Other considerations would be extra- nuclear DNA, specifically mitochondrial. As Kimberly Dunham Snary et al point out, mitochondrial – nuclear DNA mismatch matters. Pmcid pmc7238407
Did you know that this tracks with IQ deltas as well: children with a white mother and a black father have an eight-point I.Q. advantage over those with a black mother and a white father. Why? Probably for the same reason: status differences. Maybe the same impact here?
There is no such study. This is another example of the game of "telephone." Professor Caplan was citing an article by Malcolm Gladwell, who incorrectly remembered a presentation by James Flynn on race and IQ:
"If I.Q. is innate, it shouldn’t make a difference whether it’s a mixed-race child’s mother or father who is black. But it does: children with a white mother and a black father have an eight-point I.Q. advantage over those with a black mother and a white father." Gladwell, M. (2007). None of the Above. The New Yorker https://www.newyorker.com/magazine/2007/12/17/none-of-the-above
Gladwell's recollection of Flynn's presentation closely matches Flynn's article in American Psychologist. But Flynn made no comparison between BM/WF children and WM/BF children, either in that article or in any other.
Flynn was referring to the Eyferth study of illegitimate children of German mothers by American soldiers:
"The soldiers of the American occupation force in Germany, both White and Black, fathered thousands of children with German women after World War II. Eyferth (see Flynn, 1980) selected a representative sample of 181 Black children and a matching group of 83 White children and found that their mean IQs were virtually identical. In other words, children who had a White father seemed to possess no advantage whatsoever over those who had a Black father." (Flynn, 1999, p. 14)
The Eyferth study provides no information on BM/WF children. It also suffers from a number of other shortcomings:
- It was a study of young children. Other studies, notably the Minnesota Transracial Adoption Study, have shown that cognitive ability is much more malleable in children than in adults.
- Algerian soldiers were classified as "Black."
- The US army imposes minimum IQ requirements. This has the effect of narrowing the IQ difference between White and Black soldiers.
Moral of the story: Never, never take a factoid at face value. Ask to see the study that supposedly backs it.
With that said, the logic of the rebuttal still remains: there could be status differences that are hard to measure that are the fundamental reason for the disparity in your premise study as well.
Interesting...thanks for digging this up. Can you send an email to Bryan Caplan letting him know too? You would be a much better source for the email than me. Maybe he can add addendum to blog post.
Would also be good to get his take on this. He is deep in the studies as well.
In one of your posts, you cite a New Yorker article by Malcolm Gladwell, in which he refers to a presentation by James Flynn on race and IQ:
"If I.Q. is innate, it shouldn’t make a difference whether it’s a mixed-race child’s mother or father who is black. But it does: children with a white mother and a black father have an eight-point I.Q. advantage over those with a black mother and a white father."
Gladwell's description of that presentation closely matches Flynn's article in American Psychologist. But Flynn made no comparison between Black mother/White father children and White mother/Black father children, either in that article or in any other.
Gladwell was probably misremembering the following passage, which summarizes the Eyferth study of illegitimate children born to German mothers and fathered by American soldiers :
"The soldiers of the American occupation force in Germany, both White and Black, fathered thousands of children with German women after World War II. Eyferth (see Flynn, 1980) selected a representative sample of 181 Black children and a matching group of 83 White children and found that their mean IQs were virtually identical. In other words, children who had a White father seemed to possess no advantage whatsoever over those who had a Black father." (Flynn, 1999, p. 14)
The Eyferth study provides no information on Black mother/White father children, since none of the children were in that category. It also suffers from other shortcomings:
- It was a study of young children. Other studies, notably the Minnesota Transracial Adoption Study, have shown that cognitive ability is much more malleable in children than in adults.
- Algerian soldiers were classified as "Black."
- The US army imposes minimum IQ requirements. This has the effect of narrowing the IQ difference between White and Black soldiers.
In humans, fertility reaches a peak in marriages between 3rd or 4th cousins. "Closer" marriages show inbreeding depression, whereas marriages farther apart show outbreeding depression. See my article on this subject: https://www.aporiamagazine.com/p/outbreeding-depression-avenues-for
Hybrid vigor doesn't exist in our species. It is generally found in species that are developmentally less complex, particularly plants.
I know, I know. "But everybody says ..." Certain ideas gain traction because they are compatible with a certain zeitgeist.
It's the same situation in Africa. African mothers give birth earlier than European mothers:
"There is significant variation in the incidence of preterm birth worldwide. The rates of preterm birth in 184 countries in 2010 ranged from 5% in several Northern European countries to 18% in Malawi."
There seems to be a link between the SERPINH1 gene and preterm premature rupture of membranes in women of Sub-Saharan African descent.
Purisch, S. E., & Gyamfi-Bannerman, C. (2017, November). Epidemiology of preterm birth. In Seminars in perinatology (Vol. 41, No. 7, pp. 387-391). WB Saunders. https://doi.org/10.1053/j.semperi.2017.07.009
Two questions. How highly is a couple's fertility highly correlated with positive health outcomes? I'm guessing quite high, save maybe for some genetic defects that are latent? This might be too big a question for a discussion section.
Also, gestational surrogacy would avoid the harms you describe in your article. Have you written or thought much about it? Do you think it's scalable in any meaningful way?
Fertility correlates with the biological viability of the embryo or fetus. Only 40-50% of fertilized eggs make it to the blastocyst stage, and an even lower proportion make it all the way to birth (perhaps 30%). So a lot of natural selection occurs before birth.
Yes, there is a correlation between fertility and overall health:
"Our review of the existing literature suggests and association between male factor infertility and somatic health. The literature is consistent in findings that demonstrate higher risk of CVD. Similarly, infertile males appear to be at higher risk of chronic disease regardless of sociodemographic factors. However, the association with cancers varies based on the specific cancer examined and conflicting results exist."
Del Giudice, F., Kasman, A. M., Ferro, M., Sciarra, A., De Berardinis, E., Belladelli, F., ... & Eisenberg, M. L. (2020). Clinical correlation among male infertility and overall male health: a systematic review of the literature. Investigative and Clinical Urology, 61(4), 355. https://doi.org/10.4111/icu.2020.61.4.355
Gestational surrogates tend to come from a low socioeconomic background and thus are more prone to fast life history and early birth. Surrogacy is also expensive. A cheaper option would be to create a special breed of cow for this task.
I predict that the Chinese (or the North Koreans) would be the first to go this route.
Mum's a cow is a disturbing and promising prospect. And it makes sense that some cancers might be more common amongst relatively healthier people. Thanks for the thorough reply and cite.
Interesting article. I wonder if in the future similar analyses can be performed on divergent ethnic groups within the continent of Africa, where the genomic diversity is reported to be the greatest from among human subpopulations. Focus on primarily US populations may be nonrepresentative, since the entire US comprise us such a tiny proportion of the world’s population, but of course we all have to work around the availability heuristic.
I agree with you, but I'm a bit wary of the oft-cited factoid that genomic diversity is highest in Africa. Modern humans have lived longer in Africa than anywhere else, so they have accumulated a lot more "junk" variability over a longer time. I'm not convinced that African populations have more functional variability that has real-life consequences.
The African groups from whom African Americans descend comprise 85% percent of Africa's population. The very divergent groups in Africa are small populations that don't really have descendants outside of Africa. A U.S. African American is a good proxy, although with notable European ancestry.
African Americans generally have lower circulating 25-hydroxyvitamin D levels than White Americans, since their much darker skin absorbs more of the ultraviolet-B light which breaks a bond in a carbon ring of 7-dehydrocholesterol, transforming it into vitamin D3 cholecalciferol. 25-hydroxyvitamin D calcifediol (AKA "calcidiol") is made, primarily in the liver when ingested or UV-B >> skin produced vitamin D3 is hydroxylated on the 25th carbon. This 25-hydroxyvitamin D, circulating in the bloodstream is what is measured in "vitamin D" blood tests.
The kidneys need a level (concentration) of about 20 ng/mL = 50 nmol/L to play their role in regulating calcium-phosphate-bone metabolism, and governments and many doctors are happy with this. However, 50 ng/mL (125 nmol/L = 1 part in 20,000,000 by mass) is required for the proper function of the immune system. Most medical professionals and immunologists do not know this.
Many types of immune cell and some other cell types need a good supply of 25-hydroxyvitamin D to run their intracrine (inside each cell) and paracrine (to nearby cells) signaling systems, which are crucial to each cell's ability to adapt its behavior in response to its changing circumstances. These signaling systems are not known to most medical professionals and immunologists. For a tutorial and links to research: https://vitamindstopscovid.info/02-intracrine/.
These signaling systems are not related to hormonal (endocrine) signaling, which involves a signaling molecule being carried in the bloodstream, and potentially the cerebrospinal fluid, with the level of this affecting the behavior of one or more cell types all over the body.
Vitamin D3 and 25-hydroxyvitamin D do not function as hormones. They are not signaling molecules. A third compound, 1,25-dihydroxyvitamin D calcitriol functions as a hormone when the kidneys release it into the bloodstream. This is the sole hormonal function of these three compounds.
In 25-hydroxyvitamin D to calcitriol intracrine signaling, the intracellularly produced calcitriol functions as an intracrine agent, binding to "vitamin D" receptor molecules (really the "calcitriol receptor" molecules) which leads to changes in gene transcription in the nucleus, altering the cell's protein synthesis and so its behavior. Here, calcitriol is acting as an intracrine agent. This production of calcitriol in a cell is only enabled once a cell-type specific condition is detected. The changes in gene expression, and so the changes in cell behavior, also vary from one cell type to the next. Calcitriol as a paracrine agent when intracellularly produced calcitriol diffuses to nearby cells, at local levels well above the 0.05 to 0.1 ng/mL (kidney produced) hormonal background level, affecting nearby cells, also in cell-type specific ways.
This mini-tutorial should help everyone understand how important it is to maintain at least 50 ng/mL circulating 25-hydroxyvitamin D. This is generally only possible with vitamin D3 supplementation in quantities, which while small, are 5 or more times what governments and many doctors recommend.
It is common for people with dark or black skin, living far from the equator, to have significantly less circulating 25-hydroxyvitamin D than white-skinned people living alongside them - and the average levels for white-skinned people who do not supplement vitamin D3 and who have not recently had extensive UV-B skin exposure (which damages DNA and so raises the risk of skin cancer) are 15 to 25 ng/mL.
There may well be genetic reasons for African American women giving birth on average a week earlier than White women. However, some component of the observed difference would be due to their generally lower 25-hydroxyvitamin D levels.
All this can and should be corrected. See the vitamin D3 supplementation recommendations from New Jersey based Professor of Medicine, Sunil Wimalawansa, according to body weight and obesity status: https://vitamindstopscovid.info/00-evi/#00-how-much.
Vitamin D levels are low not only in African Americans but also in other dark-skinned humans. These human groups appear to have adapted accordingly by using this vitamin more efficiently. The following is an excerpt from one of my published articles:
A single UVB exposure produces less vitamin D3 in black subjects than in whites. The difference narrows, however, after liver hydroxylation to 25(OH)D and disappears after kidney hydroxylation to 1,25(OH)2D. The most active form of vitamin D is thereby kept at a constant level regardless of skin color. This may be why nearly half of African Americans are classified as vitamin-D deficient and yet few show signs of calcium deficiency. In fact, this population has less osteoporosis, fewer fractures, and a higher bone mineral density than do Euro-Americans, who generally produce and ingest more vitamin D. The same apparent contradiction emerges from a survey of East African immigrant children in Australia. None had rickets despite very low serum 25(OH)D, with 87% of them having less than 50 nmol/L and 44% less than 25 nmol/L.
These levels are apparently lower for genetic reasons. A study of African Americans found that serum 25(OH)D decreased linearly with increasing African ancestry, the decrease being 2.5-2.75 nmol/L per 10% increase in African ancestry. The study also found that sunlight and diet were 46% less effective in raising these levels among subjects with high African ancestry than among those with low/medium African ancestry.
There have been proposals to target African Americans for vitamin D supplementation, and similar proposals have been made for the Inuit of northern Canada. These proposals, though well-intentioned, may have disastrous effects on both populations. Unlike vitamin D, vitamin D is not water-soluble. If you take too much, you will not excrete it in your urine.
Frost P. (2022) The Problem of Vitamin D Scarcity: Cultural and Genetic Solutions by Indigenous Arctic and Tropical Peoples. Nutrients 14(19):4071. https://doi.org/10.3390/nu14194071
Hi Peter, Thanks very much for your reply and for your article in Nutrients, which is among the most interesting vitamin D articles I have ever read.
It would take me days to chase up the research you cite and respond properly. If and when I do, I will write to you and will also post the response to the Nutrition for Immune System Health email discussion list: https://nish.groups.io. You and anyone else seriously interested in such research are invited to join us. This is a high signal-to-noise ratio discussion group. It is not particularly busy, but everything is civil and constructive. Members include leading vitamin D researchers. We discuss vitamin D most frequently, with magnesium probably second.
It is not hard for the kidneys to maintain a very low level of circulating 1,25-dihydroxyvitamin D as a hormone to affect multiple cell types which are involved in calcium-phosphate-bone metabolism. The levels are typically 0.05 to 0.1 ng/mL (x 2.5 for nmol/L). For Europeans, they can do this quite well with 20 ng/mL (50 nmol/L) circulating 25-hydroxyvitamin D (25(OH)D).
I have not studied it, but I recall that the relevant kidney cells have an active transport system bringing 25(OH)D across their cell membrane, and that this involves transporting 25(OH)D when it is bound to the "vitamin D" binding protein DBP. This means it can raise the intracellular level higher than the total level in the bloodstream, but I am not sure what these cells' intracellular level is, or whether this can be measured.
As far as I know, 25(OH)D entry into all other cell types is from passive diffusion through the cell membrane, of the individual, unbound, molecules, from the bloodstream or from whatever fluid the cells are bathed in, such as CSF, where, as far as I know, the 25(OH)D is not bound strongly to DBP or less strongly to albumin proteins in general (VDR is a specialised albumin protein).
As far as I know, there is uncertainty and debate about the level of intracellular 25(OH)D in immune cells which require it as a raw material for intracrine and/or paracrine signaling. See my attempt at a full tutorial, since no-one else has written one: https://vitamindstopscovid.info/02-intracrine/.
Since most 25(OH)D in the bloodstream is strongly bound to VDR, does the diffusion of 25(OH)D - which must be from the small fraction which is unbound to both VDR and albumin proteins, into the extracellular fluid of tissues in general, and/or passively through the cell membranes of cells such as immune cells - result in an intracellular level which is very much lower than the total level in the bloodstream? Specifically, is the intracellular level of 25(OH)D in immune cells a small fraction of the total level? I guess it is, but I am not sure what the best research shows.
As far as I know, there is no mechanism for measuring this level in individual cells. Perhaps if a sufficient volume of them could be isolated from other cell types and the extracellular fluid, they could be lysed and the collected cytosol fluid carefully analysed. I have not read of this being done, but there is a vast amount of vitamin D research, and it would be a full time job trying to keep up with it.
While your article argues and cites research which indicates African Americans do quite well with bone density, despite their low 25(OH)D levels, you do not mention the well known terrible outcomes in numerous other immune system related conditions for African Americans with respect to those of White Americans - and White Americans would do much better if their 25(OH)D levels were at least the 50 ng/mL (125 nmol/L) their immune system needs to function properly.
This 50 ng/mL threshold is not widely known, but it is very clear, at least for immune responses to the largely bacterial pathogens which cause post-operative infections. This research needs to be very widely understood. Please see the graph, links and discussion at: https://vitamindstopscovid.info/00-evi/#00-50ngmL . The two graphs at the end of the PDF (they are not on the HTML page) of Quraishi et al. 2013/4 are the most important graphs I have ever seen for human health: https://jamanetwork.com/journals/jamasurgery/articlepdf/1782085/soi130062.pdf.
The bloodstream is perfectly capable of transporting 25(OH)D by it being dissolved in the plasma. A healthy concentration (level) is 50 ng/mL = 1 part in 20,000,000 by mass, which is surely nowhere near saturation level.
I (and I think researchers in general) regard DBP as being concerned with long-term storage of 25(OH)D, rather than transport. The more DBP there is in the plasma, and the greater its affinity for 25(OH)D, the less free 25(OH)D is in solution and so available (as best I understand it) to diffuse into cells such as the many types of immune cell which need it as raw material from which to run their 25(OH)D to calcitriol intracrine and paracrine signaling systems.
If, as you wrote, Africans have more DBP and that DBP binds more strongly to 25(OH)D, then this might be explained by several mechanisms, including:
1 - This helps the relevant kidney cells' active transport system which brings 25(OH)D into their cytosols.
2 - The need for longer term storage, so total 25(OH)D in the bloodstream lasts longer when there is little supply of vitamin D3 cholecalciferol to replenish it. (About 1/4 of ingested or UV-B produced vitamin D3 goes into circulation as 25(OH)D after hydroxylation, primarily in the liver.) This would help the person ride out the monsoon.
However, this - as far as I know - greater proportion of circulating 25(OH)D being tightly bound to DBP would make it harder for immune cells to get the intracellular 25(OH)D they need to function properly.
Your article argues against vitamin D3 supplementation for African Americans, Inuits and other populations, I think including Africans in Africa. However, African Americans suffer disproportionately from a vast range of illnesses - including dementia, autoimmune disorders, severe COVID-19 and sepsis - which would be greatly reduced if they had higher 25(OH)D levels.
Luxwolda et al. 2012 https://doi.org/10.1017/S0007114511007161 is the only research article I have ever heard of which reports 25(OH)D levels in traditionally living Africans - the people in the modern world who are most like the Africans of 50k years ago or more, who we all descended from. 50,000 years is only 2000 generations - a very short time for the evolution of fundamental changes to immune system intracellular signaling which might cope better with circulating 25(OH)D levels much lower than 50 ng/mL. So I tend to assume that all modern humans are running an immune system which coped OK with ca. 50 ng/mL levels in recent ancestral history, and which cannot work well with todays levels, which are often half, to one tenth, of this.
The lack of active transport of 25(OH)D into immune cells and the massive evidence of ill-health resulting directly from the further the 25(OH)D level is below 50 ng/mL (125 nmol/L) are arguments that the healthy state of humans, including Africans, is to have 50 ng/mL or more circulating 25(OH)D.
Luxwolda et al. don't report a majority of their subjects having more than 50 ng/mL circulating 25(OH)D, but the levels they found are much closer to this than the levels you cite in African Americans today.
"We measured the sum of serum 25-hydroxyvitamin D2 and D3 (25(OH)D) concentrations of thirty-five pastoral Maasai (34 (sd 10) years, 43 % male) and twenty-five Hadzabe hunter–gatherers (35 (sd 12) years, 84 % male) living in Tanzania. They have skin type VI, have a moderate degree of clothing, spend the major part of the day outdoors, but avoid direct exposure to sunlight when possible."
The average 25(OH)D level was 115 nmol/L = 46 ng/mL.
I made a histogram from their data, which I think has never been done before. The grey bars https://vitamindstopscovid.info/00-evi/1-Dror-Israel-14-framed.png depict much higher levels than the levels in sunny Israel for ordinary Israelis (the levels for Arab women are disastrously low).
Those very low levels for Arab men and women in Israel are about the same as those you report for present day African Americans who apparently have very healthy calcium-phosphate-bone metabolism. Those same African Americans have very poor health outcomes, I am sure, as a result of their 25(OH)D levels being so low with respect to (1) white levels, (2) the Luxwolda et al. African levels and (3) 50 ng/mL (125 nmol/L).
Ideally, one or more long-time vitamin D researchers would respond to your most interesting article, arguing to the contrary - that African Americans and Inuit would benefit from vitamin D3 supplementation to attain 50 ng/mL or more 25(OH)D.
I am an electronic technician with no articles published in this field, though I co-wrote a Letter, which can't be cited as if it was a peer-reviewed article. Ideally I would have time to do this, with one or more long-term vitamin D researchers. They are busy too!
"As far as I know, 25(OH)D entry into all other cell types is from passive diffusion through the cell membrane"
Are you sure about this point? Some human populations seem to use 25(OH)D more efficiently and more sparingly than others. An obvious means to this end would be to have more receptors that can bind to the molecule and bring it into the target tissues. I would expect to see this kind of active transport in a wide range of tissues, and not just in kidney cells.
Differences in immune response between African and Euro Americans have been attributed to differences in certain genetic variants, see:
Ogony, J. W., Radisky, D. C., Ruddy, K. J., Goodison, S., Wickland, D. P., Egan, K. M., ... & Sherman, M. E. Immune Responses and Risk of Triple-negative Breast Cancer: Implications for Higher Rates among African American Women. Cancer Prev Res (Phila) (2020) 13 (11): 901–910. https://doi.org/10.1158/1940-6207.CAPR-19-0562
The Luxwolda study is interesting. Since the Maasai and Hadzabe live at the Equator, enough UV light may enter their skin despite their high level of melanin.
Firstly, you seem unaware of studies showing that *recent* black African immigrant mothers have much better birth outcomes (closer to white). Contradicts your conclusion.
Secondly, you wrote "Moreover, if the cause is some unknown factor in the environment of Black mothers, why did it remain unchanged between 1978 and 1997? That period saw considerable social and economic gains for Black women, particularly those in interracial relationships."
Your first sentence mentions "UNKNOWN" factor(s) in the environment, but your next sentence claims its refutation as if it is KNOWN (social and economic...) If it is "unknown," how do you know it has anything to do with "social and economic" factors (and even specifically ones that remained unchanged in that period)?
Oh come on, don't start your sentence with “Nonsense”, how do you expect the conversation to go from there.
That said, “recent African immigrant mothers” aren't a monolith - we have mothers who come to the US to study and tend to be from relatively privileged backgrounds.
We also have others. It'll be interesting to know if the “better outcomes” you refer to is the same between both populations (I suspect the researchers might not separate them).
It's pretty well proven by now that parental welfare is a good predictor of children's welfare
Peter Frost is an anthropologist, so yes, I do believe he probably has this question in mind. Does he have the data to answer the question? No idea. Does he feel safe asking it? No idea either.
Research carried out on black populations is:
1 - Sorely needed
2 - A dangerous game for white researchers to play in the west. The "racism" accusations fly fast and furiously whenever this topic is broached.
I find it hard to blame the researcher if they choose not to speculate on ideas that potentially may be dangerous to their livelihoods and well-being. It's a damned if you do, damned if you don't scenario for them.
I trust that you're also doing similar (and unbiased) research that can throw some more light on these questions that we all ask.
Here's one article I recently read by ToveK, who's an African as well, based on the topic of the post, I believe also involved in some research.
It's good to hear from you Chanda! I belong to your fan club.
There is no genetic mismatch if both parents are African. Problems arise only if one parent is African and the other is European. In such a case, inconsistencies can develop between the genetic programming of the womb and the genetic programming of the fetus.
The word "if" implies a hypothesis. Personally, I don't believe the cause is unknown. It seems to be genetic, and we may have actually identified the genes in question. Please read my article to the end.
Hold on one second... The bad birth outcomes are there for black Americans even without black and white parents. Black-black American parents are still much worse than black-black African immigrant parents. Which says something else is going on.
But your ("genetic mismatch") claim can still be tested empirically. What's your prediction 1. if both parents are mixed race (both parents are like Obama), is that still a genetic mismatch? Equal to just black and white parents? 2. Does your claim predict that a recent black immigrant mother will have bad birth outcomes if she marries a white American?
As for your "if" statement, yes: I know you were not personally saying it is unknown. But you do not counter a statement saying it's unknown by giving a refutation that assumes it's known.
We're not communicating on the same wavelength. I'm talking about the difference in birth outcomes between Black mother/White father couples and White mother/Black father couples. This difference remains even when we control for a wide range of socioeconomic variables.
You're talking about the difference in birth outcomes between Black American couples and White American couples. That difference will disappear when we control for even a small number of socioeconomic variables.
Yes I know what you're talking about, and I am trying to show you that the gap is persistent in black parents in a way that undermines your explanation for the interracial pattern.
You write "the difference will disappear when we control for even a small number of socioeconomic variables." And I say NO, it won't. It reduces (obviously), but does not "disappear." This is a well-established puzzle in the field.
This is what the paper you cited in your article, to show this "disappearance," actually says:
"Results
For both very low and moderately low birth weight infants, the unadjusted risk associated with parental race showed a gradient of risk, from highest to lowest, for black mother/black father, black mother/white father, white mother/black father, and white mother/white father parents. After adjusting for other risk factors, the odds ratio associated with black mother/black father parents was reduced from 3.37 to 1.73 for very low birth weight infants and from 2.51 to 1.60 for moderately low birth weight infants, BUT BOTH REMAINED ELEVATED." [Emphasis added].
I'm surprised we're having this discussion, since you're aware of the gap in cognitive ability between African and Euro Americans.
African American parents have worse birth outcomes because they are, on average, lower in cognitive ability and more prone to doing certain unwise things. This is as true for pregnancy as it is for other areas of life. "Life is an IQ test."
In the above study, the authors adjust the data for several risk factors, including education. Yes, educational level correlates with cognitive ability, but the correlation is imperfect (many people go to college who are not really qualified for college, and many of them graduate, even though they should not graduate).
Lol, I've just seen this response now. It's even worse than your other response. No one argues that the difference in birth outcomes is ultimately due to IQ gaps. So you think the ones who have VLBW (very low birth weight) babies did even dumber things than those who have LBW babies?
Secondly, you earlier claimed the paper you cited demonstrates the gap disappears after controls. It did not disappear, in that same paper. So now you're redefining "disappeared" as "it should have disappeared"? Why can't you simply correct your earlier statement to your readers when you find that you may have misread the paper?
You're suggesting the residual difference (in birth weight) between black mother/white father and white mother black father birth outcomes is too little to support Peter Frost's speculation of a female genetic influence through the womb environment?
I am saying if a gap persists with parental black/black, after all said "environmental" controls, and yet this is not directly genetic (given non-persistence in parental black/black immigrants), then persistence in parental black mother/white father, can not implicate direct genetic causation.
Hi. I am no expert in this field, and my sources of learning about it were plebeian. I would be very grateful if you have any references or citations that you could point me to, so I could become better educated on this matter.
Thank you. Those articles look very interesting, and yes, it’s a field. I would like to learn more about. I was thinking about a topic, a little more specific to the genomic variance among humans within Africa. I think there were populations that were cut off from the rest of the continent, for example, the San people in the very southern most tip of Africa who had very little mixing with other groups for most of the last 10,000 years according to articles I found. I suspect on a big continent like Africa, especially bisected by the equator , there would be very uneven selective pressures from factors like malaria leading to selection of hemoglobin variants such as sickle cell, G6PD deficiency thalassemias, Duffy null phenotype, etc. Some of these genetic variances may have significant functional implications based on stamina and health of the various populations.
If I’m understanding the implications of the post correctly—and if biracial individuals born to Black mothers experience worse health outcomes for genetic or biological reasons—then we would expect to see an overrepresentation of those born to White mothers among high achievers too, from sports to academia. That is what we observe. I asked ChatGPT to run the numbers (NBA successful players, High-achieving academics, etx).
However, this overrepresentation appears to have a much simpler explanation.
In the United States, White mother–Black father pairings account for approximately 80% of all Black–White interracial unions. This demographic prevalence naturally produces a far greater number of biracial individuals with White mothers. According to the analysis, roughly 10% to 30% of the observed variance may be due to additional factors—such as cultural or socioeconomic dynamics—but the vast majority stems from this demographic baseline.
In short, the overrepresentation of biracial individuals with White mothers among high achievers is largely a reflection of demographic reality, not necessarily of genetic advantage. I may be missing something, but this seems to contradict the post's approach.
Developmental problems can also arise if a baby is born too late, such as a higher incidence of adolescent obesity. If I'm looking at the big picture (i.e., viability over an entire lifetime, and not just risks at birth), I can't say that one is better than the other.
The following article may be of interest:
"As indicated earlier, few studies have examined how the health of children with white mothers and black fathers compares to that of individuals with black mothers and white fathers. Exceptions are the studies of birth outcomes of black/white biracial children, which indicate that infants with white mothers and black fathers have more favorable outcomes than infants with black mothers and white fathers (Collins and David 1993; Parker 2000). These findings contradict our expectation that children with black mothers and white fathers will be healthier than children with white mothers and black fathers because they grow up in more advantaged households. Whether children with black mothers and white fathers continue to have a health disadvantage relative to children with white mothers and black fathers at older ages and whether this group has disadvantages in other health outcomes remain to be empirically tested."
Choi, K. H., & Reichman, N. E. (2019). The health of biracial children in two-parent families in the United States. Demographic Research, 41, 197-230. https://doi.org/10.4054/DemRes.2019.41.8
Do you mean the health outcomes for the mother or for the children? Younger women have fewer problems during pregnancy. Strangely enough, there is evidence that children born to younger women have shorter lives. This doesn't seem to be simply a fast life history effect:
"Consistent with prior literature, we find that children born to young and old mothers have worse adult health, are shorter, and have higher mortality than those born to mothers aged 25– 34 years. Controls for maternal education and lifespan overlap wipe out the effect for advanced maternal age up to age 45. The association between young maternal age and negative offspring outcomes, however, is robust to these controls."
Myrskylä M, Fenelon A. (2012). Maternal age and offspring adult health: evidence from the health and retirement study. Demography. 49(4):1231-57. https://doi.org/10.1007/s13524-012-0132-x.
Hi Peter, Very interesting post. I have two thoughts.
First, could 'genomic imprinting' (https://en.wikipedia.org/wiki/Genomic_imprinting) explain the diffference in outcomes observed? This is the phenomenon whereby genes are differentially expressed in offspring depending on whether they derive from the mother or the father.
Often paternally expressed genes promote offspring growth in utero at the expense of the mother. Maternal genes counteract this.
However, in hybrid offspring, this balance is often disrupted.
As a consequence, ligers (the hybrid offspring of a male lion and a female tigress) are very large, because the growth promoting paternally expressed genes of the father are not counteracted by maternally expressed genes from the mother. In contrast, tions (hybrid offspring of male tigers and female lionesses) are very small.
I recall reading that this is because in lions, prides of lionesses are regularly taken over by new males. Therefore, it is in the interest of male lions to promote the growth of offspring in the womb to the maximum extent possible, even at a cost to long-term maternal health and fertility, since the male is unlikely to have sexual access to a given lioness or pride of lionesses for a long time, and therefore her future health and fertility is of little concern to him.
In contrast, the mating system of tigers, I am told, tend to be more stable.
Could analogous differences in the mating systems of black Africans and white Europeans, together with genomic imprinting, similarly explain differences in birth weights and other among neonatal outcomes of biracial black-white offspring fathered by black and white women respectively?
___________________
A second idea:
It seems to be accepted that childbirth is especially physically traumatic (and dangerous) among humans because of our large brains, which makes it difficult for women to birth large-brained human offspring. Indeed, it is even suggested that human infants are born relatively prematurely to mitigate this risk (hence the especial helplessness of a newborn baby).
Given that race differences in brain-size are well-documented, and these differences are apparently present from birth, could the differences in neonatal outcomes therefore reflect differences in brain-size as betweeen whites and blacks, and the fact that mothers' reproductive anatomy is designed to birth offspring of her own race?
Thus, Russian author Vladimir Avdeyev, in his book 'Raciology: The Science of the Hereditary Traits of Peoples', claims
“The form of the skull of a child is directly connected with the characteristics of the structure of the mother’s pelvis—they should correspond to each other in the goal of eliminating death in childbirth. The mixing of the races unavoidably leads to this, because the structure of the pelvis of a mother of a different race does not correspond to the shape of the head of [the] mixed infant; that leads to complications during childbirth” (Raciology: p157).
Similarly, Philippe Rushton claimed in the ‘Preface to the Third Edition’ of his book 'Race Evolution and Behavior' claims that one of the reasons that blacks perform so well in sports that involve running is that they have narrower hips, which leads to a “a more efficient stride”, but that “the reason Whites and East Asians have wider hips than Blacks, and so make poorer runners, is because they give birth to larger brained babies” (Race, Evolution and Behavior: p11-12).
Could a mismatch between the reproductive anatomy and pelvises of black mothers and the larger-brained mixed-race offspring they are carrying explain the worse outcomes for black mothers of mixed race offspring? In contrast, white mothers carrying relatively smaller-brained mixed-race offspring presumably wouldn't have this problem.
I'm confused about why you see this as evidence of mismatch. Mismatch would seem to imply that mixed-race babies would have worse outcomes than single race babies of either race. I haven't read all the papers you cited, but based on the evidence you cited and my skimming some of them, it looks like the babies with black and white parents have better outcomes than babies with two black parents. Based on the evidence you cited, it looks like a case where the ancestry composition of the fetus and the race of the mother (either through genetic or environmental effects) both exert additive effects on the outcomes, but not that there is an interaction between the two. In other words, it looks like the model is (Birth Outcomes) = β_0 + β_1*(race of fetus) + β_2*(race of mother) rather than (Birth Outcomes) = β_0 + β_1*(race of fetus) + β_2*(race of mother) + β_3*(race of fetus)*(race of mother). Am I misunderstanding you or missing something? Or is there no evidence of mismatch her, just of the race of the mother having an effect in addition to the race of the fetus?
Other considerations would be extra- nuclear DNA, specifically mitochondrial. As Kimberly Dunham Snary et al point out, mitochondrial – nuclear DNA mismatch matters. Pmcid pmc7238407
I came here to make the same comment.
Did you know that this tracks with IQ deltas as well: children with a white mother and a black father have an eight-point I.Q. advantage over those with a black mother and a white father. Why? Probably for the same reason: status differences. Maybe the same impact here?
Bryan Caplan goes into detail in this very old post, Argument 1: https://www.econlib.org/archives/2007/12/gladwell_on_iq.html
I didn't know that. Can you cite the original study?
I cant but Professor Caplan likely could. Ping him via email, he is very responsive to emails.
There is no such study. This is another example of the game of "telephone." Professor Caplan was citing an article by Malcolm Gladwell, who incorrectly remembered a presentation by James Flynn on race and IQ:
"If I.Q. is innate, it shouldn’t make a difference whether it’s a mixed-race child’s mother or father who is black. But it does: children with a white mother and a black father have an eight-point I.Q. advantage over those with a black mother and a white father." Gladwell, M. (2007). None of the Above. The New Yorker https://www.newyorker.com/magazine/2007/12/17/none-of-the-above
Gladwell's recollection of Flynn's presentation closely matches Flynn's article in American Psychologist. But Flynn made no comparison between BM/WF children and WM/BF children, either in that article or in any other.
Flynn was referring to the Eyferth study of illegitimate children of German mothers by American soldiers:
"The soldiers of the American occupation force in Germany, both White and Black, fathered thousands of children with German women after World War II. Eyferth (see Flynn, 1980) selected a representative sample of 181 Black children and a matching group of 83 White children and found that their mean IQs were virtually identical. In other words, children who had a White father seemed to possess no advantage whatsoever over those who had a Black father." (Flynn, 1999, p. 14)
Flynn, J. R. (1999). Searching for justice: the discovery of IQ gains over time. American Psychologist, 54(1), 5. https://psycnet.apa.org/doi/10.1037/0003-066X.54.1.5
The Eyferth study provides no information on BM/WF children. It also suffers from a number of other shortcomings:
- It was a study of young children. Other studies, notably the Minnesota Transracial Adoption Study, have shown that cognitive ability is much more malleable in children than in adults.
- Algerian soldiers were classified as "Black."
- The US army imposes minimum IQ requirements. This has the effect of narrowing the IQ difference between White and Black soldiers.
Moral of the story: Never, never take a factoid at face value. Ask to see the study that supposedly backs it.
With that said, the logic of the rebuttal still remains: there could be status differences that are hard to measure that are the fundamental reason for the disparity in your premise study as well.
Socioeconomically, BM/WF families are better off than WM/BF families
Interesting...thanks for digging this up. Can you send an email to Bryan Caplan letting him know too? You would be a much better source for the email than me. Maybe he can add addendum to blog post.
Would also be good to get his take on this. He is deep in the studies as well.
I sent the following email to Bryan:
Dear Bryan Caplan,
In one of your posts, you cite a New Yorker article by Malcolm Gladwell, in which he refers to a presentation by James Flynn on race and IQ:
"If I.Q. is innate, it shouldn’t make a difference whether it’s a mixed-race child’s mother or father who is black. But it does: children with a white mother and a black father have an eight-point I.Q. advantage over those with a black mother and a white father."
Gladwell, M. (2007). None of the Above. The New Yorker https://www.newyorker.com/magazine/2007/12/17/none-of-the-above
Gladwell's description of that presentation closely matches Flynn's article in American Psychologist. But Flynn made no comparison between Black mother/White father children and White mother/Black father children, either in that article or in any other.
Gladwell was probably misremembering the following passage, which summarizes the Eyferth study of illegitimate children born to German mothers and fathered by American soldiers :
"The soldiers of the American occupation force in Germany, both White and Black, fathered thousands of children with German women after World War II. Eyferth (see Flynn, 1980) selected a representative sample of 181 Black children and a matching group of 83 White children and found that their mean IQs were virtually identical. In other words, children who had a White father seemed to possess no advantage whatsoever over those who had a Black father." (Flynn, 1999, p. 14)
Flynn, J. R. (1999). Searching for justice: the discovery of IQ gains over time. American Psychologist, 54(1), 5. https://psycnet.apa.org/doi/10.1037/0003-066X.54.1.5
The Eyferth study provides no information on Black mother/White father children, since none of the children were in that category. It also suffers from other shortcomings:
- It was a study of young children. Other studies, notably the Minnesota Transracial Adoption Study, have shown that cognitive ability is much more malleable in children than in adults.
- Algerian soldiers were classified as "Black."
- The US army imposes minimum IQ requirements. This has the effect of narrowing the IQ difference between White and Black soldiers.
Yours sincerely,
Peter Frost
Thanks, would appreciate it if you updated this thread if he responds.
I'm sure someone else has asked this but how does this fit with the concept of hybrid vigour?
In humans, fertility reaches a peak in marriages between 3rd or 4th cousins. "Closer" marriages show inbreeding depression, whereas marriages farther apart show outbreeding depression. See my article on this subject: https://www.aporiamagazine.com/p/outbreeding-depression-avenues-for
Hybrid vigor doesn't exist in our species. It is generally found in species that are developmentally less complex, particularly plants.
I know, I know. "But everybody says ..." Certain ideas gain traction because they are compatible with a certain zeitgeist.
Thank you. A great reply.
It will be interesting to see what these results would be if the births took place in Sub-Saharan Africa.
I'm thinking about two things here
1 - The possible feeling of belonging and community
2 - Environment (weather, amount of sunlight)
It's the same situation in Africa. African mothers give birth earlier than European mothers:
"There is significant variation in the incidence of preterm birth worldwide. The rates of preterm birth in 184 countries in 2010 ranged from 5% in several Northern European countries to 18% in Malawi."
There seems to be a link between the SERPINH1 gene and preterm premature rupture of membranes in women of Sub-Saharan African descent.
Purisch, S. E., & Gyamfi-Bannerman, C. (2017, November). Epidemiology of preterm birth. In Seminars in perinatology (Vol. 41, No. 7, pp. 387-391). WB Saunders. https://doi.org/10.1053/j.semperi.2017.07.009
Good lord. I've spoken to doctors who swear that this (low natal weight) is due to systemic racism.
Excellent article Peter, thank you.
Two questions. How highly is a couple's fertility highly correlated with positive health outcomes? I'm guessing quite high, save maybe for some genetic defects that are latent? This might be too big a question for a discussion section.
Also, gestational surrogacy would avoid the harms you describe in your article. Have you written or thought much about it? Do you think it's scalable in any meaningful way?
Fertility correlates with the biological viability of the embryo or fetus. Only 40-50% of fertilized eggs make it to the blastocyst stage, and an even lower proportion make it all the way to birth (perhaps 30%). So a lot of natural selection occurs before birth.
Yes, there is a correlation between fertility and overall health:
"Our review of the existing literature suggests and association between male factor infertility and somatic health. The literature is consistent in findings that demonstrate higher risk of CVD. Similarly, infertile males appear to be at higher risk of chronic disease regardless of sociodemographic factors. However, the association with cancers varies based on the specific cancer examined and conflicting results exist."
Del Giudice, F., Kasman, A. M., Ferro, M., Sciarra, A., De Berardinis, E., Belladelli, F., ... & Eisenberg, M. L. (2020). Clinical correlation among male infertility and overall male health: a systematic review of the literature. Investigative and Clinical Urology, 61(4), 355. https://doi.org/10.4111/icu.2020.61.4.355
Gestational surrogates tend to come from a low socioeconomic background and thus are more prone to fast life history and early birth. Surrogacy is also expensive. A cheaper option would be to create a special breed of cow for this task.
I predict that the Chinese (or the North Koreans) would be the first to go this route.
Mum's a cow is a disturbing and promising prospect. And it makes sense that some cancers might be more common amongst relatively healthier people. Thanks for the thorough reply and cite.
Interesting article. I wonder if in the future similar analyses can be performed on divergent ethnic groups within the continent of Africa, where the genomic diversity is reported to be the greatest from among human subpopulations. Focus on primarily US populations may be nonrepresentative, since the entire US comprise us such a tiny proportion of the world’s population, but of course we all have to work around the availability heuristic.
I agree with you, but I'm a bit wary of the oft-cited factoid that genomic diversity is highest in Africa. Modern humans have lived longer in Africa than anywhere else, so they have accumulated a lot more "junk" variability over a longer time. I'm not convinced that African populations have more functional variability that has real-life consequences.
The African groups from whom African Americans descend comprise 85% percent of Africa's population. The very divergent groups in Africa are small populations that don't really have descendants outside of Africa. A U.S. African American is a good proxy, although with notable European ancestry.
Look into racial differences in pelvic opening diameter. There is something there.
White are consistently larger diameter than black, somewhat expected for accomodating larger head circumference and larger birth size.
Please see the research cited and discussed at: https://vitamindstopscovid.info/00-evi/.
African Americans generally have lower circulating 25-hydroxyvitamin D levels than White Americans, since their much darker skin absorbs more of the ultraviolet-B light which breaks a bond in a carbon ring of 7-dehydrocholesterol, transforming it into vitamin D3 cholecalciferol. 25-hydroxyvitamin D calcifediol (AKA "calcidiol") is made, primarily in the liver when ingested or UV-B >> skin produced vitamin D3 is hydroxylated on the 25th carbon. This 25-hydroxyvitamin D, circulating in the bloodstream is what is measured in "vitamin D" blood tests.
The kidneys need a level (concentration) of about 20 ng/mL = 50 nmol/L to play their role in regulating calcium-phosphate-bone metabolism, and governments and many doctors are happy with this. However, 50 ng/mL (125 nmol/L = 1 part in 20,000,000 by mass) is required for the proper function of the immune system. Most medical professionals and immunologists do not know this.
Many types of immune cell and some other cell types need a good supply of 25-hydroxyvitamin D to run their intracrine (inside each cell) and paracrine (to nearby cells) signaling systems, which are crucial to each cell's ability to adapt its behavior in response to its changing circumstances. These signaling systems are not known to most medical professionals and immunologists. For a tutorial and links to research: https://vitamindstopscovid.info/02-intracrine/.
These signaling systems are not related to hormonal (endocrine) signaling, which involves a signaling molecule being carried in the bloodstream, and potentially the cerebrospinal fluid, with the level of this affecting the behavior of one or more cell types all over the body.
Vitamin D3 and 25-hydroxyvitamin D do not function as hormones. They are not signaling molecules. A third compound, 1,25-dihydroxyvitamin D calcitriol functions as a hormone when the kidneys release it into the bloodstream. This is the sole hormonal function of these three compounds.
In 25-hydroxyvitamin D to calcitriol intracrine signaling, the intracellularly produced calcitriol functions as an intracrine agent, binding to "vitamin D" receptor molecules (really the "calcitriol receptor" molecules) which leads to changes in gene transcription in the nucleus, altering the cell's protein synthesis and so its behavior. Here, calcitriol is acting as an intracrine agent. This production of calcitriol in a cell is only enabled once a cell-type specific condition is detected. The changes in gene expression, and so the changes in cell behavior, also vary from one cell type to the next. Calcitriol as a paracrine agent when intracellularly produced calcitriol diffuses to nearby cells, at local levels well above the 0.05 to 0.1 ng/mL (kidney produced) hormonal background level, affecting nearby cells, also in cell-type specific ways.
This mini-tutorial should help everyone understand how important it is to maintain at least 50 ng/mL circulating 25-hydroxyvitamin D. This is generally only possible with vitamin D3 supplementation in quantities, which while small, are 5 or more times what governments and many doctors recommend.
It is common for people with dark or black skin, living far from the equator, to have significantly less circulating 25-hydroxyvitamin D than white-skinned people living alongside them - and the average levels for white-skinned people who do not supplement vitamin D3 and who have not recently had extensive UV-B skin exposure (which damages DNA and so raises the risk of skin cancer) are 15 to 25 ng/mL.
Low 25-hydroxyvitamin D increases the risk of preeclampsia, pre-term birth, sepsis and the later development of autism, ADHD, intellectual disability and schizophrenia in children https://vitamindstopscovid.info/00-evi/#3.2. Likewise neurodegeneration in later life: https://vitamindstopscovid.info/00-evi/#3.3.
There may well be genetic reasons for African American women giving birth on average a week earlier than White women. However, some component of the observed difference would be due to their generally lower 25-hydroxyvitamin D levels.
All this can and should be corrected. See the vitamin D3 supplementation recommendations from New Jersey based Professor of Medicine, Sunil Wimalawansa, according to body weight and obesity status: https://vitamindstopscovid.info/00-evi/#00-how-much.
Vitamin D levels are low not only in African Americans but also in other dark-skinned humans. These human groups appear to have adapted accordingly by using this vitamin more efficiently. The following is an excerpt from one of my published articles:
A single UVB exposure produces less vitamin D3 in black subjects than in whites. The difference narrows, however, after liver hydroxylation to 25(OH)D and disappears after kidney hydroxylation to 1,25(OH)2D. The most active form of vitamin D is thereby kept at a constant level regardless of skin color. This may be why nearly half of African Americans are classified as vitamin-D deficient and yet few show signs of calcium deficiency. In fact, this population has less osteoporosis, fewer fractures, and a higher bone mineral density than do Euro-Americans, who generally produce and ingest more vitamin D. The same apparent contradiction emerges from a survey of East African immigrant children in Australia. None had rickets despite very low serum 25(OH)D, with 87% of them having less than 50 nmol/L and 44% less than 25 nmol/L.
These levels are apparently lower for genetic reasons. A study of African Americans found that serum 25(OH)D decreased linearly with increasing African ancestry, the decrease being 2.5-2.75 nmol/L per 10% increase in African ancestry. The study also found that sunlight and diet were 46% less effective in raising these levels among subjects with high African ancestry than among those with low/medium African ancestry.
There have been proposals to target African Americans for vitamin D supplementation, and similar proposals have been made for the Inuit of northern Canada. These proposals, though well-intentioned, may have disastrous effects on both populations. Unlike vitamin D, vitamin D is not water-soluble. If you take too much, you will not excrete it in your urine.
Frost P. (2022) The Problem of Vitamin D Scarcity: Cultural and Genetic Solutions by Indigenous Arctic and Tropical Peoples. Nutrients 14(19):4071. https://doi.org/10.3390/nu14194071
Hi Peter, Thanks very much for your reply and for your article in Nutrients, which is among the most interesting vitamin D articles I have ever read.
It would take me days to chase up the research you cite and respond properly. If and when I do, I will write to you and will also post the response to the Nutrition for Immune System Health email discussion list: https://nish.groups.io. You and anyone else seriously interested in such research are invited to join us. This is a high signal-to-noise ratio discussion group. It is not particularly busy, but everything is civil and constructive. Members include leading vitamin D researchers. We discuss vitamin D most frequently, with magnesium probably second.
It is not hard for the kidneys to maintain a very low level of circulating 1,25-dihydroxyvitamin D as a hormone to affect multiple cell types which are involved in calcium-phosphate-bone metabolism. The levels are typically 0.05 to 0.1 ng/mL (x 2.5 for nmol/L). For Europeans, they can do this quite well with 20 ng/mL (50 nmol/L) circulating 25-hydroxyvitamin D (25(OH)D).
I have not studied it, but I recall that the relevant kidney cells have an active transport system bringing 25(OH)D across their cell membrane, and that this involves transporting 25(OH)D when it is bound to the "vitamin D" binding protein DBP. This means it can raise the intracellular level higher than the total level in the bloodstream, but I am not sure what these cells' intracellular level is, or whether this can be measured.
As far as I know, 25(OH)D entry into all other cell types is from passive diffusion through the cell membrane, of the individual, unbound, molecules, from the bloodstream or from whatever fluid the cells are bathed in, such as CSF, where, as far as I know, the 25(OH)D is not bound strongly to DBP or less strongly to albumin proteins in general (VDR is a specialised albumin protein).
As far as I know, there is uncertainty and debate about the level of intracellular 25(OH)D in immune cells which require it as a raw material for intracrine and/or paracrine signaling. See my attempt at a full tutorial, since no-one else has written one: https://vitamindstopscovid.info/02-intracrine/.
Since most 25(OH)D in the bloodstream is strongly bound to VDR, does the diffusion of 25(OH)D - which must be from the small fraction which is unbound to both VDR and albumin proteins, into the extracellular fluid of tissues in general, and/or passively through the cell membranes of cells such as immune cells - result in an intracellular level which is very much lower than the total level in the bloodstream? Specifically, is the intracellular level of 25(OH)D in immune cells a small fraction of the total level? I guess it is, but I am not sure what the best research shows.
As far as I know, there is no mechanism for measuring this level in individual cells. Perhaps if a sufficient volume of them could be isolated from other cell types and the extracellular fluid, they could be lysed and the collected cytosol fluid carefully analysed. I have not read of this being done, but there is a vast amount of vitamin D research, and it would be a full time job trying to keep up with it.
While your article argues and cites research which indicates African Americans do quite well with bone density, despite their low 25(OH)D levels, you do not mention the well known terrible outcomes in numerous other immune system related conditions for African Americans with respect to those of White Americans - and White Americans would do much better if their 25(OH)D levels were at least the 50 ng/mL (125 nmol/L) their immune system needs to function properly.
This 50 ng/mL threshold is not widely known, but it is very clear, at least for immune responses to the largely bacterial pathogens which cause post-operative infections. This research needs to be very widely understood. Please see the graph, links and discussion at: https://vitamindstopscovid.info/00-evi/#00-50ngmL . The two graphs at the end of the PDF (they are not on the HTML page) of Quraishi et al. 2013/4 are the most important graphs I have ever seen for human health: https://jamanetwork.com/journals/jamasurgery/articlepdf/1782085/soi130062.pdf.
You mention that DBP is used for transporting "vitamin D". It is best to refer to the three compounds by their specific names, rather than consider them all "vitamin D". See: Reinhold Vieth 2004: https://sci-hub.se/10.1016/j.jsbmb.2004.03.037 and https://vitamindstopscovid.info/02-intracrine/#2004-vieth.
The bloodstream is perfectly capable of transporting 25(OH)D by it being dissolved in the plasma. A healthy concentration (level) is 50 ng/mL = 1 part in 20,000,000 by mass, which is surely nowhere near saturation level.
I (and I think researchers in general) regard DBP as being concerned with long-term storage of 25(OH)D, rather than transport. The more DBP there is in the plasma, and the greater its affinity for 25(OH)D, the less free 25(OH)D is in solution and so available (as best I understand it) to diffuse into cells such as the many types of immune cell which need it as raw material from which to run their 25(OH)D to calcitriol intracrine and paracrine signaling systems.
If, as you wrote, Africans have more DBP and that DBP binds more strongly to 25(OH)D, then this might be explained by several mechanisms, including:
1 - This helps the relevant kidney cells' active transport system which brings 25(OH)D into their cytosols.
2 - The need for longer term storage, so total 25(OH)D in the bloodstream lasts longer when there is little supply of vitamin D3 cholecalciferol to replenish it. (About 1/4 of ingested or UV-B produced vitamin D3 goes into circulation as 25(OH)D after hydroxylation, primarily in the liver.) This would help the person ride out the monsoon.
However, this - as far as I know - greater proportion of circulating 25(OH)D being tightly bound to DBP would make it harder for immune cells to get the intracellular 25(OH)D they need to function properly.
Your article argues against vitamin D3 supplementation for African Americans, Inuits and other populations, I think including Africans in Africa. However, African Americans suffer disproportionately from a vast range of illnesses - including dementia, autoimmune disorders, severe COVID-19 and sepsis - which would be greatly reduced if they had higher 25(OH)D levels.
Luxwolda et al. 2012 https://doi.org/10.1017/S0007114511007161 is the only research article I have ever heard of which reports 25(OH)D levels in traditionally living Africans - the people in the modern world who are most like the Africans of 50k years ago or more, who we all descended from. 50,000 years is only 2000 generations - a very short time for the evolution of fundamental changes to immune system intracellular signaling which might cope better with circulating 25(OH)D levels much lower than 50 ng/mL. So I tend to assume that all modern humans are running an immune system which coped OK with ca. 50 ng/mL levels in recent ancestral history, and which cannot work well with todays levels, which are often half, to one tenth, of this.
The lack of active transport of 25(OH)D into immune cells and the massive evidence of ill-health resulting directly from the further the 25(OH)D level is below 50 ng/mL (125 nmol/L) are arguments that the healthy state of humans, including Africans, is to have 50 ng/mL or more circulating 25(OH)D.
Luxwolda et al. don't report a majority of their subjects having more than 50 ng/mL circulating 25(OH)D, but the levels they found are much closer to this than the levels you cite in African Americans today.
"We measured the sum of serum 25-hydroxyvitamin D2 and D3 (25(OH)D) concentrations of thirty-five pastoral Maasai (34 (sd 10) years, 43 % male) and twenty-five Hadzabe hunter–gatherers (35 (sd 12) years, 84 % male) living in Tanzania. They have skin type VI, have a moderate degree of clothing, spend the major part of the day outdoors, but avoid direct exposure to sunlight when possible."
The average 25(OH)D level was 115 nmol/L = 46 ng/mL.
I made a histogram from their data, which I think has never been done before. The grey bars https://vitamindstopscovid.info/00-evi/1-Dror-Israel-14-framed.png depict much higher levels than the levels in sunny Israel for ordinary Israelis (the levels for Arab women are disastrously low).
Those very low levels for Arab men and women in Israel are about the same as those you report for present day African Americans who apparently have very healthy calcium-phosphate-bone metabolism. Those same African Americans have very poor health outcomes, I am sure, as a result of their 25(OH)D levels being so low with respect to (1) white levels, (2) the Luxwolda et al. African levels and (3) 50 ng/mL (125 nmol/L).
Ideally, one or more long-time vitamin D researchers would respond to your most interesting article, arguing to the contrary - that African Americans and Inuit would benefit from vitamin D3 supplementation to attain 50 ng/mL or more 25(OH)D.
I am an electronic technician with no articles published in this field, though I co-wrote a Letter, which can't be cited as if it was a peer-reviewed article. Ideally I would have time to do this, with one or more long-term vitamin D researchers. They are busy too!
Thanks again for your most interesting article.
"As far as I know, 25(OH)D entry into all other cell types is from passive diffusion through the cell membrane"
Are you sure about this point? Some human populations seem to use 25(OH)D more efficiently and more sparingly than others. An obvious means to this end would be to have more receptors that can bind to the molecule and bring it into the target tissues. I would expect to see this kind of active transport in a wide range of tissues, and not just in kidney cells.
Differences in immune response between African and Euro Americans have been attributed to differences in certain genetic variants, see:
Ogony, J. W., Radisky, D. C., Ruddy, K. J., Goodison, S., Wickland, D. P., Egan, K. M., ... & Sherman, M. E. Immune Responses and Risk of Triple-negative Breast Cancer: Implications for Higher Rates among African American Women. Cancer Prev Res (Phila) (2020) 13 (11): 901–910. https://doi.org/10.1158/1940-6207.CAPR-19-0562
The Luxwolda study is interesting. Since the Maasai and Hadzabe live at the Equator, enough UV light may enter their skin despite their high level of melanin.
Nonsense.
Firstly, you seem unaware of studies showing that *recent* black African immigrant mothers have much better birth outcomes (closer to white). Contradicts your conclusion.
Secondly, you wrote "Moreover, if the cause is some unknown factor in the environment of Black mothers, why did it remain unchanged between 1978 and 1997? That period saw considerable social and economic gains for Black women, particularly those in interracial relationships."
Your first sentence mentions "UNKNOWN" factor(s) in the environment, but your next sentence claims its refutation as if it is KNOWN (social and economic...) If it is "unknown," how do you know it has anything to do with "social and economic" factors (and even specifically ones that remained unchanged in that period)?
Oh come on, don't start your sentence with “Nonsense”, how do you expect the conversation to go from there.
That said, “recent African immigrant mothers” aren't a monolith - we have mothers who come to the US to study and tend to be from relatively privileged backgrounds.
We also have others. It'll be interesting to know if the “better outcomes” you refer to is the same between both populations (I suspect the researchers might not separate them).
It's pretty well proven by now that parental welfare is a good predictor of children's welfare
You really don't think it occurred to the researchers over the decades to make that distinction that occurred to you in 3 seconds?
Peter Frost is an anthropologist, so yes, I do believe he probably has this question in mind. Does he have the data to answer the question? No idea. Does he feel safe asking it? No idea either.
Research carried out on black populations is:
1 - Sorely needed
2 - A dangerous game for white researchers to play in the west. The "racism" accusations fly fast and furiously whenever this topic is broached.
I find it hard to blame the researcher if they choose not to speculate on ideas that potentially may be dangerous to their livelihoods and well-being. It's a damned if you do, damned if you don't scenario for them.
I trust that you're also doing similar (and unbiased) research that can throw some more light on these questions that we all ask.
Here's one article I recently read by ToveK, who's an African as well, based on the topic of the post, I believe also involved in some research.
https://open.substack.com/pub/woodfromeden/p/guest-post-the-global-iq-debate-a?r=600lf&utm_campaign=post&utm_medium=web
It's good to hear from you Chanda! I belong to your fan club.
There is no genetic mismatch if both parents are African. Problems arise only if one parent is African and the other is European. In such a case, inconsistencies can develop between the genetic programming of the womb and the genetic programming of the fetus.
The word "if" implies a hypothesis. Personally, I don't believe the cause is unknown. It seems to be genetic, and we may have actually identified the genes in question. Please read my article to the end.
Hold on one second... The bad birth outcomes are there for black Americans even without black and white parents. Black-black American parents are still much worse than black-black African immigrant parents. Which says something else is going on.
But your ("genetic mismatch") claim can still be tested empirically. What's your prediction 1. if both parents are mixed race (both parents are like Obama), is that still a genetic mismatch? Equal to just black and white parents? 2. Does your claim predict that a recent black immigrant mother will have bad birth outcomes if she marries a white American?
As for your "if" statement, yes: I know you were not personally saying it is unknown. But you do not counter a statement saying it's unknown by giving a refutation that assumes it's known.
[Edit: And good to see you too, Peter!]
We're not communicating on the same wavelength. I'm talking about the difference in birth outcomes between Black mother/White father couples and White mother/Black father couples. This difference remains even when we control for a wide range of socioeconomic variables.
You're talking about the difference in birth outcomes between Black American couples and White American couples. That difference will disappear when we control for even a small number of socioeconomic variables.
Yes I know what you're talking about, and I am trying to show you that the gap is persistent in black parents in a way that undermines your explanation for the interracial pattern.
You write "the difference will disappear when we control for even a small number of socioeconomic variables." And I say NO, it won't. It reduces (obviously), but does not "disappear." This is a well-established puzzle in the field.
This is what the paper you cited in your article, to show this "disappearance," actually says:
"Results
For both very low and moderately low birth weight infants, the unadjusted risk associated with parental race showed a gradient of risk, from highest to lowest, for black mother/black father, black mother/white father, white mother/black father, and white mother/white father parents. After adjusting for other risk factors, the odds ratio associated with black mother/black father parents was reduced from 3.37 to 1.73 for very low birth weight infants and from 2.51 to 1.60 for moderately low birth weight infants, BUT BOTH REMAINED ELEVATED." [Emphasis added].
https://journals.lww.com/greenjournal/abstract/1998/11000/risk_of_low_birth_weight_infants_among_black_and.15.aspx
I'm surprised we're having this discussion, since you're aware of the gap in cognitive ability between African and Euro Americans.
African American parents have worse birth outcomes because they are, on average, lower in cognitive ability and more prone to doing certain unwise things. This is as true for pregnancy as it is for other areas of life. "Life is an IQ test."
In the above study, the authors adjust the data for several risk factors, including education. Yes, educational level correlates with cognitive ability, but the correlation is imperfect (many people go to college who are not really qualified for college, and many of them graduate, even though they should not graduate).
Lol, I've just seen this response now. It's even worse than your other response. No one argues that the difference in birth outcomes is ultimately due to IQ gaps. So you think the ones who have VLBW (very low birth weight) babies did even dumber things than those who have LBW babies?
Secondly, you earlier claimed the paper you cited demonstrates the gap disappears after controls. It did not disappear, in that same paper. So now you're redefining "disappeared" as "it should have disappeared"? Why can't you simply correct your earlier statement to your readers when you find that you may have misread the paper?
You're suggesting the residual difference (in birth weight) between black mother/white father and white mother black father birth outcomes is too little to support Peter Frost's speculation of a female genetic influence through the womb environment?
I am saying if a gap persists with parental black/black, after all said "environmental" controls, and yet this is not directly genetic (given non-persistence in parental black/black immigrants), then persistence in parental black mother/white father, can not implicate direct genetic causation.
Hi. I am no expert in this field, and my sources of learning about it were plebeian. I would be very grateful if you have any references or citations that you could point me to, so I could become better educated on this matter.
By "this field," do you mean life history theory? Good articles can be found at:
https://scholar.google.com/scholar?cluster=6022679337275064043&
https://scholar.google.com/scholar?cluster=2776309909645044449&hl=fr&as_sdt=0,5
(just click on one that has a PDF)
Thank you. Those articles look very interesting, and yes, it’s a field. I would like to learn more about. I was thinking about a topic, a little more specific to the genomic variance among humans within Africa. I think there were populations that were cut off from the rest of the continent, for example, the San people in the very southern most tip of Africa who had very little mixing with other groups for most of the last 10,000 years according to articles I found. I suspect on a big continent like Africa, especially bisected by the equator , there would be very uneven selective pressures from factors like malaria leading to selection of hemoglobin variants such as sickle cell, G6PD deficiency thalassemias, Duffy null phenotype, etc. Some of these genetic variances may have significant functional implications based on stamina and health of the various populations.
Great article, many claims for referencing.
If I’m understanding the implications of the post correctly—and if biracial individuals born to Black mothers experience worse health outcomes for genetic or biological reasons—then we would expect to see an overrepresentation of those born to White mothers among high achievers too, from sports to academia. That is what we observe. I asked ChatGPT to run the numbers (NBA successful players, High-achieving academics, etx).
However, this overrepresentation appears to have a much simpler explanation.
In the United States, White mother–Black father pairings account for approximately 80% of all Black–White interracial unions. This demographic prevalence naturally produces a far greater number of biracial individuals with White mothers. According to the analysis, roughly 10% to 30% of the observed variance may be due to additional factors—such as cultural or socioeconomic dynamics—but the vast majority stems from this demographic baseline.
In short, the overrepresentation of biracial individuals with White mothers among high achievers is largely a reflection of demographic reality, not necessarily of genetic advantage. I may be missing something, but this seems to contradict the post's approach.
Well, "overrepresentation" does not mean "majority" -- not even "vast majority." But neither does it require a genetic causation.
This is why we try to rule out alternative causes, notably by controlling for socioeconomic factors.
Developmental problems can also arise if a baby is born too late, such as a higher incidence of adolescent obesity. If I'm looking at the big picture (i.e., viability over an entire lifetime, and not just risks at birth), I can't say that one is better than the other.
The following article may be of interest:
"As indicated earlier, few studies have examined how the health of children with white mothers and black fathers compares to that of individuals with black mothers and white fathers. Exceptions are the studies of birth outcomes of black/white biracial children, which indicate that infants with white mothers and black fathers have more favorable outcomes than infants with black mothers and white fathers (Collins and David 1993; Parker 2000). These findings contradict our expectation that children with black mothers and white fathers will be healthier than children with white mothers and black fathers because they grow up in more advantaged households. Whether children with black mothers and white fathers continue to have a health disadvantage relative to children with white mothers and black fathers at older ages and whether this group has disadvantages in other health outcomes remain to be empirically tested."
Choi, K. H., & Reichman, N. E. (2019). The health of biracial children in two-parent families in the United States. Demographic Research, 41, 197-230. https://doi.org/10.4054/DemRes.2019.41.8
As racial demographics, are there general disparities in health outcomes among young mother aged women?
Do you mean the health outcomes for the mother or for the children? Younger women have fewer problems during pregnancy. Strangely enough, there is evidence that children born to younger women have shorter lives. This doesn't seem to be simply a fast life history effect:
"Consistent with prior literature, we find that children born to young and old mothers have worse adult health, are shorter, and have higher mortality than those born to mothers aged 25– 34 years. Controls for maternal education and lifespan overlap wipe out the effect for advanced maternal age up to age 45. The association between young maternal age and negative offspring outcomes, however, is robust to these controls."
Myrskylä M, Fenelon A. (2012). Maternal age and offspring adult health: evidence from the health and retirement study. Demography. 49(4):1231-57. https://doi.org/10.1007/s13524-012-0132-x.
Hi Peter, Very interesting post. I have two thoughts.
First, could 'genomic imprinting' (https://en.wikipedia.org/wiki/Genomic_imprinting) explain the diffference in outcomes observed? This is the phenomenon whereby genes are differentially expressed in offspring depending on whether they derive from the mother or the father.
Often paternally expressed genes promote offspring growth in utero at the expense of the mother. Maternal genes counteract this.
However, in hybrid offspring, this balance is often disrupted.
As a consequence, ligers (the hybrid offspring of a male lion and a female tigress) are very large, because the growth promoting paternally expressed genes of the father are not counteracted by maternally expressed genes from the mother. In contrast, tions (hybrid offspring of male tigers and female lionesses) are very small.
I recall reading that this is because in lions, prides of lionesses are regularly taken over by new males. Therefore, it is in the interest of male lions to promote the growth of offspring in the womb to the maximum extent possible, even at a cost to long-term maternal health and fertility, since the male is unlikely to have sexual access to a given lioness or pride of lionesses for a long time, and therefore her future health and fertility is of little concern to him.
In contrast, the mating system of tigers, I am told, tend to be more stable.
Could analogous differences in the mating systems of black Africans and white Europeans, together with genomic imprinting, similarly explain differences in birth weights and other among neonatal outcomes of biracial black-white offspring fathered by black and white women respectively?
___________________
A second idea:
It seems to be accepted that childbirth is especially physically traumatic (and dangerous) among humans because of our large brains, which makes it difficult for women to birth large-brained human offspring. Indeed, it is even suggested that human infants are born relatively prematurely to mitigate this risk (hence the especial helplessness of a newborn baby).
Given that race differences in brain-size are well-documented, and these differences are apparently present from birth, could the differences in neonatal outcomes therefore reflect differences in brain-size as betweeen whites and blacks, and the fact that mothers' reproductive anatomy is designed to birth offspring of her own race?
Thus, Russian author Vladimir Avdeyev, in his book 'Raciology: The Science of the Hereditary Traits of Peoples', claims
“The form of the skull of a child is directly connected with the characteristics of the structure of the mother’s pelvis—they should correspond to each other in the goal of eliminating death in childbirth. The mixing of the races unavoidably leads to this, because the structure of the pelvis of a mother of a different race does not correspond to the shape of the head of [the] mixed infant; that leads to complications during childbirth” (Raciology: p157).
Similarly, Philippe Rushton claimed in the ‘Preface to the Third Edition’ of his book 'Race Evolution and Behavior' claims that one of the reasons that blacks perform so well in sports that involve running is that they have narrower hips, which leads to a “a more efficient stride”, but that “the reason Whites and East Asians have wider hips than Blacks, and so make poorer runners, is because they give birth to larger brained babies” (Race, Evolution and Behavior: p11-12).
Could a mismatch between the reproductive anatomy and pelvises of black mothers and the larger-brained mixed-race offspring they are carrying explain the worse outcomes for black mothers of mixed race offspring? In contrast, white mothers carrying relatively smaller-brained mixed-race offspring presumably wouldn't have this problem.
I'm confused about why you see this as evidence of mismatch. Mismatch would seem to imply that mixed-race babies would have worse outcomes than single race babies of either race. I haven't read all the papers you cited, but based on the evidence you cited and my skimming some of them, it looks like the babies with black and white parents have better outcomes than babies with two black parents. Based on the evidence you cited, it looks like a case where the ancestry composition of the fetus and the race of the mother (either through genetic or environmental effects) both exert additive effects on the outcomes, but not that there is an interaction between the two. In other words, it looks like the model is (Birth Outcomes) = β_0 + β_1*(race of fetus) + β_2*(race of mother) rather than (Birth Outcomes) = β_0 + β_1*(race of fetus) + β_2*(race of mother) + β_3*(race of fetus)*(race of mother). Am I misunderstanding you or missing something? Or is there no evidence of mismatch her, just of the race of the mother having an effect in addition to the race of the fetus?
White women bake their half castes for longer and sacrifice their whole lives for them.