Scooter Therapy

One of the most read posts on this blog is the one about Lego Therapy.  We have lots of small Lego sets and they are indeed great as both tools and toys.  They are not exactly cheap, once you buy many of them.

Monty, now aged 10 and with autism, is also a big fan of music therapy, which regularly shows up as a favourite therapy among parents, although it is hard to prove its value scientifically.  In fact the other day Monty went to his first grown up ballet.  He went to see Sleeping Beauty and sat transfixed throughout the performance and behaved impeccably during the interval, surrounded by all the grown-ups in the audience.  It is clear that music has a power of its own, particularly over certain children.

Scooter therapy is my invention.  All you need is one of those new type of three wheeled scooters, which can be bought very cheaply.

Now, in any ABA programme you will have to work on both fine motor and gross motor skills, so that means finely controlling your hands to write neatly, or cut shapes with scissors and gross motor skills like kicking a football or throwing a basketball.  When you apply these skills to riding a bicycle, it may, or may not work.  Typical kids start with a small bike with stabilisers and then you soon take of the stabilisers and away they go.  You take for granted that the kids have situational awareness.  So if there is a wall straight ahead, they will apply the brakes, or swerve to avoid it.  If there is a nice row of flowers on one side, the kid may glance at them, but will soon focus again on where the bike is going.  With autistic kids the world can be very different, they may have no problem pedalling, but balance, using the brakes and situational awareness can be problems.

So I decided several months ago to take a step backwards and buy a little scooter and forget about bicycles.  The new type of three wheel scooters are great, they are more stable than the old type of two wheel scooter, but you still have to lean to turn left or right.  You can scoot on one leg, lean forwards to go fast and brake using your spare foot, or stand on the rear wheel.  All this fun and you are only a few centimetres off the ground, so it is hardly dangerous.

Well, after a few months, Monty has mastered his scooter and learnt about paying attention to obstacles, like oncoming bikes and pedestrians.  When something interesting comes into sight, he dismounts to investigate.  He can even safely scoot downhill on the pavement, while holding his ice cream and remember to stop at road junctions. 

This may not sound like much, but it is quite a transformation.  Sometimes to take two steps forward,  you have to first take one step backwards.

Scooting is also fun and you can go quite a long way.  A couple of months ago we managed to go 6km around a lake, which would have been a struggle on foot.

So, if you do not already have one, invest in a scooter.  They even have them for adults.

Endothelial Dysfunction - Oxidative Stress, Inflammation and BH4

This post is rather out of sequence, but it draws together several different topics that I have been investigating and introduces another chemical often mentioned in autism research, BH4.  The factor that links them all together is something called Endothelial Dysfunction.

This blog has already established that oxidative stress and neuroinflammation are the key drivers behind autism.  It has not been clear whether the oxidative stress causes the inflammation, vice versa, or perhaps they are self perpetuating.

In my ongoing investigation into the autism comorbidities of asthma and high cholesterol (proxy for cardiovascular disease), I have come across some tantalising fact, such as:-

• Asthma research shows that cigarette smoking gives you oxidative stress and this continues even after stopping smoking.  The oxidative stress reduces the effectiveness of asthma drugs.
• Oxidative stress is a key factor in cardiovascular disease.

• BH4 also known as Tetrahydrobiopterin, THB, trade name Kuvan or sapropterin is an enzymatic cofactor that is the subject of lots of research in cardiovascular disease and even in autism research.  As a drug, BH4 is so expensive that many national health services and insurers will not pay for it.  A pack of 30 pills of 100 mg cost $900.  The typical dose is 10-20mg per kg per day.  The cost per patient was reported to be over $100,000 per year.

The BH4 drug, Kuvan, is used to treat an extremely rare, but debilitating condition called Phenylketonuria, when the body cannot produce its own BH4.  In the UK, the National Health Service will not pay for Kuvan for the very small number of people who suffer Phenylketonuria.


A very interesting chart from the American Heart Association

The following chart was meant for cardiologists, but is extremely relevant if you want to understand autism.  I highlighted the parts in yellow.

In autism, people suffer from oxidative stress and typically exhibit hypercholesterolemia (high cholesterol).  They also suffer from neuroinflammation in the brain.  In my therapy, I use NAC to reduce oxidative stress and the behavioral impact is very marked.  In some autism trials they have given BH4 and the result have been visible, but not dramatic.  From the graphic above it would seem that BH4 is an extremely expensive way to reduce oxidative stress.

The latest BH4 autism trial was funded by the drug producer with 20 mg/kg/day.
 

Tetrahydrobiopterin as a Treatment for Autism Spectrum  Disorders: A Double-Blind, Placebo-Controlled Trial

More interesting for me is to now look into Endothelial Dysfunction and see if that is occurring in autism.

Long Term Mood Improvement using NAC in Autism

A more recent post on this subject is here:

http://epiphanyasd.blogspot.com/2014/08/nac-for-long-term-use-in-autism.html

NAC (N-Acetyl Cysteine) is an anti-oxidant that is part of the autism therapy I have implemented.  I have now received feedback from other parents who are also surprised by the positive effect it has on their child with autism.  So far, it has had a positive impact in 100% of cases.

In the literature, there are several schools of thought as to why NAC is effective. 

1. As a free radical scavenger in its own right
2. As a precursor to Glutathione (GSH)
3. As a glutamate antagonist
4. Reducing homocysteine

Glutamate is one of the brain's two most important neurotransmitters, the other being GABA.  Glutamate is excitatory and so too much of it would cause you a problem.  NAC can act as an antagonist to glumate.  This is all very nicely explained by Emily Deans, a psychiatrist in Massachusetts who has a very interesting blog of her own.

• Glutathione: We Loves It (NAC and Autism)

In my research into the autism comorbidity asthma, I also came across plenty of talk about oxidative stress and anti-oxidants.  NAC is used, but it seems like they are looking for something stronger.

The main impact is as a precursor to Glutathione (GSH)

I recently learnt that in autism (or at least the one my son is affected by) the reason is without doubt number two.  The other roles (scavenger/antagonist) are irrelevant.

The reason I know this, is that after a few months NAC effectively stopped working.  This coincided with an asthma flare-up.  Now, I initially thought that the asthma attacks had released inflammatory cytokines and that these had stimulated the ever-present neuro-inflammation in the brain.

This is highly plausible and indeed I have literature showing which cytokines are released by asthma attacks.  So I thought that by firmly dealing with the asthma, I would at the same time subdue the autism.  This did not happen.

So after a few days I came up with "plan B", which did prove to be successful.  I hypothesised that the NAC had stopped working because I was not giving enough vitamin B12, which is part of the chemical process in which GSH is synthesised from NAC.  I have no means of knowing how much is needed exactly. In related processes both vitamin B6 and B9 are also involved.

I increased the B vitamins and within hours things began to revert towards the previous behavioural equilibrium.

So it was most likely the failure of NAC to produce GSH, and thus reduce oxidative stress, that had sparked the asthma flare-up. (this is will be covered on my later post of asthma as a comorbidity in autism)

But how much B12 is needed to synthesise GSH?

In your diet you have vitamins B6, B9 and B12, but it is unclear how much is needed to synthesise GSH.  A further complication is that B vitamins are not well absorbed in the gut, and some people absorb them better than others.  Older people are known to absorb B12 poorly.  There are expensive sub lingual B vitamin supplements, but there is no evidence that they actually work better.

There are at least two NAC products targeted at older people to protect them from memory loss and Alzheimer's disease:-

• Betrinac   
• Cerefolin NAC

 Both products combine NAC with vitamins B6, B9 and B12,

                                             Over the counter NAC        Cerefolin NAC        Betrinac


N-acetylcysteine (NAC)              600mg                            600mg                     600mg
Vitamin B9 (folate)                                                          1,000 mcg               800 mcg
Vitamin B6                                                                           25mg                       20mg
Vitamin B12                                                                    1,000mcg                1,000mcg



 Both products are for preventing memory loss, rather than just increasing GSH.


For a comprehensive look into B vitamins including their role in the brain, and how they are (or are not) absorbed, take a look at this link from the US Office of Dietary Supplements.


Reducing homocysteine

Homocysteine is linked with strokes, and particularly in the US there are doctors who use NAC for the purpose of lowering homocysteine.

Dr. Baum, medical director of the Mind/Body Medical Institute, a Harvard affiliate, recommends 1,000 micrograms (mcg) of folate, plus 25 milligrams (mg) of vitamin B6, 1,000 mcg of B12, and 1,800 mg of the amino acid N-acetyl-cysteine (NAC). "With folate, B6, B12, and NAC supplements, almost everyone will have normal homocysteine levels," says Dr. Baum.

There is even a discussion about the role of homocysteine in autism.  A very recent paper from Poland is: A focus on homocysteine in autism

I think think that high homocysteine, just like low GSH, is a marker of oxidative stress.  In some of the literature it is stated that homocysteine cause oxidative stress.

Here is another paper: Metabolic biomarkers of increased oxidative stress and impaired methylation capacity in children with autism

 

And yet another one:-

Folate and homocysteine metabolism in neural plasticity and neurodegenerative disorders

 

If you read all the papers you will come across various graphics showing biological cycles within the body, like the one below.  This is how I know that the various B vitamins are needed.

Vitamin B12 Therapy

I really just need to know how much B12 is needed and how to give it.  In the end the best resource turned out to be a  bulletin from a US medical insurer, and here it is:-

Clinical Policy Bulletin:  Vitamin B-12 Therapy

The document is very thorough; here are some key parts:-


Background

Vitamin B-12 belongs to the family of cobalamins. It is available in all animal-derived foods, and is absorbed at a rate of 5 mcg per day. After being ingested, vitamin B-12 becomes bound to intrinsic factor, a protein secreted by gastric parietal cells. The vitamin B-12/intrinsic factor complex is absorbed in the terminal ileum by cells with specific receptors for the complex. The absorbed complex is then transported via plasma and stored in the liver. Since the liver stores 2,000 to 5,000 mcg vitamin B-12 (adequate for up to 5 years), dietary deficiency of cobalamin (Cbl) is rare. In most cases, vitamin B-12 deficiency is due to an inability of the intestine to absorb the vitamin, which may result from an autoimmune disease that reduces the production or blocks the action of intrinsic factor, or from other diseases that result in intestinal malabsorption. The most frequent underlying cause of vitamin B-12 deficiency is pernicious anemia, which is associated with decreased production of intrinsic factor.


In a systematic review of randomized trials on vitamin B-6, B-12, and folic acid supplementation and cognitive function, Balk and colleagues (2007) stated that despite their important role in cognitive function, the value of B vitamin supplementation is unknown. A total of 14 trials met selection criteria; most were of low quality and limited applicability. Approximately 50 different cognitive function tests were assessed. Three trials of vitamin B-6 and 6 of vitamin B-12 found no effect overall in a variety of doses, routes of administration, and populations. One of 3 trials of folic acid found a benefit in cognitive function in people with cognitive impairment and low baseline serum folate levels. Six trials of combinations of the B vitamins all concluded that the interventions had no effect on cognitive function. Among 3 trials, those in the placebo arm had greater improvements in a small number of cognitive tests than participants receiving either folic acid or combination B-vitamin supplements. The evidence was limited by a sparsity of studies, small sample size, heterogeneity in outcomes, and a lack of studies that evaluated symptoms or clinical outcomes. The authors concluded that there is insufficient evidence of an effect of vitamin B-6, B-12, or folic acid supplementation, alone or in combination, on cognitive function testing in people with either normal or impaired cognitive function. This is in agreement with Clarke et al (2007) who stated that randomized trials are needed to ascertain the relevance of vitamin B-12 supplementation for the prevention of dementia.

Vitamin B-12 therapy can be administered orally or by injection. Vitamin B12 tablets of up to 5,000 mcg may be obtained over the counter without a prescription.

In a review on vitamin B-12 deficiency, Oh and Brown (2003) noted that, because most clinicians are generally unaware that oral vitamin B-12 therapy is effective, the traditional treatment for B-12 deficiency has been intramuscular injections. The authors cited evidence that demonstrates, however, that oral vitamin B-12 has been shown to have an efficacy equal to that of injections in the treatment of pernicious anemia and other B-12 deficiency states (Elia, 1998; Lederle, 1998; Kuzminski et al, 1998; Lederle, 1991). The authors explained that, although the majority of dietary vitamin B-12 is absorbed in the terminal ileum through a complex with intrinsic factor, there is mounting evidence that approximately 1 % of a large dose of oral vitamin B-12 is absorbed by simple diffusion which is independent of intrinsic factor or even an intact terminal ileum.
Kuzminzki et al (1998) reported on the outcome of 33 patients with vitamin B-12 deficiency who were randomized to receive oral or parenteral vitamin B-12 therapy. Patients in the parenteral therapy group received 1,000 mcg of vitamin B-12 intramuscularly on days 1, 3, 7, 10, 14, 21, 30, 60, and 90, while those in the oral treatment group received 2,000 mcg daily for 120 days. At the end of 120 days, patients who received oral therapy had significantly higher serum vitamin B-12 levels and lower methylmalonic acid levels than those in the parenteral therapy group.

 On treating B12 deficiency :-

Although the daily requirement of vitamin B-12 is approximately 2 mcg, the initial oral replacement dosage consists of a single daily dose of 1,000 to 2,000 mcg (Lederle, 1991; Oh and Brown, 2003). This high dose is required because of the variable absorption of oral vitamin B-12 in doses of 500 mcg or less. This regimen has been shown to be safe, cost-effective, and well tolerated by patients.


CONCLUSION


Long term high dose NAC will require careful supplementation with B vitamins.   If NAC is using up vitamin B12 faster than your child is absorbing it from food and supplements, B12 will be used up from the liver and other vitamin stores in the body.  These stores will eventually be depleted and vitamin B12 deficiency will result, if you continue to give NAC.  This is best avoided.

If money is of no concern, best to buy Cerefolin NAC or Betrinac.  If on a budget, then use the cheap NAC available on-line or in your pharmacy; but be careful to supplement far higher amounts of B6, B9 and B12 than the RDA (recommended daily amount).

Cerefolin NAC and  Betrinac have 400 times the RDA of B12, 4 times the RDA of B9 and 15 times of B6.  But each of these tablets only has 600mg of NAC.  In the autism trials the dose of NAC is 4 times higher.

It is evident that B12 is the key vitamin that acts as a precursor with NAC to form GSH (Glutathione), so this is the one to keep a close eye on should your child's NAC appear "to stop working".

It looks like 1,000 mcg of B12, of which 1% may be absorbed, is a fair place to start.  Such supplements are relatively inexpensive, and widely available.



 

Autism Drug Effectiveness in Comorbidities

The three autism comorbidities that I have chosen to investigate are asthma, high cholesterol and various types of seizure.

 

Phase 1

The first phase is the easy one.  I just need to see if my autism drugs are proven to be effective in the each comorbidity.  The results really surprised me.

With the exception of bumetanide and asthma, there is a perfect overlap.  Even more surprising, is that another loop diuretic, called furosemide, which is very similar to bumetanide, has been showed to be effective in asthma when given in the inhaled form.

In the case of cholesterol, I am looking at elevated levels in cardiology.  The use of bumetanide in people with heart problems associated with high cholesterol is to reduce blood pressure (anti-hypertensive).

 

 
You can check use of my autism drugs in each comorbidity using Google, or just look at the links I selected below.

 

Asthma/COPD

NAC improves effectiveness of the conventional corticosteroid therapy, particularly in hard to treat cases like current or past smokers. In COPD a severe form of asthma, read:  The role for N-acetylcysteine in the management of COPD

Do statins improve outcomesin patients with asthma on inhaled corticosteroid therapy?

Effect of inhaled furosemide and bumetanide on adenosine5'-monophosphate- and sodium metabisulfite-induced bronchoconstriction in asthmatic subjects

  

High Cholesterol (cardiac treatment)

NAC raises your good HDL cholesterol level, so lowering your overall cholesterol risk factor.

Dose-Related Increase of HDL-cholesterol Levels after N-acetylcysteine in Man

Statins were primarily developed to lower cholesterol as part of cardiac treatment.

 

Bumetanide is a loop diuretic and anti-hypertensive drug primarily marketed as a cardiac drug.

 

Seizures

 Glutathione peroxidase deficiency and childhood seizures

Treatment off our siblings with progressive myoclonus epilepsy of the Unverricht-Lundborg type with N-acetylcysteine

 

Role of Oxidative Stress in Refractory Epilepsy: Evidencein Patients and Experimental Models

 (then click for full version)

Can Statins Lower the Risk for Epilepsy?

Blocking seizures with the diuretic Bumetanide: Promises and pitfalls

 

Phase 2

The second phase involves understanding each comorbidity and seeing if any of their established treatments can be effective in treating autism.

This will also produce some surprises in the following posts.






 

Learning from Comorbidities in Autism

You might have been wondering why there has been a pause in my blog posts; rather than post nonsense, I have been exploring some new directions.

The current combination of bumetanide + NAC + atorvastatin does continue to be effective, but clearly there can be more.

I recently read a paper by a researcher who concluded that he thought autism was so heterogeneous there might well never be a drug therapy for autism.  I certainly see where he is coming from, but I think this tells us two things:-

 

1.      Do not expect conventional medical research to come up with an autism drug any time soon.

 

2.      It would be wise to read up on the medical research outside the realm of autism, where perhaps a more can-do approach and better resourcing might be evident.

This brings me to comorbidities.  In case you are not familiar with this term, in medicine, comorbidity is the presence of one or more disorders (or diseases) in addition to a primary disease.

In the case of autism frequent comorbidities include asthma, high cholesterol and seizures/epilepsy.

I decided to start with asthma, since Monty, aged 9 and with ASD, has mild asthma and I am already familiar with the range of treatments.

I somewhat fancifully hypothesized that there would be an overlap in effective drug therapies for autism and asthma; in other words what works for core autism treatment would be effective in asthma and vice versa.  Having been able to validate my hypothesis, I moved on to look at other comorbidities.  I am currently looking at three areas.

 

1.       Asthma and COPD

Asthma affects 300 million people worldwide and kills about 250,000 people ayear.  COPD (Chronic Obstructive Pulmonary Disease) is a more severe form of asthma and is the third leading cause of death in the US.

I figured that since these conditions are life threatening and widespread in developed counties, they would be well researched and drug therapies actively sought.

2.       High Cholesterol

The effects of high cholesterol are very well studied in cardiology, though not in autism.   The emerging understanding from cardiology is the causal link between cholesterol formation and neuroinflammation.  A little known fact is that elevated cholesterol is the norm in autism; people have asked me why, now I know and soon so will you.

 

3.       Seizures and epilepsy

 It is well known that many people with autism also have epilepsy.  There are many kinds of epilepsy and seizure; two types particularly interested me - absence seizures and non-convulsive seizures.  More of this later.

 

Subequent posts will present what I have learnt.

 

But now for a change of subject  and an interesting link ...

 

Common autism drug therapy in the US

If you do not live in the US, you may be unaware just how many drugs and supplements some autistic children receive.  It seems that in the US, 70% of autistic children take at least 10 different potions.  Not surprising, many of these can interact with each other.

If you are curious to see what some of these drugs are and what the common interactions are, you will find the following paper very interesting.  Its author, Theoharis C. Theoharides, has already appeared on this blog and he will appear again when we look at asthma and immunomodulation.

Unwanted interactions among most common treatment regimes in autism

 

 

 

The Singing Statin, the BCL-2 Gene and Epigenetics

This post has something for both the casual reader and the scientists among you.  Today I will start with the science.

Epigenetics

Epigenetics are chemical markers that can appear on your DNA as the result of some environmental exposure, like diet or stress.  Methylation is a type of epigenetic change in which methyl groups are added to DNA and switch on or off the underlying gene.  This can have severe consequences depending on which gene is affected.

Identical Twins

It seems that if one identical twin has autism, there is a 70% chance that the other twin will be autistic.  In 30% of the cases the twin is neurotypical.  Researchers have very cleverly started to analyse pairs of twins from this 30% group and look for epigenetic marks.  This would highlight genetic causes of autism.

Apoptosis

Apoptosis is a tricky word to spell, for somebody like me, but is actually something quite simple; it is programmed cell death.  Apoptosis happens in all of us, all day long.  If it gets out of control, it becomes bad and something called atrophy will occur.  Too little apoptosis can result in irregular cell growth and cancer.

 

Candidate Genes

Using the epigenetics approach, in 2010 a study was published that identified two “candidate” genes linked to autism.  They were BCL-2 and RORA.

According to that study, BCL-2 is an anti-apoptotic protein located in the outer mitochondrial membrane that is important for cell survival under a variety of stressful conditions.  In other words BCL-2 inhibits cell death.

According to another source, BCL-2 is “one of the foremost anti-apoptotic molecules”.

A very recent study has identified more such genes, using the same approach.

 

If you are really interested in the genetics of autism, there is actually a database of all the indicated genes, maintained by the Simons Foundation.

  

BCL-2 and autism

Going back to 2001, researchers had already noted that the autistic brain was deficient in BCL-2 and they suggested that:-

“These results indicate for the first time that autistic cerebellum may be vulnerable to pro-apoptotic stimuli and to neuronal atrophy as a consequence of decreased BCL-2 levels.”

The study is called :- Reduction in anti-apoptotic protein Bcl-2 in autistic cerebellum

As we have already learned, in the autistic brain the important Purkinje Cells are reduced in number by half due to atrophy.  If BCL-2 can indeed reduce this excessive apoptosis, it should be a friend indeed.

 

Stimulating production of Bcl-2

Fortunately the clever people working with Professor Wood, at the University of Minnesota, have been studying cholesterol regulation in the brain for some time.  Here is what they have been up to:-

“The lab has recently made the novel discovery that statins both in vivo and in vitro stimulate gene expression and protein levels of one of the foremost anti-apoptotic molecules, Bcl-2. Currently, studies are focused on mechanisms of statin-induction of Bcl-2”

Or in plainer English, statin drugs increase your level of BCL-2 and so reduce cell death.
 

If you want to read more here is an open access paper:-  Simvastatin Stimulates Production of the Antiapoptotic Protein Bcl-2 via Endothelin-1 and NFATc3 in SH-SY5Y Cells

 

The Singing Statin

Now we have finished with the pure science and we move back to the practical world of applied science.

Monty, aged 9, has been taking atorvastatin for a few weeks.  After day one, he developed the urge to play the piano outside of lesson time.  Every day since, he has played more and more.  Now his piano teacher says she thinks he has absolute pitch.  It turns out that this is far more common in the autistic population and there is a great deal of research that has been done on this and music/autism in general.  Here is a short article on the subject.

Now in an earlier post we established the importance of the stress hormone cortisol and also the interesting finding that you can reduce it by singing.  Then I got people asking about, “what about just listening to music” or “what about playing an instrument”.  I did not do the research, but I think nothing works like a good sing.

So yesterday I was delighted to hear that Monty has started to sing spontaneously in his room.  He put on his Mozart CD and started to sing, with his own lyrics and not just in English, but also in his second language.

I have to thank Mr Pfizer and in fact Mr Bruce Roth for bringing us Atorvastatin (called Lipitor or Sortis, depending on where you live).  Mr Roth invented it in 1985.

Perhaps BCL-2 could be better named the Singing Gene?

 

 

 

Mixed Media Messages

You may have noticed a week ago SAP, the German software giant, announced that it will in future try to ensure that 1% of its 60,000 workforce are autistic.  This attracted quite a lot of publicity.  It might have been kinder if they had referred to Asperger’s, or at least High Functioning Autism. Not all autistic people are savants or computer wizz kids.

When it comes to TV, the messages are often either trivial or sensational.  But, thanks to the internet, you can access very relevant and intelligent films, and all for free.

The MIND Institute at the University of California in Sacramento, has a rich library of material, from some very well qualified people.

 http://www.ucdmc.ucdavis.edu/mindinstitute/videos/video_autism.html

These films are typically an hour long and cover many of the subjects that have appeared in this blog.  If you are a fan of Temple Grandin, you can even watch her film.  I liked the one by Deborah Fein, halfway down the list.

As usual though, usable conclusions are rather absent; we have to add those ourselves.

 

Belgrade, Busby Babes and the Wakefield MMR Saga

On 5^th February 1958, Manchester United played away to Red Star in Belgrade.  What is remembered is not the match, but the flight home; having stopped to refuel in Munich, the plane crashed on take-off with 23 fatalities and 21 survivors.

Matt Busby, the Manager, survived the accident and ten years later he led a new team of Busby Babes to win the European Cup.  Bobby Charlton and Bill Foulkes survived the crash and played against Benfica in that final.

Why am I telling you about this?  The reason is the air crash investigation that followed.  It was convenient to blame the pilot, Captain James Thain.  The German enquiry blamed him for not deicing the wings and claimed that this ice prevented the plane from taking off, as it reached the end of the runway.

For ten years Thain tried to clear his name and insisted there had been no ice on the wings and that a deep layer of water and slush on the runway caused the accident.  Finally, Harold Wilson, the then British Prime Minister, backed his call for a new investigation.  At that second inquiry, it was shown that Thain had been right all along.  The wings were not iced up, but the runway had not been properly cleaned and the crash was inevitable.  The plane could not gather enough speed to take off and crashed into a house at the end of the runway.

Thain had been a convenient scapegoat and died aged 54, the 24^th victim of the crash.

The truth did come out in the end and it was recently the subject of an excellent documentary by National Geographic.

Do vaccines cause autism?

I was surprised last week when my mother, a retired doctor,  asked whether I thought the MMR vaccination caused autism .  My reply was along the lines of “maybe sometimes, but we will never know”.  A year ago, I would have simply said “of course not”.

Monty, autistic and aged 9, also flies from Belgrade to London, and sometimes via Munich.  Planes have got much bigger and safer and airports are much better prepared for bad weather.  Flying will always have a risk and all drugs have an element of risk; so naturally vaccines also have a risk.

From a public health perspective, it is clear that vaccines save millions of lives and so any risk is vastly outweighed by the overall benefit.

If you were Bill Gates, who is nobly trying to eradicate polio from the planet (he now has the added problem of the Taliban killing the vaccination teams in Pakistan), what would you say about Andrew Wakefield and his linking of autism to vaccines?

Not surprisingly he gets referred to as a fraud and that his research was rigged and that later research proved him wrong.  Now can we get back to eradicating polio!

In the big picture Bill is definitely right; Andrew Wakefield may also be right, but will he ever get a fair chance to prove it?  Captain James Thain waited ten years, I think Andrew Wakefield will need to wait much longer.

It sounds highly plausible that injecting a combination of vaccines preserved in a solution with mercury (the mercury has now replaced by a much larger amount of aluminium) might cause an adverse reaction in the brains of a small number of subjects; perhaps ones with a slightly permeable blood brain barrier (BBB).  Rather than trash this hypothesis, it would have been better to fully investigate it and perhaps develop safer vaccines.  As in Munich, there has been an investigation, but I was rather shocked reading comments of researchers familiar with those studies.

I would agree with Bill that Andrew Wakefield could be seen as a danger to public health, but what if he is also right.  Does it matter?  If you are touched by autism, then yes; otherwise probably not.

Back to Spock

I mentioned a few posts ago that I had been to see the latest Star Trek movie with Ted, aged 12, and his friend Adrian “Mole”.

While saving a planet, but endangering the Starship Enterprise, Spock commented that “the interests of the many outweigh the interests of the few”.  Bill would concur, and so would Peter.

The conclusion is that if you are one of the few, you are on your own.  Do not wait for the Enterprise, or anyone else, to help you.  Help yourself.

I have no idea whether Andrew Wakefield is right, but at least on my blog he gets a chance to present his case. Here he is responding to a recent measles outbreak in South Wales.

Angelina Jolie or Destiny’s Child?

At the time of writing this post Angelina Jolie’s aunt has succumbed to the same cancer that killed Angelina’s mother and she announced that she also carried the same defective gene.  She opted to take pre-emptive action and, in effect, cheat a nasty early death from breast or ovarian cancer.

I have read so much research into autism, that it is pretty clear to me, that you could calculate an Autism Risk Factor (ARF) for prospective parents, if you really wanted to.  Would you really want to?  I expect those with direct experience of autism might be in favour, the others probably would not even bother to answer the question.  Since few truly autistic people have children, it is really more of a question for their siblings; do they want Destiny’s Child?

It may sound depressing, or something to do with eugenics, but actually it does not have to be.  I am not suggesting the sort of genetic and chromosome testing that is already routinely done for conditions like Down’s syndrome.  I am talking about the kind of lifestyle changes that ideally a woman who smokes, drinks heavily or takes drugs, should take when she wants to have a child.

If your ARF puts you at risk, then you would receive a list of lifestyle changes, you should take to minimize the risk to your future child.

 

Autism Risk Factor (ARF)

I am not qualified to develop the ARF, but I am confident enough to highlight two of the factors that should go into it:

 

1.     Maternal & paternal family history of autoimmune diseases

Auto-immune diseases including, but not limited to, history of type 1 diabetes, rheumatoid arthritis, celiac disease and hypothyroidism.  Here is some supporting evidence, for those who are interested:-

·         Association of Family History of Autoimmune Diseases and Autism Spectrum Disorders

 

·         Familial Clustering of Autoimmune Disorders and Evaluation of Medical Risk Factors in Autism

 

2.     Maternal & paternal stress capacity

This risk factor is my invention.  I used to only really think about mechanical stress, but now I know all about physiological stress, psychological stress and that big one, oxidative stress.  It seems, remarkably to me, that the latter three types of stress are in fact one and the same.

Put another way, physiological stress, psychological stress and oxidative stress are reflections of each other.  If you have got one, you will have all three.

The good news is that can use obvious visible cues to spot people will a low stress capacity and you could even then confirm it with a laboratory test of their oxidative stress (GSH redox level).

I recently took four short airplane flights and I observed people with chronic nail chewing (male) and obsessive nail filing (female) sitting beside or in front of me; it looks like about 5% of the flying population.  If you added the non-autistic people with mild stereotypy (stimming) like foot flapping, and those with Trichotillomania (compulsive hair pulling, that we learned about in the posts on GSH/NAC) you would have a large proportion of those people living in some degree of potentially damaging oxidative stress.

I think the maternal stress capacity would be most relevant, but the fetus’s own stress capacity is also important, and some of that clearly comes from the paternal side.

Conclusion

So the conclusion for Ted, aged 12, is to grow up and find a nice calm girlfriend and buy a large supply of NAC, just in case.