Todd Moody wrote:
> Tell me more about "protein(glyco)" please.
In the context of our discussion on inflammogens I mentioned protein
(glyco) meaning that immune cells elaborate low weight soluble factors
which are predominently protein based. These proteins messengers are
often referred to as cytokines or interleukins. There are some cell
surface antigens of "glycoprotein type" which are low weight proteins
which have "sugar" moieties.
These cytokines/interleukins/inflammogens can be thought of as integral
components in cellular communication. Let's take a step back. nerve
cells communicate when a *neurotransitter* crosses a synaptic gap. The
synaptic gap is a small fixed distance. Neurotransmitters can be
peptides (proteins) or nonpeptides like acetylcholine. Endocrine organs
release hormones which have effects at distant tissues. Unlike nerve
communication, hormones must cross a large fixed distance to have their
effects. Now immune cells communicate by releasing
cytokines/interleukins. Cytokines must travel variable distances which
are not fixed since these cells are constantly in motion.
Traditionally, these three systems, i.e., nervous, endocrine, immune,
have been viewed as three different systems. However, each systems'
communicative messengers can cross-talk with the others' cell
populations. Cytokines serve as immune cell messengers, but they also
can act as neurotransitters and endocrine hormones as well.
Neurtransmitter can stimulate endocrine cells and immune cells. What is
clear is that there is cross talk between systems. As such, an
instigating stimuli from diet, i.e., AA and production of PGE2, PGI2,
TXA2, et al, can instigate cytokine/interleukin production which can
have profound neurological and endocrine effects.
> It suggests that it is something in
> dietary fat, rather than just immune-triggering alien protein,
> that is causing the autoimmune diseases.
Food allergy is real. Foreign proteins can wreak havoc on your immune
system, however, the gut reations to foreign protein should be rather
telltale. This is a tissue mast cell-histamine mediated mechanism. It
seems difficult to believe that food allergies are overly responsible
for organic pathologies in the absence of morphological gut changes. I
am suspicious of "food allergy" diagnoses without gut and bowel
symptoms. It appears more plausible that organic pathologies are a
neuroendocrine-immune response to macronutrient ingestion. This is not
to say that micronutrition plays no role, it clearly does. The verdict
is not in yet and I'm not suggesting that I've "cracked the code" before
anyone else. I feel strongly that diet (macronutrients) plays a
significant role in disease by disturbing the "evolutionary" tension
along the neuroendocrine-immune axes which may have both a direct and
indirect influence on gene expression. Tumor supressor genes are under
the control of sex hormones to a large degree. The hormonal axis is
strongly influenced by cytokines/interleukins. It therefore, seens
plausible that a diet which is "out of sync" with the evolved metabolic
processes presently in place can result in a neuroendocrine-immune
environment which is perfect for altered gene expression with disease
written all over it.
When one considers disease as alterations in neuroendocrine-immune
tensions and its concomitant alteration in gene expression as simply and
ADAPTATION to a changing internal environment, then it becomes clear how
diet can be viewed as an evolutionary pressure. Unfortunately, the
lessons we have learned from disease and diet is that many of the
adaptaptions to diet we presently recognize as disease are sadly
incompatible with life.
> According to Mike Kurilla (zonehome.com/zlib0008.htm), "Another
> point to consider is that LA intakes of 20 grams per day are
> sufficient to almost completely suppress D6D activity, so that
> little if any AA is made (Adam, 1992). This finding suggests
> that AA levels in the body are largely determined by dietary
> intake under conditions of typical Western diets." Kurilla also
> points out that the average American consumes about 20 g of LA
> per day. But what about the decidedly un-average paleodieter?
I'll have to look this up. I am unaware of LA down regulating D6D
activity. I believe D6D is an allosteric enzyme where the the
concentration of the products of D6D might reduce its activity.
However, my question with this is suppression of D6D prevent LA
conversion to GLA and, although this would mean a reduction of
endogenous AA production it also means a reduction of de novo synthesis
of series 1 eicosanoids. Recall that GLA is the converted to DGLA which
is converted by the enzyme cyclooxygenase into PGE1. PGE1 is very
necessary for healthy muscosa, et al.
> I agree that this is a primary strategy. I think, though, that
> there is more to it. I recall, for example, that Atkins says
> that about one third of his patients are "fat sensitive", meaning
> that their blood lipids become elevated on his diet. I have a
> feeling that these are the people who cannot tolerate the
> elevated levels of dietary AA. Now it *may* be that it is the
> effect of dietary vegetable oils that is making them intolerant.
> Maybe these people, instead of going high-protein and low-fat as
> Atkins suggests (and risking "rabbit sickness") should switch to
> NeanderThin and avoid vegetable oils altogether.
I am concerned about the undiscussed pharmacological effects of
vegetable oils. It is a widely used therapeutic technique to use
evening primrose oil (EPO) which contains LA and GLA to block pain and
reduce inflammation. I'm not suggesting that this is all bad. When you
consider how it produces its effects one might reconsider its
importance.
The GLA in EPO is readily converted to DGLA by an elongase. As levels
of DGLA build it competes with AA for cyclooxygenase (CO). CO converts
AA to PGE2 while CO also converts DGLA to PGE1. PGE2 is inflammatory
while PGE1 is non inflammatory. However, this is not my main concern.
LA, AA and other n-6 FA are readily incorporated in the cell membranes
of immune cells. This conveys "fluidity" to the cells' membranes.
However it also gives these cells a HUGH supply of proinflammatory
precursors. Precursors which I doubt where available in such quantities
for the hunter-gatherer who did not have the means to manufacture the
vegetable oils we do.
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
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