SUPPORTING RESEARCH
We’ve selected a few research articles to share with you about hyperbaric oxygen therapy and how it supports age-related conditions and anti-aging strategies.
STUDY: EFFECT OF HYPERBARIC OXYGEN ON BDNF-RELEASE AND NEUROPROTECTION
BDNF – Brain-derived neurotrophic factor – is a protein the body releases to stimulate the production of new brain cells. A process is known as neurogenesis. You need this protein to support your learning, memory, higher thinking, and other similar brain functions. Of important interest, the protein is found to be significantly reduced in the brains of people with Alzheimer’s, Parkinson’s, and Huntington’s disease. Researchers are steadily gaining in their understanding of BDNF and how it affects brain plasticity and regeneration. It is already established that hyperbaric oxygen therapy can support brain regenerative effects. A new study, published in 2017, continues to support this concept. Researchers used a lower pressure of 1.5 ATA along with 2.0 ATA, and found that both pressures were able to cause significant increases in BDNF in just 3 to 5 days of consecutive HBOT sessions.
“Both, the genetically modified NIH3T3/BDNF and native NIH3T3 fibroblasts, showed a highly significant increased proliferation after five days of HBOT in comparison to normoxic controls. “
Read the full study: “Effect of hyperbaric oxygen on BDNF-release and neuroprotection: Investigations with human mesenchymal stem cells and genetically modified NIH3T3 fibroblasts as putative cell therapeutics”.
STUDY: SKIN DAMAGE FROM ULTRAVIOLET RADIATION PREVENTED WITH HBOT
A study published in 2012 in “Cell Stress and Chaperones, A Comprehensive Journal of Stress Biology and Medicine” focused on the effects of HBOT preconditioning and its protective properties against Ultraviolet-A (UV-A) induced skin damage. Three groups of hairless mice were exposed to UV-A, three days a week for 22 weeks, with two of the groups receiving HBOT pretreatment either two or four times a week. UV-A exposure amplified skin cell death, signifying elevated levels of skin damage. Pretreatment with HBOT substantially reduced UV-A induced cell death. In addition, HBOT pretreatment prevented skin creasing and maintained skin elasticity.
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