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Relative influence of chilling versus preceding colds
- Farrel J Buchinsky (28 March 2006)
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Cold feet, cystitis and common cold: parallels between respiratory and urinary tract infections
- Ronald Eccles (19 December 2005)
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Cold feet and infections
- Anders Baerheim (8 December 2005)
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Cold exposure and the common cold
- Stephen A Hoption Cann (16 November 2005)
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Farrel J Buchinsky, Pediatric Otolaryngologist Allegheny General Hospital, Pittsburgh, PA 15212, USA
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The data presented is quite convincing that the delayed symptoms are not the same in the two groups (chilling vs. control). The authors do point out that there was a difference between those subjects that had had frequent colds in the preceding year compared to those who had not had frequent colds. So as not to negate the apparent effect of the chilling, the authors point out that "there was no difference in colds incidence between the two test groups at baseline." I am interested to know the relative influence of the two factors: chilling and frequency of colds in preceding year. Would the authors be able to model both factors simultaneously in an analysis and report the relative effect size of each factor? Incidentally, is there a mistake in the following sentence? "However, when looking at both test groups combined, those subjects who believed there were suffering from a cold had a history of more colds each year (median 2.00, range 1–10) compared to those who did not develop a cold (median 3.00, range 2–8, P = 0.007). " I would expect the numbers 2.00 and 3.00 to be interchanged, given the preceding text. Conflict of Interest:None declared |
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Ronald Eccles, Director, Common Cold Centre Cardiff University, Cardiff CF10 3US, UK
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Professor Baerheim raises an interesting parallel in his letter between the onset of symptoms of common cold and cystitis, following chilling of the feet. In our recent publication on chilling and common cold(1) we speculated that chilling of the feet caused nasal vasoconstriction that inhibited respiratory defences in the upper airway and converted a latent sub-clinical viral infection into a symptomatic common cold. Professor Baerheim has conducted research on patients with a history of cystitis and demonstrated that chilling the feet causes the onset of symptomatic cystitis with bacteriuria (2). The parallels between lower urinary tract infection (LTI) and upper respiratory tract infection (URTI) are interesting. Both URTI and LTI may be initiated by chilling the feet(1, 2); both are seasonal with increased incidence in winter (3, 4), both are associated with folk-lore that chilling causes the condition(5, 6). The link between URTI and LTI as regards chilling of the feet may be explained on the basis that both the upper respiratory tract and the lower urinary tract are involved in thermoregulatory reflexes. The nasal vasoconstriction that occurs in response to chilling the body surface conserves body heat as it reduces heat loss to the inspired air. Similarly, chilling of the body surface facilitates voiding of urine and rids the body of thermal ballast when under cooling stress. Reflex autonomic responses in the lower urinary tract in response to chilling may in some way lower local defences against infection in the same way that it is proposed that chilling lowers respiratory defences in the upper airways. The respiratory tract may harbour sub-clinical viral infections and the urinary tract may harbour faecal bacteria such as E.Coli in the periurethral area, and these sub-clinical infections may be converted to a clinical infection on chilling. In both cases it appears that thermoregulatory reflexes help to conserve body heat in response to cold stress, but there is a price to pay, with an increased susceptibility to infection. 1. Johnson C, Eccles R. Acute cooling of the feet and the onset of common cold symptoms. Fam Pract 2005;22(6):608-13. 2. Baerheim A, Laerum E. Symptomatic lower urinary tract infection induced by cooling of the feet. A controlled experimental trial. Scand J Prim Health Care 1992;10(2):157-60. 3. Eccles R. An explanation for the seasonality of acute upper respiratory tract viral infections. Acta Otolaryngologica (Stockholm) 2002;122:183- 191. 4. Elo J, Sarna S, Tallgren LG. Seasonal variations in the occurrence of urinary tract infections among children in an urban area in Finland. Ann Clin Res 1979;11(3):101-6. 5. Helman CG. "Feed a cold, starve a fever" Folk models of infection in an English suburban community, and their relation to medical treatment. Cul Med Psychiatry 1978;2:107-137. 6. Laerum E, Sandnes TW. [Urinary tract infections]. Tidsskr Nor Laegeforen 1987;107(14):1212-4. Conflict of Interest:None declared |
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Anders Baerheim, professor Department of Public Health and Primary Health Care, Kalfarveien 31, N-5018 Bergen, Norway
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I read great interest the article by Claire Johnson and Ronald Eccles.1 Also in Norway there is a common opinion among the lay population that being cold may provoke a common cold, and may cause cystitis. The latter was reflected in a case-control study on possible risk factors for cystitis, showing a high odds ratio for having been cold on the feet before start of symptoms.2 We subsequently tested the notion experimentally.3 Females 18 - 60 years with 3 or more episodes of cystitis last 12 months were placed with their feet in luke-warm water. The water was then, during 20-30 minutes, gradually cooled down to 12 degrees C. One in five of the cystitic-prone females got cystitis 55 (±5) hours afterwards. Some until now unpublished data may add to the topic. During the planning of this study, the cooling method was tested on eight healthy volunteers of both sexes. During the cooling they were asked to note all symptoms from their bodies. Six of the eight subjects experienced tingling, soreness or dryness in their throat, or tingling, stuffiness or dripping from their nose. Only two of the 29 cystitis-prone women noted soreness in their throat and/or a dry cough, and none noted any symptoms from their nose (P ≤ 0.001, Fisher exact test). Symptoms lasted 1-4 hours, and were not followed by upper respiratory infections. Cooling of the feet may act as a cold pressor. Cooling of the hand has been reported as a alpha-adrenergic task,4 and nasal congestion has previous been coupled to cooling the whole body of young healthy males.5 In both studies the legs of subjects were put in cold water or water gradually being cooled. I find it curious that the frequency of acute upper respiratory symptoms immediately after cooling is so different in the two materials, and also that cystitis-prone females react to cooling of the legs so differently, compared at least the healthy controls in our material. Further research is obviously needed. References 1. Johnson C, Eccles R. Acute cooling of the feet and the onset of common cold symptoms. Fam Pract 2005; 22: 608-613. 2. Baerheim A, Laerum E, Sulheim O. Factors provoking lower urinary tract infection in women. Scand J Prim Health Care 1992; 10: 72-75. 3. Baerheim A, Laerum E. Symptomatic lower urinary tract infection induced by cooling of the feet. A controlled experimental study. Scand J Prim Health Care 1992; 10: 157-160. 4. A comparison of cardiovascular and autonomic adjustments to three types of cold stimulation tasks. Allen MT, Shelley KS, Boquet AJ. Int J Psychophysiol 1992; 13: 59-69. 5. Nasal reaction to changes in whole body temperature. Lundquist GR, Pedersen OF, Hilberg O, Nielsen B. Acta Otolaryngol Stockh 1993; 113: 783- 788. Conflict of Interest:None declared |
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Stephen A Hoption Cann, Assistant Professor Dept. of Health Care & Epidemiology, Univ. of British Columbia, Vancouver, BC V6T 1Z3, Canada
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Johnson and Eccles (1) provide evidence that cold exposure may induce cold symptoms, presumably due to reactivation of latent viral infections. The susceptibility to viral infection of the nasal passages upon exposure to cold may explain the phenomenon of cold-induced rhinorrhea (2) as a possible means for the body to flush out the nasal passages when at a thermal disadvantage. The authors’ study (1) is consistent with a previous report by Clardy and colleagues (3) where a hypothermia regimen (30oC) was used to control cerebral edema in children. This intervention, however, was unexpectedly followed by an increased incidence of infectious complications (Haemophilus influenzae pneumonia and Streptococcus pneumoniae sepsis) in 5/13 patients (38%). Hypothermia in animals and humans can induced pancytopenia (4) and impair the functional activity of leukocytes (3). In animal models, cold temperatures may adversely affect many infectious diseases. Lillie and colleagues (5) in studying St Louis encephalitis in mice and typhus in guinea pigs observed that infectious morbidity was highest in the winter and lowest in the summer – corresponding to environmental temperature. Moreover, the incubation period (i.e. subclinical phase) for both infections was significantly shorter in the wintertime than in summer. Thus, if colder temperatures impair the ability of the host to overcome an overt infection, one could expect that the same would be true in combating subclinical infections. The fact that animals reallocate energy resources from reproduction and growth to the immune system during winter (6) further supports the concept that cold exposure impairs immunity. The idea that exposure to cold triggers the onset of cold symptoms is a belief that has persisted for millennia. In his classic medical work "De Medicina", Celsus (c. 1st century AD) states, “winter provokes headache, coughs, and all the affections which attack the throat, and the sides of the chest and lungs” (7). Stephen A Hoption Cann Department of Health Care and Epidemiology, University of British Columbia, Vancouver, BC V6T 1Z3, Canada Email:stephen.hoption.cann@ubc.ca 1 Johnson C, Eccles R. Acute cooling of the feet and the onset of common cold symptoms. Fam Pract 2005; 0: cmi072v1. 2 Jankowski R, Philip G, Togias A, Naclerio R. Demonstration of bilateral cholinergic secretory response after unilateral nasal cold, dry air challenge. Rhinology 1993; 31: 97-100. 3 Clardy CW, Edwards KM, Gay JC. Increased susceptibility to infection in hypothermic children: possible role of acquired neutrophil dysfunction. Pediatr Infect Dis 1985; 4: 379-382. 4 Lo L, Singer ST, Vichinsky E. Pancytopenia induced by hypothermia. J Pediatr Hematol Oncol 2002; 24: 681-684. 5 Lillie RD, Dyer RE, Armstrong C, Pasternack JG. Seasonal variation in intensity of brain reaction of the St. Louis encephalitis in mice and of endemic typhus in guinea pigs. Public Health Rep 1937; 52: 1805-1822. 6 Nelson RJ. Seasonal immune function and sickness responses. Trends Immunol 2004; 25: 187-192. 7 Celsus AC. De Medicina. Spencer WG (ed). London: W Heinemann 1938; II: 91. Conflict of Interest:None declared |
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