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.  

A cognitive “speed training” game that cuts dementia risk by 25 per cent alters levels of beta-amyloid, a protein that clogs up the brain in Alzheimer’s disease, in men, but not in women.

It is the first time brain training has been shown to influence the levels of a neurodegenerative marker, strengthening the evidence suggesting that mental exercises can boost brain health.

“One of the main markers that’s indicative of future dementia risk got better for men who completed cognitive speed training,” says  at Clemson University in South Carolina, who presented the research at the Alzheimer’s Association International Conference in London on 12 July.

The computer-based speed training involves recalling where objects have flashed up, with the task becoming harder as performance improves. A prior 20-year study by some of Chai’s colleagues showed that people aged 65 and older, who did the training were 25 per cent less likely to be diagnosed with Alzheimer’s disease or a related form of dementia compared with a control group.

In the latest study, Chai and her team recruited a separate group of 53 people from the US aged 65 and older, 13 of whom were male. About a third of the participants were asked to complete between 2 and 4 hours of speed training each week for 4.5 months.

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The remaining participants were either told to spend the same amount of time playing games such as Solitaire, word search and a game similar to Connect 4, or to complete another kind of brain training in which they had to strategically track objects and switch between tasks.

To explore how speed training may reduce dementia risk, the team collected blood samples from all of the participants at the start and end of the training period.

This revealed that, among men, speed training increased the ratio of two forms of beta-amyloid found in the blood, which suggests the training boosted the brain’s ability to clear beta-amyloid 42. This protein forms clumps called plaques in the brain during Alzheimer’s disease, disrupting brain function. The other two kinds of training had no effect.

“It’s a really cool finding,” says  at McGill University in Montreal. “It is definitely strengthening what they’ve [previously] shown with the reduction in dementia.”

Some Alzheimer’s treatments, such as lecanemab, have been designed to help clear amyloid from the brain, but they only marginally slow cognitive decline during Alzheimer’s disease. The limited benefit seen in trials is probably down to these treatments being taken at a relatively late stage of the condition, when substantial brain damage has already occurred, says at University College London.

Engaging in cognitive training to reduce beta-amyloid build-up before dementia develops may have a bigger effect on dementia because it would be done before much brain damage has occurred, says Castegnaro.

However, cognitive training had no effect on amyloid levels in female participants in the study. This suggests that speed training reduces dementia risk in different ways in women and men, says Chai.

The team hopes to explore how speed training may benefit women in future studies, says Chai. But first, the findings need to be verified in geographically and ethnically diverse groups, says Novozhilova.

Human eggs that contain too many or too few chromosomes can lead to miscarriage, IVF failure and conditions such as Down’s syndrome. Now, researchers have found that giving the eggs a single injection can substantially reduce the risk of chromosome error. The approach could eventually boost the chances of success for older women undergoing IVF.

“It really seems like a big deal,” says at Nilo Frantz Reproductive Medicine in Porto Alegre, Brazil, who wasn’t involved in the new research. “To my knowledge, this is the first [therapy] to show such clinical potential for correcting this major cause of IVF failure.”

During a process called meiosis, egg and sperm cells eject exactly half of their genetic material. This means that when egg and sperm combine during fertilisation, they form an embryo with a complete genome. Sometimes, however, a sperm or egg cell has slightly more or slightly less than the half genome it should contain. This is a condition known as aneuploidy.

Aneuploidy affects about in the early 30s and becomes more common with age. “Already in the late 30s, more than 65 per cent of all eggs are aneuploid,” at Ovo Labs, a biotechnology company in Germany, told the audience at the conference in London on 6 July.

Clinicians sometimes screen IVF embryos for aneuploidy when treating couples at greater risk of miscarriage or IVF failure. , conditions caused by the genetic error – which include Down’s syndrome – are only detected via blood tests and ultrasound scans taken during the first trimester of pregnancy. Until now, there have been no ways to reduce the risk of aneuploidy occurring in the first place, says Zielinska.

Now, Zielinska and her colleagues have found that the level of a protein called shugoshin-1 is substantially lower in older mouse and human eggs than in younger ones. Shugoshin-1 helps with a stage of meiosis in which two copies of each chromosome line up along the middle of an immature egg cell. The protein maintains the molecular glue that holds each pair together.

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When sperm penetrate an egg, the two copies of the egg’s chromosomes separate and move to opposite sides of the cell. One end ultimately forms the final egg cell, and the other end is discarded.

But in older eggs, the glue holding the chromosome pairs together degrades, which can cause the two copies of each chromosome to separate before fertilisation. When this happens, the chromosomes spread unevenly throughout the cell – which means the resulting egg may be aneuploid.

To explore whether replenishing shugoshin-1 could prevent aneuploidy by helping to hold chromosome pairs together, the team collected 111 spare, immature eggs from more than 30 women aged between 22 and 43 who were banking eggs or undergoing IVF.

The team injected the genetic code for shugoshin-1, in the form of mRNA, into one or more of each donor’s eggs, and left other eggs from the same donor untreated.

A few hours later, chromosomes had prematurely separated in 53 per cent of the untreated eggs, whereas this figure was nearly half – 29 per cent – in the treated ones. In eggs from nine donors who were aged over 35, aneuploidy rates were 65 per cent, on average, in untreated eggs. But in treated eggs, the average figure was just 44 per cent. This reduction wasn’t statistically significant, although this is probably because of the study’s small sample size, according to the researchers.

Common IVF test misses some genetic abnormalities in embryos

Human embryos formed with in vitro fertilisation can develop genetic abnormalities in the time between genetic testing and implantation – though this may not affect their viability

Further experiments showed the approach could prevent aneuploidy in mouse eggs, which were then successfully fertilised to produce healthy offspring.

No side effects were seen in the mouse or human studies. “We’ve achieved live births in mice, so, from that perspective, we’re confident that this approach is not interfering in the mouse model with any steps of embryo development, and it doesn’t interfere with pup health and pregnancy health,” Zielinska told the conference audience.

The researchers are now working towards testing the effects of shugoshin-1 in people. This would involve tweaking standard IVF to use immature eggs rather than mature ones, but this change would be fairly easy to implement, says Zielinska.

She hopes the therapy, which the team calls EmbryoProtect, will provide an affordable way to improve IVF for older women. “We anticipate that the treatment will cost a fraction of the cost of a full IVF cycle,” says Zielinska. “By meaningfully improving IVF success rates, especially for women over 35 where baseline success is low, we hope that fewer attempts will be needed to conceive.”

It may feel like the exhaustion of caring for a newborn leaves little room for romance. Now, researchers have found that people really do seem to love their partner less in the first year of parenthood – but there are ways to buffer against this.

Prior studies suggest that in the two years after having a baby, but these rarely account for the state of things before pregnancy. When at the University of Wrocław, Poland, started a family, she wanted to know how her relationship was set to change. “I got pregnant, and then I wrote the grant proposal to look at this,” she says.

With her colleagues, Sorokowska recruited nearly 300 heterosexual couples without children who had been together for at least two years. Every six months, for at least two years, the participants completed surveys – independently of their partner – in which they ranked on a scale from 0 to 6 how much they loved their partner and how committed they were.

The researchers analysed results from 71 of these couples who had a baby during the study and found that pregnancy itself had no impact. But – in line with the prior evidence – the participants reported loving their partners less and being less committed to maintaining the relationship within one year after childbirth. There was no change in this time among the couples who remained without children.

Sorokowska – who presented the results at the meeting in Edinburgh, UK, last month – plans to continue surveying these couples until their children reach adulthood, to determine whether the effects are long-lasting. But prior research suggests that . “There’s a steep decline in [relationship satisfaction] in the first year, only a small decline from year one to two, and then it seems to slowly recover [several years later],” says , an independent psychologist in Zurich, Switzerland.

The researchers didn’t measure how these initial changes impacted the new parents’ well-being, but Rauch-Anderegg doubts they cause substantial distress. “It’s not that we can say all these couples have relationship distress that means they need to see a therapist, but they certainly can notice something changed in their relationship,” she says.

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Some of the factors that may be responsible include the residual physical and hormonal turmoil of pregnancy after giving birth, and new parents feeling overwhelmed by childcare duties. “Simply sitting on a couch to Netflix-and-chill with your partner, or going for a walk, [often] becomes impossible,” says Rauch-Anderegg.

To prevent this, or bring some of the magic back, Rauch-Anderegg recommends asking loved ones for help and sharing any concerns with your partner. “You can make sure you’re communicating clearly about your vision for having a kid – what is the core of your relationship that you want to maintain even if there is a baby? Whether it’s a hike once a year or 20 minutes of partner time a week.”