Systemic lupus erythematosus: one disease, a thousand faces, a potent management
Author: Gar Hildenbrand
Lupus, Latin for wolf, is the word used historically to describe any chronic, usually ulcerating, skin disease. Dr. Max Gerson’s rise to medical prominence in pre-WWII Germany was owed to the curative effect in lupus vulgaris of a salt-free diet bearing his name. Lupus vulgaris, a European plague of the early part of this century, was tuberculosis of the skin, a bacterial disease that has been largely eliminated through improved public health measures and, to a lesser extent, by antibacterial drugs.
Today’s lupus is systemic lupus erythematosus (SLE), an inflammatory disorder of connective tissue which frequently targets skin (hence the designation lupus) as well as joints, kidneys, mucous membranes, the nervous system, and virtually any other organ or system in the body. Onset of the disease may be sudden and acute, with fever, painful and swollen joints, skin rash, and influenza-like symptoms; or it may smolder for years with low level malaise and intermittent fevers.
The list of symptoms attributable to SLE is extensive and astonishing. Among symptoms most frequently observed are painful joints, usually of the hands and feet, which may also include the larger joints. Of all SLE patients, 92% endure significant joint pain. Similarly, 84% of all SLE patients suffer from fevers. Skin eruptions, including round or discoid lesions, as well as a butterfly rash presenting on the cheeks below the eyes and bridging the nose, will afflict 72%. Inflammatory kidney dysfunctions, including bloody urine, loss of proteins through urine, high blood pressure, edema, and nephrotic syndrome are seen in 60%.
50% of all SLE patients will experience inflammation of the pleural sack around the lungs and the collection of effusion fluids in the pleural cavity. 50% will suffer from the symptoms of inflammation of the pericardial membrane, including chest pains, dry cough, shortness of breath, and rapid, violent, throbbing or fluttering pulse. 50% will have swollen lymph glands. 25% will experience neurologic symptoms which may include convulsive seizures, organic brain syndrome, delusions, visual and auditory hallucinations, severe depression and frank psychoses (which are too often intensified by corticosteroids). 20% are troubled by Raynaud’s disease in which small blood vessels, chiefly of the fingers, inappropriately constrict in response to cold or to emotional stress, causing pallor, then cyanotic blue coloration, and finally redness before normal circulation is restored. 10% will have a swollen spleen.
Other clinical manifestations may include: edema, Hashimoto’s thyroiditis, hemolytic anemia, blood clotting in either veins or arteries, thromocytopenic purpura including internal hemorrhages and bleeding from mouth and skin on slight injury, recurrent bronchial pneumonia, occasional temporary blindness and blurred vision, hair loss, fingertip lesions, redness around the fingernails, nail fold infarcts, dry and malformed nails, abdominal pains due to inflammation of the peritoneal membrane, and intestinal obstruction frequently involving the right colon with abdominal distention and vomiting. There are many more possible clinical features — literally, any and every internal organ may be targeted — varying widely from one individual to the next.
Survival and incidence
According to recent literature reflecting the results of conventional SLE treatment, 10% of patients will die within one year of diagnosis. Historically, nearly 25% have died within the first five years. Some community and university treatment centers have reported gains in survival, but it is not clear that these studies were free from selection and sample biases. The chief causes of death are kidney failure and intercurrent infections.
Originally thought to be a relatively rare disease, improved antinuclear antibody testing (Christian, C., Arth Rheum 25:887,’82) has shown it to occur at the rate of 1:2000. Incidence in females outweighs that in males by 9:1. It may present at any age, including childhood, but is most frequently seen in the teen and young adult years.
What is SLE?
According to Dr. Stanley Robbins’ in his Pathologic Basis of Disease (W.B. Saunders Co., Philadelphia, PA), “Systemic lupus erythematosus is the classic prototype of the multisystem disease of autoimmune origin, characterized by a bewildering array of autoantibodies, particularly antinuclear antibodies.”
Robbins also holds that “the fundamental defect in SLE is a failure of the regulatory mechanisms that sustain self-tolerance.” In terms of immunology, “tolerance” is a state in which the host will not react with an immune response against a specific antigen. Our immune systems are “self/not-self” recognition mechanisms. They keep constant surveillance against intruders, looking for signs of nonconformity and possibly checking for “secret passwords” that may identify all components of the self. “Not-self” antigens do not conform to the characteristics of the self and, perhaps, cannot give the password. “Self-tolerance” describes the ability of our cells to live together in harmony. Perhaps an apt sociological metaphor for SLE might be the U.S. Senate’s redbaiting McCarthy era, when Americans were mistaken for foreign invaders and attacked by Americans.
In SLE, antibodies are formed against antigens which are normal to the self, or host. According to Hellman, SLE’s “clinical manifestations are thought to be secondary to the trapping of antigen-antibody complexes in capillaries of visceral structures.”
Antibodies are produced by our bodies to interact with antigens. Antibodies are protein substances which are part of the serum immunoglobulins. Antigens are defined by their ability to elicit antibody responses. In SLE, interaction of autoantibodies with self antigens causes the formation of circulating immune complexes (CIC) which can form clogging deposits in the smaller vessels of the circulatory system, and in passage channels anywhere in the body. It is the collection of CIC in target tissues which is thought to be the cause of inflammation and failure at those sites.
According to Terr and Stites (“Allergic and Immunologic Disorders” (in Current Medical Diagnosis and Treatment, 1992, Appleton & Lange, Connecticut and California), “Therapy of autoimmune diseases involves a variety of approaches. Suppression of production of autoantibodies with corticosteroids and cytotoxic agents is often effective. Anti-inflammatory drugs such as aspirin, NSAIDS (nonsteroidal anti-inflammatory drugs), colchicine, and corticosteroids relieve tissue damage from immune complexes. Plasmapheresis to remove offending autoantibodies and circulating immune complexes, when combined with cytotoxic drugs, has been useful in some diseases. All of these modalities are directed at symptoms, since the underlying cause of these disorders remains unknown” (emphasis ours –ed.).
Avoidance of direct sunlight exposure is absolutely necessary for SLE patients with active disease. Topical steroids have been a mainstay of treatment for SLE skin lesions since their introduction. Aspirin and ibuprofen have been indispensable to alleviate joint pain. Hydroxychloroquine, an antimalaria drug, has been employed against joint and skin inflammations, but it has a tendency toward side effects.
Because SLE is so varied in its presentation and course from patient to patient, treatment often amounts to little more than reassurance and encouragement during quiescent periods, and escalates to firefighting during attacks. In fact, the observation of patients with active SLE can be likened to watching a droughted forest for outbreaks of fire during an electrical storm. The effects of treatment on survival have not been well established.
The Centro Hospitalario Internacional del Pacifico, S.A. (CHIPSA), is one of a number of facilities worldwide which offer alternative medical managements for SLE and other autoimmune diseases of the CIC type. During the first years of operation, CHIPSA clinicians and Gerson Institute consultants observed profound improvements in some patients with systemic lupus erythematosus (SLE) who were treated with Gerson’s diet therapy as adopted by the CHIPSA physicians. Response to treatment was unpredictable from patient to patient, and not all who were treated enjoyed benefit. Among those who did benefit, improvements regularly included normalization of laboratory parameters (sedimentation rate, ANA, red blood count, creatinine clearance) and alleviation of clinical manifestations (malar rash, oral ulcers, joint inflammation, photoallergy, serositis of the pericardium).
Follow-up revealed that even for those who benefited substantially, discontinuance of the Gerson diet therapy led to a return of symptoms. For this reason, CHIPSA physicians prescribe some aspects of the diet therapy as permanent inclusions in the ongoing lifestyle of SLE-prone persons.
The Gerson therapy is an integrated set of medical treatments. CHIPSA and the Gerson Institute inherited Gerson’s therapy, but without a deep understanding of the influence of its various components on different pathologies. Because of this, during the first years of practice, results were uneven, and mistakes were made in the management of SLE patients. In most cases, those mistakes were not life-threatening, but in a few they were.
In particular, we recall the precipitous discontinuance of steroid support for a young Canadian girl with SLE. This event was brought about by the urgings of paramedicals who wielded great influence over the family of the patient and, subsequently, over the treating physicians. These people truly believed that steroids were dangerous and should be stopped, and that Gerson’s treatment would “take over” to control the SLE inflammatory crisis. In short, in the sudden absence of steroids, the child became rapidly critical, having to be rescued by the same steroids which had been viewed as “part of the problem.” Unforgivable from a medical point of view, that experience drove home in the physicians a sense of bottom-line personal responsibility and, as a consequence, stronger reliance on their own clinical judgment and authority.
In the early years, lack of knowledge of several budding and extraordinarily important lines of research left CHIPSA and the Gerson Institute without a sense of potent rationales, and therefore without a sense of direction in the treatment of patients who did not respond easily and early on. In addition, some patients who did well while on the diet therapy experienced relapses of SLE after relaxing the practices of the treatment, and there was no way to guess which of their new dietary practices might be at fault. Was the relapse due to deficiency, or to excess? What were the cornerstones of nutritional control of SLE?
Toward the middle of the 1980s, we were fortunate to meet Dr. Nick Gonzales, who then worked in the lab of Robert A. Good. He introduced us to the protein-calorie restriction experiments conducted by Good, and we thereby became acquainted with his publications. Our first survey of the literature of Good and David G. Jose filled in many holes, provided a number of surprises, and suggested opportunities for improved clinical practice.
Although the literature reveals that experiments indicating the value of calorie restriction were conducted more than eighty years ago by Moreschi (Zeitschr.f.Immunitatsforsch., 2:651-675, 1909) and Rous (J.Exp.Med., 20:433-451, 1914), Good and collaborators keyed off of Cornell’s McCay, Crowell and Maynard (J.Nutr., 10:63-79, 1935).
Beginning in the early 1970s, Robert Good bellwethered research into the effects of malnutrition and, later, “undernutrition without malnutrition,” on immunity and disease. We have written, in general, of this work [see: How the Gerson therapy heals. Healing 6(3-4), 1990], but it is of such great value that it bears a closer look. We shall do so here, with SLE as our first focus, and also in light of the broader considerations of aging and its associated diseases.
To begin with, we offer the observation that there are no reports in the modern mainstream literature regarding nutritional control of human SLE in clinical trials. All of the literature in which solid objective evidence supports the ability of nutritional manipulation to regress SLE autoimmunity is based on animal models, notably the NZB mouse, and many others.
The value of modern animal model laboratory investigations is moot unless the measures under evaluation have been extended successfully to human clinical trials. The reasons for this are many, but the most important one is that most species react in quite different ways to any given agent. For example, morphine excites cats, penicillin kills guinea pigs, and chocolate can be lethal to dogs. Of course, none of these findings means anything in human applications.
However, restriction of calories, in the context of a diet which supplies adequate amounts of all known nutrients, provides powerful immune stimulation to a wide variety of experimental species, and early clinical experimental results suggest similar responses in man.
Good and Jose
The initial researches of Good and Jose were conducted on separate continents. Good had long been interested in nutrition, and had visited his colleague, Professor Galel Aref in Egypt in 1969 to look more closely at the immune suppressing effects of long term malnutrition in Egyptian children. These children were deficient in both humoral (antibody) and cell-mediated (T-lymphocyte) immunity, and they succumbed to numerous viral and bacterial challenges. There were many reports in the literature with similar observations in other malnourished populations.
As Good wrote (Int. J. Immunopharmac., 14(3):361-366,1992), “However, our interest was piqued especially by a report from David Jose and his colleagues in Australia. These investigators reported that Aborigines, who became malnourished upon weaning and regularly developed a decreased ability to produce antibodies, unexpectedly showed increased proliferative responses of T-lymphocytes upon stimulation with certain phytomitogens,” (Jose & Welch, Aust.Pediatr.J., 5:209-218, 1969).
Good invited Jose to join his lab, then at the University of Minnesota, Minneapolis. Together, they set out to investigate the paradox presented by the Aborigines, people whose long term “malnutrition” resulted in increased T-lymphocyte responsiveness.
Good wrote, “We showed that moderate or severe protein and protein-calorie restriction in mice inhibited development of antibody producing cells and production of circulating antibodies, regardless of the specific composition of the diets used. In contrast, cellular immunity (the thymus-dependent immune functions) was undiminished in protein or protein-calorie malnourished mice and rats, but, in some cases, was even enhanced,” (Jose, Cooper & Good, JAMA, 218:1428-1429, 1971).
As research progressed, Good showed that protein-calorie restriction could cause in animals the same enhanced response to phytomitogens seen in Australian Aborigines. In addition, he and his fellow researchers showed that even at presumably dangerously low protein levels, 3-5%, “cell-mediated immunity remained intact and in some cases appeared to be greatly increased, as in the development of cell-mediated responsiveness to stimulation with minute doses of antigen. What defects in T-cell immune responsiveness did occur were consequent to defective inflammatory expression of cellular immunity rather than to defects of T-lymphocyte-mediated immune responses. Furthermore, we noted that protein or protein-calorie restriction augmented delayed allergic reactions, increased the capacity for lymphoid cells to initiate graft-vs-host reactions, up-regulated cellular immune responses against syngeneic and allogeneic tumor cells, and even increased the capacity to resist certain types of viral infections,” (Good, Jose, Cooper, Fernandes, Kramer, Yunis, Malnutrition and the Immune Response, (ed. Suskind) 169-183, Raven, NY, 1977; Good, West, Fernandes, Fedn.Proc., 39:3089-3104, 1980).
The reason for universally depressed immunity in malnourished third-world children as opposed, in stark contrast, to enhanced immunity in laboratory experimental models under apparently similar conditions became clear. According to Good, “We reasoned that differences in the consumption of adequate levels of micronutrients might be at work in this dichotomy — the laboratory animals we had studied had been provided with all essential nutrients and trace elements, but protein-calorie malnourished children in the Third World obviously were deficient in many of these micronutrients as well as in protein and calories,” (Good, Lorenz, Int.J.Immunopharmac., 14(3):361-366, 1992).
While it was known that food restriction, per se, extended life span, it was not known whether one of the three calorie sources, protein, fat or carbohydrate, was the cause of “early” deterioration and death in full-fed animals. Several strains of mice, (NZB x NZW)F1 hybrids which develop a human analog autoimmunity and serve as an SLE model, and two other autoimmune-prone strains, MRL/MpJ-lpr/lpr and BXSB/MpJ were used to study the question (Kubo, Johnson, Gajjar, Good, J.Nutr., 117:1129-1135, 1987; Gajjar, Kubo, Johnson, Good,J.Nutr., 117:1136-1140, 1987).
Undernutrition, not malnutrition
According to Good, “The answer was clear and unmistakable. Using diets fed so that vitamin, mineral, and required protein intakes were identical between full-fed and food intake-restricted mice and only calories were limited in the restricted mice, the very large differences in survival depended solely on the calorie intake and not on the source of calories. The diets fed to the mice consuming a restricted calorie intake contained either 62% of the calories as carbohydrate (sucrose + glycerol) or 69% of the calories as fat (lard), or in the case of protein as much as 86% of the calorie intake (the higher level in this case is of course to allow adequate essential protein for the full-fed group and yet keep protein as the primary energy source in the restricted group). The groups consuming the restricted intakes were restricted to 60% of the calorie intake of the full-fed groups. In all cases, regardless of calorie source, the mice fed the 60% calorie intake lived from two to three times longer than their paired full-fed mice. There was, however, a secondary effect of fat so that the mice which consumed a restricted calorie intake of a diet proportionate in fat almost uniformly died at approximately twice the age of the full-fed mice. On the other hand, those mice placed on chronic energy intake restriction of a high carbohydrate diet that was also low in fat lived two to four times longer than full-fed mice. They lived on average three times as long as full-fed mice consuming diets relatively high in fat or carbohydrate, and the longest survivors lived more than 44 months. These results suggest a separate additional harmful effect of fat, as has been repeatedly reported” (Johnson, Good, Proc.Soc.Exp.Biol.Med. 193:4-5, 1990).
As Good observed in his experimental system (indirectly reflecting a rationale for Gerson’s diet therapy), “Thus, at least in experimental settings, if zinc and other essential nutrients were supplemented in adequate amounts, macronutrients such as protein, carbohydrates, fats, and total calories might be variously manipulated and their influence on immunity systems observed,” (Good, Lorenz, Int.J.Immunopharmac., 14(3):361-366, 1992).
As his experimentation progressed, Good came to refer to his basic nutritional manipulation as chronic energy intake restriction (CEIR). Over the course of fifteen years, he and his colleagues studied the influence of CEIR in many short-lived laboratory animals bred to develop disease. In Good’s own words, “CEIR…could double, triple, or even further extend lifespan in these inbred, short-lived mice. Moreover, CEIR delayed or, in some instances, completely inhibited development of autoimmunity diseases to which these mice succumb, particularly progressive, immunologically based hyalinizing renal disease, vascular lesions, lymphoproliferative disease, and even certain malignancies,” (Fernandes, Yunis, Good, Proc. natn.Acad. Sci. U.S.A., 73:1279-1283, 1976; ______, Nature, 263:504-506, 1976; Fernandes, Friend, Yunis, Good, Proc. natn. Acad. Sci., U.S.A., 75:1500-1504, 1978; Fernandes, Yunis, Miranda, Smith, Proc. natn. Acad. Sci. U.S.A., 75:2888-2882, 1978; Sarkar, Fernandes, Telang, Kourides, Good, Proc. natn. Acad. Sci. U.S.A., 79:7758-7762, 1982; Fernandes, Alonso, Tanaka, Thaler, Yunis, Good, Proc. natn. Acad. Sci. U.S.A., 80:874-877, 1983; Fernandes, Good, Proc. natn. Acad. Sci. U.S.A., 81:6144-6148, 1984).
In the presence of normal calorie intake levels, the source of calories had no statistically significant effect on lifespan in autoimmune mice, i.e. no difference was seen in the effects of a very high fat/no carbohydrate diet and a very low fat/high carbohydrate diet (Kubo, Johnson, Gajjar, Good, J.Nutr., 117:1129-1135, 1987; Gajjar, Kubo, Johnson, Good, J.Nutr., 117:1136-1140, 1987). However, the same diets fed at restricted calorie levels both increased lifespan in the same mice.
Low fat, low calorie best
Good stressed that, “The most dramatic shift in longevity curves occurred with a diet relatively low in fat and relatively high in carbohydrate that was fed at the CEIR level (restriction of 40% in total calories). Restriction can be imposed as late as midlife and still succeed at forestalling disease onset and greatly extending lifespan. However, for most powerful regulation of lifespan and health, CEIR is best imposed at time of weaning,” (emphases ours –ed.).
Impressive findings have accumulated rapidly over the recent decade. Although the basic mechanisms of age-related disease retardation and lifespan extension are not known, it has been shown that CEIR prevents age-related immune system deterioration and forestalls the formation of circulating immune complexes (CIC) and their accumulation in kidney glomeruli capillaries, with implications for similar benefits to other common CIC target organs and tissues (Izui, Fernandes, Hara, McConahey, Jensen, Dixon, Good, J.exp.Med., 154:1116-1124).
CEIR retards age-associated losses in interleukin-2 (IL-2) response and lowered IL-2 production levels (Jung, Palladino, Calvano, Mark, Good, Fernandes, Clin. Immun. Immunopath., 25:295- 301, 1982).
Increased attention to the role of antioxidants in the delay of aging and related illness led to studies which illuminated the selective enhancement by CEIR of radical scavenging enzymes, e.g. superoxide dismutase, and subsequent protection of the host against the destructive influences of oxidative stress (Kubo, Johnson, Misra, Dao, Good, Nutr.Rep.Int., 35:1185-1194, 1987).
Vitamin A absorption by the gastrointestinal tract is increased by CEIR, which probably adds to the above protection against oxidative stress through the antioxidative action of vitamin A (Hollander, Dadufalza, Weindruch, Walford, Expl Gerontology, 9:57-60, 1986). Additionally, CEIR increases peroxide cleaving catalase activity (Koizumi, Weindruch, Walford, J.Nutr., 117:361-367, 1987).
Insulin and glucose regulation by CEIR is a probable key mechanism in maintaining immunologic integrity and resisting age-associated disease, especially when seen in light of the role of glucose in glycation of nonenzymation protein and formation of endstage glycosylation products as proposed by Cerami, who showed a CEIR induced reduction in serum insulin and insulin-like growth factors (Cerami, Vlassara, Brownlee, Scient.Am., 256:90-94, 1987). Additionally, plasma glucose has been lowered by CEIR (Masoro, In Biological Effects of Dietary Restriction, Ed. Fishbein, Springer, NY, 1991).
An integrative hypothesis developed by Walford and Crew presents an appealing possibility, that CEIR provides greater energy to cellular and molecular repair and critical maintenance processes by decreasing energy consumption of systems of reproduction and the pituitary-hormonal axis, as well as by reducing the binding of maintenance/repair specific genes by so-called trans-acting factors (Walford, Crew, Growth Dev. Aging, 53:139-140). This view is strengthened by observed CEIR induced reduction of the basal, or nonstimulated, rate of cellular proliferation at a number of important sites, including the epithelial layer of the entire gastrointestinal tract, as well as lymphoid tissues, e.g. thymus, liver, and spleen (Ogura, Ogura, Dao, Ikehara, Good, Procl. natn. Acad. Sci. U.S.A., 86:5089-5093, 1989).
In a state of the art lecture (Del.Med.Jrl., 62(1): 743-746, 1990) Good observed, “In NZB and NZB/NZW F1 MRL lpr/lpr and BXSB mice, the composition and total amount of food eaten (total energy-intake) have profound influences on the development of disease…In short-lived autoimmune-prone mice, protein restriction delays or inhibits development of the immunological abnormalities, (the early thymic involution, splenomegaly, cellular, serological and hematological abnormalities and significantly prolonged life of mice of each of these short-lived autoimmune-prone strains. Diets low in fat and relatively high in protein (that were probably also relatively low in calories) did, however, significantly prolong life of the short-lived autoimmunity prone mice. Diets low in calories, protein and fat (total food intake) but not low in vitamins or minerals regularly doubled and sometimes even tripled life span in the short-lived autoimmune-prone B/W mice.”
Good has reasoned that CEIR promises, for humans, a way to foster longevity with good health in later life, and to delay or prevent diseases of aging, including cancer. The authors concluded that, “No other experimental influence thus far studied carries such incredible promise,” (Good, Lorenz, Int. J. Immunopharmac., 14(3):361-366, 1992).
Walford’s human trial
The Los Angeles Times reported on Tuesday, November 17, 1992, In the Arizona desert, UCLA Prof. Roy Walford is trying to delay the onset of old age through his diet.
Walford and seven other scientists who are living in a glass-enclosed three-acre greenhouse known as Biosphere II are engaged in the first human version of a well-known study in which Walford found that a severely restricted, low-calorie diet could double the life expectancy of rats and mice.
Now, Walford and the other biospherians are subsisting on 1,800 calories per day, compared to the usual 2,500. According to Walford, the group eats only what is grown in the dome — grains, vegetables, fruit and one serving of meat per week.
According to the 68-year-old Walford, who has been following the diet for more than five years, the group is exhibiting the same changes as the rodents. Each has dropped an average of 14% in body weight since the experiment began 13 months ago. Their cholesterol is lower — an average of 130, down from 200 — and their blood sugar has declined.
“This is the first well-monitored human application of the idea,” Walford said, “and it indicates that humans respond the same as animals.”
– from Unlocking the Secrets of Aging, Sheryl Stolberg, Times Medical Writer.
Diet therapy for SLE
Keen and Gershwin (Ann. N.Y. Acad. Sci., 587:208-217, 1990) have observed, “Typically, the pharmacological agents which are used in an autoimmune disease such as SLE in humans and murine lupus include both immunosuppressive and antiinflammatory drugs, most notably the corticosteroids. Unfortunately, while these drugs are often effective in retarding the development of glomerulonephritis, and they can prolong the lifespan of the animal, their long-term use is associated with a number of side effects including an increased incidence of neoplasms and potential allergic reactions to the drugs in question. In theory, the use of dietary manipulations to treat autoimmune disease in concert with more conventional drug therapy could offer an advantage over the drug therapy alone, since drug dosages could probably be reduced, thus minimizing the negative side effects associated with their use.”
In the same article, the authors noted that deficiencies of a few specific nutrients, such as the two amino acids, phenylalanine and tyrosine, as well as zinc, and phosphorus, could delay the onset of autoimmunity in certain mice. They also pointed to protein-calorie restriction and n–3 fatty acids as potent interventions in animals. They posited, “we consider it likely that diet therapy will become a powerful tool in the treatment of autoimmune disease in the near future. In our opinion, the diet therapies which will probably prove to be more useful will involve diet supplements, such as n–3 fatty acids or possibly vitamin A, rather than diet deficiencies.”
In recent years, CHIPSA doctors have come to understand the dietary treatment of rheumatoid disease in a more practical way. Demystification of predictive rationales has allowed for construction of a clinical algorithm which takes into account the varying caloric utilization rates, and other types of biodiversity, from patient to patient.
In studying the results of the first fifteen years of Good’s collaborative efforts, we came to an understanding that Gerson’s protein-calorie restricted dietary probably preserved T-cell immunities by providing ample micronutrient intake through the frequent application of raw vegetable juices as well as the crude liver extract and vitamin B-12 injections which were a standard part of his dietary therapy. Gerson’s citation (A Cancer Therapy, Results of Fifty Cases Gerson Inst., CA, 1990) of Albert Tannenbaum lends credibility to the assumption that Gerson was well aware of his findings, that calorie restriction inhibits tumor initiation and growth, and that fats promote, in most circumstances, already initiated tumors (Tannenbaum,Am.J.Cancer, 38(3):335-350, 1940; Cancer Rsrch., 2:460-467, 1942; Cancer Rsrch., 2:468-475, 1942; Cancer Rsrch., 5(11):609-615, 1945; Cancer Rsrch., 5(11):616-625, 1945).
It has become apparent, as well, that although Gerson’s sweet juices, carrot/apple and orange, contribute significantly to calorie intake (about 1,000 calories), administration of exogenous thyroid alters the ratio of calorie input to host needs, probably creating the physiological impression of reduced caloric intake and affecting host weight (Tannenbaum, Cancer Rsrch., 10:684-688, 1950). The total caloric input of Gerson’s diet therapy as described in A Cancer Therapy, Results of Fifty Cases is about 2,000/day, well below ad libitum intake levels of the general population estimated recently at 3,500/day.
An additional finding stemming from CEIR research was forwarded by Fernandes (Proc.Soc.Exper.Biol.Med., 193:16-21, 1990), “Feeding oils rich in Ω3 fatty acids, such as fish oil or linseed (flax) oil, lowers the level of arachidonic acid in phosphoglycerides of tissue membranes, including those of macrophages”, positively affecting immune function by reducing two-series prostaglandins and preventing T-cell interference with B-cell function. A number of recent studies have shown Ω3 fatty acids to protect against autoimmune disease in animals and in humans, (Buus, Sette, Colon, Science, 242:1045-1047, 1988; Lees, Brostoff, In Myelin, ed. Morell, Plenum, NY, 1984; Muckerheide, Apple, Pesce, J.Immunol., 138:833-837, 1987; Higgins, Weiner, J.Immunol., 140:440-445, 1988).
The confidence of CHIPSA physicians in the potent offerings of conventional medicine, and the development of a complementary style of treatment which allows for a cautious crossover from standard to dietary management, have yielded more consistent positive clinical results. This approach also allows for the judicious application of steroids and/or non-steroidal anti-inflammatory drugs (NSAID) during unexpected crises, and offers the assurance that the patient need not suffer in order to cross over to dietary treatment. Long term successful self-management by people with SLE, freedom from reliance on pharmaceuticals, and extended health and lifespan are reasonable goals for nutritional management of SLE.