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This could also be physiological...
- James M. Howard (27 August 2004)
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March of the allergens: cause of increasing asthma prevalence
- Davendralingam sinniah (2 September 2004)
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Further research on the aetiology of asthma
- Christos Economou (27 September 2004)
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Asthma: might it have an enteric origin?
- Richard G Fiddian-Green (28 September 2004)
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James M. Howard, independent biologist 1037 North Woolsey Avenue, Fayetteville, Arkansas 72701-2046, U.S.A.
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This could also be caused by physiological differences. It is my hypothesis that testosterone is increasing in society. Specifically, the numbers of individuals of higher testosterone are increasing more rapidly than those of lesser testosterone. This may be seen as the “secular trend,” which is the increase in size of our children and their earlier arrival at puberty. This may be why asthma is increasing in many places. Asthma may be directly linked to testosterone. Asthma is higher in males: “…boys had a 64% higher cumulative incidence of asthma…” (Acta Paediatr 1999; 88: 310). Black men produce significantly more testosterone than white men (J Nat Cancer Instit 1986; 76: 421). “Black race remained a significant predictor of active diagnosed asthma. The excess risk of asthma in black children was not appreciably altered by adjustment for other demographic and environmental factors. Black race is an important risk factor for active diagnosed asthma in these urban children, a relationship not explained by social factors.” (Am J Public Health 1996; 86: 1406). Boys produce more testosterone than girls, and blacks produce more testosterone than whites. Asthma is much higher among males and blacks than females and whites. A case may be made for negative effects of testosterone on learning ability. Therefore, increased testosterone may be connected with lower socioeconomic status. The findings of Wong, et al., may represent differences in testosterone resulting in differences in socioeconomic status and incidence of asthma. Competing interests: None declared |
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Davendralingam sinniah, professor of paediatrics penang medical college, penang, 10450 malaysia.
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It is generally concluded that the cause of the increasing prevalence of athma and allergies world-wide is largely unknown and this phenomenon is unlikely to be explained by genetic factors. But what we do know is that there has been and there continues to be an outpouring of an untold variety of new allergens and irritants into our environment which without doubt plays a significant role in the triggering and perpetuation of the scourge asthma. People in lesser developed countries having less exposure to these triggering agents have a lesser incidence of asthma until such time as development catches up and a flood of new allergens and irritants is introduced into their environment. It is the march of the allergens that precedes the march of the allergies and overwhelms the body's ability to cope that would account for the increase in the prevalence of asthma world-wide as in the rapidly developing countries such as China. Competing interests: None declared |
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Christos Economou, Paediatrician Saint Anastasios Clinic, 4 Crete Street, 1060 Nicosia, Cyprus
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I read with interest the article by Prof. G. Wong et al with regards to the increasing incidence and prevalence of paediatric asthma in the affluent societies. I would like to share a hypothesis with the Editor and your readers, who are in a position to do research. I believe we should check the hypothesis as to whether affluent societies have caused the increase in asthma through their practices. Under natural or more “primitive” circumstances a baby at the time of birth is likely to catch a mouthful of microorganisms from its mother’s vaginal and rectal fluids and these are likely to colonise the baby’s gastrointestinal tract. Usually these babies are safe from such microorganisms as they have specific passive immunity from their mothers and also added protection through breast feeding. These organisms thus can start “training” the baby’s immune system from the time of birth and this helps prevent “allergic” inflammatory reactions in the future in the baby’s respiratory track. However, if a baby is born in rich or affluent countries then it is more likely to be born under aseptic conditions whereby a lot of antiseptics are used at the time of birth eg. for episiotomy. This practice whereby babies are not given the “opportunity” to catch their mother’s vaginal and rectal flora (for which they have passive immunity) may in some way compromise the normal development of their immune system and lead to allergic inflammatory responses in their respiratory systems in the future. I have anecdotal reports of babies that were born by normal vaginal delivery and no antiseptic was applied to the mother’s genital area until after the baby was born and they didn’t develop asthma. I believe the authors of this article are ideally suited to do the retrospective or even better organize a prospective study to check on this hypothesis. If this is confirmed, then a new era in the prevention of asthma will begin. If any of your readers are interested then I could expand further on this hypothesis. Competing interests: None declared |
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Richard G Fiddian-Green, FRCS, FACS c/o Herhold, Maitland and Co, 44 Dover Street, London W1
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I share Christos Economou's concerns about the aetiology of asthma and note his comment about the possible relevance of enteral exposure with interest. Within a few seconds of my having had a sip of wine in my latter decades of life I cough. Guillermo Gutierrez, a professor of pulmonary medicine at the Hermann Hospital, University of Texas in Houston, who has observed the phenomenon repeatedly believes the coughing is a symptom of bronchial spasm. Its not an olfactory trigger because it does not happen when I sniff wine and does not stop when I hold my nose. The trigger is not in the oral cavity because swilling the wine and spitting it out does not evoke the same response. The trigger appears to be in the oesophagus, which has the same embyological origins as the trachea and bronchi, for the coughing appears to occur before the wine has had time to enter the stomach. I have on occasion had similar symptoms when suddenly exposed to fridgid air in the middle of a Michigan winter. Whilst these clearly have an intrapulmonary trigger the wine does not for it is highly unlikely that an embryological communication persists between my oesophagus and my trachea or bronchi. The similarity between these symptoms and those triggred by wine strengthens the conviction that they might indeed be due to bronchial spasm. As the response appears to be restricted to my first sip of wine and does not occur with beer or with any drink I might have after the first sip the intraoesophageal trigger has chemical specificity and is rapidly desensitised. If so the anecdotal reports of babies born by normal vaginal delivery with no antiseptic applied to the mother’s genital area until after the baby was born and didn’t develop asthma, might be due to enteral rather than to pulmonary desensitisation. Might therefore asthma have an enteral origin even if in latter life it has an intrapulmonary trigger? Putting it another way might early enteral exposure to antigens that trigger asthma in later life decrease the likelihood of that happening? Competing interests: None declared |
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