SENS Research Foundation on Approaches to the Treatment of Sarcopenia

Companies in the longevity industry that are working on ways to slow or reverse the age-related loss of muscle mass and strength that leads to sarcopenia have become attractive to the pharmaceutical industry and big investors of late. This is not because those entities have suddenly seen the light and now support the treatment of aging as a medical condition, but rather because their leadership is looking for ways to slow or reverse the muscle loss that attends the use of the suddenly popular GLP-1 receptor agonist drugs used for weight loss. How well are things going in the development of ways to slow or reverse sarcopenia, however? Not so well, perhaps, as here argued by the SENS Research Foundation staff, because researchers and developers are largely going about it the wrong way.

Suppose you were to take a group of people who were on the back end of current lifespans and give them an experimental drug to boost their muscle mass. Like most older people, they have lost a significant amount of the muscle they carried in midlife. By giving them our experimental muscle-building drug, we're hoping to restore their function, keeping them out of the nursing home and playing with their grandchildren. Excitingly, the drug seems to work. Over the course of a few months, the volunteers in our trial who receive our drug put on muscle mass, while people receiving the placebo continue to lose muscle. Mission accomplished, right?

Yet when the researchers test the volunteers on standardized tests of muscle strength and function, the newly-muscular elders are no stronger than when the trial started, and no better off than the people who were taking sugar pills. What's the drug? Actually, it's a lot of drugs. People have been trying to develop therapies to help aging people regain muscle mass and strength for decades now, and while a number of them have bulked up subjects' biceps, they have consistently failed to deliver on the functional outcomes that matter most.

As with other age-related diseases and disabilities, sarcopenia is a complex condition, driven by the collateral damage inflicted on multiple cellular and molecular structures by the processes that keep us alive. As these structural units are damaged or destroyed, we lose functional contribution to delivering muscle strength and power. To reverse this degenerative process, it isn't enough to simply add more of the dysfunctional muscle tissue aging people have. Instead, we need to develop rejuvenation biotechnologies capable of removing and repairing the range of cell and tissue damage that robs our muscles of their strength.

Link: https://www.sens.org/legs-of-iron-feet-of-clay/

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