Chronic intestinal candidiasis as a possible etiological factor in the chronic fatigue syndrome

Med Hypotheses. 1995 Jun;44(6):507-15. doi: 10.1016/0306-9877(95)90515-4.


The chronic candidiasis syndrome, also known as the Candida-related complex, putatively caused by the overgrowth of Candida albicans in the gastrointestinal tract and secondarily in the genital organs, is briefly described. Patients with this disorder have many of the same symptoms as those with the chronic fatigue syndrome, except for the recurrent flu-like symptoms of the latter disorder. The positive response of a large number of patients with the chronic fatigue syndrome (CFS) to an oral antifungal agent and a diet for intestinal candidiasis has been described by another clinician. There is evidence that Candida albicans infection of the mucous membranes depresses T cell and natural killer (NK) cell function. Similar abnormalities of immune function are found in the CFS. The function of cytotoxic T cells, T helper cells, and NK cells is important in preventing reactivation of infections from Epstein-Barr virus, cytomegalovirus, and other herpesviruses. Reactivation of one or more of these viruses could lead to the expression of the flu-like symptoms in the CFS. Yet the immune dysfunction found in this disorder has been considered the primary underlying causal factor. It is proposed that chronic intestinal candidiasis may be an agent which leads to immune depression in many CFS patients and therefore that it could be a causal factor in CFS.

MeSH terms

  • Antifungal Agents / therapeutic use
  • Candida albicans / growth & development
  • Candida albicans / isolation & purification
  • Candidiasis / drug therapy
  • Candidiasis / immunology
  • Candidiasis / physiopathology*
  • Fatigue Syndrome, Chronic / drug therapy
  • Fatigue Syndrome, Chronic / etiology*
  • Fatigue Syndrome, Chronic / microbiology
  • Humans
  • Intestinal Diseases / drug therapy
  • Intestinal Diseases / immunology
  • Intestinal Diseases / microbiology*
  • Intestinal Diseases / physiopathology
  • Models, Biological
  • Virus Activation


  • Antifungal Agents