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Saturday, 14 November 2020

Averting Autism - Antenatal Antioxidants? But Male, Female or Both?

 



 Salem College

 

Today’s post is the first of two new ones about preventing/minimizing future autism.  The second post will be about Dr Ramaekers’ idea of using Calcium Folinate, which he has already put into use in human parents seeking to avoid autism in their next child. 

Before we start, I should point out that while readers of this blog, and it seems Dr Ramaekers, likely wish that autism and its symptoms did not exist, there are some people, well paid to research autism, who think autism is a good thing. I really do wonder why such people receive any public funding and wonder what kind of University would employ such people. It is like researching deafness, but not wanting to treat it - better they stay home.


https://www.sciencedaily.com/releases/2020/08/200824091958.htm

Simon Baron-Cohen, PhD, Director of the Autism Research Centre at Cambridge, who co-led the study, added, "Some people may be worried that basic research into differences in the autistic and typical brain prenatally may be intended to 'prevent,' 'eradicate,' or 'cure' autism. This is not our motivation, and we are outspoken in our values in standing up against eugenics and in valuing neurodiversity. Such studies will lead to a better understanding of brain development in both autistic and typical individuals."

Even more odd is that Baron-Cohen's sister had a rare mutation of the GNAQ gene that led to intellectual disability and a reduced lifespan. Why would you not want to treat/prevent that?  Treating your sister would not have meant you did not value her, it would have been another sign that you loved her. 

A positive example is another autism researcher, Manuel Casanova, and his family, who set up a research effort for people who have a disorder related to the gene NGLY1.  Sadly, Manuel's grandson passed away, but the research goes on.   

If you can escape from intellectual disability, someone should make it happen.  That someone might be you.

 

I must admit I had never heard of Salem College.  It is an all-female college in Winston-Salem, North Carolina.  It is the source of another idea to avert autism, this time treating the future father with an anti-oxidant like NAC.  NAC was already on my list for future mothers.  When it comes to autism, it looks like little Salem College is going to be more useful than stuffy old Cambridge University.

I am rather surprised there still are all female colleges, but in the US, there are many.

My mother went to an all-female college at Cambridge University, back then they had no mixed colleges.  Only after 1948 could women even receive a degree at the end of their studies. Cambridge University still has three all-female colleges.

Clearly male post-conception antioxidant supplementation is not going to help.

We have already seen in the research that the future father can damage the DNA he passes on to his offspring.  This was done via epigenetic tags on his DNA caused by things like recreational drug use, or smoking tobacco.

The author of today’s paper look’s exclusively at autism risk from the father, but exactly the same therapy during pregnancy can reduce risk from the mother.  The maternal immune activation model is one of the most studied in autism. We also know that emotional stress during pregnancy increases autism risk.  Emotional stress leads to oxidative stress.

The only issue I had with this preventative approach is whether there are any negative effects from antioxidants during pregnancy.  There may well be none, since the body just adjusts production of its own antioxidants.

There was an interesting experiment I mentioned a while back about giving antioxidant or “detox” juices to healthy young people.  The anti-oxidants from the fruits just made the body reduce its own production of GSH/glutathione, so the net result of the detox juice was actually negative.  People in oxidative stress benefit from anti-oxidant therapy, everyone else is wasting their money.

There are highly conflicting reports as to whether autism tends to come from the mother’s half of the child’s DNA or from the father’s half.  In reality it does not matter, it can from either, both or neither.  What is important is to take whatever simple safe steps you can to avert future autism. 

Future parents taking NAC and Calcium Folinate, might as well join the idea of keeping pets at home during pregnancy to get exposure to the evolutionarily expected bacteria that are needed to calibrate the immune system of the fetus/baby. Humans have been living with dogs, and very importantly their bacteria, for 11,000 years.  Only very recently did humans come up with the idea of trying to kill 99.9% of bacteria in their homes. 

Dogs are humans' oldest companions, DNA shows


I really do not see anyone doing a placebo controlled clinical trial on any of this.  Nobody who agrees to participate will accept the risk of being in the placebo group.  You would have to create a control group out of people who did not want to join the trial.  The people who join the trial are self-selected and are more likely to be health conscious, or have a family history of autism or dys-something else.


Male preconception antioxidant supplementation may lower autism risk: a call for studies

Current research indicates that a sizable number of autism spectrum disorder (ASD) cases arise from de novo mutations (DNMs) occurring within the paternal germline, usually in an age-dependent manner. Andrologists have reported that somatic cells and gametes share the same pathologies that generate these DNMs—specifically, DNA hypomethylation caused by oxidative nucleoside base damage. Because many ASD researchers seek to identify genetic risk factors, teams are developing methods of assessing aberrant DNA patterns, such as parental gonadal mosaicism. Several studies propose antioxidant supplementation as a strategy to lower autism risk, and/or suggest connections between childhood neurodevelopmental disorders such as autism and paternally-derived DNMs. Actual data, however, are currently not available to determine whether male preconception antioxidant supplementation effectively lowers autism risk. The purpose of this paper is to (1) explore the mechanisms causing DNMs, specifically DNA hypomethylation; (2) explain how antioxidant supplementation may lower the risk of having a child with ASD; and, (3) advocate for the implementation of large prospective studies testing (2). These studies may very well find that male preconception supplementation with antioxidants prevents neurodevelopmental disorders in offspring, in much the same way that female prenatal consumption of folate was found to decrease the risk of birth defects. If this is indeed the case, the alarming rise in autism prevalence rates of the past few decades will slow—or even cease—upon the initiation of public awareness campaigns.

  

Antenatal antioxidants to avert autism?

Paternally derived de novo mutations (DNMs) caused by oxidative stress (OS) have been implicated in the development of autism spectrum disorders (ASDs). Whether preconception antioxidant supplementation can reduce the incidence of ASDs by reducing OS is an area of uncertainty and potentially important future scientific investigation.

The recently completed double blind, multicenter, randomized controlled Males, Antioxidants, and Infertility (MOXI) trial by the Reproductive Medicine Network (RMN), funded by the Eunice Kennedy Shriver National Institute of Child Health and Human Development (NICHD), investigated whether antioxidants improve male fertility, as measured by semen parameters and sperm DNA integrity at 3 months and pregnancy by 6 months of treatment [11]. The RMN investigators found that antioxidant treatment of the male partner does not improve semen parameters, sperm DNA integrity, or in vivo pregnancy rates in couples with male factor infertility, prompting the question whether antioxidant therapy should no longer be routinely recommended for infertile men [12]. It would be intriguing to evaluate the offspring from the participant couples of the MOXI trial for ASD. However, with only 13 live births in the antioxidant group and 21 live births in the placebo arm, the study would be vastly underpowered to demonstrate a benefit of antioxidants in the prevention of a condition with an incidence of 1 in 54 children.


The next post is about Dr Ramaeker's clinical trial of calcium folinate in children with autism and his comments about their parents and future siblings.




 


44 comments:

  1. Yes, Baron-Cohen's view is shocking, I know an aspie that believes what he says :-(

    > People in oxidative stress benefit from anti-oxidant therapy, everyone else is wasting their money.

    Yes, that is the conclusion I have been coming to. I bought some NAC ages ago (thanks for the work you do here!) and have been taking it for the last few months. As an older, male, aspie I think it has alleviated my BPH a little, which is nice. Not too surprising as I think all of those factors can suggest more OS. It seems reasonable to me that many / most people with ASD have some degree of oxidative stress, so eating a varied diet and taking something like NAC is a good idea. Unlikely to do any harm, anyway, with a decent chance of helping.

    Aspie2

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  2. Dear Peter, what is your opinion on the broader theory of dr Naviaux? Since I watched his presentation on Synchrony, for the first time I realized that it answers every single question I have ever had about the strange nature of autism (and I’ve had many). Doesn’t mean its true, but somehow it all fits, and in my mind this points towards it being true. These days, its all I can think about. I am even considering trialing Malarone on my daughter. It has a great safety profile and a similar effect on ATP compared to suramin. It is approved for up to 12 weeks of daily use in infants even, so I can probably do a 2 week trial without any worries.

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  3. Dear Peter, what is your opinion on the broader theory of dr Naviaux? Since I watched his presentation on Synchrony, for the first time I realized that it answers every single question I have ever had about the strange nature of autism (and I’ve had many). Doesn’t mean its true, but somehow it all fits, and in my mind this points towards it being true. These days, its all I can think about. I am even considering trialing Malarone on my daughter. It has a great safety profile and a similar effect on ATP compared to suramin. It is approved for up to 12 weeks of daily use in infants even, so I can probably do a 2 week trial without any worries.

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    1. Tatjana, Naviaux is very bright and has an unusually broad understanding of autism, which comes out when you read his papers.

      I hope he is right and that his theory can account for much autism. More precisely, many different types of autism may share this common feature, that is potentially treatable.

      With more than 1,000 genes implicated in autism, it is unlikely that his theory will apply to all of autism, but his cell danger response might be triggered my many different things.

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    2. But isn’t the genetic factor rendered irrelevant by his theory? It proposes that you have a ‘canvas’ upon which the cell danger response activation plays out, and depending on that you would be having autism or asthma or csf, etc. if you are blind to the existance of the cell danger response issue, you would be grouping people into conditions through genetic tests, and it would all come out nicely. I am aware that there are mouse models of autism with this or that gene affected, but according to Naviaux, ATP can turn off or turn on genes as well.

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    3. Tatjana, I do not think any theory can explain all of autism.

      We know the effect of most genes and some in great detail. Reduced expression of some of these genes will directly lead to brain abnormality; it might also trigger Naviaux's cell danger response. If you turn off this response you will still be left with a somewhat malfunctioning brain.

      I think Suramin will reduce the severity of some autism, but not "cure" it. The question is how much it can reduce severity and in what percentage of cases.

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  4. I don’t believe Simon Baron-Cohen really believes autism is just a harmless difference he`s too smart for that. I believe he`s simply trying to appease the extremists in neurodiversity by pretending autism research is just casual scientific interest.

    I believe his approach is a mistake and dangerous, such statements only encourage them & reinforce delusional anti scientific misconceptions on what autism is which feeds back to the public. It would be a tragedy if years of autism research that could yield good potential treatments were to be put on hold to pursue a pointless “anti cure woke” style neurodiversity viewpoint that only benefits a minority at the top of functionality tree.

    Moving on to the point regarding genetic mutations caused in the paternal germline, smoking has dramatically dropped but autism rates have still steadily risen.

    I am interested in the concept of delayed or accumulated gene damage from that parents’ gene line (grandfather & beyond sorry forgot the term) that may be a factor.

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    1. Ross, if your Grandparents smoked, this is likely reflected on your epigenome. These markers are accumulated and are heritable.

      In many countries smoking is indeed now less common among younger adults, but that does not erase those epigenetic tags. Drug use among younger adults is widespread and will add some new ones.

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    2. Hi Peter! Thanks for all the amazing work you have done to help us parents, it means so much.
      My son started Bumetenide in August and I noticed a slight progress in m his communication. However, like with all the treatments I have tried for my son he reaches a point when he stops responding and right is reacting badly to even 0.5mg of bumetenide - he will get more angry and frustrated as he cannot communicate his needs. His MAPS dr keeps telling us it is gut dysbiosis causing his symptoms but nothing seems to work for him. I wonder if parasites could be the culprit.

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    3. If there are GI problems, then there may well be some kind of gut dysbiosis. If diet is good and there are no GI symptoms, then gut dysbiosis is unlikely.

      There are autism doctors that have a favorite diagnosis and overuse it. Autism can be all in the gut, but it can also have nothing to do with the gut.

      Parasites have to come from somewhere. In some parts of the world it is hard to avoid parasites, but in rich western countries it is much less likely.

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  5. I find probiotics to be the hardest to get into children who don’t swallow pills. All sachets etc have a strong taste and will often be rejected. I discovered today that we have on our market a probiotic chocolate made by a company called Chocowise. Its only a strain of bifido, but for those who have no other options this is great. We spent several months this year in spain and there we were able to buy a water based kefir which had just a sweetish taste so we added it to apple juice - if you are in western europe this is a good idea too.

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  6. Hi Peter, just wanted to say I loved your presentation at Synchrony! Having failed to be able to get Bumetanide thus far, despite my best efforts, I'm hoping to go back to the relevant docs and share your video so that they can better understand both the potential benefits and low risk.

    It was also great to see you on video and hear your voice.

    Again Bravo on the presentation!

    AJ

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    1. AJ, if you do find a doctor who wants to see the video, here is a link

      https://drive.google.com/file/d/15s_1x01VR2v-iMNpgbsFtt12Ug4xbGTh/view

      Dr Ben Ari also wanted to share it, so he also has the link. He gets asked by journalists about the effect of Bumetanide in autism and it is hard to explain with scientific papers.

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    2. Hi Peter,

      Thanks very much!

      This is much easier than my trying to share the video via the Whova app

      I will definitely share the video with our developmental pediatrician. She is great, and even considered maybe offering us a script, but then conferred with a specialist (I believe a nephrologist) and then said no as she wasn't comfortable.

      I will send her the video, as I had previously shared the Ben-Ari papers and Agnieszka's write-up (which was really helpful).
      I'll hopefully wear down our developmental pediatrician ;-)

      Peter, now that I know it's possible to share the videos from Synchrony this way, do you know if there is a version of Dr. Ben-Ari's presentation available? I'd like to share it with one of the researchers I'm working with, as I think the concept may be relevant to the researcher. I've drafted an e-mail to the researcher with a few of Dr. Ben-Ari's papers, but if I could add the video, that would be terrific. If you have it, and you can e-mail it to me if it can't be shared publicly (since I did attend Synchrony)

      Thanks Peter!

      AJ (deep in Canadian snow, dreaming of a tropical holiday after covid)

      P.S. Just wanted to share a very interesting answer Dr. Ben-Ari gave with the community. It was asked if increasing KCC2 activity would be the same as inhibiting NKCC1 activity, and Dr. Ben-Ari noted that it may not actually be the same, as KCC2 may be internalized by the cell rather sitting on the cell surface, and so increasing its activity may not help push Chloride out the cell since it would also need to brought up to the cell surface. So basically it's far easier to inhibit NKCC1 than it would be get KCC2 to both get to the cell surface and then increase its activity. Just wanted to get this out there if anyone was looking at KCC2 as I think it's quite an important insight

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    3. AJ, I gave you the link that I originally gave the organizer before it went to the Whova app. I do not know how to export from Whova, they probably do not want you to do this

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  7. Hello Peter,
    I just watched your presentation at Synchrony,and I decided to pop over to the blog,which I had not done in a couple of weeks.

    I am aware of Dr. Ramaekers work in giving leucovorin to women who have already had one autistic child,who is positive for the autoantibodies,and want to have more children,and how this can prevent autism in the next child.I assume that's what this study is about.

    As he says here,Simon Baron-Cohen is a big champion of neurodiversity.It must take a great deal of mental gymnastics to champion neurodiversity,when severe autism,with intellectual disability,is a big part of your life and research.

    Your work on Bumetanide,and the work Dr. Ramaekers and Dr.Frye have done on folate and B12 are exactly the type of research advocates of neurodiversity want to wipe out.

    As you,and some other longtime readers of this blog are aware,I was diagnosed with cerebral folate deficiency,due to very high levels of both blocking and binding autoantibodies.This was a secondary result of my being found to have pernicious anaemia,which I had lived with undiagnosed for many years.I would go on to get multiple other autoimmune diagnoses,and a diagnosis.is of a very rare DNA repair disorder,and what is likely a genetic disorder of innate immunity.

    My initial treatment with leucovorin and B12 followed what was my fourth major regression,so we were beginning from a new baseline.I was verbal,but low functioning,and in my late forties when treatment started.I was able to reverse the severity by about 75%,and live independently,although I still have all my medical issues.

    Dr. Frye probably considers me one of his most remarkable patients.

    Yet,there is an element of the neurodiversity movement,that believes such treatment,whether it be for cerebral folate deficiency,or the treatments you have used with your son,are akin to genocide against autistic people,or at the very least an eradication of the autistic person's identity.I'm sure you are aware one of the main inspirations for the neurodiversity movement,was the so-called "deaf culture".We saw a similar debate several years ago,when it became possible to reverse deafness,through cochlear implants.We will no doubt see this debate escalate as treatment options for autism and prenatal screening both become more widely available.

    As with organizations like Autism Speaks,here in the US,there are a lot of people in academic and research institutions,who are staunch advocates of neurodiversity.Many of these people either have very mild autism,diagnosed as adults,or are self-diagnosed.

    Are you aware there are those in the neurodiversity movement who believe severe autism does not exist?

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  8. Hi Roger, thanks for your extensive comment.

    The world of autism is rather a shambles; perhaps half of people in the US who think they have mild autism do not even meet the diagnostic criteria. Eric Fombonne published a paper a while back in which he re-assessed people with a medical autism diagnosis and found many people did not meet the criteria. You then have to add school-diagnosed autism (which unbelievably is possible in the US) and self-diagnosed autism.

    There is small group of vocal odd people with mild autism. Since delusions and over-thinking are sometimes symptoms of mild autism, we really should not be surprised.

    We only have to worry when a tiny number of such people take out their anger in ways like the Toronto van attack killer. He hated the world and neurotypical people so much he chose to kill a bunch of people and now seeks to hide behind his diagnosis of mild autism. If he had done this in the US, he might have ended up with the ultimate potassium supplement as his punishment.

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    1. Peter,Everyting I have read says children are being diagnosed with autism earlier and earlier.I associate school diagnosis with earlier times,when we knew a lot less about autism,but I guess milder cases could be diagnosed after a child has started school.I was diagnosed as a child in school,over fifty years ago.At that time,a child had to have pretty severe autism to be diagnosed at all.

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  9. Hi Peter

    Please can I ask what dose you will advise for clemastine, for how long should it be used for? Also how would one know if it’s working/helping .
    What’s the difference between clemastine and oxatimide, what to look out for?

    I am planning to add it to my poly pill for my boy of 6 years weighing 23kg.

    Thanks

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    1. Apinke, I would just try Clemastine. In the UK you can buy this OTC from a pharmacy, if it is not in stock, it is easy to buy online from a proper UK pharmacy, it costs about £11 for 60 1 mg tablets. The allergy dose for a 6 year old is 0.5mg morning and night. I suggest you try 0.5mg in the evening.

      Clemastine has two potentially helpful effects. The immune cells in the brain are called microglia, these cells are a bit hyperactive in people with autism which may mean they neglect their real job. These cells do the "synaptic pruning" which creates a well formed adult brain, just like pruning in your garden.

      The second benefit is improving myelination. Myelin is like electrical insulation. You need myelin so that the electic signals in your brain reach their intended destination.

      I think the benefit of clemastine will depend on the age of the person, because your brain goes through many steps until it matures in your mid 20s.

      In a 6 year old you might look for changes in cognition, but also improved gross/fine motor skills.

      In my son the change was quite subtle, he started to express his own opinions, rather than just following instructions.

      I think you should try the full pack of 60 pills, so 4 months, then decide if it is beneficial. Give it in the evening because it may cause sleepiness, because it is also an antihistamine.

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    2. Thanks Peter .I got it already from a pharmacy ,I will start tonight .

      Thanks for your help .

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    3. Apinke, we have used Clemastine 0.5mg twice daily for 1½ year in a child around 20 kg, somewhat younger than yours.
      It takes a few weeks to notice the change, it is subtle. Longer sentences, standing her ground better.

      /Ling

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    4. Thanks Ling

      I will give it a try

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  10. Hi Peter,

    Couple of questions,

    1. What do you think is going on with the Bumetanide stage 3 trials so many mixed results over the years, suddenly Bumetanide trials giving very poor results ( see link), no better than placebo they say. I understand different kids may not be responders but do you think this will kill off any chance of Bumetanide being licenced for autism, or is there more tests to go in stage 3?

    https://www.jaacap.org/article/S0890-8567(20)32074-8/fulltext?rss=yes

    2. Roger Kulp experience interests me, although I live in the UK, where would you recommend getting my son a test for cerebral folate deficiency here? (even privatly?) I can’t see my nhs doctor pursuing this, or is the UK a dead end for this kind of thing.

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    1. Ross, the Dutch researchers did a trial in people with mild autism. It had a large placebo effect in the control group. These researchers seem to want to use an EEG to predict who is a responder. They have the best intentions, but they are rather muddying the water.

      We know bumetanide works for many people with severe autism, and so as not to miss a responder, the best thing to do is to let all these kids try it.

      The Dutch are not part of the stage 3 trial. I expect by 2025 it will be approved in Europe.

      Folate receptor antibodies
      ==========================

      There seems to be just one lab doing this test. You have to take a blood sample, separate out the plasma and send to the US for the test.

      http://iliadneuro.com/

      You could ask a doctor in the UK to help you do this. He/she might think you are mad, but you might meet someone helpful.

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  11. Hello Peter, Friends, and Community,

    I just wanted to share a webinar I watched a few weeks ago from several researchers here in Canada (we have a lot of really good ones here), and the link is:

    https://www.autismontario.com/civicrm/event/info?id=4323&reset=1

    I had to register to watch it, and from memory, I think I chose to say I was an interested party and not a parent as they asked way too many questions of parents. I'm hoping that it'll still play (it says it should for 90 days after the event and we're still in that period)

    The reason I wanted to share this with the community is not necessarily for main reason for the webinar (the new findings about certain base pair repeats being found within ASD genes in new and more complex patterns) but for the wonderful explanation of how genetic mutations and other factors can result in ASD.

    Ny Hoang, a genetic counsellor at Sick Kids Hospital gives the single best overview of how ASD can arise due to a combination of genetics and other factors that I've ever seen, and it's the key piece for me in this webinar. It's a very simplistic analogy (Balls of different sizes in a cup) but works really well.

    Dr. Steven Scherer, who I believe is considered one of the world's top ASD geneticists also provides some really interesting comments.

    On a side note, when we were looking to get our daughter's genetic test done initially, I had contacted Dr. Scherer directly and he was wonderfully kind. We decided not go with Sick Kids at the time because they needed blood and GeneDx could do a cheek swab, so we went with the cheek swab, but but how incredibly nice he was throughout that process to an ASD he didn't know is something I'll always remember - a true gentleman.

    I would highly recommend this video to all ASD parents, but ESPECIALLY for those who aren't sure or don't believe their child's ASD is contributed to by a genetic mutation.

    The reason is that Ny Hoang's cup and balls analogy beautifully demonstrates that the cause of ASD likely isn't necessarily a binary choice of 100% genetic or 100% environmental, but that for the majority of ASD kids, it's likely a combination of several factors in both categories. So even if a parent feels that the cause of their child's ASD id not genetic, genetics may still be (and I believe likely does) contribute in some way.

    Why do I bring this up? I've had recent conversations about genetic testing with ASD parents, and those who will recall know that I'm a big proponent of genetic testing. I used a specific test and it was successful for us, and I think my rationale for using that test still holds true.

    The test I used can be expensive (~$3,000 US) and may not turn anything up (which shouldn't exclude a genetic contributor, but to me means that the test wasn't designed to catch that specific item, and some of the items may currently be unknown to science), but if you do get a hit, that insight can be lifechanging, and easily makes the test worthwhile (in my opinion)

    I hope this is helpful!

    AJ

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  12. Ross/Peter,
    I have been in a Facebook group for cerebral folate deficiency for years.In this group,we have had families from the UK,and Germany,who have gone to Belgium,to see Dr. Ramaekers.As far I know,there are no interested specialists in the UK.

    As for genetic testing,there are some who do not think a cheek swab is as effective as a test done with whole blood.My genetic diagnosis came from a whole exome sequencing done with whole blood,and it was done through GeneDx.

    It used to be the known cases of autism with genetic causes were in the low to mid single digits of percentage points,now with whole exome and whole genome sequencing,that number has crept up to about 10-15%.Many of these genetic causes are unique forms of very rare diseases,like mine is.

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  13. Hello Peter I saw your presentation it was great! My son has been on Bumetanide for almost 8 months now, he has had great advancements, he still struggles to have a conversation but he has been gaining more vocabulary, his teacher always asks him how is he, and he never responds, but this time he said ''I'm handsome'', he has been stimming a lot and walks on his tiptoes more often, I don't know if its a coincidence but exactly one year ago he started to walk like this and his stimming worsened, before Bumetanide. He still takes Verapamil, Cetrizine, Pentoxifylline and NAC. Only his skin condition is notorious, but no other symptom of allergy or illness is noticeable, though I still think that something is going on. He is more flexible when we go walking but he is inflexible in other ways, like if he's painting a triangle and I tell him that I'll draw him a square for him to paint it and he says ''No, it's not a square, this is a triangle'' I don't know if that's Abstract thinking that he struggles with.

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    1. Lisa, did you try Ketotifen? This might help with the skin problems and the research shows that it can prevent asthma developing, when give to young children at risk. Skin problems are often followed by asthma developing. This was covered in an old post.

      If calcium folinate (Leucovorin) tablets are available in Mexico, you might want to consider this a means to increase speech. The next post has more information on this subject.

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    2. Thank you for your response Peter, I didn't know that about Ketotifen, I trialed it but only for a few days and didn't give it a chance to act because I reintroduced Pentoxifylline at that time, but I will try it again, it seems a very good option given that he has had respiratory problems before.

      I read your most recent post about Leucovorin, it's very good news that side effects can be avoided, it was great you could talk with Dr. Ramaeker's and share the information. I can get it, but it seems the FRα autoantibodies test is not done here. Could it be safe to make trial the same as with other interventions?

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    3. I recently found this online store and I can't believe it's based in Mexico, they are shipping to Europe and Canada:
      https://cuerpoymente.mx/

      Delete
  14. Hello Peter, I wanted to ask for your help on my current self diagnosed autism.I have hard time making and holding conversations, spend all of my days behind the computer watching live streams/playing video games, but even watching these streams I understand the jokes that people make, but don't understand why people laugh, why people react the way they do, have a hard time understanding politics, overall social stuff and have no inclination to learn it, just want to stay behind the computer and do nothing just watch these streams, when I dont even socialize there, feel like a complete alien/socially underdeveloped human, just watching other people, I also stim to music by dancing, have something similar to hand flapping sometimes when I'm excited. My brother exhibits strong ADHD symptoms, very hard to focus in school, but very emotional/social guy, my father is engineer/businessman, who has temper/empathy issues, but is socializing on a normal neurotypical level. I was making myself L.Reuteri 6475 yogurt, which kinda helped me understand/react to social situations more normally ( I guess?), I laugh much more in social situations, react in tune with other people, but still I am very very socially behind. I wanted your advice/opinion on possible treatments/strategies, should I get genetic testing/officially diagnosed, or are there any possible medical conditions that could be ruled out that could cause these symptoms? I am thinking of doing FMT transplant in my country, also was wondering if any of bumenatide, transcranial magnetic stimulation, stem cell therapy, parasite treatment, chelation therapy could be of any help? Would very much appreciate your help/advice.

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    1. ZZZ, I think the oxytocin from L.Reuteri DSM 17938 (in Protectis and Gastrus products) is a really good idea.

      If you had the chance to use intranasal vasopressin, that would be well worth a try.

      https://clinicaltrials.gov/ct2/show/NCT01962870

      Low doses of Psilocybin are used by many Aspies. This is not legal, but makes perfect sense from a science point of view. These are not hallucinogenic doses. You probably can find out all about this on Reddit. It is all about Serotonin 5-HT2A receptors.

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    2. Thank you for your response, one more thing i wanted your thoughts about is, I feel like I'm on a lower scale of the aspergers spectrum and it feels like compared to other aspergers people I can't socialize at all/don't really participate in socialization except from watching livestreams like I said, it feels like my head is empty in conversations/dont care about any topics unless I try really hard, it doesn't come naturally at all. My parents say I act jkinda normal but I feel like I'm not even of average aspergers level of socialization, it feels like I just watch these livestreams or twitter feed with 0 thougths on any social matter/don't care about it, just to spend time doing something to not be absolutely empty minded, it feels like hell living not understanding the social world. Could this be a representation of classic autism or is it more likely aspergers type autism?

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    3. Also was wondering if any medication thats being researched/not available on the market would be possible to get to improve symptoms, like suramin or something like that?

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    4. ZZZ Self-diagnosis is another one of those controversial areas in the autism community.I would strongly suggest that as a first step,you seek out an evaluation for a diagnosis of ASD,and then go from there.I doubt any reputable clinician is going to approve any treatments without a diagnosis.It is getting more common for doctors to order genetic testing in autism,but it is still pretty rare.I got all of the genetic,and immune,testing I did,both because I was seeing MAPS doctors,and I had such a complex history,beyond the basic criteria for autism.

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  15. Also are any of the aforementioned, TMS stimulation, FMT, stemcell therapy, parasite/chelation therapy are of any possible benefit or I should not even bother trying?

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    1. ZZZ, the term Asperger's really was for people with no speech delay and with normal to high IQ, but with mild autism. You cannot have classic autism, since you write like a typical person.

      You could also try Agmatine, which is cheap and makes some Aspies feel better. You could also try the antioxidant NAC. The more extreme therapies are for more extreme autism, your issues sound like typical Aspie ones. Many Aspies have explored ideas to make them feel better / more social etc. Look what they are saying on Reddit and post questions there.

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  16. Hi Peter!
    I was reading through older posts.
    You wrote about choosing anti-oxidants depending on the kind of oxidative stress experienced in the body.
    How does one figure this out?

    (I have ME/CFS; there is a lot of overlap in dysfunction mechanisms with autism, I learn a lot reading your blog!)

    Thank you

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    1. cats, it is rather trial and error. You might want to trial NAC and then trial a sulforaphane producing product (Avmacol, Prostaphane, Broccomax etc). You might find that taking both together is the most beneficial. You might find neither help.

      CFS features activated microglia, as does autism, so you could try a low dose of Clemastine (normally used as an antihistamine) like 1mg in the evening.

      Lethargy in some autism responds to Agmatine. This is easy to try if you live outside the EU. Try 750mg once a day and see is you have less fatigue. If this one helps, please do let us know.

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    2. Hi Peter!

      I'm interested in using melatonin. It was here that I read of using it as an antioxidant. We do have issues around serotonin in ME/CFS and fibromyalgia too. Some people don't respond well to it - I'd like to try.

      I did try NAC a while back, 600 mg only and I didn't feel it did much. After reading through your blog, I thought maybe needed to take more of it. I will be trying it again soon, and now that you mention the sulfophrane... I have started taking MSM too (I try small amounts and then titrate slowly with everything). Is there a limit to how much sulfur one can have in the body, I wonder?

      I did then move on to straight cysteine. It had immediate effects with just the first tiny dose. There was a very visible positive effect on the quality of my tissues. As I started titrating up, within a few weeks - I wasn't able to sleep at all and spent the days in a daze/lethargy. It may have exacerbated an imbalance already present, or fed the dysfunction as I started smelling ammonia soon thereafter exuding from my skin.

      Since I started taking methylfolate and taurine, my ammonia levels have come down (until the above hiccup). Is ammonia an issue in autism as well? I think its build up may be one of the things behind the lethargy in ME/CFS. There is a research group in Australia studying nitrogen products: https://www.omf.ngo/2020/10/12/nitrogen-metabolism-and-testing-nitrogen-hypothesis-in-me-cfs/

      I have found that my MCAS status calms down a lot with methylfolate and taurine as well. I recently started quercetin - I know it's used as an antioxidant, and for MCAS too. I'm interested on the effect it may have on regulating 1-carbon metabolism and transsulfuration per this paper https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4629001/

      Taurine is my lowest amino acid and metabolomic studies on ME/CFS find taurine to be low. Supplementing it brings a level of calmness I don't think I have ever experienced in my life before. If I go off it (I ran out of it once!), my neurotransmitter business gets thrown off balance. It also has allowed for my magnesium levels to go up in bloodwork - they are borderline low and years of different forms of supplementation had not worked. I started taking magnesium again and this time, it seems to be working. Taurine is an osmolyte as well. I did titrate up slowly, to avoid negative effects and let my biome adjust.

      "Taurine modulates neurotransmission by acting on several neuroreceptors such as GABA and glutamate and acetylcholine receptors." I know these are common issues with autism.
      Have you or readers had experiences supplementing taurine, positive or negative I wonder?
      These are some interesting papers on it:

      "Effect of taurine on chronic and acute liver injury: Focus on blood and brain ammonia"
      https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5615919/

      "Taurine and its analogs in neurological disorders: Focus on therapeutic potential and molecular mechanisms"
      https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6536745/

      I think the first thing I used was palmitoylethanolamide, a bit before I started the methylfolate. I took it for four months and didn't feel the need to take it again somehow - I cannot explain it, cannot put my finger on it as to why that is. You mentioning microglia makes me wonder if I should, as it has an effect on them:
      https://www.nature.com/articles/s41598-017-00342-1

      I read your blog on agmatine.
      I don't respond well to the arginine in food items high in it. My citrulline levels are slightly raised (compared to everything else) - seems to be a common finding in metabolomic studies too. There is some disfunction in urea cycle, and I'm not sure how it would go with the agmatine. I decided to wait on that one for now.

      Thank you!

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  17. zzz, reading what you write it looks to me that regardless of asperger or not, you have emotional issues (as in biological, not talk-therapy type). i think it would be helpful to visit a maps or dan doctor who could do some basic autism related tests on you, metabolism function, immunology, OAT. for starters, you care that you don’t care. as it seems there is no outside pressure for you ti change, it is your own desire. find a maps or dan in your are and start there.

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  18. cats, I use taurine in a mix called Aminoplus Burnout, its designed to fill your storages of evrrything the brain uses in stress. considering that I have an asd child, I am in long term stress. i have used it for years now and it is essential for my wellbeing. 2 years ago I discontinued it and felt really good still but a few months ago the stores I had became empty and I had to get back on it. everyone I have shown it to has tried it and literally everyone is a convert - people who don’t have long term stress use it in especially stressful weeks. taurine definitely has my voice.

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