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Although the first GLP-1 drug was approved by the US Food and Drug Administration (FDA) in the early 2000s, it wasn’t until a few years ago that its use became mainstream. Originally crafted to help people with type-2 diabetes, the class of medication was quickly recognized as a way to facilitate weight loss.
In 2023, celebrities and average Joes alike couldn’t wait to get their hands on the highly effective injectables in hopes of a lower body fat percentage.
But the drugs didn’t come without side effects, such as pancreatitis and reduced muscle mass and bone density. Strength training while using GLP-1 drugs is integral to staving off the latter. However, a study suggests there may be a loophole.
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A certain antibody known as bimagrumab could be the key to increasing muscle mass and bone density due to the use of GLP-1 drugs, according to the research originally published in the Journal of Cachexia, Sarcopenia, and Muscle.
“Bimagrumab, a drug that works by blocking activin and myostatin signaling—mechanisms known to drive muscle and bone degradation—presents a potential solution,” says head researcher Frederik Duch Bromer. “Our study investigated bimagrumab treatment in a mouse model of severe muscle and bone loss caused by botulinum toxin-induced hindlimb paralysis. This model simulates an even more extreme degree of muscle and bone deterioration than that seen with weight loss drugs.”
To perform the study, researchers broke mice into five different groups, some of which included injecting the legs of the mice with botulinum toxin to immobilize them and replicate the concurrent loss of muscle mass and bone density. Immediately after, the mice were given twice weekly bimagrumab injections for 21 days. After this, their muscle mass and skeletal muscle fiber size were analyzed.
They found the mice injected with bimagrumab had increased muscle mass, muscle fibers, and bone mineral density in the hindlimb of immobilized and unconstrained mice. Not only this, but it increased the bone formation in cortical bone (the denser variant of bone tissue).
“While bimagrumab did not completely prevent muscle and bone loss, it significantly mitigated it, suggesting that it could help counteract these effects in humans undergoing rapid weight loss,” Bromer added.
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Because the study was based on mice, researchers are still a long way off from seeing if it’s safe to use on humans. According to postdoc fellow Andreas Lodberg who was one of the researchers behind the study, more research is needed.
“Although our research did not specifically focus on bone loss in obesity, this is an important area for further investigation,” Bromer said. “Since weight loss drugs are primarily prescribed for people with obesity, understanding how bimagrumab interacts with bone health in this population is crucial.
If this advancement goes through, it could be advantageous to patients who are older, less mobile, or have physical handicaps that prevent exercise—but it could also open Pandora’s box for those who are physically abled and capable of exercising. By always turning to medication to solve a problem, do we undermine the lifestyle changes necessary to safely lose weight and keep it off? And do we encourage those on the hunt for quick fixes—who don’t medically need GLP-1 drugs—to bypass the role they play in taking their health into their own hands?