Thanks. HBOT is an interesting technology that is non invasive and in particular non chemical based so it can be added to a health and longevity stack easily. According to Scott Sherr MD (a guest on WiseAthletes), HBOT has uses for chronic (e.g., inflammation) and acute (e.g., concussion) issues.
Home HBOT chambers are available but have some functional limits.
Hereās a bit from a related paper on the paradox of oxygen. Link to paper at bottom.
2. The oxygen paradox in aging
There is a paradoxical relationship between oxygen and aging. Despite the indispensable role that oxygen plays in tissue homeostasis and organismal survival, oxygen is considered a key driver of the aging process as well. Before we discuss the therapeutic mechanisms of HBOT in aging intervention, it is necessary to delve into the delicate balance of protection versus damage by oxygen in living organisms.
Oxygen serves as a source of reactive oxygen species (ROS). Though ROS can be beneficial in some circumstances, overproduction of ROS is able to induce cumulative macromolecular oxidative damage including lipid peroxidation, protein dysfunction and DNA damage [6,7], all of which contribute to aging. Hence, it is not surprising that hypoxic conditions can ameliorate multiple hallmarks of aging in cell culture, including senescence-associated secretory phenotype (SASP) production, mitochondrial dysfunction and replicative senescence [[8], [9], [10]]. However, while it is often inappropriately assumed that the rate of aging and oxygen levels are directly proportional, the biological consequences of aging with respect to oxygen levels are actually complex and remain poorly understood. As demonstrated in Drosophila, there is a non-linear response of oxidative damage and lifespan to atmospheric oxygen levels [11]. Both extreme high and low atmospheric oxygen levels lead to increased oxidative stress and reduced longevity. On the other hand, a reduction in oxidative stress has been attributed to both increases and decreases in oxygen levels [12,13]. In another word, the truth is not a duality when it comes to the trade-off between hypoxia and hyperoxia (Fig. 2), especially when issues such as free radicals, oxidative stress and scavengers are involved [14,15]. There is actually a biphasic response induced by HBOT: although the accumulation of ROS does exist, the subsequent cytoprotective antioxidant responses tend to be more pronounced after repeated exposures, which is discussed in detail in Section 3.3. In fact, it has been already reported that systemic levels of oxidative stress are largely unaltered in healthy young volunteers after multiple HBOT sessions, with signs of depletion of ROS generation capacity [16]. Likewise, a recent study of HBOT in middle-aged males reported attenuation of oxidative stress, as reflected by circulating biomarkers [17]. These encouraging findings help alleviate concerns that HBOT results in oxidative damage. More importantly, fluctuations in oxygen concentration levels are perceived by tissues as a hypoxia trigger, allowing HBOT over several cycles to stimulate cellular protection characterized by hypoxia-inducible factor-1 (HIF-1) activation without additional detrimental effects of hypoxia [18,19]. We will discuss this problem further in Section 3.1 and Section 3.3.
https://www.sciencedirect.com/science/article/pii/S2213231722001240
