COR REGENERATE

Introduction: Aging is characterized by the progressive loss of physiological capacity. At the cellular level, two key hallmarks of the aging process include telomere length (TL) shortening and cellular senescence. Repeated intermittent hyperoxic exposures, using certain hyperbaric oxygen therapy (HBOT) protocols, can induce regenerative effects which normally occur during hypoxia. The aim of the current study was to evaluate whether HBOT affects TL and senescent cell concentrations in a normal, non-pathological, aging adult population.

Methods: Thirty-five healthy independently living adults, aged 64 and older, were enrolled to receive 60 daily HBOT exposures. Whole blood samples were collected at baseline, at the 30th and 60th session, and 1-2 weeks following the last HBOT session. Peripheral blood mononuclear cells (PBMCs) telomeres length and senescence were assessed.

Results: Telomeres length of T helper, T cytotoxic, natural killer and B cells increased significantly by over 20% following HBOT. The most significant change was noticed in B cells which increased at the 30th session, 60th session and post HBOT by 25.68%±40.42 (p=0.007), 29.39%±23.39 (p=0.0001) and 37.63%±52.73 (p=0.007), respectively.

There was a significant decrease in the number of senescent T helpers by -37.30%±33.04 post-HBOT (P<0.0001). T-cytotoxic senescent cell percentages decreased significantly by -10.96%±12.59 (p=0.0004) post-HBOT.

In conclusion, the study indicates that HBOT may induce significant senolytic effects including significantly increasing telomere length and clearance of senescent cells in the aging populations.

We are located in the heart of Spokane and offer so many wellness solutions. 

Over several decades, prestigious journals have published articles on the capacity of ozone to induce direct damage on tumor cells and, as well, to enhance the effects of radiotherapy (RT) and chemotherapy (CT). Hence, many clinicians advocate its use in cancer treatment. However, these studies have been conducted in vitro in the laboratory and in some animal models. As such, the effects of ozone on tumor cells have been demonstrated in very different conditions from those employed in clinical ozone therapy (O3T) sessions. In clinical practice, usually the ozone does not enter into direct contact with the tumor cells; i.e., the ozone does not exercise a direct effect; its multiple effects are mediated by secondary messengers (such as H2O2 and 4-hydroxynonenal) [1, 2]. Apart from this, indirect mechanism-of-action ozone stimulates adaptive mechanisms that can induce modulations in the organism by affecting the immune system, blood flow and oxygenation, and oxidative stress. These indirect effects can be potentially beneficial in anticancer therapy, as has been suggested by some studies. However, the real value of ozone as an adjuvant in oncology can only be established by conducting clinical trials specifically directed towards specific tumors, and in well-defined circumstances such as those addressing tumor status and characteristics of the patients.

We studied the effect of hyperbaric oxygen (HBO) treatment on the extent of diet-induced accumulation of lipid oxidation products in rabbit plasma and tissues, on plasma paraoxonase activity, and on the extent of progression and regression of atherosclerotic lesions in the rabbit aorta. HBO treatment of cholesterol-fed rabbits dramatically reduces the development of arterial lesions despite having little or no effect on plasma or individual lipoprotein cholesterol concentrations. Compared with no treatment in cholesterol-fed animals, HBO treatment also substantially reduces the accumulation of lipid oxidation products (conjugated dienes, trienes, and thiobarbituric acid-reactive substances) in plasma, in the low density lipoprotein and high density lipoprotein fractions of plasma, in the liver, and in the aortic tissues. In addition, HBO treatment prevents the decrease in plasma paraoxonase activity observed in rabbits fed cholesterol-rich diets. Similarly, in regression studies, HBO treatment has no effect on the rate of plasma (or lipoprotein) cholesterol decline but significantly accelerates aortic lesion regression compared with no treatment. Direct measures of aortic cholesterol content support these morphological observations. On the basis of these results, we conclude that repeated, but relatively short, exposure to HBO induces an antioxidant defense mechanism(s) that is responsible for retarding the development or accelerating the regression of atherosclerotic lesions.