What about antifungal drugs?
It must, however, be stated that there are conditions in which the use of antifungal drugs12,13 can be useful, especially if the condition suggests that the process of recovery will be a very long one. In the main, however, once we learn to recognize the symptoms that indicate Candida might be getting out of hand, the natural, non-drug methods described in this book will work, and work well.
The following modern drugs are all used effectively against various Candida infections, depending on where the infection is primarily located (for instance, urinary tract, vagina, skin or systemic): fluconazole (Diflucan), itraconazole (Sporanox), ketoconazole (Nizoral), miconazole (Daktarin, Femeron), amphotericin B (Fungilin), flucytosine (Alcobon).
Side-effects: These are minimal with many of these drugs, especially if only a single dose is prescribed (which is often the case with medications such as fluconazole). The more severe reactions listed below should be seen in context as the medication would commonly be used only in cases of severe systemic candidiasis, where the person is already very ill. When the use of antifungal drugs is prolonged or repeated, the chances of side-effects increase, including:
1 nausea, headache and stomach discomfort (fluconazole, itraconazole)
2 liver dysfunction (ketoconazole, although rarely)
3 severe pruritus (itching), gastrointestinal symptoms, fever (miconazole, especially at high doses)
4 fever, headache, backache, vomiting, thrombophlebitis and, in some cases, irreversible kidney damage (amphotericin B)
5 nausea, vomiting, diarrhoea and (rarely) fatal liver disease (flucytosine).
Nystatin is one of the main antifungals used before the availability of the modern drugs listed above. Nystatin, like amphotericin B (see above) is derived from fermentation of a fungus (Streptomyces albulus or S. noursei). Nystatin is considered relatively safe and non-toxic, although Truss and others report that, once it is stopped, when Candida is apparently under control, a rebound of yeast activity can be anticipated unless a broad anti-Candida programme has been adopted.
Nystatin is effective against certain Candida strains while others are resistant. Not being a broad-spectrum antifungal agent, it allows proliferation of yeasts, such as Trichophyton, that are resistant to it while Candida is attacked. This can lead to opportunistic overgrowth of these resistant yeasts even though Candida is controlled for the short-term.14
A variety of alternatives are discussed in Chapter 5.
The unfortunate aspect of most antifungal drug treatment is that they are seldom used together with a comprehensive antifungal dietary and supplement approach, which would encourage a healthier digestive tract and immune system.
Drugs are seldom necessary at all unless the infection is severe and widespread since the methods outlined in later chapters are safer and of proven efficacy.
A reminder
Let us not lose sight of the fact that Candida lives in every one of us and usually produces no symptoms unless the environment in which it lives (our body) has been compromised.
Diagnosis of yeast involvement in health problems is not a case of establishing whether or not yeast is present – because it always is to some extent. Rather, it is the task of the healthcare provider to advise anyone with yeast-related problems to attempt to discover what underlying factors have allowed yeast to proliferate and to focus attention on these – as well as control fungal activity.
Any approach which targets the yeast alone will result in a return of symptoms sooner rather than later. It is not just the yeasts that need to be controlled, but the causes which have allowed them to opportunistically explode into action.
In Chapter 3, we will consider just what can happen to weaken your wonderful defence mechanisms as well as additional ways in which Candida is sometimes allowed to go on the rampage, and so begin to infest other areas of your body.
REFERENCES
1 Edwards J. Candida Adherence Mycology Research, Harbor–UCLA Medical Center, Montana State University, 2002
2 Williams R. Biochemical Individuality, University of Texas Press, 1979
3 Truss C. The Missing Diagnosis, Birmingham, AL: Self-published, 1980
4 Stein J (ed). Internal Medicine, London: Little Brown, 1983
5 Odds F. Candida and Candidosis, London: Balliere-Tindall, 1988
6 Epstein J. ‘Quantative relationships between Candida albicans in saliva and the clinical status of human subjects’, J Clin Microbiol 1980; 12: 475–6
7 Cohen R. ‘Fungal flora of the normal human small intestine’, N Engl J Med 1969; 280: 638–41
8 Truss CO. J Orthomolec Psychiatry 1984; 13(2): 66–93
9 Goldberg B. Chronic Fatigue, Fibromyalgia & Environmental Illness, Tiburon, CA: Future Medicine, 1998
10 Manning BR. How Safe are Mercury Fillings? Los Angeles, CA: Cancer Control Society, 1984
11 Thompson P. ‘Assessment of oral candidiasis’, BMJ 1986; vol 292
12 O’Grady F et al. Antibiotics and Chemotherapy, 7th edn, New York: Churchill Livingstone, 1997
13 Bennett J. ‘A randomized trial comparing fluconazole with amphoterecin B for treatment of candidemia’, N Engl J Med 1994; 331: 1325–30
14 Da Prato R. ‘Fatty acid ion exchange complexes in treatment of Candida albicans’, Concord, CA: report by Arteria Co., 1985
2012 UPDATE ON ANTI-FUNGAL DRUGS
There has been an increasing incidence of widespread, systemic, Candida-related infections – particularly in hospital settings.
In Europe, in 2010, approximately 50% of systemic Candida infections occurred in intensive care units. In the USA systemic fungal infections, acquired during hospitalization, increased by over 200% between 1980 and 2000.
At the same time Candida’s resistance to the most widely used drugs (such as fluconazole) has increased. Thankfully newer antifungal drugs (such as those known as echinocandins) are now available for life-threatening infections. The general advice offered throughout this book should be seen as providing preventive as well as therapeutic benefits. Quite simply – the more efficient your immune system, the less chance Candida and other yeasts will have of proliferating.
3 How Candida gets out of hand
There are a number of predisposing factors which allow Candida to get wildly out of control. To a greater or lesser extent, these same factors may be involved in the more subtle spread of Candida, which is what happens in the majority of people affected by the symptoms described in Chapter 1.
Anyone affected by a yeast overgrowth is likely to be able to identify a number of interacting ‘causes’. Seldom will only one factor be involved. Among the main ones are the following three.
1 An underlying predisposition (a genetic tendency) in some individuals seems to be related to blood type and secretor status. As mentioned in Chapter 1, those who are non-secretors of their blood type are much more likely to be carriers of Candida and to have problems with persistent infections. Blood group O, who are also non-secretors, are the most affected of all. Candida appears to find it easier to colonize (attach to) blood type O cells. In one study, the proportion of non-secretors among patients with chronic candidiasis was 68 per cent.1
One of the protections against Candida which being a secretor