ..
>
> It states .. IN .. normal people .. the soluble transferrin receptor
...
> APPEARS .. at 25% transferrin saturation .. NOT .. "whatever" ..

Let's take a look at how one reads a study result. Reference values
always represent a group of people, therefore they are averages. We
can never ascribe a specific percentage of chemical activity to health,
and another one to illness. It just doesn't work like that. Some
people might start iron overloading at 23% transferrin saturation, but
another at 32%. The problem with reading studies so literally is that
you arrive at absolutes that don't exist. For example, no two people
in a hundred will have exactly the same percentage of transferrin
saturation. So what is "normal?" The answer is that normal is what
the greater population exhibits, but how do we know *that is OPTIMAL?*
So things gets complicated. And even THAT was not my original point.
My original point was that conditions precipiating iron saturation
levels is a factor or variable diet, variable environment, and variable
genetics. No study could ever refute that principle.

>
> Haematologica. 2005 Jan;90(1):31-7. Related Articles, Links
>
>
> The soluble transferrin receptor as a marker of iron homeostasis in
> normal subjects and in HFE-related hemochromatosis.
>
> Brandao M, Oliveira JC, Bravo F, Reis J, Garrido I, Porto G.
>
> ICBAS, Abel Salazar Institute for the Biomedical Sciences, Porto,
> Portugal.
>
> BACKGROUND AND OBJECTIVES: The soluble transferrin receptor (sTfR) is
a
> clinical marker of erythropoietic activity, also used in the
diagnosis
> of iron deficiency. In the present paper we explore the meaning of
this
> parameter in normal physiological conditions of iron homeostasis and
in
> the setting of iron overload due to hereditary hemochromatosis (HH).
> DESIGN AND METHODS: Reference values for sTfR were established in a
> population of 42 apparently healthy subjects, analyzed in relation to
> other hematologic parameters, namely, hemoglobin (Hb), mean
corpuscular
> volume (MCV), transferrin saturation (TfSat) and serum ferritin. The
> same analysis was done in a group of 45 patients with HH who were
> homozygous for the C282Y mutation of HFE and had a wide range of
TfSat
> values. In addition, individual serial profiles were analyzed in
three
> patients. RESULTS: In normal subjects circulating sTfR correlated
> significantly with the TfSat level, reflecting the systemic effect of
> iron availability on the erythropoietic activity in a normal
> physiological steady state. A TfSat of 25% appeared as a threshold
> value, below which there was a progressive increase in sTfR; this
> increase in sTfR occurred concomitantly with a decrease in Hb, MCV
and
> serum ferritin. In HH patients the up-regulation of sTfR started at
> TfSat values as high as 50%. INTERPRETATION AND CONCLUSIONS: The fact
> that sTfR up-regulation started at higher TfSat values in HH patients
> suggests that the recognition of systemic iron available for
> erythropoiesis is altered in this condition. Based on these results,
a
> new hypothesis is advanced, proposing that the HFE protein in
involved
> as a sensor of systemic iron availability, via the soluble
transferrin
> receptor.
>
> PMID: 15642666 [PubMed - in process]
>
>
--------------------------------------------------------------------------------
>
> >>So, what is the optimal balance
> of iron intake considering a variable rate of absorption, storage,
and
> consumption in myriad metabolic processes over time? <<
>
> See above ..
>
> WHEN the soluble transferrin receptors are .. UPREGULATED .. you NOW
...
> know .. iron is being ACTIVELY SOUGHT ..
>
> Contrary to what YOU seem to think of 'variable rate of absorption'
...

Variability is a constant. One in a hundred might represent the
reference value perfectly. The study abstracts don't explain this, but
it's understood. I suggest you contact a university and see if a
professor of biology doesn't agree with it. He will.

> It seems EVERYONE who is NOT .. genetically .. predisposed .. TO ..
> iron overload begins to actively seek out iron .. WHEN the
transferrin
> saturation .. is 25%.

It's just an average, and people reach it differently...

..te..

Let's take a look at how one reads a study result. Reference values
always represent a group of people, therefore they are a median value.
We can never ascribe a specific percentage of chemical activity to
health, and another one to illness. It just doesn't work like that.
Some people might start iron overloading at 23% transferrin saturation,
but another at 32%. The problem with reading studies so literally is
that you arrive at absolutes that don't exist. For example, no two
people in a hundred will have exactly the same percentage of
transferrin saturation. So what is "normal?" The answer is that
normal is what
the a studied population exhibits, it doesn't address what is
necessarily optimal. So things gets complicated. And even THAT was
not my original point. My original point was that conditions
precipiating iron saturation levels is a factor of variable diet,
variable environment, and variable genetics. No study refutes that
principle.

> Haematologica. 2005 Jan;90(1):31-7. Related Articles, Links

> The soluble transferrin receptor as a marker of iron homeostasis in
> normal subjects and in HFE-related hemochromatosis.

> Brandao M, Oliveira JC, Bravo F, Reis J, Garrido I, Porto G.

> ICBAS, Abel Salazar Institute for the Biomedical Sciences, Porto,
> Portugal.

> BACKGROUND AND OBJECTIVES: The soluble transferrin receptor (sTfR) is
a
> clinical marker of erythropoietic activity, also used in the
diagnosis
> of iron deficiency. In the present paper we explore the meaning of
this
> parameter in normal physiological conditions of iron homeostasis and
in
> the setting of iron overload due to hereditary hemochromatosis (HH).
> DESIGN AND METHODS: Reference values for sTfR were established in a
> population of 42 apparently healthy subjects, analyzed in relation to

> other hematologic parameters, namely, hemoglobin (Hb), mean
corpuscular
> volume (MCV), transferrin saturation (TfSat) and serum ferritin. The
> same analysis was done in a group of 45 patients with HH who were
> homozygous for the C282Y mutation of HFE and had a wide range of
TfSat
> values. In addition, individual serial profiles were analyzed in
three
> patients. RESULTS: In normal subjects circulating sTfR correlated
> significantly with the TfSat level, reflecting the systemic effect of

> iron availability on the erythropoietic activity in a normal
> physiological steady state. A TfSat of 25% appeared as a threshold
> value, below which there was a progressive increase in sTfR; this
> increase in sTfR occurred concomitantly with a decrease in Hb, MCV
and
> serum ferritin. In HH patients the up-regulation of sTfR started at
> TfSat values as high as 50%. INTERPRETATION AND CONCLUSIONS: The fact

> that sTfR up-regulation started at higher TfSat values in HH patients

> suggests that the recognition of systemic iron available for
> erythropoiesis is altered in this condition. Based on these results,
a
> new hypothesis is advanced, proposing that the HFE protein in
involved
> as a sensor of systemic iron availability, via the soluble
transferrin
> receptor.


> PMID: 15642666 [PubMed - in process]


------------------------------*------------------------------*--------------------


> >>So, what is the optimal balance
> of iron intake considering a variable rate of absorption, storage,
and
> consumption in myriad metabolic processes over time? <<

> See above ..

> WHEN the soluble transferrin receptors are .. UPREGULATED .. you NOW
...
> know .. iron is being ACTIVELY SOUGHT ..
> Contrary to what YOU seem to think of 'variable rate of absorption'

Variability at the macro level feeds variability at the micro level.
That's why studies don't use a single subject. One in a hundred might
represent the reference value perfectly. The study abstracts don't
explain this, it's simply understood. I suggest you contact a
university and see if a professor of biology doesn't agree with this
statement. I think you'll find he does.

> It seems EVERYONE who is NOT .. genetically .. predisposed .. TO ..
> iron overload begins to actively seek out iron .. WHEN the
transferrin
> saturation .. is 25%.

It's just a median value, and people reach it differently...

..te..

Let's take a look at how one reads a study result. Reference values
always represent a group of people, therefore they are a median value.
One individual might start iron overloading at 23% transferrin
saturation, another at 28%. The problem with reading studies so
literally is that you find yourself wanting to extrapolate to other
populations indiscriminately. No two people in a hundred will have
exactly the same percentage of transferrin saturation. What's
"normal," by the way, has nothing to do with what's "optimal," it's
simply the reference value itself, and confined to the study subjects.
My original point, though, was that conditions precipiating iron
saturation levels is a factor of variable diet, variable environment,
and variable genetics. The Macro world always impacts the micro world.
Study results don't refute that principle.

- Hide quoted text -
- Show quoted text -

> Haematologica. 2005 Jan;90(1):31-7. Related Articles, Links
> The soluble transferrin receptor as a marker of iron homeostasis in
> normal subjects and in HFE-related hemochromatosis.
> Brandao M, Oliveira JC, Bravo F, Reis J, Garrido I, Porto G.
> ICBAS, Abel Salazar Institute for the Biomedical Sciences, Porto,
> Portugal.

> BACKGROUND AND OBJECTIVES: The soluble transferrin receptor (sTfR) is
a
> clinical marker of erythropoietic activity, also used in the
diagnosis
> of iron deficiency. In the present paper we explore the meaning of
this
> parameter in normal physiological conditions of iron homeostasis and
in
> the setting of iron overload due to hereditary hemochromatosis (HH).
> DESIGN AND METHODS: Reference values for sTfR were established in a
> population of 42 apparently healthy subjects, analyzed in relation to

> other hematologic parameters, namely, hemoglobin (Hb), mean
corpuscular
> volume (MCV), transferrin saturation (TfSat) and serum ferritin. The
> same analysis was done in a group of 45 patients with HH who were
> homozygous for the C282Y mutation of HFE and had a wide range of
TfSat
> values. In addition, individual serial profiles were analyzed in
three
> patients. RESULTS: In normal subjects circulating sTfR correlated
> significantly with the TfSat level, reflecting the systemic effect of

> iron availability on the erythropoietic activity in a normal
> physiological steady state. A TfSat of 25% appeared as a threshold
> value, below which there was a progressive increase in sTfR; this
> increase in sTfR occurred concomitantly with a decrease in Hb, MCV
and
> serum ferritin. In HH patients the up-regulation of sTfR started at
> TfSat values as high as 50%. INTERPRETATION AND CONCLUSIONS: The fact

> that sTfR up-regulation started at higher TfSat values in HH patients

> suggests that the recognition of systemic iron available for
> erythropoiesis is altered in this condition. Based on these results,
a
> new hypothesis is advanced, proposing that the HFE protein in
involved
> as a sensor of systemic iron availability, via the soluble
transferrin
> receptor.
> PMID: 15642666 [PubMed - in process]
------------------------------**-----------------------------*-*--------------------

> >>So, what is the optimal balance
> of iron intake considering a variable rate of absorption, storage,
and
> consumption in myriad metabolic processes over time? <<
> See above ..
> WHEN the soluble transferrin receptors are .. UPREGULATED .. you NOW
...
> know .. iron is being ACTIVELY SOUGHT ..
> Contrary to what YOU seem to think of 'variable rate of absorption'

Again, median values are a reference point. The degree of divergence
from such a value is also unique to the marker. This is why studies
don't use a single subject. One in a hundred might represent the
reference value perfectly. The study abstracts don't explain this,
it's simply understood. I suggest you contact a university and see if
a professor of biology doesn't agree with the above statements. I
think you'll find he does.

> It seems EVERYONE who is NOT .. genetically .. predisposed .. TO ..
> iron overload begins to actively seek out iron .. WHEN the
transferrin
> saturation .. is 25%.

It's just a median value, and people reach it differently...