A metabolic hormone slowed spinal disc aging in rats — and it’s already being tested in humans for other reasons
Back pain from worn spinal discs is one of the most common consequences of getting older.
The hormone is FGF21, a growth factor that regulates energy metabolism and is already in clinical development for liver and metabolic disease. In a study published in Aging Cell, researchers found that FGF21 protects intervertebral discs — the shock-absorbing structures between spinal vertebrae — by activating SIRT1, a protein from the sirtuin family long associated with cellular maintenance, inflammation suppression, and aging.
Intervertebral disc degeneration is one of the leading causes of lower back pain worldwide. The discs act as cushions between vertebrae, consisting of a gel-like core surrounded by a fibrous ring. With age, the core loses water, the fibers stiffen, and the disc can crack or collapse, pressing on nerves and causing pain. Some degree of disc degeneration is nearly universal in people over fifty.
How SIRT1 fits in
SIRT1 is a deacetylase — an enzyme that regulates the activity of other proteins by removing chemical tags. It is activated by energy stress, fasting, and some dietary compounds including resveratrol. Prior research has linked SIRT1 to suppressing inflammatory signaling and slowing senescence in multiple tissues. In this study, administering FGF21 to rats with induced disc degeneration raised SIRT1 activity in disc cells, reduced inflammatory markers, and slowed structural deterioration. Treated rats showed less tissue damage and better preserved disc height and integrity compared to controls.
A faster path to humans than most
What makes this finding particularly interesting is that FGF21 is already in clinical trials — for nonalcoholic fatty liver disease and metabolic conditions, not back pain. Synthetic versions and analogs have reached clinical-stage testing, which lowers the bar for eventual repurposing. Still, the road from a rat model to a proven treatment in humans is long, and the field has seen many promising anti-aging interventions fail to replicate in clinical settings.
Disc degeneration is also partly a mechanical problem, not purely a biological one. Even if inflammation and senescence are suppressed, dehydrated, collapsed tissue does not simply rebuild itself. Whether a systemic treatment like FGF21 can meaningfully counteract a condition that is driven in large part by decades of physical load remains an open question — and so does the question of timing: how early would an intervention need to begin to make a real difference?