People with More Muscle Mass Tend to Suffer Less Brain Aging

The idea that muscle protects the mind has floated around gyms and medical circles for years, but new research is pushing that claim from cliché into measurable biology. Scientists are now finding that people with greater muscle mass tend to show slower brain ageing, a connection that’s becoming harder to ignore as modern weight-loss culture tilts more people toward losing not only fat but also precious lean tissue.

A large imaging study presented at a recent radiology conference examined over a thousand adults using whole-body MRI and an artificial intelligence model trained to estimate “brain age.” People with more muscle appeared to have younger-looking brains, while those with higher levels of visceral fat showed the opposite trend. The relationship held even after accounting for subcutaneous fat, which showed no meaningful link to brain ageing at all. In simple terms: the deeper the fat and the lower the muscle ratio, the older the brain looked.

This emerging science lands in the middle of an uncomfortable contradiction. GLP-1 receptor agonists (the blockbuster medications used for diabetes and rapid weight loss) are now known to cause dramatic reductions in lean mass. Peer-reviewed data show that as much as 15 to 40% of the weight lost on GLP-1s can come from muscle. The rapid drop is especially concerning for people already at risk of sarcopenia, frailty, chronic illness or nutritional deficiencies. A recent review by Zoe Memel, Stephanie Gold, Michelle Pearlman and colleagues summed up the situation with clinical bluntness: these medications work, but they can accelerate muscle decline in the very populations who cannot afford it.

The catch is subtle but significant. A skinnier body doesn’t automatically translate to a healthier brain, particularly when the weight loss includes the very tissue that drives metabolic stability. Muscle acts as a glucose sink, moderates insulin response and keeps inflammatory pathways in check. Strip it away too quickly and the body pays in ways that aren’t always visible on a scale, and now according to imaging data, the brain may pay as well.

Researchers studying GLP-1 therapies have pointed out that the problem is not the medication itself, but what happens when weight loss outpaces nutritional strategy. High-risk patients often lose muscle because they eat too little protein, perform no resistance training or enter treatment already in a fragile metabolic state. Current evidence suggests that protein-optimized diets and structured strength training can significantly blunt the muscle decline associated with GLP-1 use, though formal trials in older adults and people with chronic kidney, liver or bowel disease are still lacking.

The broader tension here mirrors the larger cultural shift around weight-loss injections. Society has embraced the idea of shrinking as fast as possible, even though biology rarely rewards shortcuts. The new brain-ageing findings highlight a less convenient truth: preserving muscle is not a cosmetic choice but a neurological one. Losing fat while clinging to every gram of lean mass may be the only version of weight loss that meaningfully supports long-term brain health.

This research is still early and the conference data will need proper peer review. But the pattern is consistent with decades of literature linking muscle mass to better metabolic control, reduced inflammation and healthier ageing overall. None of this has stopped the global enthusiasm for GLP-1 medications, but it does shift the conversation. The question is no longer whether the injections work (they do) but what else they do along the way.

Future studies will need to determine whether altering dosage, adjusting diet or pairing GLP-1 therapy with mandatory resistance training can preserve both body and brain health. For now, the message is uncomfortably simple: muscle is not optional. It is not decorative. And in an era where rapid weight loss is only a prescription away, it may be one of the most important brain-protective resources we have left.

References:

Kjaer, M. (2004) ‘Role of Extracellular Matrix in Adaptation of Tendon and Skeletal Muscle to Mechanical Loading’, Physiological Reviews, 84(2), pp. 649–698. doi: 10.1152/physrev.00031.2003.

Magnusson, S. P., Narici, M. V., Maganaris, C. N. & Kjaer, M. (2008) ‘Human Tendon Behaviour and Adaptation, in vivo’, The Journal of Physiology, 586(1), pp. 71–81. doi: 10.1113/jphysiol.2007.139105.

Wiesinger, H.‐P., Kösters, A., Müller, E. & Seynnes, O. R. (2015) ‘Effects of Increased Loading on In Vivo Tendon Properties: A Systematic Review’, Journal of Applied Physiology, 117(7), pp. 713–722. doi: 10.1152/japplphysiol.00238.2014.

Maffiuletti, N. A., Aagaard, P., Blazevich, A. J., Folland, J., Tillin, N. & Duchateau, J. (2016) ‘Rate of Force Development: Physiological and Methodological Considerations’, European Journal of Applied Physiology, 116(6), pp. 1091–1116. doi: 10.1007/s00421-016-3346-6.

Tenforde, A. S., Kraus, E., Fredericson, M. & Sawyer, S. (2021) ‘Tendon and Ligament Adaptation to Exercise, Training, and Detraining’, Sports Health, 13(1), pp. 32–40. doi: 10.1177/1941738120952076.

Tippett, S. R. & Voight, M. L. (1995) ‘Ligament: Structure, Function and Biomechanics’, Journal of Sport Rehabilitation, 4(1), pp. 66–75. doi: 10.1123/jsr.4.1.66.

Walsh, N. P. (2019) ‘Nutrition and Athlete Immune Health: New Perspectives on Connective Tissue Repair’, Sports Medicine, 49(1), pp. 153–168. doi: 10.1007/s40279-019-01160-3.

Memel, Z., Gold, S. L., Pearlman, M., Muratore, A. & Martindale, R. (2025) ‘Impact of GLP-1 Receptor Agonist Therapy in Patients High Risk for Sarcopenia’, Current Nutrition Reports, 14(1), p. 63. doi: 10.1007/s13668-025-00649-w.