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Tuesday, 25 August 2015

Vienna and some selected Autism History


  
Monty aged 12 with ASD, “You have been transformed into an Australopithecus afarensis, you walked upright more than 3 million years ago. Your picture is attached. This morphing-station is a co-production between Naturhistorisches Museum Vienna, Austria and the Smithsonian Natural History Museum in Washington”


We can never know if they had autism 3 million years ago, but it certainly is not a recent phenomenon.  Today’s post, prompted by a visit to Vienna, is a collection of historical episodes that I thought I should include in this blog, before I forget them.

Austria, as well as being home to an excellent natural history museum, where you can see what your children might have looked like had they been born 3 million years ago, is the home of autism. 

Both Hans Asperger and Leo Kanner were Austrian.  Kanner was later educated in Berlin and then, being Jewish, had the foresight to emigrate in 1924 to the US. In 1930 he developed the first child psychiatry service in an American pediatric hospital at Johns Hopkins Hospital.  He published his research on autism in 1943.  His narrowly defined type of autism became known as Kanner’s autism or classic autism; however if you read his actual case histories below you will see that they include quite high functioning people as well


                   
Kanner clearly made a valuable contribution, but he also had some odd ideas, like autism is just a childhood condition, so adults cannot have autism and that autism is extremely rare.  He thought that if a patient had epilepsy they could not be autistic. He also famously suggested that autism was caused by refrigerator mothers.

But unlike all the doctors who preceded him, at least he wrote down his findings and sought out public attention.

Hans Asperger, presumably not Jewish, eventually became chair of pediatrics at the University of Vienna.  In 1943 he published, in German, his paper on autism that focused on gifted children and what would become known as Asperger’s syndrome. 


The paper was finally rediscovered in 1991 and translated into English by Uta Frith.  Thereafter in the English speaking world, people could finally be diagnosed with Asperger’s Syndrome.  Personally I think it is a very useful/clear diagnosis: - no speech delay, no cognitive dysfunction, just the trademark differences of mild autism.

It later became known that while he may have published research on very high functioning people, he also had many patients who were low functioning.  The reason Asperger highlighted the gifted children was that during World War 2, the Nazis had a program called Aktion T4, which was set up to kill people with disabilities (unable to work).  People with Down syndrome, epilepsy, mental retardation etc. were removed from their residential institutions or homes and given a lethal injection or just carbon monoxide poisoning.  The family later received a letter that the child had sadly died of pneumonia.

At Schloss Hartheim, near Linz, two hours west on Vienna, about 30,000 people were killed, including those selected under Aktion T4.

So not surprisingly, Asperger did not write about those with autism without special gifts and talents.





Schloss Hartheim


Great Ormond Street Hospital, London 1877

Twenty years even before Johns Hopkins Hospital had been founded in Baltimore, children with epilepsy, “autism” and GI problems were being treated in London at Great Ormond Street Hospital, today of Europe's top children's hospitals.

They were using a very early drug to shift the excitatory/inhibitory balance of the neurotransmitter GABA.  It was Potassium Bromide, which is still used today in Germany to treat children with epilepsy.  Of course back in 1877 they did not know why it was effective.  Below is a link to a fascinating chapter of a book.




In 2015 this same hospital would tell you that autism is untreatable and that GI problems are not comorbid with autism.

At some point I will be writing a post all about Potassium Bromide and autism.


More History

For those of you who despair sometimes about the low level of knowledge and understanding regarding autism among healthcare providers and even supposed “experts”, I suggest you look back at the history.

As is often the case, history holds many of the answers.

Until relatively recently most children with disorders like Downs Syndrome or classic autism were sent from a very young age to live in so called “homes for the feeble minded”.  In recent times this occurs far less common and nobody uses terms like feeble-minded, but nonetheless difficult to control children are still put “into care”.

It really was a case of out sight being out of mind.

As we saw in the data on Down syndrome in the US, life expectancy was extremely short in these massive institutions where the kids lived in dormitories.  The average being only 10 years as recently as 1970.

As in Austria and Germany, in the US being sent to a home for the feeble minded was very often a death sentence, albeit a slower one.  The Germans even went as far as to financially justify their actions by quoting the cost of keeping a child in an institution for 10 years (the same life expectancy of Down's kids in the US, just 50 years ago).

Given this backdrop, not surprisingly everybody kept quiet about autism, almost nobody was interested in treating it and nobody would dream of using the word autism, for someone who was fully verbal and not mentally retarded.

So it is hardly surprising that there are/were very few older people with autism, or indeed Downs Syndrome.


Homes for the Feeble-Minded

There were numerous Homes for the Feeble-Minded in the US and across the world.  Here are some examples.





Maine School for the Feeble-Minded



Throughout its first 40 years, Belchertown operated mostly without scrutiny from outside sources. Author Benjamin Ricci (whose son lived at the school, and who later led a class-action lawsuit protesting the conditions there) referred to the conditions as "horrific", "medieval and "barbaric". Doctors at the school had little regard for patients' mental capacity, evidenced by this quote:

His method of evaluating me consisted of looking me over during the physical exam and deciding that since I couldn't talk and apparently couldn't understand what he was saying, I must be an imbecile. [...] Since I couldn't ask him to speak up or repeat what he said, he assumed I was a moron

The horrendous conditions at Belchertown were revealed in 1971 in a newspaper article entitled "The Tragedy of Belchertown". Parents sued the school, and when the state Attorney General toured the facility, he described it as "a hell hole".



In Michigan they even gave a special mention to those with epilepsy:

Michigan Home for the Feeble Minded and Epileptic



Why feeble minded?

Going back 110 years in the United Kingdom, you can see where terms like feeble minded came from:


They disallow the name of “Lunatic” and “Asylum” and classify the mentally defective as follows:-
·          Persons of unsound mind (who require care and control).
·          Persons mentally infirm (who are incapable of managing their own affairs)
·          Idiots. Defective in mind from birth.
·          Imbeciles. (Capable of guarding themselves against common physical dangers, but incapable of earning their own living).
·          Feeble-Minded. (Persons who may be capable of earning their own living under favourable conditions, but are incapable of competing with others or managing themselves).
·          Moral Imbeciles. (Persons who display some Mental Defect with vicious or criminal propensities on which punishment is no deterrent).
·          Epileptics.
·          Inebriates.  All of these three are considered Mentally Defective.
·          Deaf, Dumb and Blind.


Almost all such people were, in effect, locked up. In the UK at that time there were 149,628 such people deemed to be mentally defective.  That is 0.4% of the population at that time.




Modern Times

In rich western countries large “out of sight out of mind” institutions are a thing of the past.  They still exist in some other countries.

Now that at least some children with disabilities are educated in the community, or at least live at home many things began to change.  

The incentive to hide your disability was replaced by an incentive to promote it.  For each child with a diagnosis extra money is allocated to the school district (in the US) and in many countries families are entitled to weekly or monthly benefits payments.

Changes to diagnosis began to be made such that children with MR/ID were now diagnosed as having autism, boosting prevalence.

Then from the 1990s onwards came the boom in diagnosing Asperger’s in children and then later diagnosing Asperger’s in quite old adults.  

Finally, just to confuse everyone, in the US at least, Asperger’s has been merged into autism.

Once a rare condition, autism has become anything but; all over the period of 20 years. But it is not the same autism.

Even though the science is clearly indicating that within autism are numerous separate biological disorders and as many as 1,000 genes are involved, the US psychiatrists, with DSM5, have decided that it is all just “autism” and you are ranked on a scale of 1 to 3 for severity. I would have thought 1 to 300 might have been more reasonable.

The key discriminating factors like regressive or not, MR/ID or not, epilepsy or not, speech delay or not are not seen a relevant.

As a result the modern diagnosis of “autism” then just begs the question “what sort?”

Better to forget about “autism awareness”; much better to explain what autism really is and how certain types can be treated today based on existing hard science.



Dr Wakefield

Until Dr Wakefield published his paper in 1998, few people were familiar with autism, because nobody spoke about it.  Talk of the MMR vaccine and autism created fear among parents.

In the end Wakefield did a great deal of harm, even though much of what he said was actually true.  There is an unwritten rule that must not be challenged, “vaccines do no harm”.

As Martha Herbert pointed out, everything regarded as “Wakefield” became taboo, and research in those areas became un-fundable.  The link to GI problems is one area she highlighted and is still disputed by many, but not Boston Children’s Hospital, supposedly the number one Pediatric hospital in the world.   


Hannah Poling

As was shown in the legal case brought by US neurologist Dr Jon Poling, regarding his daughter Hannah, children with mitochondrial dysfunction can suffer an inflammatory response to multiple vaccines that can trigger mitochondrial damage leading to profound autism.  This doctor meticulously documented his case and was awarded compensation of $1.5 million plus $500,000 a year thereafter. 

It turns out that in the last 25 years the US government has paid out $3 billion dollars in compensation for childhood vaccinations (see table below).

It was expected that this case would act as a precedent to later cases, opening the flood gates so to speak.  It did not.

In this case Dr Poling was much more effective that Wakefield.  He made his point and kept his medical license.

But the public health interest in vaccination programs is immense.  Hundreds of millions of lives have been saved by vaccines and nothing is going to be let to get in the way of that.  Vaccines are effective once a critical mass of people have taken them, (Herd Immunity).  So in theory it would be fine for certain groups not to be vaccinated, like those with genetic mitochondrial dysfunctions.

As Dr Poling pointed out, quite a large minority of people with autism do have mitochondrial disorders; even Dr Kelley from Johns Hopkins has referred to this.
 




Herd Immunity

When a critical proportion of the population becomes immune, called the herd immunity threshold (HIT) or herd immunity level (HIL), the disease may no longer persist in the population





It should be noted that in about 2% of people vaccination may fail to provide immunity.   In the case of influenza you have to know which type of virus to protect against.


  
Here is Dr Poling’s response to the highly sceptical Dr Steven Novella, an American clinical neurologist and assistant professor at Yale University School of Medicine and a blogger. Novella is best known for his involvement in the skeptical movement. He had written about the Hannah Poling case on his blog.


Dear Dr. Novella,

Your assertion that the scientific question of Autism etiology belongs to the medical community rather than Hollywood Stars is correct.  I also agree that Hollywood opinions are more likely to be broadcast to millions because of their position in the media.  This heightened awareness is nothing but a positive thing for the million families struggling with this difficult, and all too common, disorder.  Jenny McCarthy is an Autism Mom looking for answers and rattling some cages—good for her.  Amanda Peet is a new mom who believes in the importance of vaccines to protect her baby—good for her too.  Don’t attack the moms, listen to them.   

These issues are very complex as we exchanged before and not amenable to soundbites.  Regarding your entry on Hannah’s case, your blog entry unfortunately propagates several of the mistakes from the media.

In criticizing the journalism of Mr. David Kirby, you wrote:

“He refers again to the Hannah Poling case, a girl with a mitochondrial disorder who developed a neurodegenerative disorder with “features of autism” after getting a fever from vaccines.”

Actually—Hannah has diagnoses of DSM-IV Autism (by JHU/KKI psychology) and mitochondrial disorder (by two metabolic experts).  The only ‘degeneration’ that occurred (along with 6mos of total growth failure) after 18mos of NORMAL development followed vaccination and nothing else! Of course, any ‘scientist’ can obviously point out that temporal correlation in a single case never proves causation. Rule number one of pediatrics though is “LISTEN TO THE MOM.”  Are 10s of thousands of autism moms over the last decade suffering from mass hysteria induced by Hollywood?  Not likely.

You also noted:

“This special case - which is not a case of autism being caused by toxins in vaccines - says nothing about the broader vaccine-autism debate.”

The only thing unique about my little girl’s case is the level of medical documentation—5 to 20% of patients with ASDs have mitochondrial dysfunction.  Many other cases where mitochondrial testing is WNL is because "we never looked" not because the testing would be "within normal limits."  Most mitochondrial experts will tell you that the dots of autism and mitochondrial disorders are strongly connected.
Finally, you say:

“The case was settled (not judged in Poling’s favor, but settled) because both sides realized it was a special case that could not be extrapolated to other vaccine-autism cases.”

The case was not settled, it was conceded by medical representatives of Sec HHS.  We are obviously pleased with the HHS decision to concede our case, but we had NOTHING to do with the concession.  This was a unilateral decision from HHS (recall that HHS is the respondent, rather than the vaccine maker, as manufacturers have blanket liability protection afforded by the Vaccine Injury Program established in 1986)  I will not speculate on the obvious question—why concede?   Hannah’s case was positioned to set precedent as a test case in the Omnibus Autism Proceedings for potentially thousands of other cases.
With regard to the science of Autism, I have no argument with the assertion that a single case does not prove causation of a generalized autism-vaccine link.  What the case does illustrate though is a more subtle point that many physicians cannot or do not want to comprehend (ostensibly because vaccines are too important to even question).  Autism is a heterogeneous disorder defined by behavioral criteria and having multiple causes.  Epidemiological studies which have not found a link between autism and aspects of vaccination do not consider the concept of autism subgroups.  Indeed, in a heterogeneous disorder like Autism, subgroups may indeed be ‘vaccine-injured’ but the effect is diluted out in the larger population (improperly powered study due to inability to calculate effect size with unknown susceptible subpopulation).   I think former NIH Director, Dr. Bernadine Healey explained it best in that population epidemiology studies are not “granular” enough to rule-out a susceptible subgroup. 

Furthermore, ‘science’ has not systematically studied the children who fell ill following vaccination to determine what the cause(s) for their adverse reaction was.  It would follow that if you never tried to understand why a single child developed encephalopathy following vaccination—you wouldn’t have the first clue as to what aspects of vaccination you could alter which could increase the relative risk of that adverse event (whether it be thimerosal, live virus, or ‘too many’). Could the susceptibility be a mitochondrial genetic haplogroup similar to Chloramphenicol toxicity—sure it could!  Why did a few Alzheimer’s patients die of fatal encephalitis following administration of the failed AN-1792 vaccine, but the majority had no ill effects (vaccine didn’t work though)? 

Definition:  Autism is a heterogeneous systemic disorder with primary neuropsychiatric manifestations due to complex genetic and gene-environmental interactions likely affecting synaptic plasticity early in childhood development.  This new theory of Autism is rapidly replacing the ‘old guard’ dictum that Autism is a genetically predetermined developmental brain disorder of synaptic formation/pruning that is set in motion prenatally.  By the ‘10 year rule of science,’ your time is about up! 

Until the biological basis of ASD subgroups are better understood, further epidemiological and genetic studies regarding “Autism” causation will be relatively meaningless.  We need good science to be able to address these complex issues which parallel nicely the emerging story of genetic and environmental influences in Parkinson’s disease.  Perhaps some Parkinson’s researchers want to take a crack at Autism?
Recommended SCIENCE reading for the evening:
 
Altered calcium homeostasis in autism-spectrum disorders: evidence from biochemical and genetic studies of the mitochondrial aspartate/glutamate carrier AGC1. Mol Psychiatry 2008 Jul 8.  (The discussion includes thimerosal as a potential toxin that could trigger further perturbations of calcium homeostasis leading to neuronal injury—and in a mainstream Nature publication no less)

Thank-you Dr. Novella and his band of skeptics for continuing the debate.

Dr. Jon Poling
Jon S. Poling MD PhD
Managing Partner, Athens Neurological Associates
Clinical Assistant Professor, Department of Neurology, Medical College of Georgia
Diplomate, American Association of Neuromuscular and Electrodiagnostic Medicine
ASN Certified in MRI and CT Neuroimaging
                               


In the US there is $0.75 levy on childhood vaccines to fund a compensation scheme.









By the 1980/90s almost all of the huge institutions for “feeble minded” children had been closed in the US and other Western countries.  The understanding of autism among medical practitioners did not really change.  Finally Asperger’s old papers were translated from German into English and in the 1990s large numbers of children started to get diagnosed with Asperger’s syndrome.  The stigma of such a diagnosis was no longer as it would have been a few decades before.




Conclusion

It is rather odd that many people’s points of reference regarding autism still date back to those two Austrians, Kanner and Asperger, from 1943.

Neuroscience has moved on a fair way since world war two, but in many ways autism has not.  In some ways it is now going backwards.

The main change is the surge of interest in Asperger’s, which is now, unhelpfully, being referred to simply as autism.  This does a great disservice to those with what used to be known as autism.  They generally cannot speak up for themselves and really do need customized medical treatment.

People with Asperger’s are more than capable enough to decide for themselves whether they want/need to treat their condition.

Fortunately researchers probably pay little attention to what is (mis)reported in the mass media regarding autism and the so those research papers will keep coming.

Drug firms have been struggling for decades to come up with new treatments for neurological disorders.  Apparently the disease likely to be first “overcome” is Parkinson’s.  Dr Poling did suggest in his commentary above that autism might benefit from some Parkinson’s researchers; maybe there will be some surplus ones sometime soon.

It is clear that no serious investigation of the type suggested by Dr Poling into the effect of vaccines on specific sub-types of autism will happen.  The link with mitochondrial disease and its treatment remains almost hushed up, even though the clinicians involved are at leading institutions (Johns Hopkins, Harvard etc.).  As one reader commented to me, “why is Dr Kelley’s work on mitochondrial disease and autism not published in the literature?”.

In reality, I expect that only a tiny percentage of autism can be traced back to vaccines, so there should be nothing for public health authorities to be fearful about.  Even Dr Poling remains pro-vaccines.

I am still shocked that in the US over $3 billion has already been paid out in compensation for damage caused by childhood vaccines.
 






Wednesday, 19 August 2015

Low Dose Clonazepam for Autism - SFARI Webinar with William Catterall








This post will be mainly of interest to the small number of people using low-dose clonazepam for autism and those considering doing so.

This therapy modifies the excitatory/inhibitory (im)balance between the GABA and Glutamate neurotransmitters.  The big advantage is that it should be very safe, is extremely inexpensive and, unlike Bumetanide, does not cause diuresis.   The disadvantage is that the effective dose is only in a narrow window, and you have to find it by trial and error.


Does it work?

It certainly does work in some children with autism.

It also appears to have an additional effect over Bumetanide alone, at least my son.

Questions remain:

·        Does it work with everyone who responds to bumetanide?
·        Does it only work in people with a Nav1.1 dysfunction?
·        Will bumetanide work in everyone who responds to Clonazepam?


One of my earlier, detailed, posts on this subject is this one:-



Just google “clonazepam epiphany” or use the site index, for the other posts.


Professor Catterall

I have already covered the science behind low-dose Clonazepam and Professor Catterall’s trials in two mouse models.  It is quite a complex subject and in the end most people just want to know does it work in humans with autism or not.

Catterall’s research was funded by the Simons Foundation, so no surprise really that he made a Webinar for SFARI.  It covers the ground of those two papers and indicates the next steps for his research.

It is a bit lighter going than his papers, but it is a full hour of science.

Catterall plans to trial it in humans with autism, starting with those known to have sodium channel dysfunction. So he is following the same pattern he used with his mice.

The first mouse model he used was Dravet syndrome, a rare condition leading to epilepsy and autism which is caused by a sodium ion channel (Nav1.1) dysfunction.  The second experiment used a standard mouse model of autism called the BTBR mouse model, so no connection with sodium channels.

My question to Catterall was whether this therapy would only work in people with a Nav1.1 dysfunction.  He did respond via the comments on the post, but did not really answer the question.  The fact that he plans to trial his idea on humans with autism with a known sodium ion channel dysfunction, does suggest something at least.

I think that since the actual mechanism of the drug is on a sub-unit of the GABAA receptor, sodium channels may actually be more of a coincidence, meaning that while autism Nav1.1 dysfunction may indeed indicate this therapy, it may be applicable in other autism where GABA is dysfunctional.


Bumetanide Use

The downside of bumetanide use to correct the E/I imbalance often found in autism is the diuresis and excessive loss of potassium in about 20% of people.

If you revisit the original paper suggesting an  E/I imbalance might be fundamental to many kinds of autism, you will see that this E/I imbalance is not just an ongoing issue, it is potentially an avoidable cause of disruption at key points in the brain’s development prior to maturation. In simpler terms, an E/I imbalance during development may cause the physical brain abnormalities often observed in autism.

That would suggest you should try and reverse E/I imbalance as soon as possible, well before maturation of the brain. 

One day an analog of bumetanide may be developed, that avoids the diuresis;  it is already being discussed.


Bumetanide (or low dose Clonazepam) use, even before autism has become established ?


In something like 30% of cases of classic autism there is macrocephaly (a big head), which even shows up on ultrasound scans of the pregnant mother.  A big head does not necessarily mean autism, but specific types of autism are clearly associated with big heads.

There are many other well known risk factors, like siblings with autism, siblings with other disabilities, older parents, family history (schizophrenia, bipolar, auto-immune conditions, COPD, Nobel Laureates, math prodigies) etc.

Since we also know that an indicator of this kind of E/I imbalance is that benzodiazepine drugs can show paradoxical effects (they work in reverse), it should be possible to make some kind of predictive diagnostic test.


So it would not be rocket science to identify many babies at elevated risk of autism and then treatment could be started very early and well before brain maturation.

This is rather like the Japanese researchers in the previous post suggesting that sulforaphane consumption in childhood might prevent susceptible people developing schizophrenia in adulthood.








Thursday, 13 August 2015

Sulforaphane Research in Japan – Cognitive Deficits and Schizophrenia






I recently received some papers about Sulforaphane from a reader of this blog and also comments from people with schizophrenia looking for therapies

Sulforaphane is already a valued part of my autism Polypill for Monty, aged 12 with ASD.  Just google "Sulforaphane Epiphany", or use the site index tab on this blog.

Sulforaphane has been patented for various purposes by John Hopkins, however even after twenty years they have not brought to market a standardized product.  The Sulforaphane (SFN) used in their research is made in the lab and then has to be kept deep frozen.

Sulforaphane is not a stable substance and so you are wasting your money buying most supplements.  Even most types of broccoli powder, which should be a precursor to Sulforaphane (SFN), were shown to be ineffective in independent lab tests.

In Japan it seems they are far more advanced, they already have a standardized SFN-glucosinolate tablets, no mention of the need to keep them frozen.


Japanese Sulforaphane (SFN) research

What is interesting in the Japanese research into cognitive deficits in schizophrenia is that SFN shows has both prophylactic and therapeutic effects.  This suggests that even if there is no immediate benefit from taking SFN in some people, there may be some long term preventative/protective benefits.




Oxidative stress and inflammation play a role in cognitive impairment, which is a core symptom of schizophrenia. Furthermore, a hallmark of the pathophysiology of this disease is the dysfunction of cortical inhibitory γ-aminobutyric acid (GABA) neurons expressing parvalbumin (PV), which is also involved in cognitive impairment. Sulforaphane (SFN), an isothiocyanate derived from broccoli, is a potent activator of the transcription factor Nrf2, which plays a central role in the inducible expressions of many cytoprotective genes in response to oxidative stress. Keap1 is a cytoplasmic protein that is essential for the regulation of Nrf2 activity. Here, we found that pretreatment with SFN attenuated cognitive deficits, the increase in 8-oxo-dG-positive cells, and the decrease in PV-positive cells in the medial prefrontal cortex and hippocampus after repeated administration of phencyclidine (PCP). Furthermore, PCP-induced cognitive deficits were improved by the subsequent subchronic administration of SFN. Interestingly, the dietary intake of glucoraphanin (a glucosinolate precursor of SFN) during the juvenile and adolescence prevented the onset of PCP-induced cognitive deficits as well as the increase in 8-oxo-dG-positive cells and the decrease in PV-positive cells in the brain at adulthood. Moreover, the NRF2 gene and the KEAP1 gene had an epistatic effect on cognitive impairment (e.g., working memory and processing speed) in patients with schizophrenia. These findings suggest that SFN may have prophylactic and therapeutic effects on cognitive impairment in schizophrenia. Therefore, the dietary intake of SFN-rich broccoli sprouts during the juvenile and adolescence may prevent the onset of psychosis at adulthood.

  


After giving written informed consent, participants received 3 tablets of SFN prepared by Kagome Co., Ltd. (Nagoya, Japan), totaling 30 mg of SFN-glucosinolate per day, for 8 weeks. It is known that SFN-glucosinolate is metabolized to SFN in the body.

Objective

Schizophrenia is a mental disorder characterized by severe cognitive impairment. Accumulating evidence suggests a role for oxidative stress in the pathophysiology of schizophrenia. Sulforaphane (SFN) extracted from broccoli sprout is an agent with potent anti-oxidant and anti-inflammatory activity. In this study, we attempted to evaluate the effect of SFN on cognitive impairment in medicated patients with schizophrenia.

Methods

We recruited a total of 10 outpatients with schizophrenia, all of whom gave informed consent. Participants took 3 tablets of SFN, consisting of 30 mg of SFN-glucosinolate per day, for 8 weeks. Clinical symptoms using the Positive and Negative Syndrome Scale (PANSS) and cognitive function using the Japanese version of CogState battery were evaluated at the beginning of the study and at week 8.

Results

A total of 7 patients completed the trial. The mean score in the Accuracy component of the One Card Learning Task increased significantly after the trial. However, we detected no other significant changes in participants.

Conclusion

This result suggests that SFN has the potential to improve cognitive function in patients with schizophrenia.

   
I do get comments from people with schizophrenia on this blog and there is clearly a big overlap between some schizophrenia and some autism.  More and more therapies are being shown to be effective in both; it seems to be the SFN is one of those therapies.

What would be nice would be a commercially available, standardized product that genuinely could be relied upon to produce SFN in the body.  The Japanese appear to have already mastered this.  No need for Johns Hopkins patents.

For the time being, I am happily using my Supersprouts broccoli sprout powder which does indeed seem to produce SFN.  If one day they stop making it, I have already found that you would just need to add heat stable myrosinase (in the form of daikon radish root) to otherwise ineffective broccoli sprout powder.

For those of you who tried other products claiming to contain/produce SFN, and found them ineffective, you do not know whether the child does not respond to SFN, or your product produced none.

  
Conclusion

SFN really does look worth a try, or perhaps even a second try for those who tried one of those “false” supplements.  Price does not always indicate quality.


One day I hope that the Japanese firm Kagome, chooses to sell its SFN tablets worldwide and not just their tomato ketchups and juices.