The Hygiene Hypothesis or Old Friends Hypothesis

The hygiene hypothesis proposes that several chronic inflammatory disorders (allergies, autoimmunity, inflammatory bowel disease) are increasing in prevalence in developed countries because a changing microbial environment has perturbed immunoregulatory circuits which normally terminate inflammatory responses.

What the hygiene hypothesis says is that our bodies are ecosystems that have been damaged by a rapid reduction in number and variety of microorganisms that populate our bodies and immediate environment. That alteration of those environments has been so rapid in genetic terms that we have not had time to adapt, and the consequence is the rise of autoimmune diseases and immunological disorders.

The hygiene hypothesis is the theory upon which practical therapies like helminthic therapy (worm therapy) are based. The use of benign infectious organsims to treat or prevent diseases involving immune dysregulation, autoimmunity or chronic inflammation.

Some stress-related psychiatric disorders, particularly depression and anxiety, are associated with markers of ongoing inflammation, even without any accompanying inflammatory disorder. Moreover, pro-inflammatory cytokines can induce depression, which is commonly seen in patients treated with interleukin-2 or interferon-a. Therefore, some psychiatric disorders in developed countries might be attributable to failure of immunoregulatory circuits to terminate ongoing inflammatory responses. This is discussed in relation to the effects of the immune system on a specific group of brain serotonergic neurons involved in the pathophysiology of mood disorders.

The incidences of several chronic inflammatory disorders have been increasing strikingly in the developed countries. These include allergic disorders (asthma, hay fever), some autoimmune diseases (for example, type 1 diabetes and multiple sclerosis) [1] and inflammatory bowel diseases (IBD; ulcerative colitis and Crohn’s disease) [2].

The ‘hygiene,’ or ‘old friends’ hypothesis attributes some of these increases to a failure of immunoregulation [3]. We know that a failure of immunoregulatory mechanisms can lead to simultaneous increases in all these diverse types of pathology, because genetic defects of Foxp3, a transcription factor that plays a crucial role in the development and function of regulatory T cells (Treg), lead to a syndrome known as X-linked autoimmunity–allergic dysregulation syndrome (XLAAD) that includes aspects of all of them [4].


Next Page