July 13 | 2018
3 Things Microbes in Space Can Teach Us About Our Health on Earth
Kristina Campbell is a Canadian writer who covers microbiome science for digital and print media around the world. She is author of The Well-Fed Microbiome Cookbook (Rockridge Press, 2016) and co-author of an academic textbook for health professionals, Gut Microbiota: Interactive Effects on Nutrition and Health (Elsevier, 2018).
A 3D rendering of an astronaut in outer space.
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We all know the typical astronaut accessories—the EVA suit, the oxygen tanks, the radio assembly. But there's an invisible part of each space mission that's often overlooked: the trillions of microorganisms that hitch a ride.
Observing responses of pathogens in space could help scientists figure out how to outsmart them when they cause trouble on Earth.
Dr. Sarah Wallace is a NASA microbiologist who aims to keep microbes from causing problems for U.S. astronauts aboard the International Space Station. According to Wallace, research on microorganisms in space has more than cosmic importance. It can also reveal things about our health here on Earth:
1) Avoiding disease isn't all about maintaining a sterile environment.
NASA has a great track record of keeping the crew healthy on space missions. But surprisingly, it's not from having kept the space flight environment as sterile as possible.
Wallace says, "We [monitor] the environment but unless we find something that's medically significant, or [in] super high numbers, we're not going to do anything."
Not only is it impossible for astronauts to live in completely sterile quarters—crew members, after all, are microbe-shedding machines—but it may not even be desirable, given what we now know about the human microbiome. Scientists have found that the entire community of microorganisms (bacteria, archaea, fungi, and viruses) living in and on us likely have an active role in keeping us healthy. This means that down on the ground we need to let go of the germophobe idea that eradicating all microbes is always better for our health.
2) Disease-causing microbes change their behavior under different conditions.
Remember the recent E. coli O157:H7 outbreak linked to romaine lettuce? We're still grappling with a lot of pathogen problems here on Earth. One reason is that scientists are still learning which strategies these disease-causing microorganisms are capable of employing under different conditions.
Space missions are associated with a major shift in gut microbiome composition—as shown in NASA's twin study.
Wallace says experiments with Salmonella Typhimurium showed that the pathogen became more virulent in space. Yet curiously, the opposite seemed to happen to Staphylococcus aureus under space-flight-like conditions—it became more benign.
"The way these organisms have evolved, certain triggers [in the space flight environment] might be dictating how they're responding," Wallace says.
Observing these responses could help scientists figure out how to outsmart the pathogen when it causes trouble on Earth. "It's giving us some great insights into how we could target them differently in the future," she explains.
3) Major shifts in the gut microbiome could affect health in specific ways.
Scientists still have a lot to learn about which changes in an adult's gut microbiome actually cause a change in health status. In fact, microbiome-focused therapeutics companies are in hot pursuit of these connections.
Space missions are associated with a major shift in gut microbiome composition—as shown in NASA's twin study, which followed astronaut Scott Kelly during a year aboard the ISS while his identical twin brother Mark (a retired astronaut) stayed on the ground. Scott experienced simultaneous changes in telomere length and bone formation; were these related to the gut microbial differences?
Wallace says a soon-to-be-published study of nine additional astronauts could help answer this question. The research may reveal how closely gut microbiome shifts track health outcomes, and the reversibility of the changes.
She emphasizes the science from her lab isn't meant to help only the small minority of humans who will ever go to space: "That's always our goal—that our research is helping people on Earth."
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Kristina Campbell is a Canadian writer who covers microbiome science for digital and print media around the world. She is author of The Well-Fed Microbiome Cookbook (Rockridge Press, 2016) and co-author of an academic textbook for health professionals, Gut Microbiota: Interactive Effects on Nutrition and Health (Elsevier, 2018).
October 23 | 2023
Gene Transfer Leads to Longer Life and Healthspan
In August, a study provided the first proof-of-principle that genetic material transferred from one species to another can increase both longevity and healthspan in the recipient animal.
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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.
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Eve Herold is an award-winning science writer and consultant in the scientific and medical nonprofit space. A longtime communications and policy executive for scientific organizations, she currently serves as Director of Policy Research and Education for the Healthspan Action
Coalition. She has written extensively about issues at the crossroads of science and society, including regenerative medicine, aging and longevity, medical implants, transhumanism, robotics and AI, and bioethical issues in leading-edge medicine. Her books include Stem Cell Wars and
Beyond Human, and her latest book, Robots and the People Who Love Them, will be released in January 2024. Her work has appeared in Vice, Medium, The Washington Post and the Boston Globe, among others. She’s a frequent contributor to Leaps.org and is the recipient of the 2019
Arlene Eisenberg Award from the American Society of Journalists and Authors.
A new study provides key insights in what causes Alzheimer's: a breakdown in the brain’s system for clearing waste.
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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
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Matt Fuchs is the host of the Making Sense of Science podcast and served previously as the editor-in-chief of Leaps.org. He writes as a contributor to the Washington Post, and his articles have also appeared in the New York Times, WIRED, Nautilus Magazine, Fortune Magazine and TIME Magazine. Follow him @fuchswriter.