The dominant diseases of modernized societies as omega-3 essential fatty acid deficiency syndrome: substrate beriberi.

About 1900, modern food selection and processing caused widespread epidemics of the B vitamin deficiency diseases of beriberi and pellagra which, for genetic reasons, often expressed as different diseases ranging from bowel and heart disease to dermatoses and psychoses. But the B vitamins merely help convert essential fatty acids (EFA) into the prostaglandin (PG) tissue regulators and it now turns out that, through hydrogenation, milling and selection of w3-poor southern foods, we have also been systematically depleting, by as much as 90%, a newly discovered trace Nordic EFA (w3) of special importance to primates and sole precursor of the PG3(4) series, even as a concurrent fiber deficiency increases body demand for EFA. Since substrate EFA is processed by many B vitamin catalysts, an EFA deficiency will mimic a panhypovitaminosis B, i.e., a mixture of substrate beriberi and substrate pellagra resembling vitamin beriberi and pellagra but exhibiting as even more diverse endemic disease. This would constitute a second stage of the Modern Malnutrition and explain why some workers now hold the dominant diseases of modernized societies to be new, nutritionally based, pellagraform yet lipid-related and to range, once again, from heart disease to psychosis. It is an assumption that our dominant diseases are unrelated to each other or are merely revealed by out diagnostic acumen and therapeutic success; and that hydrogenating millions of tons of food oils annually, to destroy the rancidity producing w30EFA, is safe for primates. Extensive beriberiform disease is reported here in 32 typical cases taken from medical practice which responds strikingly to linseed oil supplements (60% w3-EFA) in confirmation of identical results in Capuchins.

The major psychoses and neuroses as omega-3 essential fatty acid deficiency syndrome: substrate pellagra.

Pellagra was once a major cause of three behaviorally different mental disorders-schizophreniform, manic-depressive-like, and phobic neurotic - plus drying dermatoses, autonomic neuropathies, tinnitus, and fatigue. In this preliminary study all three of the corresponding present-day mental diseases are found to exhibit, statistically, the same pellagraform physical disorders but to ameliorate not so much with vitamins as with supplements of a newly discovered trace omega-3 essential fatty acid (w3-EFA), which provides the substrate upon which niacin and other B vitamin holoenzymes act uniquely to form the prostaglandin 3 series tissue hormones regulating neurocircuits en block. Since present-day refining and food selection patterns, as well as pure corn diets, deplete both the B vitamins and W3-EFA, the existence of therapeutically cross-reacting homologous catalyst and substrate deficiency forms of pellagra are postulated, the first contributing to the B vitamin deficiency epidemics of 50-100 years ago, the second to the more recent endemic "Diseases of Western Civilization" which express in certain genetic subgroups as the major mental illnesses of today.

The choroid plexus and system disease in mental illness. III. The exogenous peptide hypothesis of mental illness.

Based on the apparent existence of a second (choroid plexial) blood-brain barrier offering a new brain attack mechanism on the periventricular primary personality brain (Rudin, 1980) and which may be breached to produce the schizophreniform psychosis characteristic of systemic lupus erythematosus (Rudin, 1981), we here assess the evidence that viruses and exogenous peptides, including especially the glutens of cereal grains, may be the primary triggers for schizophrenia. Schizophrenia would then be supposed to result as one expression of gene-determined combined transport organ dysfunction with underlying basal laminar immunopathy at the tissue level and possibly a prostaglandin disorder at the chemical and membrane level in turn, finally disrupting neurotransmission in the periventricular limbic system. We conclude that the evidence warrants test of the hypothesis, including a clinical trial under national auspices employing an elemental diet, plasmapheresis, immunosuppression together with an antiviral regimen.

The choroid plexus and system disease in mental illness. II. Systemic lupus erythematosus: a combined transport dysfunction model for schizophrenia.

Carr et al. (1978) and Rudin (1979) independently suggested tat systemic lupus erythematosus (SLE) might provide a model for schizophrenia since SLE is strongly associated with schizophreniform psychoses and exhibits only a covert CNS pathology revealed by immunofluorescent immune complex deposits in the choroid plexus. To carry the concept forward we here examine SLE employing the ideas developed in the preceding paper (Rudin, 1980) indicating that the choroid plexus is part of a second blood-brain barrier guarding the periventricular primary personality brain, the limbic system, and that the choroid plexus is also but one of a set of "transport organs" sharing common vulnerability to covert basal lamina immune complex pathology. In this context both SLE and schizophrenia are viewed as expressions of combined transport dysfunction syndromes, resulting from polygenic-induced sensitivity to exogenous peptides or viruses causing basal laminar immune complex disease, but exhibiting differing statistical expressions over the transport organ group due to difference in genes which elicit different transport organ sensitivities to different exogenous viruses or peptide antigens. Immune disease processes are briefly reviewed.

The choroid plexus and system disease in mental illness. I. A new brain attack mechanism via the second blood--brain barrier.

Schizophrenia and certain idiopathic neuroses and retardations may be caused by polygenic sensitization to exogeneous peptide antigens or viruses causing a covert immune complex basal lamina disease of the choroid plexus. This organ has the general structure and disease susceptibility of many other transport organs but acts as a second blood--brain barrier putting at risk to contamination and dysfunction the periventricular primary personality (limbic) brain now thought to be centrally involved in schizophrenia. Genetic variability selects different antigens and different target organs so that a complex statistical structure of disease expression can result over the transport organ group as well as between this group and the endocrines and exocrines. This leads to the concept of intra- and intercombined system diseases all of which may have a covert biphasic (hyper-hypo) time course. To this extrinsic combinatorial complexity may be added an intrinsic or neural combinatorial complexity resulting from the fact that the choroid plexus is threaded throughout the limbic system and subject to spotty disease characteristic of many immunopathies. In this way a wide range of behavioral disorders may arise as well as mental retardations if the process occurs during development. In this paper we discuss basic mechanisms. In the next paper of the series we examine systemic lupus erythematosus, the prototypical "combined transport dysfunction," as a model for schizophrenia. In the last paper we search for specific exogeneous peptide triggers for schizophrenia viewed as one expression of combined transport organ dysfunction. We conclude that immunofluorescent and virological surveys should be conducted in all mental illnesses as well as clinical trials of interferon therapy and elemental diets.

Glaucoma, "auditory glaucoma", "articular glaucoma" and the third eye.

Galucoma may be one of a set of "baropathic" disorders including tinnitus, Meniere's disease, arthritis and bursitis caused by transport dysfunction in the "tissue membranes" of the set of closed "tissue cells" envisioned by The Tissue Cell Theory of Metazoa and which result, in turn, from prostaglandin disturbances induced by primary or secondary essential fatty acid deficiencies possibly coupled with immunopathic effects.

Covert transport dysfunction in the choroid plexus as a possible cause of schizophrenia.

Schizophrenia and certain forms of idiopathic mental retardation may result from covert immune complex disease of the basal lamina of the choroid plexus, a process already known to cause covert transport dysfunction in similar structures of, for example, skin, bowel, kidney, and endocrines. Plexial attack could lead to cerebrospinal fluid contamination and then, via an "open" ependyma, to neurotransmitter dysfunction in the periventricular limbic brain. The immune complex mechanism implies polygenic induction, direct or autoimmune, of immune sensitivity to exogenous agents and is thus compatible with the genetic picture in schizophrenia. Candidate agents include viral coat peptides and cereal grain glutens. The glutens are known to cause immune complex skin and bowell disease variants, and some empirical evidence links them to schizophrenia. Only newer immunofluorescence methods can detect the pathology, which is otherwise silent. Systemic lupus erythematosus provides a model since it is a genetic immune complex disease strongly associated with schizophreniform psychoses, exhibits choroid plexial immunofluorescence but no central nervous system pathology by ordinary methods, and may be triggered by viruses.