Glutathione (GSH) Part I

Today’s post is where I am going to get seriously scientific.  There is another Epiphany at the end, but you will read about it in Part II.  Part I is the primer.  To fully understand Part II and see why it really does lead to another epiphany moment, you should read it.  If you plan on actually implementing this at home, I suggest you read Part I, Part II and go and see your paediatrician.  My research should not be seen as medical advice.  Doctor always knows best and I am not a doctor.

Introduction

I mentioned earlier, that in January 2013,when I decided to launch my ANA project, the plan was as follows; start work first with my own observations and look for a hypothesis that I could develop entirely myself.  Having found a treasure trove of existing scientific research, I decided that I would also develop a Plan B.  Plan B is very simple, to just read the research and apply my own little grey cells.

Plan A went very fast and with a few days I had developed my first hypothesis.  I have not given it a name yet, but the letters TRH will feature prominantly.  Having developed a hypothesis you then have to figure out what to do with it.  In the case of my second hypothesis, concerning Hypokalemic Sensory Overload, it was really easy to test it.  For me, it is proven, although maybe one day I will do a double-blind, randomized, placebo-controlled study, to prove it to the rest of the world.

One weekend in early February, I had an evening off at home with no kids nor any obligations.  So I thought this would be a good time to tinker away on Google Scholar.  This is a special kind of search that only lists serious scientific research.

If it was not for Google Scholar, I would have a lot more free time and you would be doing something much more fun and read my ramblings.

I started reading some research into the pseudo-science of autism.  Having travelled through hyperbaric oxygen  therapy, I arrived at methyl B12 treatment.  It turns out that in the US, parents are injecting their autistic kids with vitamin B12 in their rears.  There are whole discussions on various websites as to how best to do this.  Apparently, the best way is to wait till the kid is asleep, apply lidocaine cream to numb the skin and then jab in the needle.  This is not something I plan doing to Monty, nor I hope him to me.  Then I found some research dedicated to see if methyl B12 treatment actually works.

Well, the study concluded that “methyl B12 is ineffective in treating behavioral symptoms of autism”.  But then the author a caveat “However, detailed data analysis suggests that methyl B12 may alleviate symptoms of autism in a subgroup of children, possibly by reducing oxidative stress”

I was aware that I was in the dreaded territory of  “DAN Doctors” and the paper was published in a something called The Journal of Alternative and Complimentary Medicine, so big red warning lights were flashing.  I could buy the full paper for $51 or live with the abstract.  I choose the latter and moved on.

Now after 20 munites of "Google Scholaring" I had something juicy to investigate.  What is oxidative stress? what is glutathione redox status (GSH/GSSG)? and what was the relevance of the subgroup that had increased plasma concentrations of GSH?

My new book on Human Physiology has yet to arrive, but I have pretty much figured it out anyway.  I do love Amazon and I guess they must love me, by now.

So what is Glutathione (GSH)? Well, if you live in the world of  pseudo-science, it is very easy;  it’s an antioxidant “period”.

I’d be wasting my time and yours if I left it at that.

 

First a bit of chemistry

A thiol is a type of compound that contains  the following bond   R–SH, where R is a carbon containing group of atoms. (Hopefully, from schooldays you will recall that S is sulphur and H is hydrogen).

Thiols tend to smell terrible, like rotten eggs or garlic and thiols are readily oxidized

Thiols play a very important role in human biology.  I took a quick look at a list thiols, to see if any bells starting ring between my ears. They did.

You have guessed that Glutathione is a thiol, make a mental note of another important one, cysteine.

 

Selected Thiols

 

Glutathione  C₁₀H₁₇N₃O₆S

Cysteine   C₃H₇NO₂S

Thioctic acid  C₈H₁₄O₂S₂

  

I included the third thiol for a reason;  I used to buy vials of the stuff on business trips to Romania.  It was not cheap, maybe EUR 300 for a whole box, I do not remember.  I do remember that it is used as a therapy for peripheral diabetic neuropathy.  It is known to be a powerful antioxidant.

Having got the suspicious items through customs they finally ended up going to the military hospital, along with my father in law, the final recipient. It is administered intravenously.  As you will see from the study, only when give IV was there an effect, the oral version had no beneficial therapeutic effect.  This is a very common problem, crossing the BBB (blood brain barrier) and the same you will notice later, will apply to GSH.  In US and  UK, this treatment for peripheral diabetic neuropathy is not used and is merely experimental.  In some east European countries, it has been a standard therapy for decades.

I told you that this particular thiol is called Thioctic acid, but just confuse the lay person, it has a further three names - Thiotacid, Lipoic acid and Alpha Lipoic Acid (ALA).

Now did I choose to add ALA to my list of three thiols to talk about, because I already knew something else about it?  It often seems to be the case, in my 5 weeks reading about human physiology, that it's a very small world, full of coincidences.

ALA has another quite unrelated use, in heavy metal chelation.  I read that "Lipoic acid administration can significantly enhance biliary excretion of inorganic mercury in rat experiments".  It is the agent of choice of some DAN Doctors for their young patients with autism.

Do not confuse alpha lipoic acid with alpha-Linolenic acid, which is an omega 3 fatty acid.

By the way, we are actually doing some research currently into omega 3 oil.  Please note that there is no such thing as omega 3 oil as such, it is the name to a big group of quite different individual polyunsaturated fatty acids. It is believed that three are important in human physiology, those being alpha-linolenic acid (ALA), eicosapentaenoic acid (EPA), and docosahexaenoic acid (DHA). More of this and what to make of them, will be in a later post.

Summary so far

• So we know that GSH is a thiol, thiols incorporate a sulphur-hydrogen bond. Thiols are great antioxidants and thiols tend to stink.

• GSH’s formula is  C₁₀H₁₇N₃O₆S and it looks like:-

• In its oxidized form GSH becomes GSSG
• GSSG’s formula is C₂₀H₃₄N₆O₁₃S₂

 

As you would expect GSSG goes by numerous aliases, namely :-

Glutathione Hydrate Oxidized, Glutathione Oxidized GSSG Hydrate;GSSG Hydrate Oxidize; and even Glutathione Disulphide

If you compare the molecular formulas of GSH and GSSG,  you will notice that one molecule of GSSG = 2 molocules of GSH plus  O²⁻

Redox (reduction- oxidation)

You may have learnt about his at school.  The process often involves oxygen, hence oxidation, but it does not have to.  The strict definitions are :

Oxidation = all processes that involve loss of electrons

Reduction = all processes that involve the gain of electrons

In redox processes, the reductant or reducing agent loses electrons and is oxidized, and the oxidant or oxidizing agent gains electrons and is reduced. The pair of  oxidizing agent and reducing agent is called a redox pair. A redox couple is a reducing species and its corresponding oxidized form, e.g., Fe²⁺/Fe³⁺.

 So when a piece of your caste iron fence rusts, you get:

 

4 Fe + 3 O₂ → 2 Fe₂O₃

 

(the next part is taken from Colorado State University’s fantastic web resource covering Pathophysiology and more)  I just added maybe 5% and corrected the spelling.

 

A radical (aka free radical)  is an atom or group of atoms that have one or more unpaired electrons. Radicals can have positive, negative or neutral charge. They are formed as necessary intermediates in a variety of normal biochemical reactions, but when generated in excess or not appropriately controlled, radicals can wreak havoc on a broad range of macromolecules. A prominent feature of radicals is that they have extremely high chemical reactivity, which explains not only their normal biological activities, but how they inflict damage on cells.  Their chief danger comes from the damage they can do when they react with important cellular components such as DNA, or the cell membrane. Cells may function poorly or die if this occurs. To prevent free radical damage the body has a defence system of antioxidants.

Oxygen Radicals

There are many types of radicals, but those of most concern in biological systems are derived from oxygen, and known collectively as reactive oxygen species. Oxygen has two unpaired electrons in separate orbitals in its outer shell. This electronic structure makes oxygen especially susceptible to radical formation.

Sequential reduction of molecular oxygen (equivalent to sequential addition of electrons) leads to formation of a group of reactive oxygen species:

• superoxide anion
• peroxide (hydrogen peroxide)
• hydroxyl radical

The structure of these radicals is shown in the figure below, along with the notation used to denote them. Note the difference between hydroxyl radical and hydroxyl ion, which is not a radical.

Another radical derived from oxygen is singlet oxygen, designated as ¹O₂. This is an excited form of oxygen in which one of the electrons jumps to a superior orbital following absorption of energy.

Formation of Reactive Oxygen Species

Oxygen-derived radicals are generated constantly as part of normal aerobic life. They are formed in mitochondria as oxygen is reduced along the electron transport chain. Reactive oxygen species are also formed as necessary intermediates in a variety of enzyme reactions. Examples of situations in which oxygen radicals are overproduced in cells include:

• White blood cells such as neutrophils specialize in producing oxygen radicals, which are used in host defence to kill invading pathogens.
• Cells exposed to abnormal environments such as hypoxia or hyperoxia generate abundant and often damaging reactive oxygen species. A number of drugs have oxidizing effects on cells and lead to production of oxygen radicals.
• Ionizing radiation is well known to generate oxygen radicals within biological systems. Interestingly, the damaging effects of radiation are higher in well oxygenated tissues than in tissues deficient in oxygen.

Biological Effects of Reactive Oxygen

It is best not to think of oxygen radicals as "bad". They are generated in a number of reactions essential to life and, as mentioned above, phagocytic cells generate radicals to kill invading pathogens. There is also a large body evidence indicating that oxygen radicals are involved in intercellular and intracellular signaling. For example, addition of superoxide or hydrogen peroxide to a variety of cultured cells leads to an increased rate of DNA replication and cell proliferation - in other words, these radicals function as mitogens.

Despite their beneficial activities, reactive oxygen species clearly can be toxic to cells. By definition, radicals possess an unpaired electron, which makes them highly reactive and thereby able to damage all macromolecules, including lipids, proteins and nucleic acids.

One of the best known toxic effects of oxygen radicals is damage to cellular membranes (plasma, mitochondrial and endomembrane systems), which is initiated by a process known as lipid peroxidation. A common target for peroxidation is unsaturated fatty acids present in membrane phospholipids.

Reactions involving radicals occur in chain reactions. Note that a hydrogen is abstracted from the fatty acid by hydroxyl radical, leaving a carbon-centered radical as part of the fatty acid. That radical then reacts with oxygen to yield the peroxy radical, which can then react with other fatty acids or proteins.

Peroxidation of membrane lipids can have numerous effects, including:

• increased membrane rigidity
• decreased activity of membrane-bound enzymes
• altered activity of membrane receptors.
• altered permeability

In addition to effects on phospholipids, radicals can also directly attack membrane proteins and induce lipid-lipid, lipid-protein and protein-protein crosslinking, all of which obviously have effects on membrane function.

Mechanisms for Protection Against Radicals

Life on Earth evolved in the presence of oxygen, and necessarily adapted by evolution of a large battery of antioxidant systems. Some of these antioxidant molecules are present in all life forms examined, from bacteria to mammals, indicating their appearance early in the history of life.

Many antioxidants work by transiently becoming radicals themselves. These molecules are usually part of a larger network of cooperating antioxidants that end up regenerating the original antioxidant. For example,vitamin E becomes a radical, but is regenerated through the activity of the antioxidants vitamin C and glutathione.

Enzymatic Antioxidants

Three groups of enzymes play significant roles in protecting cells from oxidant stress:

Superoxide dismutases (SOD) are enzymes that catalyze the conversion of two superoxides into hydrogen peroxide and oxygen. The benefit here is that hydrogen peroxide is substantially less toxic that superoxide. SOD accelerates this detoxifying reaction roughly 10,000-fold over the non-catalyzed reaction.

SODs are metal-containing enzymes that depend on a bound manganese, copper or zinc for their antioxidant activity. In mammals, the manganese-containing enzyme is most abundant in mitochondria, while the zinc or copper forms predominant in cytoplasm. Interestingly, SODs are inducible enzymes - exposure of bacteria or vertebrate cells to higher concentrations of oxygen results in rapid increases in the concentration of SOD.

Catalase is found in peroxisomes in eucaryotic cells. It degrades hydrogen peroxide to water and oxygen, and hence finishes the detoxification reaction started by SOD.

Glutathione peroxidase is a group of enzymes, the most abundant of which contain selenium. These enyzmes, like catalase, degrade hydrogen peroxide. They also reduce organic peroxides to alcohols, providing another route for eliminating toxic oxidants.

In addition to these enzymes, glutathione transferase, ceruloplasmin, hemoxygenase and possibly several other enzymes may participate in enzymatic control of oxygen radicals and their products.

Non-enzymatic Antioxidants

Three non-enzymatic antioxidants of particular importance are:

Vitamin E is the major lipid-soluble antioxidant, and plays a vital role in protecting membranes from oxidative damage. Its primary activity is to trap peroxy radicals in cellular membranes.

Vitamin C or ascorbic acid is a water-soluble antioxidant that can reduce radicals from a variety of sources. It also appears to participate in recycling vitamin E radicals. Interestingly, vitamin C also functions as a pro-oxidant under certain circumstances.

Glutathione may well be the most important intracellular defense against damage by reactive oxygen species. It is a tripeptide (glutamyl-cysteinyl-glycine). The cysteine provides an exposed free sulphydryl group (SH) that is very reactive, providing an abundant target for radical attack. Reaction with radicals oxidizes glutathione, but the reduced form is regenerated in a redox cycle involving glutathione reductase and the electron acceptor NADPH.

 

 ** Now we have left Colorado ** 
 
(Colorado State University is located in Fort Collins, Colorado, in case you were wondering) 
You kept that one quiet Colin, I thought an Englishman's home was supposed to be a castle, and preferably in North London, not over there where Eric Cartman and Stan Marsh come from)

An antioxidant is a molecule inhibits the oxidation of other molecules

Oxidation reactions can produce free radicals. In turn, these radicals can start chain reactions. When the chain reaction occurs in the cell, it can cause damage or death to the cell. Antioxidants terminate these chain reactions by removing free radical intermediates, and inhibit other oxidation reactions. They do this by being oxidized themselves, so antioxidants are often reducing agents such as thiols.

Oxidative Stress

I found a great definition:-

An imbalance between oxidants and antioxidants, in favour of the oxidants, potentially leading to damage is called oxidative stress.

Wikipedia itself has gone for a dumbed down version:-

Oxidative stress reflects an imbalance between the systemic manifestation of reactive oxygen species and a biological system's ability to readily detoxify the reactive intermediates or to repair the resulting damage

 

I prefer the former definition. Every time I hear “detoxify, toxins or detox”  I assume I am talking to somebody who does not know which end of a screwdriver to hold.

Pro-oxidant

A pro-oxidant helps induce oxidative stress.

Let’s sum up again:-

• Glutathione (GSH) and Glutathione (GSSG) are dating, they are a redox couple.
• GSH is a reducing agent and antioxidant, during redox it loses electrons and is itself oxidized to form GSSG.
• GSH is the most important of the 3 most important antioxidants in your body.
• Free radicals are not always bad. They have both a positive/necessary role plus a negative/redundant role.
• Oxidative stress is always bad. The oxidants have got the whip hand.

 

Coming up in Part II

 

• Brain region-specific glutathione redox imbalance in autism

 

• Regulation of cellular glutathione

 

• Clinical trial of glutathione supplementation in autism spectrum disorders

 

• Glutathione precursors to raise GSH levels in plasma (N-acetylcysteine, whey protein)

 

• N-acetylcysteine in psychiatry

 

• And finally, having understood the science behind it, what you have all been waiting for, and what I was shocked find had already been tested:-  A Randomized Controlled Pilot Trial of Oral N-Acetylcysteine in Children with Autism

Glutathione (GSH) Part II

Glutathione (GSH) Part III


 

 

What's Up Doc?

Can you fix something without truly understanding it?

 

 

If you ask a brainy engineer, the type that designs jet engines or nuclear reactors, can you solve a problem without understanding it; the answer is likely to be negative.  If you ask the guy that fixes your car, he might say “dunno, but let’s have a go”.  I have never met a white coated medical researcher, so I cannot tell you how they would reply.

 

A long time ago I gave up on expecting experts to fix types of unusual problems.  Like the illuminated “engine malfunction” light that sometimes appears in my car, like why did the radiators in my house bang and clank as they warmed up and later as they cooled down (it's not air in the system).  Why did my environmentally friendly solar panels make a noise like they were about to explode? The list grows longer.  Having solved all these problems and some others, I moved on to healthcare.  Why did my chest hurt when I sneezed? very funny to watch, instead of my reflex being to cover my mouth, I would hold my chest.  Then I even started giving medical advice to my Mother, a doctor herself.  But I digress.

 

If somebody had asked me, prior to Christmas 2012, "so Peter can you fix Monty?" then the best I could have said would have been something dull like:-

  

Autism is an incurable condition that you can manage, but you cannot reverse or cure it pharmacologically. Maybe one day there will be a cure, but too late for us.  Using behavioural techniques Monty has made great strides forward.  He can walk, run, ski, swim, read, write, do basic addition and subtraction.  He has emerging understanding of Wh- questions.  When asked a specific question he may make a short verbal reply, or he might totally ignore the questioner and the question.  A lot depends on who asks the question.  He sometimes suffers from stereotpy (aka stimming) particularly at school and this can makes it hard to complete simple academic work.  He may sometimes disrupt the class, even though he has a 1:1 assistant.  When his brother, Ted, asked if Monty will ever learn to drive I answered “maybe, maybe not, let’s hope for the best”

 

 

 

Three months later, and two months after everybody now knows about the Bumetanide Epiphany, my wife says to me out of the blue “Do you think you can really fix Monty” and even “What’s up, Doc”. Well, I never said I could or would fix him, but at least I am going to have a dam good try. Ted’s odds of getting Dad’s old Triumph Spitfire all to himself are slipping daily from odds-on favourite. If they slip to 50% my job will be complete.

 

 

So, can I fix something without truly understanding it?

Well, quite possibly, but the more I understand the problem, the better are my chances.

In neurobiology nobody fully understands the subject.  It is a work in progress. By the time Monty and Ted draw their pensions, it will still be a work in progress.

 

 

We speak your language - Ми говоримо ваш језик

I am pleased to  see that most people reading this blog are not native English speakers.

Dule ("Doolay", for those English speakers)  has very kindly offered to translate the useful parts of the blog for his friends into their language.  The nice people at Google have fortunately made that job a little easier, but as you can see below, they know some languages much better than others.
 
This blog has a translate feature.  Just look under the duck on the skateboard and you will see a Google Translate button.  (Sadly, the Google search this blog feature is not yet working)

           TRANSLATE

Select Language  

 Click the little down arrow and take your choice.

  

Ми говоримо ваш језик

Видим да већина људи читају овај блог нису Енглески матерњи језик.

Овај блог има за превод функцију. Само погледајте под патком на скејтборд и видећете Гоогле Транслате дугме.

         ТРАНСЛАТЕ

         Изаберите језик

Кликните на малу стрелицу надоле и да свој избор.

  

 

Акожелите да чујете нешто врло смешно, идите до главног Гоогле транслате вебстранице и кликните на малу слику говорника.Тада ћете добити аудиопревод. Звучи као кинески са веома лошимпрехладе.

 

 

Nous parlons votre langue

Je vois que la plupart des gens qui lisent ce blog ne sont pas de langue maternelle anglaise.

Ce blog a une fonction de traduction. Il suffit de regarder sous le canard sur la planche à roulettes et vous verrez un bouton Google Translate.

TRADUIRE

Sélectionnez la langue

Cliquez sur la petite flèche vers le bas et faites votre choix.

 

Google parle très bien français. Moi, je fais de mon mieux. Mais je peux apercevoir quelques erreurs. (traduit par Google)

 

 

 

 

私達はあなたの言語を話す



私はこのブログを読んで、ほとんどの人が英語のネイティブスピーカーではないことがわかります。

このブログは翻訳機能を持っています。ちょうどスケートボードのアヒルの下を見て、あなたはGoogle翻訳のボタンが表示されます。

TRANSLATE

言語を選択

少し下向き矢印をクリックし、あなたの選択を取る。

If you are looking for a clever comment in Japanese, dream on !

 

Nom de guerre, Mon frère - Manchopathy

Today’s post had better be a quick one.  The desk research in the background is getting complicated and I have just ordered a 900 page book on Human Physiology, so as not to spout complete nonsense.  Worse still, a couple of days ago, I received in the mail, a big brown envelope from Tokyo with a juicy report on the use of Ceredist, a TRH analog.  It is 20 pages long, and the bad news is that 18 pages are in Japanese.  The good news is that I had expected all 20 pages to be in Japanese.

To business.   You are slowly being introduced to the cast members of this blog.

The star of course is “Monty”, aged 9.

His supposedly “typical” big brother, aged 12, is going to be called “Ted”.

Head of Applied Research, part-time biker and Speech Therapist will be called Dule (“Doolay”)

Last week I decided that it was time for some good old fashioned primary research, to test a hypothesis that I had formulated.  This is what we presented to the in-house ethics committee, for approval:-

1.    Many children with autism exhibit what appears as sensory overload.  On hearing a moderately loud sound, they will cover their ears, almost as if in pain.  Bright lights, darkness, certain smells, even touch can trigger similarly strong reactions.  Entire books have been written documenting these odd behaviours, but I never read an explanation for them.

2.    In my trawl through the literature, I noted that a disorder with surprisingly similar symptoms has been documented -   Hypokalemic sensory overstimulation

This disorder manifests itself as an overwhelming feeling of sensory stimulation.  But then disappears 20 minutes after a dose of oral potassium.  A related, but much more severe, disorder that causes temporary paralysis also exists -  Hypokalemic periodic paralysis

3.    The recommended daily amount of potassium for adults is 3,500mg.  A typical banana contains 400 mg of potassium. A dissolvable tablet of Potassium Citrate contains 500mg of potassium.  So 500mg is a safe dose to experiment with.

4.    A laboratory experiment is proposed using an MP3 file of a baby crying. Dule will first establish a baseline volume (VB) at which Monty will cover his ears. Monty will be sitting in a fixed position in the lab. This test will be repeated over a few days to see if VB varies.

 

5.    Then the subject will receive 500mg of oral potassium and wait for 20 minutes. The MP3 file will be played again while he is sitting in the identical test position. Dule will crank up the volume and note the new threshold volume (VT).

 

6.    The same test will be repeated with Ted and Dule as subjects.

 

Prior to providing Dule with the oral potassium solution, Peter suggested to Dule that he would perhaps prefer if the test did not show up anything worthy of further investigation.  Since that would again drive Peter crazy, that no serious scientist had noticed this, done something about it and published their work.

Here is the raw data from the test:-

 

Volume * at which sound becomes disturbing
	7-Mar-13	8-Mar-13		11-Mar-13		11-Mar-13
						after K+
Monty	9	9		9		16
Ted				23		26
Dule				21		23
* sound level on digital display of Philips mini HiFi
room is about 20 m2, subjects were 2.5 m from HiFi unit

 

Discussion

As you see, Monty is far more sensitive to sound than both Ted and Dule.  Monty experiences a sharp increase in his capacity to cope with sound stimulation after drinking the potassium.  Ted and Dule show a small increase in capacity, that may be just down to measurement tolerance/error. (Dule was testing himself, after all)

Mon Dieu!  It looks like we have to do a serious follow on study with more subjects and some flashy equipment.  Worse still, now I have to be able to explain scientifically why this is happening !

 

The cause is related to something called VDCC (voltage dependent calcium channels) these are like little valves that open to let  Ca²⁺ ions in or out; they are misbehaving.   Recall that Bumetanide works in a similar way by triggering NKCC1 and NKCC2 (Sodium, Potassium, Chloride Cotransporters) to let in/out  Cl^- ions.  The subject of misbehaving ion channels has already been given a fancy name by scientists, its Channelopathy.  Now I was wondering how I was going to explain my use of French in this post.  It's all about the English Channel or should I say la Manche, and so we'll call it Manchopathy.

 

 

 

Beware of Men in White Coats - plus some interesting research

I am not quite ready yet to start presenting my own research findings.  They will start appearing in a few days.  In the meantime there are a couple of very readable papers from two different sources that are well worth looking at.

The first paper is a review of drug therapy in autism.  It was written in 20102 and includes more drugs than appear in comparable literature written in the US.  As a matter of interest, it was written by Indian scientists, but published by the Polish Academy of Science.  It is open access, so you can download it in full.

It is highly readable and even includes Bumetanide, my original epiphany drug.

Well done Baldeep Kumar et al from Chandigarh.  If it was up to me, all parents of kids with autism would get a copy of your paper Drug therapy in autism: a present and future perspective.  At least they would then have a sound factual understanding of what is available and what is on the horizon.

 

The second paper sounds even better:- Novel and emerging treatments for autism spectrum disorders: A systematic review.  It is also free to acces the complete paper.

It is published by the American Academy of Clinical Psychiatrists.  I have no idea who they are, but the name sounds very impressive.  The paper is certainly worth your time to read and undoubtedly took a great deal of desk research.

However, as I pointed out in my earlier post, about primary and secondary research you have to be very careful who is analysing the data.  It is best to do it yourself, whenever possible, or failing that contact Baldeep in Chandigarh.  Always read the label, even if you are one of those people that cut them off.  The paper is written by an author who is so prolific even my desk has got 5 of his papers lurking on it.  He is a big believer in the merits of hyperbaric oxygen therapy. The problem is I also have 2 papers on my desk that are highly critical of how he interprets his research data.  I think he may be suffering from Autistic Stress Syndrome (ASS) that I introduced in an earlier rather harsh post.

In her paper, Doreen Granpeesheh really lays into his powers of analysis and data interpretation.  Look at the bottom of page 272 if you are interested.

The other paper I have, really trashes the author.  Enough said.

Beware of Men in White Coats.

 

The risk of doing nothing

Everything you do entails some level of risk.  What is important is to understand the risk and takes steps, where necessary, to mitigate it.  We do this every day, even if we do not realise it.

 In the field of autism there are many risks to consider in daily life.  Many of them are the same risks that apply to very young typical children;  running out into the road without paying attention to the traffic, falling into an unattended swimming pool, even touching a hot iron, or hot pan on the cooker.  These are risks you can mitigate by good parenting.

When it comes to chemical/pharmacological interventions extreme care should be taken by the parents.  This puts them in an awkward question.  They undoubtedly want a miracle cure and thanks to the internet there is no difficulty in accessing them.  When such therapies are put forward by actual medical doctors, mainly from North America, you can hardly blame the parent for turning off their built-in risk assessor.  The doctor must know best.

I am not going to give you a list of the various chemicals/supplements/drugs that some parents are even injecting into their kids.

I think you need to do your own risk assessment of whatever intervention(s) you are going to use, be it behavioural, chemical, musical, swimming with dolphins etc.  If you are not able to assess the risk, then best not to take it.

If there is no downside, it is not going to be the end of the world if there turns out to be no benefit.  It may just lighten your wallet a little.

For me, the biggest issue has always been the risk of doing nothing.

 

My own experience with risk

I have taken some seemingly big risks in my time, but because I usually took mitigating action, I never came to regret them.  I travelled once from Delhi, up through floods in Nepal, across the Himalayas to Tibet, across to Hong Kong, then back to Beijing and across what was then Soviet Russia, to Moscow, then East Berlin over to the English Channel and home.  This was all done over land with public transport.  I came back without even a scratch, although several kilos lighter.

When you stop thinking about the risks, is when trouble will find you. A year after graduating from Imperial College, I heard that my favourite professor, Neil Watson, a world renowned expert on turbochargers (page 2 of link), had fallen off a ladder at home and killed himself.  Many years later, I nearly killed myself, on my own building site, falling backwards into an empty swimming pool.