Written by Ana Valdes
The difference in COVID-19 death rates between white people and black, Asian and minority ethnic (BAME) people in the UK is shocking. One recent report found that, between the beginning of February and the end of April 2020, black people in England were 71% more likely than white people to die from COVID-19 while Asians were 62% more likely.
From the start of the coronavirus pandemic, there has been an attempt to use science to explain the disproportionate impact of COVID-19 on different groups through the prism of race. This disparity has led to an inquiry by Public Health England and funding for urgent academic research into the issue. Data from the UK and the US suggests that people categorised as black, Hispanic (Latino) and south Asian are more likely to die from the disease. The way this issue is often discussed, but also the response of some scientists, would suggest that there may be some biological reason for the higher death rates based on genetic differences between these groups and their white counterparts. However, there are clear links between people’s racial groups, their socioeconomic status, what happens to them once they are infected and the outcome of their infection.
There are many social reasons why ethnic minorities may generally be more vulnerable to disease, including a greater chance of malnutrition, more exposure to pollution due to where they live, or greater likelihood of working in less healthy environments. Inequality and poverty also play a role in the fact that BAME people are more likely to suffer conditions that we know are linked to a greater chance of dying from COVID-19, such as diabetes and heart disease. But that won’t change the fact that the generally worse health among BAME groups in western societies is strongly linked to socioeconomic factors that are known to play a very significant role in this pandemic.
Initial data suggests that BAME healthcare workers are more likely to die from COVID-19 than their white colleagues. British Medical Association research has found that BAME doctors are twice as likely as white doctors to feel pressured into working with inadequate PPE when they are at risk of infection. And they are twice as likely not to feel confident enough to raise concerns about workplace safety. However, all these established facts alone do not seem to explain why the risks of COVID-19 vary between different ethnic groups and are lowest among white people.
But the reality is there is no evidence that the genes used to divide people into races are linked to how our immune system responds to viral infections. There are certain genetic mutations that can be found among specific ethnic groups that can play a role in the body’s immune response. But because of the loose definition of race (primarily based on genes for skin colour) and recent population movements, these should be seen as unreliable indicators when it comes to susceptibility to viral infections.
You only have to look at how the statistics are gathered to understand how these issues are confused. The research reveals that data from the UK’s Office for National Statistics that has been used to highlight the disparate death rates separates Indians from Pakistanis and Bangladeshis, and yet groups all Africans (including black Caribbeans). This makes no sense in terms of race, ethnicity or genetics. The data also shows those males categorised as black are over 4.6 times more likely to die than their white counterparts from the virus. They are followed by Pakistanis/Bangladeshis (just over four times more likely to die), and then Chinese and Indians (just over 2.5 times).
This problem arises even with recent analysis that purportedly show people from ethnic minorities are no more likely to die once you consider the effects of other illnesses and deprivation. Meanwhile, in the US the groups most disproportionately affected are African Americans and Hispanics/Latinos. All these groups come from very different population groups. We’ve also seen high death rates in Brazil, China and Italy, all of whom have very different populations using the classical definition of race. The idea that COVID-19 discriminates along traditional racial lines is created by these statistics and fails to adequately portray what’s really going on. These kinds of assumptions ignore the fact that there is as much genetic variation within racialised groups as there is between the whole human population.
There are some medical conditions with a higher prevalence in some racialised groups, such as sickle cell anaemia, and differences in how some groups respond to certain drugs. But these are traits linked to single genes and all transcend the traditional definitions of race. Such “monogenetic” traits affect a very small subset of many populations, such as some southern Europeans and south Asians who also have a predisposition to sickle cell anaemia. Death from COVID-19 is also linked to pre-existing conditions that appear in higher levels in black and south Asian groups, such as diabetes. The argument that this may provide a genetic underpinning is only partly supported by the limited evidence that links genetics to diabetes. The way people’s immune systems work depends on genetic factors, not just environmental and social ones. There are effectively two parts to our immune systems. One is the part that produces antibodies, called the “adaptive immune system”. When our body has never seen a virus before, it can take several days for it to produce them, which is why some people get sick in the first place. We also have an “innate immune system” that acts before our body has had time to make antibodies. This system is strong in children and young people, but not very good after the age of 65. This is likely to be one reason why older people are at higher risk of dying of COVID-19.
However, the ONS figures confirm that genes predisposing people to diabetes cannot be the same as those that predispose to COVID-19. Otherwise, Indians would be affected as much as Pakistanis and Bangladeshis, who belong to the same genome-wide association group. Any genetic differences that may predispose you to diabetes are heavily influenced by environmental factors. There isn’t a “diabetes gene” linking the varying groups which are affected COVID-19. But the prevalence of these so-called “lifestyle” diseases in racialised groups is strongly linked to social factors. Other evidence suggests higher death rates from COVID-19 including among racialised groups might be linked to higher levels of a cell surface receptor molecule known as ACE2. But this can result from taking drugs for diabetes and hypertension, which takes us back to the point about the social causes of such diseases.
According to scientific researches, women can have a more effective innate immune response to other viruses such as HIV than men, and that oestrogen, the female hormone, enhances this type of immune response. Women are also less likely to die from COVID-19 than men. The research also reveals that human populations from different parts of the planet have had to adapt to different types of infections. Ethnic differences in the risk to other respiratory viral diseases have been linked to genetic variation, and these variants are different in BAME groups and white people in these same pathways. However, the role of ethnicity in genetic susceptibility to viral diseases is still controversial.
In the absence of any genetic link between racial groups and susceptibility to the virus, we are left with the reality, which seems more difficult to accept, that these groups are suffering more from how our societies are organised. There is no clear evidence that higher levels of conditions such as type-2 diabetes, cardiovascular disease and weakened immune systems in disadvantaged communities are because of inherent genetic predispositions. But there is evidence they are the result of structural racism. All these underlying problems can be directly connected to the food and exercise you have access to, the level of education, employment, housing, healthcare, economic and political power within these communities. The evidence suggests that this coronavirus does not discriminate but highlights existing discriminations. The continued prevalence of ideas about race today – despite the lack of any scientific basis – shows how these ideas can mutate to provide justification for the power structures that have ordered our society since the 18th century.
Edited by Pa Modou Faal