Intestinal Fermentation Syndome (False Candida)

Dr Orion Truss of Birmingham, Alabama first brought the Candida (16) hypothesis forward in 1978. Dr. Truss is a psychiatrist with a special interest in clinical ecology; his seminal papers in the Journal of Orthomolecular Psychiatry (‘Tissue Injury Induced by Candida Albicans’, vol. 7, no 1, 1978, pp 17-37 and ‘Restoration of Immune Competence to Candida Albicans’, vol. 9, no 4, 1980, pp 287-301) certainly revealed an extensive and fascinating area of personal investigation. His work was taken up enthusiastically by Dr Bill Crook, who has done more than any single individual to popularize the Candida hypotheses, or what has now become known as ‘the yeast connection’, taken from the title of his book (The Yeast Connection, Professional Books, 1983)

Since that time, the whole theory seems to have gripped the public’s imagination and clinical ecologists have been keen to extol the existence of the problem and the enormous benefits to be gained from tackling it vigorously. The fact is there are health gains to be made by  following an anti-Candida programme, taking antifungal drugs and excluding sugar and yeast foods from one’s diet. Yet Truss’s idea is no more than a theory.

If there is one valid complaint that members of the medical profession have against clinical ecologists it is their tardiness in backing up ideas with research. It has been 15 years not since Truss’s innovative papers – ample time to carry out detailed studies that would validate his claims. Yet they are singularly lacking. A catalogue of startling recoveries does not constitute scientific study. We may be getting the right results for the wrong reason.

Despite a degree of ‘brand identification’, Truss was in fact far from being the first investigator in this field. His ideas were anticipated almost 70 years earlier by Turner, who presented a paper on what he called ‘intestinal germ carbohydrate fermentation’ (proceedings of the Royal Society of Medicine Symposium of Intestinal Toxaemia, 1911). In 1931 Hurst was in his footsteps, writing about ‘intestinal carbohydrate dyspepsia’. In the 1930s and 1940s this dyspepsia was being treated with Lactobacillus acidophilus, B vitamin supplements and a low-starch diet (remarkably like modern anti-Candida treatment except that legumes are no longer banned, as they were at that time).

Medical literature has tried to define the patient-type who suffers with this syndrome. A major text on gastroenterology in 1976 described victims as ‘Essentially unhappy people  . . . . . any suggested panacea or therapeutic straw is grasped . . .  no regime is too severe and no programme too difficult  . . . with the tenacity of the faithful, they grope their way from one practitioner to the next in the search for a permanently successful remedy.’ This disparaging description shows a lamentable weakness on the part of doctors for blaming any patient they cannot help.

The ‘problem patient’ attitude was probably what sank the condition in the 1950s. At that time, the psychosomatic theory of disease was enjoying a great revival. The tendancy was to dismiss all patients with vague, ill-defined symptoms as psychiatric cases. Unlike today, there were no physical findings to disprove the psychiatric label and so it stuck. It’s still with us, to a large degree.

ON-BOARD BREWERY

So the idea of a yeast-like organism that lives on starches and sugars and causes bowel disturbance is far from new. It seems to enjoy a vogue in medical circles every few decades and then lapses out of sight once again. The reason is probably that, as in the 1980s, some doctors become convinced they know what causes the syndrome, but then can’t seem to find a workable proof that affords a satisfactory explanation. This casts doubt on the basis of the theory. So it is today with ‘Candida’.

The success of antifungal drugs may have fed a myth. In some cases, anti-Candida therapeutic agents such as Nystatin seem to work only in very high doses (10 to 100 times the usual dose). This has led to the speculation that it may be helping by some other mechanism than just that of eradicating the yeast micro-organism; possible by blocking bowel permeability.

One thing is certain, there is virtually no correlation between Candida in the stool sample and the existence of the ‘yeast syndrome’. Indeed, Candida albicans is rarely identified in specimens, despite its known very wide occurrence. This lack of correlation is disappointing but hardly surprising, especially if we are looking for the wrong culprit.

It is true: treatment directed towards this type of organism can be highly effective in selected individuals, so clearly a real phenomenon exists. But that doesn’t prove that Candida is to blame. In fact I’d like to set the debate alight with the claim that the culprit may not be Cnadida at all, or that Candida is only one of many potential suspects.

Other available flora that might be at work include the ordinary yeasts of the genus Saccharomyces (food yeasts), certain species of E. Coli, Pseudammonas (pyruvate fermentation) and, most fascinating of all, Sarcina ventriculi.

Historically, Sarcina is an important organism. In the old days, when surgeons operated in frock coats and quite often smoked cigars at the same time, once in a while they would literally blow up their patients!: as the alcoholic gases generated by sarcina were released from the patient’s stomach when cut open, the cigar would ignite the fumes and a fireball was the disastrous result!

These ‘on-board breweries’ are probably quite common. Dr Keith Earton called my attention to the speculation that so-called ‘spontaneous combustion’ may be due to this microbe. Puzzling cases have been documented of human beings literally vanishing in a sheet of fire, for no apparent reason. Perhaps Sarcina, or some other organism, and its inflammable gaseous excreta could be to blame.

Incidentally just as Candida isn’t the only contender for the role of pathogen, ordinary ethyl alcohol is not the only product of fermentation we seem to be dealing with. Many other products can be derived from the breakdown of sugars and starches, including short-chain fatty acids such as acetate, proprionate, succinate and bdutyrate, and other alcohols such as iso-propanol, butanol and 2,3 – butylenes glycol. Testing for these substances is now available commercially in the UK under the expertise of Dr John Howard at Biolab UK (see Useful Addresses).

Further, if detoxification pathways are blocked due to overload, other unwanted metabolites are produced, such as epoxies, aldehydes and even chloral hydrate, ingredient of the classic ‘Mickey Finn’. Typically this chemical produces a tired and ‘spacey’ feeling. Here is at least part of the reason these patents can’t take alcoholic drinks. Naturally, these by-products too have a bad effect on the patient; most are quite toxic.

For treatment of this condition, all that is written about Candida is probably valid, at least until we know the truth about what we are dealing with. Antifungals usually help, but probiotics are more logical. Avoidance of fermentable sugars is important.

Paradoxically, antibiotics occasionally solve the problem; presumably when the culprit is a fermenting bacillus.

HYPERSENSITIVITY TO GUT BACTERIA  AND PARASITES

A great many allergy patients are sensitized to organisms growing within their own intestines; so-called ‘gut flora’. Candida (16), which has risen to prominence recently, is just one aspect of this important and at times baffling phenomenon. It is as if the patient had a permanent ‘on-board’ food allergen and is unable to get rid of it. Unless the diagnosis is suspected, it can block all progress and interfere with treatments such as enzyme potentiated desensitization (EPD) and Miller’s method.

In 1962 Dr Len McEwen started to investigate the medical histories of ‘intrinsic’ asthma patients. He identified a group who were improved by taking tetracycline. These patients could have their symptoms made worse by challenge with old-style bacterial vaccines and made better particularly reliably when treated with Enterovioform, making it clear that the offending antigen had something to do with gut flora.

Interestingly, careful stool sample studies from patients taking tetracycline, ampicillin or Enterovioform showed no detectable change when compared to controls. In  particular, McEwen found no increase in the Candida counts, which is what might be expected to happen. He deduced that although the antibiotics did not kill the bacteria they somehow prevented the release of antigenic substances and he hit upon the idea that the trouble might be coming from the upper gut, in particular the stomach. He reasoned that since this area is normally sterile, the mucosa would not be adapted to antigens from bacterial flora. Thus if organisms were to be found there, it might be that the normal defence mechanisms were being by-passed and that allergic reactions were being set up.

Thus there are patients who will be improved allergically by taking antibiotics, in contrast to the majority, who get worse.

In the late 1970s Orion Truss was working with allergic symptoms associated particularly with psychological illness. Gradually it become evident that people with Candida seemed to develop multiple food allergies. A possible mechanism for this effect, apart from the Candida itself acting as an antigen, was that hyphae from the yeast cells penetrated the gut wall and caused it to become permeable to food products. These food products could then reach the bloodstream in much larger quantities than normal. This in itself would increase the likelihood of an allergic reaction without the Candida acting as a ‘bystander antigen’.

All these are no more than hypothetical explanations. Regardless of the theories, the fact remains that many patients improve with either antifungals or, in some cases, antibiotics. It may even be that the effect is not achieved by means of reducing the flora stabilizing cell membranes in the gut. This might explain why some practitioners have noticed that although routine therapeutic quantities of the anti-fungal Nystatin have no effect, very substantial doses may keep the patient’s allergic symptoms in check. Alternatively, in these large doses the Nystatin may be having a stabilizing prophylactic effect on the mast cells of the gut mucosa in much the same way that sodium cromoglycate protects the lungs (see drugs for allergies). MeEwen says: ‘The real effect of Nystatin may have fed a myth.’ We shall have to wait and see. In the meantime, as MeEwen allows, it makes sense to go on using it, since manifestly it works in many cases.

ANTIBIOTICS

Note: Enterovioform has been withdrawn for safety reasons. It led to 10,000 cases of disastrous sub-acute neuropathy in Japan. A possible replacement is nifurozazide. It is licensed in France, Germany and Belgium, where it is sold under two trade-names: Ercefuryl and Pentofuryl (currently the drug is not licensed for use in Britain or approved by the US Food and Drug Administration).

 In the meantime, according to McEwen, the most effective treatment is a 10-day course of De-Nol (two tablets, twice daily, about 30 minutes before food), which eliminates the gastric flora, combined with one of the systemic antifungals to reduce colon Candida. Remember De-Nol and Nystatin (or amphotericin) interact  and so should be taken separately.

 Tetracycline can be considered as an alternative (500 mg twice daily).