<<Disclaimer: Verify this information before applying it to your situation.>>
The risk of osteoporosis and bone fracture in celiacs may not only be due
to calcium deficiency. A new study shows that vitamin B12 and folate
deficiency and the resulting elevated circulating homocysteine level can
contribute to increased fracture risk as well as increased stroke risk.
This study is discussed in the Medscape and JAMA articles below. Also,
while on the subject of mineral and vitamin deficiencies due to celiac
disease, it is interesting to note the profound effects a zinc deficiency
can have on organs, the immune system, metabolism, growth and development
as outlined in the abstract also included below.
----------
Medscape Medical News
Folate, Vitamin B12 May Reduce Fracture Risk in Elderly After Stroke
Laurie Barclay, MD
"March 1, 2005 - Supplementation with folate and vitamin B12 reduces the
risk of fracture in the elderly who have had a stroke, according to the
results of a randomized study published in the March 2 issue of JAMA."
(JAMA. 2005;293:1082-1088, 1121-1122)
Access to this article may require free registration with Medscape:
http://www.medscape.com/viewarticle/500550
----------
JAMA. 2005;293:1082-1088.
Effect of Folate and Mecobalamin on Hip Fractures in Patients With Stroke
A Randomized Controlled Trial
Yoshihiro Sato, MD; Yoshiaki Honda, MD; Jun Iwamoto, MD; Tomohiro Kanoko,
PhD; Kei Satoh, MD
Author Affiliations: Department of Neurology, Mitate Hospital, Tagawa (Drs
Sato and Honda); Department of Sports Medicine, Keio University School of
Medicine, Tokyo (Dr Iwamoto); and Departments of Rehabilitation Medicine
(Dr Kanoko) and Vascular Biology (Dr Satoh), Institute of Brain Science,
Hirosaki University School of Medicine, Hirosaki, Japan.
ABSTRACT
Context: Stroke increases the risk of subsequent hip fracture by 2 to 4
times. Hyperhomocysteinemia is a risk factor for both ischemic stroke and
osteoporotic fractures in elderly men and women. Treatment with folate and
mecobalamin (vitamin B12) may improve hyperhomocysteinemia.
Objective: To investigate whether treatment with folate and vitamin B12
reduces the incidence of hip fractures in patients with hemiplegia
following stroke.
Design, Setting, and Patients: A double-blind, randomized controlled study
of 628 consecutive patients aged 65 years or older with residual hemiplegia
at least 1 year following first ischemic stroke, who were recruited from a
single Japanese hospital from April 1, 2000, to May 31, 2001. Patients were
assigned to daily oral treatment with 5 mg of folate and 1500 µg of
mecobalamin, or double placebo; 559 completed the 2-year follow-up.
Main Outcome Measure: Incidence of hip fractures in the 2 patient groups
during the 2-year follow-up.
Results: At baseline, patients in both groups had high levels of plasma
homocysteine and low levels of serum cobalamin and serum folate. After 2
years, plasma homocysteine levels decreased by 38% in the treatment group
and increased by 31% in the placebo group (P<.001). The number of hip
fractures per 1000 patient-years was 10 and 43 for the treatment and
placebo groups, respectively (P<.001). The adjusted relative risk, absolute
risk reduction, and the number needed to treat for hip fractures in the
treatment vs placebo groups were 0.20 (95% confidence interval [CI], 0.08-
0.50), 7.1% (95% CI, 3.6%-10.8%), and 14 (95% CI, 9-28), respectively. No
significant adverse effects were reported.
Conclusion: In this Japanese population with a high baseline fracture
risk, combined treatment with folate and vitamin B12 is safe and effective
in reducing the risk of a hip fracture in elderly patients following
stroke.
----------
J Nutr. 2005 Mar;135(3):359-62.
Roles for cell death in zinc deficiency.
Fraker PJ.
Department of Biochemistry and Molecular Biology and Department of Food
Science and Human Nutrition, Michigan State University, East Lansing, MI
48823.
Studies of zinc deficiency (ZD) have become important for demonstrating
that nutritional imbalances can readily induce programmed cell death (PCD)
or apoptosis in a variety of kinds of cells. In mice, ZD caused a 300%
increase in the amount of apoptosis among pre T-cells, which was a major
cause of thymic atrophy that alters host defense. Embryogenesis was
significantly altered in ZD mice due to increased apoptosis in the neural
crest, optic, and head regions. Insufficient zinc initiated PCD in
hepatocytes, glioma, kidney, monocytes, fibroblasts, and testicular cells,
demonstrating the scope of this phenomenon. New forms of cell death
continue to emerge. For example, autophagy is initiated by starvation and
various nutritional and metabolic imbalances. Autophagy is a form of PCD
whereby the cell digests some of its own organelles to provide needed
nutrients. Understanding the interplay between these different forms of
cell death and nutritional imbalances is very important because of their
profound impact on development, growth, immune function, and health.
PMID: 15735063 [PubMed - in process]
* * *
*Please provide references to back up claims of a product being GF or not GF*
|
