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Scientists confirm fruit and vegetable skin really is good for you
Fruit and vegetable skin is often rich in fibre
Ekaterina Vasileva-Bagler/Getty Images
Some people are convinced that fruit and vegetable skin are particularly nutritious, and now scientists have confirmed the idea. They have discovered that these parts of fruits and vegetables often contain far more fibre than the flesh we normally consume.
The finding suggests cooks are unwittingly discarding fibre-rich food by chucking out the seeds, skins and stems of fruits and vegetables when preparing a meal.
Home cooks and caterers should adopt “root to tip” eating and start cooking with squash peel, watermelon rind and pepper stalks to improve the public’s intake of dietary fibre, the team says.
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“We’ve really got to shift our purchasing habits to buy whole fruits and vegetables, and then use all of the fruits and vegetables in dishes,” says Rachel Gibson at King’s College London.
Gibson and her colleagues tested the fibre content of 12 fruits and vegetables, including butternut squash, kiwi fruit, watermelon, broccoli and bell pepper. The team measured the fibre content both in the parts typically consumed and the parts that usually go to waste.
They found that, in 10 of the 12 produce types, the normally wasted components contain more fibre than the commonly consumed parts. Butternut squash seeds and skin, for example, contained 9.25 grams of fibre per 100 grams, compared with 2 g of fibre per 100 g of squash flesh. Meanwhile, the skin and core of a pineapple core contains 450 per cent more fibre than the flesh. These skin and core components are often tough to chew, but the researchers say they can be blended, grated or roasted to make them more palatable.
Just 4 per cent of British adults meet the recommended minimum daily intake of 30 g of dietary fibre, with the average adult consuming around half that per day.
Gibson suggests caterers could use the findings to design fibre-rich meals using more produce that would otherwise go to waste. This could reduce food waste and cut costs for commercial kitchens, as well as increasing dietary fibre intake, she says.
King’s College London’s canteen piloted a “root to tip” menu in May 2025. Meals included a West African peanut stew made with all of a butternut squash, kale stalks and leek tops, and a watermelon salad featuring pickled watermelon rind.
Eating a larger proportion of harvested fruit and vegetables will also improve the resilience of the food system in the face of climate shocks, says Gibson. “Everything we pull out of the ground that we can eat, we should be eating.”
Christian Reynolds at City St George’s University of London says the research is an “exciting investigation”. But he points out that the most carbon-intensive food waste is meat and dairy products. Reducing fruit and vegetable waste is therefore “part of the solution, but it’s not the only thing we need to do”, he says.
Journal Reference:
International Journal of Food Sciences and Nutrition
DOI: 10.1080/09637486.2026.2734852
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Inhaling CO2 may rescue nerves’ ability to regrow
Breathing out after birth switches off the ability of tissues to regenerate, a study in mice suggests. But the pathway seems to be reversible
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Why the world’s first spinal cord transplant is so controversial
Shutterstock/PeopleImages
The virologist Jonas Salk said that “hope lies in dreams, in imagination and in the courage of those who dare to make dreams into reality”. Salk was certainly daring – he risked paralysing himself, his wife and their children while testing his polio vaccine. Thankfully, it paid off. None of them experienced any ill effects and his work is credited with saving millions.
Risks have to be taken for medicine to advance, and someone is always the first to receive a treatment. But there are risks, and then there are risks.
Salk tested his vaccine on cells, monkeys and children who had already had polio before turning his unexposed family into guinea pigs. His approach is far from standard protocol today, but he did a lot to reduce the risk of something going wrong.
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There is less evidence to justify an operation that took place this month in Russia. Details are scant, but the procedure involved cutting out a section of spinal cord from someone with a complete spinal cord injury and gluing in a replacement piece from a donor. The transplant was a world first, but there is little evidence to believe it will have worked or that now was the time to try it.
The transplant was a world first, but there is little evidence to believe it will have worked
History tells us that acting ahead of medical evidence can have catastrophic results. Take the first synthetic organ transplants, which replaced tracheas with plastic tubes. The surgeon who fitted them admitted they hadn’t been tested on large animals because they “didn’t have the time”. Complications and deaths followed.
With new medical procedures, the gold standard is randomised controlled trials, which are costly and take time, but they aren’t the only route. When someone is critically ill, there are compassionate-use protocols that make interventions available before they are fully tested. Pig kidney transplants are currently being trialled this way, for example.
The dream of spinal cord transplants will surely become a reality one day, but only if the science underpinning them is built first. Courage, dreams and imagination are of course good, yet with experimental surgeries, evidence is better.
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Transplanted ovaries adjust to the recipient’s biological age
Ovaries from older mice, which were no longer able to reproduce, seemed to become active again when transplanted into younger animals, suggesting the new host’s body lowered the organs’ molecular age
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Hannah Fry: I lost my dad to Alzheimer’s. New research into its origins is amazing
Fran Pulido
I was sitting in a conference in August, drifting as I so often do between listening to what was on stage and pretending to be doing important work on my laptop (by which I mean sending memes on WhatsApp).
All of a sudden, from the stage, the renowned biologist Aviv Regev came out with a sentence that made every single person in the room sit up and pay attention: “Of course,” she said, “we now know that Alzheimer’s starts in the nose.”
I’m sorry, what? Starts in the nose? I didn’t know Alzheimer’s starts in the nose.
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My own lovely dad died from Alzheimer’s last year, and ever since his diagnosis, I’ve done an incredible amount of digging into the disease, trying to understand what was happening to him. I was astonished I’d never come across this idea.
And perhaps you haven’t either. Which is why I want to share my astonishment at discovering that Aviv Regev was right – not only is Alzheimer’s closely associated with our sense of smell, but there is a growing body of research suggesting that our noses might have something to do with why the disease develops in the first place.
The first bit you might already know: people with Alzheimer’s tend to lose their sense of smell, sometimes years before any symptoms of memory loss start to show up. But it turns out that our ability to smell is a surprisingly good indicator of our overall health (looking at you, covid-19). One study from 2014 found that smell loss in older people was a better predictor of whether they would be dead within five years than a cancer diagnosis.
Could pollution find its way to the brain via smell receptors?
STEVE GSCHMEISSNER/Science Photo Library/Alamy
It’s not that losing your sense of smell itself will kill you. More that the olfactory nerves are deeply intertwined with some of the most important memory structures in the brain, so when they start to deteriorate, it can be an early warning that something much more serious is going on.
And this connection seems to work in both directions. One intriguing study (admittedly with quite a small sample size) put a diffuser with essential oils by older people’s beds, thus exposing them to all kinds of wonderful scents while they slept. After six months, the people who had the olfactory enrichment performed better on memory tests than those in a control group.
All very interesting. But not what Regev had been suggesting. Her words seemed to imply that noses are actually responsible for the trouble in the first place.
It turns out that the reason scientists are even entertaining this possibility is because of how fiercely our brains are protected from the outside world. Our skulls are like an actual fortress: even our blood isn’t allowed in without passing a particularly fussy bouncer called the blood-brain barrier.
One of the only real exceptions is a little bit of bone right at the top of your nose that is riddled with holes. It’s called the cribriform, and it’s where the olfactory fibres dangle down into your nose to give you your sense of smell – a bit like if you pushed some Play-Doh through a sieve.
And that means that, despite all the elaborate defences protecting your brain, there is a potential route in, sitting right in the middle of your face.
So, here’s the idea. Maybe the beta-amyloid plaques, the sticky little protein fragments that appear to play such a key role in the cascade of Alzheimer’s in the brain, are what’s left over after the brain has fought an infection. And maybe the nose is how the infection arrives.
To see if this held any water, in 2022, a group of scientists squirted some chlamydia up the noses of some mice.
(I should add, for the sake of the mice’s reputation, that it was actually Chlamydia pneumoniae, a cousin of the bacterium that causes the STI. But I hope you’ll forgive me the less scientifically accurate version. In a long career, you get very few chances to write sentences that good, and I wasn’t about to waste mine.)
The remarkable thing, though, was that within 72 hours, the bacteria had travelled up the nerves in the nasal cavity and got through to the brain. What’s more, the infection triggered the accumulation of beta-amyloid. Now that’s not definitive proof of how Alzheimer’s starts in humans. But there is some other, rather unsettling evidence that infections aren’t the only unwelcome visitors that manage to get in that way.
A group in Mexico studied stray dogs that spent their lives breathing in polluted air. Inside the dogs’ brains, they found microscopic particles of metals – that seem to have entered through the nose – wrapped in pockets of inflammation and that same beta-amyloid protein. You don’t see the same thing in dogs that lived in cleaner, more rural environments.
Now these studies have been extended to look at the brains of very small children and young adults who died from gun violence or car accidents – and they find something similar. Tiny, metal–rich particles, thought to originate from exhausts and brake dust, turned up in their brain tissue, alongside inflammation and accumulations of beta-amyloid. The very sorts of changes associated with Alzheimer’s, appearing in brains that were sometimes only a few years old. Put together, it implies that the disease might have an environmental cause, one that begins much much earlier than we thought.
So, where does Alzheimer’s start? The answer is no one nose (pun very much intended). There is still a great deal we don’t understand, but the implications from all this research are rather extraordinary. What if the beta-amyloid plaques we’ve spent so long trying to get rid of are, at least sometimes, the aftermath of the brain trying to protect itself? And what if, rather than focusing entirely on clearing up the damage, we could work out what set it off in the first place?
But more than anything, I can’t help but laugh as I think about all this in the context of my dad, who had many wonderful qualities, but a discreet nose wasn’t one of them. We used to say that his nose would enter a room 15 minutes before he did. He would have found it very funny indeed if it turned out to have been the cause of his downfall.
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How vaccines could be about to revolutionise acne treatments
Acne could be caused by our immune systems overreacting to proteins released by skin bacteria. Columnist Michael Le Page looks into the experimental treatments aiming to block this process and prevent or reduce acne
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Personalised cancer vaccine expected to be approved next year
A scanning electron micrograph of a melanoma cell
Science Photo Library/Alamy
A personalised mRNA vaccine for melanoma, the deadliest form of skin cancer, is expected to be approved for use in the US, Europe and the UK next year. The vaccine is designed to stimulate immune responses against genetic mutations that are unique to an individual’s cancer. When used alongside standard treatment in a late-stage trial, it substantially cut the risk of cancer recurrence or death within the next two years.
“I think approval could be quick, and next year sounds reasonable,” says Alan Melcher at the Institute of Cancer Research in London, who wasn’t involved in the trial.
“It is a huge deal,” says Rebecca Lee at the University of Manchester, who also wasn’t involved. Thousands of people in the UK alone could benefit from this, based on the trial’s patient population, she says. “It’s highly likely the US and Europe [including the UK] will approve it next year”. However, producing the vaccine is very expensive, and it may not be deemed cost-effective for use on the UK’s National Health Services (NHS), she says.
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In August, drugmaker Modern announced that the vaccine had positive results in a late-stage trial. More specific findings have now been released.
The trial recruited more than 1100 adults who had surgery to remove high-risk melanomas that were likely to recur or spread to distant sites. In the UK, 19,400 melanoma cases are diagnosed annually, of which about 25 per cent are deemed high risk.
Two-thirds of the participants were randomly assigned to receive a bespoke vaccine on top of standard immunotherapy, called pembrolizumab, which helps the immune system find and destroy cancer. Both were delivered every 3 weeks for up to a year. The remaining participants received placebo injections plus pembrolizumab.
The vaccine is made by genetically sequencing a small sample of a person’s cancer and comparing that sequence with the DNA in the individual’s healthy blood cells. This enables researchers to pinpoint mutations specific to the cancer.
Based on the same technology used in covid-19 vaccines, the cancer vaccine contains mRNA molecules that encode for proteins with up to 34 of those mutations. “The jab contains a fingerprint of proteins specifically associated with the cancer,” says Lee. “This helps [immune] T cells recognise the cancer better, and then pembrolizumab prevents those T cells from becoming exhausted once they’ve started attacking the cancer cells.”
About two years after the start of treatment, 82 per cent of the participants who received the vaccine plus pembrolizumab were alive without their cancer recurring, on average, compared with 70 per cent among those on pembrolizumab alone. “It’s a really exciting result,” says Lee. Side effects were similar between the two groups.
The results combine cancer recurrence and death rates into one figure, but since a treated cancer has to recur for it to cause death, this combined measure should be interpreted mostly as a sign of the vaccine reducing recurrence, says Melcher. The participants haven’t been tracked for long enough to robustly determine whether the vaccine improves survival rates. These results should be available within a few years, says Lee.
But because the vaccine has to be tailored to and manufactured for each individual, it is expected to be very costly, which could affect NHS access. “If it was a cheap drug, I’d definitely say it will get approved [for NHS use], but it’s going to be expensive,” says Lee. In January, a report by Reuters suggested it would cost around $200,000 per treatment. Merck and Moderna did not respond to a request about its cost.
Further research is needed to better understand who is mostly likely to benefit from the vaccine, says Melcher. Some people may have mutations included in their vaccine that fail to stimulate anti-cancer immunity as predicted, or pembrolizumab could work so well that the vaccine can’t lead to further improvement. “If we can find immune markers in the blood or tumour that predict patient responses, we could use those to determine who to give the jab to,” says Melcher.
James Larkin, also at the Institute of Cancer Research, says personalised vaccines could also work for other types of cancer, such as those affecting the lungs, bladder and kidneys, which are also routinely treated with immunotherapy. Further research is needed to verify this and explore whether the vaccines could work as standalone treatments.
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Body temperature may drive the higher risk of autoimmune conditions in women
Autoimmune conditions are much more common in women than men, which could partly be due to the fluctuating body temperatures that occur during the menstrual cycle and menopause
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Cholesterol may disrupt the brain’s cleaning system in Alzheimer’s disease
The glymphatic system flushes toxins out of the brain, but this seems to be disrupted in Alzheimer’s disease, and cholesterol may be involved
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1 in 4 cases of depression may be caused by off-kilter body clocks
Disturbed sleep is a common depression symptom
chaiyan Anuwatmongkonchai / Alamy
A quarter of depression cases are caused by people’s body clocks being out of whack, a large study suggests. This newly identified “circadian depression” responds poorly to standard antidepressants, but might be eased by taking melatonin or adopting behavioural strategies, like going outside in the early morning sun.
“The coordination of [your body clocks] underpins your mood, your metabolism, your concentration, your sleep-wake cycle and many other key factors,” says Ian Hickie at the University of Sydney. “When it’s well, you feel really well, you get up in the morning full of energy. When it’s off, you feel jet-lagged all the time, you feel tired, you feel exhausted, you gain weight, you can’t concentrate, you sleep poorly and your behaviour changes.”
Hickie and his colleagues asked more than 10,000 people in Australia with severe, recurrent depression to fill out surveys about their sleep patterns and other characteristics, such as whether their symptoms change seasonally. The participants also provided saliva samples for DNA analysis.
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Of these participants, 23 per cent were identified as having circadian depression. This meant they exhibited at least three of six signs of body clock dysregulation: being an “evening type”, going to sleep later than most people, feeling very tired when getting up regardless of sleep duration, sleeping more during bouts of depression, sleeping in late on non-work days, and experiencing strong seasonal changes in mood, energy, sleep and appetite. “It’s not only about the quantity or the amount of sleep, it’s really about the rhythm and the regularity of sleep,” says team member Emiliana Tonini, also at the University of Sydney.
Those with circadian depression tended to have more severe symptoms than those with non-circadian depression, including more suicidal thoughts. They also developed symptoms at an earlier age – the average age of onset was 18 in the circadian-depression group and 23 in the non-circadian group.
Body clock dysregulation and the resulting mood disturbances may be caused by genetic factors, the study found. The participants with circadian depression were more likely to have genetic variants linked to sleep problems, higher body weight, inflammatory markers and ADHD. “There is an underlying biology that is quite distinct from other forms of depression,” says Tonini.
Another contributing factor may be our modern lifestyles, says Hickie. Our body clocks need to be reset each morning by light exposure to maintain steady, 24-hour rhythms and can be destabilised by artificial light exposure at times when we would have historically been in the dark, he says. “We live in the 21st century, which says, you know, ‘Stay inside, be on a computer all day, avoid the light and then stay up at night and expose yourself to light’”. This is “a complete reverse of what we’re built for”.
The participants identified as having circadian depression reported less efficacy and more side effects when they took common antidepressants like selective serotonin reuptake inhibitors. This may be because these SSRIs target a form of depression related to the neurotransmitter serotonin.
The researchers are about to launch a clinical trial to investigate whether taking a synthetic form of the hormone melatonin, which regulates sleep-wake cycles, might be more effective for treating circadian depression. They previously found that an antidepressant called agomelatine, which mimics melatonin’s effects in the brain, improved sleep and reduced general depression.
The trial will also explore whether behavioural strategies for body clock regulation reduce depression. These include waking up at the same time every morning around sunrise and going outside, spending time outside again in the middle of the day when the sun is brightest, and having regular mealtimes and exercise times during daylight hours.
Once it gets dark, Hickie recommends not eating large meals, exercising or being exposed to bright lights. “They are all the wrong signals,” he says.
Aside from helping with depression, rejigging body clocks may also reduce inflammation and promote healthy weight, says Hickie. He hopes that, in the future, early identification of circadian depression will allow people to be treated more effectively and spare them from taking medications that are inappropriate for them. “If you get on the right track first off, you’re more likely to get out of the hole you’re in and more likely to have better longer-term mental health, but also physical health,” he says.
The findings are “really useful because they advance the field in terms of understanding the whole circadian rhythm aspect of depression and how it might be related to biological measures like genetics and inflammatory markers”, says Colleen Loo at the University of New South Wales in Sydney.
However, more research is needed before circadian depression can be formally recognised as a new subtype of depression, says Loo. “As a clinical psychiatrist, I don’t think it’s time for us to say, ‘Right, based on this, we’re going to say that, if you have these symptoms, we should treat you with this medication rather than that medication,’” she says.
Nevertheless, people with depression could consider trying melatonin and behavioural strategies in addition to their current treatments if they believe their body clocks aren’t functioning optimally, says Loo. Melatonin is available only on prescription in the UK and Australia, but not in the US. “Melatonin is a safe medication and things like low lighting before bed is sensible anyway,” says Loo. “All clinicians should be talking to patients about these things if they have sleep disturbances.”
Journal Reference:
British Journal of Psychiatry
DOI: 10.1192/bjp.2026.10798
Need a listening ear? UK Samaritans: 116123; US 988 Suicide & Crisis Lifeline: 988; hotlines in other countries.
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