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Metabolic Reset Protocol

Summary

A four-phase clinical framework that repairs mitochondrial function, activates AMPK, and moves patients to oral maintenance without dependency.

Overview

A comprehensive, multi-phase clinical framework to stabilize mitochondrial bioenergetics, clear accumulated oxidative stress, and restore metabolic homeostasis. The protocol uses targeted peptides, coenzymes, and amino acids to repair cellular energy production, then moves the patient to sustainable, endogenous maintenance.

By targeting the inner mitochondrial membrane (IMM), optimizing the NAD+ salvage pathway, and modulating the folate–AICAR–AMPK axis, this step-by-step approach takes patients from acute exogenous intervention to long-term biological resilience without creating physiological dependency.

Phase 1 agents: mitochondrial repair and oxidative clearance

AgentRouteDoseFrequencyDuration
SS-31 (MTP-131)Subcutaneous (SubQ) injection40 mg per dose, dailyRepeat 2 times per year10 days
GlutathioneIntravenous (IV)600 mg to 1,200 mg per treatment, 1–2 days per weekRepeat as needed8 weeks
Bioavailable B-complexOral capsuleOngoingOngoingOngoing
TMG (trimethylglycine)Oral capsule250 mg, dailyOngoingOngoing

Phase structure

1

Phase 1: Mitochondrial repair and oxidative clearance

Goal: Stabilize the inner mitochondrial membrane (IMM), restore electron transport chain (ETC) efficiency, and rapidly clear systemic oxidative stress to stop ongoing cellular damage at its source.
  • SS-31 subcutaneously
  • Glutathione intravenously
  • Bioavailable B-complex orally
  • TMG orally

Why: Before metabolic pathways are activated, the foundational cellular machinery must be secured. SS-31 binds directly to cardiolipin, sealing leaks in the mitochondrial membrane and restoring ATP production efficiency. At the same time, high-dose IV glutathione acts as a systemic "mop," neutralizing the oxidative stress (ROS) that has accumulated in the cytosol. This phase stops the damage at its source while clearing the existing inflammatory burden.

2

Phase 2: Metabolic acceleration and AMPK activation

Goal: Move from cellular repair to metabolic optimization by inhibiting the NNMT enzyme, activating the AMPK pathway, and driving fatty acid oxidation to mimic the physiological effects of exercise.
  • Add 5-Amino-1MQ
  • Add MOTS-c on a strict cycle
Stop
  • SS-31
Continue
  • Glutathione IV
  • TMG
  • B-complex

Why: With the mitochondrial engines repaired, this phase pushes the cells to burn stored energy. MOTS-c acts as an "exercise mimetic," creating a state of metabolic stress through the AMPK pathway. 5-Amino-1MQ inhibits the NNMT enzyme, which prevents the drain of nicotinamide (NAM) and primes the body's salvage pathway to recycle NAD+ more efficiently. Strict cycling of MOTS-c is clinically essential to keep the immune system from forming neutralizing antibodies against the patient's own natural peptides.

3

Phase 3: Transition to maintenance

Goal: End acute exogenous interventions and hand off to oral precursors, sustaining bioenergetic gains while preventing biological dependency and downregulation of natural synthesis pathways.
  • Give a single NAD+ IV loading dose
  • Introduce GlyNAC
Stop
  • Glutathione IV
  • 5-Amino-1MQ
  • MOTS-c
Continue
  • TMG
  • B-complex

Why: Prolonged use of high-dose exogenous antioxidants and peptides can cause the body to downregulate its own production. Stopping IV glutathione and the injected peptides, and giving a single NAD+ IV "loading dose," moves the patient smoothly to oral maintenance. GlyNAC supplies the rate-limiting amino acids that push the cells to synthesize their own glutathione, which supports long-term redox homeostasis.

4

Phase 4: Ongoing maintenance

Goal: Provide long-term, sustainable support of DNA methylation, redox balance, and the NAD+ salvage pathway without overwhelming the patient's biological systems.
Continue
  • NMN/NR (500 mg), daily
  • GlyNAC (600 mg–1,200 mg), daily
  • TMG, daily
  • B-complex, daily

Why: As the body metabolizes daily NMN, it continually generates nicotinamide (NAM), which requires large amounts of methyl donors. A continuous supply of TMG and B-complex is needed to prevent systemic methyl depletion and the resulting buildup of homocysteine, which protects long-term cardiovascular and metabolic health.

Contraindications

  • Active malignancy (specifically for MOTS-c)
  • Evaluate patient-specific medical history, current medications, and other contraindications before starting
Clinical disclaimer. This protocol framework is provided for informational and educational purposes for licensed healthcare professionals. The statements and therapies described have not been evaluated by the Food and Drug Administration. These products and protocols are not intended to diagnose, treat, cure, or prevent any disease. Patient-specific medical history, current medications, and contraindications must be evaluated thoroughly before initiation.
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