If you are trying to lose weight, knowing what fuel your body is burning is largely guesswork. Bathroom scales may take weeks to register any change, and even then, they can’t distinguish between loss of fat, muscle and water. Smartwatches and gym equipment can also only infer whether you are in a “fat-burning zone” from measures such as heart rate.

But now researchers have developed a handheld breathalyser that detects whether you are burning fat from a single exhalation.

When carbohydrate supplies run low, the body increasingly relies on fat for energy, converting some of it into molecules called ketones. This process also produces a molecule called acetone, which passes into breath.

Although breath acetone has long been used as a window into metabolism, measuring it has typically required bulky laboratory equipment. Blood-ketone tests are also widely used, but require repeated finger pricks.

In recent years, several companies have developed breathalyser-style devices that detect acetone, but accurately measuring the tiny amounts in exhaled breath is challenging. This is because humidity, variations in breathing technique and chemically similar compounds, including alcohol, can interfere with the sensors.  

To overcome these problems, at ETH Zurich in Switzerland and his colleagues have combined an acetone-specific sensor with miniature filters that remove moisture and other interfering compounds. An accompanying smartphone app also guides users on the correct breathing technique to capture acetone at the end of the third breath, when it most closely resembles levels in the bloodstream.

To test the device, which is commercially available under the name Nutrion, the researchers compared its readings with laboratory measurements of breath-acetone and blood-ketone levels in 12 volunteers, who had no known health problems, under a range of dietary and exercise conditions.

They found that the device closely tracked both laboratory breath-acetone measurements and blood-ketone levels.

The researchers – some of whom are shareholders or on the board of Alivion, a spin-off of ETH Zurich that makes Nutrion – also found that it was sensitive enough to detect subtle short-term fluctuations in metabolism, which is important because the body continually switches between fuels during everyday activities.

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“We were able to resolve even the finest changes in breath as someone started to burn fat,” says Güntner, who is an advisor to Alivion. “After more intensive exercise, we saw breath acetone increase, but if someone then drank a sugary drink or ate a carbohydrate-rich meal, we could see it immediately fall again.”

Such information could be useful when dieting or intermittently fasting, when the goal is to extend the periods during which the body burns fat. But it could also have applications beyond weight loss. Ketogenic diets – high-fat, very low-carbohydrate diets that trigger ketone production – are used to treat some forms of drug-resistant epilepsy, particularly in children. But monitoring ketosis usually involves repeated finger-prick blood tests. An ongoing trial is evaluating Nutrion as an alternative.

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“It is really good to hear that they have moved into clinical trials in epilepsy, which would take some logistical strain off home testing for blood-ketone monitoring and potentially make management of epilepsy easier going forward, while still providing objective data,” says at Elevate Performance Testing in Wymondham, UK, which provides personalised testing to athletes.

The effects of Nutrion are also being investigated alongside , GLP-1 weight-loss therapy and ketogenic diets during cancer treatment, says Güntner. “There are many situations where monitoring ketone production is important, and it would be useful to have this information immediately available.”

Dugdale-Duwell – who has that measures metabolism via exhaled carbon dioxide – adds that athletes might benefit if Nutrion enables them to tailor their carbohydrate intake to their metabolic responses. But it remains unclear whether this would improve performance. “I wouldn’t be surprised to see the device used from a marginal-gains perspective,” he says.

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.

The best treatment for multiple sclerosis (MS) might be antivirals that target the Epstein-Barr virus. Pharmaceutical companies are now being called on to develop such drugs after researchers studied the immune responses of people with and without the condition.

“There aren’t good Epstein-Barr virus drugs currently available, but they can be developed,” says at Harvard Medical School. “That might be the most useful specific therapy for MS in the future.”

MS is caused by an immune attack on myelin, a fatty sleeve that wraps around nerves. The loss of myelin reduces their ability to transmit signals and can cause a wide range of symptoms, including muscle weakness. Drugs that suppress the immune system can slow the progression of the condition.

There is strong evidence that the Epstein-Barr virus (EBV), which causes mononucleosis, or glandular fever, is also the cause of MS. “I think most MS researchers now would agree that EBV plays a major role in the development of the disease,” says team member at the Harvard T.H. Chan School of Public Health.

But exactly how remains a mystery. Almost everyone is infected with EBV during their childhood or teen years. It mainly infects immune cells known as B-cells, where it can remain dormant for the rest of a person’s life. But in some cells, the virus can reactivate.

The big question is why only around 1 in 1000 people develop MS when nearly everyone gets EBV. This suggests there is something different about the immune response to EBV in people who go on to develop MS, says team member at Massachusetts General Hospital. “Our question for this study was: in people with MS, what parts of EBV does the immune system respond to? And do those responses look different from people who don’t have MS?”

The team focused on immune cells known as CD4 T-cells, which circulate in the body. Although these aren’t the cells that directly attack myelin, there are multiple lines of evidence suggesting they play a role in MS, says Drosu.

The team found that, in 30 people with MS, most of the CD4 T-cells targeting EBV were specifically targeting viral proteins produced when the virus is actively replicating, rather than the proteins associated with its dormant stage. What’s more, people with MS produced twice as many of these cells, on average, as 30 people without the condition.

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The researchers then looked at CD4 T-cells in 60 people with MS before and after they began drug treatments that reduce their number of B-cells. They found these treatments reduced the T-cell response to EBV almost to the levels seen in people without MS.

In addition, the team found low levels of EBV in the saliva of these people before they were treated to reduce their number of B-cells, which shows that the virus was replicating in their bodies. After treatment, viral levels dropped below detectable levels in most people.

The thinking has been that B-cells help drive the harmful immune response in people with MS, says Levy, and this is why drugs that reduce B-cell levels are effective. But the results suggest these drugs also work by eliminating B-cells infected with EBV, he says, thereby reducing the immune response caused by active viral replication. “We’re thinking that depleting B-cells is also depleting the reservoir of the Epstein-Barr virus.”

If so, targeting EBV directly with antivirals might be just as effective as B-cell-depleting drugs, but without the undesirable side effects of treatments that weaken the immune system, such as an increased risk of infections. “I think a lot of patients would prefer a specific drug,” says Bjornevik. “If we can show that an antiviral had a similar effect as the most effective MS drugs, I think there will be a big market for that drug.”

Another approach already being trialled for treating MS is using modified immune cells called CAR T-cells. While existing drugs merely reduce B-cell levels, CAR T-cells can temporarily eliminate them altogether. Dozens of people with MS have gone into remission after CAR-T treatment, says Levy.

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But EBV might linger in some other cell types and reinfect B-cells as they slowly recover in the years after the CAR T-cell treatment, he says. “Then we would need the antivirals… so we just have to wait and see.” CAR T-cells can also have serious side effects, says Bjornevik, so antivirals could be safer as well.

There are also vaccines against EBV under development. “If people don’t get infected with EBV, their risk of MS would be virtually zero,” says Drosu. “So I think vaccines are [a] very promising strategy to eradicate MS.”

But 1000 people would have to be vaccinated to prevent just one case of MS, Levy points out. However, EBV causes many other problems, including a number of cancers, and has also been linked to other autoimmune conditions, such as lupus and rheumatoid arthritis.