Would You Eat These Futuristic Foods?
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 rendering of a 3D-printed burger.
Imagine it's 2050. You wake up and make breakfast: fluffy scrambled eggs that didn't come from a chicken, but that taste identical to the ones you remember eating as a kid. You would never know that the egg protein on your plate, ovalbumin, was developed in an industrial bioreactor using fungi.
"We have this freedom to operate, freedom to engineer way beyond what we have now with livestock or plants."
For lunch, you head to your kitchen's 3D printer and pop in a cartridge, select your preferred texture and flavor, then stand back while your meal is chemically assembled. Afterward, for dessert, you snack on some chocolate that tastes more delicious than the truffles of the past. That's because these cocoa beans were gene-edited to improve their flavor.
2050 is not a random year –it's when the United Nations estimates that the world population will have ballooned to nearly 10 billion people. That's a staggering number of mouths to feed. So, scientists are already working on ways to make new food products that are unlike anything we consume today, but that could offer new, potentially improved nutritional choices and sustainable options for the masses. To whet your appetite, here are three futuristic types of food that are currently in development around the world:
1) Cellular Agriculture
Researchers at VTT Technical Research Centre of Finland, a leading R&D organization in Europe, are on the cutting-edge of developing a whole new ecosystem of food with novel ingredients and novel functionality.
In the high-tech world of cellular agriculture, single-cell organisms can be used in contained environments to produce food ingredients that are identical to traditionally sourced ingredients. For example, whey protein can be developed inside a bioreactor that is functionally the same as the kind in cow's milk.
Ditto for eggs without a chicken – so the world will finally know which came first.
The steel tank bioreactors in VTT´s piloting facility are used to grow larger amounts of plant cells or to brew dairy and egg proteins with microbes.
(VTT)
"We take the gene from a chicken genome, and place that in a microbe, and then the microbe can, with those instructions, make exactly the same protein," explains Lauri Reuter, a Senior Specialist at VTT who holds a doctorate in biotechnology. "It will swim in this bioreactor and kick out the protein, and we get this liquid that can be purified. Then you would cook or bake with it, and the food you would eat tastes and looks like food you would eat right now."
But why settle for what chickens can do? With this technology, it's possible, for example, to modify the ovalbumin protein to decrease its allergenicity.
"This is the power of what we can do with modern tools of genetic engineering," says Christopher Landowski,a Research Team Leader of the Protein Production Team. And the innovative potential doesn't stop there.
"We have this freedom to operate, freedom to engineer way beyond what we have now with livestock or plants," Reuter says. Future foods sourced from cells could include meat analogues, sugar substitutes, dairy substitutes, nutritious veggies that don't taste bitter, personalized nutrition – ingredients designed for individual needs; the list goes on. It could even be used one day to produce food on Mars.
The researchers emphasize the advantages of this method: their living cell factories are efficient – no care of complex animals is required; they can scale up or down in reaction to demand; their environments are contained and don't require antibiotics; and they provide an alternative to using animals.
But the researchers also readily admit that the biggest obstacle is consumer acceptance, which is why they seek to engage with people along the way to alleviate any concerns and to educate them about the technology. Novel foods of this sort have already been eaten in research settings, but it may take another three to five years before the egg and milk proteins hit the market, probably first in the United States before Europe.
Eventually, the researchers anticipate widespread adoption.
Emilia Nordlund, who directs the Food Solutions team, predicts, "Cellular agriculture will revolutionize the food industry as dramatically as the Internet revolutionized many other industries."
Jams made of culture cells of various plants: strawberry, scurvy grass, arctic bramble, tobacco, cloudberry and lingonberry.
(VTT/Lauri Reuter)
2) 3D-printed foods
In South Korea, researchers are developing 3D-printed foods to help solve a problem caused by aging. Elderly people often rely on soft foods which are easier to chew, but aren't always healthy, like Jello and pudding.
With 3D printing, foods of softer textures can be created with the same nutritional value as firmer food, via a processing method that breaks down the food into tiny nutrients by grinding it at a very low temperature with liquid nitrogen.
"The goal is that someone at home can print out food with whatever flavor and texture they want."
The micro-sized food materials are then reconstructed in layers to form what looks like a Lego block. "The cartridges are all textures, some soft and some stiff," explains Jin-Kyu Rhee, associate professor at Ewha Womans University, whose project has been funded for the last three years by the South Korean government. "We are developing a library of food textures, so that people can combine them to simulate a real type of food."
Users could then add powdered versions of various ingredients to create customized food. Flavor, of course, is of prime importance too, so the cartridges have flavors like barbecue to help simulate the experience of eating "real" food.
"The goal is that someone at home can print out food with whatever flavor and texture they want," Rhee says. "They can order their own cartridge and digital recipes to generate their own food, ready to cook with a microwave oven." It could also be used for space travel.
Rhee expects the prototype of the printer to be completed by the end of this year and will then seek out a commercial partner. If all goes well, you might be able to set up your 3D printer next to your coffee pot by 2025.
3) CRISPR-edited foods
You may not know that the cocoa plant is having a tough time out there in nature. It's plagued by fungal disease; on farms, about 30 to 40 percent of the potential cocoa beans are lost every year. For all the chocolate lovers of the world, this means less to go around.
Conventional plant breeding is very slow for trees, so researchers like Mark Guiltinan at Penn State University are devising ways to increase the plants' chances for survival – without moving any genes between species, as in genetically modified organisms (GMOs).
"Because society hasn't really embraced [GMOs] very much, we're trying to develop ways that don't use transgenic plants and speed up breeding," Guiltinan says.
He and his colleagues are using CRISPR-cas9, the precise method of editing DNA, to imbue cocoa plants with immunity to fungal disease.
How does it work? Similar to humans, the plants have an immune system. Part of it functions like brakes, repressing the whole system so it's only working when it needs to.
"Like when you get a fever, your immune system is working full blast, but your body shuts it down when it doesn't need it," he explains. "Plants do exactly the same thing. One idea is if we can reduce or eliminate that brake on the immune system, we could make plants that have a very high immunity."
A CRISPR-edited npr3 mutant cacao plantlet, not too much to see yet, but soon it will become a happy plant in the greenhouse.
(Photo credit: Mark Guiltinan)
The CRISPR-cas9 system allows "a really amazing little protein" to go into the cocoa plant cell, find a specific gene, and shut it off to put the whole immune system into overdrive. This confers the necessary immunity, and though the plant burns through a lot of energy, as if it has a fever all the time, this method would allow for more plants to fend off the fungal attacks every year. Which means more chocolate. It could also greatly reduce the need for pesticides.
"Replacing chemicals with genetics is one part of our goal," Guiltinan says. "And it's totally safe." Another goal of his project is to improve the cocoa beans' quality and flavor profile through gene editing.
Yum. Is your mouth watering yet?
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.
Pioneering XPRIZEs, Longevity and Mindset with Dr. Peter Diamandis
XPRIZE founder and chairman Peter Diamandis launches XPRIZE Healthspan at an event on November 29.
A new competition by the XPRIZE Foundation is offering $101 million to researchers who discover therapies that give a boost to people aged 65-80 so their bodies perform more like when they were middle-aged.
For today’s podcast episode, I talked with Dr. Peter Diamandis, XPRIZE’s founder and executive chairman. Under Peter’s leadership, XPRIZE has launched 27 previous competitions with over $300 million in prize purses. The latest contest aims to enhance healthspan, or the period of life when older people can play with their grandkids without any restriction, disability or disease. Such breakthroughs could help prevent chronic diseases that are closely linked to aging. These illnesses are costly to manage and threaten to overwhelm the healthcare system, as the number of Americans over age 65 is rising fast.
In this competition, called XPRIZE Healthspan, multiple awards are available, depending on what’s achieved, with support from the nonprofit Hevolution Foundation and Chip Wilson, the founder of Lululemon and nonprofit SOLVE FSHD. The biggest prize, $81 million, is for improvements in cognition, muscle and immunity by 20 years. An improvement of 15 years will net $71 million, and 10 years will net $61 million.
In our conversation for this episode, Peter talks about his plans for XPRIZE Healthspan and why exponential technologies make the current era - even with all of its challenges - the most exciting time in human history. We discuss the best mental outlook that supports a person in becoming truly innovative, as well as the downsides of too much risk aversion. We talk about how to overcome the negativity bias in ourselves and in mainstream media, how Peter has shifted his own mindset to become more positive over the years, how to inspire a culture of innovation, Peter’s personal recommendations for lifestyle strategies to live longer and healthier, the innovations we can expect in various fields by 2030, the future of education and the importance of democratizing tech and innovation.
In addition to Peter’s pioneering leadership of XPRIZE, he is also the Executive Founder of Singularity University. In 2014, he was named by Fortune as one of the “World’s 50 Greatest Leaders.” As an entrepreneur, he’s started over 25 companies in the areas of health-tech, space, venture capital and education. He’s Co-founder and Vice-Chairman of two public companies, Celularity and Vaxxinity, plus being Co-founder & Chairman of Fountain Life, a fully-integrated platform delivering predictive, preventative, personalized and data-driven health. He also serves as Co-founder of BOLD Capital Partners, a venture fund with a half-billion dollars under management being invested in exponential technologies and longevity companies. Peter is a New York Times Bestselling author of four books, noted during our conversation and in the show notes of this episode. He has degrees in molecular genetics and aerospace engineering from MIT and holds an M.D. from Harvard Medical School.
Show links
- Peter Diamandis bio
- New XPRIZE Healthspan
- Peter Diamandis books
- 27 XPRIZE competitions and counting
- Life Force by Peter Diamandis and Tony Robbins
- Peter Diamandis Twitter
- Longevity Insider newsletter – AI identifies the news
- Peter Diamandis Longevity Handbook
- Hevolution funding for longevity
XPRIZE Founder Peter Diamandis speaks with Mehmoud Khan, CEO of Hevolution Foundation, at the launch of XPRIZE Healthspan.
Hevolution Foundation
Matt Fuchs is the editor-in-chief of Leaps.org and Making Sense of Science. He is also a contributing reporter to the Washington Post and has written for the New York Times, Time Magazine, WIRED and the Washington Post Magazine, among other outlets. Follow him @fuchswriter.
Important findings are starting to emerge from research on how genes shape the human response to the Covid virus.
From infections with no symptoms to why men are more likely to be hospitalized in the ICU and die of COVID-19, new research shows that your genes play a significant role
Early in the pandemic, genetic research focused on the virus because it was readily available. Plus, the virus contains only 30,000 bases in a dozen functional genes, so it's relatively easy and affordable to sequence. Additionally, the rapid mutation of the virus and its ability to escape antibody control fueled waves of different variants and provided a reason to follow viral genetics.
In comparison, there are many more genes of the human immune system and cellular functions that affect viral replication, with about 3.2 billion base pairs. Human studies require samples from large numbers of people, the analysis of each sample is vastly more complex, and sophisticated computer analysis often is required to make sense of the raw data. All of this takes time and large amounts of money, but important findings are beginning to emerge.
Asymptomatics
About half the people exposed to SARS-CoV-2, the virus that causes the COVID-19 disease, never develop symptoms of this disease, or their symptoms are so mild they often go unnoticed. One piece of understanding the phenomena came when researchers showed that exposure to OC43, a common coronavirus that results in symptoms of a cold, generates immune system T cells that also help protect against SARS-CoV-2.
Jill Hollenbach, an immunologist at the University of California at San Francisco, sought to identify the gene behind that immune protection. Most COVID-19 genetic studies are done with the most seriously ill patients because they are hospitalized and thus available. “But 99 percent of people who get it will never see the inside of a hospital for COVID-19,” she says. “They are home, they are not interacting with the health care system.”
Early in the pandemic, when most labs were shut down, she tapped into the National Bone Marrow Donor Program database. It contains detailed information on donor human leukocyte antigens (HLAs), key genes in the immune system that must match up between donor and recipient for successful transplants of marrow or organs. Each HLA can contain alleles, slight molecular differences in the DNA of the HLA, which can affect its function. Potential HLA combinations can number in the tens of thousands across the world, says Hollenbach, but each person has a smaller number of those possible variants.
She teamed up with the COVID-19 Citizen Science Study a smartphone-based study to track COVID-19 symptoms and outcomes, to ask persons in the bone marrow donor registry about COVID-19. The study enlisted more than 30,000 volunteers. Those volunteers already had their HLAs annotated by the registry, and 1,428 tested positive for the virus.
Analyzing five key HLAs, she found an allele in the gene HLA-B*15:01 that was significantly overrepresented in people who didn’t have any symptoms. The effect was even stronger if a person had inherited the allele from both parents; these persons were “more than eight times more likely to remain asymptomatic than persons who did not carry the genetic variant,” she says. Altogether this HLA was present in about 10 percent of the general European population but double that percentage in the asymptomatic group. Hollenbach and her colleagues were able confirm this in other different groups of patients.
What made the allele so potent against SARS-CoV-2? Part of the answer came from x-ray crystallography. A key element was the molecular shape of parts of the cold virus OC43 and SARS-CoV-2. They were virtually identical, and the allele could bind very tightly to them, present their molecular antigens to T cells, and generate an extremely potent T cell response to the viruses. And “for whatever reasons that generated a lot of memory T cells that are going to stick around for a long time,” says Hollenbach. “This T cell response is very early in infection and ramps up very quickly, even before the antibody response.”
Understanding the genetics of the immune response to SARS-CoV-2 is important because it provides clues into the conditions of T cells and antigens that support a response without any symptoms, she says. “It gives us an opportunity to think about whether this might be a vaccine design strategy.”
Dead men
A researcher at the Leibniz Institute of Virology in Hamburg Germany, Guelsah Gabriel, was drawn to a question at the other end of the COVID-19 spectrum: why men more likely to be hospitalized and die from the infection. It wasn't that men were any more likely to be exposed to the virus but more likely, how their immune system reacted to it
Several studies had noted that testosterone levels were significantly lower in men hospitalized with COVID-19. And, in general, the lower the testosterone, the worse the prognosis. A year after recovery, about 30 percent of men still had lower than normal levels of testosterone, a condition known as hypogonadism. Most of the men also had elevated levels of estradiol, a female hormone (https://pubmed.ncbi.nlm.nih.gov/34402750/).
Every cell has a sex, expressing receptors for male and female hormones on their surface. Hormones docking with these receptors affect the cells' internal function and the signals they send to other cells. The number and role of these receptors varies from tissue to tissue.
Gabriel began her search by examining whole exome sequences, the protein-coding part of the genome, for key enzymes involved in the metabolism of sex hormones. The research team quickly zeroed in on CYP19A1, an enzyme that converts testosterone to estradiol. The gene that produces this enzyme has a number of different alleles, the molecular variants that affect the enzyme's rate of metabolizing the sex hormones. One genetic variant, CYP19A1 (Thr201Met), is typically found in 6.2 percent of all people, both men and women, but remarkably, they found it in 68.7 percent of men who were hospitalized with COVID-19.
Lung surprise
Lungs are the tissue most affected in COVID-19 disease. Gabriel wondered if the virus might be affecting expression of their target gene in the lung so that it produces more of the enzyme that converts testosterone to estradiol. Studying cells in a petri dish, they saw no change in gene expression when they infected cells of lung tissue with influenza and the original SARS-CoV viruses that caused the SARS outbreak in 2002. But exposure to SARS-CoV-2, the virus responsible for COVID-19, increased gene expression up to 40-fold, Gabriel says.
Did the same thing happen in humans? Autopsy examination of patients in three different cites found that “CYP19A1 was abundantly expressed in the lungs of COVID-19 males but not those who died of other respiratory infections,” says Gabriel. This increased enzyme production led likely to higher levels of estradiol in the lungs of men, which “is highly inflammatory, damages the tissue, and can result in fibrosis or scarring that inhibits lung function and repair long after the virus itself has disappeared.” Somehow the virus had acquired the capacity to upregulate expression of CYP19A1.
Only two COVID-19 positive females showed increased expression of this gene. The menopause status of these women, or whether they were on hormone replacement therapy was not known. That could be important because female hormones have a protective effect for cardiovascular disease, which women often lose after going through menopause, especially if they don’t start hormone replacement therapy. That sex-specific protection might also extend to COVID-19 and merits further study.
The team was able to confirm their findings in golden hamsters, the animal model of choice for studying COVID-19. Testosterone levels in male animals dropped 5-fold three days after infection and began to recover as viral levels declined. CYP19A1 transcription increased up to 15-fold in the lungs of the male but not the females. The study authors wrote, “Virus replication in the male lungs was negatively associated with testosterone levels.”
The medical community studying COVID-19 has slowly come to recognize the importance of adipose tissue, or fat cells. They are known to express abundant levels of CYP19A1 and play a significant role as metabolic tissue in COVID-19. Gabriel adds, “One of the key findings of our study is that upon SARS-CoV-2 infection, the lung suddenly turns into a metabolic organ by highly expressing” CYP19A1.
She also found evidence that SARS-CoV-2 can infect the gonads of hamsters, thereby likely depressing circulating levels of sex hormones. The researchers did not have autopsy samples to confirm this in humans, but others have shown that the virus can replicate in those tissues.
A possible treatment
Back in the lab, substituting low and high doses of testosterone in SARS-COV-2 infected male hamsters had opposite effects depending on testosterone dosage used. Gabriel says that hormone levels can vary so much, depending on health status and age and even may change throughout the day, that “it probably is much better to inhibit the enzyme” produced by CYP19A1 than try to balance the hormones.
Results were better with letrozole, a drug approved to treat hypogonadism in males, which reduces estradiol levels. The drug also showed benefit in male hamsters in terms of less severe disease and faster recovery. She says more details need to be worked out in using letrozole to treat COVID-19, but they are talking with hospitals about clinical trials of the drug.
Gabriel has proposed a four hit explanation of how COVID-19 can be so deadly for men: the metabolic quartet. First is the genetic risk factor of CYP19A1 (Thr201Met), then comes SARS-CoV-2 infection that induces even greater expression of this gene and the deleterious increase of estradiol in the lung. Age-related hypogonadism and the heightened inflammation of obesity, known to affect CYP19A1 activity, are contributing factors in this deadly perfect storm of events.
Studying host genetics, says Gabriel, can reveal new mechanisms that yield promising avenues for further study. It’s also uniting different fields of science into a new, collaborative approach they’re calling “infection endocrinology,” she says.