Technology’s Role in Feeding a Soaring Population Raises This Dilemma
When farmer Terry Wanzek walks out in his fields, he sometimes sees a grove of trees, which reminds him of his grandfather, who planted those trees. Or he looks out over the pond, which deer, ducks and pheasant use for water, and he knows that his grandfather made a decision to drain land and put the pond in that exact spot.
Growing more with fewer resources is becoming increasingly urgent as the Earth's population is expected to hit 9.1 billion by 2050.
"There is a connection that goes beyond running a business and making a profit," says Wanzek, a fourth-generation North Dakota farmer who raises spring wheat, corn, soybeans, barley, dry edible beans and sunflowers. "There is a connection to family, to your ancestors and there is a connection to your posterity and your kids."
Wanzek's corn and soybeans are genetically modified (GM) crops, which means that they have been altered at the DNA level to create desirable traits. This intervention, he says, allows him to start growing earlier and to produce more food per acre.
Growing more with fewer resources is becoming increasingly urgent as the Earth's population is expected to hit 9.1 billion by 2050, with nearly all of the rise coming from developing countries, according to the Food and Agriculture Organization of the United Nations. This population will be urban, which means they'll likely be eating fewer grains and other staple crops, and more vegetables, fruits, meat, dairy, and fish.
Whether those foods will be touched in some way by technology remains a high-stakes question. As for GM foods, the American public is somewhat skeptical: in a recent survey, about one-third of Americans report that they are actively avoiding GMOs or seek out non-GMO labels when shopping and purchasing foods. These consumers fear unsafe food and don't want biotechnologists to tamper with nature. This disconnect—between those who consume food and those who produce it—is only set to intensify as major agricultural companies work to develop further high-tech farming solutions to meet the needs of the growing population.
"I don't think we have a choice going forward. The world isn't getting smaller. We have to come up with a means of using less."
In the future, it may be possible to feed the world. But what if the world doesn't want the food?
A Short History
Genetically modified food is not new. The first such plant (the Flavr Savr tomato) was approved for human consumption and brought to market in 1994, but people didn't like the taste. Today, nine genetically modified food crops are commercially available in the United States (corn, soybean, squash, papaya, alfalfa, sugar beets, canola, potato and apples). Most were modified to increase resistance to disease or pests, or tolerance to a specific herbicide. Such crops have in fact been found to increase yields, with a recent study showing grain yield was up to 24.5 percent higher in genetically engineered corn.
Despite some consumer skepticism, many farmers don't have a problem with GM crops, says Jennie Schmidt, a farmer and registered dietician in Maryland. She says with a laugh that her farm is a "grocery store farm - we grow the ingredients you buy in products at the grocery store." Schmidt's father-in-law, who started the farm, watched the adoption of hybrid corn improve seeds in the 1930s and 1940s.
"It wasn't a difficult leap to see how well these hybrid corn seeds have done over the decades," she says. "So when the GMOs came out, it was a quicker adoption curve, because as farmers they had already been exposed to the first generation and this was just the next step."
Schmidt, for one, is excited about the gene-editing tool CRISPR and other ways biotechnologists can create food like apples or potatoes with a particular enzyme turned off so they don't go brown during oxidation. Other foods in the pipeline include disease-resistant citrus, low-gluten wheat, fungus-resistant bananas, and anti-browning mushrooms.
"We need to not judge our agriculture by yield per acre but nutrition per acre."
"I don't think we have a choice going forward," says Schmidt. "The world isn't getting smaller. We have to come up with a means of using less."
A Different Way Forward?
But others remain convinced that there are better ways to feed the planet. Andrew Kimball, executive director of the Center for Food Safety, a non-profit that promotes organic and sustainable agriculture, says the public has been sold a lie with biotech. "GMO technology is not proven as a food producer," he says. "It's just not being done anywhere at a large scale. Ninety-nine percent of GMOs are corn and soy, and they allow chemical companies to sell more chemicals. But that doesn't increase food or decrease hunger." Instead, Kimball advocates for a pivot from commodity agriculture to farms with crop diversity and animals.
Kimball also suggests a way to use land more appropriately: stop growing so much biofuel. Right now, in the U.S., more than 55 percent of our crop farmland is in corn and soy. About 40 percent of that goes into cars through ethanol, 40 percent is fed to animals and a good bit of the rest goes into high-fructose corn syrup. That leaves only a small amount to feed people, says Kimball. "If you want to feed the world, not just the U.S., you want to make sure to use that land to feed people," he says. "We need to not judge our agriculture by yield per acre but nutrition per acre."
Robert Streiffer, a bioethicist at the University of Wisconsin at Madison, agrees that GMOs haven't really helped alleviate hunger. Glyphosate resistance, one of the traits that is most commonly used in genetically engineered crops, doesn't improve yield or allow crops to be grown in areas where they weren't able to be grown before. "Insect resistance through the insertion of a Bt gene can improve yield, but is mostly used for cotton (which is not a food crop) and corn which goes to feed cattle, a very inefficient method of feeding the hungry, to say the least," he says. Important research is being done in crops such as cassava, which could help relieve global hunger. But in his opinion, these researchers lack the profit potential needed to motivate large private funding sources, so they require more public-sector funding.
"A substantial portion of public opposition is as much about the lack of any perceived benefits for the consumers as it is for outright fear of health or environmental dangers."
"Public opposition to biotech foods is certainly a factor, but I expect this will slowly decline as labels indicating the presence of GE (genetically engineered) ingredients become more common, and as we continue to amass reassuring data on the comparative environmental safety of GE crops," says Streiffer. "A substantial portion of public opposition is as much about the lack of any perceived benefits for the consumers as it is for outright fear of health or environmental dangers."
One sign that the public may be willing to embrace some non-natural foods is the recent interest in cultured meat, which is grown in a lab from animal cells but doesn't require raising or killing animals. A study published last year in PLOS One found that 65 percent of 673 surveyed U.S. individuals would probably or definitely try cultured meat, while only 8.5 percent said they definitely would not. In the future, lab-grown food may become another way to create more food with fewer resources.
Danielle Nierenberg, president of the Food Tank, a nonprofit organization focused on building a global community of safe and healthy food, points to an even more immediate problem: food waste. Globally, about a third of food is thrown out or goes bad before it has a chance to be eaten. She says simply fixing roads and infrastructure in developing countries would go a long way toward ensuring that food reaches the hungry. Focusing on helping small farmers (who grow 70 percent of food around the globe), especially female farmers, would go a long way, she says.
Innovation on the Farm
In addition to good roads, those farmers need fertilizer. Nitrogen-based fertilizers may get a boost in the future from technologies that release nutrients slowly over time, like slow-release medicines based on nanotechnology. In field trials on rice in Sri Lanka, one such nanotech fertilizer increased crop yields by 10 percent, even though it delivered only half the amount of urea compared with traditional fertilizer, according to a study last year.
"I'm not afraid of the food I grow. We live in the same environment, and I feel completely safe."
One startup, the San-Francisco-based Biome Makers, is profiling microbial DNA to give farmers an idea of what their soil needs to better support crops. Joyn Bio, another new startup based in Boston and West Sacramento, is looking to engineer microbes that could reduce farming's reliance on nitrogen fertilizer, which is expensive and harms the environment. (Full disclosure: Joyn Bio and this magazine are funded by the same company, Leaps by Bayer, though leapsmag is editorially independent. Also, Bayer recently acquired Monsanto, the leading producer of genetically engineered seeds and the herbicide Roundup.)
Terry Wanzek, the farmer in North Dakota, says he'd be willing to try any new technology as long as it helps his bottom line – and increases sustainability. "I'm not afraid of the food I grow," he says of his genetically modified produce. "We eat the same food, we live in the same environment, and I feel completely safe."
Only time will tell if people several decades from now feel the same way. But no matter how their food is produced, one thing is certain: those people will need to eat.
How Leqembi became the biggest news in Alzheimer’s disease in 40 years, and what comes next
A few months ago, Betsy Groves traveled less than a mile from her home in Cambridge, Mass. to give a talk to a bunch of scientists. The scientists, who worked for the pharmaceutical companies Biogen and Eisai, wanted to know how she lived her life, how she thought about her future, and what it was like when a doctor’s appointment in 2021 gave her the worst possible news. Groves, 73, has Alzheimer’s disease. She caught it early, through a lumbar puncture that showed evidence of amyloid, an Alzheimer’s hallmark, in her cerebrospinal fluid. As a way of dealing with her diagnosis, she joined the Alzheimer’s Association’s National Early-Stage Advisory Board, which helped her shift into seeing her diagnosis as something she could use to help others.
After her talk, Groves stayed for lunch with the scientists, who were eager to put a face to their work. Biogen and Eisai were about to release the first drug to successfully combat Alzheimer’s in 40 years of experimental disaster. Their drug, which is known by the scientific name lecanemab and the marketing name Leqembi, was granted accelerated approval by the U.S. Food and Drug Administration last Friday, Jan. 6, after a study in 1,800 people showed that it reduced cognitive decline by 27 percent over 18 months.
It is no exaggeration to say that this result is a huge deal. The field of Alzheimer’s drug development has been absolutely littered with failures. Almost everything researchers have tried has tanked in clinical trials. “Most of the things that we've done have proven not to be effective, and it's not because we haven’t been taking a ton of shots at goal,” says Anton Porsteinsson, director of the University of Rochester Alzheimer's Disease Care, Research, and Education Program, who worked on the lecanemab trial. “I think it's fair to say you don't survive in this field unless you're an eternal optimist.”
As far back as 1984, a cure looked like it was within reach: Scientists discovered that the sticky plaques that develop in the brains of those who have Alzheimer’s are made up of a protein fragment called beta-amyloid. Buildup of beta-amyloid seemed to be sufficient to disrupt communication between, and eventually kill, memory cells. If that was true, then the cure should be straightforward: Stop the buildup of beta-amyloid; stop the Alzheimer’s disease.
It wasn’t so simple. Over the next 38 years, hundreds of drugs designed either to interfere with the production of abnormal amyloid or to clear it from the brain flamed out in trials. It got so bad that neuroscience drug divisions at major pharmaceutical companies (AstraZeneca, Pfizer, Bristol-Myers, GSK, Amgen) closed one by one, leaving the field to smaller, scrappier companies, like Cambridge-based Biogen and Tokyo-based Eisai. Some scientists began to dismiss the amyloid hypothesis altogether: If this protein fragment was so important to the disease, why didn’t ridding the brain of it do anything for patients? There was another abnormal protein that showed up in the brains of Alzheimer’s patients, called tau. Some researchers defected to the tau camp, or came to believe the proteins caused damage in combination.
The situation came to a head in 2021, when the FDA granted provisional approval to a drug called aducanumab, marketed as Aduhelm, against the advice of its own advisory council. The approval was based on proof that Aduhelm reduced beta-amyloid in the brain, even though one research trial showed it had no effect on people’s symptoms or daily life. Aduhelm could also cause serious side effects, like brain swelling and amyloid related imaging abnormalities (known as ARIA, these are basically micro-bleeds that appear on MRI scans). Without a clear benefit to memory loss that would make these risks worth it, Medicare refused to pay for Aduhelm among the general population. Two congressional committees launched an investigation into the drug’s approval, citing corporate greed, lapses in protocol, and an unjustifiably high price. (Aduhelm was also produced by the pharmaceutical company Biogen.)
To be clear, Leqembi is not the cure Alzheimer’s researchers hope for. While the drug is the first to show clear signs of a clinical benefit, the scientific establishment is split on how much of a difference Leqembi will make in the real world.
So far, Leqembi is like Aduhelm in that it has been given accelerated approval only for its ability to remove amyloid from the brain. Both are monoclonal antibodies that direct the immune system to attack and clear dysfunctional beta-amyloid. The difference is that, while that’s all Aduhelm was ever shown to do, Leqembi’s makers have already asked the FDA to give it full approval – a decision that would increase the likelihood that Medicare will cover it – based on data that show it also improves Alzheimer’s sufferer’s lives. Leqembi targets a different type of amyloid, a soluble version called “protofibrils,” and that appears to change the effect. “It can give individuals and their families three, six months longer to be participating in daily life and living independently,” says Claire Sexton, PhD, senior director of scientific programs & outreach for the Alzheimer's Association. “These types of changes matter for individuals and for their families.”
To be clear, Leqembi is not the cure Alzheimer’s researchers hope for. It does not halt or reverse the disease, and people do not get better. While the drug is the first to show clear signs of a clinical benefit, the scientific establishment is split on how much of a difference Leqembi will make in the real world. It has “a rather small effect,” wrote NIH Alzheimer’s researcher Madhav Thambisetty, MD, PhD, in an email to Leaps.org. “It is unclear how meaningful this difference will be to patients, and it is unlikely that this level of difference will be obvious to a patient (or their caregivers).” Another issue is cost: Leqembi will become available to patients later this month, but Eisai is setting the price at $26,500 per year, meaning that very few patients will be able to afford it unless Medicare chooses to reimburse them for it.
The same side effects that plagued Aduhelm are common in Leqembi treatment as well. In many patients, amyloid doesn’t just accumulate around neurons, it also forms deposits in the walls of blood vessels. Blood vessels that are shot through with amyloid are more brittle. If you infuse a drug that targets amyloid, brittle blood vessels in the brain can develop leakage that results in swelling or bleeds. Most of these come with no symptoms, and are only seen during testing, which is why they are called “imaging abnormalities.” But in situations where patients have multiple diseases or are prescribed incompatible drugs, they can be serious enough to cause death. The three deaths reported from Leqembi treatment (so far) are enough to make Thambisetty wonder “how well the drug may be tolerated in real world clinical practice where patients are likely to be sicker and have multiple other medical conditions in contrast to carefully selected patients in clinical trials.”
Porsteinsson believes that earlier detection of Alzheimer’s disease will be the next great advance in treatment, a more important step forward than Leqembi’s approval.
Still, there are reasons to be excited. A successful Alzheimer’s drug can pave the way for combination studies, in which patients try a known effective drug alongside newer, more experimental ones; or preventative studies, which take place years before symptoms occur. It also represents enormous strides in researchers’ understanding of the disease. For example, drug dosages have increased massively—in some cases quadrupling—from the early days of Alzheimer’s research. And patient selection for studies has changed drastically as well. Doctors now know that you’ve got to catch the disease early, through PET-scans or CSF tests for amyloid, if you want any chance of changing its course.
Porsteinsson believes that earlier detection of Alzheimer’s disease will be the next great advance in treatment, a more important step forward than Leqembi’s approval. His lab already uses blood tests for different types of amyloid, for different types of tau, and for measures of neuroinflammation, neural damage, and synaptic health, but commercially available versions from companies like C2N, Quest, and Fuji Rebio are likely to hit the market in the next couple of years. “[They are] going to transform the diagnosis of Alzheimer's disease,” Porsteinsson says. “If someone is experiencing memory problems, their physicians will be able to order a blood test that will tell us if this is the result of changes in your brain due to Alzheimer's disease. It will ultimately make it much easier to identify people at a very early stage of the disease, where they are most likely to benefit from treatment.”
Learn more about new blood tests to detect Alzheimer's
Early detection can help patients for more philosophical reasons as well. Betsy Groves credits finding her Alzheimer’s early with giving her the space to understand and process the changes that were happening to her before they got so bad that she couldn’t. She has been able to update her legal documents and, through her role on the Advisory Group, help the Alzheimer’s Association with developing its programs and support services for people in the early stages of the disease. She still drives, and because she and her husband love to travel, they are hoping to get out of grey, rainy Cambridge and off to Texas or Arizona this spring.
Because her Alzheimer’s disease involves amyloid deposits (a “substantial portion” do not, says Claire Sexton, which is an additional complication for research), and has not yet reached an advanced stage, Groves may be a good candidate to try Leqembi. She says she’d welcome the opportunity to take it. If she can get access, Groves hopes the drug will give her more days to be fully functioning with her husband, daughters, and three grandchildren. Mostly, she avoids thinking about what the latter stages of Alzheimer’s might be like, but she knows the time will come when it will be her reality. “So whatever lecanemab can do to extend my more productive ways of engaging with relationships in the world,” she says. “I'll take that in a minute.”
How to have a good life, based on the world's longest study of happiness
What makes for a good life? Such a simple question, yet we don't have great answers. Most of us try to figure it out as we go along, and many end up feeling like they never got to the bottom of it.
Shouldn't something so important be approached with more scientific rigor? In 1938, Harvard researchers began a study to fill this gap. Since then, they’ve followed hundreds of people over the course of their lives, hoping to identify which factors are key to long-term satisfaction.
Eighty-five years later, the Harvard Study of Adult Development is still going. And today, its directors, the psychiatrists Bob Waldinger and Marc Shulz, have published a book that pulls together the study’s most important findings. It’s called The Good Life: Lessons from the World’s Longest Scientific Study of Happiness.
In this podcast episode, I talked with Dr. Waldinger about life lessons that we can mine from the Harvard study and his new book.
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More background on the study
Back in the 1930s, the research began with 724 people. Some were first-year Harvard students paying full tuition, others were freshmen who needed financial help, and the rest were 14-year-old boys from inner city Boston – white males only. Fortunately, the study team realized the error of their ways and expanded their sample to include the wives and daughters of the first participants. And Waldinger’s book focuses on the Harvard study findings that can be corroborated by evidence from additional research on the lives of people of different races and other minorities.
The study now includes over 1,300 relatives of the original participants, spanning three generations. Every two years, the participants have sent the researchers a filled-out questionnaire, reporting how their lives are going. At five-year intervals, the research team takes a peek their health records and, every 15 years, the psychologists meet their subjects in-person to check out their appearance and behavior.
But they don’t stop there. No, the researchers factor in multiple blood samples, DNA, images from body scans, and even the donated brains of 25 participants.
Robert Waldinger, director of the Harvard Study of Adult Development.
Katherine Taylor
Dr. Waldinger is Clinical Professor of Psychiatry at Harvard Medical School, in addition to being Director of the Harvard Study of Adult Development. He got his M.D. from Harvard Medical School and has published numerous scientific papers he’s a practicing psychiatrist and psychoanalyst, he teaches Harvard medical students, and since that is clearly not enough to keep him busy, he’s also a Zen priest.
His book is a must-read if you’re looking for scientific evidence on how to design your life for more satisfaction so someday in the future you can look back on it without regret, and this episode was an amazing conversation in which Dr. Waldinger breaks down many of the cliches about the good life, making his advice real and tangible. We also get into what he calls “side-by-side” relationships, personality traits for the good life, and the downsides of being too strict about work-life balance.
Show links
- Bob Waldinger
- Waldinger's book, The Good Life: Lessons from the World's Longest Scientific Study of Happiness
- The Harvard Study of Adult Development
- Waldinger's Ted Talk
- Gallup report finding that people with good friends at work have higher engagement with their jobs
- The link between relationships and well-being
- Those with social connections live longer