A thorough inspection of an old Viking latrine in Denmark has confirmed what we all sort of suspected: the lives of early Scandinavians were not especially sanitary. These otherwise hardy people were crawling with intestinal parasites, mostly due to the food they ate, and because they kept their livestock close. Like, roommate close.
The outhouse in question was active a thousand years ago, but a recent study by researchers at the Liverpool School of Tropical Medicine (LSTM) shows the genes of some modern people are still haunted by the ghosts of those Viking parasites. They may even contribute to the reason lung diseases like chronic obstructive pulmonary disease (COPD) and emphysema are so prevalent worldwide, affecting around 300 million people — nearly 5 percent of the global population.
Of course, these types of diseases are most common in smokers, but there is one inherited risk factor, which is compounded by smoking, that’s found in people who have slightly different forms of a protein called alpha-1-antitrypsin (A1AT). These deviant forms of A1AT are particularly common in Scandinavian populations.
A1AT protects the liver and lungs from enzymes called proteases, which are produced by our immune cells, but they’re also produced by parasitic worms. The explanation for why some people have deviant forms of A1AT has stumped researchers for years, but this study shows that they can be traced back to the way Vikings adapted over generations to being completely overrun by parasites.
“Vikings would have eaten contaminated food and parasites would have migrated to various organs, including lungs and liver, where the proteases they released would cause disease,” says study lead author Richard Pleass in a press release.
These deviant forms of A1AT were a helpful adaptation for Vikings a couple thousand years ago because they bonded to an antibody called immunoglobulin E (IgE) found in the lungs, and which protects against the proteases introduced by parasites.
“The deviant forms appear to bind IgE very well and protect the antibody from cleavage by proteases,” says Pleass in an email.
And as Vikings didn’t smoke tobacco and lived relatively short lives anyway (your average Viking would have been unbelievably fortunate to make it to the age of 50), the fact that the deviant forms of A1AT didn’t protect them as effectively from lung disease was not as important as the fact that they helped them deal with their worms.
These days, however, things are different. Some people smoke tobacco, and in most places in the world, we’ve got a decent grasp on food safety and appropriate social boundaries with our farm animals. We also regularly live past the age of 50. We need A1AT to prevent the protease from corroding our lung tissue, yet some of us are still living in the Viking Age.