23/07/2025
We need to stop thinking of osteoarthritis (OA) as just a “wear-and-tear” disease. The science now tells a more nuanced story—one where metabolic dysfunction plays a central role. Not the only role. But an important one.
Yes, obesity increases joint load, particularly in weight-bearing joints such as the knees. In fact, for every 5-point increase in BMI, the risk of knee OA rises by 35%. But the connection doesn’t stop there.
Hand osteoarthritis is also significantly more common in individuals with obesity. The hands don’t bear weight—so clearly, something more than load is at play.
That “something” is a constellation of metabolic abnormalities:
-Chronic hyperglycemia
-Insulin resistance
-Dyslipidemia
-Hypertension
-Systemic inflammation
These factors fuel joint degeneration from within. Elevated glucose levels stimulate the production of proinflammatory cytokines and matrix metalloproteinases (MMPs), which damage cartilage and degrade joint tissue. Insulin resistance and visceral fat contribute to chronic, low-grade inflammation, which in turn alters joint biology.
The same metabolic dysfunction that damages blood vessels, nerves, and organs also erodes joint integrity.
So no, osteoarthritis is not just a mechanical disease. It’s a metabolic one too.
The implications?
Managing OA means addressing load and biology. That includes: – Reducing visceral adiposity – Improving insulin sensitivity – Controlling inflammation – Engaging in strength training and aerobic movement – Prioritizing sleep and stress management.
OA is not always inevitable. It’s often modifiable. However, only if we understand what is driving it.
