Monty’s First Joke

Today at 6.30 in the morning something very unexpected happened;  Monty, aged 10 with ASD, made his first joke.  For a boy of few words this is quite a big step.

“I hit my head and now I can see birdies”

Elder brother Ted, when he finally arose, was impressed. It was very much his kind of humour, making a joke about your own weaknesses.

Regular readers will know that we are currently investigating the role of the vagus nerve in autism; all I can say is that nobody mentioned that the vagus nerve also mediates your sense of humour.  It may just be a happy coincidence, but this happened within 24 hours of our latest little experiment.  


 

Epsom salts, Autism and Hypokalemic Sensory Overload

Early on in this blog I wrote about a supposedly rare condition, where somebody suffers from sensory overload, usually from sound, but it could be light or even smell.  That condition has fancy sounding name, Hypokalemic Sensory Overload.  The cure is very simple, just to give oral potassium and within 20 minutes there is a full recovery.  Here is one research study.

 

I felt it odd that nobody had compared this to sensory overload in autism.  I did my own experiment at home and found to my surprise that sensory overload in autism could also be treated with oral potassium.

In the last few weeks I received two very thoughtful comments on this blog, from adult sufferers who have found the same remedy as I have.  So at least I am no longer in a minority of one.

The interesting thing about potassium in the human body is that it relies on another electrolyte, magnesium.  Without sufficient magnesium, the body cannot maintain an adequate level of potassium.  This is why supplements normally contain both potassium and magnesium.  A problem with both potassium and magnesium is that they very easily upset the stomach, indeed some laxatives are based on magnesium.

Epsom salts

I have noted that the long list of autism interventions used in the US, frequently includes having a bath in Epsom salts.  Epsom salts are named after a town near London, England, from which they were originally mined.  Epsom salts are just magnesium sulphate (MgSO4).

In the “biomedical” community it is proposed that magnesium does great things for autism and/or sulphur does.

The sulphur part at least has a scientific explanation.  It was long ago shown that there is an apparent abnormality in the sulphur metabolism in autism. 

In effect there is greater loss than normal of sulphur in the urine, resulting in lower plasma levels than in typical people.

So people are dipping their kids in Epsom salts on that basis that either the magnesium or the sulphur will do some good, not sure of which.

Interestingly, on the web, I found one mother writing about the Epsom salts baths she gives her child; she says she know when it is time for another one, where her child starts to cover her ears (sound sensory overload).

Trans-dermal Magnesium

Since magnesium supplements are in-effect laxatives, other ways have been sought to administer this electrolyte.  There are several transdermal creams and sprays that do indeed seem to work, but they can irritate the skin.  Interestingly, also on the web, some autistic adults talk about using such supplements and benefiting. 
 

Making the Connection

Well I hope this is all obvious to you, at least one of the things that is going on is an ion channel disease, the result of which is sensory overload in autism.  By chance, some people have stumbled upon magnesium supplementation as a therapy.  The extra magnesium is making whatever potassium there is in that person’s diet more effective, and hence reducing their symptoms.  Since the condition is actually Hypokalemic Sensory Overload, they would do even better to add some extra potassium as well.

The sulphur part may, or may not be, a red herring.  Sadly there are many of them in autism.

Conclusion

I have completed this part of my autism investigation.  If you want to treat autistic sensory overload, that seems to affect almost all people with ASD and most with ADHD, the options are:-

1.     Reduce the body’s daily loss of potassium and magnesium, with a potassium sparing diuretic, like Spironolactone

2.     Increase consumption of potassium and magnesium in diet.  Bananas, oranges and kiwis are rich in potassium, for example.

3.     Use small doses of oral potassium and magnesium supplements throughout the day

4.     Use expensive transdermal magnesium treatments.  Nobody seems to make a potassium version.

5.     Take a soak in the bath with an added cup of Epsom salts.

There should be a second reason to try option (1).  For entirely unrelated reasons, this drug is proposed to help in autism due to its secondary anti-inflammatory and hormonal effects.
Spironolactone might be a desirable immunologic and hormonal intervention in autism spectrum disorders

 I have to say that, having done my field research, I will be sticking with (2), (3) and the occasional (5)

 

Hormonal Remedy for Brain Injuries

Autism is a non-traumatic type of brain injury; the kind you typically see in the Emergency Room is TBI (Traumatic Brain Injury), after a car crash or, in the US, a shooting.

TBIs are very common and frequently fatal; when not fatal they often produce grave ongoing physical and psychological consequences, some of which may be life-long.  As a result there is a great deal of research into understanding TBIs and how to best treat them.

In this blog we have already mentioned that statins are being used to successfully treat TBI.  As I discovered, they have an impact in autism as well.

My renewed interest in TBI is two fold:-

1. Does TBI cause ongoing hormonal changes in the brain? (as does ASD)
2. Are there hormone therapies for TBI? (there are experimental ones for ASD)

The answer is yes and yes.

After a TBI there frequently are hormonal changes and they have even been given a name.

Post TBI Hormonal Deficiency Syndrome

The most frequently affected hormones are reported to be growth hormone (GH) and insulin-like growth factor (IGF-1).  This is interesting because these same hormones appear to be affected in autism.

There is a hormone therapy for TBI and it is currently undergoing a third stage clinical trial at 67 hospitals across the US. 

Progesterone for the Treatment of Traumatic Brain Injury (ProTECT III)

You can read all about the study with the above link.  If you are curious as to how Progesterone can reduce neuroinflammation and be neuroprotective, here is another paper:-
Progesterone as a neuroprotective factor in traumatic and ischemic brain injury

Regular readers of this blog will know that I like charts.  Here is a neat summary of how progesterone helps in TBI.

Progesterone is indeed a female hormone, but it is also present in small amounts in the male brain.  It is a fringe therapy for ADD and ADHD with the hormone given transdermally.

In TBI, progesterone is being given intravenously in the ER, as soon as possible after the accident.

In autism we are working many years after the brain injury occurred, but that should not stop us looking further.  The same applies to statins.


 

Endocrinology & Autism - the Final Frontier

When I started this blog 85 posts ago, I could not even spell endocrinology, let alone know how important it might be in my quest to figure out autism and how best to manage it.  Endocrinology is all about the biosynthesis, storage, chemistry, biochemical and physiological function of hormones and with the cells of the endocrine glands and tissues that secrete them.

What does that have to do with autism?

Well, 85 posts later, I think I can safely tell you that while oxidative stress and neuroinflammation in the damaged autistic brain are the two drivers of autism, most of the behavioural consequences are likely mediated by you child's endocrine system. 

Like me, you can try as hard as you like to minimize oxidative stress and neuroinflammation and this will take you a long way; but the ultimate goal would be to give the endocrine system a little help to switch from autistic homeostasis towards neurotypical homeostasis.  Is this really possible?  A year ago I would have said this was pure fantasy; now I am not so sure.

There are numerous well documented hormonal imbalances in autism, only some of which have been investigated and none very thoroughly. 

Medicine is full of "-ologies" and you would have thought autism had most to do with Neurology, but I have a feeling that Endocrinology will give me the final piece of the puzzle that I am looking for.

For this next stage in my investigation I will be taking advice from an Endocrinologist.








 

Piracetam for Autism, Comrades

Piracetam was first synthesized in 1964 by a Romanian scientist called Corneliu Giurgea, who was highly unusual.  He was educated in then communist Romania, followed by research in Russia and then at the University of Rochester in the US, before ending up in Belgium, eventually as the Head of Research at drug firm UCB and being a Professor at a Belgian university.  How this was possible under the strict form of communism followed in Romania,  I do not really understand.

Anyway, Giurgea was clearly very resourceful and he decided to invent a new class of drugs, to be called Nootropic.

He stated that Nootropic drugs should have the following characteristics:

1.     They should enhance learning and memory.

2.     They should enhance the resistance of learned behaviors/memories to conditions which tend to disrupt them (e.g. electroconvulsive shock, hypoxia).

3.     They should protect the brain against various physical or chemical injuries.

4.     They should increase the efficacy of the tonic cortical/subcortical control mechanisms.

5.     They should lack the usual pharmacology of other psychotropic drugs (e.g. sedation, motor stimulation) and possess very few side effects and extremely low toxicity.

Piracetam was soon followed by other drugs developed by competitors.

This class of drug seems never to have been licensed in the US, but was used widely in the Soviet Union, Eastern Europe and some western European countries.

As seems all too common in medicine, nobody knows for sure how Piracetam works.  There are many proposed mechanisms and I was attracted by one of them.

Autism in Ukraine

The internet does give the impression of giving you all the answers.  Often it gives you far too much information, much of it of dubious quality.  In reality, you are only seeing what is written in English, and although it is the international language of science and medicine, you will never see the majority of Russian, Japanese and Chinese knowledge/research.  Medical practice varies widely between Western medicine and the others.

In Japan for example, the MMR vaccination has been banned since 1993 and Prozac, the anti-depressant prescribed in huge quantities in the US, is a banned substance.  

So it was not a surprise to find only passing references to apparently widespread use of Piracetam for autism in the Ukraine, going back for decades.  I have no doubt if you could access the Russian research you would find studies on this.

Side Effects

There is no shortage of drugs prescribed in the US for autism, such as Ritalin, Prozac and Risperidone.  I have no doubt that they have some very good qualities; however they all have very real side effects, some of which are permanent.  Giurgea was very wise to only consider drugs with very few side effects and low toxicity.

In the 50 years since he synthesized Piracetam, one thing everyone seems to agree on, is that either it has no side effects, or it has very minor side effects.

Does Piracetam work?

In the 1970s there were numerous studies on Piracetam in a wide range of neurological conditions.  Today Piracetam is extensively used “off label” as a treatment for many of those conditions.  Does Piracetam work in autism?

I guess the doctors in the Ukraine must think it works.  Dr Akhondzadeh, a researcher into autism, ADHD, and other mental health conditions in Iran, found it to be effective.  Kelly Dorfman of the Development Delay Resources in Pittsburgh thinks it is effective for learning disabilities and dyspraxia, but less so for autism.

Olga Bogdashina, President of the Autism Society of Ukraine, notes that piracetam is widely used as an autism treatment in the Ukraine. Having conducted her own small-scale study, she found that piracetam improved the attention spans and mental capabilities in the majority of participating children. She also says that her autistic son became more sociable and flexible and less aggressive on the supplement. She does warn that during the initial phase of treatment, hyperactivity and tantrums may increase. However, researcher Stephen Fowkes notes that these side effects are only common with high doses, and asserts that they are rare with standard doses (both cited in “Letters to the Editor, Autism Research Review International, 1996).

I thought Bogdashina’s name was familiar.  I read her book on sensory issues in autism.  It is a good read, but it does not really tell you what to do.

Piracetam’s claimed possible methods of action

·        It is NOT a sedative or a stimulant

·        Piracetam is a positive allosteric modulator of the AMPA receptor.

^·         It is hypothesized to act on ion channels or ion carriers; thus leading to increased neuron excitability

^·         GABA brain metabolism and GABA receptors are not affected by piracetam.

^·         Piracetam improves the function of the neurotransmitter acetylcholine via muscarinic cholinergic (ACh) receptors, which are implicated in memory processes

·        Furthermore, piracetam may have an effect on NMDA glutamate receptors, which are involved with learning and memory processes.

·        Piracetam is thought to increase cell membrane permeability

·        Piracetam may exert its global effect on brain neurotransmission via modulation of ion channels (i.e., Na⁺, K⁺).

·        It has been found to increase oxygen consumption in the brain, apparently in connection to ATP metabolism, and increases the activity of adenylate kinase in rat brains.

·        Piracetam, while in the brain, appears to increase the synthesis of cytochrome b5, which is a part of the electron transport mechanism in mitochondria.

·        But in the brain, it also increases the permeability of the mitochondria of some intermediaries of the Krebs cycle.

In 2005 there was an interesting review carried out in Poland; it is very readable.

Piracetam - An old drug with novel properties? 

"Piracetam is generally reported to have minimal or no side effects. It is interesting to note, however,  that piracetam is occasionally reported side effects of anxiety, insomnia, agitation, irritability  and tremor are identical to the symptoms of excessive acetylcholine/glutamate neuroactivity. In spite of these effects, piracetam is generally not considered to be a significant agonist or inhibitor of the synaptic action of most   neurotransmitters. The piracetam-type nootropic drugs might exert their

effect on some species of molecules present in the plasma membrane. It would seem that they act as potentiators of an already present activity, rather than possessing any neurotransmitter-like activity of  their own."

It would seem to me that we have come back to the vagus nerve and the Cholinergic system

http://epiphanyasd.blogspot.com/2013/10/biomarkers-in-autism-cholinergic-system.html

I learnt in that post that there are two main classes of acetylcholine receptor (AChR), nicotinic acetylcholine receptors (nAChR) and muscarinic acetylcholine receptors (mAChR).  Mostly it seems to be the nicotinic type that is targeted by medical science, but piracetam has an effect on the other type of receptor.  This would explain excessive use of piracetam causing symptoms of too much acetylcholine.

If this is indeed the case, that would add yet another method of “correcting” the known biomarker of autism that is “diminished acetylcholine and nicotinic receptor activity”.  Of all the methods I have so far investigated, this might actually be the safest;  it is certainly inexpensive.

Effect on Comorbidities

My method of separating fact from fiction in autism now includes looking at the effect of therapies on the principal comorbidities of autism.  Most genuinely effective drugs seem to work across many comorbidities.  Epilepsy is the most prevalent comorbidity.
 

Piracetam relieves symptoms in progressive myoclonus epilepsy: a multicentre, randomised, double blind, crossover study comparing the efficacy and safety of three dosages of oral piracetam with placebo

"CONCLUSIONS—This study provides further evidence that piracetam is an effective and safe medication in patients with Unverricht-Lundborg disease. In addition, it shows that a dose of 24 g is highly beneficial, more effective than lower doses and that a dose-effect relation exists. There is considerable variation in optimal individual dosage. "

Note:  Unverricht–Lundborg disease is the most common form of an uncommon group of epilepsy called the progressive myoclonus epilepsies.

Conclusion

Piracetam seems to be a safe supplement/drug that improves mood and reduces aggression (and SIBs).  I thought it was worthwhile testing and indeed I was not disappointed.  The dosage suggested is 50-100 mg/kg, but the optimal dose seems to vary by child.  If you follow my vagus nerve/neuroinflammation/ cholinergic way of thinking, then Piracetam would be acting (via acetylcholine) to reduce pro-inflammatory cytokines and hence reduce inflammation in the autistic brain.  This would mean that Piracetam would be a useful tool to control autism flare-ups, be they triggered by pollen allergy, intestinal inflammation, or even stress.  I shall use it as such.

As for why Piracetam seems more effective in the Ukraine than in Pittsburgh - that I can answer.  Much of what passes as autism in Pittsburgh, would be completely ignored in Kiev.  It would not be diagnosed as autism; only if it is disabling would it be called autism.  If you have "autism-lite", the symptoms are mild and you probably do not need Piracetam and it would likely have little effect.   The same would apply for the majority of ADHD/ADD cases, outside of the US they would not be diagnosed as such.

If you are on Ritalin for your severe ADHD, you might want to try Piracetam.  If you Google ADHD and Piracetam, you will find adults using Piracetam to avoid the side effects of Ritalin.

If your child suffers from SIBs (self-injurious behaviours) then Piracetam, along with nicotine patches, would be well worth investigating.

 

 

 

 

 

Medicine - More Art than Science

Today's post is only indirectly about autism, it is more to do with what expectations are realistic from medical science in 2013.

I come from a family full of doctors and two engineers.  As one of the engineers, I know that engineering is a true science, and I had assumed that so was medicine.  In engineering the answers are either right or wrong, maybe or sometimes is not acceptable.  If you build 100 aeroplanes, full of maybe millions of components, you expect them work (ie not crash) everyday for 30 years.  An acceptable failure is much less than 1%, over the entire life of the planes.  So the science needs to be fully understood to the tiniest detail.

The more I am reading about medical science, the more clear it becomes how little is really understood and how trial and error is behind many breakthroughs.  Many drugs, particularly in neuroscience, work for reasons not fully understood; or there are several proposed methods of action, perhaps one of which is correct.  This really is not science.

Once you start thinking about medicine as an art rather than a science, things become clearer.  It also means that the old fashioned approach of 20-50 years ago might actually be more appropriate, than that of today.    

This also means that medicine is more about probability.  So, some new hi-tech anti-cancer drug may work in 60% of patients, but if you are one of the 40%, why suffer those horrible side effects? or indeed pay for it.  Or, for your allergy medicine, the doctor may prescribe you say, Claritin, but he probably does not tell you that in X% of patients it will not work.  Perhaps he should say, here are four antihistamines try them all and choose the two that work best, then just alternate between them.

I have been reading about thyroid hormones.  I am amazed by all the nonsense written about them, including in mass market books by experts.  The question is actually very simple, there is a prohormone called T4 with a long half-life and an active hormone called T3 with a much shorter half-life.  To optimally treat hypothyroidism you just need balance the dosage and frequency of T3 and T4 and you need to know that T3 is needed throughout the body and for it to be produced locally from T4, requires special enzymes (D1, D2, D3) to be present in sufficient quantities.  As a result, some people may need to be given T3 in addition to (or instead of) T4.   How complicated is that?

So how does this apply to autism?  Well, it means that perhaps we should not be critical of the "trial and error" approach of some US autism doctors.  "Trial and error" does need to have boundaries and safety is clearly the most important issue.  It also means that it is totally "normal" to find therapies that work in one group and yet are ineffective in another.  It means that applying complex statistical analysis, from sciences like engineering, to evaluate tiny clinical trials in autism is really a waste of time.  Not surprisingly, none of these trials stand up to scrutiny later.  Those scrutinising these mini studies are making the same mistake I did, thinking medicine is a "hard" science.  Maybe it will be in 500 years, but not in 2013.

Much can be learnt from Monty, age 10 with ASD, whose piano teacher tells me  "if a pill works, keep taking it". Hundreds of millions of people have benefited from taking statins, but as I learnt, 99% for the wrong reason.












 

Cytokine Theory of Disease & the Vagus Nerve

If you are a regular reader of this blog you will know that the key to controlling autism is reducing oxidative stress and neuroinflammation.  One of the key drivers of the on-going neuroinflammation are signalling molecules called cytokines; if you can limit the release of harmful cytokines you can reduce neuroinflammation.  This appears to be easier said than done.  I learnt that some statins limit the release of pro-inflammatory cytokines and neuroscientists in the US are researching their use, but not yet in autism.  I did some home research and found a positive effect within 24 hours.

It turns out there is an entire field of neuroscience relating to cytokines as a mediator of disease and this is all channelled through the Vagus nerve.  There is an eminent  neuroscientist, Kevin Tracey, who dominates this field; he is credited with discovering that vagus nerve stimulation inhibits inflammation by suppressing pro-inflammatory cytokine production.   Tracey is also an inventor, he is seeking to apply the science and has an interesting start-up company.  So I have found a kindred spirit and if you read his papers, you will find that often missing element, a sense of humour.

Tracy has even written a book, which explains his discoveries.

Fatal Sequence: The Killer Within

For those scientists among you, a very readable paper is:- 

Physiology and immunology of the cholinergic  Anti-inflammatory pathway

For those in a hurry, here is summary

The cytokine theory of disease is a concept that cytokines produced by the immune system can cause the signs, symptoms, and damaging aftereffects of disease.

One example is the case of TNF, a cytokine implicated as a necessary and sufficient mediator of lethal septic shock. Administration of TNF to healthy humans reproduces the metabolic, immunological, and pathological manifestations of the disease and the gene knockout or pharmacological blockade of TNF activity prevents the development of lethal septic shock. Other pathophysiological activities ascribed to TNF are the capacity to cause fever and localized inflammation. Clinical successes in the 1990s using drugs that specifically inhibit TNF for patients with inflammatory bowel disease or rheumatoid arthritis directly implicated a pathogenic role of this cytokine in other diseases and validated in humans the fundamental premise of the cytokine theory of disease.

 

 

The cholinergic anti-inflammatory pathway

Tracey reasoned that, since the CNS coordinates major physiological responses via innervated circuits, it might also use neural input to control a potentially deadly cytokine response. In classical physiological systems, the sensory projections of the autonomic nervous system provide input to brain networks about essential bodily functions. These elicit a coordinated neural output from the CNS to maintain homeostasis for parameters as varied as heart rate, blood pressure, digestion, body temperature, organ perfusion, and blood glucose levels. Accordingly, it seemed possible to posit the existence of a comparable mechanism to control cytokine release that could, at least in theory, function as an extremely fast, reflex-like anti-inflammatory pathway controlled by brain networks.  Stimulation of vagus nerve signals was shown to significantly inhibit TNF release in animals receiving lethal amounts of endotoxin. Subsequent work established that vagus nerve signaling inhibits cytokine activities and improves disease endpoints in experimental models of sepsis, schemia/reperfusion, hemorrhagic shock, myocardial ischemia, ileus, experimental arthritis, and pancreatitis. The cellular molecular mechanism for inhibition of cytokine synthesis is attributable to acetylcholine (ACh), the major vagus nerve neurotransmitter. Macrophages and other cytokine-producing cells express acetylcholine receptors (AChRs), which transduce an intracellular signal that inhibits cytokine synthesis. The best characterized of these cholinergic receptors that suppress cytokines is the α7 subunit of the nicotinic AChR (α7 nAChR).

 

 

It takes nerve to restrain cytokines: anatomy of an innervated cytokine system

Recent studies of the physiology, functional anatomy, and cellular molecular mechanisms of the cholinergic anti-inflammatory pathway indicate that the principal components for cytokine suppression by the vagus nerve converge in the spleen. Endotoxin localizes to macrophages primarily in the spleen and liver, thereby activating an immediate early cytokine response. The spleen is the major source of both hepatic and systemic TNF during endotoxemia; it releases newly synthesized TNF into the splenic vein, which drains into the liver, and from there, TNF crosses into the systemic circulation.

 Vagus nerve stimulation, or administration of α7 nAChR agonists, inhibits not only TNF but also IL-1, IL-6, IL-8, and high mobility group box 1 (HMGB1)

 

Preclinical efficacy of experimental therapeutics

Preclinical studies are in progress to determine whether it may be possible to develop therapeutics based upon either devices that stimulate vagus nerve activity or drugs that activate the cholinergic anti-inflammatory pathway to suppress cytokine damage. A significant number of studies indicate that the cholinergic anti-inflammatory pathway is a robust regulator of cytokine-mediated damage in local and systemic experimental disease.

The role of exercise

Exercise reduces levels of TNF and other cytokines, confers protection against cardiovascular disease and type 2 diabetes, increases vagus nerve activity, and confers protection against the development of atherosclerosis. It is possible that the mechanism of these exercise effects is at least in part attributable to exercise-induced increases in cholinergic anti-inflammatory pathway activity. Obesity, on the other hand, is characterized by diminished vagus nerve output and elevated cytokine levels, which have been implicated in mediating insulin resistance and atherosclerosis. Since weight loss and exercise are each associated with increasing vagus nerve activity, one can consider whether enhanced activity in the cholinergic anti-inflammatory pathway might decrease cytokine production and reduce the damage and metabolic derangements mediated by chronic, low-grade systemic inflammation that is characteristic of the metabolic syndrome

His conclusion:-

“It is bemusing to think that one of the fundamental premises of the ancient Greeks was that dietary manipulation controlled humoral balances. This concept is now, at least in principle, supported by new evidence of a direct link between dietary composition and the regulation of cytokines by the cholinergic anti-inflammatory pathway. Modern clinical studies have advocated supplementing diet with fish oil, soy oil, olive oil, and other fats to significantly increase vagus nerve activity, reduce inflammatory markers, and improve disease severity in inflammatory bowel disease, rheumatoid arthritis, and cardiovascular disease. These clinical anti-inflammatory responses may be linked to the fat-induced stimulation of the cholinergic anti-inflammatory pathway, as is the case in rats. And now it appears that a major source of systemic TNF during lethal challenges is the spleen, the source of Galen’s black bile. One can’t help but wonder: How did the ancient Greeks know?”

 

Anti-inflammatory activities of vagus nerve stimulation

The discovery by Tracey that vagus nerve stimulation inhibits inflammation by suppressing pro-inflammatory cytokine production has led to significant interest in the potential to use this approach for treating inflammatory diseases ranging from arthritis to colitis, ischemia, myocardial infarction, and congestive heart failure. Action potentials transmitted in the vagus nerve activate the efferent arm of the Inflammatory Reflex, the neural circuit that converges on the spleen to inhibit the production of TNF and other pro-inflammatory cytokines by macrophages there. This efferent arc is also known as the Cholinergic anti-inflammatory pathway Because this strategy targets the release of TNF and other pro-inflammatory cytokines, it may be possible to use vagus nerve stimulation instead of anti-inflammatory antibodies (e.g., Remicade or Enbrel) to treat inflammation. SetPoint Medical, Inc. is an early-stage medical device company, set up by Tracey, developing an implantable  neurostimulation platform for the treatment of inflammatory diseases.

Remicade and Enbrel are ultra-expensive drugs, costing about $20,000 per year.  Not surprisingly, some US autism doctors are wondering what they would do in autism.

My Conclusion

I was wondering if Kevin Tracey might be related to Jeff Tracy, in which case, can Brains please make Monty, aged 10 with ASD,  a vagus nerve stimulation device, preferably with a built-in nuclear power pack.  (I refer to a cult British TV series from the 1960s called Thunderbirds, a favourite of both Monty and his big brother, Ted.)