The figures are startling. The mortality rate from Covid 19 among black Americans is 2.6 times that of Caucasians.
https://www.apmresearchlab.org/covid/deaths-by-race
In the UK, the figures are even more stark. Blacks are more than 4 times likely to die from COVID than whites.
https://www.ons.gov.uk/peoplepopulationandcommunity/birthsdeathsandmarriages/deaths/articles/coronavirusrelateddeathsbyethnicgroupenglandandwales/2march2020to10april2020
Although in general, Asians and Hispanics do worse than Caucasians as well, the differences are far less pronounced.
What accounts for this difference? There are various possibilities including genetic differences, acquired co-morbidities (diseases) or perhaps the way those co-morbidities are managed by physicians. The last one interests me the most.
Mendelian randomisation is nature's way of demonstrating differences in outcome due to a putative risk factor. For example, subjects with familial hypercholestrolaemia, the commonest autosomal dominant condition in the population, have a higher risk of heart disease and stroke than those without the condition, due to the fact that they have high LDL cholesterol. So far, no such signals have emerged in COVID.
However, differences could be acquired. Black subjects have a higher prevalence of hypertension and obesity than other races. Both of these have emerged as significant risk factors for COVID related mortality.
While the above is undoubtedly true, I believe (I haven't seen this in the medical press yet) that there is another factor- how hypertension is managed in Black subjects. For unknown reasons, Black people with hypertension respond poorly to a class of drugs called ACE inhibitors (yes, it's the same ACE you read about in the context of COVID receptors). In fact, there is evidence to suggest that Black subjects have a higher risk of death from MI (heart attack), stroke and heart failure when treated with ACE inhibitors than when not.
https://www.thecardiologyadvisor.com/home/topics/hypertension/ace-inhibitors-may-not-be-as-effective-in-black-patients/
As a result, ACE inhibitors are used far less often to treat hypertension in Blacks than in other races, and herein, I believe, lies the rub. I have cautioned here in the past against discontinuing ACE inhibitors in hypertensive subjects during the pandemic, as this is likely to lead to harm, an inference that was later confirmed by NEJM.
https://www.nejm.org/doi/full/10.1056/NEJMsr2005760 (free to access)
This is a case of unintended iatrogenic (physician induced) randomisation. If you are obese, and hypertensive, you are more likely to die from COVID 19. However, if you are obese, hypertensive and not taking ACE inhibitors, as in the majority of Black subjects, that risk is far higher.
https://www.apmresearchlab.org/covid/deaths-by-race
In the UK, the figures are even more stark. Blacks are more than 4 times likely to die from COVID than whites.
https://www.ons.gov.uk/peoplepopulationandcommunity/birthsdeathsandmarriages/deaths/articles/coronavirusrelateddeathsbyethnicgroupenglandandwales/2march2020to10april2020
Although in general, Asians and Hispanics do worse than Caucasians as well, the differences are far less pronounced.
What accounts for this difference? There are various possibilities including genetic differences, acquired co-morbidities (diseases) or perhaps the way those co-morbidities are managed by physicians. The last one interests me the most.
Mendelian randomisation is nature's way of demonstrating differences in outcome due to a putative risk factor. For example, subjects with familial hypercholestrolaemia, the commonest autosomal dominant condition in the population, have a higher risk of heart disease and stroke than those without the condition, due to the fact that they have high LDL cholesterol. So far, no such signals have emerged in COVID.
However, differences could be acquired. Black subjects have a higher prevalence of hypertension and obesity than other races. Both of these have emerged as significant risk factors for COVID related mortality.
While the above is undoubtedly true, I believe (I haven't seen this in the medical press yet) that there is another factor- how hypertension is managed in Black subjects. For unknown reasons, Black people with hypertension respond poorly to a class of drugs called ACE inhibitors (yes, it's the same ACE you read about in the context of COVID receptors). In fact, there is evidence to suggest that Black subjects have a higher risk of death from MI (heart attack), stroke and heart failure when treated with ACE inhibitors than when not.
https://www.thecardiologyadvisor.com/home/topics/hypertension/ace-inhibitors-may-not-be-as-effective-in-black-patients/
As a result, ACE inhibitors are used far less often to treat hypertension in Blacks than in other races, and herein, I believe, lies the rub. I have cautioned here in the past against discontinuing ACE inhibitors in hypertensive subjects during the pandemic, as this is likely to lead to harm, an inference that was later confirmed by NEJM.
https://www.nejm.org/doi/full/10.1056/NEJMsr2005760 (free to access)
This is a case of unintended iatrogenic (physician induced) randomisation. If you are obese, and hypertensive, you are more likely to die from COVID 19. However, if you are obese, hypertensive and not taking ACE inhibitors, as in the majority of Black subjects, that risk is far higher.
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