March 09 | 2022
How dozens of men across Alaska (and their dogs) teamed up to save one town from a deadly outbreak
In 1925, health officials in Alaska came up with a creative solution to save a remote fishing town from a deadly disease outbreak.
Photo by Ugur Arpaci on Unsplash
During the winter of 1924, Curtis Welch – the only doctor in Nome, a remote fishing town in northwest Alaska – started noticing something strange. More and more, the children of Nome were coming to his office with sore throats.
Initially, Welch dismissed the cases as tonsillitis or some run-of-the-mill virus – but when more kids started getting sick, with some even dying, he grew alarmed. It wasn’t until early 1925, after a three-year-old boy died just two weeks after becoming ill, that Welch realized that his worst suspicions were true. The boy – and dozens of other children in town – were infected with diphtheria.
A DEADLY BACTERIA
Diphtheria is nearly nonexistent and almost unheard of in industrialized countries today. But less than a century ago, diphtheria was a household name – one that struck fear in the heart of every parent, as it was extremely contagious and particularly deadly for children.
Diphtheria – a bacterial infection – is an ugly disease. When it strikes, the bacteria eats away at the healthy tissues in a patient’s respiratory tract, leaving behind a thick, gray membrane of dead tissue that covers the patient's nose, throat, and tonsils. Not only does this membrane make it very difficult for the patient to breathe and swallow, but as the bacteria spreads through the bloodstream, it causes serious harm to the heart and kidneys. It sometimes also results in nerve damage and paralysis. Even with treatment, diphtheria kills around 10 percent of people it infects. Young children, as well as adults over the age of 60, are especially at risk.
Welch didn’t suspect diphtheria at first. He knew the illness was incredibly contagious and reasoned that many more people would be sick – specifically, the family members of the children who had died – if there truly was an outbreak. Nevertheless, the symptoms, along with the growing number of deaths, were unmistakable. By 1925 Welch knew for certain that diphtheria had come to Nome.
In desperation, Welch tried treating an infected seven-year-old girl with some expired antitoxin – but she died just a few hours after he administered it.
AN INACCESSIBLE CURE
A vaccine for diphtheria wouldn’t be widely available until the mid-1930s and early 1940s – so an outbreak of the disease meant that each of the 10,000 inhabitants of Nome were all at serious risk.
One option was to use something called an antitoxin – a serum consisting of anti-diphtheria antibodies – to treat the patients. However, the town’s reserve of diphtheria antitoxin had expired. Welch had ordered a replacement shipment of antitoxin the previous summer – but the shipping port that was set to deliver the serum had been closed due to ice, and no new antitoxin would arrive before spring of 1925. In desperation, Welch tried treating an infected seven-year-old girl with some expired antitoxin – but she died just a few hours after he administered it.
Welch radioed for help to all the major towns in Alaska as well as the US Public Health Service in Washington, DC. His telegram read: An outbreak of diphtheria is almost inevitable here. I am in urgent need of one million units of diphtheria antitoxin. Mail is the only form of transportation.
FOUR-LEGGED HEROES
When the Alaskan Board of Health learned about the outbreak, the men rushed to devise a plan to get antitoxin to Nome. Dropping the serum in by airplane was impossible, as the available planes were unsuitable for flying during Alaska’s severe winter weather, where temperatures were routinely as cold as -50 degrees Fahrenheit.
In late January 1925, roughly 30,000 units of antitoxin were located in an Anchorage hospital and immediately delivered by train to a nearby city, Nenana, en route to Nome. Nenana was the furthest city that was reachable by rail – but unfortunately it was still more than 600 miles outside of Nome, with no transportation to make the delivery. Meanwhile, Welch had confirmed 20 total cases of diphtheria, with dozens more at high risk. Diphtheria was known for wiping out entire communities, and the entire town of Nome was in danger of suffering the same fate.
It was Mark Summer, the Board of Health superintendent, who suggested something unorthodox: Using a relay team of sled-racing dogs to deliver the antitoxin serum from Nenana to Nome. The Board quickly voted to accept Summer’s idea and set up a plan: The thousands of units of antitoxin serum would be passed along from team to team at different towns along the mail route from Nenana to Nome. When it reached a town called Nulato, a famed dogsled racer named Leonhard Seppala and his experienced team of huskies would take the serum more than 90 miles over the ice of Norton Sound, the longest and most treacherous part of the journey. Past the sound, the serum would change hands several times more before arriving in Nome.
Between January 27 and 31, the serum passed through roughly a dozen drivers and their dog sled teams, each of them carrying the serum between 20 and 50 miles to the next destination. Though each leg of the trip took less than a day, the sub-zero temperatures – sometimes as low as -85 degrees – meant that every driver and dog risked their lives. When the first driver, Bill Shannon, arrived at his checkpoint in Tolovana on January 28th, his nose was black with frostbite, and three of his dogs had died. The driver who relieved Bill Shannon, named Edgar Kalland, needed the owner of a local roadhouse to pour hot water over his hands to free them from the sled’s metal handlebar. Two more dogs from another relay team died before the serum was passed to Seppala at a town called Ungalik.
THE FINAL STRETCHES
Seppala and his team raced across the ice of the Norton Sound in the dead of night on January 31, with wind chill temperatures nearing an astonishing -90 degrees. The team traveled 84 miles in a single day before stopping to rest – and once rested, they set off again in the middle of the night through a raging winter storm. The team made it across the ice, as well as a 5,000-foot ascent up Little McKinley Mountain, to pass the serum to another driver in record time. The serum was now just 78 miles from Nome, and the death toll in town had reached 28.
The serum reached Gunnar Kaasen and his team of dogs on February 1st. Balto, Kaasen’s lead dog, guided the team heroically through a winter storm that was so severe Kaasen later reported not being able to see the dogs that were just a few feet ahead of him.
Visibility was so poor, in fact, that Kaasen ran his sled two miles past the relay point before noticing – and not wanting to lose a minute, he decided to forge on ahead rather than doubling back to deliver the serum to another driver. As they continued through the storm, the hurricane-force winds ripped past Kaasen’s sled at one point and toppled the sled – and the serum – overboard. The cylinder containing the antitoxin was left buried in the snow – and Kaasen tore off his gloves and dug through the tundra to locate it. Though it resulted in a bad case of frostbite, Kaasen eventually found the cylinder and kept driving.
Kaasen arrived at the next relay point on February 2nd, hours ahead of schedule. When he got there, however, he found the relay driver of the next team asleep. Kaasen took a risk and decided not to wake him, fearing that time would be wasted with the next driver readying his team. Kaasen, Balto, and the rest of the team forged on, driving another 25 miles before finally reaching Nome just before six in the morning. Eyewitnesses described Kaasen pulling up to the town’s bank and stumbling to the front of the sled. There, he collapsed in exhaustion, telling onlookers that Balto was “a damn fine dog.”
A LIVING LEGACY
Just a few hours after Balto’s heroic arrival in Nome, the serum had been thawed and was ready to administer to the patients with diphtheria. Amazingly, the relay team managed to complete the entire journey in just 127 hours – a world record at the time – without one serum vial damaged or destroyed. The serum shipment that arrived by dogsled – along with additional serum deliveries that followed in the next several weeks – were successful in stopping the outbreak in its tracks.
Balto and several other dogs – including Togo, the lead dog on Seppala’s team – were celebrated as local heroes after the race. Balto died in 1933, while the last of the human serum runners died in 1999 – but their legacy lives on: In early 2021, an all-female team of healthcare workers made the news by braving the Alaskan winter to deliver COVID-19 vaccines to people in rural North Alaska, traveling by bobsled and snowmobile – a heroic journey, and one that would have been unthinkable had Balto, Togo, and the 1925 sled runners not first paved the way.
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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.