Article Text


Concurrent trends in asthma and obesity
  1. S Chinn
  1. Correspondence to:
    Professor S Chinn
    Department of Public Health Sciences, King’s College London, London SE1 3QD, UK;

Statistics from

Is the concurrent rise in the prevalence of asthma and obesity a red herring?

Studies that have reported an association between asthma and obesity have mostly been single cross sectional studies, although an increased incidence of asthma in participants who were overweight at baseline has been reported in several longitudinal studies. The latter have contributed to the debate about the nature of the association, showing that the reverse causality explanation—that decreased physical activity as a result of asthma leads to increased weight—is not plausible. Cohort studies have the potential to determine whether increased symptoms of asthma are an immediate consequence of weight gain or, if not, to establish the lag, but frequent follow up would be required. However, pure cohort studies cannot answer the question of how much of the increase in the prevalence of asthma in a population can be explained by an increase in obesity, as age and period are completely confounded. Repeated cross sectional studies in the same population are needed to answer this question.


Some countries have regular cross sectional population health surveys, such as the National Health and Nutrition Examination Surveys (NHANES) in the United States and the Health Survey for England. Such surveys routinely include height and weight, as increased body mass index (BMI) in adults is a risk factor for a number of diseases, but the Health Survey for England has included respiratory symptoms only in selected surveys. Increases in asthma and in overweight (BMI 25–<30 kg/m2) or obesity (BMI ⩾30 kg/m2) have been reported many times over the last 20 years, but rarely in the same study. This has led to speculation that the rise in obesity might explain some of the increase in the prevalence of asthma, but there has been little direct evidence to support or refute the hypothesis.1–4


Some direct evidence is provided in this issue by Wickens et al.5 They studied comparable groups of 11–12 year old children in New Zealand in 1989 and 2000 and found an increased prevalence of symptoms, asthma, and medication in 2000 compared with 1989, but little difference in the corresponding odds ratios unadjusted or adjusted for BMI. They also found a stronger relation between most outcomes and BMI in 2000 than in 1989, particularly for wheeze and medication in the last 12 months, which remained statistically significant in the 2000 data after adjustment for a number of potential confounders.

The results are similar to those of Chinn and Rona from the National Study of Health and Growth (NSHG),6 who found that virtually none of the increase in wheeze or asthma in 8 and 9 year old children in the UK from 1982 to 1994 was explained by the rise in overweight and obesity, and also reported a stronger association between asthma and obesity in the later than in the earlier year in children aged 5–11 years. The UK and New Zealand studies were each carried out in a school population with symptoms and medication reported by parent or caregiver. Height and weight were measured, unlike in many adult studies from which an association between asthma and obesity has been reported. However, in children BMI is a poorer measure of fatness than skinfold thickness. In the NSHG there was a weaker association of asthma and persistent wheeze with skinfold measurements than with BMI.7


Wickens et al considered that there was insufficient evidence to conclude that the association in children is of recent origin.5 They argued that comparisons of studies over time are hampered by changing definitions of asthma. Certainly, comparison is difficult as the lack of definition of overweight and obesity in children before 2000 led to a variation in reporting results. However, the NSHG had identical symptom questions over time, and there is no doubt that the association of persistent wheeze with BMI was stronger in the representative sample in 1993/1994 than in 1977.7,8 Neither the NSHG6 nor the New Zealand study5 was able to show an interaction between year of survey and the association of asthma and BMI, possibly due to lack of power but, taken together, the evidence is strengthened that the association in children is recent.


No direct information on the BMI adjusted trend in the prevalence of asthma has been published in adults, although data on asthma and BMI were obtained in NHANES (at least in surveys II and III).9,10 There is also a lack of information on when the association between asthma and obesity arose in adults, or whether it is long standing but only noticed once obesity became more prevalent. The earliest studies to report an association were carried out in the early 1980s and were studies of chronic disease in general.11,12

A rough estimate of the maximum likely effect on the rise in asthma can be obtained, for a given increase in prevalence of overweight and obesity, on the assumption that the association is causal. For example, a change in BMI distribution from 85% normal weight, 10% overweight and 5% obese to 75% normal, 15% overweight and 10% obese would, at most, increase the prevalence of asthma by 6.8% over baseline, given the published estimates of relative risks. A baseline prevalence of 5% would increase to 5.3%, a very modest rise compared with most of those reported. So we should not expect the rise in overweight and obesity to explain more than a very small amount of the increase in asthma.


Ideally, trends should be calculated from more than two time points. Long term trends in asthma and BMI can show whether the increase in asthma started close to, or soon after, the beginning of the major increase in obesity. Parallel trends, or points of inflexion close in time, tell us little in themselves other than that a direct causal role is possible. The contrary—especially a reversal of one trend in the absence of a change in the other—is evidence against a direct causal relation provided the data are representative of the same populations. There is now some evidence for a recent slowing down or cessation of the increase in asthma in children and in adults.13–16 Data on BMI were not collected in the individual studies and three of the studies were carried out in selected areas.13,14,16 The fourth study used data from 1990 to 1998 from the UK General Practice Research Database and showed a levelling off of trends in managed asthma from about 1995.15 Recent trends in BMI in Italy or Switzerland are not available but in England there is evidence from the Health Survey for England for an increase in obesity in adults from 1993 to 1998. While England is not the whole of the UK, and neither study may be fully representative as the General Practice Research Database may have practice participation bias and the Health Survey for England individual non-response bias, taken together the results suggest that the trends are not parallel.


There is little doubt that there was a concurrent rise in the prevalence of asthma and obesity in many developed countries in the 1980s and early 1990s, and this led to the speculation that the increase in obesity might explain some of the trend in asthma. Even without more direct evidence that the trend in overweight and obesity explains little or none of the trend in asthma, we can conclude that controlling the weight of the population would do little to reduce the prevalence of asthma as the associated relative risks are too small. However, it may take more direct evidence to convince the whole of the scientific community of this and, if further data exist to establish whether the association is recent or long standing in adults, this would be of interest. A long standing association in adults would contrast with that in children and would make changes in the population in diet and physical activity less likely as an explanation.

Is the concurrent rise in the prevalence of asthma and obesity a red herring?


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