“Toward a Unified Theory of Black America“ is an interesting NY Times Magazine article by Stephen J. Dubner, co-author of Steven D. Levitt’s Freakonomics, about one of Levitt’s research partners, an ambitious 27-year-old Harvard economist named Roland G. Fryer Jr.
When he presents a paper, Fryer is earnest and genial and excitable, sometimes carrying on like a Southern preacher. While he denies that his work is united by a grand thesis — he is a scientist, he explains, devoted to squeezing truths from the data, wherever that may lead — he does admit to having a mission: ”I basically want to figure out where blacks went wrong. One could rattle off all the statistics about blacks not doing so well. You can look at the black-white differential in out-of-wedlock births or infant mortality or life expectancy. Blacks are the worst-performing ethnic group on SAT’s. Blacks earn less than whites. They are still just not doing well, period.”
To Fryer, the language of economics, a field proud of its coldblooded rationalism, is ideally suited for otherwise volatile conversations. ”I want to have an honest discussion about race in a time and a place where I don’t think we can,” he says. ”Blacks and whites are both to blame. As soon as you say something like, ‘Well, could the black-white test-score gap be genetics?’ everybody gets tensed up. But why shouldn’t that be on the table?”
Fryer said this several months ago, which was well before Lawrence H. Summers, the president of Harvard, wondered aloud if genetics might help explain why women are so underrepresented in the sciences. Summers — who is also an economist and a fan of Fryer’s work — is still being punished for his musings. There is a key difference, of course: Summers is not a woman; Fryer is black.
Fryer grew up in a bad environment:
How many of his close family members, I asked him, had either died young or spent time in prison? He did a quick count: 8 of 10. ”Suppose you can separate people into two camps: geneticists and environmentalists,” he said. ”Coming up where I came up, it’s hard not to be an environmentalist.”
But then Dubner takes the young professor to reunite with his estranged father (a Xerox salesman who went to prison for rape) and estranged mother (a singer).
Fryer finds out that his father had been a high school math teacher, and that his mother’s family had been big wheels in Tulsa’s famously prosperous black community. His maternal grandmother had studied classical music at the Julliard Academy.
Later that night, over Scotch and soda at an airport hotel in Tulsa, Fryer sifted through the discoveries of his trip. He hadn’t known that his father was a math teacher. He hadn’t known that so much accomplishment ran in his mother’s family. ”I used to consider myself a genetic aberration or maybe an impostor,” he said. ”But I actually have some pretty good genes.”
Unfortunately, what passes for fresh new ideas in economics these days are rather stale. For example, Fryer is trying to revive Clarence E. Grim’s 1987 salt sensitivity-slave ship theory:
Fryer well appreciates that he can raise questions that most white scholars wouldn’t dare. His collaborators, most of whom are white, appreciate this, too. ”Absolutely, there’s an insulation effect,” says the Harvard economist Edward L. Glaeser. ”There’s no question that working with Roland is somewhat liberating.”
Glaeser and Fryer, along with David M. Cutler, another Harvard economist, are the authors of a paper that traffics in one form of genetic theorizing. It addresses the six-year disparity in life expectancy for blacks versus whites, arguing that much of the gap is due to a single factor: a higher rate of salt sensitivity among African-Americans, which leads to higher rates of cardiovascular disease, stroke and kidney disease.
Fryer’s notion that there might be a genetic predisposition at work was heightened when he came across a period illustration that seemed to show a slave trader in Africa licking the face of a prospective slave. The ocean voyage from Africa to America was so gruesome that as many as 15 percent of the Africans died en route, mainly from illnesses that led to dehydration. A person with a higher capacity for salt retention might also retain more water and thus increase his chance of surviving. So it may have been that a slave trader would try to select, with a lick to the cheek, the ”saltier” Africans. Whether selected by the slavers or by nature, the Africans who did manage to survive the voyage — and who then formed the gene pool of modern African-Americans — may have been disproportionately marked by hypertension. Cutler, a pre-eminent health economist, admits that he thought Fryer’s idea was ”absolutely crazy” at first. (Although the link between the slave trade and hypertension had been raised in medical literature, even Cutler wasn’t aware of it.) But once they started looking at the data, the theory began to seem plausible.
Economists know almost nothing about evolutionary genetics (Paul Krugman is an honorable exception), so it’s not surprising that they’d trip over this molehill and ignore the mountain. It’s not implausible that there would be a Darwinian effect in the theorized direction, but it seems unpromising to focus on a unique selection pressure experienced for just one generation and ignore the relentless selection pressure on the countless generations of Africans in Africa. Peoples who have been evolving for hundreds of generations in sweaty tropical climates handle salt differently than peoples who have been evolving in cool climates.
Greg Cochran told me:
The reason it wouldn’t have an important effect is that you don’t get a lot of genetic change in one generation unless you try _really_ hard. If they lost the bottom 15% of the people (in terms of salt retention) during the Middle Passage, a cutoff of about one std below average, the increase in salt retention would be about a tenth or so of a standard deviation, assuming a narrow-sense heritability of 50%. You’d never notice the difference. [And, of course, genetic differences in salt retention didn’t cause all the deaths in the Middle Passage, so this estimate is optimistic.]
But there is a real difference in salt retention between Africans and non-Africans, and it may well have something to do with cardiovascular problems (although other differences like an increased tendency to inflammation may be as important). It’s been around for a long, long time. See the following account, based on a recent article in The American Journal of Human Genetics:
Here’s the press release from the U. of Chicago about the article about Africans’ tendency to retain salt:
Researchers at the University have found genetic evidence to support the sodium-retention hypothesis, a controversial 30-year-old theory that the high rate of hypertension in certain ethnic groups is caused, in part, by an inherited tendency to retain salt.
In the online edition of the December  issue of the American Journal of Human Genetics, the researchers show that the frequency of one version of a gene that is crucial to salt retention correlates with distance from the equator.
Populations that live in hot, humid climates near the equator tend to have the normal version of that gene, which produces a very effective protein. Populations that adapted to cooler climates tend to have a mutant gene that codes for a totally dysfunctional protein.
“The surprise,” said study author Anna Di Rienzo, Associate Professor in Human Genetics, “was finding that as populations moved away from the tropics, the original or normal version of the gene became less and less common and the ‘broken’ version more frequent, which suggests it is protective. There seems to be a strong selective advantage conferred by the non-functioning protein, and that advantage increases with latitude.
“This could change the way we look for disease genes,” she added. “Historically, we have searched for mutations, altered or damaged versions of genes that cause rare disorders, like cystic fibrosis or phenylketonuria. Now, we are starting to look for common genes that may have been beneficial in an environment of scarcity, but have become harmful in a world of plenty. In the modern setting, it may often be the genes that aren’t damaged that predispose to disease, such as the ‘thrifty genes’ associated with type 2 diabetes.”
Humans need salt, sodium chloride, to transport nutrients, transmit nerve impulses or contract muscles, such as the beating heart. The average adult contains about 250 grams of salt, enough to fill three small salt shakers. This salt is constantly lost through sweat and urine and replaced through the diet.
Salt is now “so common, so easy to obtain and so inexpensive,” according to Mark Kurlansky, author of a recent history of salt, “that we have forgotten that from the beginning of civilization until about 100 years ago, salt was one of the most sought-after commodities in human history.”
In the sub-Saharan African regions where humans first appeared, available salt must have been limited and quickly lost through sweat. People who were better at retaining salt may have had a significant survival advantage.
This advantage decreased as humans spread to cooler climates…
Too much salt has become the norm. Despite a recommended daily allowance of less than six grams of salt, the average American consumes about 10 grams daily.
Since 1972, a series of studies has attempted to connect excess salt intake to high blood pressure, but that connection remains uncertain. But Di Rienzo’s team of evolutionary biologists took a different approach, looking at the genetics of salt processing. They focused on a gene called CYP3A5, part of a family known as cytochrome P450 genes, which help the body break down and eliminate a wide range of compounds, including many drugs and salt.
In the kidney, CYP3A5 acts to retain salt. One version of this gene, however, a mutation known as CYP3A5 *3, produces a truncated, non-functional protein.
The researchers looked at variations of this gene in 1,064 individuals drawn from 52 populations scattered around the world. The mutation was least common in some natives of sub-Saharan Africa, ranging from a low of only 6 percent of Yorubans in Nigeria (Latitude 8ºN) to 31 percent among the Mandenka of Senegal (12ºN). Rates were higher among populations in East Asia, ranging from 55 percent among the Dai of China (21ºN) to 75 percent among Han Chinese (32ºN) to 77 percent among Japanese (38ºN) and 95 percent among the Uygur of China (44ºN).
Rates in Europe were uniformly high, ranging from 80 to 95 percent in Italy, France and Russia. The highest rate, 96 percent, was found among the Basque, an isolated ethnic group of uncertain origins now concentrated in the Pyrenees Mountains (43ºN)…
The researchers found one other gene, for a hormone called AGT (angiotensin) that followed a similar distribution pattern, with different versions that correlated with distance from the equator. AGT also is involved in salt retention and has been associated with hypertension and pre-eclampsia, a complication of pregnancy. One variation of this gene, known as AGT M235, was closely correlated with CYP3A5 *3.
This correlation of two unlinked gene variants with similar effects “is remarkable,” the authors note, “and suggests a shared selective pressure.”
More generally, if Dr. Fryer truly wants to “figure out where blacks went wrong,” if he wants to develop new insights into African-Americans, he should look at Africans. People who study African-Americans almost always adopt a condescending “blank slate” assumption that says that Africans didn’t bring anything with them from Africa. American intellectuals’ disdain for learning anything at all about Africa could be called the Black Slate theory.
In particular, I would suggest Fryer look into the continuity between family structures in Africa and in African-American communities. This has largely disappeared from American consciousness, but James Q. Wilson’s recent book “The Marriage Problem” has a couple of chapters on the vast literature about African family structures and their similarities to African-American ways of life that could introduce him to some of the facts and sources.
Of course, I’m the last person to listen to for career advice!