The Rationale for use of HBOT as an intervention for age related functional decline
THE RATIONAL FOR USE OF HBOT AS AN INTERVENTION FOR AGE RELATED FUNCTIONAL DECLINE
Shai Efrati
The Sagol Center for Hyperbaric Medicine and Research, Assaf-Harofeh Medical Center, Israel. Sackler School of Medicine and Sagol School of Neuroscience, Tel-Aviv University, Israel.
Beginning at birth, developmental programs results in age-related changes in gene expression, growth and organs physiological function. With ageing, from a certain stage, organ functions start to deteriorate. There are 4 major denominators common to most age related physiological deterioration:
- Atherosclerosis-
- Mitochondria dysfunction- During aging, mitochondria number and function decline. Mitochondrial dysfunction accelerates atherosclerosis, which by itself increases mitochondrial damage. This vicious cycle seen in many of the age related diseases .
- Inflammation- Inflammation is a natural and highly regulated response that provides protection when infection occurs. However, if left unregulated, these same processes can cause tissue injury and damage. Inflammatory processes, particularly those resulting in chronic inflammation, have been implicated in most age related diseases.
- Stem cells- Age related depletion and reduce functionality of stem cells contributes to decrease regenerative capacity along the aging process shifting the net balance from regeneration to deterioration.
In recent years, there is growing evidence on the regenerative effects of hyperbaric oxygen therapy (HBOT). Even though many of the beneficial effects of HBOT can be explained by improvement of tissue oxygenation, it is now realized that intermittent increase of oxygen concentration can induce many of the mediators and cellular mechanism that are usually induced during hypoxia but without the hazardous hypoxia – termed Hyperoxic-hypoxic paradoxes. The intermittent hyperoxic exposure during HBOT can affect HIF-1 levels, MMP activity, VEGF, induce stem cells proliferation, augmented circulating levels of endothelial progenitor cells (EPCs) and angiogenesis factors. HBOT can decrease the inflammatory response in endothelial and thus promote vascular recovery. The fluctuations in the dissolved oxygen, generated by HBOT, directly sensed and affect the mitochondria and several animal and human studies have demonstrated the beneficial effects of HBOT on the mitochondrial level.
In this lecture we will review and discus the rational for the use of HBOT as an intervention that can target important aspects of age related functional decline.
