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Why black people die more from Covid-19

DrZoidberg

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In the latest episode of This Week in Virology they are joined by the sociomedical scientist Robert Fullilove. They discuss why Covid-19 impacts minorities more.

https://www.microbe.tv/twiv/twiv-655/

It's interesting having him being cross examined by four virologists.

His explanation is quite simple. Poor people can't afford to give a shit about being infected, and if they did care there's nothing they can do about it anyway. Where's poor people supposed to socially isolate?

While pretty damn obvious, it's always nice to have it explained by experts.
 

I hadn't thought about that before. Anything that messes with the circulatory system combined with sickle-cell is bad news.



Two thoughts:

First maybe there's a relationship with those who suffer from aplastic anemia, the other bad adaptation to malaria, and maybe there's a relationship to malaria itself. The latter could mean we will have to develop a maintenance solution. The first could mean there is a genetic relationship we need to consider.

It's good that people are looking at such as genetic links. However I think the sociological explanations seema more appropriate since they reflect the results sociological material consequences one might expect, availability of medical support, need for resources to survive, etc.
 

I hadn't thought about that before. Anything that messes with the circulatory system combined with sickle-cell is bad news.



Two thoughts:

First maybe there's a relationship with those who suffer from aplastic anemia, the other bad adaptation to malaria, and maybe there's a relationship to malaria itself. The latter could mean we will have to develop a maintenance solution. The first could mean there is a genetic relationship we need to consider.

It's good that people are looking at such as genetic links. However I think the sociological explanations seema more appropriate since they reflect the results sociological material consequences one might expect, availability of medical support, need for resources to survive, etc.

The sociological explanation is the one people want. The Occam’s razor explanation is the one you don’t say in public.
 
Two thoughts:

First maybe there's a relationship with those who suffer from aplastic anemia, the other bad adaptation to malaria, and maybe there's a relationship to malaria itself. The latter could mean we will have to develop a maintenance solution. The first could mean there is a genetic relationship we need to consider.

It's good that people are looking at such as genetic links. However I think the sociological explanations seema more appropriate since they reflect the results sociological material consequences one might expect, availability of medical support, need for resources to survive, etc.

The sociological explanation is the one people want. The Occam’s razor explanation is the one you don’t say in public.

The sociological explanation is the one Occam's razor favours. There may be genetic factors that cause black people to suffer more severe cases on average, all else equal, or their may be none, or there may even be genetic factors that would cause white people to suffer (slightly) more severe cases on average, all else equal, but with the effects swamped by other factors. There is no way to tell just from the raw death rates because all else isn't equal.

We do however know that black people in the US tend to be poorer, have less insurance coverage, are concentrated in urban areas where they are reliant on public transport, are more often employed in jobs that do not accomodate working from home, and live in larger households than white people. Those known factors alone predict higher rates for blacks (and Latinos).

If you want to make the case that a not directly demonstrated genetic factor also plays an important role, you have to do one of two things:

- directly demonstrate it, e.g. identify genetic variants that are reliably correlated with severe outcomes and that are more common among blacks, and quantify their contribution to the racial disparity in outcomes, or

- positively show that the upper bound for the expected effect size of the known (sociological) factors is insufficient to explain the observed disparity in outcomes.
 
Two thoughts:

First maybe there's a relationship with those who suffer from aplastic anemia, the other bad adaptation to malaria, and maybe there's a relationship to malaria itself. The latter could mean we will have to develop a maintenance solution. The first could mean there is a genetic relationship we need to consider.

It's good that people are looking at such as genetic links. However I think the sociological explanations seema more appropriate since they reflect the results sociological material consequences one might expect, availability of medical support, need for resources to survive, etc.

The sociological explanation is the one people want. The Occam’s razor explanation is the one you don’t say in public.

The sociological explanation is the one Occam's razor favours. There may be genetic factors that cause black people to suffer more severe cases on average, all else equal, or their may be none, or there may even be genetic factors that would cause white people to suffer (slightly) more severe cases on average, all else equal, but with the effects swamped by other factors. There is no way to tell just from the raw death rates because all else isn't equal.

We do however know that black people in the US tend to be poorer, have less insurance coverage, are concentrated in urban areas where they are reliant on public transport, are more often employed in jobs that do not accomodate working from home, and live in larger households than white people. Those known factors alone predict higher rates for blacks (and Latinos).

If you want to make the case that a not directly demonstrated genetic factor also plays an important role, you have to do one of two things:

- directly demonstrate it, e.g. identify genetic variants that are reliably correlated with severe outcomes and that are more common among blacks, and quantify their contribution to the racial disparity in outcomes, or

- positively show that the upper bound for the expected effect size of the known (sociological) factors is insufficient to explain the observed disparity in outcomes.

Also, Africa, Arabia and Europe were connected via a landbridge from the dawn of man until today. That means about the same exposure to the same transmissable diseases and therefore, in general, comparable immunity. The differences will be small and not have statistically significant impacts. The genetic diseases that are unique to each community are all rare, and will therefore not lead to statistically significant differences?
 
The sociological explanation is the one Occam's razor favours. There may be genetic factors that cause black people to suffer more severe cases on average, all else equal, or their may be none, or there may even be genetic factors that would cause white people to suffer (slightly) more severe cases on average, all else equal, but with the effects swamped by other factors. There is no way to tell just from the raw death rates because all else isn't equal.

We do however know that black people in the US tend to be poorer, have less insurance coverage, are concentrated in urban areas where they are reliant on public transport, are more often employed in jobs that do not accomodate working from home, and live in larger households than white people. Those known factors alone predict higher rates for blacks (and Latinos).

If you want to make the case that a not directly demonstrated genetic factor also plays an important role, you have to do one of two things:

- directly demonstrate it, e.g. identify genetic variants that are reliably correlated with severe outcomes and that are more common among blacks, and quantify their contribution to the racial disparity in outcomes, or

- positively show that the upper bound for the expected effect size of the known (sociological) factors is insufficient to explain the observed disparity in outcomes.

Also, Africa, Arabia and Europe were connected via a landbridge from the dawn of man until today. That means about the same exposure to the same transmissable diseases and therefore, in general, comparable immunity. The differences will be small and not have statistically significant impacts. The genetic diseases that are unique to each community are all rare, and will therefore not lead to statistically significant differences?

Evolution isn't strongly modular. A gene variant can be selected because it offers e. g. a better ability to metabolize certain sugars or proteins and thus be selected because those are present in quantities in one group's diet, independently of a slight unrelated effect it has on the receptors the virus docks to or on the immune system. So there might be significant differences even if the immune system itself has evolved under similar selection pressures.

We just don't have any good reason to believe there is, nor any strong indication in which direction it would work if it does exist.
 
Also, even if Africa and Eurasia where never fully isolated,there's the issue of tropical diseases, often transmitted by animal vectors that only thrive in hot climates. This can go both ways too: there could be a positive interaction with resistance to a different disease, or a trade-off where a selected specific resistance comes at the cost of a weaker generic immune response. So I don't think it's a priori implausible that European and African populations have innate differences in their response to the coronavirus - we just don't know that it is so, or which population shows a better response if so.

The fact that African Americans in 2020 suffer at higher rates than European Americans just doesn't cut it as evidence. At least not until we control for known sociological factors and/or quantify their expected effect size and find it clearly insufficient to explain the full extent of the disparity.

It's also worth noting that the data underlying the sociological explanation is pretty rock solid. This isn't just some one-off study by a grad student based on informal interviews with a couple dozen or hundred self-selected informants. Household sizes income, insurance coverage etc can all be learned from census data, with sample sizes in the millions.
 
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