Health-behavior Induced Disease: Return
of the Milk-alkali Syndrome
Caruso Jb; Patel RM; Julka K; Parish DC.
J Gen Intern Med, July 2007; 22(7):1053-5.
The milk-alkali syndrome is a well-documented consequence of
excessive calcium and alkali intake first
recognized in association with early 20th century antacid
regimens. The syndrome became rare after widespread
implementation of modern peptic ulcer disease therapies.
With recent trends in osteoporosis therapy coupled with
widely available calcium-containing supplements, the
milk-alkali syndrome has reemerged as an important clinical
entity. Our case illustrates a patient who self-medicated
his peptic ulcer disease with a regimen resembling a common
early 20th century dyspepsia regimen. When superimposed upon
chronic high calcium supplementation, the patient became
acutely ill from the milk-alkali syndrome. When taken to
excess, or used inappropriately, medications and supplements
ordinarily considered beneficial, can have harmful effects.
Our case underscores the importance of
obtaining a thorough medication history including use of
over-the-counter supplementation.
Zinc and the Liver: An Active Interaction
Stamoulis I ; Kouraklis G ; Theocharis S.
Dig Dis Sci ; 2007 ; 52(7) :1595-612.
Zinc is an essential trace element, exerting important
antioxidant, anti-inflammatory, and antiapoptotic effects.
It affects growth and development and participates in
processes such as aging and cancer induction. The liver is
important for the regulation of zinc homeostasis, while zinc
is necessary for proper liver function. Decreased zinc
levels have been implicated in both acute and chronic liver
disease states, and zinc deficiency has been implicated in
the pathogenesis of liver diseases. Zinc supplementation
offers protection in experimental animal models of acute and
chronic liver injury, but these hepatoprotective properties
have not been fully elucidated. In the present review, data
on zinc homeostasis, its implication in the pathogenesis of
liver diseases, and its effect on acute and chronic liver
diseases are presented. It is concluded that zinc could
protect against liver diseases, although up to now the
underlying pathophysiology of zinc and liver interactions
have not been defined.
Vitamin D and Calcium Supplementation
Reduces Cancer Risk: Results of a
Randomized Trial
Lappe Jm ; Travers-Gustafson D ;
Davies Km ; Recker RR.
Am J Clin Nutr; June 2007; 85(6):1586-91.
Numerous observational studies have found supplemental
calcium and vitamin D to be associated with reduced risk of
common cancers. However, interventional studies to test this
effect are lacking. The purpose of this analysis was to
determine the efficacy of calcium alone and calcium plus
vitamin D in reducing incident cancer risk of all types.
This was a 4-y, population-based, double-blind, randomized
placebo-controlled trial. The primary outcome was fracture
incidence, and the principal secondary outcome was cancer
incidence. The subjects were 1179 community-dwelling women
randomly selected from the population of healthy
postmenopausal women aged >55 y in a 9-county rural area of
Nebraska centered at latitude 41.4 degrees N. Subjects were
randomly assigned to receive 1400-1500 mg supplementa
calcium/d alone (Ca-only), supplemental calcium plus 1100 IU
vitamin D3/d (Ca + D), or placebo. When analyzed by
intention to treat, cancer incidence was lower in the Ca + D
women than in the placebo control subjects (P < 0.03). With
the use of logistic regression, the unadjusted relative
risks (RR) of incident cancer in the Ca + D and Ca-only
groups were 0.402 (P = 0.01) and 0.532 (P = 0.06),
respectively. When analysis was confined to cancers
diagnosed after the first 12 mo, RR for the Ca + D group
fell to 0.232 (CI: 0.09, 0.60; P < 0.005) but did not change
significantly for the Ca-only group. In multiple logistic
regression models, both treatment and serum
25-hydroxyvitamin D concentrations were significant,
independent predictors of cancer risk. Improving calcium and
vitamin D nutritional status substantially reduces
all-cancer risk in postmenopausal women.
Cardiac Nitric Oxide Synthases are
Elevated in Dietary Copper Deficiency
Saari Jt ; et al.
J Nutr Biochem; 2007; 18(7):443-8.
Dietary copper (Cu) deficiency leads to cardiac
morphological and functional defects suggestive of heart
failure. However, simultaneous cytoprotective events also
appear to occur. The molecular mechanisms responsible for
this complex alteration of cardiac function by Cu deficiency
have not been elucidated. Because prior work has implicated
altered nitric oxide (NO) metabolism in this altered
function, we have examined this pathway in further detail.
Male Sprague-Dawley rats were fed diets that were either Cu
adequate (6 mg Cu/kg diet) or Cu deficient «0.5 mg Cu/kg
diet) for 5 weeks. Endothelial NO synthase (NOS) and
inducible NOS (iNOS) protein expressions, as measured by
Western blot analysis, were 58% and 40% higher,
respectively, in Cu-deficient than in Cu-adequate rat
hearts. Cardiac NOS activity, as measured by conversion of
(3)H-arginine to (3)H-citrulline, was 130% higher in
Cu-deficient than in Cu-adequate rats.
NFkappaB is a known transcription factor for iNOS.
Activation of NFkappaB, determined by an ELISA for the p65
subunit, was found to be 33% higher in Cu-deficient than in
Cu-adequate rats. Coupled with prior evidence of elevated
cardiac nitrate/nitrite production in Cu-deficient rats,
these data suggest multiple pathways for enhanced NO
production that may contribute to altered cardiac function
under dietary Cu deficiency.
Copper
Deficiency Causes Reversible Myelodysplasia
Huff JD, et al.
Am J Hematol; 2007; 82(7):625-30.
Copper deficiency is a recognized but often overlooked
cause of anemia and neutropenia. We began checking serum
copper levels on patients referred for evaluation for
unexplained anemia and neutropenia or myelodysplasia.
Eight patients were identified as copper deficient
(serum copper less than 70 mug/dL). The anemia was
normochromic and normocytic in seven patients.
Neutropenia was present in seven patients. Seven
patients had been referred for evaluation of
myelodysplasia. Three were seen for consideration for
allogenic stem cell transplant. Five patients had
concomitant peripheral neurological symptoms. Seven
patients were treated with oral copper gluconate. All
treated patients demonstrated a hematological response;
seven had a complete remission. The improvement in
anemia and neutropenia was rapid with normalization of
blood counts within three to four weeks. In one patient,
normalization of the underlying marrow dysplasia was
demonstrated by bone marrow histology eight months after
copper replacement. The cause of copper deficiency was
felt to be gastrointestinal malabsorption in five of our
patients. We conclude that copper deficiency should be
considered in all patients with unexplained anemia and
neutropenia or myelodysplasia.
Magnesium and C-Reactive Protein
in Heart Failure: An Antiinflammatory
Effect of Magnesium Administration?
Almonznino-Sarafian D, et al.
Eur J Nutr; June 2007; 46(4):230-7.
Little is known about the relationship between
serum magnesium (Mg) and C-reactive protein (CRP) in
heart failure
(HF). The researchers wanted to investigate the
relationship, if any, between serum Mg and CRP in HF
patients and,
concomitantly, to test a hypothesis that Mg
supplementation might affect serum CRP levels. Serum
Mg and CRP were evaluated in 68 patients with
chronic systolic HF leading to hospital admission
and 65 patients requiring hospitalization for other
causes. Following 5 weeks, serum Mg, CRP and
intracellular Mg were reevaluated in 17 HF patients
after administration of oral Mg citrate 300 mg/day
(group A), and 18 untreated HF patients (group B).
In order to obtain Gaussian distribution,
logarithmic transformation of CRP was performed.
Inverse correlation was found between serum Mg and
log CRP (r = -0.28, P = 0.002). Compared to
controls, patients with HF demonstrated higher
baseline CRP levels, independent of coexisting
conditions, and lower serum Mg values. Following Mg
treatment, log CRP decreased from 1.4 +/- 0.4 to 0.8
+/- 0.3 in group A (P < 0.001). No significant
changes in log CRP were
demonstrable in group B. Serum Mg (mmol/l) rose
significantly in group A (0.74 +/- 0.04-0.88 +/-
0.08, P < 0.001),
and to a lesser extent in group B (0.82 +/-
0.08-0.88 +/- 0.08, P = 0.04). Intracellular Mg
significantly increased only
in Mg-treated group A (P = 0.01). The researchers
found that oral Mg supplementation to HF patients
significantly
attenuates blood levels of CRP, a biomarker of
inflammation. Targeting the inflammatory cascade by
Mg administration might prove a useful tool for
improving the prognosis in HF.
|
|
