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Diabetes Masterclass

Course Description

Conventional diabetes management is built around one goal: bring the blood sugar number down, by whatever mechanism gets there. Metformin-class drugs improve mitochondrial function somewhat; insulin secretagogues pressure the pancreas to release more insulin; SGLT2 inhibitors simply spill sugar out through the kidneys. All three can lower a number without addressing why the blood sugar was high in the first place — and two of the three actively burden organs that are often already struggling.

This masterclass, part of the AIC Functional Medicine Training Program, reframes diabetes through a mitochondrial lens: the engine (mitochondria) is what actually burns the fuel (glucose), and when the engine is compromised — by toxins, chronic infection, nutrient depletion, or circadian disruption — fuel backs up in the blood regardless of how much insulin is available. Dr. Ashwani Garg walks through a practical, fasting-insulin-based framework for distinguishing true type 2 diabetes (reversible, high insulin) from type 1.5 and type 1 presentations (declining pancreatic function, much harder to reverse), and for spotting when a case that looks metabolic is actually being driven by something else entirely (the session includes a real case of fungal overgrowth producing a falsely low HbA1c).

From there, the session builds a complete root-cause protocol: identifying and removing what’s damaging mitochondrial function (heavy metals, microplastics, chronic gut infections and LPS/endotoxemia, antibiotic overuse, blue light and circadian mismatch, chronic stress, dehydration and unstructured water), sequencing diet and lifestyle changes before supplementation, a foundational supplement layer (B-complex, magnesium, zinc, probiotics, berberine, alpha lipoic acid, NAC), and — for select cases — bioregulatory peptides (thymus, pancreatic, thyroid glandular peptides, and mitochondrial biogenesis peptides like MOTS-c and SS-31) as an advanced intervention layer. Extensive practitioner Q&A covers testing sequences, insulin titration during reversal, intermittent fasting, and managing diabetes that develops after chemotherapy.

The depth, terminology, and case-based teaching are calibrated for a practitioner audience, though informed patients who want a clinical-depth understanding of their own metabolic presentation are welcome to enroll.

What You’ll Learn?

  • Why diabetes is best understood as mitochondrial and metabolic dysfunction, not simply "high blood sugar" — using the engine/fuel-tank framework
  • How conventional diabetes drug classes actually work — metformin-type mitochondrial support, insulin secretagogues that pressure the pancreas, and SGLT2 inhibitors that spill glucose through the kidneys — and where each falls short of addressing root cause
  • A fasting-insulin-based framework for distinguishing true type 2 diabetes (high insulin, reversible) from type 1.5 and type 1 presentations (declining pancreatic function, much harder to reverse)
  • Why "pre-diabetes" as a category is questionable, and why HbA1c above 5.6 already indicates metabolic dysfunction
  • Root causes that damage mitochondrial function: heavy metals, microplastics, chronic gut infections, dysbiosis and LPS/endotoxemia, antibiotic overuse, herbicides/pesticides, and chronic emotional or physical stress
  • The role of circadian biology, blue light exposure, and sleep timing (10pm–2am repair window) in leptin resistance, insulin resistance, and metabolic dysfunction
  • Why processed sugar depletes the body's own nutrient reserves during metabolism, while whole foods like jaggery bring cofactors along with the fuel
  • A sequenced treatment protocol: diet and lifestyle changes first, foundational nutrient support second (B-complex, magnesium, zinc, probiotics, berberine, alpha lipoic acid, NAC), advanced detox and peptide therapy only where needed
  • How grounding, structured water, and reducing non-native EMF exposure fit into a metabolic recovery protocol
  • Where bioregulatory peptides — thymus, pancreatic, and thyroid glandular peptides, and mitochondrial biogenesis peptides like MOTS-c and SS-31 — fit as an advanced intervention for organ-specific repair
  • Practical case-based guidance: testing sequences for new diabetes diagnoses, insulin titration during reversal, evaluating intermittent fasting as an intervention, and managing diabetes that develops after chemotherapy

Blood sugar is the symptom; mitochondrial and metabolic dysfunction is usually the disease. Bringing a number down with a drug that punctures the kidney or exhausts the pancreas can look like progress while the actual engine — the mitochondria — stays damaged.

This masterclass gives practitioners a fasting-insulin-based framework for knowing what kind of diabetes they’re actually looking at, why it developed, and a sequenced, root-cause protocol for reversing what’s reversible and supporting what isn’t, as part of the AIC Functional Medicine Training Program. Informed patients auditing this course will walk away with a clearer, evidence-grounded picture too — but the training is built, first, for the practitioner in the room.