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CALCIUM ABSORPTIVE EFFICIENCY IS
POSITIVELY RELATED TO BODY SIZE
Barger-Lux, Heaney RP
J Clin Endocrinol Metab 2005; 90(9):5118-20.
The efficiency of calcium absorption is more important
to calcium balance than calcium intake. All is not known
about the causes of absorption variability. This study looks
into the relationship between body size and calcium
absorption efficiency.
The study was conducted at an inpatient metabolic unit in an
academic health sciences center. The study included 178
women of average age 50.2 years. Calcium absorption fraction
was measured via dual tracer method. Observed values were
expressed as residuals from predicted values for each
woman’s actual calcium intake, using the previously
published relationship between intake and absorption. The
absorption residuals were significantly positively
correlated with height, weight, and surface area, and after
adjusting for estrogen status, these body size variables
accounted for about 4% of the total variability. The
magnitude of this effect is such that a woman 1.8 meters in
height would absorb 30% more calcium from a given intake
than a woman 1.4 meters tall.

CALCIUM FORTIFICATION SYSTEMS DIFFER
IN BIOAVAILABILITY
Heaney RP, et al
J Am Diet Assoc 2005; 105(5):807-9
This study tries to compare the
bioavailability of calcium from two different fortification
systems used in orange juice. Study design was randomized
crossover, within-subject. The study subjects were 25
healthy premenopausal women in an academic health sciences
center. The dosage of calcium was 500 mg in two different
commercially available orange juice products, taken at
breakfast after an overnight fast. One product uses calcium
citrate malate as its fortification system, while the other
uses a combination of tricalcium phosphate and calcium
lactate. The main outcome measure was the area under the
curve (AUC) for the increase in serum calcium seen from 0 to
9 hours after ingesting the calcium source. The AUC for the
calcium citrate malate product was 48% greater than that
seen for the tricalcium phosphate/calcium lactate product.
These results indicate that equivalent calcium contents on a
nutritional label do not guarantee equivalent nutritional
value. Manufacturers should be encouraged to provide
bioavailability information on their fortified products.

DIETARY IRON DEFICIENCY INDUCES
VENTRICULAR DILATION, MITOCHODRIAL ULTRASTRUCTURAL
ABERRATIONS AND CYTOCHROME C RELEASE: INVOLVEMENT OF NITRIC
OXIDE SYNTHASE AND PROTEIN TYROSINE NITRATION.
Don F, et al
Clin Sci (Lond). 2005; 109(3):277-86
Iron deficiency results in
multiple health problems, including problems involving
the cardiovascular system. The mechanism by which iron
deficiency damages the cardiovascular system needs to be
elucidated. This study examines the effect of dietary
iron deficiency on cardiac ultrastructure mitochondrial
cytochrome c release, NOS (nitric oxide synthase) and
several stressrelated protein molecules, including
protein nitrotyrosine, the p47phox subunit of NADPH
oxidase, caveolin-1 and RhoA.
Male weanling rats were fed with either a control or an
iron-deficient diet for 12 weeks. The rats on the
iron-deficient diet were found to have increased heart
weight and size over the control group. Left ventricular
dimension and chamber volume were significantly larger
in the iron deficient group. Iron deficient ventricular
tissues revealed mitochondrial swelling and abnormal
sarcomere structure. Cytochrome c release was enhanced,
and protein expressions of endothelial NOS and inducible
NOS , and protein nitrotyrosine formation were elevated
in the cardiac tissue of the iron deficient group. NADPH
oxidase, caveolin-1, and RhoA expression were
upregulated in the ventricular tissue of the iron
deficient. These results suggest that iron deficiency
may induce cardiac hypertrophy, characterized by
aberrant mitochondrial and irregular sarcomere
organization – accompanied by increased reactive
nitrogen species and RhoA expression.

IRON STATUS OF FEMALE COLLEGIATE
ATHLETES INVOLOVED IN DIFFERENT SPORTS.
Sareen S. Gropper, et al.
Biological Trace Element Research, Vol 109, 206, pp 1-13.
This study involved 70 female
athletes, ages 18-15, who were involved in collegiate
cross-country track, tennis, softball, swimming, soccer,
basketball, and gymnastics. No significant differences were
seen in mean hemoglobin, hematocrit, serum iron, total
iron-binding capacity, transferrin saturation, and ferritin
were found among the teams. All of the mean concentrations
of each parameter for every team were inside normal ranges.
Several athletes, however, from a variety of spots had
suboptimal iron status indices. Seventeen athletes with low
serum ferritin concentrations (<15mcg/L), also exhibited low
serum iron (<60mcg/L) and low transferrin saturation (<16%).
Thirteen of the athletes failed to consume ⅔ of the RDA for
iron and exhibited suboptimal serum concentrations of
ferritin, iron, and/or transferrin saturation. Out of nine
athletes taking iron supplements, one exhibited suboptimal
iron status. In summary, nonanemic iron depletion was seen
among the female collegiate athletes in all sports, and the
female athlete should continue to be individually and
routinely evaluated fro nutritional deficiencies throughout
their athletic careers.

ABNORMAL DEVELOPMENT AND INCREASES
3-NITROTYROSINE IN COPPER-DEFICIENT MOUSE EMBRYOS.
Beckers-Trapp ME, et al.
Free Radic Biol Med, 2006; 40(1):35-44.
Copper deficient rat embryos are characterized by low
superoxide dismutase activity and high superoxide anion
concentrations, and result in brain and heart anomalies.
High superoxide anions can lead to the formation of the
strong biological oxidant, peroxynitrite. In the study,
embryos from copper-adequate and copper-deficient dames were
cultured in media that were adequate or deficient in copper.
After 48 hours, the copper-deficient exhibited brain and
heart anomalies, as well as a high incidence of yolk sac
vasculature abnormalities. Protein nitration(3-nitrotyrosine
levels) were markedly higher in the copper deficient’s
anterior neural tube epithelium. Correction of the
deficiency did not ameliorate the abnormal development, but
did decrease the 3-nitrotyrosine levels mentioned. Study
shows that copper-deficiency compromises oxidant defense and
increases protein nitration and may contribute to
copper-deficiency-induced teratogenesis.

IRON BIOAVAILABILITY FROM FORTIFIED FLUID MILK AND PETIT
SUISSE CHEESE DETERMINED BY THE PROPHYLACTIC-PREVENTIVE
METHOD
Salgueiro J, et al.
Biological Trace Element Research, Vol 109, pp 91-96, 2006.
This study measures the iron
bioavailabity of micronized ferric orthophosphate when used
to fortify low fat fluid milk enriched with calcium and
Petit Suisse cheese using the prophylactic-preventive method
in rats. There were four groups of rats in the study, a
basal diet group (control diet; 6.5 ppm Fe), a reference
standard diet (ferrous sulfate micronized; 18.2 ppm Fe), a
basal diet with fortified milk supplying the iron (17.9 ppm
Fe, from micronized ferric orthophosphate), and a basal diet
with iron fortified Petiti Suisse as the iron source (18 ppm
Fe from micronized ferric orthophosphate). The iron
bioavailability for the groups were calculated as the ratio
between the mass of iron incorporated into the hemoglobin
during the study and the total iron taken in per animal. The
relative bioavailability, as compared to the reference
standard of micronized ferrous sulfate was 61% and 69% for
the milk source and cheese source respectively (both
containing the micronized ferric orthophosphate). These are
considered to be of medium bioavailability.

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