Although there’s some question about the conclusions, the study of selection pressures in the European genome makes sense to me: Europeans have undergone some evolutionary changes just in the last couple or three millennia. As one with European ancestry, I wonder, “In what ways am I different from, say, Europeans from the Apennines to the Alps, the general region from which I assume my ancestors originated? Do I differ from them in skin pigmentation, dietary traits, and body measurements as hinted at by Weichen Song and fellow genetic researchers?” *
Song writes that his group found changes in 88% of 870 polygenic traits. Surprising? No. Look at all the possible genetic influences. Look at them in your own genealogy. I think of the historical interactions among migrating, warring, and what I call Montague-Capelet matings, that is, matings across cultural barriers, you remember, the Romeo-Juliet-type relationships. As anthropologist Clyde Kluckhohn argued later in his career, there are apparently no “pure races,” and people reflect the properties of their gene pools. All the historical mixing of peoples in Europe over three millennia has had an effect: It produced me, an embodiment of appearance, physical strengths and weaknesses, resistances and susceptibilities, potential talents and noticeable limitations.
I cannot, of course, undo my genetic inheritance. No one can. Little but idle speculation can come from asking, “What if?” I am what I am; you are what you are; both of us are susceptible of and resistant to polygenic conditions, such as arthritis, or diabetes, or high blood pressure. We were born with stamps of resistance or susceptibility. We were all born with a skin color and a programmed set of body measurements (unless someone administers growth hormones artificially). So, biologically, we’re predetermined in such polygenic traits that might have originated in some unknown set of ancestors. For some, even dietary traits reveal a distinct heritage as alcohol or milk intolerance can indicate. Those nineteenth-century statements about Native Americans and “firewater,” bespeak a polygenic truth. Just as some people have little tolerance for milk, others have little tolerance for hard liquor. Throw in the pressures of culture and walla! Tempting advertisements for ice cream and whiskey and the easy availability of both prove to be roads to suffering.
The study of European polygenics by Song is a rudimentary step toward understanding the roles played by cooperating genes. But there’s a danger in taking too much from such studies. Nevertheless, I’m going to go full hypothetical here and in the process maybe explain why in African countries the COVID-19 pandemic has not devastated populations. I might mix and match info here, so recognize that in hypothesizing I’m only guessing, but sometimes, as we have all discovered, guesses, even bad ones, can lead to discoveries of one kind or another.
Here’s my hypothesis in the form of a general question: Is there a polygenic protection against severe or deadly COVID in some populations? The hypothesis emerges from my having read “A version of this gene doubles the risk of dying from COVID-19,” published in LIVESCIENCE.COM. The gene, designated as LZTFL1 regulates lung cells’ reaction to infections. The presence of the gene lowers the defensive response of the cells. Now, this is where the hypothesis comes in: “The gene version that raises COVID-19 risk is present in 60% of people of South Asian ancestry, 15% of people of European ancestry, 2.4% of people with African ancestry, and 1.8% of people with East Asian ancestry.” ** Born to be vulnerable to the ravages of COVID infection? Not so much in the African genes, it seems.
Now, I’m not proclaiming that I have a causal link between one gene and COVID susceptibility. Rather, I’m suggesting that an explanation for the low numbers of deaths in African nations might derive from the absence of that gene or from its inability to work in a polygenic group to the detriment of the gene holder. Unfortunately, I have neither the wherewithal nor the expertise to pursue the matter scientifically. So, my hypothesis will probably die like wild grape on a vine in the Pennsylvanian forests. It’s not going to be turned into a fine wine.
And I know the objections you will raise: 1) the average age in Africa is lower than the average age in Europe and North America; 2) as a consequence of a younger population, fewer people are severely affected or even infected, as was the case in, for example, the American population that had over a half million deaths, mostly in the older population; 3) in general the African population spends more time outdoors and indoors, one of the drawbacks or advantages, depending on a perspective of one’s economic assessments that separate First and Third Worlds—those who spend more time outside have the distinct advantage of more Vitamin D in their bloodstreams, a vitamin that appears to protect against severe COVID reactions; and finally, 4) maybe the data on African COVID cases are erroneous; maybe the cases are underreported.
If you are a medical researcher, I just handed you a possible topic to pursue. It would be a complex task because it would entail trying to connect lifestyle to an individual gene and to a group of genes that might work in unison for a single effect. I happen to think there’s much to come from polygenic research. But it won’t come from me. This is where I meet my genetic, mental, and psychological limitations, and those, in turn, meet my life choices. I never particularly cared much for staring down microscopes even when I learned micropaleontology or eventually had to teach the subject with, I now admit, feigned enthusiasm. I might not have had the interest, but I could see the value and I could see that others did, in fact, have genuine interest in little things. That I never pursued the subject of microbiology beyond micropaleontology—which is more descriptive than experimental—doesn’t mean I haven’t asked a good question about the predisposition of a population to withstand the ravages of a disease that killed so many. The follow up question would be: “Is there a gene therapy for COVID that one could derive from an African immunity?” We know, for example, that sickle cell anemia seems to afford a protection against malaria, though in the long run, does little good in other biological interactions. There are many lessons to learn about who we are and how we got to be where we are today.
If COVID-19 and other pandemic diseases were not so tragic, we might say like a comedian opening his gig, “A funny thing happened to me on my way here today.”
Notes:
*Song, Weichen, et al. A selection pressure landscape for 870 human polygenic traits, Nature Human Behavior (2021). DOI: 10.1038/s41562-021-01231-4
**Pappas, Stephanie. Online at https://www.livescience.com/covid-gene-death-risk?utm_source=SmartBrief&utm_medium=email&utm_campaign=368B3745-DDE0-4A69-A2E8-62503D85375D&utm_content=AFB6D9DE-4D5E-4C6E-92F1-00E6B6414E83&utm_term=b84f2fa7-0d47-430c-a9c6-894ced980d93 Accessed November 20, 2021. See Downes, Damien J. Et al. Identification of LZTFL1 as a candidate effector gene at a COVID-19 risk locus. Nature Genetics 53, 1606-1615 (2021). Online at https://www.nature.com/articles/s41588-021-00955-3?utm_medium=affiliate&utm_source=commission_junction&utm_campaign=3_nsn6445_deeplink_PID100052172&utm_content=deeplink Accessed November 20, 2021.
Song writes that his group found changes in 88% of 870 polygenic traits. Surprising? No. Look at all the possible genetic influences. Look at them in your own genealogy. I think of the historical interactions among migrating, warring, and what I call Montague-Capelet matings, that is, matings across cultural barriers, you remember, the Romeo-Juliet-type relationships. As anthropologist Clyde Kluckhohn argued later in his career, there are apparently no “pure races,” and people reflect the properties of their gene pools. All the historical mixing of peoples in Europe over three millennia has had an effect: It produced me, an embodiment of appearance, physical strengths and weaknesses, resistances and susceptibilities, potential talents and noticeable limitations.
I cannot, of course, undo my genetic inheritance. No one can. Little but idle speculation can come from asking, “What if?” I am what I am; you are what you are; both of us are susceptible of and resistant to polygenic conditions, such as arthritis, or diabetes, or high blood pressure. We were born with stamps of resistance or susceptibility. We were all born with a skin color and a programmed set of body measurements (unless someone administers growth hormones artificially). So, biologically, we’re predetermined in such polygenic traits that might have originated in some unknown set of ancestors. For some, even dietary traits reveal a distinct heritage as alcohol or milk intolerance can indicate. Those nineteenth-century statements about Native Americans and “firewater,” bespeak a polygenic truth. Just as some people have little tolerance for milk, others have little tolerance for hard liquor. Throw in the pressures of culture and walla! Tempting advertisements for ice cream and whiskey and the easy availability of both prove to be roads to suffering.
The study of European polygenics by Song is a rudimentary step toward understanding the roles played by cooperating genes. But there’s a danger in taking too much from such studies. Nevertheless, I’m going to go full hypothetical here and in the process maybe explain why in African countries the COVID-19 pandemic has not devastated populations. I might mix and match info here, so recognize that in hypothesizing I’m only guessing, but sometimes, as we have all discovered, guesses, even bad ones, can lead to discoveries of one kind or another.
Here’s my hypothesis in the form of a general question: Is there a polygenic protection against severe or deadly COVID in some populations? The hypothesis emerges from my having read “A version of this gene doubles the risk of dying from COVID-19,” published in LIVESCIENCE.COM. The gene, designated as LZTFL1 regulates lung cells’ reaction to infections. The presence of the gene lowers the defensive response of the cells. Now, this is where the hypothesis comes in: “The gene version that raises COVID-19 risk is present in 60% of people of South Asian ancestry, 15% of people of European ancestry, 2.4% of people with African ancestry, and 1.8% of people with East Asian ancestry.” ** Born to be vulnerable to the ravages of COVID infection? Not so much in the African genes, it seems.
Now, I’m not proclaiming that I have a causal link between one gene and COVID susceptibility. Rather, I’m suggesting that an explanation for the low numbers of deaths in African nations might derive from the absence of that gene or from its inability to work in a polygenic group to the detriment of the gene holder. Unfortunately, I have neither the wherewithal nor the expertise to pursue the matter scientifically. So, my hypothesis will probably die like wild grape on a vine in the Pennsylvanian forests. It’s not going to be turned into a fine wine.
And I know the objections you will raise: 1) the average age in Africa is lower than the average age in Europe and North America; 2) as a consequence of a younger population, fewer people are severely affected or even infected, as was the case in, for example, the American population that had over a half million deaths, mostly in the older population; 3) in general the African population spends more time outdoors and indoors, one of the drawbacks or advantages, depending on a perspective of one’s economic assessments that separate First and Third Worlds—those who spend more time outside have the distinct advantage of more Vitamin D in their bloodstreams, a vitamin that appears to protect against severe COVID reactions; and finally, 4) maybe the data on African COVID cases are erroneous; maybe the cases are underreported.
If you are a medical researcher, I just handed you a possible topic to pursue. It would be a complex task because it would entail trying to connect lifestyle to an individual gene and to a group of genes that might work in unison for a single effect. I happen to think there’s much to come from polygenic research. But it won’t come from me. This is where I meet my genetic, mental, and psychological limitations, and those, in turn, meet my life choices. I never particularly cared much for staring down microscopes even when I learned micropaleontology or eventually had to teach the subject with, I now admit, feigned enthusiasm. I might not have had the interest, but I could see the value and I could see that others did, in fact, have genuine interest in little things. That I never pursued the subject of microbiology beyond micropaleontology—which is more descriptive than experimental—doesn’t mean I haven’t asked a good question about the predisposition of a population to withstand the ravages of a disease that killed so many. The follow up question would be: “Is there a gene therapy for COVID that one could derive from an African immunity?” We know, for example, that sickle cell anemia seems to afford a protection against malaria, though in the long run, does little good in other biological interactions. There are many lessons to learn about who we are and how we got to be where we are today.
If COVID-19 and other pandemic diseases were not so tragic, we might say like a comedian opening his gig, “A funny thing happened to me on my way here today.”
Notes:
*Song, Weichen, et al. A selection pressure landscape for 870 human polygenic traits, Nature Human Behavior (2021). DOI: 10.1038/s41562-021-01231-4
**Pappas, Stephanie. Online at https://www.livescience.com/covid-gene-death-risk?utm_source=SmartBrief&utm_medium=email&utm_campaign=368B3745-DDE0-4A69-A2E8-62503D85375D&utm_content=AFB6D9DE-4D5E-4C6E-92F1-00E6B6414E83&utm_term=b84f2fa7-0d47-430c-a9c6-894ced980d93 Accessed November 20, 2021. See Downes, Damien J. Et al. Identification of LZTFL1 as a candidate effector gene at a COVID-19 risk locus. Nature Genetics 53, 1606-1615 (2021). Online at https://www.nature.com/articles/s41588-021-00955-3?utm_medium=affiliate&utm_source=commission_junction&utm_campaign=3_nsn6445_deeplink_PID100052172&utm_content=deeplink Accessed November 20, 2021.
RSS Feed