Summary: It only takes three days of poor eating to damage the aging brain. A new study reveals that a lack of dietary fiber is a major driver of memory impairment and inflammation in older adults.
The research found that refined diets—regardless of fat or sugar content—specifically target the amygdala, the brain’s emotional memory center. When fiber is missing, the gut produces less butyrate, a key molecule that protects the brain from inflammation. This biological breakdown makes older brains less capable of learning from bad experiences, potentially increasing the risk of financial scams and physical harm.
Key Facts
- The Three-Day Window: Refined, fiber-poor diets can impair emotional memory in as little as 72 hours.
- The Amygdala’s Vulnerability: Unlike the hippocampus, which is primarily affected by high-fat diets, the amygdala is uniquely sensitive to any refined diet lacking fiber.
- The Butyrate Connection: Fiber breakdown in the gut produces butyrate, an anti-inflammatory molecule that crosses the blood-brain barrier. Low fiber leads to low butyrate and unregulated brain inflammation.
- Mitochondrial Burnout: In aging brains, the mitochondria within microglia (immune cells) fail to adapt to refined diets, leading to depressed cellular respiration and memory loss.
- Financial Risk: Because the amygdala helps associate risky actions with bad outcomes, dietary-induced impairment may leave seniors more vulnerable to scams and exploitation.
Source: Ohio State University
Past studies in animals have shown that a highly processed diet is linked to memory problems and inflammation in the aged brain – and the effect can happen fast, after just three days of poor eating.
A new study suggests another dietary pitfall could have a similar damaging effect in a similarly short amount of time in older adults: a lack of fiber.
The study in rats also points to the amygdala – the small structure governing emotional memories, especially related to bad experiences – as a brain region that is particularly sensitive to a highly processed diet.
Every type of refined diet fed to old animals was associated with cellular and behavioral signs of cognitive problems traced to this emotional memory center of the brain.
“The amygdala is important for learning the association between something fearful and a bad outcome. And we found that all of the refined diets, whether they were high fat, high sugar, low fat, low sugar, it didn’t matter. They all impaired memory that’s governed by the amygdala,” said co-lead author Ruth Barrientos, an investigator in the Institute of Brain, Behavior and Immunology at The Ohio State University.
“And when we looked to see the common thread among all of those diets, the one thing that became very obvious was that they all lack fiber.”
Not learning the association between an action and its outcome, especially when it’s dangerous or risky, may increase the risk for physical or financial harm, said Barrientos, also an associate professor of psychiatry and behavioral health and neuroscience in Ohio State’s College of Medicine.
“The amygdala plays a role in that kind of awareness and learning,” she said. “Its vulnerability to a refined diet is therefore concerning for older adults who are at greater risk of financial exploitation and scams.”
The research was published recently in the journal Brain, Behavior, and Immunity.
Barrientos has studied the effects of high-fat and highly processed diets on the aged brain for several years, seeing behavioral results and related indications of inflammation in both the amygdala and the hippocampus, which is important for spatial, autobiographical and episodic memory.
In this work, she and colleagues focused on disentangling the diet contents to see whether fat or sugar, or something else, had the strongest link to cognitive impairment in rats.
Young and aged male rats were fed either normal chow or one of five experimental diets for three days: low fat, low sugar; low fat, high sugar; medium fat, low sugar; medium fat, high sugar; or high fat, low sugar.
Behavioral tests showed that old animals that were fed all of the refined diets – no matter the level of fat or sugar – had impaired long-term emotional memory based in the amygdala compared to young rats on the same diets. In contrast, memory-related behavior traced to the hippocampus was negatively affected only by the high-fat, low-sugar diet.
And then there was the no-fiber factor. All of the experimental diets lacked fiber, and examination of the rats’ guts and blood showed a significant reduction in a key molecule, called butyrate, that is produced in the gut and circulated in the blood when dietary fiber is broken down by gut microbes.
Previous research by other labs has shown that butyrate has anti-inflammatory effects and can cross the blood-brain barrier, which may mean a deficiency in butyrate caused by a lack of dietary fiber could be linked to unregulated inflammation in the brain, Barrientos said.
“What our study really brings to light is the complexity of diet and how it affects so many different things, even the brain,” said co-lead author Kedryn Baskin, assistant professor of physiology and cell biology at Ohio State.
“There’s not a magic bullet, but in this case, low butyrate, as a result of a lack of fiber, is a culprit.”
At the cellular level, the researchers found the most compelling evidence of refined diet-related damage in the mitochondria of microglia, cells that have multiple functions important to memory function. When exposed to experimental energy demands in cell cultures, mitochondria from young brains could adapt to the changes, but these power centers in aged brain cells were not able to rise to the challenge.
“The mitochondria are still functioning, but they’re showing depressed respiration and are functioning at a much, much lower rate in the aged compared to the young,” Baskin said.
Though the refined diets caused some weight gain, Barrientos said the findings put to rest the notion that obesity brought on by a highly processed diet is the primary driver of impaired cognition.
“These effects on the brain after you eat something are pretty rapid,” she said. “You can experience this unhealthy cognitive dysfunction well before you reach obesity.”
And while she and Baskin said the data imply increasing fiber in the diet could be beneficial to the brain, the team plans to study whether fiber or butyrate supplementation in animals could reverse the age-related cognitive problems that follow poor eating.
Funding: This work was supported by the National Institute on Aging, the National Center for Advancing Translational Sciences, the Foods for Health Research Initiative at Ohio State, and the National Heart, Lung, and Blood Institute.
Additional co-authors were Michael Butler, Jade Blackwell, Andrew Sanchez, Hannah Sanders, Dominic Kolonay, Jeferson Jantsch, Stephanie Muscat, Sabrina Mackey-Alfonso and Bryan Alvarez, all of Ohio State; and Maria Elisa Caetano-Silva, Akriti Shrestha, Casey Kin Yun Lim, Robert McCusker and Jacob Allen of the University of Illinois Urbana-Champaign.
Key Questions Answered:
A: Not necessarily. The study found that it didn’t matter if the diet was high or low in fat/sugar—if it lacked fiber, the amygdala suffered. Fiber is the common thread that protects your emotional memory.
A: The amygdala is responsible for “fear learning”—recognizing when a situation might have a bad outcome. When inflammation impairs this region, your brain struggles to flag risky or suspicious behavior, like a suspicious phone call or a “too good to be true” financial offer.
A: While the researchers are currently studying whether supplements can reverse the damage, the best defense is a whole-food, fiber-rich diet. The goal is to keep your gut producing butyrate, which acts as a natural shield for your brain cells.
Editorial Notes:
- This article was edited by a Neuroscience News editor.
- Journal paper reviewed in full.
- Additional context added by our staff.
About this diet, aging, and emotional memory research news
Author: Emily Caldwell
Source: Ohio State University
Contact: Emily Caldwell – Ohio State University
Image: The image is credited to Neuroscience News
Original Research: Open access.
“The aged amygdala’s unique sensitivity to refined diets, independent of fat or sugar content: A brain region and cell type-specific analysis” by Michael J. Butler, Jade A. Blackwell, Andrew A. Sanchez, Hannah F. Sanders, Dominic W. Kolonay, Jeferson Jantsch, Stephanie M. Muscat, Maria Elisa Caetano-Silva, Akriti Shrestha, Casey Kin Yun Lim, Sabrina E. Mackey-Alfonso, Bryan D. Alvarez, Robert H. McCusker, Jacob M. Allen, Kedryn K. Baskin, and Ruth M. Barrientos. Brain, Behavior, and Immunity
DOI:10.1016/j.bbi.2025.106220
Abstract
The aged amygdala’s unique sensitivity to refined diets, independent of fat or sugar content: A brain region and cell type-specific analysis
Western-style diets, high in saturated fats and refined carbohydrates and low in dietary fiber, are strongly linked to cognitive decline, particularly in aging. However, the specific macronutrient contributions and mechanisms underlying these effects remain unclear.
Here, we investigated how short-term exposure to refined-ingredient diets (RDs) varying in fat and sugar content impacts memory, mitochondrial function, and metabolic signaling in young adult and aged male rats.
A key finding was that amygdala-dependent memory was broadly impaired in aged rats across all RDs, regardless of fat or sugar content, suggesting a unique vulnerability of the aging amygdala to refined dietary ingredients. In contrast, hippocampal-dependent memory impairments were observed only in aged rats fed a high-fat, low-sugar RD.
Functional mitochondrial assays revealed significant RD-induced reductions in oxygen consumption in amygdalar and hippocampal mitochondria isolated from aged rats. Cell-type–specific analyses identified aged microglia as particularly susceptible, showing widespread suppression of mitochondrial respiration with limited metabolic flexibility.
Astrocytes and synaptic mitochondria exhibited more region- and age-specific effects. All RDs lacked dietary fiber, and consistent with prior findings, butyrate, a microbial-derived short-chain fatty acid, was rapidly and robustly depleted in both gut and circulation, especially in aged animals.
Proteomic and phosphoproteomic analyses identified diet-induced disruptions in mitochondrial proteins and synaptic signaling pathways, including complex I subunits and glutamate receptor signaling.
Together, these findings reveal that the aged amygdala is especially sensitive to refined diet exposure and highlight microbial, metabolic, and inflammatory pathways that may underlie diet-induced cognitive decline.
