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Nathan Goodyear

Hyperbaric oxygen therapy promotes neurogenesis: where do we stand? - 0 views

www.ncbi.nlm.nih.gov/...PMC3231808

hbot hyperbaric therapy hyperbaric brain TBI stroke neurogenesis neuorplasticity

shared by Nathan Goodyear on 18 May 17 - No Cached
  • Numerous in vivo and in vitro studies confirm that HBOT induces neurogenesis
  • HIF-1α is the principal mediator of cellular hypoxia adaptations
  • activated by hypoxia, HIF-1α causes the transcription of its regulated downstream genes, including erythropoietin (EPO) and VEGF which are known to promote neurogenesis
  • ...10 more annotations...
  • The safety of HBOT was also evaluated and it was pointed out that, if given at proper paradigms, like 1.5 ATA for 60 minutes, HBOT will not cause oxygen toxicity
  • Rockswold et al., on the other hand, found that HBOT might be potentially beneficial for severe TBI patients
  • McDonagh et al., concluded that there was insufficient evidence to establish the effectiveness of HBOT in the treatment of TBI
  • The first multicenter, randomized, double-blind, controlled trial in 2009 found that 40-hour HBOT of 24% oxygen at 1.3 ATM produced significant improvement in children's overall functioning, receptive language, social interaction, eye contact, and sensory/cognitive awareness compared to those received slightly pressurized room air
  • Another study in 2010 on 16 autism patients, adopting a similar treatment paradigm, showed no effect on a wide array of behavioral evaluations
  • To date, there is little evidence that HBOT causes malignant growth or metastasis. A history of malignancy should therefore not be considered as a contraindication for HBOT
  • HBOT enhances the production of reactive oxygen species (ROS) and causes oxidative stress in body tissues
  • Excessive accumulation of oxidative stress may contribute to neurodegenerative processes and cell death in the brain, as seen in diseases like Alzheimer's disease (AD) and Parkinson's disease (PD)
  • Hormesis
  • process that results in a functional improvement of cellular stress resistance, survival, and longevity in response to sub-lethal levels of stress
  • Nathan Goodyear on 18 May 17
     
    great review of hbot, brain injury, neuroplasticity and neurogenesis.
Nathan Goodyear

Frontiers | Management of Glioblastoma Multiforme in a Patient Treated With Ketogenic M... - 0 views

www.frontiersin.org/...full

press-pulse therapy hyperbaric ketogenic metabolic therapy cancer ketogenic diet Glioblastoma glioblastoma multiforme HBOT nutrition

shared by Nathan Goodyear on 01 Apr 18 - No Cached
  • The SOC for GBM was modified in this patient to initiate KMT prior to surgical resection, to eliminate steroid medication, and to include HBOT as part of the therapy
  • the greatest therapeutic benefit for patients (near 1.0)
  • The observed reduction in blood glucose in our patient would reduce lactic acid fermentation in the tumor cells, while the elevation of ketone bodies would fuel normal cells thus protecting them from hypoglycemia and oxidative stress
  • ...30 more annotations...
  • Previous studies showed that GBM survival and tumor growth was correlated with blood glucose levels
  • Evidence indicates that glioma cells cannot effectively use ketone bodies for energy due to defects in the number, structure, and function of their mitochondria
  • The accuracy of the GKI as a predictor for therapeutic efficacy, however, is better when ketone bodies are measured from the blood than when measured from the urine
  • A reduction of glucose-driven lactic acid fermentation would not only increase tumor cell apoptosis, but would also reduce inflammation and edema in the tumor microenvironment thus reducing tumor cell angiogenesis and invasion
  • Besides serving as a metabolic fuel for GBM, glutamine is also an essential metabolite for normal immune cells
  • therapies that inhibit glutamine availability and utilization must be strategically employed to avoid inadvertent impairment of immune cell functions
  • we used the non-toxic green tea extract, EGCG, and chloroquine in an attempt to limit glutamine availability to the tumor cells
  • EGCG is thought to target the glutamate dehydrogenase activity that facilitates glutamine metabolism in GBM cells
  • Chloroquine, on the other hand, will inhibit lysosomal digestion thus restricting fermentable amino acids and carbohydrates from phagocytosed materials in the tumor microenvironment
  • HBOT to increase oxidative stress in the tumor cells
  • As glucose and glutamine fermentation protect tumor cells from oxidative stress, reduced availability of these metabolites under ketosis could enhance the therapeutic action of HBOT, as we recently described
  • Prior to subtotal tumor resection and standard of care (SOC), the patient conducted a 72-h water-only fast
  • Following the fast, the patient initiated a vitamin/mineral-supplemented ketogenic diet (KD) for 21 days that delivered 900 kcal/day
  • KD (increased to 1,500 kcal/day at day 22
  • the patient received metformin (1,000 mg/day), methylfolate (1,000 mg/day), chloroquine phosphate (150 mg/day), epigallocatechin gallate (400 mg/day), and hyperbaric oxygen therapy (HBOT) (60 min/session, 5 sessions/week at 2.5 ATA)
  • Biomarkers showed reduced blood glucose and elevated levels of urinary ketones with evidence of reduced metabolic activity (choline/N-acetylaspartate ratio) and normalized levels of insulin, triglycerides, and vitamin D
  • This is the first report of confirmed GBM treated with a modified SOC together with KMT and HBOT, and other targeted metabolic therapies
  • Glioblastoma multiforme (GBM) is the most common and malignant of the primary adult brain cancers
  • less than 20% of younger adults generally survive beyond 24 months
  • glucose and glutamine are the primary fuels that drive the rapid growth of most tumors including GBM
  • Glucose drives tumor growth through aerobic fermentation (Warburg effect), while glutamine drives tumor growth through glutaminolysis
  • The fermentation waste products of these molecules, i.e., lactic acid and succinic acid, respectively, acidify the tumor microenvironment thus contributing further to tumor progression
  • Glucose and glutamine metabolism is also responsible for the high antioxidant capacity of the tumor cells thus making them resistant to chemo- and radiotherapies
  • The reliance on glucose and glutamine for tumor cell malignancy comes largely from the documented defects in the number, structure, and function of mitochondria and mitochondrial-associated membranes
  • These abnormalities cause the neoplastic GBM cells to rely more heavily on substrate level phosphorylation than on oxidative phosphorylation for energy
  • dexamethasone not only increases blood glucose levels but also increases glutamine levels through its induction of glutamine synthetase activity
    • Nathan Goodyear
      Nathan Goodyear on 21 May 18
       
      use mannitol instead
  • Calorie restriction and restricted KD are anti-angiogenic, anti-inflammatory, anti-invasive, and also kill tumor cells through a proapoptotic mechanism
  • Evidence also shows that therapeutic ketosis can act synergistically with several drugs and procedures to enhance cancer management improving both progression free and overall survival
  • hyperbaric oxygen therapy (HBOT) increases oxidative stress on tumor cells especially when used alongside therapies that reduce blood glucose and raise blood ketones
  • The glutamine dehydrogenase inhibitor, epigallocatechin gallate (EGCG) is also proposed to target glutamine metabolism
  • Nathan Goodyear on 01 Apr 18
     
    Case study of Glioblastoma treated with ketogenic metabolic therapy as an adjuct to modified standard therapy.
Nathan Goodyear

Hyperbaric Oxygen Therapy Can Improve Post Concussion Syndrome Years after Mild Traumat... - 0 views

www.ncbi.nlm.nih.gov/...PMC3829860

hbot hyperbaric therapy hyperbaric brain concussion post concussion syndrome TBI traumatic brain injury

shared by Nathan Goodyear on 17 May 17 - No Cached
  • The changes in SPECT images after treatment indicate that HBOT led to reactivation of neuronal activity in stunned areas that seemed normal under CT and MRI imaging. While SPECT imaging has a limited spatial resolution (compared, for example, to fMRI), the changes in activity were sufficiently robust to be clearly detected by the SPECT images.
  • HBOT might initiate a cellular and vascular repair mechanism and improve cerebral vascular flow
  • HBOT induces regeneration of axonal white matter [61], [62], [63], [64], has positive effect upon the myelinization and maturation of injured neural fibers [65], and can stimulate axonal growth and increase the ability of neurons to function and communicate with each other
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  • HBOT was found to have a role in initiation and/or facilitation of angiogenesis and cell proliferation processes needed for axonal regeneration [67].
  • The observed reactivation of neuronal activity in the stunned areas found here, along with similar results in post-stroke patients
  • At the cellular level, HBOT can improve cellular metabolism, reduce apoptosis, alleviate oxidative stress and increase levels of neurotrophins and nitric oxide through enhancement of mitochondrial function (in both neurons and glial cells)
  • HBOT may promote the neurogenesis of endogenous neural stem cells
  • With regard to secondary injury mechanisms in mTBI, HBOT can initiate vascular repair mechanism and improve cerebral vascular flow [58], [59], [68], [69], promote blood brain barrier integrity and reduce inflammatory reactions [28] as well as brain edema
  • It might be possible that HBOT enables the metabolic change simply by supplying the missing energy/oxygen needed for those regeneration processes.
  • Nathan Goodyear on 17 May 17
     
    Hbot therapy, according to study, induces neuroplasticity and improves brain function in post concussion syndrome and those with mTBI.  The important point about this study was that the study was done years after the injury; what if the therapy was employed immediately after...
Nathan Goodyear

Long Course Hyperbaric Oxygen Stimulates Neurogenesis and Attenuates Inflammation after... - 0 views

www.hindawi.com/...512978

hbot hyperbaric hyperbaric therapy brain MPO stroke neurogenesis BDNF brain derived neurotrophic factor

shared by Nathan Goodyear on 18 May 17 - No Cached
  • Nathan Goodyear on 18 May 17
     
    animal study finds that HBOT reduced stroke infarct size, increased neurogenesis, increased BDNF, and reduced MPO.
Nathan Goodyear

Hyperbaric oxygen therapy for traumatic brain injury - 0 views

www.ncbi.nlm.nih.gov/...PMC3231802

TBI brain traumatic brain injury hbot hyperbaric hyperbaric therapy

shared by Nathan Goodyear on 17 May 17 - No Cached
  • Nathan Goodyear on 17 May 17
     
    great review article on the positive effects of hbot in TBI
Nathan Goodyear

Hyperbaric oxygen as an adjunctive therapy in treatment of malignancies, including brai... - 0 views

www.ncbi.nlm.nih.gov/...PMC4971045

HBOT hyperbaric oxygen therapy cancer radiation chemotherapy brain

shared by Nathan Goodyear on 09 Mar 18 - No Cached
  • Nathan Goodyear on 09 Mar 18
     
    great review of HBOT in cancer therapies
Nathan Goodyear

Hyperbaric oxygen suppressed tumor progression through the improvement of tumor hypoxia... - 0 views

www.nature.com/...s41598-021-91454-2

HBOT hyperbaric oxygen therapy cancer

shared by Nathan Goodyear on 01 Sep 23 - No Cached
  • Nathan Goodyear on 01 Sep 23
     
    2.5 ata for cancer
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