Re: Dietary iron is not dangerous, even heme

On Dec 24, 7:18 am, Taka <taka0...@xxxxxxxxx> wrote:1997 <<

You use studies which seem to be .. dated.

The latest studies are beginning to show the methods / laboratory
technicians have not been doing their jobs.
They have not been testing the iron levels properly .. and therefore
any studies before Jan/07 have been thrown into the trash ..

Didn't you hear that .. ?

Does the calcein-AM method assay the total cellular 'labile iron
pool'
- or only a fraction of it?
Tenopoulou M, Kurz T, Doulias PT, Galaris D, Brunk UT
Biochem J. 2007 Jan 18;

The calcein-AM (acetoxymethyl ester) method is a widely used
technique
that is supposed to assay the intracellular 'labile iron pool' (LIP).
When cells in culture are exposed to this ester, it passes the plasma
membrane and reacts with cytosolic unspecific esterases. One of the
reaction products, calcein, is a fluorochrome and a hydrophilic
alcohol
to which membranes are non-permeable and which, consequently, is
retained within the cytosol of cells. Calcein fluorescence is
quenched
following chelation of low mass labile iron, and the degree of
quenching gives an estimate of the amounts of chelatable iron.
However,
a requirement for the assay to be able to demonstrate cellular LIP in
total is that such iron be localized in the cytosol and not in a
membrane-limited compartment. For some time it has been known that a
major part of cellular redox-active labile, low mass iron is
temporarily localized in the lysosomal compartment as a result of the
autophagic degradation of ferruginous materials, such as
mitochondrial
complexes and ferritin. Even if some calcein-AM may escape cytosolic
esterases and enter lysosomes to be cleaved by lysosomal acidic
esterases, resulting calcein does not significantly chelate iron at
pH
<5. Here we show that the calcein-AM method does not capture
lysosomal
low mass iron and, therefore, that the method seriously
underestimates
total cellular labile iron.


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Am J Clin Nutr. 1997 Aug;66(2):347-56.

Iron absorption from the whole diet in men: how effective is the
regulation of iron absorption?

Hallberg L, Hultén L, Gramatkovski E.
Department of Clinical Nutrition, Göteborg University,
Annedalsklinikerna, Sahlgrenska University Hospital, Sweden.

Iron absorption from the whole diet, which contained a highly
bioavailable form of iron, was measured for 5 d in 31 health men,
including 12 blood donors. Nonheme iron in all meals was labeled with
an extrinsic, inorganic radioiron tracer added in amounts to ensure
uniform specific activity in all meals. Heme iron was labeled
similarly by using hemoglobin biosynthetically labeled with another
radioiron tracer. There was a good inverse relation between total
absorption and concentration of serum ferritin up to approximately 60
micrograms/L. In subjects with serum ferritin > 60 micrograms/L there
was no relation to iron absorption. At this serum ferritin
concentration, absorption decreased to a level just sufficient to
cover basal iron losses, implying that at a serum ferritin
concentration > or = 60 micrograms/L no further accumulation of iron
stores will occur by dietary iron absorption. The findings thus
suggest that in normal subjects there is no risk of developing iron
overload by iron absorption from the diet even if the diet is
fortified. Similar findings were made previously in two studies in
women, both of which indicated an effective control of absorption. At
the same serum ferritin concentration the absorption per kilogram body
weight was the same in men and women served identical diets with a
high iron bioavailability. These new observations strongly suggest
that translation of serum ferritin concentration into amounts of
stored iron should be made with caution and that in subjects with high
serum ferritin concentrations, other causes than increased iron stores
should be considered. There was effective control of both heme- and
nonheme-iron absorption but their relations to iron status were
different.
PMID: 9250114

J Intern Med. 1995 Sep;238(3):223-30.

Body iron stores, dietary iron intake and coronary heart disease
mortality.

Reunanen A, Takkunen H, Knekt P, Seppanen R, Aromaa A.
Research and Development Centre, Social Insurance Institution,
Helsinki, Finland.

OBJECTIVES. To assess whether increased body iron stores and dietary
iron intake are associated with an increased risk of coronary heart
disease mortality. DESIGN. A prospective population study with a mean
mortality follow-up time of 14 years. SETTING. Participants attending
a health screening examination carried out in several localities in
Finland. SUBJECTS. All 6086 men and 6102 women aged from 45 to 64
years at the baseline examination without known heart disease, who had
had serum iron and total iron binding capacity (TIBC) assessed. In a
random fifth of these people, dietary iron intake was assessed by a
dietary history. INTERVENTIONS. The study was observational without
any interventions. MAIN OUTCOME MEASURES. Mortality from coronary
heart disease. RESULTS. Altogether, 739 of the men and 245 of the
women died from coronary heart disease. No relationship between TIBC
and coronary mortality was observed in the men; in the women, an
inverse although not significant association was found. Transferrin
saturation was inversely but not significantly associated with
coronary mortality in men; in women, the relationship was U-formed
with a higher mortality at both the lower and higher ends of the
distribution. Adjustment for other risk factors did not alter the
results. No association was found with dietary iron intake and
coronary mortality. CONCLUSIONS. The results do not corroborate
earlier findings that excess body iron stores and increased iron
intake are associated with an elevated risk of coronary heart
disease.

Wikipedia:http://en.wikipedia.org/wiki/Human_iron_metabolism

Absorbing iron from the diet

Like most mineral nutrients, iron from digested food or supplements is
almost entirely absorbed in the duodenum by enterocytes of the
duodenal lining. These cells have special molecules that allow them to
move iron into the body.

To be absorbed, dietary iron must be in its ferrous Fe2+ form. A
ferric reductase enzyme on the enterocytes' brush border, Dcytb,
reduces ferric Fe3+ to Fe2+. A protein called divalent metal
transporter 1 DMT1, which transports all kinds of divalent metals into
the body, then transports the iron across the enterocyte's cell
membrane and into the cell.

These intestinal lining cells can then either store the iron as
ferritin (in which case the iron will leave the body when the cell
dies and is sloughed off into feces) or the cell can move it into the
rest of the body, using a protein called ferroportin. The body
regulates iron levels by regulating each of these steps. For instance,
cells produce more Dcytb, DMT1 and ferroportin in response to iron
deficiency anemia. [5]

Our bodies' rates of iron absorption appear to respond to a variety of
interdependent factors, including total iron stores, the extent to
which the bone marrow is producing new red blood cells, the
concentration of hemoglobin in the blood, and the oxygen content of
the blood. We also absorb less iron during times of inflammation. In
fact, recent discoveries demonstrate that hepcidin regulation of
ferroportin (see below) is responsible for the syndrome of anemia of
chronic disease.

While Dcytb and DMT1 are unique to iron transport across the duodenum,
ferroportin is distributed throughout the body on all cells which
store iron. Thus, regulation of ferroportin is the body's main way of
regulating the amount of iron in circulation.

Taka

.

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