Enhancing Humans: Should We or Shouldn’t We?
Kira Peikoff was the editor-in-chief of Leaps.org from 2017 to 2021. As a journalist, her work has appeared in The New York Times, Newsweek, Nautilus, Popular Mechanics, The New York Academy of Sciences, and other outlets. She is also the author of four suspense novels that explore controversial issues arising from scientific innovation: Living Proof, No Time to Die, Die Again Tomorrow, and Mother Knows Best. Peikoff holds a B.A. in Journalism from New York University and an M.S. in Bioethics from Columbia University. She lives in New Jersey with her husband and two young sons. Follow her on Twitter @KiraPeikoff.
A panel of leading experts gathered this week at a sold-out event in downtown Manhattan to talk about the science and the ethics of enhancing human beings -- making people "better than well" through biomedical interventions. Here are the ten most memorable quotes from their lively discussion, which was organized by the New York Academy of Sciences, the Aspen Brain Institute, and the Hastings Center.
1) "It's okay for us to be enhanced relative to our ancestors; we are with the smallpox vaccine." —Dr. George Church, iconic genetics pioneer; professor at Harvard University and MIT
Church was more concerned with equitable access to enhancements than the morality of intervening in the first place. "We missed the last person with polio and now it's spread around the world again," he lamented.
Discussing how enhancements might become part of our species in the near-future, he mentioned the possibility of doctors slightly "overshooting" an intervention to reverse cognitive decline, for example; or younger people using such an intervention off-label. Another way might be through organ transplants, using organs that are engineered to not get cancer, or to be resistant to pain, pathogens, or senescence.
2) "All the technology we will need to fundamentally transform our species already exists. Humans are made of code, and that code is writable, readable and hackable." —Dr. Jamie Metzl, a technology futurist and geopolitical expert; Senior Fellow of the Atlantic Council, an international affairs think tank
The speed of change is on an exponential curve, and the world where we're going is changing at a much faster rate than we're used to, Metzl said. For example, a baby born 1000 years ago compared to one born today would be basically the same. But a baby born 1000 years in the future would seem like superman to us now, thanks to new capabilities that will become embedded in future people's genes over time. So how will we get from here to there?
"We will line up for small incremental benefits. By the time people are that changed, we will have adapted to a whole new set of social norms."
But, he asked, will well-meaning changes dangerously limit the diversity of our species?
3) "We are locked in a competitive arms race on both an individual and communal level, which will make it very difficult to put the brakes on. Everybody needs to be part of this conversation because it's a conversation about the future of our species." —Jamie Metzl
China, for one, plans to genetically sequence half of all newborns by 2020. In the U.S., it is standard to screen for 34 health conditions in newborns (though the exact number varies by state). There are no national guidelines for newborn genomic screening, though the National Institutes of Health is currently funding several research studies to explore the ethical concerns, potential benefits, and limitations of doing so on a large scale.
4) "I find freedom in not directing exactly how my child will be." —Josephine Johnston, Director of Research at the Hastings Center, the world's oldest bioethics research institute
Johnston cautioned against a full-throttled embrace of biomedical enhancements. Parents seeking to remake nature to serve their own purpose would be "like helicopter parenting on steroids," she said. "It could be a kind of felt obligation, something parents don't want to do but feel they must in order to compete." She warned this would be "one way to totally ruin the parenting experience altogether. I would hate to be the kind of parent who selects and controls her child's traits and talents."
Among other concerns, she worried about parents aiming to comply with social norms through technological intervention. Would a black mom, for example, feel pressure to make her child's skin paler to alleviate racial bias?
5) "We need to seriously consider the risks of a future if a handful of private companies own and monetize a map of our thoughts at any given moment." – Meredith Whittaker, Research Scientist, Open Research Lead at Google, and Co-Director of New York University's AI Now Institute, examining the social implications of artificial intelligence
The recent boom in AI research is the result of the consolidation of the tech industry's resources; only seven companies have the means to create artificial intelligence at scale, and one of the innovations on the horizon is brain-computer interfaces.
Facebook, for example, has a team of 60 engineers working on BCIs to let you type with your mind. Elon Musk's company Neuralink is working on technology that is aiming for "direct lag-free interactions between our brains and our devices."
But who will own this data? In the future, could the National Security Agency ask Neuralink, et al. for your thought log?
6) "The economic, political, and social contexts are as important as the tech itself. We need to look at power, who gets to define normal, and who falls outside of this category?" – Meredith Whittaker
Raising concerns about AI bias, Whittaker discussed how data is often coded by affluent white men from the Bay Area, potentially perpetuating discrimination against women and racial minorities.
Facial recognition, she said, is 30 percent less accurate for black women than for white men. And voice recognition systems don't hear women's voices as well as men's, among many other examples. The big question is: "Who gets to decide what's normal? And how do we ensure that different versions of normal can exist between cultures and communities? It is impossible not see the high stakes here, and how oppressive classifications of normal can marginalize people."
From left: George Church, Jamie Metzl, Josephine Johnston, Meredith Whittaker
7) "We might draw a red line at cloning or germline enhancements, but when you define those or think of specific cases, you realize you threw the baby out with the bathwater." —George Church, answering a question about whether society should agree on any red lines to prohibit certain interventions
"We should be focusing on outcomes," he suggested. "Could enhancement be a consequence of curing a disease like cognitive decline? That would concern me about drawing red lines."
8) "We have the technology to create Black Mirror. We could create a social credit score and it's terrifying." —Meredith Whittaker
In China, she said, the government is calculating scores to rank citizens based on aggregates of data like their educational history, their friend graphs, their employment and credit history, and their record of being critical of the government. These scores have already been used to bar 12 million people from travel.
"If we don't have the ability to make a choice," she said, "it could be a very frightening future."
9) "These tools will make all kinds of wonderful realities possible. Nobody looks at someone dying of cancer and says that's natural." —Jamie Metzl
Using biomedical interventions to restore health is an unequivocal moral good. But other experts questioned whether there should be a limit in how far these technologies are taken to achieve normalcy and beyond.
10) "Cancer's the easy one; what about deafness?" —Josephine Johnston, in retort
Could one person's disability be another person's desired state? "We should be so suspicious" of using technology to eradicate different ways of being in the world, she warned. Hubris has led us down the wrong path in the past, such as when homosexuality was considered a mental disorder.
"If we sometimes make mistakes about disease or dysfunction," she said, "we might make mistakes about what is a valid experience of the human condition."
Kira Peikoff was the editor-in-chief of Leaps.org from 2017 to 2021. As a journalist, her work has appeared in The New York Times, Newsweek, Nautilus, Popular Mechanics, The New York Academy of Sciences, and other outlets. She is also the author of four suspense novels that explore controversial issues arising from scientific innovation: Living Proof, No Time to Die, Die Again Tomorrow, and Mother Knows Best. Peikoff holds a B.A. in Journalism from New York University and an M.S. in Bioethics from Columbia University. She lives in New Jersey with her husband and two young sons. Follow her on Twitter @KiraPeikoff.
Gene Transfer Leads to Longer Life and Healthspan
The naked mole rat won’t win any beauty contests, but it could possibly win in the talent category. Its superpower: fighting the aging process to live several times longer than other animals its size, in a state of youthful vigor.
It’s believed that naked mole rats experience all the normal processes of wear and tear over their lifespan, but that they’re exceptionally good at repairing the damage from oxygen free radicals and the DNA errors that accumulate over time. Even though they possess genes that make them vulnerable to cancer, they rarely develop the disease, or any other age-related disease, for that matter. Naked mole rats are known to live for over 40 years without any signs of aging, whereas mice live on average about two years and are highly prone to cancer.
Now, these remarkable animals may be able to share their superpower with other species. In August, a study provided what may be the first proof-of-principle that genetic material transferred from one species can increase both longevity and healthspan in a recipient animal.
There are several theories to explain the naked mole rat’s longevity, but the one explored in the study, published in Nature, is based on the abundance of large-molecule high-molecular mass hyaluronic acid (HMM-HA).
A small molecule version of hyaluronic acid is commonly added to skin moisturizers and cosmetics that are marketed as ways to keep skin youthful, but this version, just applied to the skin, won’t have a dramatic anti-aging effect. The naked mole rat has an abundance of the much-larger molecule, HMM-HA, in the chemical-rich solution between cells throughout its body. But does the HMM-HA actually govern the extraordinary longevity and healthspan of the naked mole rat?
To answer this question, Dr. Vera Gorbunova, a professor of biology and oncology at the University of Rochester, and her team created a mouse model containing the naked mole rat gene hyaluronic acid synthase 2, or nmrHas2. It turned out that the mice receiving this gene during their early developmental stage also expressed HMM-HA.
The researchers found that the effects of the HMM-HA molecule in the mice were marked and diverse, exceeding the expectations of the study’s co-authors. High-molecular mass hyaluronic acid was more abundant in kidneys, muscles and other organs of the Has2 mice compared to control mice.
In addition, the altered mice had a much lower incidence of cancer. Seventy percent of the control mice eventually developed cancer, compared to only 57 percent of the altered mice, even after several techniques were used to induce the disease. The biggest difference occurred in the oldest mice, where the cancer incidence for the Has2 mice and the controls was 47 percent and 83 percent, respectively.
With regard to longevity, Has2 males increased their lifespan by more than 16 percent and the females added 9 percent. “Somehow the effect is much more pronounced in male mice, and we don’t have a perfect answer as to why,” says Dr. Gorbunova. Another improvement was in the healthspan of the altered mice: the number of years they spent in a state of relative youth. There’s a frailty index for mice, which includes body weight, mobility, grip strength, vision and hearing, in addition to overall conditions such as the health of the coat and body temperature. The Has2 mice scored lower in frailty than the controls by all measures. They also performed better in tests of locomotion and coordination, and in bone density.
Gorbunova’s results show that a gene artificially transferred from one species can have a beneficial effect on another species for longevity, something that had never been demonstrated before. This finding is “quite spectacular,” said Steven Austad, a biologist at the University of Alabama at Birmingham, who was not involved in the study.
Just as in lifespan, the effects in various organs and systems varied between the sexes, a common occurrence in longevity research, according to Austad, who authored the book Methuselah’s Zoo and specializes in the biological differences between species. “We have ten drugs that we can give to mice to make them live longer,” he says, “and all of them work better in one sex than in the other.” This suggests that more attention needs to be paid to the different effects of anti-aging strategies between the sexes, as well as gender differences in healthspan.
According to the study authors, the HMM-HA molecule delivered these benefits by reducing inflammation and senescence (cell dysfunction and death). The molecule also caused a variety of other benefits, including an upregulation of genes involved in the function of mitochondria, the powerhouses of the cells. These mechanisms are implicated in the aging process, and in human disease. In humans, virtually all noncommunicable diseases entail an acceleration of the aging process.
So, would the gene that creates HMM-HA have similar benefits for longevity in humans? “We think about these questions a lot,” Gorbunova says. “It’s been done by injections in certain patients, but it has a local effect in the treatment of organs affected by disease,” which could offer some benefits, she added.
“Mice are very short-lived and cancer-prone, and the effects are small,” says Steven Austad, a biologist at the University of Alabama at Birmingham. “But they did live longer and stay healthy longer, which is remarkable.”
As for a gene therapy to introduce the nmrHas2 gene into humans to obtain a global result, she’s skeptical because of the complexity involved. Gorbunova notes that there are potential dangers in introducing an animal gene into humans, such as immune responses or allergic reactions.
Austad is equally cautious about a gene therapy. “What this study says is that you can take something a species does well and transfer at least some of that into a new species. It opens up the way, but you may need to transfer six or eight or ten genes into a human” to get the large effect desired. Humans are much more complex and contain many more genes than mice, and all systems in a biological organism are intricately connected. One naked mole rat gene may not make a big difference when it interacts with human genes, metabolism and physiology.
Still, Austad thinks the possibilities are tantalizing. “Mice are very short-lived and cancer-prone, and the effects are small,” he says. “But they did live longer and stay healthy longer, which is remarkable.”
As for further research, says Austad, “The first place to look is the skin” to see if the nmrHas2 gene and the HMM-HA it produces can reduce the chance of cancer. Austad added that it would be straightforward to use the gene to try to prevent cancer in skin cells in a dish to see if it prevents cancer. It would not be hard to do. “We don’t know of any downsides to hyaluronic acid in skin, because it’s already used in skin products, and you could look at this fairly quickly.”
“Aging mechanisms evolved over a long time,” says Gorbunova, “so in aging there are multiple mechanisms working together that affect each other.” All of these processes could play a part and almost certainly differ from one species to the next.
“HMM-HA molecules are large, but we’re now looking for a small-molecule drug that would slow it’s breakdown,” she says. “And we’re looking for inhibitors, now being tested in mice, that would hinder the breakdown of hyaluronic acid.” Gorbunova has found a natural, plant-based product that acts as an inhibitor and could potentially be taken as a supplement. Ultimately, though, she thinks that drug development will be the safest and most effective approach to delivering HMM-HA for anti-aging.
In recent years, researchers of Alzheimer’s have made progress in figuring out the complex factors that lead to the disease. Yet, the root cause, or causes, of Alzheimer’s are still pretty much a mystery.
In fact, many people get Alzheimer’s even though they lack the gene variant we know can play a role in the disease. This is a critical knowledge gap for research to address because the vast majority of Alzheimer’s patients don’t have this variant.
A new study provides key insights into what’s causing the disease. The research, published in Nature Communications, points to a breakdown over time in the brain’s system for clearing waste, an issue that seems to happen in some people as they get older.
Michael Glickman, a biologist at Technion – Israel Institute of Technology, helped lead this research. I asked him to tell me about his approach to studying how this breakdown occurs in the brain, and how he tested a treatment that has potential to fix the problem at its earliest stages.
Dr. Michael Glickman is internationally renowned for his research on the ubiquitin-proteasome system (UPS), the brain's system for clearing the waste that is involved in diseases such as Huntington's, Alzheimer's, and Parkinson's. He is the head of the Lab for Protein Characterization in the Faculty of Biology at the Technion – Israel Institute of Technology. In the lab, Michael and his team focus on protein recycling and the ubiquitin-proteasome system, which protects against serious diseases like Alzheimer’s, Parkinson’s, cystic fibrosis, and diabetes. After earning his PhD at the University of California at Berkeley in 1994, Michael joined the Technion as a Senior Lecturer in 1998 and has served as a full professor since 2009.
Dr. Michael Glickman