Evolutionary Discordance of Grains/Legumes in Diet - PART B
Up to this point, we have only briefly touched upon the role cereal grains have in inducing autoimmune disease (except for a brief look at celiac disease). There is substantial evidence (both epidemiological and clinical) showing the role cereal grains may play in the etiology of such diverse autoimmune diseases as multiple sclerosis (MS), insulin-dependent diabetes mellitus (IDDM), rheumatoid arthritis, sjogrens syndrome, dermatitis herpetiformis, and IgA nephropathy.
Although this proposal may at first seem preposterous, there is strong data to suggest that cereal grains may be involved in all of these diseases through a process of molecular mimicry whereby certain amino acid sequences within specific polypeptides of the gramineae family are homologous to (have the same structural form as) a variety of amino acid sequences in mammalian tissue. These homologous amino-acid (AA) sequences can ultimately confuse our immune systems so that it becomes difficult to recognize "self" from "non-self." When this happens, T-cells, among other immune-system components, launch an autoimmune attack upon a body tissue with AA sequences similar to that of the dietary antigen.
It seems that grass seeds (gramineae) have evolved these proteins with similarity to mammalian tissue to protect themselves from predation by mammals, vertebrates, and even insects. This evolutionary strategy of molecular mimicry to deter predation or to exploit another organism has apparently been with us for hundreds of millions of years and is a quite common evolutionary strategy for viruses and bacteria. It has only been realized since about the mid-1980s [Oldstone 1987] that viruses and bacteria are quite likely to be involved in autoimmune diseases through the process of molecular mimicry. Our research group has put together a review paper compiling the evidence (and the evidence is extensive) implicating cereal grains in the autoimmune process, and with a little bit of luck it should be published during 1998. [Editorial note as of June 1999: The paper has now been published; the citation is: Cordain L (1999) "Cereal grains: humanity's double-edged sword." World Review of Nutrition and Dietetics, vol. 84, pp. 19-73.]
Without the evolutionary template and without the evidence provided us by the anthropological community showing that cereal grains were not part of the human dietary experience, the idea that cereal grains had anything to do with autoimmune disease would probably have never occurred to us. This new electronic medium has allowed instant cross-fertilization of disciplines which probably would have rarely occurred as recently as five years ago.
Up to this point, we have only briefly touched upon the role cereal grains have in inducing autoimmune disease (except for a brief look at celiac disease). There is substantial evidence (both epidemiological and clinical) showing the role cereal grains may play in the etiology of such diverse autoimmune diseases as multiple sclerosis (MS), insulin-dependent diabetes mellitus (IDDM), rheumatoid arthritis, sjogrens syndrome, dermatitis herpetiformis, and IgA nephropathy.
Although this proposal may at first seem preposterous, there is strong data to suggest that cereal grains may be involved in all of these diseases through a process of molecular mimicry whereby certain amino acid sequences within specific polypeptides of the gramineae family are homologous to (have the same structural form as) a variety of amino acid sequences in mammalian tissue. These homologous amino-acid (AA) sequences can ultimately confuse our immune systems so that it becomes difficult to recognize "self" from "non-self." When this happens, T-cells, among other immune-system components, launch an autoimmune attack upon a body tissue with AA sequences similar to that of the dietary antigen.
It seems that grass seeds (gramineae) have evolved these proteins with similarity to mammalian tissue to protect themselves from predation by mammals, vertebrates, and even insects. This evolutionary strategy of molecular mimicry to deter predation or to exploit another organism has apparently been with us for hundreds of millions of years and is a quite common evolutionary strategy for viruses and bacteria. It has only been realized since about the mid-1980s [Oldstone 1987] that viruses and bacteria are quite likely to be involved in autoimmune diseases through the process of molecular mimicry. Our research group has put together a review paper compiling the evidence (and the evidence is extensive) implicating cereal grains in the autoimmune process, and with a little bit of luck it should be published during 1998. [Editorial note as of June 1999: The paper has now been published; the citation is: Cordain L (1999) "Cereal grains: humanity's double-edged sword." World Review of Nutrition and Dietetics, vol. 84, pp. 19-73.]
Without the evolutionary template and without the evidence provided us by the anthropological community showing that cereal grains were not part of the human dietary experience, the idea that cereal grains had anything to do with autoimmune disease would probably have never occurred to us. This new electronic medium has allowed instant cross-fertilization of disciplines which probably would have rarely occurred as recently as five years ago.
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