HBOT Conversations:
Dr. Paul Harch & Inflammation
Dr. Paul G. Harch, M.D. has used hyperbaric oxygen therapy to treat more than 100 different conditions, including stroke, dementia, autism, and traumatic brain injury. His goal is to help his patients get their lives back using hyperbaric oxygen therapy.
He is the author of The Oxygen Revolution and is considered an International expert and pioneer in the field of Hyperbaric Oxygen Therapy (HBOT). His informative, and comprehensive guide on HBOT has helped countless souls better understand what HBOT is and how it directly affects the body at the genetic level.
This episode on Inflammation is the first in a 9 episode series that will be released weekly with Dr. Harch.
Watch the Podcast
HBOT News podcast host, Edward di Girolamo, talks with special guest and HBOT expert, Dr. Paul G. Harch, MD. This is the first of nine episodes with Dr. Harch examining the God-given miracle of Hyperbaric Oxygen Therapy.
In this episode, we dive into how HBOT is a game-changer for inflammation. Harch explains that inflammation is the driving factor for countless chronic illnesses, but thankfully Hyperbaric Oxygen Therapy is a natural proven way to suppress inflammation.
Harch summarizes a fascinating study done in 2008, by Dr. Cassandra Godman. Her team took skin biopsies and extracted the normal tissue, then they examined the cells that lined the tiniest blood vessels in the tissue. Next, they put these cells in a petri dish and put them in a hyperbaric chamber and gave him a single hyperbaric treatment. Afterwards, they did a mass gene array analysis for 48 hours. What happened next was ground-breaking in better understanding the role that HBOT has on inflammation.
At the end of 24 hours 8,101 of our 19,000 protein coding genes in our 23 chromosomes were either significantly turned on or turned off & suppressed. That single HBOT treatment turned on the anti-inflammatory genes and the growth and repair hormone genes, and the largest cluster suppressed were the pro-inflammatory genes.
Our inflammatory reaction is inescapable when an injury occurs. But, when the patient receives hyperbaric oxygen therapy treatment after an injury (the sooner the better), it can have an overwhelming positive influence on the inflammatory reaction at any place along the spectrum. Harch continues to explain that the anti-inflammatory effects of hyperbaric oxygen are wide-ranging.
Harch spoke of the Navy’s experience with Hyperbaric Oxygen Therapy, as the Navy really kind of dominated this field for many years. The Navy reported that if you can get someone in a chamber within one hour of coming out of the water – when they’re symptomatic for decompression sickness – then the first hyperbaric treatment is curative in 90% of cases. Everyone thought that HBOT was treating bubbles in the brain at that point, but the reality is they were treating inflammation. We now know that it’s the inflammatory reaction in the brain after the bubbles passed that Hyperbaric Oxygen Therapy is treating; not the bubbles.
HBOT isn’t new, it dates back well over a hundred years. It’s still misunderstood, because many believe that HBOT therapy is a treatment for diseases. But, the reality is that HBOT is a treatment for disease processes, and it’s these processes that cause the diseases. We treat the inflammation that causes the disease processes, and in turn we treat the disease. That’s the power of Hyperbaric Oxygen Therapy.
Stay tuned for all nine episodes that will be release each Friday for the next eight weeks.
Guest

Dr. Paul G. Harch, MD
Dr. Paul G. Harch, M.D. is a clinician in emergency medicine and hyperbaric medicine who is the former director of the University Medical Center Hyperbaric Medicine Department and LSU Hyperbaric Medicine Fellowship. Currently, he is a Clinical Professor of Medicine in the Section of Emergency Medicine at LSU School of Medicine in New Orleans. He graduated from the Johns Hopkins University School of Medicine after graduating from the University of California at Irvine with magna cum laude/Phi Beta Kappa honors.
Dr. Harch initiated and continues to be a private practice that has resulted in the largest case experience in neurological hyperbaric medicine in the world. In this practice, he adapted the concepts of conventional hyperbaric oxygen therapy to wounds in the central nervous system, which spawned the subsequent academic and research practice. Harch HBOT is the best place to receive oxygen therapy treatments, and patients have traveled from more than 50 countries to be treated by Dr. Harch himself.
Harch HBOT – Hyperbaric Oxygen Therapy Clinic
5216 Lapalco Blvd.
Marrero, LA
504-309-4948
hbot@hbot.com
https://hbot.com/
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Recent HBOT News
Adjunctive hyperbaric oxygen therapy in radiation-induced non-healing wound.
Abstract: Korpinar, Cimsit, Cimsit, Bugra, Buyukbabani, , , , (2006). Adjunctive hyperbaric oxygen therapy in radiation-induced non-healing wound. The Journal of dermatology, 2006 Jul;33(7):496-7. https://www.ncbi.nlm.nih.gov/pubmed/16848825
Impact of perioperative hyperbaric oxygen therapy on the quality of life of maxillofacial patients who undergo surgery in irradiated fields.
Abstract: From 2001 to 2005, 66 patients referred for perioperative hyperbaric oxygen therapy (HBO2) for debridement of necrotic tissue or prevention of radionecrosis were assessed with quality of life measures, before and after completion of HBO2 and surgery. The...
Apoptosis of T-leukemia and B-myeloma cancer cells induced by hyperbaric oxygen increased phosphorylation of p38 MAPK.
Tumor cells with different origins have different threshold to apoptosis. Hematopoietic (Jurkat, NCI-H929) cells and non-hematopoietic (A549, MCF-7) cells were received hyperbaric oxygen (HBO(2)) treatment from 2.5 to 3.5 atmosphere absolute (ATA) of 100% oxygen for 6h, and a significant percentage of apoptosis were shown only in hematopoietic Jurkat and NCI-H929 cells by either Annexin V or TUNEL assay. Oxidative stress was illustrated higher in HBO(2)-treated hematopoietic cells by superoxide fluorochrome detectors. HBO(2) treatment leads to caspase-3, caspase-7 activation and further cleavage of PARP within cells. Furthermore, the increased phosphorylation of p38 MAPK was demonstrated in both Jurkat and NCI-H929 cells.
