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.

Lamming 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 is mixed evidence on whether a higher protein intake helps with ageing, says Lamming.

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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 the University of Nottingham, 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.  

As we age, our body loses its ability to clear out zombie-like cells that have stopped dividing, instead dripping out poison and turning other cells rogue. Restoring the ability to remove these “senescent” cells prevented signs of cognitive decline and frailty in older mice, with hints that the same outcomes could occur in people.

“What’s attractive about this study is that it is not trying to kill [senescent] cells directly,” says at University College London, who wasn’t involved in the research. “It is repairing the body’s own waste-disposal system that should have removed them in the first place.”

To better understand why this system goes awry, at Stanford University, California, and her colleagues compared mice aged 6 to 8 months (roughly equivalent to people in their 20s) with mice aged 23 to 25 months (equivalent to people in their late 60s or 70s). They found that the older mice had more of these senescent cells in their organs, including the liver and spleen, as well as in their bone marrow.

Specifically, the senescent cells were neutrophils, immune cells that are normally the body’s first line of defence against infection. These would normally be cleared away by macrophages residing in tissue, which remove damaged cells and debris, but this ability .

Andreasson and her colleagues traced this decline to prostaglandin E2, a signalling molecule that increases with age. They found that higher prostaglandin E2 activity overstimulates a receptor called EP2 on tissue-resident macrophages, which leaves them less able to remove senescent cells.

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Next, the team tested whether blocking this overstimulation could improve signs of ageing by genetically modifying the EP2 gene from tissue-resident macrophages in older mice. These animals went on to clear more senescent neutrophils and showed signs of healthier ageing, including lower levels of inflammation, reduced muscle loss, less visceral fat and better mobility, compared with unmodified mice of the same age. They also performed almost as well as young mice in memory tests.

“We were very surprised at the magnitude of the effect,” says Andreasson. “The paradox is that we had only reduced the level of [the receptor protein] EP2 by 50 per cent.”

The researchers also tested an experimental drug that blocks the EP2 receptor protein. When given orally to older mice for two months, this caused similar age-related improvements to those experienced by the genetically modified mice.

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“This is a very promising study, but we need to be careful,” says Gilroy. “[The EP2 receptor] is part of a normal signalling system, and blocking it throughout the body could have unwanted effects.” The mice experienced no known side effects, but Gilroy says it may be safer to target the EP2 receptor in ageing macrophages specifically.

Finally, the team found similar patterns in human tissue, with liver samples from older people showing higher EP2 receptor activity and more senescent neutrophils. “The human data are supportive, but still correlative,” says Gilroy. “We haven’t yet shown that blocking [the EP2 receptor] can restore neutrophil clearance in aged human tissue.” 

The researchers are now planning to study whether this process affects the onset of conditions such as Alzheimer’s disease.

Resting body temperature rises a little bit each year in women from the age of 18 to 42, for reasons that are still being figured out. The finding opens up the possibility of using temperature-sensing wearables to track ageing and detect perimenopause or potential health problems.

“We think there is a lot of information about health in the temperature signal,” says  at SRI International, a research institute headquartered in California. “We hope this facilitates investigations to identify novel markers of conditions – it may be an untapped resource of information about our health.”

Gombert-Labedens and her colleagues analysed data from a  that asked more than 750 women aged 18 to 42 to measure their oral or rectal temperature with a thermometer every day when they first woke up.

The readings showed that, on average, body temperature was lower during the first half of the participants’ menstrual cycles and higher during the second half, after ovulation occurred. Many fertility-tracking apps use this temperature jump to predict a user’s fertile window.

Gombert-Labedens and her colleagues re-examined the data in more detail to investigate the effect of age on temperature across different stages of the menstrual cycle. They found that each year from age 18 to 42, the participants became a fraction warmer, on average. As a result, those aged 35 and older tracked about 0.05°C hotter than the younger subjects across both halves of the menstrual cycle.

This is consistent with the team’s previous research that found that finger skin temperature, measured continuously by a smart ring, was  than in those aged 18 to 35.

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Further research is required to explain why this temperature increase occurs, but it probably has something to do with hormonal changes, especially towards the end of the reproductive years, says Gombert-Labedens. When perimenopause begins, temperature can increase suddenly and cause hot flushes and night sweats, but it’s unclear whether this is linked to the same mechanisms, she says.

The study only included women who did not use hormonal contraception and did not have hormonal conditions such as PMOS (polyendocrine metabolic ovarian syndrome, previously known as PCOS), so we don’t yet know how these factors might affect body temperature over time.

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Other research has found that after menopause, body temperature in women tends to  and become similar to that of men.

The higher temperature around midlife may explain why anecdotally, some women at this age say they don’t feel the cold as much as they used to, says Gombert-Labedens. “We speculate that the higher temperature in midlife women could influence their perception and reaction to environmental temperature,” she says.

As smart rings and other temperature-sensing wearables become more popular, it may be possible to identify patterns or deviations in individuals’ temperature trends that signal the approach of menopause, provide an estimate of their rate of biological ageing or detect early signs of ovarian cancer or other conidtions, says Gombert-Labedens.