I'm at the halfway point now! Today I start week 3 of my 6.
Week 2 of my hyperbaric oxygen treatment was certainly more eventful than week 1, even at this early stage! This is both good and bad.
I had experience of an oxygen toxicity seizure towards the end of HBOT last Monday and I was able to reverse this just in time before it became more serious. I knew this was a risk as I have reflex epilepsy but there are some interesting findings that I am documenting. Increase in ROS and RNS (among other complex mechanisms) obviously affects the epileptic brain and stimulates the central nervous system but we can manage this to get the benefits rather than increase risky complications using some clever management techniques I learned from research as I will explain.
We must also remember that antioxidants have anticonvulsant benefits but reduce the efficacy of HBOT so a patient with reflex epilepsy must try to find a balance that is therapeutic to get the benefits of HBOT and not dangerous. I don't take any antioxidants now including vitamin D which I usually take regularly and can be a useful anticonvulsant at therapeutic doses. If I have problems I will take magnesium chloride orally to act as a central nervous system depressant to ward off seizures when I experience an aura. I just slip off my mask and have a drink and rest for a few minutes, then continue using biofeedback techniques to stay calm.
Now, I could have been really negative here if I was misinformed by thinking that this treatment was just not for me and may be making things worse but I see the seizure activity as a great thing even though its terrifying and makes me anxious. Interestingly as the week went on, my tolerance to the oxygen increased and I needed less 'air breaks'. The 'air break' technique is commonly described in the literature as a method of managing seizure activity and improving tolerance for those who experience oxygen toxicity seizures. From Wednesday onwards I breezed through and felt great! I was even able to reduce my air breaks and on Friday I really noticed the positive differences.
The risk of seizures is higher as the pressure in the chamber increases and that is precisely what happened with my when we reached a depth of 33 feet on Monday. As the week went on my tolerance improved and I was able to take less air breaks under the same pressure. It reminded me of when I came off antiviconvulsant drugs (withdrawal effects-breakthrough seizures before adapting), its absolutely terrifying and could easily be life threatening but if you understand what is happening and how to manage the symptoms you can achieve things that others will say you can't.
My experience in this area helped me a great deal and I'm really looking forward to the challenge that will present itself as we maintain this depth over the next couple of weeks. The benefit of being in a multiplace chamber (more than 1 person in the chamber) as opposed to a monochamber (1 person) is that I have a mask I can take of at any time for 'air breaks'. I still get the benefits of increased oxygen uptake from normal air as it is a pressurised environment and my lungs and central nervous system is learning to adapt to this increased stimulation from the greater amounts of oxygen used at these pressures.
Some may think its insane to be thinking like that but I am really starting to learn about what is happening in this part of my brain. It is difficult to describe so for this update I will simply present the facts from the reading I have done to explain my thinking. If you look at the research and put 2 and 2 together you can understand that the increased seizure activity is a good sign because it means the treatment is doing what its supposed to- increase in oxidative stress- reactive oxygen species and reactive nitrogen species. I also purposely don't have antioxidants during treatment to improve efficacy even though this leaves me more vulnerable to having seizures. The fact this is improving is greatly encouraging and may in time also help to promote healing of stubborn scar tissue in that area of my brain.
Some research that caught my eye. I have highlighted mentioned topics in bold:
Seizures and HBOT for those who are at risk:
The risk here is higher for me compared to the general population obviously but I can try to see this as a positive because I am getting instant feedback of what is happening inside my head. Its good to see the positive side of this.
'Hyperbaric oxygen treatment (HBOT)
involves some risk of central nervous system (CNS) oxygen toxicity, which may be revealed by various signs and symptoms including
seizures in patients breathing O2 at pressures of 2 ATA or higher.'
Seizure incidence in 80,000 patient treatments with hyperbaric oxygen (PDF Download Available). Available from:
https://www.researchgate.net/publication/8168355_Seizure_incidence_in_80000_patient_treatments_with_hyperbaric_oxygen [accessed Feb 1, 2016].
'CNS oxygen toxicity, as manifest by GTC seizure activity, is a rare but recognized side effect of HBO2.' It goes on to say that the mechanisms probably vary but makes for interesting reading. Makes perfect sense to me and I believe epileptic patients can certainly adapt. Giving up should not be the first option! I'm seeing great benefits now from not giving up.'
http://onlinelibrary.wiley.com/doi/10.1111/j.1528-1167.2005.69804.x/pdf
This review has emphasized the positive aspects of HBO2-induced reactive species, but there is clearly a potential for negative effects. The risks for O2 toxicity depend on the concentration and intracellular localization of reactive species. Because exposure to hyperoxia in clinical HBO2 protocols is rather brief, studies show that antioxidant defenses are adequate so that biochemical stresses related to increases in reactive species are reversible (8, 10, 153, 154).
'Air breaks':
Treatments often include so-called air breaks, where a patient breathes just air for 5 minutes once or twice through the course of a treatment. This intervention has been demonstrated to enhance pulmonary O2 tolerance (1). CNS O2 toxicity is manifested as a grand mal seizure. This occurs at an incidence of approximately 1 to 4 in 10,000 patient treatments. (155–157) Pathological changes in association with isolated O2-mediated seizures have not been found in studies with guinea pigs, rabbits and humans. (158) http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3058327/#!po=31.6216
Mechanisms for cancer management:
'One unique feature of tumors is the presence of hypoxic regions, which occur predominantly at the tumor center. Hypoxia has a major impact on various aspects of tumor cell function and proliferation. Hypoxic tumor cells are relatively insensitive to conventional therapy owing to cellular adaptations effected by the hypoxic microenvironment. Recent efforts have aimed to alter the hypoxic state and to reverse these adaptations to improve treatment outcome.
One way to increase tumor oxygen tensions is by hyperbaric oxygen (HBO) therapy. HBO therapy can influence the tumor microenvironment at several levels. It can alter tumor hypoxia, a potent stimulus that drives angiogenesis. Hyperoxia as a result of HBO also produces reactive oxygen species, which can damage tumors by inducing excessive oxidative stress.' http://www.ncbi.nlm.nih.gov/pubmed/17102915
It is well accepted that
breathing greater than 1 ATA O2 will increase production of reactive oxygen species (ROS). (
2) This is critically important as it is the molecular basis for a number of therapeutic mechanisms.
ROS and also reactive nitrogen species (RNS) serve as signaling molecules in transduction cascades, or pathways, for a variety of growth factors, cytokines and hormones. (
3–
5) ROS is a collective term for O
2-derived free radicals as well as O
2-derived non-radical species such as hydrogen peroxide and hypochlorous acid. ROS are generated as part of normal metabolism by mitochondria, endoplasmic reticulum, peroxisomes, various oxidase enzymes and phospholipid metabolism. ROS act in conjunction with several redox systems involving glutathione, thioredoxin and pyridine nucleotides, and play central roles in coordinating cell signaling and also anti-oxidant, protective pathways. (
3,
4,
6) (
5) This point is central to the ensuing discussion –
oxidative stress is not synonymous with oxygen toxicity.
RNS include nitric oxide (·NO) and agents generated by reactions between ·NO, or its oxidation products, and ROS. Peroxide-dependent enzymes such as myeloperoxidase can catalyze reactions between nitrite, a major oxidation product of ·NO, and hydrogen peroxide or hypochlorous acid to generate oxidants such as nitryl chloride and nitrogen dioxide that are capable of nitration and S-nitrosylation reactions. (
11–
13)There are three nitric oxide synthase. The effect of hyperoxia on catalytic activity is reflected by values for the apparent Michaelis-Menten constant for O
2 and it differs among the three NOS isoforms. In part this is because enzyme activity is constrained by ferric-ferrous conversion at the active site. As a general statement, however, hyperoxia augments RNS production. (
14–
18)
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3058327/
And I just added this about melatonin because I found it interesting and because melatonin has anticonvulsant benefits. My seizure threshold is lower in the hours after waking, rises, and then levels off throughout the day. Circadian rythms and epilepsy have an interesting relationship. This post is poorly written and all over the place but I just wanted to write something about my experiences. :p
Proof perhaps that in the WRONG environment reactive oxygen species and reactive nitrogen species could do more harm than good even with HBOT. Improtant therefore to keep blood glucose relatively low and to add more stress with higher ketones?:
I'm still tracking my blood ketones, glucose, and everything else. Looking forward to my session this afternoon and looking forward to improving my tolerance to the oxygen! My next MRI scan in May should be very interesting. I'm having MRI spectroscopy and we will be looking at biomarkers to see what changes my ketogenic diet and HBOT is having on the microenvironment in brain tissue. Fun stuff in a way, I just have to stay determined because I have a lot of university work to do and other projects.
