Autoimmune diseases

Autoimmune diseases (AD) are examples of immune mediated or hypersensitivity diseases. All involve immune attacks on host cells. Often self-tissues are attacked as if they were transplanted organs being rejected. This terrible mistake has a number of inter-related causes.

Systemic Lupus Prototype of Type III -IV Illness

Systemic Lupus Erythematosis (SLE) is an immune-mediated disease which serves as a model of hypersensitivity disease. The peak incidence of SLE is in women between the ages of 20 and 40 and who present with a typical malar rash, lymphadenopathy, arthralgias, fever, fatigue and will often complain of recurrent flu-like illness. As the disease advances, increased evidence of target organ damage can be found with protein and red cells in the urine, raised ESR, pleurisy, pericarditis, hair loss, associated with the appearance of circulating auto-antibodies, especially antinuclear.

A number of prescription drugs and several industrial chemicals are known to trigger auto-immune disease. Hydralazine, isoniazid, penicillamine, practolol and other drugs can induce SLE. While they may act as incomplete antigens and contribute to immune complex formation, the toxic effects of certain drugs on the complement system may also interfere with immune complex clearing and induce SLE indirectly. SLE can be considered a disease of immune complex handling - immune complexes containing non-cellular antigens are inappropriately deposited in tissues which are then damaged by inflammatory responses. A general thesis would suggest that drugs and chemical in the environment which promote the formation of immune complexes or impair the clearing of complexes would tend to induce autoimmune disease. Hydralazine, marketed as an anti-hypertensive drug, also occurs naturally in tobacco, smoke, mushrooms and may enter the food supply through contamination with plastics, dyes, and herbicides. Individual susceptibility would be influenced by the ability to metabolize the toxic chemical. Slow acetylators, for example, are more prone to hydralazine-induced SLE.

Bardana et al reported on autoimmune reactions induced by food antigens. They recalled that Sr. Wm. Osler had first suggested that dietary proteins were important in the pathogenesis of Henoch-Schonlein purpura and arthritis. They reported on an investigation of alfalfa-induced illness in monkeys A non-nutrient amino acid, L-canavanine, found in alfalfa seeds and sprouts, was identified as a trigger of an SLE-like syndrome. The severity of illness produced by canavanine in monkeys is remarkable; a hemolytic anemia was a consistent effect. Cooking alfalfa-containing foods may remove the problem since canavanine is heat labile.

In SLE-prone mice, removing milk protein, casein, from a standard laboratory diet had a dramatic benefit - 8% of the casein-fed mice survived at 24 months; 100% of the casein-free group survived. When the milk protein, casein, is digested, protein fragments or peptides can be potent players in immune networks. A casein peptide, beta-casomorphin 4-9, stimulates immune activity, creating hypersensitivity.

Strategy Over Time

Diet revision and medication can work together. In the following example a patient with systemic lupus and advanced arthritis improved substantially with diet revision by had frequent flare-ups after eating the wrong foods and also had persisting but minimal inflammatory activity even on an elemental formula. Prednisone, used judiciously, helped to control the self-generated aspect of SLE but food control was responsible for a major remission of the disease.

Time-course of a 35 year old female patient with SLE: Her starting lab values were ANA 640 - homogeneous, IgG 23.0 (8-18.00), Hg 103 with low iron. She had an aggressive inflammatory arthritis pattern involving mostly hands, feet, and knees with constant pain, swelling, and deformity. She was frequently ill with sweating, flushing, chills, fatigue and irritability. Both prednisone and imuran had been used to control her disease without much success. She started diet revision therapy with an elemental formula off medication; after 14 days of Alpha ENF, swelling and pain subsided about 70 %; feet remained tender and her hands were still aching. Symptoms would flare periodically (bouncing-ball path) over the next 40 days - apparent reactions to food reintroduction; prednisone re-introduced after a major flare-up at 20 mg/day + ENF with clearing of symptoms over the next week; reintroduced P1 foods and reduced prednisone to 10 mg per day over the next month with increasing comfort; IgG down and Hg up... to day 60, then reduced prednisone 5 mg P1 with Alpha ENF 4 times per day. Food boundaries remained strict; some P2 foods introduced - about 1 per week. After 6 months still required prednisone 5 mg per day but doing well -working full time with minimal joint pain and no swelling. At 18 months she remained remarkably stable eating P1 and P2 foods mostly; boundaries still strict - hands and feet flare 1st with any reactive foods (especially milk and wheat). Still using Alpha ENF times per day and prednisone 5.0 mg per day. ANA 160; IgG 16.7. Busy, physically active life, working and mother' s duties.

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