Vitamin B12 deficiency results from a failure of intestinal
absorption or subsequent transport to the tissues;
it is rarely, if ever, caused by a lack of B12 in the diet.
Disorders of vitamin B12 absorption and transport
have been discussed by Kapadia & Donaldson (1985)
and just a few examples of malabsorption are mentioned
here.
• Elderly people are prone to atrophic gastritis, a
condition in which the gastric oxyntic mucosa
atrophies to such an extent that virtually no hydrochloric
acid or intrinsic factor is secreted.
• In patients with diverticula, strictures and fi stulas
of the small intestine, stagnant regions of the lumen
may become contaminated with colonic bacteria
which can take up much of the dietary vitamin B12
passing by. Bacteria can take up vitamin B12 bound
to intrinsic factor, although not as avidly as they can
take up the free vitamin. Intrinsic factor and bacteria
have a similar affi nity for B12, so it is possible
that bacterial uptake could take place following the
vitamin’s release from haptocorrin but before its
transfer to intrinsic factor.
• The fish tapeworm Diphyllobothrium latum competes
with the host for B12, making it less available
for absorption.
• A common inherited disorder is an auto-immune reaction
with formation of antibodies against intrinsic
factor. Such cases involve two types of antibody: type
I prevents intrinsic factor from binding to cobalamin
and type II blocks the binding of the intrinsic factor–
cobalamin complex to the ileal receptor.
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As a middle aged male (66) I have long been concerned about the reduction in efficiency of absorbing vitamins amd minerals with age.
In the case of B-12, I consume it sublingually from tablets which have been allowed to dissolve in my mouth, with the residues being allowed to stay in the mouth for an extended time.
Oddly, it is the timed-release tablets which are the least convenient to do this with. They tend to leave a pasty residue which is absent in the other B-12 tablets.
I came here looking for a better picture of what is going on in the cellular structures of the lens of the eye. I am working on ways to arrest the development of a cataract, and perhaps even reverse the existing level of opacity.
The current medical model is that nothing other than surgery which includes the removal of the entire opaque lens is likely to restore vision.
It is amazing how little is available to the public about the cellular structures. the development and the metabolic processes of the lens. If anyone else has thoughts along these lines, I would like to hear them. I am not yet ready to accept that surgery is the only option, that no other options have merit.
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