True Health Medical Center in Naperville Illinois is also the same location for Richard Gelband of Gelband Natural Health and Chiropractic. It is also the location of Pure Compounding Pharmacy. Look them up. They’re all the same address.

Dr. Usman’s main scam is chelation of autistic children, but she also does HBOT, she orders vacuous tests and now sells a full range of unnecessary vitamins and useless supplements.

Dr. Stoller is simply exposing his lack of knowledge. Although gas laws and hyperbaric medicine may have not been taught where he went to medical school, in the US (as well as the UK and Europe), the gas laws are not only part of the required chemistry and physics pre-requisites, but are also taught – again – in the sections on pulmonary physiology and blood physiology. Hyperbaric medicine is discussed in these sections, as well.

While Dr. Stoller is somewhat correct that normobaric oxygen is not as effective in treating carbon monoxide poisoning, he neglects to mention (or perhaps was unaware) that these patients are given 100% oxygen at pressures of 2 – 3 atmospheres. He also neglects to mention (or, again, is unaware) that there are studies that fail to show any advantage to HBOT in carbon monoxide poisoning.

Dr. Stoller goes on to claim:

“In the case of autistic children and children with CP, the therapeutic window, or that pressure that will effect DNA signaling, appears to be very low – in many cases less than 1.3 ATA.”

HBOT therapy in CP (cerebral palsy) has been – at best – “controversial”. A large multicenter (real “centers”) trial of HBOT in 111 children with CP (Collet et al, 2001) showed no difference. The data supporting its use in autism is too flimsy to even reach the level of “controversial”.

I assume that by “DNA signalling”, Dr. Stoller means gene expression – a testable hypothesis which has, to date, not been tested by practitioners (like Dr. Stoller) who make a living treating patients with HBOT. If Dr. Stoller has some data to support his claims, I encourage him to make it public. Otherwise, it looks as though he is simply being self-serving in his assertions.

Dr. Stoller goes on to claim:

“Breathing in normobaric oxygen, regardless of the concentration is not comparable to using oxygen under pressure.”

Cellular respiration operates on the partial pressure of oxygen – the product of the total pressure and the fraction (concentration) of oxygen. In the “study” discussed above, the partial pressure of oxygen in the “treatment” group was 237 mm Hg (for those at or near sea level) and the “control” group was breathing 164 mm Hg partial pressure of oxygen (again, if they were at or near sea level).

The partial pressure of oxygen experienced by the “treatment” group could have been attained – easier and will far less expense – by having them breath 31% oxygen at sea level pressure. If Dr. Stoller doesn’t understand this, perhaps he should attend a refresher course on the gas laws.

Prometheus

Carbon monoxide poisoning occurs because heme holds CO a lot stronger than it does O2. You have to increase the O2 partial pressure to get the chemical potential of O2 high enough for it to displace the CO. In a review that Stoller wrote,

http://hbotnm.com/articles/CON.....search.pdf

he talks about the levels of HBO2 used for CO poisoning are 2.5 to 3 atmospheres of pure O2. That is 10 times higher than the 0.31 atmospheres of O2 used in this study. I think what he says is misleading to compare less than 100% O2 given at higher atmospheric pressure to 100% O2 given at 1 atm.

He gets the NO stuff wrong in his review, NO binds to hemes more strongly than does CO (in general). The association binding constants of O2, CO and NO to sperm whale myoglobin are 1.2, 27 and 220,000 respectively.

HBO2 will eventually cause injury and eventually will cause seizures. The use of O2 at one atmosphere for CO poisoning between episodes of HBO2 is associated with adverse outcomes in CO poisoning. So what? What does that have to do with autism?

What exactly is HBO2 doing in autism? Without a hypothetical physiological mechanism, there is no hypothesis of how HBO2 is going to do anything to improve autism symptoms. We know that autism is not a novel form of CO poisoning. What exactly is the “therapeutic window” that he says appears to be lower in autism?

The statements about Gas Laws not being taught/understood are ludicrous, as is this statment:

Breathing in normobaric oxygen, regardless of the concentration is not comparable to using oxygen under pressure.

At the FIO2 (24%), and added pressure (.23-.27 ATM) of the study, they are comparable, and I’d venture to guess that Stoller is unhappy about that being pointed out by several commenters so far.

I wonder what you think about this from the comment section at BMS:

Normobaric oxygen vs Hyperbaric Oxygen

Kenneth Stoller (06 April 2009) International Hyperbaric Medical Association email

Oxygen dosing (which is modulated by pressure far more than absolute concentration)is what provides the signaling at a cellular level, including the subcellular level in the mitochondria, to facilitate the changes observed using a hyperbaric environment.

No where was this made more clear than in a 163 patient prospective study of carbon monoxide poisoning patients who were given different doses of supplemental normobaric oxygen. Six week post-treatment cognitive sequelae were unchanged – contrast that to the results when hyperbaric oxygen is used. (Weaver et al in reply to Scheinkestal et al: The role of hyperbaric oxygen in carbon monoxide poisoning. Emerg Med Australa 2004;16;394-399).

The gas laws and hyperbaric medicine are not taught in medical school, so it is unfortunate that these questions have to come up, because there is a fundamental lack of understanding about what oxygen under pressure does. This problem is far greater than treating autistic children – this endemic lack of understanding about what hyperbaric oxygen does and when to use it has kept hyperbaric chambers out of Emergency Departments everywhere when there should be a chamber in every trauma center.

In the case of autistic children and children with CP, the therapeutic window, or that pressure that will effect DNA signaling, appears to be very low – in many cases less than 1.3 ATA. That has been my experience with dozens of children so affected. However that is not the appropriate pressure (oxygen dose) for treating other conditions.

Oxygen dose is poorly understood in hyperbaric medicine and even less understood outside of the field, again there is a lot of misapplication. Breathing in normobaric oxygen, regardless of the concentration is not comparable to using oxygen under pressure.

Competing interests

President of the International Hyperbaric Medical Association

Second the comment above:

Peer review is not a panacea – it is only as good (or as “tough”) as the reviewers and the editor make it.

Many classic examples of dismal “peer” review can be found, needless to say, in the journals devoted to “alternative” therapies.

As I’ve said before, peer review will never be infallible until we remove humans from the process.

Heh.

– pD

The pressure change in the Shiratsuch et al (2005) study was 20 mmHg, roughly equal to 0.03 atm, the increased pressure the control group was exposed to. This is equivalent to a 740 foot change in altitude. In a more recent study – Shiratsuch et al (2007) – they investigated the mechanisms behind the observed increase in phagocytosis in macrophages at slightly increased pressure (20 mmHg).

An review of the literature reveals that this degree of increased pressure (20 mmHg) – which is equivalent to the increased tissue pressure seen during inflammation – actually seems to stimulate an inflammatory response, but the data are too sparse to claim that the transient increase in pressure seen in the control group (20 mmHg) could be stimulating neuroinflammation.

Rather than explaining any improvements seen in the control group, these studies further reinforce my concernt that the increased blood flow seen after HBOT may be the result of increased neuroinflammation. At the very least, it is a weak “alibi” for not finding a greater difference between the two groups.

pD,

Biomed Central (BMC) Pediatrics chages $1515 per article for publication. It does this so that it can remain “open-access” and still pay the bills. Instead of the readers paying the freight, the authors do.

However, BMC journals do have peer review. This is in contrast to Medical Hypotheses – another journal that charges for publication – which does not use peer review.

Peer review is not a panacea – it is only as good (or as “tough”) as the reviewers and the editor make it. Clearly, the editor fell down on the job in this case because a serious flaw (failure to correct for multiple comparisons) was left uncorrected.

This is not a problem seen only in Biomed Central journals. Reviewers may not notice problems because they are reading too many articles or because they lack sufficient expertise in a certain area. Since the editor decides if the corrections made by the authors are good enough and will only send them to the reviewers if he/she has concerns, the expertise and work-load of the editor plays a role as well.

Finally – and this isn’t discussed enough, I think – a journal that is paid by the authors is under significant pressure to fill the “pages” in order to pay the bills. It tends to make the journal more “sensitive” to the authors, possibly at the expense of good peer review. “Old style” journals – which get their revenue from subscribers and advertisers – are under different pressures, but generally tend to err on the side of keeping the journal’s reputation intact in order to attract readers (and thereby advertising revenue).

In truth, I’ve read crap studies in “traditional” paper journals and I’ve read a lot of good studies in the open access online journals. As I’ve said before, peer review will never be infallible until we remove humans from the process.

Prometheus

Could you speak towards the differences in “toughness” in the peer review process? For example, when one reviewer apparently wanted better statistics, as opposed to just removal of a table, would other journals have resubmitted the paper back to the reviewers to determine if they felt the changes were sufficient to warrant publication? The devil is in the details, I suppose.

– pD

http://www.ncbi.nlm.nih.gov/pubmed/12974755

Previous investigations have shown that increased atmospheric pressure can affect such cellular functions as interferon- g secretion [16] and apoptosis [17,18]. To assess the effects of increased atmospheric pressure on cytokine production, monocytemacrophages were cultured in 8.75% O2, 2.1% CO2 at 2.4 ATA (increased atmospheric pressure). We used 8.75% O2 and 2.1% CO2 so that cells at 2.4 ATA would be exposed to the equivalent of 21% O2, 5% CO2 at sea level. When compared to cells cultured in normoxia at sea level, up to 12 h of increased atmospheric pressure did not affect IL-1 b or TNF- a synthesis (data not shown).

Actually, my question number two was referring to this citation.

Shiratsuch H, Basson MD:
Differential regulation of monocyte/
macrophage cytokine production by pressure.
Am J Surg 2005, 190(5):757-762.

http://www.ncbi.nlm.nih.gov/pubmed/16226954

The authors apparently cited this in support of the observed improvement effect in the “placebo” group.

If you don’t mind, I’d still like to post the question.

What is your take on this study with respect to any likely clinical significance in autism in either the treatment or control group?