Dr. Steenblock’s Treatment Program for ALS

Dr. Steenblock’s Innovative Treatment Approach for ALS

When it comes to chronic and degenerative diseases such as ALS, Dr. David Steenblock and his medical team’s passion is to innovate. This is in keeping with Dr. Steenblock’s decades long in-office exploration and experimentation (The very things that history shows are drivers of medical progress).

ALS is a case-in- point: Dr. Steenblock did a retrospective analytic study of 54 sporadic ALS patients he treated from 2011 to 2015. What he discovered was that 52 of these 54 had spinal injuries and reinjuries that caused damage to their blood-spinal cord barriers. This damage creates openings through which flow neurotoxic and proinflammatory compounds (some coming from bacterial and fungal microorganism in the GI tract and elsewhere), activated and damaged immune cells that secrete misfolded SOD1, as well as other cell and nerve cell toxic players (Some of which are selectively lethal to motor neurons).

This discovery naturally gave Dr. Steenblock specific targets for treatment. Depending on exactly what he finds in each patient, his therapeutic approach typically includes: intravenous EDTA chelation to remove toxic heavy metals and to help bust up biofilms in the gut and elsewhere; intravenous nutrients and supplements to reduce endotoxins in the gut and blood stream; hyperbaric oxygen therapy; and the revitalization of each patient’s bone marrow stem cells and then the harvesting of marrow which is minimally processed and administered (This kind of treatment is referred to as bone marrow aspirate concentrate or BMAC and is used to foster repair of spinal-blood barrier breaches and affected motor neurons).

Supporting references  

Blood-Spinal Cord and Brain Barriers in Health and Disease (Book) Edited by:Hari Shanker Sharma and Jan Westman  ISBN: 978-0-12-639011-7

Blood-spinal cord barrier disruption contributes to early motor-neuron degeneration in ALS-model mice Proc Natl Acad Sci U S A. 2014 Mar 18;111(11):E1035-42. doi: 10.1073/pnas.1401595111. Epub 2014 Mar 3.

Alterations of the blood-spinal cord barrier in sporadic amyotrophic lateral sclerosis. Sasaki S., Neuropathology. 2015 Aug 4. doi: 10.1111/neup.12221. PMID:26242689

The effect of mild traumatic brain injury on peripheral nervous system pathology in wild-type mice and the G93A mutant mouse model of motor neuron disease. Evans TM, Jaramillo CA, Sataranatarajan K, Watts L, Sabia M, Qi W, Van Remmen H.Neuroscience. 2015 Jul 9;298:410-23. doi: 10.1016/j.neuroscience.2015.04.041. Epub 2015 Apr 25. PMID: 25921732

Expression of the ALS-causing variant hSOD1(G93A) leads to an impaired integrity and altered regulation of claudin-5 expression in an in vitro blood-spinal cord barrier model. Meister S, Storck SE, Hameister E, Behl C, Weggen S, Clement AM, Pietrzik CU. J Cereb Blood Flow Metab. 2015 Jul;35(7):1112-21. doi: 10.1038/jcbfm.2015.57. Epub 2015 Apr 8. PMID: 25853911

Blood-spinal cord barrier breakdown and pericyte reductions in amyotrophic lateral sclerosis. Winkler EA, Sengillo JD, Sullivan JS, Henkel JS, Appel SH, Zlokovic BV. Acta Neuropathol. 2013 Jan;125(1):111-20. doi: 10.1007/s00401-012-1039-8. Epub 2012 Sep 1. PMID:22941226