Low-dose suramin temporarily improves symptoms of autism in small-scale study

Many people believed it to be a psychological disorder.

There was an infamous clinical trial called "PACE" that purported to show that psychotherapy (CBT), along with exercise ("graded exercise therapy", or "GET") gradually increased beyond one's initial limits, was an effective treatment for chronic fatigue. The idea is that CFS patients do not have a metabolic illness; rather, they are suffering from self-reinforcing "unhelpful beliefs" that cause them to fear and avoid physical activity. Even the very act of attributing one's chronic fatigue to a physical illness is itself pathologised (and is to be attenuated via CBT) under this framework.

However, the PACE trial was a complete bodge; the protocol and criteria for classifying "recovery" were changed during the trial (to the point that a patient that got worse could nevertheless be classified as having "recovered), the outcome measures were subjective and self-reported (which are liable to be affected by CBT or other forms of social pressure), and conflicts of interest were not reported to participants.

Re-analyses of the data were thwarted by the fact that the researchers did not publish anonymised trial data, which violated the requirements of one of their funding sources and the requirements of one of the journals in which they published. There were plenty of methodological criticisms of the trial (http://www.virology.ws/2015/10/21/trial-by-error-i/) but the actual trial data was still not available. Academicians and patients alike unsuccessfully tried to get access to anonymised PACE data for years, and the PACE researchers did their absolute best to prevent that from happening -- including labelling legitimate requests for anonymised trial data (that they were obliged to publish) and criticism of their study as "vexatious" and "harassment" in a BMJ feature article (https://doi.org/10.1136/bmj.d3780). The Information Commissioner's Office ordered the PACE researchers to release the trial data, the researchers appealed that decision -- and got laughed out of court. The tribunal concluded that there indeed was a very strong academic interest in the data being released, that it was sufficiently anonymised to prevent re-identification, and went as far as to say that the PACE researchers were overly disparaging of patient groups and skeptical researchers -- and that legitimate requests for trial data and criticism of the PACE study did not constitute harassment.

Given how hard the PACE researchers tried to prevent release of the anonymised trial data, the results of the independent re-analysis (http://dx.doi.org/10.1080/21641846.2017.1259724) should not be too surprising. There was no basis for an in-flight change to criteria and protocols and CBT/exercise did not provide a statistically significant change in recovery. There are other serious issues with the PACE study's methods that are addressed in http://www.virology.ws/2017/03/13/an-open-letter-to-psycholo... or in the independent reanalysis linked (and there's a quite decent timeline and overview of the PACE trial here: http://me-pedia.org/wiki/PACE_trial).

Serious biological research (not nonsense by CBT-obsessed wankers who lie with statistics) into CFS continues and there's indeed many findings on potential biomarkers for CFS -- more keeps getting published, 10.1186/s40168-017-0261-y nor 10.1186/s12967-017-1161-4 weren't there last time I looked into this, for example. There's robust evidence of biomedical anomalies in CFS patients -- far more than enough for CFS to be considered a legitimate medical syndrome and not a psychiatric/psychological/"somatic" syndrome. That we haven't yet identified a biomarker useful for diagnosis nor know an aetiology certainly shouldn't disqualify CFS from being a medical syndrome!

Since there's plenty of evidence against the PACE trials' findings -- why do CFS patients object to it? After all, papers regularly do get proven wrong or have their findings revised, it's kinda how science operates. It's not the actual publication of the PACE results that have caused harm -- it's how the results were used. Since PACE was the first clinical trial of its scale on CFS patients, its findings ended up single-handedly defining clinical policy, treatment recommendations, and public policy relating to welfare and insurance. CBT and making patients do physical exercise is infinitely cheaper than any sort of medical treatment; and if the PACE trial happened to find that those will help people with CFS "recover" and get back to work, well, that's just a happy coincidence. That CBT is useless and excessive physical exercise harmful to CFS patients is immaterial; there's research that says it helps, so if you're a recalcitrant patient who complains, you're clearly not doing the CBT or the exercise enough! Similarly, the mere belief that CFS has a physical (and not psychological) cause is explicitly called out as one of the "harmful beliefs" that CBT is to neutralise -- disagreement with the treatment method (or familiarity with current medical research) is itself a sign that you're not taking CBT seriously.

It is not just through treatment guidelines (and denial of medical access beyond CBT and forced exercise) that the PACE results have materially harmed patients. Extremely unusually for a clinical trial, PACE was funded by the UK DWP -- and could not have returned better results to justify the DWP's agenda of cutting disability spending: http://www.centreforwelfarereform.org/uploads/attachment/492... . The DWP wanted findings to show that CBT and GET would get disabled people off benefits; and the PACE researchers (by changing the protocol/criteria halfway through) handed that to DWP on a silver platter. That CBT/GET are, in reality, useless (at best) is immaterial here -- DWP doesn't give a flying fuck whether people actually do get better or even manage to survive without disability benefit, they only needed these published findings to justify benefit cuts.

This might win the gold medal for loose associations in a non-schizophrenic context.

> It is also common to experience various sensations in the skin, from crawling or tingling sensations, tenderness of palms and the soles, and numbness of hands, arm, legs or feet.

That's an intriguing symptom, given that many inflammatory/autoimmune conditions cause peripheral neuropathy. I wonder if what is being described is the "unblocking" of peripheral nerves, causing a flood of signal-distorting noise as they re-join the nervous system.

In this case, for example: "We had four non-verbal children in the study, two 6-year-olds and two 14-year-olds. The six-year-old and the 14-year-old who received suramin said the first sentences of their lives about one week after the single suramin infusion. This did not happen in any of the children given the placebo." That seems promising and worth further study.

Rabies is an objective pathology, so it is far more easily/accurately classified than subjective social conditions like autism.

We could just Google this....but ATP adenosine triphosphate is the preferred energy source in the cellular energy cycle. A phosphate gets broken off when a cell uses it leaving ADP which is... Something something, I forget the rest. It's more expensive for the body to extract energy from ADP.

As one of the aformentioned caretakers I can attest that a certain narrowing of focus on one's own issues is part of the deal. I also have an autistic adult friend who is constantly dismayed by the focus on child autisim, so I can relate to what you are saying.

The focus on children is likley caused by the medical siloing of patients into pediactric and adult. Also researchers may want to focus on harm reduction, ie by preventing or amelirating autisitic symptoms in children it is likley to also prevent the downstream effects to their nervous systems. But certainly if researchers want to get a better understanding of treatment efficacy, adults should also be included in trials.

Our current diagnostic grouping of symptoms into an autisic spectrum is imperfect, I would be very supprised if autisim as we understand it today is caused by one thing. So if this research becomes a treatment it will likley only be benificial for a certain percentage.