PALEOFOOD Archives

Paleolithic Eating Support List

PALEOFOOD@LISTSERV.ICORS.ORG

Options: Use Forum View

Use Monospaced Font
Show Text Part by Default
Show All Mail Headers

Message: [<< First] [< Prev] [Next >] [Last >>]
Topic: [<< First] [< Prev] [Next >] [Last >>]
Author: [<< First] [< Prev] [Next >] [Last >>]

Print Reply
Subject:
From:
"Andrew S. Bonci, BA, DC, DAAPM" <[log in to unmask]>
Reply To:
Paleolithic Eating Support List <[log in to unmask]>
Date:
Sun, 1 Jun 1997 11:00:55 -0500
Content-Type:
text/plain
Parts/Attachments:
text/plain (94 lines)
Todd Moody wrote:

> Such as diarrhea, for example?  My son Dylan gets diarrhea for a
> few days every two weeks or so.  I can't figure it out, and can't
> even get the doctor interested in it.

I'd say yes to diarrhea.  The first encounter a foreign gut protein
(let's say antigen) has with immunoregulatory cells is the tissue mast
cell (TMC) which lines the gut.  Upon contact with the TCM these cells
degranulate and release histamines (HA).  The HA release causes a large
degree of vasodilation and subsequent extravasation of fluids into the
bowel.  So yes, diarrhea would be an indication of a food allergy
especially if the offending food and its antigen has been seen before by
your immune system.  Once your immune system sees this antigen, it is
now sensitive to is.  This occurs by TMC IgE (immunoglobulin E)
complexes.  Now, the TMC having released HA and its attendant
extravasation the bowel is attempting to "wash out" the antigeninc
triggers.  This mechanism is particular effective against intestinal
parasites.  However good this mechanism is against parasites it may
leave the bowel permeable to the very antigens it has reacted against.

This antiparasitic mechanism is understood to be a very "old" host
defense mechanism.  When I consider it more deeply, it antedates the
development of agriculture and the bulk intoduction of monocotylodon
antigens into the bowel.  This may be anexample of a paleolithic host
defense mechanism which "could not have predicted" the advent of foreign
plant proteins.  This stuff sure keeps you wondering!

I've been sifting through the available Medline citations and
abstracts.  I have found some hints and clues that insulin causes an
elevation of HA in histaminergic neurons (these are nerves that
predominantly use HA as a neurotransmitter).  I am looking for info
which might suggest or refute the contention that insulin challenge also
results in an elevation in the HA of the TMC.

> Very interesting.  You may not be aware that a large percentage
> of people with autism are low in an enzyme called
> phenolsulfotransferase (PST), which in turn plays a role (I don't
> understand this part) in maintaining the lining of the gut.  So,
> low PST leads to leaky gut.  This in turn leads to undigested
> proteins getting into the system to cause other problems.

Curious, would like to hear more on this enzyme and its role in gut
integrity.

> The fact that PGE1 plays a role here is another reason to think
> carefully about macronutrient manipulation.

I strongly feel that keeping the insulin load down will "shunt" fatty
acid metabolism away from AA production and toward PGE1 when dealing
with n-6 FA.  It seems that as exogenous AA decreases with a concomitant
rise in exogenous starch and insulin load, the body compensates by
manufacturing a steady supply of its own (endogenous) AA.  This seems to
be provided by insulin's influence over D5D (among other enzymes).

> And I have recently read that many autistic people have quite
> elevated levels of arachidonic acid.  All this leaves me thinking
> very hard about the links between AA, food allergy, leaky gut,
> and autism.

There may be an food allergy-starch-insulin-AA-HA-immune axis(?)
interaction.  I wonder how deep foreign proteins are allowed to
penetrate the organism with a healthy immune system.  My view on this
food allergy phenomenon is that the antigen does not penetrate deeply at
all, but that there may be a "hyperimmune reaction" to the antigen.  I'd
use the case of rheumatic fever/heart disease as a model.  In rheumatic
heart disease the patient has a step infection which sensitizes the
immune system.  Long after the strep infection is gone the immune cells
are still very active.  This activity is no longer directed at the
invading strep but rather is directed at host cells.  Immune complexes
are found on joint tissue and heart valves to name a few.  This is what
I believe is occuring in food allergy.

> In addition to low-carb diet (very hard to implement for a
> child), what else would help to tip the scale toward PGE1?  I
> have read that sesame oil downregulates D5D, but in both n-6 and
> n-3 series FA, so that may not be a winner.

This is tough.  I feel the best solution is the one which you indicate
is difficult to implement in a child.  Perhaps the best way to implement
a low-insulin-load diet is to remove the craving for it.  This may be a
blind fold given the media assault from TV and print advertisments.
You've got the rock road to walk.  It's easy for the guy juggling ideas,
so that's mostly what I offer.

Andrew  =8-)
--
Andrew S. Bonci, BA, DC, DAAPM
Assistant Professor, Department of Diagnosis
Cleveland Chiropractic College
6401 Rockhill Road
Kansas City, Missouri   64131
(816) 333-7436 ex39

ATOM RSS1 RSS2