In patients with kidney disease, specifically a large amount of protein in the urine, with elevated cholesterol levels, those consuming a vegetarian soy diet for eight weeks experienced significant falls in blood cholesterol and in urinary protein excretion. As soon as they returned to normal diets, their blood cholesterol and urine protein levels returned to what they’d been before.

According to the study, conducted by the University of Milan, the “soy diet induced a moderate but significant reduction in urinary protein excretion that. . . could not be attributed to spontaneous improvement.” This study has meaning for kidney patients whose cholesterol abnormalities increase the risk of heart disease.

At the same time the Department of Clinical Chemistry, University of Helsinki, demonstrated that the fact that Japanese women have a much lower incidence of hot flushes and other meno pausal symptoms may have something to do with the traditional Japanese low fat diet.

In studying the women from a village south of Kyoto the researchers found the women were excreting isoflavonoids, or weak oestrogens, 100-1000 fold higher than women consuming a typical western diet.

The excretion of iso flavonoids in urine is associated with eating soy products such as tofu and miso.

“Such high amounts [of isoflavonoids] could have biological effects, especially in postmenopausal women with low oestrogen levels,” said the report.

Two other studies demonstrated the value of a vegetable rich diet. The Tottori University in Japan found that when a young woman with the autoimmune disease lupus erythematosus was taken off steroids and placed on a vegetarian diet, she significantly improved.

Finally, a study in northeastern Italy (International Journal of Cancer: 50:223-229) found an association between cancer of the colon and rectum and high consumption of white bread, cheese, eggs and red meat. The study also found a protective effect in a high consumption of carrots, spinach, wholegrain bread and pasta.

Although few orthodox treatments are much beyond a shot in the dark, many other cultures have treated SLE successfully. In central, east and southern Africa, sangomas (better known in the West as “witchdoctors”) treat with the South African pennywort. At least three comprehensive historical accounts exist of the medicinal uses of this plant, including two written fairly recently (eg, Medicinal and Poisonous Plants of Southern and Eastern Africa, 2nd ed, Edinburgh: E & S Livingstone Ltd, 1962: 1035-6). In one naturopathic textbook, there are 37 references for the clinical use of the SA pennywort for SLE (Text Nat Med, Bastyr University Publ, 1989, Seattle, Washington). It’s important that the African subspecies of the SA pennywort be employed, however, since varieties from other parts of the world have been shown not to contain the same chemical constituents.

Oriental medicine has frequently made successful use of Triptrerygium wilfordi when the symptom picture has resembled SLE, a common ailment in the Far East. In an experimental study of 103 patients with SLE given a daily dose of a tea brewed with the roots and stems of the plant, more than half had symptoms substantially improve or disappear; in some cases, lab tests had returned to normal and drug therapy could be stopped (Chin Med J, 1981; 94: 827-34).

In homeopathy, Cistus canadensis can be indicated for SLE when the skin is involved (Tyler, Homeopathic Drug Pictures, Health Science Press, Rustington, Sussex, 1970), although the usual remedy of choice is Thuja. In one retrospective study admittedly not the most rigorous where 14 homeopathic medical practitioners prescribed Nux vomica alone (in various potencies) or in combination with other remedies for 62 patients, the success rate (as judged by both practitioner and patient) was 80 per cent (J of Liga Medic Homoeo Inter, 1987, 2 (1): 27-31).

Nutritionally, a low-calorie, low-fat diet can help some SLE patients (The Lancet, Jan 26, 1985), as may supplementation with selenium (Acta Derm Venereal (Stockh), 1982; 62 (3): 211-4).

You should also get tested for gastric acid deficiency. One study showed that none of the SLE patients examined had normal stomach acid levels. Supplements of hydrochloric acid and vitamin B complex brought improvement (J Immuno, 1984; 133(1): 222-6).

In my own practice, I find that many SLE symptoms are produced when “immune complexes”, formed by food molecules, are deposited in the tiny capillary blood vessels. Excess food molecules find their way into your circulatory system if your intestinal gut wall is “leaky”. So the first port of call in investigating this disease should be a test for gut permeability, which can be easily remedied once identified.

!AHarald Gaier

Harald Gaier is a registered naturopath, osteopath and homeopath.

The test

The ANA test is straightforward: a blood sample is taken, then tested for the presence of autoantibodies. Autoantibodies may attack different parts of a cell, but the ANA test is particularly good at detecting those that attack the cell nucleus.

Is the test accurate?

Not especially. A positive result is only an indication of the likelihood of your having the disease – it is not a definite confirmation of its presence.

The ANA test result is reported as a titre – a measure of how much the blood sample can be diluted and yet still show the presence of antibodies. The higher the titre, the more likely the presence of a connective tissue disorder such as SLE (Postgrad Med, 1993; 94: 55-66).

But what constitutes a positive result? In some studies, a titre of less than 1 in 40 was regarded as a positive result. However, a higher titre is usually considered more conclusive. For example, a titre of 1 in 80 suggests that an autoimmune disease is highly likely, and at least one commercial lab (Arup Laboratories, owned by the University of Utah) states in its guidelines that only titres of 1 in 160 or higher are to be considered significant positives.

How specific is the test?

At best, a positive ANA test only tells the doctor that there’s a likelihood of connective tissue disease, but it can’t tell you which one as a number of such conditions will produce a positive result. Whereas 95 per cent of SLE sufferers will test positive with the ANA (Rheum Dis Clin North Am, 1990; 16: 617-39), only 30-50 per cent of those with rheumatoid arthritis, 40-70 per cent with Sjögren’s syndrome, 60-80 per cent with scleroderma and 20-50 per cent with chronic juvenile arthritis will (Arch Pathol Lab Med, 1999; 124: 71-81).

Healthy people can also show a positive result: around 2 per cent of the population have mildly elevated antibodies without symptoms (Adv Immunol, 1989; 44: 93-151). One study involving 15 international laboratories found that ANA tests of the general population were positive in 32 per cent of cases at a titre of 1 in 40, and in 5 per cent of people at a dilution of 1 in 160 (Arthritis Rheum, 1982; 25: 1271-7).

Drugs used to treat other disorders, such as procainamide (for heart arrhythmias), hydralazine (a vasodilator) and even the tetanus vaccine can return a positive result (Science, 1994; 266: 810-3), as can a form of lupus that is drug-induced.

Viral or bacterial infections, lung diseases (such as pulmonary hypertension), ulcerative colitis, cancers (of the skin, breast, lung and kidney) and even skin conditions like psoriasis can cause an increase in the number of antibodies produced.

Diagnosis is further complicated by the considerable overlap in symptoms of many connective-tissue diseases as well as the presence of various antibodies. For example, ‘mixed connective-tissue disease’ displays the symptoms of SLE, scleroderma and myositis, leading some to ask whether this is truly a separate entity at all (Arthritis Rheum, 1998; 41: 768-77).

Moreover, there is a high potential for false negatives (an all-clear result when you have the disease.) As autoimmune disorders often evolve over time, a significant number of patients produce negative ANA tests early on (Arthritis Rheum, 1999; 42: 1785-96), and only repeat testing at a later date can verify the disease status (Arch Pathol Lab Med, 1999; 124: 71-81).

Yet more inaccurate tests

If your ANA test results are positive, another set of tests can be ordered to differentiate between diseases by looking at specific nuclear proteins. But these tests are also low in sensitivity. So, while a positive result for double-stranded DNA and SM antibodies may confirm SLE, a negative test doesn’t necessarily rule it out (Arch Pathol Lab Med, 1999; 124: 71-81).

Although these tests are not harmful in themselves, their biggest danger is their huge room for error. An incorrect diagnosis can set you off on a treatment you don’t need, often requiring drugs with debilitating side-effects of their own.

The allergist Dr John Mansfield has shown that allergies are responsible for much arthritic disease. I have found that areas with low soil boron such as Jamaica, Mauritius and Fiji have high levels of arthritis of up to 70 per cent. But in areas with high soil boron, there is little or no arthritis.

These two factors must work together: boron does something to alleviate the effect of allergies. In plants, boron will make cell walls more permeable to other ions, so possibly this also happens to humans and animals. Boron will correct adjuvant arthritis in animals and the adjuvant is generally a mineral oil. Similar oils are found in some baby oils and boron will correct arthritis in babies. Possibly a substance like histamine is influenced by boron. Much more research is needed to solve the problem completely, but the information is exciting. Rex Newnham, Nutritional Consultant, Cracoe, N Yorkshire…….

So a carefully researched report that has just landed on our desk sheds some amazing light on these – and many other – debilitating diseases. It may even provide you with the key to a mystery illness that could be wrecking the life of someone you know.

The report has been prepared by Carolyn Thompson of Toronto, and it concerns her sister who, in October last year, suddenly became very sick. Her sister began suffering stomach spasms, and even walking became a major problem. By last March, she had undergone biopsies and was on 24 different medications.

Her sister was convinced she was going to die, and doctors could offer no hope. They thought she must have multiple sclerosis, but couldn’t find any signs of it in tests.

Then, Carolyn mentioned a report she had read about the possible effects of diet colas, which are full of the artificial sweetener aspartame. Her sister regularly drank them, and had one in her hand as she was talking to Carolyn.

Carolyn told her to throw it away, and not to drink any more. Within 32 hours, her sister was walking again. Three days later and she was holidaying in Florida, and she’d thrown away her wheelchair.

Her sister is still not completely better, but she’s well on the road to recovery, and every day she is seeing slight improvements.

Carolyn points out that there are epidemics of MS and systemic lupus in the United States – and there is an epidemic of diet cola drinks. Is there a definitive link?

Carolyn is convinced so. Anyone who has fibromyalgia symptoms, spasms, shooting pains, numbness in the legs, cramps, vertigo, dizziness, headaches, tinnitus, joint pain, depression, anxiety attacks, slurred speech, blurred vision or memory loss should stop drinking diet drinks, she says.

You never know, things could get better.

* Buy the WDDTY special report on Aspartame by visiting our web site http://www.wddty.co.uk

To reach this conclusion, Spanish researchers studied the prevalence of HCV in 134 consecutive SLE patients and compared this with HCV prevalence in healthy controls. Eleven per cent of the SLE patients had antibodies to HCV compared with only 1 per cent of the controls.

In addition, the researchers found that, when found together, the diseases seemed to have modified each other. For example, HCV infection in SLE patients involves more liver symptoms and immunological disorders than in non-SLE subjects. Also, SLE patients with HCV show fewer skin symptoms and a different DNA profile.

What remains unclear is whether there is a link between HCV and SLE or whether HCV can, under

certain circumstances, mimic SLE. Although small, this study represents one of the largest studies ever done into the association between SLE and HCV. Currently, however, it raises more questions than it answers (Arthritis Rheum, 2000; 43: 2801-6).

I’d also be interested in your comments on my medication, which includes cyclophosphamide, prednisolone, ranitidine, nifedipine, frusemide and carbamazepine (the latter because I suffer from petit mal epilepsy). What alarms me is that all the tablets say they should not be taken with kidney impairment, which I have. It was suggested that I may live five years. I’m 46. Well, I think if I don’t die from lupus, I’ll die from the medicine. U J S, Newcastle-on-Tyne…

A:As you know, SLE is an auto immune disease, in which the immune system begins to attack the body’s own cells. There is much that medicine doesn’t know about this condition for instance, what causes it or even how to devise a test to definitely diagnose it.

In most cases, diagnosis is made on the basis of a collection of symptoms: arthritic like joint and muscle pain, swelling of hands and feet, a red rough “wolverine” rash over the skin hence the name, which means, literally “red wolf”.

In some cases, the disease can progress to attack the kidneys and central nervous system. Although the treatment and diagnosis of the disease hasn’t changed much in 10 years, we do know that certain things such as ultraviolet light, hormones (such as the Pill) and infections can cause a flare up. Luckily, the arthritis accompanying SLE is rarely permanently crippling and the rashes can heal without scarring.

In the 1970s the late American medical critic Dr Robert Mendelsohn called SLE one of the most important of the modern iatrogenic (doctor produced) diseases (The People’s Doctor, vol 5 no 2). He identified a number of drugs which can precipitate lupus. Significantly, in your case, these include drugs to control epilepsy, such as carbamazapine the drug you are taking. Phenytoin, methsuximide and ethosuximide also may bring on SLE. If you were taking an anti convulsant before your symptoms of SLE started, it is possible that one of those drugs triggered (or worsened) the disease.

Other drugs which can cause lupus include antihypertensives such as methyldopa drugs, those for irregular heartbeat like procainamide hydrochloride, the anti tuberculosis drug isoniazid, anti psychotic drugs such as chlorpromazine, certain antibiotics like penicillin, streptomycin and tetracycline, phenelzine sulfate, for anxious and depressed patients, or the antihypertensive hydralazine hydrochloride.

Conventional treatment assumes that lupus can’t really be cured, and so seeks to suppress symptoms and control them through maintenance therapy. The mainstay of treatment is steroids, such as prednisone or prednisolone whose anti inflammatory affects control many of the more obvious symptoms.

According to a review of lupus treatment in the British Medical Journal (11 September 1993), Patrick Venables, senior lecturer at the Kennedy Institute of Rheumatology in London, says that in the 1970s and 1980s it became fashionable to give high doses of intravenous prednisolone in a “pulsed” way to avoid cumulative side effects from steroids (everything from osteoporosis and diabetes to an increased likelihood of infections, and even sudden death).

However, several studies, he said, showed no difference in terms of effect on kidney function between the two groups and no long term benefit.

Cyclophosphamide is a powerful cytotoxic drug used to treat leukemia and some forms of cancer. It acts as an immunosuppressant to stop the body from rejecting transplant drugs and is given in cases of severe rheumatoid arthritis. Recently, these sorts of drugs have been flavour of the month in treating autoimmune diseases.

According to Venables, it can be of some benefit in kidney lupus, but its use is often cut short by almost invariable side effects. These include nausea, and vomiting, hair loss, an early menopause in women and permanent sterility in men, bladder cancer, cystitis and bone marrow suppression.

It has been found, says Venables, that pulsed intravenous treatment and the concurrent use of the drug mensa can help to avoid some of these side effects.

In reviewing treatment of SLE, Venables says in essence that although more people with lupus are surviving the disease, an increased number are now suffering from the side effects of the drugs. Hence, the emphasis now is in trying to modify current regimens to cut down the number of problems caused by the treatment itself.

You rightfully say that the cocktail of powerful drugs should not be used in people with kidney damage. Presumably you are taking the nifedipine, an antihypertensive, and frusemide, a powerful diuretic, for hypertension, and ranitidine (Zantac) for peptic ulcers or disturbance of stomach function.

As you say, the main worry is that all of these drugs aren’t supposed to be given to someone with kidney impairment.

The first thing you might do is to investigate with your doctor whether your SLE could have been caused or exacerbated by your anti convulsant drugs.

Ask your doctor to change to a milder anti convulsant drug or see if you can lower the dose or be weaned off it altogether. This alone may help your symptoms.

You might also wish to have a session with him in which you review the potential for kidney damage of all these drugs and try to cut out any which aren’t essential. For instance, is it absolutely necessary to have the cyclophosphamide, clearly the most potent? Is it at all possible to simply stick to a low dose of steroids?

Also clarify why are you being given the other drugs. Do they have a legitimate function in controlling your disease or are they only there to combat side effects of your other medication?

As for an alternative approach, Dr Jonathan Brostoff, honorary consultant physician at the Middlesex Hospital Medical School and a leading international authority on food allergy and the immune system, is one of a number of medics who believe that SLE is aggravated and possibly even caused by food intolerance. He finds that some of his patients with SLE do much better if a classic elimination diet is tried on them and they are subsequently treated for reactions to food or other environmental chemicals.

You may wish to try this approach with a very experienced doctor like Brostoff, who can see if the dietary method will halt SLE sufficiently for you to quit some of the drugs.

It has been shown that a combination of subtotal fasting for 7-10 days plus a subsequent one year vegetarian diet, seems to be a useful supplement to conventional treatment for rheumatoid arthritis (Lancet, 1991; 338: 899-904; Am Rheum Dis, 1983; 42: 45-51).Evidence is also beginning to trickle in about the benefits of a low protein, low fat diet in those with SLE (Lancet, May 1992, Vol 339). It is unfortunate that most of the studies into diet and SLE have been conducted on animals, yet even here there evidence is strong (J Gerson Inst, 1992;8(1-2):22-8). Those studies which do exist in humans have shown a strong correlation between fatty acids and the inflammatory process (Arth Rheum, 1990; 33:810-20). A vegetarian diet has been shown to lower an individual’s fatty acid profile (Am J Clin Nutr, 1990; 51:585-95).

In addition, there is research to show that certain amino acids such as phenylalanine and tyrosine can cause flare ups of discoid lupus erythematosus, rheumatoid arthritis and progressive systemic scelrosis (AMA Archs Dermatol, 1959; 80: 46-77).

This seems to square with the findings of Dr. Chris Reading in Sydney, Australia. He also believes that when someone is highly allergic to grains, milk, eggs, beef and yeast, the substances which actually do the damage are what he calls “subfractions” components of these foods such as the gluten, alphagliaden, alphacasien, secalin and hordein in grains and yeast and alphalactalbumins and betalactoglobulins in milk eggs and beef (see Chris Reading and Ross Meillon, Your Family Tree Connection, Keats, 1984).

Lupus is a connective tissue disease. Some 30 per cent of our body’s cell protein is made up of collagen. Research from the All India Institute of Medical Sciences has found that fluoride disrupts the synthesis of collagen and leads to the breakdown of collagen in skin, muscle, tendon, ligament, bone, lungs, kidneys, trachea, cartilage and more (Toxicological Letters, 1982; 10: 97-100; Toxicol Euro Res, 1981; 2: 99-104).Many steroid preparations contain fluoride as a means of transporting them round the body. Steroids have already been shown to cause osteoporosis, and the fluoride element is likely to exacerbate this action.

Lupus sufferers should do all they can to avoid ingesting fluorides, including switching to a non fluoride toothpaste, washing all fruit and vegetables (pesticides contain fluoride). If your have kidney lupus, and kidney function is impaired, your body may retain up to two thirds of all the fluoride you take in.

This frightening discovery, which seems to have been universally ignored, comes from the nurses’ health study, involving 69,435 women.

They found that 30 women on HRT developed the illness, against 15 who had never taken hormones (Annals of Internal Medicine 1995; 122:430-3).