Blog by Professor Mike Kelly.
In the UK, there has been considerable comment in the medical and other media about the shortcomings of government actions in response to the COVID-19 pandemic, as well as sometimes bitter exchanges between public health experts. One element that has been largely absent from the arguments has been exploration of the implications of the observed relationships between the severity of the disease and mortality and social factors.
It has been apparent since the early days of the pandemic that ethnicity, occupation, housing tenure, social deprivation, and age were linked to risk. It was also apparent early on, that type 2 diabetes, hypertension, cardiovascular disease, COPD, chronic kidney disease, obesity and dementia seemed to increase risk. These same diseases have of course been the principal drivers of health inequalities in the UK for decades, overlapping as they do with the same risk factors for COVID – ethnicity, occupation, housing tenure and social deprivation. That this might happen was already strongly suggested in the scientific literature. Studies dating from the SARS outbreak at the beginning of the century showed the additive way that these familiar pre-existing medical diseases interacted with a corona virus.
Health and social inequalities created the perfect breeding ground for COVID 19. This was entirely predictable. This was a perfect storm, and a perfectly predictable one.
As data became clearer, the NHS was encouraged to engage with the at risk groups, and to deal with the emerging problem of health inequalities. Of course, the inequalities were not emerging; it was just that the virus was amplifying the existing pattern of inequalities in health.
In a recently published paper, I outline the important evidence that needs to be interrogated in order to understand the mechanisms involved here, an evidence base that, I argue, has been underutilised in the response to the pandemic. In spite of very clear knowledge about associations, the implications have not been acted upon.
First, we need to harness knowledge derived from the social sciences about the nature of social variations in the population and about the everyday social practices which make up the rich and highly granulated texture of social life. It is no good referring to the BAME community, or the socially disadvantaged, or the elderly, as if they were homogenous groups. They are not. There are multitudes of different communities, neighbourhoods, and localities across the land. The social differences and the meanings that they have for people living in communities, are the bedrocks of individual and population lives, and therefore of responses to the disease. Descriptions of the variegated nature of the population is not just to be found in the social scientific evidence base. Most importantly, it is well known to local public health teams. It should have been corralled in efforts at prevention, messaging, contact tracing, supporting, and helping communities from the very beginning. It is not as if we have to go out and capture this knowledge anew. It is grist to the mill of the world of local public health teams. Unfortunately, for much of 2020 this deep understanding of local communities was side-lined, in favour of centralised directives, based on modelling which for the most part seemed to assume that the population was homogeneous or used gross and unwieldy categories like social disadvantage, or ethnicity, or age, as if they told you all you needed to know.
Second, the nature of the knowledge about local communities should be treated as an equal with the epidemiology, virology, and immunology. The knowledge about the social is not mere background and context. It is the reality that determines the degree to which preventive strategies will or will not be successful.
Third, the evidence concerning the mechanisms operating between the social factors, pre-existing disease and COVID-19 needs to fully explored, again, not with the social as background and context, but as something interacting directly with the human biology. This too is not new. Many of the mechanisms are described in the literature. Unfortunately, although there is widespread acknowledgement that the social factors play a role in the aetiology and progress of many diseases, the social factors tend to be treated either as background and context, or as an external triggers. They are both, but they are also in a syndemic interaction with the virus and the pre-existing medical conditions.
With a death toll in the UK now nearly reaching twice the number of civilians killed by enemy air raids in the Second World War, we need to remember that while vaccines provide protection for some, vaccines really only give us respite. As the virus continues to mutate and new variants undermine efforts to try to get society moving again, we must use the evidence we already have relating to the social and to the mechanisms linking the social with the biological. This must be placed front and centre along with the local knowledge and understandings embedded in the communities we seek to help. Unless we do this, we will get more surprises like vaccine hesitancy among some neighbourhoods and communities.
Professor Mike Kelly is Senior Visiting Fellow at the Primary Care Unit. University of Cambridge.
Read the paper
M.P. Kelly The relation between the social and the biological and COVID-19. Public Health. July 2021. https://doi.org/10.1016/j.puhe.2021.05.003
Image credit: Tim Dennell