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Jean E. Pierog R.N.,M.S. , NC


Systemic lupus erythematosus (SLE) is an autoimmune disease in which the body’s defense system attacks its own tissues. The term "lupus" comes from the Latin word meaning "wolf" because the characteristic rash that spreads across the bridge of the nose and cheeks resembles a wolf bite (Bosche, 1988; Dibner & Colman, 1994). Since the facial rash is bright red, "erythematosus" which is Latin for "red", also describes the affliction. "Systemic" was added to differentiate it from two other forms of lupus, discoid and drug-induced.

Discoid lupus is a skin disease that is limited primarily to the face, neck and scalp. It does not affect the internal organs, but if it is untreated it can cause scars and baldness. Approximately 10% of those with discoid lupus will progress to mild SLE (Dibner & Colman, 1994). Drug-induced lupus is caused by specific drugs, primarily hydralazine and procainamide (treat hypertension and irregular heart beats, respectively) and disappears when the drugs are eliminated. The cause of this is an inherited malfunction of the way the drugs are metabolized. This paper will concentrate on the systemic form which means it affects the body’s internal organs as well as the skin.


The prevalence of lupus is about 4,280 cases per 100,000 population, with Afro-Caribbeans having the highest prevalence followed by Asians then Caucasions (Emery, 1994). The very highest prevalence is in the Sioux, Crow and Arapahoe Indian tribes (Klinman & Steinberg, 1988). Women have 13 times the chance of developing lupus as men do. The disease usually strikes women of childbearing age with 70% having an onset of the illness between ages 13 and 40 years. It can strike children and the elderly, but the symptoms are usually milder. Blacks have a worse prognosis, due in large part to the increased prevalence of renal disease (Bosche, 1988; Emery, 1994; Klinman & Steinberg, 1988). It currently affects one million Americans and is more common than leukemia, multiple sclerosis, cystic fibrosis, muscular dystrophy, pernicious anemia, rheumatic fever or Hodgkin’s disease.

As recently as the 1950’s, lupus was considered to be a fatal disease and less than 50% of all patients were alive 4 years following diagnosis. Now, however, as a result of better diagnostic criteria and early and better treatments, 76-90% of all patients will live ten years or more after diagnosis. Many, with good self care and early recognition of flare-ups will live a normal lifespan (Dibner & Colman, 1994; Emery, 1994).


Generally speaking, lupus is an over reaction of the immune system as opposed to AIDS and cancer which occur when the immune system is underactive (Remtulla, 1995). In 1957, researchers discovered autoantibodies in the blood of people with SLE. Until that time, very little was known about the cause of lupus.

The following is the most widely accepted version of the autoimmune reaction, but the precise mechanism has yet to be absolutely verified. Lymphocytes are white blood cells and are of two types: B- cells and T-cells. The B lymphocytes reside in the thymus and produce antibodies which are formulated to neutralize specific antigens. Some T lymphocytes are called Helper T cells since they promote immune responses, in part by encouraging the B- cells to produce more antibody. Other T lymphocytes known as Suppressor T cells inhibit the immune response and signal the B lymphocytes to slow down antibody production. It is thought that in active lupus, the Suppressor T cells are unable to tell the B- cells to stop antibody production so that the entire immune response is thrown out of balance and there is excessive production of autoantibodies. It has been shown that during a lupus flare-up, there is a lower number of Suppressor T cells in the bloodstream but in times of remission there is a normal amount (Dibner & Colman, 1994). (Refer to Immune Diagram in Appendix)

Therefore, in lupus, the body extends the elimination of antigens (usually foreign invaders) to antigens which are a part of the body’s self. These antigens and antibodies form complexes called immunocomplexes which lodge onto various organs and are eventually attacked by the immune system. This in turn results in inflammation of the various organs causing eruptions on the skin, painful joints, kidney problems, enlargement of the spleen and fevers (Remtulla, 1995).


What makes the immune system malfunction and actually attack "self"? In lupus, there is currently no known cause, but it is generally accepted that it may be a multifactorial, complex interaction. Researchers lean toward a combination of heredity and environmental factors.

There seems to be a genetic predisposition to develop lupus since so far the number one risk factor is a family history of the disease. According to Dr. Arthur Kreg, (lupus researcher and professor of Medicine at the University of Iowa), there are at least six as yet unidentified genes responsible for lupus (Hales, 1992). About 10% of all persons who develop lupus have a close relative who also has it. On the other hand, only 5% of children born to a parent with lupus actually develop it. Among identical twins, if one has lupus, the other has a 24% chance of contracting the illness (Bosche, 1988). This points out that other factors are important, perhaps environmental. In fact, there is a higher rate of lupus among nonrelated members who live in the same household than in the population at large. In addition, there is even a greater risk of nonrelated members of the same household developing the autoantibodies without actually developing lupus (Dibner & Colman, 1994). Therefore, something in the environment may trigger the lupus response in a person who is genetically predisposed.

Some researchers believe that a virus is responsible for the breakdown in communication between the T- Helper cells and the B lymphocytes, but lupus is known not to be contagious. However, just as the HIV virus deactivates the immune system, it may be possible that an unidentified virus is responsible for "hyperacting" the immune system.

Yet another cause or at least contributing factor may be hormonal. Since 90% of lupus cases are women, especially during the childbearing years, researchers believe that increased estrogen levels may play a role. In addition, high estrogen birth control pills and pregnancy (increased estrogen levels) can induce flare-ups in women with lupus. After menopause, many women go into prolonged remission. Some studies have shown that estrogens activate the immune system whereas androgens (male hormones) deactiviate it. Additionally, people without lupus break down estrogen differently than those with lupus (Dibner & Colman, 1994).

Other contributing factors may be as yet unidentified metabolic and environmental ones. Physical and emotional stress may also play a role in the development of lupus. Sunlight, especially ultraviolet light, exacerbates lupus. Perhaps chemicals or environmental toxins and/or foods can cause lupus. Allergic reactions to substances in the environment or ingested foods or medications (such as BCPs, sulfa, penicillin, barbiturates, hydralazine and procainamide) are possible factors. Some researchers believe that silicone breast implants can trigger lupus because some women develop autoantibodies and symptoms of connective tissue disease following breast implants. Those whose implants rupture experience more severe symptoms and experience them quicker than those whose implants remain intact (Dibner & Colman).


Symptoms of SLE are very broad and vary greatly, in fact, no two people present with the same symptoms. The severity and extent of symptoms also vary widely and any part of the body can be involved. (Refer to "Frequency of Symptoms" chart in appendix). The typical lupus victim will present with only a few signs/symptoms such as fatigue and arthritis and no definitive diagnosis can be made in such a limited clinical presentation. It may be weeks, months or even years later that additional features of lupus will surface.

Fatigue. This is the most common of all the symptoms. Patients complain of extreme lethargy and having to take naps daily. Almost 100% of lupus patients have fatigue.

Fever. Fever is common in about 80% of cases but it can be of two types: a constant low grade fever of about 100 degrees F or a high fever >100 degrees F that is intermittent.

Pain. Primarily arthritis type pain and flulike aches in the joints especially. Joint swelling usually occurs in the smaller joints of the hands or feet. Unlike Rheumatoid arthritis, there is no deformity and the pain is usually worse at night, although in both cases stiffness of the joints is present on awakening. About 95% of lupus patients experience pain.

Sun sensitivity. Approximately 60% of patients develop a rash, fever or aches following intense sun exposure.

Rashes. The most common area to get a red rash is on the face in a butterfly formation over the nose and cheeks. This occurs in 50% of patients.

Chest pain. This is a sharp pain over the chest area which can be due to inflammation of the lining of the heart (pericarditis) and/or lining of the lungs (pleuritis). Occasionally, the lining of the abdominal cavity can become inflamed and is known as peritonitis.

Cold hands and/or feet. Also known as Raynaud’s phenomenon, this is a sensitivity to cold, most commonly in the fingers followed by the toes. When the temperature is cold (usually < 60 degrees F), the fingers and toes become blanched and painful. When they are rewarmed, they become a bright red. Twenty percent of patients have this symptom.

Edema/swelling. This usually occurs around the eyes, ankles or legs. It may indicate kidney disease caused by the lupus which affects 50% of all lupus patients. The kidney’s filtration system becomes clogged by the antigen/antibody complexes thereby causing inflammation, functional impairment and occasionally permanent scarring. Kidney damage is one of the most serious complications of lupus and may result in hypertension, fluid and electrolyte imbalances and sometimes death (Bosche, 1988).

Depression. Many patients, about half, will suffer from a profound organic depression with helpless/hopeless manifestations. Involvement of the central nervous system (CNS) can also cause symptoms ranging from headaches and seizures to chronic confusion and memory loss.

Dry eyes, Dry mouth. Also known as Sjogren’s syndrome, the autoantibodies attack the glands that make the tears, saliva and other lubricants such as the vaginal lubricant.

Easy bruising. This is a sign of a low platelet count since they may also be destroyed by the autoantibodies.

Premenstrual flares. Most women say that all their symptoms are worse just before menses.

Additional symptoms include alopecia (hair loss), nausea, vomiting and/or gastrointestinal problems, pneumonias, weight loss (prior to diagnosis), and miscarriages.


It is important to note that the traditional assessment is a medical diagnostic one, whereas the nutritional assessment evaluates dietary and lifestyle factors so that recommendations can be made to improve health by modifying lifestyle choices. The difference is that the first is diagnostic and the second (nutritional) determines the direction of support for someone with the lupus diagnosis.


There is no one symptom or medical test that is indicative of a definitive lupus diagnosis. Evaluation consists of a combination of presenting symptoms, laboratory results, physical findings and a family history.

Lupus is often called the "great imitator" as it mimics so many other illnesses (American Lupus Society, 1993). Some of these diseases include connective tissue diseases like rheumatoid arthritis, Lyme’s, syphilis, tuberculosis, mononucleosis, AIDS and chronic fatigue syndrome. Other disorders include psychotic problems, leukemia, lymphoma or fibromyalgia. Oftentimes the patient will present with only a few symptoms and months to even years latter may develop different or additional symptoms in the range of SLE related problems.

The following are the assessments most typically performed in the traditional medical approach.


The "Revised Criteria for the Classification of Lupus" developed by the American College of Rheumatology in 1982 is a useful guide (refer to appendix for chart). It consists of 11 of the most common abnormalities that are specific to lupus. A positive diagnosis is the presence of 4 out of 11 of the criteria (in combination with other tests), but they need not be present at the same time (Klinimen & Steinberg, 1988).

1. Malar rash (butterfly shape over nose & cheeks)

2. Discoid rash (round, scaly spots on face & upper body)

3. Photosensitivity (light sensitive)

4. Oral ulcers (usually painless small erosions)

5. Arthritis (especially in hands, wrists, toes)

6. Serositis (inflammation of linings of heart, lungs or abdominal cavity)

7. Renal disorder (kidney abnormality)

8. Neurological disorder (seizures, psychosis, schizophrenia, etc.)

9. Hematological disorder (hemolytic anemia, thrombocytopenia, leukopenia, and lymphocytopenia; see chart for significant values)

10. Immunologic abnormalities (presence of 4 antibodies in the blood: Anti-DNA, lupus erythematosus cell prep, antibodies to Sm {Smith}, false positive serologic test for syphilis)

11. Antinuclear antibodies (ANA) (autoantibodies to the cell nuclei)


Checks for genetic predisposition, any relatives with SLE or a related disorder.


List of symptoms, current and past as well as previous illnesses, surgeries, allergies and medications.


Includes a head to toe exam, looking for hair loss, eye inflammation, mouth ulcers, swollen lymph nodes, skin rashes, chest problems, organ enlargement, edema, joint pain and cool discolored extremities. A neurological exam is also done.


CBC- Complete Blood Count. Looks at red and white blood cells and platelets.

Blood Chemistry Screen- Tests kidney function, electrolytes.

Urinalysis- Looks for protein and blood in the urine.

Sedimentation Rate- Screens for active inflammation.

ANA- Screens for autoantibodies to cell nuclei in the blood.

Rheumatoid Factor- Test for arthritis.

Serologic Test for Syphilis- False positive in 20% of SLE patients.

Lyme Titer- Mimics SLE; may have false positive.

HIV Test- Rule out AIDS. May lead to more specific testing.

Anti-DS (Double-Stranded) DNA Antibodies- Patients produce antibodies to their own DNA (70% of cases).

Anti-Sm (Smith) Antibodies- Very specific to SLE; an antibody to a protein in the cell nucleus.

Antibodies to Ribonuclear Protein- Indicates connective tissue disease.

Antibodies to RO and LA- Found in 30-40% of SLE patients and important to know if pregnant.

Antiphospholipid Antibodies- Antibodies directed against phospholipids, specifically lupus anticoagulant and anticardiolipin antibodies. At risk for clotting problems.

Serum Complement Levels- Proteins in the blood that fight infection and inflammation. SLE patients have lower levels.

(Dibner & Colman, 1994)

All routine tests are repeated at regular intervals or when the start of a flare is suspected. Early treatment is critical in order to prevent a severe exacerbation (American Lupus Society, 1993).


Since SLE is such a broad spectrum illness affecting many different body systems and touching on every aspect of the client’s lifestyle, a wide range of nutritional assessments are recommended.

According to Jonathan Wright, MD, 100% of all SLE patients have food allergies and improve with appropriate identification and therapy (Burton Goldberg Group, 1993). In addition, Bauman (1994) states that 80% of people with food sensitivities have enzyme insufficiency and hypoglycemia. He also says that low energy (fatigue is present in almost 100% of SLE clients) indicates that nutrients are not reaching the cells of the endocrine glands and vital organs. The acid/base balance is disrupted by waste products in the interstitial fluids and a person’s enzymes are consumed in scavenging which means that nutrient absorption is lessened. Leon Chaitow, ND, DO, emphasizes that hydrochloric acid (HCL) deficiency is common in patients with lupus (Burton Goldberg Group, 1993).

Because of the above information, clients should be tested for food and environmental allergies as well as for acid/base balance and gastrointestinal disturbances.


It is important to note that the traditional approach is primarily a medication regime which treats the symptoms of lupus (since the cause is unknown). The nutritional approach seeks not only to enhance the immune system by introducing nutritional, environmental and lifestyle support systems, but the goal is also to mitigate the side effects caused by the traditional medical approach. Thus it is very important to have an understanding of the traditional drugs used in order to better consult on nutritional boosters!


*Nonsteroidal AntiInflammatory Drugs- These are the most commonly prescribed drugs and include aspirin, advil, motrin, etc. These are the drugs of choice of patients with no organ involvement who require antiinflammatory properties. Side effects include GI upset, bleeding, ulcers, decreased blood flow to the kidneys, liver toxicity, allergies and fluid retention.

*Antimalarial Drugs- Seem to be effective in treating SLE related rashes, mouth ulcers, and arthritis. The mechanism is unknown, but they seem to have antiinflammatory and immuno-suppressive properties. The side effects include retinopathy, increased photosensitivity, hair loss, and peripheral neuropathy.

*Corticosteroids- These are used when patients’ symptoms do not improve with NSAIDs or antimalarials. These drugs are related to cortisone, a hormone produced by the adrenal gland, but are synthetic. They are usually prescribed for extreme fatigue, severe arthritis, pericarditis, pleuritis, kidney disease or uncontrolled fever. They reduce inflammation, relieve muscle and joint pain and fatigue and suppress the immune system. Side effects include weight gain, susceptibility to infection, hypertension, diabetes, edema, excess hair growth, thin skin, diabetes, poor wound healing, increased blood lipids, early osteoporosis, muscle fatigue, psychiatric problems and cataracts (Mayo Clinic Health Letter, 1990).

*Immunosuppressive Drugs- These were initially used for cancer patients and are considered chemotherapy. They depress the immune system and affect every cell, and are therefore reserved for patients with major organ involvement or intractable arthritis. Side effects include severe nausea, hair loss, increased risk of infection, blood in the urine, late malignancies, premature menopause and infertility and bone marrow suppression.

The above are considered the traditional treatments, but the following is a list of treatments considered experimental at this point in time.

*IV Gamma Globulin*


*Plasmapheresis combined with IV Cytoxin*


*Hormonal Therapy*

*Monoclonal Antibody Treatment*

*Omega-3 Fatty Acid*

*Combined Immunosuppressive Therapy*

*Total Lymph Node Irradiation*

(from Dibner & Colman, 1994)

In 1992 the International Lupus Conference in London reported that the Chinese use an Asian shrub called Tripterygium wilfordii to treat lupus, RA and other autoimmune disorders (Blau, 1993). At the Shanghai Medical University, 200 lupus patients reported results on a level equal to corticorsteroids for reducing inflammation with many less side effects. Further studies are underway.


There have been several investigational studies of mice and humans which suggest an association between dietary factors and lupus. However, no studies have been conclusive in demonstrating a real link between diet and SLE (Bay Area Lupus Foundation, Inc., 1988).

Several studies have shown a promising link between omega-3 fatty acids found in fish oil and flax seeds and a reduction in SLE symptoms. It is presumed to be due to the anti-inflammatory properties of the omega-3 fats. In 1994, Chandrasekar and Fernundes showed that mice with lupus had delayed onset and slower progression of renal disease if they were fed fish oil versus corn oil. In addition, the fish oil mices’ lifespan was significantly lengthened compared to the corn oil mice. In 1993, Hall et. al. studied 55 lupus mice, approximately half of which were fed a 15% flaxseed diet and the other half a standard rodent diet (minus flaxseed). The findings showed a significant decrease in renal and spleen compromise and a lower mortality in flax fed mice.

In 1994, Clark and Parbtani published a study using humans with lupus and flaxseed (n=26 and they were followed for 2 years, 10 weeks in a double-blind, cross-over study). They found a significant decrease in serum lipid levels, thereby lowering the rate of atherosclerotic and inflammatory changes of the cardiovascular system.

Other studies have shown the following relationships:

*Human lupus-52 females in Japan followed for 1 year showed that frequent intake of meat was associated with an increased risk of onset and progression of SLE (Minami, et. al, 1993).

*Human lupus-Confirmation of the association between high dose steroids in lupus patients and the development of an atherogenic plasma lipid profile in 64 patients with SLE (MacGregor, et. al., 1992).

*Human lupus-Showed that participants given the Systemic Lupus Eythematosus Self Help course had significant increases in enabling skills and the use of relaxation and exercise activities (Braden, et. al., 1993).

*Human lupus-41 of 160 lupus patients developed end stage renal disease and those who smoked or who had hypertension had shorter times to renal failure (Ward & Studeski, 1992).

*Human lupus-This study confirmed the role of ultraviolet B light in the initiation and potentiation of lupus skin lesions (Jones, 1992).

*Mice lupus-Six Chinese herbs, atractylodes ovata, angelica sinensis, cordyceps, liqustrum, codonopsis and homosapiens improved defective in vitro (human) interleukin-2 production and in mice they prolonged the lifespan (Chen, et. al., 1993).

*Human and animal lupus-In a study of the cholesterol lowering effect of alfalfa, a lupus syndrome emerged in mice, monkeys and one human. Two humans had flare-ups of lupus after ingesting alfalfa tablets. The substance canavanine, a non-protein amino acid, is found in large amounts in alfalfa and has toxic properties. Canavanine in mice seemed to interfere with the interaction between B and T cells and resulted in increased autoantibody production and a decrease in suppressor T cells (Shils, et. al., 1994).

Several other studies, according to Werbach (1988), show benefits for lupus patients from:

*a low calorie, low fat diet

*limited beef and dairy products

*beta carotene supplementation

*pantothanic acid supplementation

*vitamin B12 1000 mcg IM 2 times a week

*vitamin E, 1200-1600 I.U. daily

*selenium supplementation

*omega-3 and omega-6 fatty acids

The following nutritional approach to enhancing the health of lupus patients is a general one, developed from a number of sources. The approach is based primarily on immune enhancement and anti-inflammatory properties of foods, nutrients and herbs. It should be understood that each client with lupus will present with different SLE related problems and nutritional support will vary according to the priority of the problem (that is support for kidneys, hair loss, fatigue, skin problems, poor circulation, nervous system, heart problems, etc.). The following recommendations are from: Bauman, 1994; Balch&Balch, 1993; Bay Area Lupus Foundation, 1988; Blau, 1993; Burton Goldberg Group, 1993; Klinman & Steinberg, 1988; Dibner & Colman, 1994; Rector-Page, 1992.

*Start with therapeutic fast

*No dairy products

*No gluten

*Decrease or eliminate animal products except for cold water marine animals, especially mackeral, salmon, fish high in omega-3 EFAs.

*Whole foods diet such as "Eating for Health Regenerative 5 Food Group System" minus the "occasional foods". See Appendix.

*Reduce or eliminate salt

*Kidney disease patients should limit protein intake (no dairy, no meat, limited beans).

*Less than 20% fat intake

*No caffeinated beverages (interferes with calcium absorption)

*Avoid foods that contain psoralens (celery, parsnips, figs, and parsley) since they increase photosensitivity.

*No alfalfa sprouts (contains canavanine)

*Take aloe vera juice 1-2 glasses a day

*Avoid all refined foods

*Avoid mushrooms (contain hyrazines/amines)

*Drink green drinks (barley, wheat grass, etc. to diminish internal toxicities)

*Take a potassium broth (Rector-Page) which benefits the kidneys

*Take enzymes to aid digestion, especially HCL tablets, and ensure absorption of nutrients.

*Identify the allergens and avoid them


*Vitamin C and bioflavenoids (about 5000 mg daily)

*Proteolytic enzymes (away from meals on an empty stomach; anti-inflammatory and anti-viral agents)

*Digestive enzymes with meals

*Calcium 1500-3000 mg daily

*Quercitin Plus with bromelain 3 times a day (anti-inflammatory)

*Flaxseed/flaxseed oil or high omega fish oil

*Betacarotene 100,000 I.U.

*Vitamin D up to 1000 I.U. daily

*Magnesium 750 mg 2 times a day

*Zinc 50-100 mg daily

*Vitamin E up to 1500 I.U. daily

*L-cysteine, L-methionine, L-cystine amino acids for cell protection, skin formation and white blood cell activity.

*Garlic capsules- 2 with meals (immune enhancers)

*Germanium, 100-150 mg daily

*Sun Chlorella 1 packet daily

*CoQ10 60 mg daily

*Internasal B12 or 1000 mcg IM 2 times a week

*Raw thymus glandular

*Shark cartilage

*Egg yolk lecithin

*Enzymatic therapy liquid liver with Siberian ginseng

*Vitamin B complex

*Selenium 50-100 mg daily

*Vitamin B-6 in high doses (500mg 3 times a day; reduces symptoms of lupus)

*Acidophilus (protects intestinal bacteria balance)

*Kelp tablets 5 daily

*Superoxide Dismutase (powerful antioxidant)

Note that some of the above nutrients can be combined in a multi-complex supplement.


*Mix equal parts of the tinctures of the Chinese herbs Bupleurum falcatum, licorice and wild yam. Take 1 teaspoonful 3 times a day.

*Drink an infusion of nettle 2 times a day.

*Relevant herbs should be used to treat symptoms as they arise. The herb should match the symptom at the time: echinacea, goldenseal, pan d’ arco, red clover, gotukola, carnivora extract and yucca for arthritic symptoms.

*Royal jelly 40,000 mg 2 teaspoons daily

*Crystal Star Ginseng 6 Defense Restorative tea or capsules

*Crystal Star Liv-Alive capsules and tea daily for one month to start

It should be emphasized that herbs should not be taken on a daily maintenance schedule like vitamins. Combinations work better than single herbs. Therapeutic herbs work best on an as-needed basis and so should be taken when you are experiencing symptoms. Rotate and alternate herbal combinations according to changing health needs. Best results occur by taking herbs in descending strength for six days, rest on the seventh. That is, take 6 capsules day 1, 5 on day 2, etc. until you take 1 capsule on day 6. The body then needs to rest to restore its own balance. (Rector-Page, 1992)


This may be promoted by both the traditional and nutritional approaches.

*Avoid strong sunlight and use clothing and sunscreens that block all UVA & UVB rays.

*Do not take tetracycline (increases sun sensitivity) or gantrisin, penicillin, ampicillin (causes rashes) or BCPs.

*Get a lot of rest, especially when the disease is active (sleep has an anti- inflammatory effect)

*Exercise regularly but not to the point of exhaustion

*Identify and avoid stressors including surgery, infections, abortions, psychological stressors, environmental chemicals, toxins and stressors.

*Avoid crowds and people with suspected or known contagious illnesses.

*Consider avoiding immunizations (may initiate flare-ups)

*Get support as in a local Lupus Support group

*Arrange for help with housework, if possible

*If you have Sjogren’s Syndrome (5%) you may need artificial tears, artificial saliva and a vaginal lubricant.

*Avoid recreational drugs and excessive alcohol intake

*Get hypertension under control, if applicable

*Don’t smoke


*Biofeedback training

*Guided imagery



*Juice therapy (carrot, celery and add flax seed oil, black currant oil and garlic)

*Reflexology--all glands, intestines, liver, whole spine

*Distraction therapy

*Transcutaneous electrical nerve stimulation (TENS)

*Relaxation therapy and stress reduction techniques


*Hot or cold treatments with and without massage


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Balch, J.F., M.D. & Balch, P.A. Prescription for Nutritional Healing. NY: Avery Publishing Group, Inc. 81-85; 231-32. 1993.

Bauman, Ed. Lectures and Readings from Diet Counselor and Nutrition Educator Courses, 1994-95.

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Bay Area Lupus Foundation, Inc. "Vitamins, Mineral Supplements and the Lupus Patient" in Lupus Newsletter. 3-5. Spring, 1988.

Bay Area Lupus Foundation, Inc. "New Research Directions" in Lupus Newsletter. 5-7. Spring, 1988.

Blau, S.P., M.D. with Schultz, D. Living with Lupus. Mass.: Addison-Wesley Publishing Co. 1993.

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Clark, W.F. & Parbtani A. "Omega-3 Fatty Acid Supplementation in Clinical and Experimental Lupus Nephritis" in American Journal of Kidney Diseases. 23(5). 644-7. May, 1994.

Dibner, R.M., M.D. & Colman, Carol. The Lupus Handbook for Women. NY: Simon & Schuster. 1994.

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MacGregor, A.J., et. al. "Fasting Lipid and Anticardiac Lipin Antibodies as Risk Factors for Vascular Disease in SLE" in Annals of the Rheumatic Diseases. 51(2). 152-5. February, 1992.

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Miller, B. B., M.D. The Immune System: Nutrition for Optimal Wellness. Texas: Bruce Miller Enterprises, Inc. 1989.

Minami, Y., et. al. "Female Systemic Lupus Erythematosus in Miyagi Prefecture, Japan: A Case-Control Study of Dietary and Reproductive Factors" in Tohoku Journal of Experimental Medicine. 169(3). 245-52. March, 1993.

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