CONDITIONS WE TREAT
Peripheral neuropathy involves progressive damage to the peripheral nervous system — producing pain, sensory loss, weakness, and autonomic dysfunction that can be profoundly disabling. SynergyO3 investigates the upstream biological drivers of nerve damage: oxidative stress, microvascular ischemia, mitochondrial dysfunction, and chronic inflammation.
CLINICAL PRESENTATION
Peripheral neuropathy affects multiple nerve types — sensory, motor, and autonomic — producing a diverse symptom spectrum. Causes range from diabetes and chemotherapy to heavy metals, Lyme disease, autoimmunity, and idiopathic factors. Individual results vary — Dr. Volpp evaluates each patient's complete clinical picture.
Dr. Volpp evaluates diabetic neuropathy, chemotherapy-induced peripheral neuropathy (CIPN), idiopathic small fiber neuropathy (SFN), Lyme-associated neuropathy, toxic neuropathy (heavy metals, medications), autoimmune neuropathy, and post-viral neuropathy patterns.
Testing may include nerve conduction studies (NCS), electromyography (EMG), skin punch biopsy for intraepidermal nerve fiber density (small fiber neuropathy), inflammatory markers, comprehensive metabolic panel, heavy metal screen, autoimmune neuropathy antibodies, and vascular markers assessing nerve blood supply.
COMMONLY OVERLAPPING CONDITIONS
CLINICAL EDUCATION
Peripheral nerve damage is driven by a convergence of vascular, metabolic, and inflammatory mechanisms. Endoneurial microvascular ischemia reduces nerve blood supply. Oxidative stress damages Schwann cells and axons. Mitochondrial dysfunction impairs axonal energy transport. Chronic inflammation activates nociceptors and sustains central sensitization.
Peripheral nerves depend on a rich blood supply through tiny endoneurial capillaries. Microvascular disease — from diabetes, inflammation, toxins, or oxidative injury — reduces this blood supply, creating nerve ischemia. Restoring microvascular function is a key mechanism for neuropathy symptom improvement.
Reactive oxygen species directly damage Schwann cells — the myelin-producing cells that insulate peripheral nerves. Oxidative damage impairs myelin synthesis and nerve conduction velocity, while also damaging axonal mitochondria and reducing the ATP needed for electrical signal transmission.
Peripheral axons must transport mitochondria over very long distances from cell bodies to nerve endings. Impaired mitochondrial function reduces this transport capacity, creating energy deficits at nerve terminals that manifest as sensory abnormalities, pain, and progressive axonal degeneration.
KEY STATISTICS
Comprehensive intake, targeted labs, and biomarker assessment to map biological drivers.
Physician-designed sequenced protocol combining EBOO, HOCATT, and IV nutrients.
Follow-up labs, functional benchmarks, and protocol refinement based on response.
ROOT CAUSE INVESTIGATION
Dr. Volpp evaluates each patient's complete picture — identifying which biological mechanisms are most active — before any protocol is designed. Individual results vary.
Elevated blood glucose glycates proteins throughout the body, including nerve myelin. Advanced glycation end-products (AGEs) activate inflammatory pathways, impair microvascular function, and directly damage the Schwann cells and axons of peripheral nerves.
Activated macrophages and inflammatory cytokines within peripheral nerve tissue drive ongoing nerve damage in autoimmune, Lyme, and inflammatory neuropathies. Neuroinflammation can self-perpetuate even after the initial trigger (infection, toxin) is removed.
Platinum-based and taxane chemotherapy agents generate massive oxidative stress that depletes glutathione reserves and directly damages peripheral nerve mitochondria. This mechanism underlies CIPN — and glutathione repletion is a key therapeutic target in prevention and treatment.
TREATMENT APPROACH
All protocols are physician-designed and supervised by Dr. Heather Volpp, MD. Therapies are selected based on each patient's evaluation. Results may vary.
EBOO ozone therapy may support neuropathy by improving endoneurial microvascular circulation, reducing the oxidative stress that damages Schwann cells and axons, and upregulating the antioxidant defenses depleted in chronic neuropathic conditions.
The HOCATT's far-infrared and carbonic acid therapy promotes peripheral vasodilation and improved microvascular circulation in extremities — directly targeting the endoneurial ischemia that drives neuropathic symptoms.
YOUR PATH FORWARD
Every patient begins with a comprehensive physician evaluation. No protocol begins before Dr. Volpp has reviewed your complete clinical picture.
A comprehensive intake with Dr. Volpp reviewing your symptom timeline, prior lab work, medications, and functional status. Targeted lab panels are ordered to identify active biological drivers.
Based on your evaluation findings, Dr. Volpp designs a sequenced treatment protocol — typically combining EBOO sessions, HOCATT therapy, and IV nutrient support at clinically appropriate intervals.
Functional benchmarks and symptom tracking guide protocol adjustments. Follow-up labs assess inflammatory markers and key biomarkers. Treatment frequency is adjusted as you progress toward your goals.
COMMON QUESTIONS
TAKE THE NEXT STEP
Begin with a comprehensive consultation with Dr. Heather Volpp, MD — Board-Certified Internal Medicine. Your evaluation will review your full clinical picture and identify which biological mechanisms may be driving your symptoms.
Book Your Appointment →Physician-Supervised · SynergyO3 Medical · Encinitas, CA · (760) 450-4602
Individual results vary. Consult with Dr. Volpp during your evaluation.
