Abstract
Background. There is a common folklore that chilling of the body surface causes the development of common cold symptoms, but previous clinical research has failed to demonstrate any effect of cold exposure on susceptibility to infection with common cold viruses.
Objective. This study will test the hypothesis that acute cooling of the feet causes the onset of common cold symptoms.
Methods. 180 healthy subjects were randomized to receive either a foot chill or control procedure. All subjects were asked to score common cold symptoms, before and immediately after the procedures, and twice a day for 4/5 days.
Results. 13/90 subjects who were chilled reported they were suffering from a cold in the 4/5 days after the procedure compared to 5/90 control subjects (P = 0.047). There was no evidence that chilling caused any acute change in symptom scores (P = 0.62). Mean total symptom score for days 1–4 following chilling was 5.16 (±5.63 s.d. n = 87) compared to a score of 2.89 (±3.39 s.d. n = 88) in the control group (P = 0.013). The subjects who reported that they developed a cold (n = 18) reported that they suffered from significantly more colds each year (P = 0.007) compared to those subjects who did not develop a cold (n = 162).
Conclusion. Acute chilling of the feet causes the onset of common cold symptoms in around 10% of subjects who are chilled. Further studies are needed to determine the relationship of symptom generation to any respiratory infection.
Johnson C and Eccles R. Acute cooling of the feet and the onset of common cold symptoms. Family Practice 2005; 22: 608–613.
Introduction
The common cold is a mild self-limiting illness usually confined to the upper respiratory tract.1 The disease is self-diagnosed from a range of symptoms such as nasal stuffiness, sneezing, throat irritation and mild fever.2 There is a common folklore that associates the development of symptoms of common cold with exposure to a cold environment, and that the onset of a cold is a direct result of wet clothes, feet and hair.3 Throughout the clinical literature of the last three hundred years there have been many reports that acute cooling of the body surface causes the onset of symptoms of common cold, and historically it has been generally accepted that acute exposure to cold is a direct cause of these symptoms.4,5
However, studies involving inoculation of cold viruses into the nose and periods of cold exposure have failed to demonstrate any effect of cold exposure on susceptibility to infection with common cold viruses.6–8 Although modern textbooks of virology dismiss any cause-and-effect relationship between cold exposure and common cold as erroneous folklore,9 the belief is so widespread and longstanding it is difficult to completely dismiss this idea as having no validity.
In 1919 Mudd and Grant studied the reactions of the nasal mucosa in response to chilling the body surface and showed that cooling the body surface causes a reflex vasoconstriction of blood vessels in the nose and a decrease in temperature of the mucous membrane.10 They speculated that this reflex vasoconstriction of the airway epithelium could decrease resistance to infection and allow bacterial infection of the tonsils.10 Some years later Sir Christopher Andrewes suggested that exposure to a cold environment may trigger the development of a cold but only in people who are carrying the latent cold virus.6 Eccles developed these early observations by proposing a hypothesis that acute cooling of the body surface causes a reflex vasoconstriction in the nose and upper airways, and this vasoconstrictor response may inhibit respiratory defence and cause the onset of common cold symptoms by converting an asymptomatic viral infection (sub-clinical infection) into a symptomatic viral infection (clinical infection).11 The novel idea in this hypothesis was that when common cold viruses are circulating in the community a proportion of those infected will have sub-clinical infections, and that when any of this sub-group are exposed to chilling of the body surface this could aid conversion of a sub-clinical infection to a clinical infection. This study was aimed at testing this hypothesis, by studying the onset of common cold symptoms after acute chilling of healthy asymptomatic subjects, during the winter, when common cold viruses are circulating in the community.
The aims of the study were to determine if acute chilling caused: acute onset of common cold symptoms within minutes of chilling; delayed onset of common cold symptoms over a 4/5 days period after chilling; the perception that the subjects were suffering from a common cold over a 4/5 days period after chilling. The study also aimed to investigate any relationship between the history of colds incidence in the previous year and the onset of common cold symptoms.
Methods
Subject population
180 healthy subjects were recruited from the student population of Cardiff University. All subjects attended the Common Cold Centre, Cardiff. All procedures were carried out under standard conditions at a room temperature of eighteen to twenty-five degrees centigrade. Subjects were not permitted to smoke or consume food or drink during the study period. All subjects were given a patient information leaflet to read and were asked to sign the consent form. After signing the consent form the subjects completed a questionnaire about their medical history and their suitability for inclusion into the study was checked. Subjects were deemed suitable for inclusion in the study if the subject was over eighteen years old and healthy as determined by medical history. Subjects were not enrolled in the study if the subject had suffered with acute upper respiratory tract infection in the previous two weeks, or if the subject had a history of seasonal or perennial rhinitis.
Experimental procedures
Once enrolled into the study subjects were randomized to receive chilling or control procedures. A computer generated randomization list was used to assign subjects to either the chill or control procedure with subjects stratified according to the number of common colds reported by the subject in the previous year. Subjects with 0–3 colds in the previous year were allocated to the next available procedure at the start of the randomisation list and subjects with 4 or more colds were assigned to the next available procedure at the end of the list. Ninety subjects were allocated to receive the chill procedure and ninety subjects to receive the control procedure. If allocated to the chilling procedure, the subject was asked to remove their shoes and socks and place their feet in a bowl containing 9–10 litres of water at a temperature of 10°C for twenty minutes. The temperature of the cold bath was monitored (Pen shape digital multi-stem thermometer, Scientific Laboratory Supplies Ltd, Wilford Industrial Estate, Nottingham, UK) and ice was added if necessary to maintain the water temperature at 10°C. If allocated to the control procedure the subject was asked to keep their shoes and socks on and place their feet in an empty bowl for twenty minutes. Warm water was not used as a control as it was believed that this stimulus could have influenced nasal blood flow.
Symptom scores
All subjects were asked if they were suffering with a cold and to score symptoms of runny nose, blocked nose, sore throat, sneezing and cough on a scale of 0–3 with 0 = not present, 1 = mild, 2 = moderate, 3 = severe before and immediately after the procedure. The same common cold question and symptom scores were also used in a daily diary. The method of symptom scores has been widely used in previous studies on common cold.12,13 All subjects were provided with a diary, in which they were instructed to score symptoms and at the same time to indicate if they believed they were suffering from a common cold (day 1 PM, days 2 and 3 AM/PM, day 4 AM, and on visit two which occurred on day 4 or 5).
Nasal airflow was measured as a Nasal Partitioning Ratio (NPR) as described by Cuddihy and Eccles14 before the procedures and on day 4/5 using the GM NV1 spirometer (GM Instruments Ltd, Unit 6 Ashgrove, Ashgrove Rd, Kilwinning, Scotland, UK). NPR was believed to be useful as an objective measure to confirm the presence of acute rhinitis. However the measurements of NPR proved to be too variable to provide any meaningful data and these results are not presented in the present paper.
Previous history of colds
As part of the clinical history subjects were asked how many colds they had suffered from in the previous year.
Statistics
This was a pilot study and it was therefore not possible to perform a power calculation, but the ratio of sub-clinical to clinical infection was considered in order to determine the sample size required for the study. It was predicted that 29 subjects in the chilled group would develop colds and 9 subjects in the control group giving a maximum difference between the groups of 20 and a minimum of 10 depending on the distribution of spontaneous colds. Statistical comparisons were made between the two experimental groups of subjects; chilled and control. The hypotheses were tested at a 0.05 level of significance. The Mann-Whitney test was used to test for differences in symptom scores and history of colds incidence. The immediate effects of chilling were studied by comparing the differences from baseline to immediately after the test procedures in total symptom scores, between chilled and control groups. The delayed effects of chilling were studied by comparing the differences in total symptom scores between chilled and control groups over the 4/5 days period after the test procedures. Mean total symptom scores have been used to describe the symptom score data in the text as this descriptive shows a change in the symptom score, whereas the median does not due to the large number of zero scores. The total symptom scores (days 1 + 2 + 3 + 4/5, maximum score 120) were also analysed as dichotomous data using the Chi-squared test, with total scores of 0–8 indicating absence of a cold and 9–120 indicating presence of a cold. The Chi-squared test was used to test for differences in the number of colds reported by the two test groups in their diaries. A subject was deemed to have experienced a cold if they reported they were suffering from a cold on any occasion after the test procedures on days 1 + 2 + 3 + 4/5.
Results
Subject demographics
180 subjects were enrolled in the study between October 2003 and March 2004, 90 were randomized to the chill procedure, and 90 to the control procedure. The flow diagram in Figure 1 shows the flow of participants through each stage of the study. The demographics of the two test groups are provided in Table 1 that demonstrates that the test groups were balanced and there was no significant difference in any of the baseline characteristics.
Flow of subjects through each stage of the study
Flow of subjects through each stage of the study
Demographics of test groups
| Control n = 90 | Chill n = 90 | Significance | |
|---|---|---|---|
| Median age (range) | 20.0 (18–43) | 20.0 (18–39) | P = 0.598 (MW) |
| Male | 29 | 25 | P = 0.515 (Chi-squared) |
| Female | 61 | 65 | |
| Median colds per year (range) | 2.0 (1–10) | 2.0 (1–8) | P = 0.859 (MW) |
| Control n = 90 | Chill n = 90 | Significance | |
|---|---|---|---|
| Median age (range) | 20.0 (18–43) | 20.0 (18–39) | P = 0.598 (MW) |
| Male | 29 | 25 | P = 0.515 (Chi-squared) |
| Female | 61 | 65 | |
| Median colds per year (range) | 2.0 (1–10) | 2.0 (1–8) | P = 0.859 (MW) |
MW = Mann Whitney test.
Demographics of test groups
| Control n = 90 | Chill n = 90 | Significance | |
|---|---|---|---|
| Median age (range) | 20.0 (18–43) | 20.0 (18–39) | P = 0.598 (MW) |
| Male | 29 | 25 | P = 0.515 (Chi-squared) |
| Female | 61 | 65 | |
| Median colds per year (range) | 2.0 (1–10) | 2.0 (1–8) | P = 0.859 (MW) |
| Control n = 90 | Chill n = 90 | Significance | |
|---|---|---|---|
| Median age (range) | 20.0 (18–43) | 20.0 (18–39) | P = 0.598 (MW) |
| Male | 29 | 25 | P = 0.515 (Chi-squared) |
| Female | 61 | 65 | |
| Median colds per year (range) | 2.0 (1–10) | 2.0 (1–8) | P = 0.859 (MW) |
MW = Mann Whitney test.
Acute effects of chilling
The test procedures did not cause any significant changes in symptom scores, and all the mean scores were close to zero indicating few or no symptoms were present before or immediately after the procedures as illustrated in Table 2. The small difference in symptom scores between the two groups prior to the procedures was not significant (P = 0.245). The difference in total symptom score pre and post chill procedure was not significantly higher than the difference in total symptom score pre and post control procedure (P = 0.62).
Immediate effects of chilling
| Baseline | Immediately after procedure | Difference | Statistics | |
|---|---|---|---|---|
| Control (n = 90) | 0.02 (0.15) | 0.13 (0.37) | 0.11 (0.35) | Comparison of differences P = 0.62 (MW) |
| Chill (n = 90) | 0.07 (0.29) | 0.21 (0.51) | 0.14 (0.41) |
| Baseline | Immediately after procedure | Difference | Statistics | |
|---|---|---|---|---|
| Control (n = 90) | 0.02 (0.15) | 0.13 (0.37) | 0.11 (0.35) | Comparison of differences P = 0.62 (MW) |
| Chill (n = 90) | 0.07 (0.29) | 0.21 (0.51) | 0.14 (0.41) |
Figures are mean (standard deviation) of total symptom scores, before and immediately after control and chill procedures. Differences are differences from baseline.
MW = Mann Whitney test.
Immediate effects of chilling
| Baseline | Immediately after procedure | Difference | Statistics | |
|---|---|---|---|---|
| Control (n = 90) | 0.02 (0.15) | 0.13 (0.37) | 0.11 (0.35) | Comparison of differences P = 0.62 (MW) |
| Chill (n = 90) | 0.07 (0.29) | 0.21 (0.51) | 0.14 (0.41) |
| Baseline | Immediately after procedure | Difference | Statistics | |
|---|---|---|---|---|
| Control (n = 90) | 0.02 (0.15) | 0.13 (0.37) | 0.11 (0.35) | Comparison of differences P = 0.62 (MW) |
| Chill (n = 90) | 0.07 (0.29) | 0.21 (0.51) | 0.14 (0.41) |
Figures are mean (standard deviation) of total symptom scores, before and immediately after control and chill procedures. Differences are differences from baseline.
MW = Mann Whitney test.
Delayed effects of chilling
Table 3 shows the mean daily scores and total score for days 1 to 4/5 following each procedure. Total symptom scores for days 1–4/5 following the chill procedure (5.16 ± 5.63 s.d.) were significantly higher than the total symptom scores for days 1–4/5 following the control procedure (2.89 ± 3.39 s.d.) (P = 0.013). When the total symptom scores for the 4/5 days were analysed as dichotomous data, 26/90 (28.8%) of the chilled subjects and 8/90 (8.8%) of the control subjects were deemed to be suffering from a cold (total symptom score 9–120), and this difference was significant (P = 0.001).
Delayed effects of chilling
| Day 1 | Day 2 | Day 3 | Day 4/5 | Total | Statistics | |
|---|---|---|---|---|---|---|
| Control (n = 88) mean score | 0.32 (0.70) | 0.73 (1.11) | 0.48 (0.77) | 1.36 (1.95) | 2.89 (3.39) | Comparison of total symptom scores P = 0.013 |
| Chill (n = 87) mean score | 0.57 (1.12) | 1.38 (1.84) | 1.28 (1.48) | 1.93 (2.83) | 5.16 (5.63) |
| Day 1 | Day 2 | Day 3 | Day 4/5 | Total | Statistics | |
|---|---|---|---|---|---|---|
| Control (n = 88) mean score | 0.32 (0.70) | 0.73 (1.11) | 0.48 (0.77) | 1.36 (1.95) | 2.89 (3.39) | Comparison of total symptom scores P = 0.013 |
| Chill (n = 87) mean score | 0.57 (1.12) | 1.38 (1.84) | 1.28 (1.48) | 1.93 (2.83) | 5.16 (5.63) |
Figures are mean (standard deviation) of daily symptom scores and total scores for days 1–4/5 following each procedure.
Delayed effects of chilling
| Day 1 | Day 2 | Day 3 | Day 4/5 | Total | Statistics | |
|---|---|---|---|---|---|---|
| Control (n = 88) mean score | 0.32 (0.70) | 0.73 (1.11) | 0.48 (0.77) | 1.36 (1.95) | 2.89 (3.39) | Comparison of total symptom scores P = 0.013 |
| Chill (n = 87) mean score | 0.57 (1.12) | 1.38 (1.84) | 1.28 (1.48) | 1.93 (2.83) | 5.16 (5.63) |
| Day 1 | Day 2 | Day 3 | Day 4/5 | Total | Statistics | |
|---|---|---|---|---|---|---|
| Control (n = 88) mean score | 0.32 (0.70) | 0.73 (1.11) | 0.48 (0.77) | 1.36 (1.95) | 2.89 (3.39) | Comparison of total symptom scores P = 0.013 |
| Chill (n = 87) mean score | 0.57 (1.12) | 1.38 (1.84) | 1.28 (1.48) | 1.93 (2.83) | 5.16 (5.63) |
Figures are mean (standard deviation) of daily symptom scores and total scores for days 1–4/5 following each procedure.
The total number of subjects that reported they were suffering from a common cold in their diaries during the 4/5 days following the chill or control procedures is shown in Figure 2 and this illustrates that significantly more subjects believed they were suffering from a cold in the chilled group (13/90, 14.4%) compared to the control group (5/90, 5.6%, P = 0.047). There was no sex difference in the development of colds with 9.3% of males and 10.3% of females developing colds (P = 0.828, Chi-squared). Of those in the chilled group that developed colds 4/13 were male (31%) and 9/13 female (69%), but this sex difference merely reflects the proportions of males (28%) and females (72%) exposed to the chill procedure and is not significant (P = 0.749, Fisher Exact).
Numbers of subjects that reported they were suffering from a common cold in their diaries during the 4/5 days period following control or chill procedures. The shaded area represents those subjects reporting colds
Numbers of subjects that reported they were suffering from a common cold in their diaries during the 4/5 days period following control or chill procedures. The shaded area represents those subjects reporting colds
Colds history in previous year
There was no difference in colds incidence between the two test groups at baseline as illustrated in Table 1. 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).
Discussion
Acute effects of chilling
The present study provides no evidence for an acute effect of chilling on the development of common cold symptoms. Symptom scores were close to zero in both the control and chilled groups.
Delayed effects of chilling
A delayed effect of chilling on the incidence of colds and symptoms was observed in the 4/5 days following the chill procedure. Significantly more chilled subjects than control subjects reported they were suffering from colds in the 4/5 days following the test procedures. The difference in the incidence of colds between the two test groups was also supported by a significant difference in total symptom scores over the 4/5 days following the test procedures. Analysis of the symptom scores as dichotomous data also demonstrated a significantly greater symptom score (more colds) in the chilled group. The increased incidence of reports of colds and higher symptom scores in the chilled subjects compared to the control subjects may be due to several factors.
Belief in the folklore that acute chilling of the body surface, in some way precipitates a common cold could have caused some bias in the reporting of colds and symptoms. The subjects were not questioned about their beliefs but the idea was introduced and then dismissed in the informed consent information in the following way:
If the common cold symptoms reported after chilling were solely a result of subject bias caused by belief in the effects of chilling then one would have expected an acute effect of chilling on the scoring of common cold symptoms rather than a delayed effect.“This study is designed to investigate the effects of acute chilling on the development of common cold symptoms. It is a popular belief that the development of an upper respiratory tract infection such as the common cold is a result of a chill. However, previous studies have failed to demonstrate that exposure to a cold environment increases the incidence of the common cold.… Common cold symptoms are very common during the winter period and it is expected that some subjects will develop symptoms because they have been previously exposed to infected persons. Therefore the development of any common cold symptoms may be unrelated to any experimental procedures in this study”.
The differences between the chilled and control groups could have occurred as a chance finding, as it was expected that some subjects would develop cold symptoms due to natural exposure to common cold viruses. The probability value for the different reporting of colds was just below P = 0.05 (P = 0.047) but the P-value for the difference in total symptom scores was more convincing with P = 0.013, and for the dichotomous analysis was P = 0.001. With two different measures of the incidence of common cold providing significant differences between the two test groups it is unlikely that the results are solely due to chance.
Chilling of the feet in cold water (12°C ± 1°C) has been previously reported to cause an intense vasoconstriction of both the cutaneous and upper airway blood vessels15 and the vasoconstriction of the upper airways has been proposed as a mechanism that reduces respiratory defence against infection.10,11 When common cold viruses are circulating in the community a proportion of subjects will have sub-clinical infections, and chilling of these subjects may cause vasoconstriction in the upper airway epithelium and conversion of a sub-clinical to a clinical infection. In these cases the subject links the causality of the common cold symptoms to the chill and does not realise that they were already infected before they ‘caught’ a cold. Laboratory studies using viral challenge and cold exposure do not provide any evidence that chilling increases susceptibility to the development of common cold symptoms7,8 but these studies do not mimic the natural exposure to common cold viruses and they can be criticised for the small numbers of subjects used to power the studies.
An interesting finding in the present study was that the subjects who reported they developed a cold after the chill or control procedures also reported that they suffered from significantly more colds each year, than the subjects who did not report a cold after the procedures. This finding may indicate that there is a sub population in the general population who are more susceptible to developing common cold symptoms each year and that they may have a ‘common cold constitution’.16
The results of the present study demonstrate that chilling is associated with the onset of common cold symptoms but the study does not provide any objective evidence, such as virology, that the subjects were infected with a common cold virus. Because of the great variety of viruses causing the common cold syndrome it is difficult to identify the causative agent responsible for common cold symptoms in any subject when viruses are circulating in the community. For this reason it was decided to first study the relationship between chilling and symptoms, and then to consider the use of virology in a subsequent study.
In summary the results of the present study support the folklore that exposure to chilling may cause the onset of common cold symptoms, perhaps by some change in respiratory defence caused by reflex vasoconstriction of the blood vessels of the upper airways. Further studies in this area are needed to determine if the development of common cold symptoms following cold exposure are associated with infection.
Declaration
Funding: the study was funded by Cardiff University. The study sponsor had no involvement in the study design, the collection, analysis and interpretation of data, in the writing of the report or in the decision to submit for publication. The corresponding author had full access to all the data in the study and had final responsibility for the decision to submit for publication.
Ethical approval: the study was approved by the South East Wales Local Research Ethics Committee.
Conflicts of interest: none.
References
Johnston S, Holgate S. Epidemiology of viral respiratory infections. In Myint S, Taylor-Robinson D (eds). Viral and other infections of the human respiratory tract. London: Chapman & Hall;
Helman CG. “Feed a cold, starve a fever” Folk models of infection in an English suburban community, and their relation to medical treatment.
Dowling HF, Jackson GG, Spiesman IG, Inouye T. Transmission of the common cold to volunters under controlled conditions. II. The effect of chilling of the subject upon susceptibility.
Douglas RGJ, Lindgren KM, Couch RB. Exposure to cold environment and rhinovirus common cold. Failure to demonstrate effect.
White DO, Brown L. Respiratory viruses. In Gronoff A, Webser R (eds). Encyclopedia of virology. San Diego: Academic Press;
Mudd S, Grant SB. Reactions to chilling of the body surface. Experimental study of a possible mechanism for the excitation of infections of the pharynx and tonsils.
Jackson G, Dowling H, Spiesman I, Boand A. Transmission of the common cold to volunteers under controlled conditions. 1 The common cold as a clinical entity.
Macknin ML, Piedmonte M, Calendine C, Janosky J, Wald E. Zinc gluconate lozenges for treating the common cold in children—A randomized controlled trial.
Cuddihy PJ, Eccles R. The use of nasal spirometry for the assessment of unilateral nasal obstruction associated with changes in posture in healthy subjects and subjects with upper respiratory tract infection.
Drettner B. Vascular reactions of the human nasal mucosa on exposure to cold. Acta Otolaryngologica (Stockholm)
Comments
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
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
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
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
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7 Celsus AC. De Medicina. Spencer WG (ed). London: W Heinemann 1938; II: 91.
Conflict of Interest:
None declared