The most useful thing to understand about visceral fat is that it is not a storage depot. It is active tissue that secretes signalling molecules into the bloodstream continuously, and a substantial proportion of those signals are inflammatory.
That single fact reorganises a great deal of what otherwise looks like unrelated illness.
The immune connection is not a metaphor
Fat cells and immune cells share an evolutionary lineage. In Drosophila, the fat body performs the functions that in mammals are split between adipose tissue and the innate immune system — the same organ does both jobs. The separation in humans is more of a division of labour than a clean break, and adipose tissue retained a great deal of immune signalling capability.
This is why adipose tissue secretes the molecules it does:
- TNF-α, IL-6, IL-1β — classical pro-inflammatory cytokines
- Leptin — the satiety hormone, which is structurally related to the cytokine family and behaves like one
- Adiponectin and resistin — adipokines with opposing metabolic effects
One consequence deserves emphasis. C-reactive protein, the inflammatory marker measured routinely, is produced by the liver largely under the direction of circulating IL-6 — and a major source of that IL-6 is adipose tissue. When CRP is elevated in a patient with central adiposity, a good deal of what is being measured originates in the fat itself.
Leptin resistance travels with insulin resistance
Leptin signals satiety. In sustained excess, the receptors become less responsive — the same pattern insulin follows, and the two typically appear together.
The practical result is a patient with high circulating leptin who does not experience satiety, and high circulating insulin that is driving storage rather than mobilisation. That is not a willpower state. It is a signalling failure, and it is measurable. The mechanism on the insulin side is covered in hyperinsulinemia and chronic pain.
Why this reaches pain
A persistently raised inflammatory baseline lowers the threshold at which ordinary tissue signals register as pain, slows resolution after injury, and sustains central sensitization. That is the mechanistic link between metabolic dysfunction and pain that does not settle — and it explains a clinical pattern most chronic pain patients recognise: the same procedure that helped someone else helps them less, and for less time.
There is a second loop worth naming. Highly palatable processed food drives dopamine release through the brain’s reward pathway, in a pattern that overlaps with other reinforcing substances. Animal models in which dopamine signalling is disrupted show markedly reduced overconsumption of palatable food — evidence that the reward pathway, not appetite alone, is doing the driving. These are animal-model findings and should not be read as directly established in humans.
The loop, as we see it clinically: reward-driven intake raises adiposity, adiposity raises inflammation, inflammation raises pain, and pain increases the pull toward the most available source of dopaminergic relief — which for most people is food. We wrote about that convergence in addiction, chronic pain and type 2 diabetes share one substrate.
Where the evidence is contested — and where it is not
Two claims frequently made in this area need to be separated, because they carry very different evidentiary weight.
Well established: adipose tissue is endocrine and immune-active; IL-6 from adipose tissue drives hepatic CRP; leptin and insulin resistance co-occur; central adiposity associates strongly with metabolic syndrome and its downstream disease.
Genuinely contested: the proposition that industrial seed oils are a primary driver of the rise in metabolic disease.
The timeline presented in the talk is specific. Industrial seed oil entered the human diet in commercial quantities from around 1917 — against two to three million years of human history without it. The sharp uptake came after the 1977 dietary guidelines, which promoted reduced fat consumption and tolerated increased carbohydrate in its place. Canola oil adoption followed shortly after, and diabetes prevalence began climbing roughly five to seven years behind it. The proposed mechanism is oxidised linoleic acid.
That correlation is real and the mechanism is biologically plausible. It also cannot be separated from the simultaneous rise in refined carbohydrate, total energy intake, ultra-processing and sedentary behaviour — all of which moved in the same decades. We present this as a hypothesis under investigation, not as settled science. Dr. Padda’s own framing is a prediction rather than a finding: that industrial seed oils will eventually be regarded with the disdain now reserved for cigarettes. Patients should know which parts of this are established and which are forecast.
On prevalence, the same talk puts adverse metabolic syndrome at more than 25% of US adults by formal criteria, and plausibly 60–70% once clinically identifiable metabolic derangement is counted rather than the diagnostic checklist alone. The gap between those two numbers is the point: the formal criteria are a diagnostic convention, and a great many people are metabolically unwell before they satisfy it.
Prevalence figures and the seed-oil timeline as presented by Dr. Padda in a professional educational presentation to a clinical audience.
One correction, because this one is a misstatement rather than a contested position. The talk describes roughly 22 teaspoons of sugar a day as falling “within the recommended guidelines.” It does not. That figure approximates average American consumption; no dietary guideline recommends it, and the American Heart Association’s limits are far lower — around 6 teaspoons a day for women and 9 for men. There is no dietary requirement for added sugar at all. A source being authoritative does not make a misspoken number correct, so we have fixed it here rather than reproduced it.
What we actually ask patients to do
Deliberately, none of this is calorie counting.
- Shorten the eating window. Fewer eating occasions means fewer insulin excursions and a lower area under the insulin curve. That is the target, not the calorie total.
- Stop snacking before worrying about anything else. It is the single change with the largest effect on insulin exposure.
- Eat real food rather than avoiding categories. Framing a change as deprivation reliably increases the pull of whatever was removed.
- Eat to about eight parts in ten full — the Okinawan hara hachi bu convention. It changes the relationship with the meal rather than adding another number to track.
We avoid calorie counting because it is imprecise in principle — resting metabolic requirement varies substantially day to day, and the gut microbiome materially affects what is extracted from a given intake — and because it consumes the willpower that is better spent on food quality. See treating metabolic disease at the dietary root cause.
Frequently asked questions
I am not overweight. Can I still have this problem?
Yes. Visceral fat is not always visible externally, and the inflammatory state can be present in people at normal body weight. It is identified by biomarkers rather than by appearance — see hyperinsulinemia and chronic pain.
Is my elevated CRP coming from my fat?
Frequently, in part. Hepatic CRP production is driven largely by circulating IL-6, and adipose tissue is a major IL-6 source. CRP is non-specific, so it has to be interpreted alongside the rest of the picture.
Are seed oils the cause of all this?
That is an open question, not a settled one. The correlation exists and the mechanism is plausible, but it cannot be separated from the simultaneous rise in refined carbohydrate and ultra-processed food. We treat it as a hypothesis worth taking seriously, not as established fact. See treating metabolic disease at the dietary root cause.
Why no calorie counting?
Because it is inaccurate in practice, spends willpower that food quality needs, and reliably produces self-reward behaviour that cancels the deficit. Shortening the eating window addresses insulin exposure more directly.
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
- Adipose tissue is endocrine and immune-active; it shares lineage with the innate immune system.
- Much of a raised CRP in central adiposity traces back to adipose-derived IL-6.
- Leptin resistance and insulin resistance appear together and are signalling failures, not willpower failures.
- The food-reward loop is supported by animal models; do not overstate it as established in humans.
- The seed-oil hypothesis is plausible and unproven — we label it as contested.
- The intervention is eating window and food quality, not calorie arithmetic.
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
