“Eat less, live longer” has a firm footing in the laboratory: dietary restriction extends lifespan across species, from yeast to mammals. But a review published in The Innovation Nutrition argues that the slogan travels badly to the dinner table—and that what people eat may matter at least as much as how much.

Drawing on more than thirty large prospective cohorts and meta-analyses, the authors—Jintao Huang, Dejian Huang, and corresponding author Ziyun Wu of Shanghai Jiao Tong University—assemble a case for “precision diets”: optimizing macronutrient quality, sources, and proportions rather than cutting total energy.

Severe restriction, they note, is hard to sustain and carries risks including reproductive impairment, menstrual irregularities, osteoporotic fractures, and cardiac arrhythmias.

The evidence is organized around four nutrients. Carbohydrates follow a U-shaped curve: in several populations, moderate intake—about 50 to 55 percent of energy—is associated with lower all-cause mortality, with whole grains, legumes, vegetables, and whole fruits consistently outperforming refined grains and sugar-sweetened beverages.

Protein shifts with age: in midlife, higher intake of animal protein correlates with higher mortality risk, whereas plant protein shows favorable associations; after 65, when sarcopenia and frailty take over, the recommendation flips toward moderately more high-quality protein from fish, legumes, and other sources.

For fats, type beats quantity—unsaturated fats from nuts, olive oil, and fish are linked to better cardiovascular outcomes, while industrial trans fats should be limited. Dietary fiber, at roughly 25 to 29 grams per day, shows one of the most stable associations with lower mortality, likely mediated through short-chain fatty acids produced by gut microbes.

The authors caution repeatedly against overreach. Cohort studies show associations, not causation. Clinical ketogenic diets are not ordinary low-carb diets and belong, they argue, in medically supervised, time-limited treatment rather than everyday longevity practice.

The framework’s age-stratified ratios—19 to 35, 36 to 64, and 65 onward—are research scaffolding, not validated prescriptions.

The review’s most forward-looking section is a feedback loop: because postprandial glucose, insulin, and triglyceride responses can differ up to tenfold between individuals eating identical meals, precision nutrition should mean continuous assessment—continuous glucose monitors, microbiome and multi-omics profiling, wearables, and artificial-intelligence-assisted diet design—rather than one personalized menu generated once.

Time-restricted eating adds a temporal dimension. Early personalized-nutrition trials have improved short-term metabolic markers, but the authors stress that no tool has yet demonstrated longer healthspan; that will take multi-year randomized trials, enriched for adults over 75, non-European genetic backgrounds, and low- and middle-income regions.

The public-health message that survives the caveats is deliberately unglamorous: choose high-quality carbohydrate sources, partially replace red and processed meat with plant proteins, favor unsaturated fats, eat enough fiber—and treat diet as one strand of a life woven together with sleep, circadian rhythm, exercise, and social connection. 

Dance training can influence how we perceive not only movement but also everyday emotional expressions, according to new research from the Centre for Cognition and Neuroscience at City St George’s, University of London.

The study, published in the journal Cerebral Cortex, found that dance expertise influences the brain’s early visual and somatosensory responses when observing emotional facial expressions.

The findings build on Professor Beatriz Calvo-Merino’s previous research, which showed for the first time that motor training, such as dance expertise, can modulate how we perceive actions. This latest study broadens that understanding, suggesting that the effects of dance training extend beyond familiar, dance-specific movements to influence the perception of emotions in other people’s faces.

Professor Calvo-Merino, Professor of Cognitive Neuroscience at City St George’s, said: “The impact of dance expertise goes beyond movement and taps into social perception mechanisms, such as face processing and emotions. This is fascinating as it provides direct evidence for the impact of the arts on social cognition.” 

To investigate the relationship between dance expertise and emotion processing, the researchers recruited 26 professional or trainee ballet dancers from dance schools across London, alongside 26 people without dance experience.

The team, formed by Dr Vasiliki Meletaki, Professor Bettina Forster and Professor Calvo-Merino, recorded participants’ brain activity using specialised equipment as they completed a task involving the identification of emotions and whether faces were perceived as male or female. Participants were shown images of happy, afraid and neutral facial expressions.

Professor Forster developed the EEG analysis approach used to examine when and where brain responses to emotional expressions differed between dancers and non-dancers, allowing the researchers to investigate how dance expertise influences both visual and somatosensory processing.

The results revealed distinct patterns of brain activity between dancers and non-dancers, indicating that dance expertise influences how emotional expressions are processed through both visual and somatosensory systems.

In particular, dancers showed early differences in their brain responses to neutral and emotional faces, suggesting a distinctive way of processing emotional expressions. They also demonstrated early somatosensory responses to facial emotions, particularly neutral and afraid faces.

By contrast, non-dancers showed emotional effects primarily at later stages of emotional processing compared to dancers.

As a result, the findings suggest that dance expertise shapes both the visual and embodied perception of emotions, providing new evidence of how specialised motor and artistic training can influence human perception.

Professor Bettina Forster said: “What is particularly interesting is that dance expertise appears to influence how the somatosensory cortex responds to emotions expressed by others. This suggests that our own bodily experiences can shape how the brain processes other people’s emotions, providing further evidence for the embodied nature of emotion perception.”

Dr Vasiliki Meletaki added: “It was exciting for us to find empirical evidence for the profound impact professional dance training has on how dancers perceive not only their bodies and dance movements but also other people’s emotional expressions.” 

Antibodies that coat the lining of your gut may be playing an important role in preventing colon cancer from developing, Rockefeller University scientists have discovered.

Mice that lack a specific class of antibodies, called immunoglobulin A (IgA), develop more than twice as many colon tumors as usual, the team reported in Nature. The study also explained why: When the antibodies bind to the cells lining the inside of the gut, it keeps those cells from dividing too quickly—which could lead to cancer.

When the researchers gave IgA-deficient mice oral doses of the antibodies, they no longer had a higher risk of developing tumors.

“One intriguing aspect of this work is that it shows how a natural defense in the gut restrains the cell division that can lead to cancer,” says senior author Daniel Mucida, head of Rockefeller’s Laboratory of Mucosal Immunology. “Most cancer research focuses on trying to destroy a tumor that already exists, but what if we could intervene before tumors form?”

The discovery illuminates why people with IgA deficiency—who have few or none of these antibodies—are at a higher risk of developing colorectal cancer but also could shed light on other aspects of the complex interplay between the gut microbes, immune system, and cancer—even in otherwise healthy people.

A common antibody filling the gut

Scientists and clinicians have long known that the gut has high levels of IgA. Unlike many antibodies that are highly specific for one pathogen at a time, IgA is a broad-acting first line of defense in the immune system. A single IgA molecule can bind to a wide range of gut bacteria—as well as some healthy human cells—but researchers had long wondered why there were such high levels of IgA in the digestive system.

Mucida and his colleagues study how the intestine strikes a balance between protecting the body against invading pathogens and absorbing the nutrients the body needs. In the past, for instance, the lab has discovered the role that gut immune cells play in food intolerances and allergies.

In the new work, former Rockefeller postdoctoral fellow Gregory Donaldson—now an assistant professor at UCLA—wanted to tease out exactly how IgA antibodies interact with gut bacteria, and whether that could be relevant to colon cancer.

“We know these antibodies bind bacteria and by doing so can shape the microbiome,” he says. “And because IgA deficiency, which affects about 1 in 500 people in the U.S., is linked to colorectal cancer, I wondered whether these interactions might be relevant to the disease.”

Donaldson began by studying IgA-deficient mice that were raised alongside normal mice, ensuring that they were exposed to the same germs and food. The mice without IgA developed more colorectal cancers than those who had IgA—echoing what was already known to occur in humans.

“We found this was true for several different kinds of models of colon cancer, so that was a really convincing effect,” says Donaldson.

Moreover, giving these mice an oral treatment of IgA molecules eliminated the increased risk of cancer.

Keeping the brakes on cell division

Mucida, Donaldson, and the rest of their group zoomed in to the cells lining the gut, called epithelial cells—where colon cancers first form—to see how they were different in the mice lacking IgA. They discovered that changes in gene expression included ones related to cell division, or proliferation, and that these changes came before any tumors ever emerged.

“We assumed there must be some sort of receptor on the epithelial cells that was mediating this,” Donaldson says.

Second author Gabriella Lima dos Reis, a graduate student in Gabriel Victora’s lab, homed in on one receptor that is found on the surface of epithelial cells and that IgA can bind to. Called DMBT1, it had already been linked in multiple ways to some cancers, but its exact role in colon cancer was unclear.

The team went on to show that DMBT1, in the presence of gut bacteria, acts as a gas pedal for cell proliferation. But IgA, when it binds to DMBT1, acts as a brake. If IgA is completely absent, DMBT1 signaling is unrestrained, letting gut epithelial cells divide more than usual and form tumors. But without gut bacteria, without DMBT1 signaling, or with normal IgA levels, the epithelial cells are kept in check.

“If IgA is missing, epithelial cells that are performing their normal function—responding to bacteria by producing new cells—can keep dividing unchecked, leading to cancer,” Mucida says. “We think this homeostatic effect is IgA’s main function. This was a big surprise.”

Lessons for colon cancer

By establishing DMBT1’s natural function in epithelial cells for the first time, the findings may lay the groundwork for new interventions to reduce colon cancer risk.

“Based on the mechanism we discovered, perhaps we could influence epithelial cells to be less likely to develop into a tumor,” Mucida says. “We know, for example, that having polyps increases your chances of getting colon cancer, so we think that there could be an opportunity to target this pathway after polyps are removed. Right now, there are no interventions available at that point.”

“What is potentially even more exciting is that there is evidence that individual species of bacteria can have really specific effects on epithelial cells as well,” Donaldson notes. “A lot of research has focused on bacteria that induce tumors or can exacerbate their growth, but we have some evidence that there are bacteria that could do the opposite, just as IgA does. To that end, perhaps we could develop a probiotic supplement that induces a protective IgA response. This is all very speculative, but it’s one direction that we could look towards in the future.”

Mucida adds, “Overall, there is a lot more to learn about how the dance between bacteria, antibodies, and epithelial cells in the gut works to maintain health.”