Why We Treat Insulin Before We Treat the Joint

Patients arrive at a pain clinic expecting the conversation to be about their back, their knee, or their neuropathy. They are frequently surprised when the first thing we order is a fasting insulin.

That is not a detour. For a large fraction of chronic pain patients, insulin resistance is the substrate the pain is running on, and treating the joint without treating the substrate produces the result those patients have already experienced repeatedly: temporary relief, then return.

The number most patients are told is fine

The conventional thresholds are familiar. An HbA1c under 5.7% is normal. Between 5.7 and 6.4% is prediabetes. At 6.5% and above, the diagnosis is type 2 diabetes.

Those cut-points are diagnostic conventions, not biological cliffs. A patient at 6.1% has not been well until the moment they crossed 5.7. What has actually happened, often for years before the HbA1c moved at all, is a steady rise in fasting insulin as the pancreas works progressively harder to hold glucose in the normal range.

That is why we aim lower than the diagnostic threshold, and why we look at fasting insulin alongside HbA1c rather than glucose alone. Insulin moves first. Glucose is the lagging indicator, and by the time it is abnormal a great deal of the inflammatory damage is already underway.

We treat this as disease modification rather than as a number to manage. The mechanism linking high insulin to pain is set out in hyperinsulinemia and chronic pain.

Why this belongs in a pain clinic

Adipose tissue is not inert storage. It is an endocrine and immune organ that secretes pro-inflammatory signalling molecules continuously, and the more visceral fat present, the higher that baseline signal runs. We go through that biology in visceral fat and the metabolic problem you cannot see.

A raised inflammatory baseline changes the pain experience directly. It lowers the threshold at which tissue signals become painful, slows the resolution of injury, and sustains the central sensitization that keeps pain going after the original problem has healed.

The practical consequence is that an injection into an inflamed joint in a metabolically inflamed patient does less, and does it for less time. The same procedure in a patient whose insulin has been brought down does more, and lasts longer. That is the clinical observation that drives the sequencing, and it is why the metabolic work is not an adjunct to the pain treatment — it frequently is the pain treatment.

There is a further link worth naming: the overlap between obesity, chronic pain and addiction is not coincidental. All three run through the same inflammatory and dopaminergic territory. We wrote about that convergence in addiction, chronic pain and type 2 diabetes share one substrate.

Cerebral blood flow, and why this is not only about joints

Imaging work using SPECT has reported reduced regional cerebral blood flow across a range of brain regions in association with rising body mass, including in people who are overweight rather than obese. Reduced perfusion is one of the more consistently observed antecedents of cognitive decline.

That finding should be read as an association in cross-sectional imaging, not as demonstrated causation — but it aligns with what we see clinically, and it is part of why we treat metabolic dysfunction aggressively in patients whose presenting complaint is pain rather than cognition. The related mechanism is covered in what untreated chronic pain does to the brain.

The bias problem, in both directions

A point from the video that deserves to be repeated plainly: clinician bias about weight affects the quality of care patients receive, and it runs in both directions.

Clinicians who are themselves carrying excess weight are less likely to raise the subject at all. Clinicians who are lean and have never struggled with it frequently underestimate how difficult the problem is, and communicate in ways that land as judgement rather than help. Both failures end at the same place — the patient does not get useful counselling.

The remedy is not to pretend the bias is absent. It is to examine it directly, understand the patient’s actual circumstances, and recognise that the metabolic environment most people live in was not designed by them.

The food environment is not an accident

The modern American food supply was shaped by policy decisions taken for reasons that made sense at the time. Mid-century agricultural subsidy and distribution programmes were built to move calories reliably across a large country and to stockpile against scarcity — an objective driven by national security rather than by nutrition.

That system was optimised for shelf stability and efficiency. Shelf stability favours refined carbohydrate and industrial oils, which do not spoil. It does not favour nutrient density.

The system is therefore not broken. It is functioning exactly as designed — the design simply did not have the current problem in view. Recognising that changes the conversation with patients, because it moves the frame from personal failure to environment. See treating metabolic disease at the dietary root cause.

What that looks like at street level

The argument stops being abstract when the geography narrows. A household survey commissioned by the City of St. Louis, covering a nine-square-block area, found overweight or obesity in very nearly every adult woman surveyed.

Two things need saying about that number. It is a small, geographically specific sample and it is not a figure for St. Louis, for Missouri, or for any demographic group nationally — anyone quoting it that way is misusing it. And read as what it actually is, a snapshot of one neighbourhood, it is more damning rather than less.

Several hundred adults living within nine blocks of each other did not independently arrive at the same metabolic outcome through several hundred independent failures of willpower. Something in that environment — what is sold there, at what price, within what walking distance, on what budget — is producing a consistent result. That is what a food environment is, and it is why the clinical conversation cannot stop at individual advice.

Figure presented by Dr. Padda in a professional educational presentation, sourced to a City of St. Louis household survey.

The inversion, in one comparison

The clearest way to see what changed is to look at why the country originally cared about nutrition at all.

In the 1940s, the concern driving federal food policy was that roughly 40% of military recruits were ineligible for service because of malnutrition — they were underweight. Today the figure that disqualifies recruits has inverted: on the order of 70% of Americans cannot qualify for military service, substantially because of overweight and obesity.

Same policy machinery. Opposite failure mode. What we have now is the malnutrition of excess — energy-dense, nutrient-poor, and abundant.

The subsidy structure that produced it has not been retired. By Dr. Padda’s account, around 10% of every SNAP dollar is spent on sugar-sweetened beverages — roughly $7 billion a year, which functions as a downstream subsidy to the sugar industry. About two-thirds of SNAP recipients are also on Medicaid, so the same public purse pays for the exposure and then for the disease.

What this costs, and where it is heading

The projections presented in the same talk:

• Around 85% of US adults overweight or obese by 2030.
• Roughly 80% of those patients becoming insulin resistant, prediabetic or diabetic.
• Insulin therapy exceeding $800 per month, and about $10,000 per year in total cost per insulin-dependent patient — before renal dysfunction, before dialysis, before anything else downstream.
• Obesity and insulin resistance accounting for somewhere between a third and two-thirds of national healthcare expenditure — on the order of $1.7 trillion a year.

These figures were presented by Dr. Padda in a professional educational presentation to a clinical audience. Projections are projections; the wide band on the expenditure share reflects genuine disagreement about how much disease to attribute to metabolic dysfunction.

There is one more number worth sitting with, because it changes the time horizon. Roughly 8% of our genes carry environmental edits — including dietary ones — that persist for life and may carry forward into subsequent generations. If that is right, the food environment is not only a problem for the person eating in it.

That is the argument for treating insulin resistance as disease modification rather than as a number to be managed. The compounding runs in one direction unless something interrupts it.

Frequently asked questions

My HbA1c is normal. Why are you testing my insulin?

Because insulin rises years before glucose does. A normal HbA1c with a high fasting insulin means the pancreas is compensating successfully — for now. Catching that stage is the entire point. See hyperinsulinemia and chronic pain.

What does my weight have to do with my back pain?

Less than you would think mechanically, and more than you would think chemically. Visceral fat secretes inflammatory signals that lower pain thresholds and slow healing, independent of load. See visceral fat and the metabolic problem you cannot see.

Will treating this get me off pain medication?

It is frequently part of how that happens. Reducing the inflammatory baseline makes interventional treatment work better and last longer, which is what creates room to reduce medication. See opioid tapering: medication is a bridge, not a destination. Do not start, stop, or change any medication without consulting your physician.

Is this a weight-loss programme?

No. The target is insulin resistance and inflammation, not a number on a scale. Weight often changes as a consequence, but it is not the endpoint we track.

Where can I be evaluated?

Padda Institute, 4477 Woodson Rd, Suite 100, St. Louis, MO 63134, serving the St. Louis region across Missouri and Illinois. Call (314) 481-5000 or text (314) 886-5902.

Key takeaways

• Insulin rises years before glucose; a normal HbA1c does not rule out metabolic dysfunction.
• Adipose tissue is an immune organ, and its inflammatory output changes pain thresholds directly.
• Metabolic treatment makes interventional pain treatment work better and last longer.
• Clinician bias about weight degrades counselling in both directions and has to be addressed openly.
• The food environment was optimised for shelf stability, not nutrition — which reframes patient blame.

Medically reviewed by Gurpreet Singh Padda, MD, MBA, MHP — Board Certified in Anesthesiology, Pain Medicine, Interventional Pain Management, Addiction Medicine, and Obesity Medicine. Last reviewed August 2026.

This article is educational and is not a substitute for evaluation, diagnosis, or treatment by a physician. Individual results vary. Do not start, stop, or change any medication without consulting your physician.

Dr. Gurpreet Singh Padda, MD, MBA, MHP