This clinic began as an interventional pain practice. It became clear quickly that chronic pain was rarely an isolated pathology. The tools available here relieve symptoms well; they do not reverse the course of a disease whose driver is metabolic inflammation.
What metainflammation is
Inflammation is a biological response launched by the immune system against assaults that threaten normal physiology. It is essential. It becomes pathological when it fails to resolve: excessive acute inflammation damages tissue, and non-resolving inflammation produces chronic tissue malfunction. The balance between an effective response and collateral damage is delicate.
Chronic nutrient overload disturbs that balance. When adipose tissue expandability is low and the nutrient load keeps arriving, the tissue becomes irregular and inflamed. That is overnutrition-induced inflammation — metainflammation.
Fat tissue is an endocrine organ
Obesity is characterized by a low-grade chronic inflammatory state in which pro-inflammatory cytokines including TNF-α, IL-6 and CRP are elevated. Over-accumulated subcutaneous and abdominal adipose tissue stops behaving as inert storage and begins signaling.
The proteins adipose tissue releases that affect inflammation include TNF-α, IL-6, IL-1β, leptin, adiponectin, resistin, acylation-stimulating protein, SAA3, α1 acid glycoprotein, pentraxin-3, IL-1 receptor antagonist and macrophage migration inhibitory factor. That is not a waste depot; it is an organ with an output.
Lactate is a signal, not a waste product
A study published in Nature demonstrated that lactate is a key regulator of cell function in Warburg-associated disease rather than simply a metabolic by-product. Lactate rewires macrophages, changing how immune cells behave, and it drives histone lactylation — a modification that alters which genes are expressed.
The Warburg effect itself, described by Otto Warburg ninety years ago, is the observation that cancer cells consume glucose differently from healthy cells, generating energy in a way that supports rapid growth. The metabolic and oncologic literatures are describing the same underlying machinery.
Why a pain physician cares about metabolism
The question arrives regularly: why worry about a patient’s weight or metabolic function — why not just treat the pain? Because more than 90% of the chronic pain patients seen here have metabolic dysfunction, including many whose waist circumference would not flag them.
Multi-joint pain, including in non-weight-bearing joints, tracks the inflammatory cascade independently of mechanical load. Treating the joint while the inflammatory environment persists produces relief that does not hold.
Dopamine, motivation and anhedonia
The brain’s dopamine system, which drives motivation, is directly affected by chronic inflammation. That offers an explanation for reduced motivation in metainflammation, and for why many patients with diabetes develop chronic pain accompanied by anhedonia.
Nearly 77% of the US population is now overweight. That change over fifty years correlates with the availability of highly processed food and with a marked rise in chronic pain. In mouse models, high-calorie foods that induce dopamine release disrupt normal feeding signals.
Where the vascular disease fits
Heart disease correlates closely with the global incidence of obesity and type 2 diabetes, and attention has shifted toward metainflammation as the primary pathophysiology. Early metabolic abnormalities appear to precede the vascular changes rather than follow them — atherosclerosis behaving more like atheroscleritis.
And it is not solved by removing meat
Patients frequently presume the Standard American Diet is entirely to blame and that a plant-based diet resolves it. Long-term vegan diets carry their own risks — metainflammation can persist, and sarcopenia becomes a genuine concern where protein intake and quality are inadequate. The variable that matters is the metabolic environment, not the category of food.
