Georg Ivanovas From Autism to Humanism - systems theory in medicine

5.5 Homeopathy

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b) atopic disease and psora

Another chronic disease described by Hahnemann is the so called psora. It has a short incubation time of 1-2 weeks, starts with fever as in a cold, shows eczematic eruptions and has the tendency to cause later a generalized disturbance (Hahnemann 1835: 50). In contrast to syphilis, psora has spontaneously the tendency to become chronic. No suppression of the skin lesions is necessary, although this might promote the chronification. The cases Hahnemann described for psora (Hahnemann, 1835: 22-24) are mostly identical with what is called today atopic disease.

In modern terms atopic disease starts mainly with dermatitis. Children having atopic skin alterations will later develop allergic rhinitis or asthma with a 80% probability (Leung/Bieber 2003), the so called ‘atopic march’ (Demehri et al 2009). A connection of atopic dermatitis with fever has not been observed in orthodox medicine, but the incidence of atopic disease rises with the incidence of childhood infections (Benn et al. 2004).

Theoretically, there is a multitude of causes for the atopic disease. The genes attributed to asthma are, among others, ADAM 33 (Shapiro/Owen 2002), ADRB2 (Ridley 2000), DPP10 (Allen et al 2003). Also the silent congenital infection with Ureaplasma urealyticum has been claimed as its cause (Day 1997), but is probably only one germ in a whole spectrum.

The use of antibiotics in the first year of life has been accused for the rise of asthma and other allergic diseases, as well (Bach 2002; Dotinga 2003, Motluk 2003; Randerson 2004; Noverr et al 2004a), denied by others (Benn et al 2004).

Fever has been seen as protective (Williams et al 2004), or as harmful (Benn et al 2004).

The prevalence of house dust mite shall be causal (Sears et al 2003). But measurements of house dust mite in the environment of newborns cannot predict asthma (Martinez 2003).

Endotoxin, found, e.g., in the faecal flora of larger mammals is associated with wheezing during the first year of life, even at low doses. But in animal models and in studies in humans, exposure to endotoxin in early life, during the development of the immune system, seems to prevent the development of allergic disease (Weiss 2002). However, cleanness protects if the disease is present (Morgan et al 2004).

Pollution was accused (Gauderman et al 2004). But Athens, Greece, long had a relatively low asthma incidence, despite its high levels of air pollution (Bach 2002). Asthma was also quite low in former Eastern Germany, despite a horrible pollution. But asthma rose to Western levels after reunion, although pollution declined.

Another explanation are the preservatives, stabilisators, colourings etc. of Western food industry, also discussed for the development of ADHD (Eigenmann/ Haenggeli 2004). Even global warming was attributed to the rise of asthma (Ault 2004).

Welcome to pleiotropy and pluralism. Your looks are affected not by a single "looks" gene but by lots of them – and by nongenetic factors as well, with fashion and free will figuring prominently among them…. Nearly every statement we might care to make about asthma can be challenged, including the assertion that it is getting worse” (Ridley 2000).

Indeed, a look at the scientific news service of covering only one year (accessed 4.3.02) shows such confusing results as: Bacteria ameliorate (30.10.01), or worsen (12.6.02) or are causal (14.6.01), bovine tuberculosis ameliorates (28.2.02), cats worsen (6.7.02), or not (14.3.01), dogs ameliorate (6.11.01), gas cookers worsen (14.8.01), passive smoking worsens (27.9.01), margarine and fried food worsens (20.7.01), harmonic families ameliorate (5.7.01), but asthmatic children strengthen the family (23.3.01), etc. Up to 68% of the cases are caused genetically (23.10.01), something that does not explain the rise of asthma in children of 33% in the German town of Munster in the years from 1995 to 2000 (13.6.01), or only if one assumes that these are all the not genetically caused cases.

Epidemiological studies differ from a 20 % incidence in British isles with a falling tendency (Anderson et al 2004) to over 60% incidence in Aberdeen with a rising tendency (Devenny et al 2004). This might be due to different definitions or to special local conditions (Rees 2005), or to the observed population (Zauli et al. 2005). The general trend seems to be that asthma rises with the adaptation of a Western living style remaining then on a high level (Asher et al 2006).

The comparison of results is often difficult as it is not always obvious whether they refer to atopic disease, asthma or allergy. These different terms represent often more a certain approach of the observer leading to different categories than distinct diseases (Wenzel 2006). However, there is a major difference between eosinophilic (atopic) asthma and not atopic asthma in children. Whereas atopic asthma has the tendency to become worse (and thus represents a chronic disease as defined by Hahnemann), children with non atopic asthma lose their symptoms over school age (Illi et al 2006).

This typical autistic-undisciplined picture is due to the nonlinear nature of atopic disease and asthma which is a network pathology with a predominance of Th2 helper cells (chap. 6.3).

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