The Importance of Social Intervention in England's Mortality Decline: The Evidence Reviewed

Citation: Guha (1994) The Importance of Social Intervention in England's Mortality Decline: The Evidence Reviewed.
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Summary

Notes: Szreter (1988) published an attack on McKeown's thesis that the mortality decline in England over the eighteenth and nineteenth centuries was due to improved standards of living and, especially, better nutrition. Rather than nutrition, Szreter championed the hypothesis that improved public health measures greatly reduced exposure to diseases. Because industrialization and urbanization were full swing in England by the middle of the nineteenth century, Szreter argued that improved public health measures were the most important mechanism to combat diseases that were promoted by the conditions of the new urban environment (e.g., overcrowding). In response to Szreter's public health hypothesis, Guha cites evidence that reaffirms the importance of McKeown's nutritional hypothesis. Mortality started to decline, fitfully at times, in London beginning around 1750. As Szreter admits, public health measures were completely inadequate during the eighteenth and early nineteenth centuries. Nevertheless, mortality improved during this time period, indicating that improvements could occur in highly unsanitary urban environments without the creation of that infrastructure which Szreter regards as being the only possible source of alleviation (p. 94). Interestingly, the height of an average British male over this period increased, with a pause in growth for cohorts born just before the Napoleonic Wars. This evidence strongly suggests that the cause of mortality decline during this era was due to improved living conditions and better nutrition, just as McKeown postulated initially. Because mortality conditions were improving in London does not mean that it was an innocuous place to live-it actually had higher mortality rates than rural locations until the twentieth century due to its deleterious epidemiological environment. But, the fact that mortality was actually improving in such an environment lends credence to the importance of nutritional status. Szreter juxtaposes airborne diseases to water- and food-borne diseases in a manner that was never intended by McKeown. In fact, McKeown argues that improvements in nutritional status should reduce mortality from all or nearly all the common infections (cited in McKeown, p. 98). But in Szreter's view, if the nutritional hypothesis is correct, then the primary cause of mortality decline must be a reduction in airborne diseases (especially tuberculosis). If, on the other hand, the public health view is correct, then the primary cause of mortality decline must be a reduction in water- and food-borne diseases (e.g., diarrhea). Guha argues that exposure to tuberculosis was nearly universal in the late nineteenth century and even well into the twentieth, but that the case-fatality rate dropped considerably. This, again, indicates that reduced mortality from TB must be due to better nutrition and not reduced exposure due to improved public health initiatives. Especially damaging to Szreter's argument is Guha's finding that morbidity from diarrhea did not decline substantially in the nineteenth century. That is, people were still exposed to food- and water-borne infection, but they began to survive infection at much greater rates. For instance, in Mansfield, England, 338 people were infected during the diarrhea epidemic of 1908. Only two of these people died, both of them infants. Guha concludes that Victorian public health technology may have had some benefits, but only improved nutritional status, which enables the host to combat the disease more effectively, can account for reduced mortality during this era.