The mechanism, specifically

Three connective-tissue effects do most of the work, and none of them is visible on a scan:

• Glycation and cross-linking of collagen. Sustained high insulin and glucose modify collagen so the annulus of a disc and the capsule of a facet joint become stiffer and less able to distribute load. Stiffer tissue fissures at loads it used to tolerate.
• Impaired microvascular perfusion. The disc has no blood supply and is fed by diffusion across the vertebral endplates. The same small-vessel damage that harms kidneys and retinas degrades that supply line, and endplate calcification blocks it outright.
• A degradative rather than reparative state. Elevated inflammatory tone keeps tissue turning over toward breakdown, so the microdamage of an ordinary week does not clear before the next week starts.

Add a nervous system effect on top: metabolic inflammation lowers the threshold at which mechanical contact becomes symptomatic, which is a large part of why the same disc protrusion is silent in one person and disabling in another.

The confession this practice is built on

Dr. Padda spent roughly twenty years telling patients whose numbers were drifting that they were not too bad. He has said so publicly, in front of rooms of colleagues, because the alternative is pretending the model was always right. He was also, for years, a strict vegetarian defending guidelines he now dismantles.

That correction is why the intake here asks for an A1C alongside your leg symptoms. A physician who has already been wrong about the terrain once is more careful about calling a back a purely mechanical problem and stopping there. More on that.

What we look at

• Fasting insulin, not only glucose. Insulin rises years before glucose does, so a normal fasting glucose with a high insulin is an early signal that a glucose-only panel misses entirely.
• A1C, with the caveat that it is an average and can hide substantial variability.
• Triglyceride to HDL ratio, a cheap and useful proxy for insulin resistance.
• hs-CRP for inflammatory tone.
• Vitamin D, which is widely insufficient and matters for bone and muscle.

The part that is not about individual discipline

The population arriving here is disproportionately working schedules they do not control, eating what is available at the hour they are free, and sleeping less than repair requires. The food environment on a late shift is engineered around acellular carbohydrate and industrial seed oil, and that is an incentive problem before it is a willpower problem.

We subsidize the crop that drives the disease and then means-test the treatment. Saying so is not a political position; it is the reason a back clinic ends up looking at bloodwork, and the reason lecturing a patient about discipline is both unkind and inaccurate.

Common questions

Why does a pain doctor want my A1C?

Because the tissue we are being asked to fix is maintained by that system, and a structural plan built on an inflamed terrain underperforms. Better to know at the start.

That is the subject of The load matters. It is not the main reason your back hurts, and being told it is has probably ended a few appointments early..

Will fixing this make my back pain go away?

Rarely on its own, and it changes what everything else achieves. It is the difference between relief that holds and relief that resets.

See You have explained it four times. Nobody wrote it down..

Do I have to lose weight first?

No. Nothing here is conditional on it, and metabolic health improves with changes to food quality, sleep and movement well before the scale moves. On weight specifically.

Related reading

• Weight and the lumbar spine
• Sleep and back pain
• Degenerative disc disease
• About Dr. Padda

What changes at menopause pulls bone and metabolism in the same direction.