Concern is growing that early evidence suggests people from the BAME community (Black, Asian and Minority Ethnic) are disproportionately dying from COVID-19. Twelve UK doctors have so far died from COVID-19 and all were men over the age of 50 and of BAME origin. 44% of NHS staff are black, Asian or of ethnic minority so it is worrying that all 12 deaths are from that sector of the workforce. (I will address the age and gender differences also emerging in a separate post).
Elsewhere, Michigan in the US has confirmed that of their COVID-19 deaths, 41% of patients were African American yet they only make up 14% of the state’s population. And in Chicago more than 70% of COVID-19 deaths have been in black residents yet they make up just 30% of the population.(1)
Meanwhile in Stockholm, Sweden of the first 15 deaths reported there, 6 (or 40%) were people of Somali origin despite the fact the Somali community accounts for less than 1% of the population.(2)
Here in the UK the head of the British Medical Association, Dr Chaand Nagpaul, has called on the government to begin an investigation into why BAME people appear to be more vulnerable to Covid-19.
In an interview he said “At face value, it seems hard to see how this can be random – to have the first 10 doctors {author's note: now 12} all being of BAME background. Not only that, we also know that in terms of the BAME population, they make up about a third of those in intensive care. There’s a disproportionate percentage of BAME people getting ill."
He went on to say “We have heard the virus does not discriminate between individuals but there’s no doubt there appears to be a manifest disproportionate severity of infection in BAME people and doctors. This has to be addressed – the government must act now.” (3)
On 10th April 2020, ICNARC (Intensive Care National Audit & Research Centre) released its data on the comparison of COVID-19 deaths on ITUs (Intensive Care Units) with viral pneumonia deaths on ITUs between 2017 and 2019. (COVID-19 patients on ITU have a pneumonia caused by the coronavirus so this comparison is the closest researchers can get to comparing like with like.)
Their data showed a distinct difference in deaths by ethnic origin. (4)
Percentage breakdown of deaths from COVID-19 by ethnicity:
White 66.4 %
Asian 14.4 %
Black 11.9 %
Other 6.0 %
Mixed 1.3 %
Percentage breakdown of deaths from viral pneumonia between 2017 and 2019 by ethnicity:
White 88.4 %
Asian 5.8 %
Black 2.8 %
Other 2.1 %
Mixed 0.9 %
In the COVID-19 deaths 12% of patients were black and 14% Asian but from the typical figures for a viral pneumonia we would have expected them to be 3% and 6% respectively. Likewise the figure for deaths in white people is lower for COVID-19 at 66% rather than the expected 88% for a viral pneumonia.
Why is this happening? Is it a reflection of inequalities in healthcare and primarily socio-economic in origin, do the BAME community have more of the high risk co-morbidities associated with an adverse outcome from COVID-19 or is there an underlying genetic predisposition? We need to know because if the answer lies in a genetic vulnerability the implications for African and Asian countries are immense.
Certainly Dr Nagpaul suggested that there may be several underlying reasons rather than a singular cause saying, “You’ve got a high proportion of BAME people not able to stay at home, serving the nation, putting themselves at risk. If you add that to overcrowded and multigenerational occupancies, the infections can be brought back home and spread to other members of the family.”
He also highlighted the importance of translating the COVID-19 information leaflets for those who do not speak English and drew attention to the higher prevalence of diabetes, heart disease and kidney disease among BAME communities and as he rightly points out, “Previous inequalities will be greater at a time of crisis. This [coronavirus] may be bringing into focus historic inequalities facing BAME communities.” (3)
Socio-economic Causes
Like Italy and Spain, both badly affected by COVID-19, BAME cultures include their elderly population more than their white counterparts with multi-generational living and social gatherings the norm. They are more likely than white populations to live in the urban areas and in more crowded housing. Variations in diet, smoking and drinking are all possible confounding factors.
There is also the very real difference between the white and BAME communities in access to healthcare. In the USA, with no NHS to provide provision for all, those with few financial resources struggle to afford healthcare and the BAME population are over-represented in the poorer communities. It would be naive to not acknowledge the ongoing role racism may be playing, not only as to who can access healthcare but also the treatment received within it, something that has been well documented. (5) (6)
Co-Morbidities
Many diseases, including infections, can be more common in certain groups. Differences between male and female, young and old and different races are well documented. (7) (8)
Some of the underlying conditions that increase an individual's risk to COVID-19 include diabetes, high blood pressure and heart disease all of which are more prevalent in BAME people. This would predispose the BAME community to an adverse outcome from COVID-19.
Genetic Differences
Data from China showed that blood type A was associated with higher mortality from COVID-19 and blood type O the lowest. Our blood type is determined by our genetics so it is reasonable to question if other genetic variations increase or decrease an individual's risk from COVID-19.
One of the key areas of interest is called the ACE2 receptor. This is something found sitting on the surface of the cells in the lungs, kidneys, heart and gut. It helps regulate blood pressure in humans by changing a protein called angiotensin I into angiotensin II.
Imagine the ACE2 receptor as a house with a large front door. The protein angiotensin I knocks on the “door” which opens allowing the protein into the “house”. Once in the house the protein goes through the change from version I to version II. Version II is then sent back out through the door and into the blood stream where, amongst other things, it increases our blood pressure. One of the drugs used to control high blood pressure is called an ACE inhibitor and it interferes with this conversion of the angiotensin I into version II. It does this by keeping the door “locked” so that when angiotensin I knocks on the door it no longer opens. It can’t go through the door, into the house and change into angiotensin II, it is “locked out”. This means there is less angiotensin II made so there is less circulating through the body and blood pressure drops.
The COVID-19 coronavirus is getting into the body’s cells via the ACE2 receptor. It has discovered that when it “knocks” on the door it too is let in. Once in the “house” (the cell) it takes over. It destroys the contents of the house and refurnishes it with its own belongings....in more scientific terms it destroys the genetic content of the host cell replacing it with its own. It then divides again and again to make more of itself and as it does this it causes damage to the surrounding area.
In the lungs this damage causes the cough and respiratory symptoms associated with COVID-19. In some people the damage worsens and they begin to notice breathing difficulties. In the worst cases the damage is so severe the person cannot breathe on their own and needs mechanical assistance, in other words ventilation on ITU. All because the virus is invading cell after cell through the ACE2 receptor.
It is well documented that ACE inhibitor drugs do not work as well in black people as in white people and one theory as to why is that black people naturally have higher levels of ACE2 receptors. Research in China showed a higher number of ACE2 receptors in Asian patients compared with white patients. (9)
At the start of the COVID-19 outbreak there was concern that taking an ACE inhibitor drug increased the risk of serious illness. However it now seems more probable that the prevalence of the ACE2 receptor is the underlying connection, not the drug. Indeed one line of ongoing research is to see if ACE inhibitor drugs could be used as a treatment for COVID-19 with the theory being they may be able to “mop up” the virus by tricking it into binding with the drug rather than the body’s cells.
What is clear is that if some people are predisposed to have more ACE2 receptors then it follows that the coronavirus has more opportunity to attack and infiltrate in those particular people.
In conclusion
It is clear that there are many factors that could be contributing to the higher number of deaths from COVID-19 in the BAME population but whilst there is any possibility that there is a racially determined genetic variant making this population vulnerable this needs to be the priority for investigation.
