Losing deep belly fat may slow brain aging and protect memory

Losing deep belly fat rather than just overall body weight is linked to slower brain aging and better cognitive function years later. The research, published in Nature Communications, suggests that targeting this specific type of fat might help protect the brain from age-related decline.

Visceral fat wraps deep around internal organs, while subcutaneous fat sits just beneath the skin and is more visible. Visceral fat is highly metabolically active and frequently releases inflammatory molecules that can travel and affect the whole body, including the brain. Previous research linked high visceral fat to cognitive decline, but it remained unknown if actively losing this fat could protect brain structure over the long term. Scientists needed to determine if reducing this specific fat depot offered lasting neurological benefits.

Lead authors Dafna Pachter and Hadar Klein, along with corresponding author Iris Shai and colleagues from Ben-Gurion University of the Negev in Israel, conducted the research. They wanted to understand if sustained reductions in specific fat depots could preserve brain health. To investigate this, they utilized a wealth of long-term data from several earlier clinical trials.

The researchers first looked at 533 adults who had participated in four dietary and lifestyle trials five to sixteen years earlier. These participants, who were mostly male and in their early sixties, underwent magnetic resonance imaging to measure both their brain volume and abdominal fat. They also completed the Montreal Cognitive Assessment, a standard test used to detect cognitive impairment.

The team found that individuals with lower amounts of visceral fat scored consistently higher on the cognitive tests. This relationship was heavily influenced by brain volume, with the negative association between visceral fat and cognitive scores appearing most pronounced in people who had relatively preserved brain structures. Body mass index, a standard measure of weight relative to height, did not show these same relationships with cognitive performance or brain structure. This suggests that body mass index alone might not capture the specific neurodegenerative risks posed by deep abdominal fat.

Next, the team examined a subset of 295 participants who had complete abdominal fat data across three time points. These measurements were taken at the start of their original trial, at eighteen months, and at a final follow-up several years later. The researchers calculated the cumulative exposure to abdominal fat over the years for each individual.

The results showed that long-term exposure to high levels of visceral fat predicted lower cognitive test scores. In contrast, cumulative exposure to subcutaneous fat did not show this negative relationship with memory and cognition. This difference highlights the unique metabolic risks associated with visceral fat compared to fat stored under the skin.

The researchers then analyzed whether the initial fat lost during the eighteen-month trials predicted later brain health. For 297 participants, they compared the change in fat during the intervention to brain scans taken five to ten years later. A greater reduction in visceral fat during the trial predicted higher total brain volume at the long-term follow-up.

Reductions in visceral fat also predicted greater gray matter volume. Gray matter contains most of the brain’s neuronal cell bodies and is highly involved in processing sensory information, muscle control, and decision making. The analysis also showed that reductions in the proportion of visceral fat were associated with a healthier hippocampus. The hippocampus is a brain region central to learning and memory, and it is often one of the first areas affected by cognitive decline.

Reductions in superficial and deep subcutaneous fat during the intervention showed no such relationship with later brain structure. The relative change in body mass index during the intervention also did not predict long-term brain volume. This points to the specific role of visceral fat in neurodegeneration.

The team also evaluated 188 participants who underwent repeated brain scans at baseline, eighteen months, and five years. They tracked the rate at which the brain shrank over time, comparing it to the participants’ cumulative visceral fat exposure. People with higher long-term visceral fat experienced a faster rate of brain atrophy across multiple regions.

These individuals also showed a faster expansion of the brain’s ventricles. Ventricles are fluid-filled spaces in the brain that grow larger as surrounding brain tissue is lost. To understand the biological mechanism at play, the researchers tested various blood markers to see how they related to longitudinal brain changes.

They found that baseline levels of fasting blood sugar and a marker of long-term blood sugar control were the only metabolic factors related to the long-term brain changes. Lipid and inflammatory markers did not show this relationship over time. This suggests that the way visceral fat disrupts blood sugar regulation and insulin sensitivity may be the primary path through which it harms the brain. When visceral fat levels drop, improved glycemic control might alleviate stress on brain tissues.

Readers should note that the study population was eighty-six percent male and mostly overweight or obese. This might limit how well the findings apply to women or individuals with lower body weight. While the initial fat loss occurred during randomized controlled trials, the long-term follow-up was observational.

Because the participants’ habits after the trials ended were not strictly controlled, the study cannot definitively prove cause and effect for the long-term data. The researchers accounted for the participants’ diets during the follow-up period, but post-trial lifestyle choices could still influence the outcomes. The study also did not measure fat accumulation in organs like the liver and pancreas, which could play a role in brain health.

Future studies incorporating these measurements and specific biomarkers for neurodegenerative diseases like Alzheimer’s will help clarify the exact biological pathways linking abdominal fat to brain aging. These findings address a gap in the field, identifying visceral fat as a distinct, modifiable risk factor for neurodegeneration.

The study, “Sustained visceral fat loss is associated with attenuated brain atrophy and improved cognitive function in late midlife,” was authored by Dafna Pachter, Hadar Klein, Omer Kamer, Dana Tamar Goldberg Toren, Liav Alufer, Noa Ebstein Karamani, Tomer Atlas, Amit Yaary, Idan Hagbi, Yoash Chassidim, Ilan Shelef, Moti Salti, Frauke Beyer, Veronica Witte, Assaf Rudich, Uri Yoel, Gal Ben-Arie, Anat Yaskolka Meir, Alon Kaplan, Gal Tsaban, Hila Zelicha, Carmi Bartal, Lu Qi, Matthias Blüher, Michael Stumvoll, Uta Ceglarek, Berend Isermann, Dong D. Wang, Meir J. Stampfer, Frank B. Hu, Galia Avidan, and Iris Shai.