This is a guest appearance rather than a clinical explainer — a long-form conversation on someone else’s podcast, addressed to that host’s audience. The register is different from our usual posts, and some of it is personal.
It is worth reading for the argument about food environments, and it needs reading with attention to which claims are established and which are the speaker’s own position. We have marked those distinctions throughout.
The background, because it explains the argument
Dr. Padda was born in India and arrived in the United States at eight or nine, in the period after Partition, when his family left a country they believed was moving toward communism. His father is a physicist; his mother a mathematician.
The family landed in public housing in downtown St. Louis City. He has described not initially realising there was a white population in America — the children around him were Black, he was brown, he wore a turban, and he did not yet speak English. He learned the country from that vantage point, and later completed his education in the county, moving between three distinct communities before adulthood.
That trajectory is the origin of the argument he makes now. Watching the same person do better or worse depending on which neighbourhood they lived in — what was sold there, what it cost, what was within walking distance — is a different education from reading about health disparities. It is why his framing consistently lands on environment rather than individual choice, and why he speaks about the community that first took his family in.
The remarks in this interview are addressed to that audience directly, at the host’s invitation, and we have preserved that context rather than genericising it.
The food environment argument
The core claim is that the modern food supply is not neutral background — it is an active input, and it was optimised for shelf stability rather than nutrition. We set that history out in why we treat insulin before we treat the joint.
Several specific mechanisms come up in the conversation, and they sit at different levels of evidence:
Reasonably supported. Highly processed, energy-dense food drives dopamine release through reward pathways in a manner that overlaps with other reinforcing substances, and that reinforcement — rather than hunger alone — sustains overconsumption. Covered in fat is an immune organ.
Emerging, not settled. Intestinal permeability allowing bacterial lipopolysaccharide into the circulation, with downstream inflammatory consequences, is an active research area. The proposition that this causes specific autoimmune diseases — lupus, rheumatoid arthritis — goes beyond what the evidence currently establishes. It is a hypothesis worth taking seriously and it is not a finding.
Investigational, animal-model. The suggestion that components of industrial vegetable oil suppress oxytocin signalling, with consequences for bonding, derives from rodent work. It has not been established in humans, and the extension from a mouse hypothalamus to human parent–child attachment is a long one. We report it as the speaker’s position, clearly labelled, because it is stated strongly in the interview and readers deserve to know its status.
A reframing with growing support. The interview describes fibromyalgia as “fundamentally a disorder of metabolism,” with the pain as a secondary consequence rather than the primary disease.
Multiple studies now report associations between fibromyalgia and metabolic dysfunction — insulin resistance in particular — and this is the model under which we treat it: address the metabolic driver, and the pain follows. That is a meaningful departure from the conventional account, which treats fibromyalgia primarily as a disorder of central pain processing.
Two honest caveats for patients reading this. Formal diagnostic classification has not changed, so you will still encounter the older framing in most clinical settings and should not be surprised by it. And most of the supporting work reports association rather than demonstrated causation — which is what “correlate” means and is worth knowing when you weigh it. We are not reproducing any specific prevalence percentage here, because the figure most often quoted in this area has not survived our own citation checking.
What follows practically is straightforward regardless of where the classification debate lands: if you have fibromyalgia, your metabolic status is worth measuring. See why we treat insulin before we treat the joint.
What “reversal” means, and what it does not
The strongest claims in the conversation concern type 2 diabetes, and they need careful separation.
The published figure quoted concerns conventional advice. Cohort analysis of routine primary care data has produced strikingly low annual probabilities of a person with obesity attaining normal body weight through standard “eat less, move more” counselling — probabilities in the range of one in a few hundred, varying substantially by sex and starting BMI. Whatever one thinks of the methodology, it is a published finding rather than an opinion, and it is the honest baseline against which anything else should be measured.
The claim that this practice achieves substantially better results — including patients coming off insulin within a few months — is a practice-reported outcome. It reflects this clinic’s own experience with its own patients under its own protocols. It has not been through independent trial, it is not a guarantee, and individual results vary.
What it is not is a claim that type 2 diabetes is trivially reversible for everyone. The relevant mechanism is set out in hyperinsulinemia and chronic pain and addiction, chronic pain and type 2 diabetes share one substrate.
On the injectables
The interview declines to use GLP-1 receptor agonists, and gives a specific reason: they reduce intake indiscriminately, protein included, so lean mass is lost alongside fat. On discontinuation, fat is regained more readily than muscle — leaving a patient at a similar weight with a worse body composition than they started with.
The underlying concern is real and increasingly discussed: loss of lean mass with GLP-1 therapy is documented, and it is why resistance training and adequate protein are now routinely recommended alongside these drugs. The specific ratios cited in the interview for how long muscle takes to rebuild are the speaker’s own figures rather than published values.
This is a position, not a consensus. These medications have substantial evidence behind them and they are the right choice for many patients. If you are taking one, this is a conversation to have with your prescriber — do not start, stop, or change any medication without consulting your physician.
Frequently asked questions
Is fibromyalgia really a metabolic disease?
Multiple studies now report associations between fibromyalgia and metabolic dysfunction, particularly insulin resistance, and that is the model we treat under — metabolic driver first, pain as a consequence. Formal diagnostic classification has not changed, so most clinicians will still describe it as a central pain processing disorder. Either way, your metabolic status is worth measuring. See why we treat insulin before we treat the joint.
Can type 2 diabetes actually be reversed?
Remission is achievable for a meaningful proportion of patients, particularly earlier in the disease. The specific results described in this interview are this practice’s own reported experience, not trial data. Individual results vary. See addiction, chronic pain and type 2 diabetes share one substrate.
Should I stop my GLP-1 medication after watching this?
No — not without speaking to your prescriber. The lean-mass concern is legitimate and worth discussing, and it is usually addressed with protein intake and resistance training rather than by stopping. Do not start, stop, or change any medication without consulting your physician.
Do vegetable oils really affect bonding?
That comes from animal research and has not been demonstrated in people. We have flagged it as investigational because it is stated strongly in the interview and its evidentiary status is easy to miss. See fat is an immune organ.
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
- The environment-over-choice argument comes from lived observation across three St. Louis communities.
- Food reward and overconsumption is the best-supported mechanism discussed.
- Intestinal permeability and autoimmunity is an emerging area, not established causation.
- The vegetable oil and oxytocin claim is animal-model only.
- Fibromyalgia as a metabolically driven disorder has growing support and is how we treat it; formal classification has not yet changed, and we publish no prevalence figure.
- Diabetes reversal results described here are practice-reported, not trial data. Individual results vary.
- The GLP-1 lean-mass concern is real; the conclusion drawn from it is a position, not consensus.
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.
Find out what is actually driving your pain
Evaluation at the Padda Institute starts by identifying the pain generator and the metabolic terrain it is running on — not by adding another prescription.
Book an appointment or call (314) 481-5000 · text (314) 886-5902
Padda Institute Center for Interventional Pain Management, 4477 Woodson Rd, Suite 100, St. Louis, MO 63134 — serving the St. Louis region across Missouri and Illinois.
Dr. Gurpreet Singh Padda, MD, MBA, MHP
