Paleolithic Diet Symposium List


Paleolithic Diet Symposium Listserver carries a continual discussion about the absence of grains in the early Man's diet.
The letter below was posted to this list group:


Date: Mon, 16 Jun 1997 14:07:00 -0600
Reply-To: Paleolithic Diet Symposium List <PALEODIET@MAELSTROM.STJOHNS.EDU>
From: Loren Cordain <cordain@CAHS.COLOSTATE.EDU>
Subject: Re: Response to molecular mimicry comments

In the human immune system, there are a number of individual mechanisms
which allow the body the ability to determine self from non self so that foreign
proteins (i.e. bacteria, viruses etc) can be recognized, destroyed and
eliminated.
Perhaps the most complex system which nature and evolution have engineered
to accomplish this is the human leukocyte antigen (HLA) system. This system
was discovered when early physicians found out that tissue from one human could
not be grafted to another without rejection. The physiological function of
this system was not to foil the efforts of transplant surgeons, but to initiate
an immune response to parasites (viruses, bacteria).
All cells of the body manufacture HLA proteins, whose function is to bind
short peptides (protein fragments) and display them on the cell surface. Most
of the peptides are derived from the body's own proteins (self peptides),
however when the body is infected by a virus or bacteria, the HLA molecules pick
up peptides derived from broken down proteins of the virus or bacteria and
present them to T lymphocytes.
The purpose of T-lymphocytes is to continually scan the surfaces of other
cells to recognize foreign peptides while ignoring self peptides. Once a
T-cell receptor "recognizes" a foreign peptide, a complex series of steps is set
into play which ultimately destroys the cell presenting the foreign peptide as
well as living viruses or bacteria in the body which also have peptide sequences
similar to those which were presented. When the HLA system loses the ability
to recognize self (self peptides) from non-self (foreign peptides),
T-lymphocytes attack self-tissue resulting in what is known as an autoimmune
disease (i.e. celiac disease, IDDM, MS, Dermatitis Herpetiformis, ankylosing
spondylitis etc).
The HLA proteins which present foreign peptides to circulating T-lymphocytes
are coded by DNA sequences on chromosome 6. The entire HLA system includes
more than 100 genes and occupies a region more than four million base pairs in
length which represent 1/3,000 of the total human genome. On chromosome 6,
the HLA is sub-divided into Class I (HLA-A, HLA-B, HLA-C) and Class II segments
(HLA-DR, HLA-DQ, HLA-DP).
Individuals with autoimmune disease inherit characteristic HLA combinations
which identify their disease. People with celiac disease have genetic markers
(HLA-DR3, HLA -B8 and HLA-DQ2) which are associated with the disease; people
with insulin dependent diabetes mellitus (IDDM) almost always have DQ and DR
genotypes. Thus, the manner in which foreign proteins are presented to
circulating T cells by HLA proteins tends to be different for individuals with
auto-immune diseases compared to those without these maladies.
As I mentioned in a previous post, the incidence of a variety of autoimmune
diseases follows a southeasternly gradient from northern Europe (highest
incidence) to the Mideast (lowest incidence) - can provide citations if wanted.
This gradient occurs because the incidence of susceptible HLA haplotypes
increases as one moves north westerly from the Mideast. This gradient which
occurs for both the incidence of autoimmune diseases and HLA haplotypes is not a
serendipitous relationship but occurred as a result of the spread of agriculture
from the Mideast to northern Europe (Simoons FJ. Celiac disease as a geographic
problem. In: Food, Nutrition & Evolution. DN Walcher & N Kretchmer (Eds), NY
Masson Pub, 1981, 179-199).
Consequently, as agriculture spread into Europe there were environmental
elements associated with this demic expansion which progressively selected
against HLA haplotypes (combinations of HLA genes inherited from the two
chromosomes in each cell) which were originally present in the pre-agrarian
peoples of Europe. Now, the question is, what were those environmental
selective elements? In the case of celiac disease, it doesn't take a rocket
scientist to determine that it was wheat.
Increasing consumption of wheat caused increased mortality from celiac
disease - thus, the incidence of celiac disease and its susceptible HLA
haplotypes (HLA-B8, HLA-DQ, HLA-DR) are lowest in those populations with the
most chronologic exposure to wheat (Mideasterners and southern Europeans) and
greatest in those populations with the least exposure (northern Europeans).
Similar arguments can be made for IDDM and a host of other autoimmune
diseases. There are a substantial number of animal studies showing that
consumption of wheat by rats increases the incidence of IDDM - citations
available if wanted.
How is it that wheat can wreak such havoc with the autoimmune system? Our
group believes that wheat contains peptide sequences which remain undigested and
which can enter into systemic circulation. These peptide sequences are
homologous to a wide variety of the body's tissue peptide sequences and hence
induce autoimmune disease via the process of molecular mimicry (e.g. macrophages
ingest the circulating wheat peptides and HLA molecules within the macrophage
present amino acid sequences of the fragmented peptide to circulating
T-lymphocytes which through clonal expansion create other T cells to "attack"
the offending dietary antigen and any other self antigen which has a similar
peptide sequence - i.e. the bodies own tissues). The original
non-agricultural HLA haplotypes conferred selective advantage because these
genotypes provided enhanced immunity from certain types of infectious diseases,
however with the advent of cereals in the diet they represented a liability.
Thus, the genetic data clearly shows that a recently introduced food type
has resulted in genetic discordance between our species and those from the
gramineae family.

        Cordially,

        Loren Cordain, Ph.D.
        Professor, Colorado State University


        -And yep! I'm not a her, but a him!




Another letter from the discussion is placed here:
Enig & Fallon Reply to Dr. Cordain - 29 Jun 1997



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