Atopic disease is characterized by inflammation. This inflammation is mainly IgE-induced. According to linear assumptions IgE was a long time considered as the cause of atopic disease, but IgE deficient mice can became allergic, as well (Mehlhope et al 1997). As seen before, the search for causes is often futile in nonlinear systems. A study of the pattern might be much more promising.

Atopic disease concerns two main organs, the skin and the lungs. Although the inflammatory process is maintained by different cells in the two organs - mast cells in asthma, Langerhans cells in atopic eczema (Leung/Bieber 2003, Kaplan et al. 2005), there is a comparable pattern. Two components seem to be crucial for the development of the atopic disease, a slow and a quick factor, although there is only little knowledge about these two different rhythms for the skin (Leung/Bieber 2003).

The situation is better in asthma. The quick regulative inflammation is triggered by animal fur, pollen, cigarette smoke or house dust mite faeces (Brown 2004). The slow process involves the thickening of the smooth muscle that might become about three or four times as thick and contains many mast cells (Brightling et al 2002). This thickening is a long term process (Shore 2004) which does not correlate with the amount of inflammation in the airways (Brown 2004). It is a structural abnormality of the so-called remodelling process. As asthma progresses, the chronic inflammation leads to a further remodelling. But although inflammation and the remodelling process influence each other reciprocally, the two mechanisms are somehow separate (Brown 2004, Holgate/Polosa 2006).

What we see here is a regulative process on two different levels

• a quick positive feedback mechanism of mediator cascades leading to an asthma attack
  
• a long term, structural process based on a slow positive feedback leading to thickened smooth muscle with a higher density of mast cells.
  

These two layers of disease are about what Hahnemann descried with his concept of chronic disease. The quick mechanism which can be influenced quite easily is more definite and precise. The slow mechanism which remains untouched by specific therapies, worsens with time and leads to a continuous decline of health and vitality.

Exactly this can be observed in steroid therapy. It is effective in suppressing inflammation and reducing the frequency of asthma attacks, but makes no long-term difference to how well people's lungs work (Brown 2004, Guilbert et al 2006, Murray et al 2006, American Thoracic Society 2007).

Moreover, the quick cascade mechanism that provokes symptoms gives not necessarily a hint onto the development of the underlying chronic disease. It could be shown that asthma (or better the chronic process) starts quite early in life. It might remain silent for some time and can reoccur after long periods of absence (Sears et al 2003). Those who had consistently low peak flow measures at ages 18 and 26 had already had a low peak flow by the age 9 (Rassmussen et al 2002). That is, early alterations remain over decades without symptoms and without ‘disease-value’. The chronic process continues, despite short term incidences of worsening or amelioration.

This is a very simple pattern. The factual processes are probably much more complex. But already this plain model shows how systemic tools might be used to come to new conclusion and hypotheses which might eventually lead to a different understanding of the development of the atopic disease in special and of chronic diseases in general. Such conclusions might be:

• There are different levels in the development of disease which represent somehow Russell’s logical types (chap. 3.2). Probably the principles of emergence (chap. 4.10) are also applicable here and it would be most helpful to conceptualise the interrelation between fast and slow mechanisms with this epistemological tool.
  
• The two types of alterations seen in atopic disease (fast and slow) correspond to the criteria of Bateson’s network pathologies (chap. 6.7). There is a monotone increase in the remodelling process and quick runaways in the fast process.
  
• Quick runaways result – according to the theory – from fixed variables, from intervention into a homeostatic process. This theoretical model is supported by a lot of observations of empirical medicine, especially by homeopathy.
  
• The monotonous change of the remodelling process corresponds to the lack of rhythms.
  

These four points do not constitute different categories. They are different approaches to state the same fact. For example, the lack of rhythms is not only an expression of a chronic disease. It reveals also a rigidity of the organism (chap. 6.4), which might be the consequence of local therapeutic interventions, and so on.