Dr. Rob Henning and his team in the Netherlands are working on a way to induce hibernation, making surgery safer and slowing disease.
Dr. Rob Henning's job as an anaesthesiologist includes keeping a patient's circulation and oxygenation steady in order to minimize the amount of damage inflicted during surgery. So it's not entirely surprising that at some point in the early 90s, he started thinking about hibernation.
The appeal of induced hibernation is clear: a patient under the knife would have a slower heartbeat, meaning less bleeding, and would need less oxygen to feed their organs. Their immune system also wouldn't overreact to lesions and other trauma.
Learning how to induce hibernation could also lead to medications and treatments that could mitigate the damage done by diseases like diabetes and Alzheimer's. And in the longer term, induced hibernation could even help humans in things like space travel.
"Hibernation is great for general anaesthesia," Henning told me on the phone in Dutch. "But as our knowledge grew, we kind of segued into [looking at] the whole issue of organ damage."
There is just one problem: even today, nobody really understands how hibernation works. Biologists researching hibernating animals only measure certain bodily functions, like heart rate or body temperature. The mechanism that causes hibernation—exactly how these animals slow down all these essential processes in their cells—is a complete unknown.
The cell culture contained a high concentration of hydrogen sulphide, or H2S, which gave it that peculiar smell. The team suspected this might be what was protecting cells
The research Dr. Henning is doing now at the UMCG in Groningen in the Netherlands could change that, however.
Non-hibernating animals subjected to extreme cold will sustain major damage to their cells and organs. Hibernating animals, by contrast, suffer barely any damage.
When, say, a hamster, gets the right signals—shortening days, scarcity of food, and dropping temperatures—it starts to prepare for hibernation. It stuffs itself with food, essentially to the point that it develops the same symptoms as someone suffering from Type II diabetes. It then finds a cozy place and starts its long sleep.
If a person lays in bed too long, the results can get pretty nasty. Blood starts clotting and muscles start wasting away. Hamsters don't suffer these consequences, however, even though they show signs of the same damage humans would suffer: the lungs go through changes that are similar to asthmatics, and the brain is damaged much in the same way as with Alzheimer's. But when the hamster wakes up, all this damage disappears without a trace.
The lowered metabolism couldn't be the only explanation for this phenomenon, Henning told me—there had to be processes in the hamster's cells that protected them from damage. One of those processes was accidentally discovered by Henning's team.
Usually, refrigerating cells is the same as signing a death certificate. Pop a few human or rat cells into a fridge, and they won't survive for long. So you can imagine the surprise when a group of hamster cells was forgotten in a fridge by one of the students, and then rediscovered, still alive, a week later. Smelling like rotten eggs, but alive.
The cell culture contained a high concentration of hydrogen sulphide, or H2S, which gave it that peculiar smell. The team suspected the production of this molecule could play a large role in protecting the cells.
Their suspicions turned out to be correct. An enzyme that stimulates the production of H2S stays active in cells of hibernators when they're cooled. In non-hibernators, the enzyme switched off below a certain temperature.
When the researchers started experiments on rat cells, activating the enzyme during cooling, they found that the cells could be left at 5ºC for a few days and survive. In further experiments they found out which compounds stimulated the production of H2S, and developed a series of experimental medicines that have the same effect.
For people who work with cell cultures, this discovery was pretty revolutionary. Previously, cells could be preserved only by freezing them. This process damages the cells, and also forms ice crystals that kill a lot of them. Now, cells can be kept cooled in a sort of hibernation for a few days, allowing experiments to be pushed over the weekend, which probably led to much rejoicing among scientists.
But wait—there's more.
Henning and his team are testing out these compounds on living rats—species that do not hibernate. "We're looking at the effects of the compounds we developed, and they seem to protect the animals from organ damage," he said.
The rat is anaesthetized and injected with the compound. When researchers then cooled the rat, they found it was suddenly protected from blood clotting, organ damage, and other effects of deep cooling.
"Cooling and heating damage is very similar to the damage caused by inflammations," Henning told me. "The damage is caused by the same mechanism in both cases: oxygen radicals."
Type II diabetes is an illness that is characterized by large quantities of oxygen radicals that cause damage to the body. The same goes for obesity and Alzheimer's disease. This compound could stop that damage.
"Please note that the compound does nothing against the diabetes itself, but it stops or strongly slows the damage that would normally occur from occurring," Henning adds.
It will take a while before we'll see these kinds of medicines on the market though. The development has been taken over by a company called Sulfateq, which will validate the compound on non-hibernators, like rats, before applying for human trials.
The next step would be to use these compounds and processes during major surgeries to safely lower the patient's temperature. And after that? The European Space Agency asked Henning to be an advisor for its long space missions think tank—so if everything works out, even the sky isn't the limit.
Modern Medicine is a series on Motherboard about how health care and medical technology can move forward so rapidly while still being stuck in the past. Follow along here.