[Editor's Note: This essay is in response to our current Big Question, which we posed to experts with different perspectives: "How should DNA tests for intelligence be used, if at all, by parents and educators?"]
It's 2019. Prenatal genetic tests are being used to help parents select from healthy and diseased eggs. Genetic risk profiles are being created for a range of common diseases. And embryonic gene editing has moved into the clinic. The science community is nearly unanimous on the question of whether we should be consulting our genomes as early as possible to create healthy offspring. If you can predict it, let's prevent it, and the sooner, the better.
There are big issues with IQ genetics that should be considered before parents and educators adopt DNA IQ predictions.
When it comes to care of our babies, kids, and future generations, we are doing things today that we never even dreamed would be possible. But one area that remains murky is the long fraught question of IQ, and whether to use DNA science to tell us something about it. There are big issues with IQ genetics that should be considered before parents and educators adopt DNA IQ predictions.
IQ tests have been around for over a century. They've been used by doctors, teachers, government officials, and a whole host of institutions as a proxy for intelligence, especially in youth. At times in history, test results have been used to determine whether to allow a person to procreate, remain a part of society, or merely stay alive. These abuses seem to be a distant part of our past, and IQ tests have since garnered their fair share of controversy for exhibiting racial and cultural biases. But they continue to be used across society. Indeed, much of the literature aimed at expecting parents justifies its recommendations (more omegas, less formula, etc.) based on promises of raising a baby's IQ.
This is the power of IQ testing sans DNA science. Until recently, the two were separate entities, with IQ tests indicating a coefficient created from individual responses to written questions and genetic tests indicating some disease susceptibility based on a sequence of one's DNA. Yet in recent years, scientists have begun to unlock the secrets of inherited aspects of intelligence with genetic analyses that scan millions of points of variation in DNA. Both bench scientists and direct-to-consumer companies have used these new technologies to find variants associated with exceptional IQ scores. There are a number of tests on the open market that parents and educators can use at will. These tests purport to reveal whether a child is inherently predisposed to be intelligent, and some suggest ways to track them for success.
I started looking into these tests when I was doing research for my book, "Social by Nature: The Promise and Peril of Sociogenomics." This book investigated the new genetic science of social phenomena, like educational attainment and political persuasion, investment strategies, and health habits. I learned that, while many of the scientists doing much of the basic research into these things cautioned that the effects of genetic factors were quite small, most saw testing as one data point among many that could help to somehow level the playing field for young people. The rationale went that in certain circumstances, some needed help more than others. Why not put our collective resources together to help them?
Good nutrition, support at home, and access to healthcare and education make a huge difference in how people do.
Some experts believed so strongly in the power of DNA behavioral prediction that they argued it would be unfair not to use predictors to determine a kid's future, prevent negative outcomes, and promote the possibility for positive ones. The educators out in the wider world that I spoke with agreed. With careful attention, they thought sociogenomic tests could help young people get the push they needed when they possessed DNA sequences that weren't working in their favor. Officials working with troubled youth told me they hoped DNA data could be marshaled early enough that kids would thrive at home and in school, thereby avoiding ending up in their care. While my conversations with folks centered around sociogenomic data in general, genetic IQ prediction was completely entangled in it all.
I present these prevailing views to demonstrate both the widespread appeal of genetic predictors as well as the well-meaning intentions of those in favor of using them. It's a truly progressive notion to help those who need help the most. But we must question whether genetic predictors are data points worth looking at.
When we examine the way DNA IQ predictors are generated, we see scientists grouping people with similar IQ test results and academic achievements, and then searching for the DNA those people have in common. But there's a lot more to scores and achievements than meets the eye. Good nutrition, support at home, and access to healthcare and education make a huge difference in how people do. Therefore, the first problem with using DNA IQ predictors is that the data points themselves may be compromised by numerous inaccuracies.
We must then ask ourselves where the deep, enduring inequities in our society are really coming from. A deluge of research has shown that poor life outcomes are a product of social inequalities, like toxic living conditions, underfunded schools, and unhealthy jobs. A wealth of research has also shown that race, gender, sexuality, and class heavily influence life outcomes in numerous ways. Parents and caregivers feed, talk, and play differently with babies of different genders. Teachers treat girls and boys, as well as members of different racial and ethnic backgrounds, differently to the point where they do better and worse in different subject areas.
Healthcare providers consistently racially profile, using diagnostics and prescribing therapies differently for the same health conditions. Access to good schools and healthcare are strongly mitigated by one's race and socioeconomic status. But even youth from privileged backgrounds suffer worse health and life outcomes when they identify or are identified as queer. These are but a few examples of the ways in which social inequities affect our chances in life. Therefore, the second problem with using DNA IQ predictors is that it obscures these very real, and frankly lethal, determinants. Instead of attending to the social environment, parents and educators take inborn genetics as the reason for a child's successes or failures.
It is time that we shift our priorities from seeking genetic causes to fixing the social causes we know to be real.
The other problem with using DNA IQ predictors is that research into the weightiness of DNA evidence has shown time and again that people take DNA evidence more seriously than they do other kinds of evidence. So it's not realistic to say that we can just consider IQ genetics as merely one tiny data point. People will always give more weight to DNA evidence than it deserves. And given its proven negligible effect, it would be irresponsible to do so.
It is time that we shift our priorities from seeking genetic causes to fixing the social causes we know to be real. Parents and educators need to be wary of solutions aimed at them and their individual children.
[Editor's Note: Read another perspective in the series here.]
At age 52, Glen Rouse suffered from arm weakness and a lot of muscle twitches. “I first thought something was wrong when I could not throw a 50-pound bag of dog food over the tailgate of my truck—something I use to do effortlessly,” said the 54-year-old resident of Anderson, California, about three hours north of San Francisco.
In August, Rouse retired as a forester for a private timber company, a job he had held for 31 years. The impetus: amyotrophic lateral sclerosis, or ALS, a progressive neuromuscular disease that is commonly known as Lou Gehrig’s disease, named after the New York Yankees’ first baseman who succumbed to it less than a month shy of his 40th birthday in 1941. ALS eventually robs an individual of the ability to talk, walk, chew, swallow and breathe.
Rouse is now dependent on ventilation through a nasal mask and uses a powerchair to get around. “I can no longer walk or use my arms very well,” he said. “I can still move my wrists and fingers. I can also transfer from my chair to the toilet if I have two of my friends help me.”
It’s “shocking” that modern medicine has very little to offer to people with this devastating condition, Rouse said. But there is hope on the horizon. Yesterday, the U.S. Food and Drug Administration approved Relyvrio, a drug made up of two parts, sodium phenylbutyrate and taurursodiol, to treat patients with ALS.
“This approval provides another important treatment option for ALS, a life-threatening disease that currently has no cure,” said Billy Dunn, director of the Office of Neuroscience in the FDA’s Center for Drug Evaluation and Research, in a statement. “The FDA remains committed to facilitating the development of additional ALS treatments.”
Until this point, the FDA had approved only two other medications—Riluzole (rilutek) in 1995 and Radicava (edaravone) in 2017—to extend life in patients with ALS, which typically kills within two to five years after diagnosis. That’s why earlier this week, Rouse was optimistic about the FDA’s likely approval of a controversial new drug for ALS.
When Relyvrio is taken in addition to Riluzole, it appears to slow functional decline by an additional 25 percent and extend life by another 6 to 10 months, said Richard Bedlak, director of the Duke ALS Clinic. “It is not a cure, but it is definitely a step forward.”
“The whole ALS community is extremely excited about it,” he said the day before Relyvrio’s expected approval. “We are very hopeful. We’re on pins and needles.”
A study of 137 ALS patients did not result in “substantial evidence” that Relyvrio was effective, the agency’s Peripheral and Central Nervous System Drugs Advisory Committee concluded in March. However, after some persuasion from FDA officials, patients and their families, the committee met again and decided to recommend approving the drug.
In January 2019, following an ALS diagnosis in October the previous year, Jeff Sarnacki, of Chester, Maryland, was accepted into a trial for Relyvrio. “Because of the trial, we did experience hope and a greater sense of help than had we not had that opportunity,” said Juliet Taylor, his wife and caregiver. They both believed the drug “worked for him in giving him more time.”
In June 2019, Sarnacki chose an open-label extension, offered to patients by drug researchers after a study ends, and took the active drug until he died peacefully at home under hospice care in May 2020, five days after his 60th birthday. A retired agent with the federal Bureau of Alcohol, Tobacco, Firearms and Explosives who later worked as a security consultant, Sarnacki lived about 19 months after diagnosis, which is shorter than the typical prognosis.
His symptoms had begun with leg cramps and foot drop in late fall 2017. At the end of life, he could only move a few fingers on his left hand and could not speak or eat by mouth; a feeding tube became necessary, Taylor said. He also took Radicava and Riluzole, the two previously approved drugs, for his ALS. “We were both incredulous that, so many years after Lou Gehrig’s own diagnosis, there were so few treatments available,” she said.
The dearth of successful treatments for ALS is “certainly not for lack of trying,” said Karen Raley Steffens, a registered nurse and ALS support services coordinator at the Les Turner ALS Foundation in Skokie, Ill. “There are thousands of researchers and scientists all over the world working tirelessly to try to develop treatments for ALS.”
Unfortunately, she adds, research takes time and exorbitant amounts of funding, while bureaucratic challenges persist. The rare disease also manifests and progresses in many different ways, so many treatments are needed.
As of 2017, the Centers for Disease Control and Prevention estimated that more than 31,000 people in the U.S. live with ALS, and an average of 5,000 people are newly diagnosed every year.
Most cases of ALS are sporadic, meaning that doctors don’t know the cause. There is about a one-year interval between symptom onset and an ALS diagnosis for most patients, so many motor neurons are lost by the time individuals can enroll in a clinical trial, said Richard Bedlack, professor of neurology and director of the Duke ALS Clinic in Durham, North Carolina.
Bedlack found the new drug, Relyvrio, to be “very promising,” which is why he testified to the FDA in favor of approval. (He’s a consultant and disease state speaker for multiple companies including Amylyx, manufacturer of Relyvrio.)
The “drug has different mechanisms of action than the currently approved treatments,” said Bedlack, who is also chief of neurology at the Durham Veterans Affairs Medical Center. He adds that, when Relyvrio is taken in addition to Riluzole, it appears to slow functional decline by an additional 25 percent and extend life by another 6 to 10 months. “It is not a cure, but it is definitely a step forward.”
T. Scott Diesing, a neurohospitalist and director of general neurology at the University of Nebraska Medical Center in Omaha, said he hopes the drug is “as good as people anticipated it should be, because there are not too many options for these patients.”
So far, Rouse's voice is holding up, but he knows the day will come when ALS will steal that and much more from him.
ALS is 100 percent fatal, with some patients dying as soon as a year after diagnosis. A few have lasted as long as 15 years, but those are the exceptions, Diesing said.
“If this drug can provide even months of additional life, or would maintain quality of life, that’s a big deal,” he notes, adding that “the patients are saying, ‘I know it’s not proven conclusively, but what do we have to lose?’ So, they would like to try it while additional studies are ongoing.” The drug has already been approved in Canada.
As his disease progresses, Rouse hopes to get a speech-to-text voice-generating computer that he can control with his eyes. So far, his voice is holding up, but he knows the day will come when ALS will steal that and much more from him. He works at I AM ALS, a patient-led community, and six of his friends have already died of the disease.
“Every time I lose a friend to ALS, I grieve and am sad but I resolve myself to keep working harder for them, myself and others,” Rouse said. “People living with ALS find great purpose in life advocating and trying to make a difference.”
The Friday Five covers important stories in health and science research that you may have missed - usually over the previous week, but today's episode is a lookback on important studies over the month of September.
Most recently, on September 27, pharmaceuticals Biogen and Eisai announced that a clinical trial showed their drug, lecanemab, can slow the rate of Alzheimer's disease. There are plenty of controversies and troubling ethical issues in science – and we get into many of them in our online magazine – but this news roundup focuses on scientific creativity and progress to give you a therapeutic dose of inspiration headed into the weekend and the new month.
This Friday Five episode covers the following studies published and announced over the past month:
- A new drug is shown to slow the rate of Alzheimer's disease
- The need for speed if you want to reduce your risk of dementia
- How to refreeze the north and south poles
- Ancient wisdom about Neti pots could pay off for Covid
- Two women, one man and a baby