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:
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  This page revised & info accurate as of |
