Minerals in the News
From Albion Advanced Nutrition
Vol 3, Issue 6, June 2005

 

 

CALCIUM FROM DIET AND SUPPLEMENTS IS ASSICIATED WITH RUDUCED RISK OF COLORECTAL
CANCER IN A PROSPECTIVE CHOHORT OF WOMEN [IN PROCESS CITATION].
Cancer Epidemiol Biomarkers Prev, 2005 Jan;14(1):126-32.
Flood A., et al.


Researchers investigated the association between calcium intake and colorectal cancer in a prospective
cohort of 45,354 women without a history of colorectal cancer who successfully completed a 62-item
National Cancer Institute/Block food-frequency questionnaire. Women were followed for an average of 8.5
years, during which time 482 subjects developed colorectal cancer. Cut points between quintiles of energyadjusted
dietary calcium were 412, 529, 656, and 831 mg/day. They created categories for calcium from
supplements as follows: 0 mg/day (n=25,441), 0 to 400 mg/day (n=9,452), 401 to 800 mg/day (n=4,176),
and >800 mg/day (n-6,285). Risk ratios and confidence intervals (95% CI) for increasing quintiles of
dietary calcium relative to the lowest quintile were 0.79, 0.77, 0.78, and 0.74, P(trend) = 0.05. For
increasing categories of calcium from supplements, the risk ratios (and 95% CI) relative to no supplement
use were 1.08, 0.96, and 0.76, P(trend) = 0.09. Simultaneously high consumption of calcium from diet and
calcium from supplements resulted in even further risk reduction, RR = 0.54 (95% CI, 0.37-0.79) compared
with low consumption of both sources of calcium. These data indicate that a difference of <400 to >800 mg
of calcium per day was associated with an approximately 25% reduction in risk of colorectal cancer, and
this reduction in risk occurred regardless of the source of the calcium (i.e., diet or supplements).


 

 

WHAT ARE THE CAUSES OF HYPOMAGNESEMIA? [IN PROCESS CITATION].
J Fam Pract 2005 Feb;54(2):174-6.
Mouw DR and Latessa RA.
 

The causes of magnesium depletion and hypomagnesemia are decreased gastrointestinal (GI) absorption and
increased renal loss. Decreased GI absorption is frequently due to diarrhea, malabsorption, and inadequate
dietary intake. Common causes of excessive urinary loss are diuresis due to alcohol, glycosuria, and loop
diuretics. Medical conditions putting persons at high risk for hypomagnesemia are alcoholism, congestive
heart failure, diabetes, chronic diarrhea, hypokalemia, hypocalcemia, and malnutrition. Evidence suggests
that magnesium deficiency is both more common and more clinically significant than generally appreciated.

 

EFFECTIVENESS OF SELENIUM SUPPLEMENTS IN A LOW-SELENIUM AREA OF CHINA.
Am J Clin Nutr 2005;81:829-34.
Yiming X., et al.
 

Researchers carried out a supplementation trial in a selenium-deficient population in China to assess the
requirement for selenium as selenite and as selenomethionine. 120 subjects with an average selenium intake
of 10 µg/d were randomly assigned and administered tablets containing no selenium or amounts as high as
66 µg Se/day for 20 weeks. Plasma was sampled before supplementation and at 4-week intervals during
supplementation and was assayed for the two plasma seleno-proteins, gluthathione peroxidase and
selenoprotein P. Full expression of gluthatione peroxidase was achieved with 37 µg Se/d as
selenomethionine and with 66 µg/d as selenite. Full expression of selenoprotein P was not achieved at the
highest doses of either form. Full expression of selenoprotein P requires a greater selenium intake than does
full expression of plasma glutathione peroxidase. This suggests that selenoprotein P is a better indicator of
selenium nutritional status than is glutathione peroxidase and that the recommended dietary allowance of
selenium, which was set with the use of glutathione peroxidase as the index of selenium status, should be
revised. Selenium as selenomethionine had nearly twice the bioavailability of selenium as selenite.

 

DUODENAL ASCORBATE AND FERRIC REDUCTASE IN HUMAN IRON DEFICIENCY.
Am J Clin Nutr 2005;81:130-3.
Atanasova BD., et al.
 

The first step in iron absorption requires the reduction of ferric iron to ferrous iron, a change that is
catalyzed by duodenal ferric reductase. Iron deficiency is associated with high iron absorption, high ferric
reductase activity, and high duodenal ascorbate concentrations in experimental animals, but it is not known
whether a relation between reductase and ascorbate is evident in humans. The objective of the study was to
assess the relation between ferric redutase activity in human duodenal biopsy specimens and ascorbate
concentrations in iron-replete and iron-deficient subjects. Patients and control subjects were overnightfasted
adults presenting sequentially for upper gastrointestional endoscopic investigation. Ferric reductase
activity in duodenal biopsy specimens was assayed by using nitroblue tetrazolium. Ascorbate was assayed
in duodenal biopsy specimens and plasma. Iron-deficient patients had significantly higher reductase activity
and duodenal and plasma ascorbate concentrations than did control subjects. Incubation of biopsy
specimens with dehydroascorbate (to boost cellular ascorbate) increased reductase activity in the tissues that
initially had normal activity, but inhibited reductase activity in the tissues that already had high reductase
activity. Iron deficiency in humans is associated with increased duodenal ascorbate concentrations. This
finding suggests that increased reductase activity is partly due to an increase in this substrate for duodenal
cytochrome b reductase 1.

 

LOW DIETARY ZINC DECREASES ERYTHROCYTE CARBONIC ANHYDRASE ACTIVITES AND IMPAIRS
CARDIORESPIRATORY FUNCTION IN MEN DURING EXERCISE.
Am J Clin Nutr 2005;81:1045-51.
Henry C. Lukaski.


This study determined the effects of low zinc intake on carbonic anhydrase activity in red blood cells
(RBCs) and cardiorespiratory function during exercise. In this double-blind, randomized crossover study,
14 men aged 20-31 years old were fed low-zinc and supplemented (3.8 and 18.7 mg/d) diets made up of
Western foods for 9-weeks periods with a 6-week washout. Peak work capacity, determined by using a
cycle ergometer and a graded, progressive protocol, and a prolonged submaximal test (70% peak intensity
for 45 minutes) were administered during the second and ninth weeks of each diet period. Dietary zinc did
not affect hemoglobin or hematocrit. Low dietary zinc resulted in lower serum and erythrocyte zinc
concentrations, zinc retention, and total carbonic anhydrase and isoform activities in RBCs. Peak oxygen
uptake, carbon dioxide output, and respiratory exchange ratio were lower and ventilatory equivalents for
metabolic responses during exercise were greater with low than with supplemental zinc intake. Similar
functional responses were observed during prolonged, submaximal exercise. These findings indicate that
low dietary zinc is associated with significant reductions in zinc status, including RBC carbonic anhydrase
activities, and impaired metabolic responses during exercise.