Kathleen Bruce's post from an unnamed contributor and Dr. Dettwyler's post
on
iron and cognitive development have aroused a great deal of concern in me.
The information is a biased, unbalanced combination of limited facts and
anecdotal information presented to this group as if they overturn the
larger,
established body of knowledge on the detrimental effects of iron deficiency.

While I am sure that the proponents of this viewpoint have the best of
intentions, I believe there is a great deal of danger in espousing this
viewpoint to an audience that does not understand the underlying issues.
Unfortunately, the claims in these posts (and those of Dr. Stuart-Macadam)
are widely scattered and require five times the effort to either factually
refute some claims or place other claims in perspective.  As a clinical/
laboratory research scientist, I only have a limited amount of time to take
away from my work to devote to this effort, but, because this is an issue of

concern in this group (based on private E-mail I have received), I will do
what I can.

Worldwide and in economically-developed countries (U.S., Europe, and Japan
included), iron deficiency is the most prevalent nutritional problem.
Because I believe that most of the subscribers on this list practice in the
economically-developed world, I will try to focus this discussion on iron
deficiency issues in among children and women of childbearing age in this
population.  Approximately 10-20% of women of childbearing age in the
developed world are anemic, the most prevalent "cause" being iron deficiency

secondary to insufficient dietary iron intake (Scrimshaw, Sci Am 265:46-52,
1991).

A certain proportion of the iron in your diet is absorbed into the cells
lining the intestines, the rest is lost in the feces (to answer Dr.
Dettwyler's question, the amount of iron in the feces is directly
proportional to the amount consumed and does not include iron from anywhere
in the body beyond the brush-border epithelial cells of the intestines).
 The
proportion absorbed (usually between 5-20%) increases and decreases in
response to how much iron you have stored in your bone marrow and other
tissues.  Some of the iron is transported from the intestinal lining to
the body's tissues by a molecule called transferrin, the rest is lost
when the old cells are sloughed off and new cells grow.  In the tissues,
iron is taken up, used for any immediate needs, and the rest is stored in a
molecule called ferritin for later use.  Most of the iron in your body is in

the red blood cells where it is used to transport oxygen in the blood.  When

the body doesn't have enough iron available, it can't synethesize normal red

blood cells.  Those that are synthesized are small (microcytic) and lack the

coloration associated with iron bound to hemoglobin (hypochromic).  As a
result, hemoglobin and hematocrit levels drop (standard diagnostic tools
used
in the clinical situation, especially in prenatal care).  Underlying
infections, several nutrient deficiencies and other pathologies can also
cause hemoglobin or hematocrit levels to fall when one's iron status is just

fine.  It is up to the health-care provider to recognize this and perform
the
necessary additional tests to determine if iron deficiency is the cause of
the fall in hemoglobin and hematocrit (unfortunately, I think only two or
three medical schools in the U.S. teach a course in nutrition).  At this
time, the best second test for iron deficiency is serum ferritin levels
(which rise and fall in proportion to the amount of iron stored in ferritin
in the tissues), but one can also test the status of serum transferrin as
well for more diagnostic power.  Serum ferritin rises during infections
(which can mask underlying iron deficiency), so a person with low
hemoglobin and ferritin in all likelihood doesn't have an underlying
infection causing low iron status (a factual contradiction of the "iron
deficiency only reflects underlying infections" view).  When hemoglobin,
serum ferritin, and another test of iron status are below what they should
be
(IN THE ABSENCE ANOTHER PATHOLOGY which must be confirmed by the health-care

provider) then the person has an extremely high probability of having some
degree of iron deficiency and/ or iron-deficiency anemia (see R. Gibson's
"Principles of Nutritional Assessment" 1990 for more diagnostic
information).

Any believeable study on the effects of iron deficiency on some outcome has
excluded people with underlying infections or pathologies.  Survey data on
the prevalence of iron deficiency in the U.S. (and probably other developed
countries) is based on low hemoglobin levels confirmed by low ferritin
levels.  The usual "causes" of confirmed iron deficiency in the developed
world vary by group.  Women usually develop iron deficiency from having
higher menstrual losses of blood iron relative to insufficient dietary iron
intake (pathological blood losses are a completely different subject).
Pregnant women usually develop iron deficiency because the fetus will
generally absorb all the iron it needs from the mother regardless of her own

iron status or dietary intake of iron.  Children usually develop iron
deficiency because they have periods of growth when they are synthesizing
blood cells and tissue relatively faster than they are taking in iron from
the diet.  While there are numerous other "causes" that are much more
infrequently encountered, the typical "causes" I have given have nothing to
do with infection or parasitism.

The link between iron deficiency and poor physical performance, increased
mortality, poor cognitive development or impaired immune function are based
on three very strong experimental methods.  After excluding patients with
infections or other pathologies (generally less than 1-5% of those you want
to study in the developed world), one can 1) monitor changes when animals ar
e
made iron deficient from an iron-poor diet and after an iron-rich diet is
supplied, 2) for less severe outcomes, make volunteers iron deficient by
dietary iron restriction, monitor changes, and follow up after an iron
supplement is given, or 3) for more severe problems, give iron supplements
to
iron deficient women or children and monitor changes as iron status
improves.  These kinds of studies have essentially "proven" the effects of
iron deficiency (secondary to low dietary iron intake) on the outcomes in
question (I say "essentially" because even gravity is only a theory).  Other

theories, like Dr. Weinburg's studies of the body's iron conservation during

infection, have come along and been incorporated (with open arms) into the
larger body of information on iron and health, but must always be viewed in
perspective.

From this information, I hope you can see the dangers of ignoring the risks
associated with iron deficiency and the proven benefit of iron supplements
or
a more iron-enriched diet in "curing" or avoiding these problems.  Because
there is no real benefit of storing up LARGE quantities of iron in your body

(unless you plan a REALLY long fast), one must not go to the other extreme.

If you have not been soundly diagnosed as having iron deficiency, you don't
need iron supplements, unless you have become pregnant and are at risk of
becoming iron deficient due to fetal needs and delivery blood losses.  If
you
need iron, lower doses of oral iron supplement have been found to be just as

effective as higher doses without as many gastrointestinal side-effects
(read
the Institute of Medicine's "Nutrition During Pregnancy", 1990, for more
info
on iron and pregnancy).  Exclusively breastfed, full-term infants should not

need supplemental iron for several months (how many months is hotly
debated),
if ever, given the availability of iron-enriched transitional foods for
infants.  Lactating women have a number of benefits when it comes to iron
status: 1) lactational amenorrhea reduces the amount of iron lost from the
body, 2) because pregnancy generally depletes the mother's iron stores,
postpartum women have an increased ability to absorb what iron is in their
diet, and 3) not much iron at all is lost in producing milk (which has
surprised some OB/GYNs I've worked with).

For more information, the most readable treatment of the topic is an article

by Dr. Nevin Scrimshaw called "Iron Deficiency" in volume 265, pages 46-52
of
the 1991 Scientific American magazines.  Dr. Scrimshaw is truly an eminent
scientist with credentials including: member, National Academy of Sciences;
founder, Institute of Nutrition for Central America and Panama; and
professor
emeritus, MIT.  My discussions with him on my own work in iron and lactation

were inspiring and humbling.

Paul Zimmer, Ph.D.


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