Twenty years after Orion Truss discovered candida, many practitioners now believe the story is more complicated and that natural alternatives are better than anti fungal drugs.
It is now almost 20 years since C Orian Truss, an American clinician, first introduced the world to an unlikely medical monster a yeast fungus in the gut which, he said, was responsible for a vast range of human ailments. Since then, the name of that tiny yeast, Candida albicans, has become a watchword for the many millions of people who have sought unorthodox answers when conventional medicine has failed them.
Today, two decades on, “candida” has in a sense come of age, but has maturity brought wisdom? Some would say no, and that the syndrome has turned out to be much more complex than Truss thought.
For conventional doctors, “candidiasis” still means primarily a localised invasion of the vagina or mouth, commonly called “thrush”. Few of them have taken on board Truss’s radical notion that candida can also proliferate in the gut and cause “a syndrome of almost unlimited scope”, in the words of US physician Richard Passwater. Traditional medical prejudice and conservatism may be the reason, or it may be, as some specialists like Dr Keith Eaton believe, because the “candida syndrome” has not yet been proven and may be a misnomer.
Recently, some clinicians have begun to question the whole idea. “Although it is possible that Candida albicans may be the cause, it has never been proved to be the culprit,” says Dr Keith Eaton, a leading specialist. Naturopath Harald Gaier, director of medical research at London’s Hale Clinic, agrees. “Clearly, other similar organisms such as Candida utilis, Torulopsis glabrata or even Crytococcus hystolticus may be responsible, or indeed parasites like Giardia
lamblia or Blastocystis hominis,” he says.
Dr Eaton has coined the term “Fungal type Dysbiosis”, but Dr Gaier favours the even less specific “Dysfunctional Gut Syndrome”. Both agree that the primary diagnosis is through a test that shows up abnormal production of ethanol in the gut. This, according to Dr Eaton, is the only strong evidence pointing to yeast as the culprit.
“We still have no proof, however, that it’s Candida albicans. Truss claimed that because anti fungal drugs worked, the syndrome must have a fungal cause; he then jumped to the conclusion that it must be C albicans. Neither he nor anyone else has come up with a shred of evidence to support it. The fact that anti fungal drugs work could be explained by the fact that they are good gut wall stabilisers; they also kill bacteria and parasites. That’s why I call it ‘fungal type dysbiosis’ (FTD) it looks like a fungus is involved, but we can’t be sure.”
Dr Eaton believes bacteria may be at least partly responsible. He has found elevated levels of hydrogen in the breath of his “dysbiosis” patients, and hydrogen is produced by bacteria, not yeast. Another reason for the symptoms could be an allergic reaction to bacteria or yeast. Allergic reactions produce an excess of histamine, which metabolises into histadine and can be measured in the urine. In a study on 21 patients with “dysbiosis”, Dr Eaton showed that they had the similar levels of histadine to patients with food allergy (JNutr Biochem, Oct 1998).
In fact, he has found some patients with FTD can be helped by food intolerance treatments, such as low dose neutralisation and enzyme potentiated desensitisation.
It was once thought to inhabit primarily the large intestine, but now it’s understood to live primarily in the small intestine, according to Dr Gaier. When candida is permitted to proliferate, it can perform an astonishing metamorphosis, changing from a simple yeast cell into a much more harmful “mycelial” fungal form. Under the microscope, the cell appears to sprout roots and branches; these burrow their way into the walls of the intestine, and ultimately can spread throughout the body, with potentially widespread adverse effects (Current Biology, 1997; 7: 691-94).
In fact, we all have antibodies to candida in our blood, which suggests that symptomless, low level systemic invasions may be commonplace. However, when the immune system is under pressure, say, as a result of stress, illness or medication, the infection can take hold, causing a wide variety of symptoms apparently unrelated to the gut (see box, p 1). In particular, if the candida infection reaches the brain, it will cause a host of cerebral and mental symptoms, which again tends to reinforce the conventional dismissive diagnosis that the patient’s problems are psychogenic in origin.
Dr Leo Galland, the noted US nutritional doctor, says there is new evidence suggesting that the antibodies directed against candida may cross react with organ tissues, particularly in the thymus gland and ovaries, producing a kind of auto immune reaction. This can lead, he says, to ovarian failure, premature menopause and infertility. Antithymus antibodies may interfere with immune function and lead to a vicious cycle: yeast infection leads to immune suppression, which leads to worse yeast infection (Lancet, 1991; 338: 1238-40; NE J Med, 1989; 320: 245-6).
Perhaps the most insidious damage, however, is to the lining of the gut. Besides penetrating the gut wall in its mycelial fungal form, candida overgrowth is often associated with an increase of toxins called polyamines, which attack the mucosal cells of the gut wall. This results in excessive intestinal permeability popularly known as “leaky gut”. Because the gut wall leaks, it can no longer function as an effective barrier. Thus, all manner of substances, some toxic, can pass through in particular undigested food molecules (See WDDTY vol 8 no 5). Such foreign bodies, circulating in the blood, will sensitise the immune system and often cause adverse reactions to food, showing up as either as allergy or intolerance. These, in turn, can result in a bewildering array of symptoms, many of which overlap with those from C albicans. Diagnostically separating food sensitivity from candidiasis is therefore complex. Two recent laboratory tests, however, have made the clinician’s life easier the ethanol test and the hydrogen breath test (available from Biolab in London: 0171 636 5959).
C albicans has also been found to be a major allergen in its own right, which can produce a hay fever type of reaction, resulting in hives, asthma and irritable bowel syndrome. Many women with chronic vaginitis have an allergic vaginitis provoked by candida (L Galland in R Jenkins et al, Post Viral Fatigue Syndrome, John Wiley & Sons, 1991).
The evidence is also building that C albicans either contains or produces toxic substances, which can interfere both with the immune system and brain function. Many of these toxins are alcohols which are produced by the reaction of sugars in the food and yeasts in the gut. One of the main “sugar alcohols” is arabinitol, which recent studies have shown to be a powerful neurotoxin. In America, two laboratories now offer tests for the presence of these alcohols in the blood. Dr Galland finds them particularly useful for patients complaining of neuropsychiatric disorders or autism.
The connection between autism and candida is new and highly controversial, but backed by the findings of US laboratory director Dr William Shaw of the Great Plains Laboratory in Kansas. He became interested in the connection after noticing abnormal metabolites in the urine of two autistic children. He noticed that both had extremely high levels of tartaric acid 600 times more than normal children. Tartaric acid is a known toxin, so he wondered whether the tartaric acid could be causing symptoms of autism. He reasoned that, because humans do not produce this chemical and the only source of tartaric acid is yeast, reducing yeast in the gut might reduce the autistic behaviour. Treatment with the anti fungal drug nystatin was tried, with enough success to justify its further use. To date, over a thousand children with autism have been treated with anti fungal agents, with, Dr Shaw reports, “good clinical response in 80 to 90 per cent”. In the absence of clinical trials, however, these results must be seen as anecdotal.
Although Truss’s treatments have stood the test of time, numerous clinicians are beginning to modify his original therapy. Diets are now becoming less severe, partly because they are difficult to follow and partly because of practitioners’ own preferences. There’s a difference of opinion, for example, over whether milk and yeast products should be totally excluded (Environmental Medicine in Clinical Practice, BSAENM 1997). How long the diet should be maintained also differs between practitioners; Dr Keith Eaton still maintains a strict diet for three to six months, but Dr Harald Gaier says he now finds three weeks is all that is necessary.
Over the years, conventional anti fungals such as nystatin have gradually tended to fall out of favour. An increasing number of practitioners are now turning towards natural therapies. First and foremost are the “probiotics”. These are specially cultured bacteria, identical to the ones in the gut that normally keep the C albicans yeast under control. Once the candida has been cleared by diet or drugs, probiotics are prescribed to repopulate the gut.
Chief among these are species of Lactobacillus and Bifidobacteria (see box, p 2). Apart from competing with C albicans for space, they have also been shown to increase intestinal acidity, creating a less favourable environment for candida. Probiotics can be taken either as dry capsules or liquid yoghurts. Although the anecdotal evidence for their effectiveness is overwhelming, there have been few clinical trials for their use in candidiasis.
A recent year long, crossover trial on candidal vaginitis, however, showed a three fold decrease in symptoms in patients who ate yoghurt containing Lactobacillus acidophilus (Annals of Internal Medicine 1992; 116: 353-7).
Besides using probiotics, many of today’s candida practitioners are turning to new sources of anti fungal drugs, most of them extracted from plants. Caprylic acid, for example, is a fatty acid found in coconuts and palm oil; it was shown to have remarkable anti fungal properties 50 years ago (Bull Johns Hopkins Hospital, 1946; 78: 333-9). Eight years later, three cases of “severe intestinal candidiasis” were reported to be successfully treated (Arch Intern Med, 1954; 93: 53-60). Caprylic acid has since been shown to be harmless to friendly gut flora, and yet to kill both the yeast form of candida and the invasive mycelial form, because it is absorbed by the intestinal mucosal cells.
Another plant product which is gaining in popularity is goldenseal (Hydrastis canadensis). Its principal active ingredients are berberine, canadine and hydrastine. An Indian journal confirmed that berberine is a powerful anti fungal (Sabouradia, 1982; 20: 79-81).
It is also claimed to kill many kinds of harmful bacteria, viruses and other parasitic organisms.
Goldenseal appears to have two other properties that make it particularly useful against candida: it inhibits the destructive polyamines that go along with candida and eliminates the “die off” toxins produced when it is killed. Goldenseal can be taken internally as a capsule or used as a vaginal douche or mouthwash.
Dr Gaier favours a radically new technique, which has transformed his treatment programme. One of the concomitants of yeast overgrowth is an infestation of anaerobic gut bacteria which take the place of the lactobacilli, but do not consume the yeasts, he says. Although it is a fairly easy matter to clear out the yeasts by drugs, the anaerobic bacteria often hinder the repopulation of the gut by lactobacilli, thus running the risk of the yeast infection recurring.
Dr Gaier recently came across a French product called Gastropax, which is usually prescribed as an antacid. One of its modes of action is to release oxygen in the gut. Anaerobic (which means “without oxygen”) bacteria are killed by oxygen, so Dr Gaier now prescribes Gastropax for five days and then starts them on a three week course of treatment with special diet and tincture of Berberis vulgaris, another candida terminator with remarkable results, he says. Patients are completely better in six weeks to several months.