Protein-rich products – from cereal to crisps to coffee – are all over supermarket shelves, but mounting evidence in non-human animals suggests that restricting our intake could slow ageing and extend lifespan. So, does that mean eating too much protein is harmful?

“We have this impression that dietary protein is sort of a universally good thing,” says at the University of Wisconsin-Madison. But according to the latest review of the evidence, “increasing dietary protein, beyond what’s needed, for sedentary individuals or animals leads to metabolic problems and can lead to shorter lifespan as well”, he says.

But others point out that nutritional studies in animals like mice and rats don’t readily translate to people, and a high protein intake has been linked to benefits in humans.

Lamming and his colleagues sifted through more than 300 studies, mostly in sedentary rodents, that explored how restricting protein intake to the minimum required to prevent deficiency affects ageing and lifespan.

In these studies, rodents generally either ate the equivalent of the minimum protein requirement recommended by US guidelines – 0.8 grams of protein per kilogram of body weight – or about double that. The latter is similar to the intake recently recommended by US dietary guidelines for optimal health, 1.2 to 1.6 grams of protein per kilogram of body weight.

In one study, rats that ate around the minimum protein intake lived nearly 120 days, or more than 50 per cent, longer than those that ate about double that.

This may be because protein restriction increases levels of the hormone FGF21, says Lamming. In rodents, this acts on the brain, fat tissue and the liver to improve blood sugar levels and reduce the number of senescent cells. These cells, which accumulate with age, have stopped dividing and cause chronic inflammation.

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Restricting protein intake has also been shown to dampen the activity of a protein called mTORC1 in mice. mTORC1 ordinarily stimulates cell growth, but reducing its activity boosts cellular repair. “It essentially switches cells from a proliferative state, where they’re growing and engaging a lot of metabolism, to one where they’re dividing more slowly, if at all, and focusing on repair,” says Lamming. Studies suggest this in mice, he says.

All this suggests that the recent trend to up our protein intake is probably fine among people who exercise regularly, because they may need more protein to repair muscle damage, but eating more than is needed could cause harm in sedentary individuals, says Lamming.

But at the University of Illinois Urbana-Champaign points out that rodents vary hugely from people when it comes to protein metabolism. For instance, mTORC1 is activated by feeding, and while people tend to a have a few big meals a day, rodents graze more regularly. Protein restriction may therefore affect mTORC1 pathways differently between the different species, he says. We are also more exposed to factors that accelerate ageing, like infections and extreme heat, than lab animals, says Layman.

What’s more, the review does not include most of the studies in people that suggest that upping our protein intake beyond the minimum , he says.

Dudley says no studies were intentionally omitted. “We were focused on protein restriction, not the many studies looking at higher levels of protein intake,” he says. Beyond building muscle and preventing frailty, there’s mixed evidence on whether a higher protein intake helps with ageing, says Dudley.

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For instance, one study linked this to a reduced risk of age-related muscle loss, or sarcopenia, among . But the rates of sarcopenia were so low that the link is unreliable, says at the University of Sheffield in the UK.

Still, some studies showed that restricting intake of certain amino acids – such as isoleucine and valine, which are highest in meat, fish and dairy – in mice has a similar effect to limiting overall protein intake, says at Nottingham University, UK.

Atherton says he is planning a study to investigate whether drugs that deplete specific amino acids in people improve outcomes like blood sugar control, with results expected in the next few years.  

DNA samples collected from Inca mummies have confirmed the presence of a strain of smallpox that first emerged in Europe.

“We interpreted this as the first direct molecular evidence of smallpox introduction into the Americas through European colonisation,” says at Trinity College Dublin, Ireland.

Smallpox was the scourge of humanity for centuries until its eradication in the 1980s, through vaccination, from all but a few high-security medical laboratories. Severe strains of the virus had a mortality rate of up to a third and left survivors with scars from the blisters and scabs that cover the skin and fill with pus.

The disease was particularly brutal in parts of the world colonised by Europeans, such as and the Americas, where Indigenous populations had no natural immunity, resulting in millions of deaths.

In the Americas, historical reports record that smallpox began devastating Indigenous communities in the early 16th century, after the arrival of European colonists.

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at the University of Dundee in the UK, who wasn’t involved in the new research, says the waves of epidemics, including smallpox, that spread across the Americas were some of the most important events in history. “These diseases killed perhaps 95 per cent of the Indigenous population of the Americas and allowed for European colonisation,” he says.

Nakagome and his colleagues studied samples of bone from mummies found at an archaeological site known as Camarones 9 in northern Chile, discovered in 1957. Over subsequent decades, 41 mummified bodies wrapped in blankets and buried with grave goods were recovered from the site.

“While the original aim was to study the human DNA, we also searched for DNA from ancient pathogens,” says Nakagome. “That is when we discovered fragments matching the smallpox virus in two individuals.”

The first was a woman who was 30 to 35 years old at the time of death, and the second, an 18-to-20-year-old man, was revealed by carbon dating to have died between 1492 and 1631.

By reconstructing the virus’s genomes and comparing them with other ancient and modern smallpox viruses, the team found that they belonged to a lineage of smallpox that includes early medieval and early modern European strains.

The discovery adds weight to the possibility that small skin lesions on the trunks of the mummies, previously attributed to chronic arsenic exposure, may in fact have been the distinctive pustules that scar the skin of smallpox victims.

“This finding allowed us to identify a small group of people impacted by the virus for which no historical record exists,” says team member at the University of Chile in Santiago. Before the new research, the pathogen was known only from historical accounts of large-scale outbreaks, she says.

The work was particularly sensitive because of the disturbance of the original remains and the loss of material during analysis, both considered extremely controversial subjects to Indigenous people and the scientific community. “We never forget that behind every DNA extraction is a person, not a data point,” says de la Fuente Castro.

Ward welcomed the new research. “Understanding exactly what was killing native peoples and why they were so susceptible to epidemic disease is a vitally important issue,” he says.

Historians are now trying to understand how Europeans deliberately or inadvertently fuelled the spread of epidemics like smallpox, he says. “Without these epidemics, colonisation of the Americas would have been very different.”