From: russ@wpg.com (Russell Lawrence)
Subject: B12 deficiencies  Was: Starting an alternative group...
Organization: WP Group
Date: Thu, 15 Oct 1992 05:30:18 GMT

Steve Dyer writes:
sd> B12 formed by microorganisms, 
sd> if at all, seems to appear so late in the gut that absorption 
sd> isn't an important factor in preventing deficiency.  

Russell Lawrence writes:
rl> Would you mind pointing me to some evidence to convince me that 
rl> this is true in persons who are not suffering from malnutrition, 
rl> gastric disorder, or inadequate reabsorption?  

From article <16953@pitt.UUCP>, by geb@cs.pitt.edu (Gordon Banks):
gb> I'm not quite clear about what you are questioning, but the
gb> facts are that persons who have the disorder of the parietal
gb> cells of the stomach which prevents them from making intrinsic
gb> factor become vitamin B12 deficient, once their body stores
gb> of the vitamin are depleted.  Oral B12 given to them is
gb> not absorbed in sufficient quantities to reverse the manifestations
gb> of disease produced by the deficiency.  If intrinsic factor
gb> is administered orally along with the B12 (as in the Shilling
gb> test), then they do absorb the B12 given simultaneously.
gb> This is the basis for diagnosing the disease pernicious
gb> anemia.  People with disease of the terminal ileum, such
gb> as Crohn's disease can also develop B12 deficiency due to
gb> the fact that is the portion of the gut to which the intrinsic
gb> factor bound B12 is absorbed.  The solution to both problems
gb> is to inject the B12 instead of taking it orally.  B12 deficiency
gb> is very uncommon in people with normal gut.  One would have
gb> to be a strict vegan and not take any supplementation.

Let's not overlook the fact that absence of intrinsic factor also 
inhibits re-absorption of the B12 (up to six micrograms) that is
excreted daily in bile.  It seems clear that the pharmacologic 
mechanism of absorption (ie diffusion) cannot cope with such a 
loss without high-dose supplements, but this wouldn't support 
the conclusion that diffusion should be written off in healthy 
individuals with normal reabsorption of biliary B12.  That's why 
I excluded persons with gastric disorders in the question that I 
posed for Steve.  

While such questions may seem nit-picky, the answers may help 
explain why traditional vegans typically have normal B12 status.  
Another possible explanation that's been running through my head 
since we began a recent discussion of B12 in s.m.n. is that 
traditional vegans have diets with significantly lower amounts of 
fat and oil than one might expect to find in americans who've 
recently switched to veganism.  The reduced consumption of fats 
and oils might reduce the daily turnover of B12 by reducing the 
total amount of bile secreted daily.  While the amounts we'd be 
dealing with here may not seem significant to affluent omnivores 
consuming 4+ micrograms of B12 per day, they could make quite a
difference to traditional vegans as well as primates living in 
the wild.  

Incidently, Victor Herbert claims that the mechanism of 
absorption involving intrinsic factor is capable of handling a 
maximum of 1.5 to 3.0 micrograms at any one time.  Any idea
how such a figure would be calculated?   Which particular
stage(s) of the absorption process set the limit?

-- 
Russell Lawrence, WP Group, New Orleans (504) 443-5000
russ@wpg.com   uunet!wpg!russ
Newsgroups: sci.med