As the world wrestles with a global pandemic, a study of tens of thousands of ancient skeletons has revealed how the human body evolves to fight disease, and how the diseases also evolve to become less deadly over time. Its conclusions could teach experts more about how we’ll adapt to cope with diseases in the future.
The researchers behind the new study say that it shows how germs mutate to replicate and ensure survival across as many human hosts as possible – but that this behaviour also then reduces the severity of the disease over time. In the end, the harmful microorganisms or pathogens end up reaching a sort of truce with the human body.
Leprosy, tuberculosis, and treponematoses (a group of diseases including syphilis) were the diseases analysed in the research. They can all leave marks on bones and teeth that indicate infection, and thanks to the human remains and the medical records that are available, they can be traced back as far as 200 generations.
“Each of these three diseases shows a decline in prevalence resulting from co-adaptation that is mutually beneficial for the disease and human host,” says anthropologist Maciej Henneberg, from Flinders University in Australia.
“In the last 5,000 years, before the advent of modern medicine, skeletal signs of tuberculosis become less common, skeletal manifestations of leprosy in Europe declined after the end of the Middle Ages, while skeletal signs of treponematoses in North America declined, especially in the last years before contact with invading Europeans.”
The researchers looked at three previous studies of the three diseases, covering 69,379 skeletons in total. Across the studies looked at, the ages of these skeletons varied from as far back as 7250 BCE right up until the present day.
Not all of these skeletons were from people with tuberculosis, treponematoses, or leprosy, and not all of the skeletons from people who did have these diseases would have shown physical signs on the bones. While this means the new study isn’t a strict epidemiological meta-analysis, it does mean that the sample size was large enough for the team to make some useful speculations.
None of the three diseases kills their human hosts immediately, which helps the pathogens live on and spread. But the statistically significant decline in the prevalence of tuberculosis, treponematoses, or leprosy over time suggests that either humans became more immune or tolerant or that the disease became less damaging.
“From an evolutionary perspective, it makes sense for a pathogen to cause less harm to the host on which it depends for its survival so high levels of transmission appear to be a temporary evolutionary trait which reduces as time goes on when we look at leprosy, tuberculosis and syphilis,” says anthropologist Teghan Lucas, from Flinders University.
While there are some caveats to mention – such as the different ways the three studies reported their respective results, and the need to consider other factors that can affect disease spread besides those covered here – it’s an interesting overview of the progress of diseases over time.
The COVID-19 coronavirus has only been with us a short time, but we’ve already seen the viruses mutating and changing in order to ensure its survival and to reach more human hosts. Even as vaccinations get the spread of the virus under control, experts will have to keep a close eye on how it evolves in the future.
The new research is part of the growing field of palaeopathology, the study of ancient human diseases through evidence such as skeletons, mummified remains, ancient documents and literature, and art.
“Palaeopathology is becoming an increasingly popular discipline which allows diseases which manifest on hard tissues to be studied in past populations because the diseases preserved for as long as the skeletal remains exist,” says Lucas.
“Due to the preservation of pathological signs on skeletons, it is possible to trace the process of co-evolution of the three major infectious diseases as far back as specimens have been found.”
The research has been published in PLOS One.
