My improvement seems to be continuing, even at altitude. I had an episode six days ago that was probably a sugar reaction, not common for me anymore. I was sick for a couple of hours followed by a kind of sleep I call “coma”. Other than that, I have been remarkably stable. The travel didn’t cost me much at all. I went out for dinner with my husband last night and realized it was the first night out I’ve had in years where I just had fun without struggling at all, after working most of the day. No faking being all right or overlooking symptoms in order to appreciate the moment.
Ali has been struggling with MCS (multiple chemical sensitivity), as a new symptom cluster. She’s had little bits of it before, but nothing like this. It was triggered by an exposure to a new cat litter about a month ago. Since then other chemicals have been triggering her, especially deodorants, perfumes, laundry products. The episodes aren’t medically scary, but involve a dramatic mood shift to blacker than black, ill-defined intolerable, sick feeling. No POTS symptoms particularly, or anything else really. The odd thing to me is that otherwise, she is doing well. Not much OI (orthostatic intolerance). Baseline mood pretty good. With avoidance of the things triggering her, she actually feels fairly well and would be thinking of getting out of the house, but for now, any outings are particularly threatening and would need to be outdoors. We are dealing with eliminating the things she needs us to from the environment.
MCS is a horribly isolating symptom. It makes a hug dangerous. It affects everyone in a household in a more direct way than other symptoms. It comes with tons of psychic overlay. Easy to disbelieve. Looks psychiatric to the uninitiated. Very, very difficult to be a canary in the coal mine.
We recently ran a bunch of labs that were not particularly illuminating, other than our Vitamin D levels are still very low despite replacement. We both still have macrocytosis from AZT, but less than before, expecting it to take 6 months overall to get back to a baseline, because that’s how long it takes to replace all of your red blood cells. Neither of us have serology suggestive of activated EBV, HHV6 or CMV. I have completely negative serology for EBV, strangely given all my years in the ER. We both had high IGF-1’s at baseline, normal now. Ali’s PCOS parameters have improved on treatment (lower LH/FSH ratio), as has my blood sugar on Actos (fasting glucose from 110 to 93, non-fasting from 140 to 110). IgG subunits were normal, my IgG and IgM borderline low. C4a’s and TGF beta-1’s were lost, again; we need to have them redrawn. We’ve been planning to send cytokine and NK cell profiles, but we don’t have baselines, so I doubt that it will tell us much we don’t know.
Our baseline labs consisted of extensive hormone testing and Richie Shoemaker’s panel, which includes all of the very few tests we’ve had that were abnormal in the past, outside of TBD (tick borne disease) testing, and a few fleeting auto-antibodies; I’ve had a mildly elevated nucleolar ANA and we’ve both had mildly elevated anti-cardiolipins. TGF beta-1 was the only test we found that was very high for both of us. When I first learned of the virus, I expected that there would be a viral load measure, but it seems all we have to monitor is downstream effects.
I’ve been receiving questions about my meds. Except for stopping AZT a couple of months ago, nothing has changed significantly since I last reported. I’ve fiddled with my hormones a little. Tried natural menopause for a little while, but it wasn’t pretty, convincing me that bioidentical HRT (hormone replacement therapy) is very important for me. Here’s my current regimen, once daily unless otherwise specified:
Isentress 400mg twice
Actos 15 mg twice
B12 5000 units chewable
Armour thyroid 30mg for years, now 15mg
Estradiol cream 5mg
Testosterone cream 2mg
Selegilene .5mg cream
Low dose aspirin
Sublingual Zofran 4mg prn nausea
Topical D3 10,000 units, now increasing and adding oral
Meriva SR, undenatured whey protein, L carnitine, glutamine, ALA, Vitamin C, CoQ-10, irregularly
Specific Carbohydrate Diet yogurt, super-fermented to reduce lactose, included here because I think it is a valuable treatment in the setting of inflammatory bowel problems: Making SCD Yogurt
We are both planning to step it up again with supplements, including some we haven’t tried before. It’s a big subject. I will post about this soon.
In consultation with our family doctor, Ali and I are about to start weekly intravenous pushes consisting of a modified Meyers’ cocktail and glutathione. Here is the formula we are planning to use:
Vitamin B complex – 100
Pyridoxine HCL 100mg
Leucovorin (folinic acid) 10mg
Vitamin C 500mg
Magnesium Chloride 800mg
We have also decided to rent a mild hyperbaric chamber (aka soft chamber, altitude sickness or Gamow bag) and supplement with an oxygen concentrator via mask. This safe technology delivers up to 90% FiO2 (fraction inspired oxygen) at 1.3 ATA (atmospheres of pressure), by non-rebreather mask, with a 10 L/min oxygen concentrator. I’ve been meaning to write a post about oxygen for some time. Because of the observation that CFS patients have redox problems (elevated free radicals), some practitioners think that the use of even low dose oxygen, which produces free radicals during administration, is toxic in this setting. I even heard from a patient that they had been afraid to take oxygen when they were in the ER for chest pain. This seems to be completely incorrect thinking to me. Regardless of the downstream difficulties, oxygen is essential and you have to feed the stream, especially in the face of tissue hypoxia and vascular instability, a hallmark of the disease, causing local ischemia. There are too many anecdotal reports of benefit from low flow oxygen, without added pressure, during downswings, to ignore. It is a very simple, safe thing to try. Supplemental oxygen has helped me through some bad moments. I saw too many benefits from HBOT (hyperbaric oxygen therapy) in practice with related chronic conditions, including autism and chronic Lyme Disease, to dismiss it now.
- Normobaric hyperoxia therapy for traumatic brain injury and stroke: a review. Kumaria
- Normobaric hyperoxia–induced improvement in cerebral metabolism and reduction in intracranial pressure in patients with severe head injury: a prospective historical cohort-matched study. Tolias
- A prospective, randomized clinical trial to compare the effect of hyperbaric to normobaric hyperoxia on cerebral metabolism, intracranial pressure, and oxygen toxicity in severe traumatic brain injury. Rockswold
- Oxygen therapy in acute ischemic stroke – experimental efficacy and molecular mechanisms. Poli
Administering oxygen is one of the most powerful supportive interventions that we have. Repeated doses of hyperoxia has a salutary effect on the injured brain, whether the injury is ischemic, demyelinating or traumatic. Used therapeutically, repeated exposure to oxygen under pressure is antiinflammatory and antimicrobial. HBOT produces revascularization of ischemic tissues and may encourage mitochondrial biogenesis. Oxygen is regulated like a drug, the argument being that if the dose is high enough, it can kill you, although so can too much water. High dose oxygen can cause CNS hyperexcitability (seizures) in susceptible people. HBOT is “approved” for 13 indications that are treated in hospitals. Approved means reimburseable. Hospital hyperbaricists can be pretty territorial, but using it beyond the approved conditions is legal off-label use of a drug, like using antiretrovirals approved for HIV to treat a different retrovirus, and like the majority of prescriptions written. HBOT probably has broad applicability and nobody wants to pay for it. The technology isn’t patentable, so it hasn’t been studied and optimal dosing for various applications is largely unknown.
The following papers provide important clues for ME/CFS. The last link will take you to slides of Dr. Rossignol’s lecture for the Autism One conference, this coming week.
- Mitochondrial dysfunction in autism spectrum disorders: a systematic review and meta-analysis. Rossignol/Frye
- The effects of hyperbaric oxygen therapy on oxidative stress, inflammation, and symptoms in children with autism: an open-label pilot study. Rossignol/Mumper
- Hyperbaric treatment for children with autism: a multicenter, randomized, double-blind, controlled trial. Rossignol/Mumper
- Hyperbaric oxygen therapy might improve certain pathophysiological findings in autism. Rossignol
- Oxygen-induced mitochondrial biogenesis in the rat hippocampus. Gutsaeva/Piantadosi
- Hyperbaric oxygen therapy may improve symptoms in autistic children.
- Dr. Rossignol’s slides
Dr. Rossignol’s work seems to me to be hitting on all cylinders. He is beginning to explain why clinically there is an independent pressure effect, since the pO2 (partial pressure of oxygen) for the treatment he is using (FiO2 24% 1.3 ATA) can be reproduced with normobaric oxygen delivered by mask. He is also working on the methylation block question, and his work is suggesting that rather than, or in addition to, a conversion defect, it is yet another (in a long list) of receptor insensitivities, eg insulin, LH, Vitamin D and leptin, overrepresented in ME/CFS patients. This is beginning to get to the heart of the methylation defect. It should be remembered, that methylation is important for retroviral latency.
There are two related neuroimmune diseases with which we already have significant HBOT experience:
Autism. I personally had wonderful experiences treating autism with low pressure HBOT. Autistic children have many of the same metabolic problems that ME/CFS patients do, including the mitochondrial defect. They have similar brain vulnerabilities as well. I treated children who demonstrated remarkable cognitive gains and improved sensory processing over a very short period of time.
MS. In the UK there is a network of charity chambers, salvaged military chambers that aren’t rated to go to the depth required to treat wounds or acute carbon monoxide poisoning. At the time I closed my chamber, they had done more than a million treatments over a couple of decades. Their experience is completely uncontrolled. But it’s not that much fun, and people don’t keep doing it for years and years if they aren’t pretty sure it’s helping. There were a couple of studies that indicated benefit, but a negative Cochrane report shut down serious study. Also there’s a medical society, called the UHMS, controlled by the insurers, that exists to be sure nobody gets HBOT for anything but a short list of reimburseable conditions. They also want to make sure that nobody gets treated in anything but a hard chamber, declaring on their website that HBOT requires 1.4 ATA when soft chambers are only rated to go to 1.3 ATA. Rather transparent I would say.
Here is a potpourri of literature that in my opinion collectively support the use of HBOT as part of a coherent treatment strategy for ME/CFS:
- Hyperbaric oxygen therapy in Thai autistic children.
- Hyperbaric oxygen therapy improves spatial learning and memory in a rat model of chronic traumatic brain injury. Harch
- Evaluation of hyperbaric oxygen treatment of neuropsychiatric disorders following traumatic brain injury. Shi
- Chronic hyperbaric oxygen treatment elicits an anti-oxidant response and attenuates atherosclerosis in apoE knockout mice. Kudchodkar
- Hyperbaric oxygen treatment attenuates the pro-inflammatory and immune responses in apolipoprotein E knockout mice. Kudchodkar
- HIV: reactive oxygen species, enveloped viruses and hyperbaric oxygen. Baugh
- Hyperbaric oxygen treatment induces antioxidant gene expression. Godman
- Involvement of the mitochondrial ATP-sensitive potassium channel in the neuroprotective effect of hyperbaric oxygenation after cerebral ischemia. Lou
- Oxygen therapy in stroke: past, present, and future. Singhal
- Effect of large dose hyperbaric oxygenation therapy on prognosis and oxidative stress of acute permanent cerebral ischemic stroke in rats. Xue
- Hyperbaric oxygen preconditioning induces neuroprotection against ischemia in transient not permanent middle cerebral artery occlusion rat model. Xiong
- Optimal dosing as a necessary condition for the efficacy of hyperbaric oxygen therapy in acute ischemic stroke: a critical review. Rogatsky
- Effect of hyperbaric oxygen on the expression of proteins Bcl-2 and Bax in the gerbil hippocampus CA1 following forebrain ischemia reperfusion. Zhou
- Neuroprotection by hyperbaric oxygenation after experimental focal cerebral ischemia monitored by MRI. Schäbitz
- Integrated brain restoration after ischemic stroke–medical management, risk factors, nutrients, and other interventions for managing inflammation and enhancing brain plasticity. Kidd
- Effects of hyperbaric oxygen exposure on experimental hepatic ischemia reperfusion injury: relationship between its timing and neutrophil sequestration. Kihara
- Hyperbaric oxygen therapy for reduction of secondary brain damage in head injury: an animal model of brain contusion. Palzur
- Low pressure hyperbaric oxygen therapy and SPECT brain imaging in the treatment of blast-induced chronic traumatic brain injury (post-concussion syndrome) and post traumatic stress disorder: a case report. Harch
- Hyperbaric oxygen in the treatment of patients with cerebral stroke, brain trauma, and neurologic disease. Al-Waili
- Effects of hyperbaric oxygenation therapy on cerebral metabolism and intracranial pressure in severely brain injured patients. Rockswold
- Effects of hyperbaric oxygen therapy on facial nerve regeneration. Vilela
- Hyperbaric oxygen limits infarct size in ischemic rabbit myocardium in vivo. Sterlin
We know that changing the environment, internally, externally, in this way or that, has made the difference for some people. We also know that there are many people who stay relatively well, at least well enough to function, doing nothing at all, except living their lives within the limits of their disease. I speak to many patients who have had essentially no medical care for years who describe what for ME/CFS is a pretty good course, stable with periods of very mild symptoms only. That makes it unwise to choose a therapy that might do significant harm. Or at least, save the heroics for the sickest patients. It is ironic that using extra oxygen is more questionable than prescribing dangerous drugs for symptom relief. There was a time when prescribing B12 shots was tantamount to quackery, but how many ME/CFS patients have been helped by B12 shots? Lots. When I was in practice, I was struck by how controversial it was to prescribe oxygen for an autistic child, but SSRI’s, tricyclics, benzodiazepines, speed, whatever pharmaceutical was acceptable. I was also struck by how much some patients improved just by stopping medications. When things are going south, always consider what you can stop. I can’t know of course if this next leg of the journey will help us or not, but I’m pretty sure that it won’t hurt, except in the pocketbook. I’ll keep you posted.