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See Inside Scientific American Volume 307, Issue 2

Readers Respond to "Food Poisoning's Hidden Legacy" and Other Articles

Letters to the editor from the April 2012 issue of Scientific American


FOOD POISONING'S EFFECTS

Maryn McKenna does not mention controls for medical history in her article on evidence that foodborne pathogens cause lifelong consequences, “Food Poisoning's Hidden Legacy.” An elevated incidence of renal impairment and circulatory problems within six years after individuals suffered severe immediate symptoms of Escherichia coli ingestion, as compared with those suffering mild or no symptoms, does not prove their E. coli exposure was the cause. That conclusion assumes that there was no preexposure renal or circulatory dysfunction. For instance, a compromised excretory system could cause a more severe response to E. coli ingestion and, if not identified a priori, could later be perceived as a consequence of the exposure. Alternatively, those with a propensity for development of these medical conditions may have a heightened sensitivity to E. coli. Correlation alone does not prove causality.

Peter Irwin
via e-mail

Affected joints after infection with Salmonella bacteria, reported by McKenna, are an old, but apparently forgotten, problem. Those of us who have worked in developing countries have seen, treated and followed up on patients with typhoid fever, a severe infection caused by Salmonella typhi. Pain and swelling of the joints may continue long after discharge and apparent recovery. The different types of joint problems following typhoid infection listed by surgeon William W. Keen in 1898 included joint infection during the illness, rheumatic typhoid arthritis and septic typhoid arthritis. And Charles W. Wilson reported patients developing swollen joints after typhoid infections in the Journal of Bone and Joint Surgery in May 1899. We now see that other salmonellae can produce the same long-term problems.

Alan Dugdale
Brisbane, Australia

BREATH-DEFYING

On reading “The Limits of Breath Holding,” by Michael J. Parkes, I was reminded that in 1958 I decided to see how long I could hold my breath underwater. I found that if I floated face down and relaxed, I could flex my diaphragm muscles repeatedly to delay the urge to take a breath. Eventually I was able to do so for almost four minutes.

Jon Otterson
Madison, Wis.

There is a counterpart to holding one's breath: expelling air completely and seeing how long one can go before inhaling. There is a break point there, but the diaphragm is “held” in a state of complete relaxation instead of contraction. Does the same mechanism affect both sides of this coin?

Bryon Moyer
via e-mail

My foster mom claims that one late evening I was too quiet, and she found me unresponsive and turning blue. I was fortunate in not becoming another statistic of sudden infant death syndrome (SIDS). Could the role of a not so fully developed or underdeveloped diaphragm explain “involuntary breath holding” in infants and thus SIDS?

Bennett A. Wallace
Louisville, Ky.

PARKES REPLIES: The last two questions both highlight the need for more research on the diaphragm. Regarding Moyer's comments, we know that people can perform only very short breath holds with deflated lungs. Yet is the diaphragm “held” at its relaxed length with an isometric contraction or just completely relaxed? Further, these short breath holds neither confirm nor refute the hypothesized role of the diaphragm in the break point. Its chemoreceptors could still be stimulated by the rapid rise in carbon dioxide or the fall in oxygen. As for Wallace's question, many hypotheses attempt to explain SIDS. Experimentally testing the hypothesis of a “not so fully developed or underdeveloped diaphragm” in infants is not easy.

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