The existence of morphological and physiological abnormalities in the autism brain was recognized in the 1960s. Today, in view of many such extensive pathological findings, it has been stated and reiterated that autism spectrum disorder (ASD) has a biological rather than a psychological basis. Despite this, other than pharmacologic agents that address limited aspects of symptoms, development of therapies for ASD has been focused primarily on psychosocial measures based on principles of applied behavioral analysis. With this latter approach, however, a generally accepted intervention or group of interventions which consistently and comprehensively address the needs of most individuals with autism in a cost-effective and time-efficient manner has not yet been established.
While examining reports of another medical intervention, hyperbaric oxygen therapy with inspired oxygen partial pressures typically ranging from 0.31 to 1.5 atm. for neurological conditions such as autism, we wondered if increased oxygen partial pressure, alone, without the encumbrance, risk, and cost of hyperbaric exposure would produce useful clinical outcomes. In five pilot cases, therefore, a normobaric hyperoxic treatment we have called Microbaric® Oxygen Therapy (MBO2) was administered to preteen and teenage boys with ASD. All results were positive, some remarkably so, and addressed the full scope of the subject’s symptoms. Also, follow-up for over seven years in several cases suggests these outcomes are permanent.
To help encourage controlled research on MBO2 for ASD, we have laid out a hypothetical basis for its efficacy using our own pilot study outcomes and observations together with relevant information from the scientific literature, the most important of which we believe relates to regional brain hypoperfusion, neuroinflammation, and angiogenesis. In investigating research on angiogenesis and autism, we found a 2016 publication concerning autism postmortem brains which identified persistent splitting angiogenesis, as opposed to sprouting angiogenesis, in some regions of all donated autism brains and in none of the age-matched control brains. With this finding and the established effects of hyperoxia on angiogenesis and inflammation, we have developed a hypothesis that potentially accounts for regional cerebral hypoperfusion; delayed, progressive onset of ASD over the early years of life; increased perfusion in hypoperfused regions of the brain following hyperoxic therapy; the broad range of oxygen partial pressures that seem to have impact; permanent reduction in the symptoms of autism resulting from MBO2; and perhaps, a time-efficient and cost-effective method of treating autism that will help upgrade the long-term prognosis for affected individuals.
Published Date: 2020-04-27; Received Date: 2020-01-27