Most physicians who end up practicing metabolic medicine arrive there deliberately. Dr. Gurpreet Singh Padda arrived there because his pain patients did not make sense. In a conversation with Sharon Fekety on The Doctor Whisperer, he traced the path from pediatric anesthesia to interventional pain to diabetes reversal, and explained the observation that forced the turn. This article summarizes the medical ideas from that discussion.
The observation that did not fit
Dr. Padda started in anesthesia, working with heart, liver and lung transplant cases. At Cardinal Glennon Children’s Hospital in St. Louis he noticed that patients on the bone marrow transplant unit were in significant pain that was going largely untreated. Solving that pulled him into pediatric pain, then into adult pain, and eventually out of academic medicine into private practice.
Then came the observation that redirected everything. His patients were, in many cases, financially incapacitated by their pain. They were not working. They did not have money. And they were overweight.
That combination breaks the usual story. If obesity tracked with affluence and abundance, this was the population least likely to show it. Something else was driving it, and whatever that was appeared to be operating in the same patients whose pain would not resolve.
What the biomarkers showed
When he looked at the laboratory picture rather than the imaging, a pattern emerged. Almost all of these patients carried markers of severe systemic metabolic inflammation: elevated high-sensitivity CRP, and badly skewed omega-6 to omega-3 fatty acid ratios.
The significance is directional. This was not inflammation as a consequence of being in pain. It looked like part of the underlying milieu that made the pain persistent in the first place — a terrain that kept the signal switched on. That framing is the through line of his clinical work, and it is why this practice treats the drivers behind chronic pain rather than the signal alone.
He also made a point about training: nutrition is barely taught in medical school. Pursuing it meant going outside conventional medical education, which eventually led to board certification in addiction medicine and to speaking on the nutritional dimension of care for Low Carb USA and the American Society of Interventional Pain Physicians.
Nine square blocks in North St. Louis
The most striking thing in the conversation is a piece of analysis he ran on his own patient population’s neighborhood.
Using geographic mapping of household income combined with healthcare outcome data and DRG codes, he modeled what happens to a nine-square-block area of North St. Louis over time, then had a statistician independently check the result because he did not trust his own conclusion. By his account, the projection for 2035 is this: 99 percent of that population overweight, 60 percent with type 2 diabetes, and half progressing to end-stage renal disease and dialysis.
The figure he returns to is the cost. On that trajectory, caring for the people living in those nine blocks would exceed the state of Missouri’s disposable budget by 2035.
This is his own analysis rather than a published study, and it is offered here as such. But the reason he cites it is not to be alarming. It is the reason he moved into diabetes reversal at all: a projection like that describes a problem no clinic can treat its way out of one patient at a time.
The wider context he gives is that roughly six to seven percent of the United States population is metabolically healthy, which leaves something like 93 to 94 percent metabolically dysfunctional.
Why an addiction model applies to sugar
His approach to diabetes reversal came from applying what he already knew about addiction.
The concept he leans on is hedonic substitution: human behavior is substantially driven by the pursuit of pleasure, and when one source of reward is removed, another is substituted for it. Treating sugar consumption as a purely informational problem — telling someone what to eat — ignores the reward system doing the actual driving, and ignores the neuroinflammatory state that shapes how strongly that system pulls.
That is why his interventions target behavior and biology together rather than relying on dietary instruction alone.
Glycogen, insulin, and why eating frequency matters
The mechanical part of his explanation is the most useful for patients, and it is not the one most people have heard.
The liver holds a glycogen store of roughly 2,000 kilocalories. That store is a buffer, and it has a ceiling. Americans move considerably less than they used to, which means most people never meaningfully deplete it.
Insulin is usually described as the hormone that moves sugar from the bloodstream into cells. Dr. Padda’s framing is more specific about the order of operations: insulin fills glycogen first, and once that store is full, the surplus is directed into fat storage. So the problem is not any single meal. It is the combination of a glycogen buffer that never empties and an eating pattern of six or seven occasions a day, each one raising insulin again. Under those conditions the system is being told to store, more or less continuously.
This is also the connection back to pain. Visceral fat is not inert; it is metabolically active tissue that releases inflammatory signals, which is the same inflammation showing up in those pain patients’ bloodwork.
Membrane fluidity and the 1971 shift
Then there is the part of insulin resistance that gets left out of most explanations.
High circulating insulin does desensitize receptors. But receptors sit in cell membranes, and a membrane has to remain fluid for the receptors embedded in it to function. When membrane composition changes, receptor function degrades everywhere at once — brain, liver, muscle.
Membrane composition is substantially a function of the omega-6 to omega-3 ratio, which is a function of dietary oil. He points to about 1971 as the inflection point, when American consumption shifted heavily toward vegetable oils. A ratio that was once roughly balanced is now, in his description, closer to 15 to 1.
That mechanism is worth sitting with, because it reframes the dietary fat conversation. The argument is not that seed oils are inflammatory in the abstract. It is that they change the physical medium your receptors operate in.
What he asks patients to do first
The interventions he described are deliberately ordered simplest-first:
- Narrow the eating window. Time-restricted nutrition creates enough of a gap to actually draw down some glycogen.
- Add simple movement. Walking depletes glycogen. The intervention does not have to be athletic to work.
- Reduce the carbohydrate load. His point on this is physiological rather than ideological: there are essential fatty acids and essential amino acids, but there is no essential dietary sugar. Through gluconeogenesis the body manufactures what glucose it requires.
- Then address the reward side, since hedonic substitution is what undoes plans built on willpower alone.
Frequently asked questions
What is metainflammation?
It is chronic, low-grade systemic inflammation arising from metabolic dysfunction rather than from infection or acute injury. It is measurable through markers such as high-sensitivity CRP and fatty acid ratios, and it is the mechanism that links chronic pain, metabolic disease and addiction in Dr. Padda’s clinical model.
Why would a pain doctor care about diabetes?
Because in his patient population the two arrived together. Inflammation from metabolic dysfunction changes how the nervous system processes pain signals, so treating a painful structure while ignoring the metabolic environment around it addresses only part of the problem.
Does this mean my pain is caused by my diet?
Not on its own. There is usually a real structure generating the pain, and identifying it is the diagnostic work interventional pain medicine exists to do. The metabolic argument is about why that pain is louder and more persistent than the imaging alone would predict.
Is cutting carbohydrate the whole intervention?
No. Eating frequency and glycogen depletion matter alongside composition, movement is part of it, and the reward-driven side of eating has to be addressed or the plan will not hold.
Key takeaways
- Patients incapacitated by pain were also overweight and without financial resources, which decouples obesity from abundance and points at a different driver.
- Those patients carried measurable markers of systemic metabolic inflammation, including elevated hs-CRP and skewed omega-6 to omega-3 ratios.
- Insulin fills the roughly 2,000-kilocalorie liver glycogen store first and directs the surplus to fat, so eating frequency matters, not just what is eaten.
- Receptors need fluid membranes to work, and membrane composition tracks dietary oil, which is why the omega ratio affects far more than inflammation alone.
- Simple interventions come first: a narrower eating window, walking, and less carbohydrate.
Find the source of your pain — not just the signal
If your pain has outlasted the injury that started it, the useful question is what is keeping it switched on. Request an appointment or call (314) 481-5000.
Related reading
- Why medications, procedures, and surgery may not fix chronic pain
- How inflammation and diet drive chronic pain and hormone problems
- Insulin resistance comes years before diabetes
- Sugar, refined grain and seed oil: the mechanism behind each one
- How the 1977 dietary guidelines went wrong
- About Dr. Gurpreet Singh Padda, MD, MBA, MHP
Dr. Gurpreet Singh Padda, MD, MBA, MHP
