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Mice given processed fats struggled to adapt to winter.
In A Nutshell
- Mice eating processed fats got stuck in “summer mode”; their body clocks took twice as long to adjust when the lights changed to mimic winter
- It’s not about how much fat you eat, but what kind: The ratio of different fat types acts like a seasonal calendar for the brain
- Hydrogenated oils (the stuff in most processed foods) erase the “winter signal” that naturally occurs in seasonal foods
- Humans have the same biological pathway, but scientists don’t yet know if our bodies react to fats the same way
Struggling to understand why your metabolism seems out of sync with the seasons? Your body might be stuck thinking it’s still summer, thanks to the types of fats lurking in processed foods. A study from the University of California, San Francisco, suggests it’s not just how much fat you eat, but rather the ratio of different fat types that may tell your internal clock what season it is.
Scientists discovered that mice fed diets low in certain types of fats showed a summer-like pattern, taking longer to sync with winter light cycles. These animals kept warmer body temperatures, a sign their metabolism stayed in summer mode. Diets with the same calories but different fat types produced completely different effects on how bodies tracked seasons.
Published in Science, the study shows that mouse brains have a built-in seasonal timer that reads the fats they eat. This discovery suggests modern diets rich in hydrogenated oils and processed fats might create similar confusion in humans, though scientists haven’t tested that yet.
Why Fat Type Acts Like a Seasonal Signal
In nature, many plants and animals pack more polyunsaturated fats (PUFAs) into their tissues during winter. It helps them stay flexible in cold temperatures. So a diet high in PUFAs signals winter, while a diet low in PUFAs signals summer—the season when animals naturally store energy for leaner times ahead.
Lead researcher Daniel Levine and colleagues zeroed in on a molecular switch that controls the body’s internal clock. Earlier work from the same lab had connected this switch to how mice and humans sense nutrients and regulate sleep timing.
When researchers fed mice high-fat diets that differed only in their fat composition, the differences were clear. Animals eating fewer polyunsaturated fats adjusted their daily patterns more slowly to winter lighting, taking about 40% longer than mice eating more of these fats. During summer lighting, these same mice adjusted faster, as if their bodies expected abundant food.
Looking at brain tissue, the team found that diets lower in polyunsaturated fats flipped this molecular switch in the hypothalamus, the brain’s control center for daily rhythms and metabolism. The change affected how cells produced signaling molecules and raised body temperature.
Mice given a low fat, low calorie diet were much quicker to adapt to seasonal changes. (Credit: pexels.com)
Genes Prove Fat Types Actually Control the Clock
To make sure this switch actually caused the effects rather than just happening alongside them, the team studied genetically modified mice. These animals were engineered so the switch couldn’t flip.
The results were clear: These mice adjusted to seasonal lighting at steady rates no matter what they ate. Regular mice? Their adjustment speed changed dramatically based on fat type.
The genetic evidence proved dietary fat composition actively controls how bodies track seasons, not just correlates with it. Mice unable to flip this switch became immune to the seasonal signals hiding in their food.
Fasting experiments revealed another layer. When mice went without food, the switch flipped to winter mode, and animals shifted their daily schedules earlier. Analyzing which genes turned on and off showed this change affected hundreds of genes involved in processing polyunsaturated fats into signaling molecules.
How Food Processing Erases Winter
To isolate what fat saturation does, researchers made two high-fat diets with identical calories. One used regular corn oil, naturally high in polyunsaturated fats. The other used partially hydrogenated corn oil, where industrial processing converts polyunsaturated fats into more saturated types.
Mice fed the hydrogenated oil showed the flipped switch, warmer bodies, fewer signaling molecules, and slower adjustment to winter lighting. The genetically modified mice? No diet-related changes at all.
Partial hydrogenation, the same process that creates trans fats, strips away the seasonal signal that would normally say “winter is here.” What’s left is a metabolism displaying summer patterns: warmer body temperature and delayed clock adjustment.
The experiments tracked male mice for weeks as they adapted to new lighting schedules mimicking seasonal changes. Researchers even used computer-controlled feeding devices to test calorie restriction, which had opposite effects, helping mice adjust faster to winter. This suggests total calories and fat type send separate seasonal messages to the body.
What This Might Mean for Humans
Processed foods are available year-round with altered fat compositions. Combined with artificial lighting, this could create “seasonal confusion” between internal clocks and the actual environment. Many processed foods go through hydrogenation or contain different fat ratios than seasonal whole foods. Even products without trans fats might have fat profiles that signal the wrong season.
The research team points out that humans with a genetic mutation affecting the same molecular switch develop a sleep disorder where they crash early and wake at dawn. This proves the pathway exists in humans—but whether dietary fats affect human daily rhythms the same way needs direct testing.
The study authors note that obesity rates and sleep problems have shot up in industrialized countries. Lots of factors contribute, but their findings suggest fat composition deserves attention as a possible piece of the puzzle.
This summer-like pattern seen in mice might connect to how bodies regulate energy across seasons. Whether any of this applies to human metabolism, weight patterns, or seasonal changes in people remains unknown and needs human studies.
Polyunsaturated fats, the winter-signaling type in this research, have multiple weak spots in their chemical structure. That makes them fragile, which is exactly why food companies process them. Many packaged snacks, baked goods, and fried foods contain oils altered for shelf stability, unintentionally changing their seasonal signals.
Disclaimer: This research was done in mice, not humans. We don’t yet know if people’s bodies work the same way. Talk to your doctor before changing your diet based on this study.
Paper Summary
Limitations
The experiments used only male mice of a single genetic strain, which limits generalizability. Environmental conditions in laboratory settings differ substantially from natural habitats where animals face variable temperatures, food availability, and social conditions. The study primarily examined activity rhythms measured by running wheels, which represent just one output of the circadian system. Effects on other physiological processes remain unknown. Body temperature changes caused by high-fat feeding could independently affect circadian rhythms separate from the molecular mechanism studied.
Funding and Disclosures
This research received support from the National Institute of Neurological Disorders and Stroke through grants R01NS117929, R35NS132160, and R01NS104782. Additional funding came from the Sandler Program for Breakthrough Biomedical Research, partially funded by the Sandler Foundation, the Novo Nordisk Foundation Project Grant in Bioscience and Basic Biomedicine NNF17OC0028702, the Lundbeck Foundation Danish-American Research Exchange Fellowship, the Danish Cardiovascular Academy funded by the Novo Nordisk Foundation grant NNF17SA0031406, and the Danish Heart Foundation. Daniel Levine conducted this research as a Glenn Foundation for Medical Research Postdoctoral Fellow. The authors declared no competing financial interests.
Publication Details
The study was authored by Daniel C. Levine, Rasmus H. Reeh, Thomas McMahon, and Thomas Mandrup-Poulsen from the Department of Neurology, University of California San Francisco, along with Ying-Hui Fu and Louis J. Ptáček, who hold additional affiliations with the Institute for Human Genetics, Weill Institute for Neuroscience, and Kavli Institute for Fundamental Neuroscience at UCSF. Rasmus H. Reeh and Thomas Mandrup-Poulsen also maintain affiliations with the Department of Biomedical Sciences at the University of Copenhagen in Denmark. The paper appears in Science, volume 390, published October 23, 2025, with DOI 10.1126/science.adp3065. Correspondence should be directed to Louis J. Ptáček at [email protected] or Ying-Hui Fu at [email protected].