Wednesday, 14 December 2016

Refining Antioxidant (ROS & RNS) Therapy in Autism -  Selenium and Molybdenum

Today’s post is about further refining antioxidant therapy.

As we saw in a recent post, oxidative and nitrosative stress is a very common feature of autism and is treatable with OTC products.

The cheapest antioxidant, N-acetylcysteine (NAC), looks to be the best one, but there are numerous others with exotic names and equally exotic prices.

Today we just look at selenium and molybdenum.  Selenium was on my to-do list for a long time because it affects some key enzymes call GPX (glutathione peroxodases).
Molybdenum was enthusiastically recommended in a recent comment and this blog has previously touched on Molybdenum Cofactor Sulfurase (MOCOS).

Rather surprisingly, there is a commercial product that contains NAC, Selenium and Molybdenum. 

Selenium and GPX (glutathione peroxodases)

There are eight different glutathione peroxodases, but GPx1, GPx2, GPx3, and GPx4 are all made from selenium.

GPX speeds up the antioxidant reactions that involve glutathione (GSH).

In autism we know that both GSH and GPX are lacking.

We know how to make more GSH, just take some NAC.  But what about the catalyst GPX? 
There may be an equally easy way to increase that. 

Selenium and Thyroid  Enzymes

Selenium is also part of the three deiodinase enzymes D1, D2 and D3.

The active thyroid hormone is called T3, but most of what is circulating in your body is the inactive pro-hormone form called T4.

Deiodinase 1 (D1)  both activates T4 to produce T3 and inactivates T4. Besides its increased function in producing extrathyroid T3, its function is less well understood than D2 or D3.

Deiodinase 2 (D2), located in the ER membrane, converts T4 into T3 and is a major source of the cytoplasmic T3 pool.  It looks like some people with autism may lack D2 in their brain.

Deiodinase 3 (D3) prevents T4 activation and inactivates T3. It looks like some people with autism have too much D3 in their brain.

D2 and D3 are important in homeostatic regulation in maintaining T3 levels at the plasma and cellular levels.

·        In hyperthyroidism D2 is down regulated and D3 is upregulated to clear extra T3

·        in hypothyroidism D2 is upregulated and D3 is downregulated to increase cytoplasmic T3 levels

Serum T3 levels remain fairly constant in healthy individuals, but D2 and D3 can regulate tissue specific intracellular levels of T3 to maintain homeostasis since T3 and T4 levels may vary by organ.  

It appears that some people with autism may have central hyperthyroidism, meaning in their brain.

Regular readers may recall this post:-

The major source of the biologically active hormone T3 in the brain is the local intra-brain conversion of T4 to T3, while a small fraction comes from circulating T3. 

As evidence derived from in vitro studies suggests, in response to oxidative stress D3 increases while D2 decreases (Lamirand et al., 2008; Freitas et al., 2010).  As we know in the autistic brain we have a lot of oxidative stress.

Furthermore, in ASD, the lower intra-brain T3 levels occur in the

Absence of a systemic T3 deficiency (Davis et al., 2008), most likely due to the increased activity of D3.

So in some autistic brains we have too much D3 which is inactivating T3 and preventing T4 being converted to T3.

Reduced D2 is reducing the conversion of T4 to T3. 

We would therefore want to increase D2 in some autism.

This can be achieved by:-

·        Reducing oxidative stress, which we are already sold on. 

·        We can also potentially upregulate the gene that produces D2 using some food-based genetic therapy. Kaempferol (KPF) appears to work and may explain why broccoli sprout powder makes some people go hyper and some others cannot sleep  

The cAMP-responsive gene for type 2 iodothyronine deiodinase (D2), an intracellular enzyme that activates thyroid hormone (T3) for the nucleus, is approximately threefold upregulated by KPF

·        Perhaps low levels of selenium differentially affect the synthesis of D1, D2 and D3?


Where does selenium come from? 

We know from Chauham/James that selenium levels are reduced in autism, but we also know that selenium levels vary widely by geography.  

You get selenium from your diet and the level of selenium in the soil varies widely.  It is widely held that most healthy people should have plenty selenium in their diet. 

In the following paper there is an analysis of Selenium status in Europe and the Middle East.
Since we have plenty of Polish readers I have included the chart with the Polish data (on the left).  It shows that Polish people may be a little deficient in selenium.
You can see the level of selenium in Poland is below that needed to optimise plasma GPx activity.
So if you already have reduced GPx activity, because of autism, and you really need to make the most of your limited glutathione (GSH) because you have oxidative/nitrosative stress, then a little extra selenium could be just what the doctor should have ordered.


Se is an essential non-metal trace element [3] that is required for selenocysteine synthesis and is essential for the production of selenoproteins [4]. Selenoproteins are primarily either structural or enzymatic [2], acting as catalysts for the activation of thyroid hormone and as antioxidants, such as glutathione peroxidases (GPxs) [5]. GPx activity is commonly used as a marker for Se sufficiency in the body [6], where serum or plasma Se concentrations are believed to achieve maximum GPx expression at 90–100 μg/L (90.01 μg/L as proposed by Duffield and colleagues [7] and 98.7 μg/L according to Alfthan et al. [8]). However, plasma selenoprotein P (SEPP1) concentration is a more suitable marker than plasma GPx activity [9]. Prospective studies provide some evidence that adequate Se status may reduce the risk of some cancers, while elevated risk of type 2 diabetes and some cancers occurs when the Se concentration exceeds 120 μg/L [10]. Higher Se status has been linked to enhanced immune competence with better outcomes for cancer, viral infections, including HIV progression to AIDS, male infertility, pregnancy, cardiovascular disease, mood disorders [2] and, possibly, bone health [11–14].


Selenium and NAC for Rats with TBI

Perhaps not surprisingly, selenium and NAC have been found beneficial for Rats unfortunate enough to have sufferred a traumatic brain injury (TBI).

It has been suggested that oxidative stress plays an important role in the pathophysiology of traumatic brain injury (TBI). N-acetylcysteine (NAC) and selenium (Se) display neuroprotective activities mediated at least in part by their antioxidant and anti-inflammatory properties although there is no report on oxidative stress, antioxidant vitamin, interleukin-1 beta (IL)-1β and IL-4 levels in brain and blood of TBI-induced rats. We investigated effects of NAC and Se administration on physical injury-induced brain toxicity in rats. Thirty-six male Sprague–Dawley rats were equally divided into four groups. First and second groups were used as control and TBI groups, respectively. NAC and Se were administrated to rats constituting third and forth groups at 1, 24, 48 and 72 h after TBI induction, respectively. At the end of 72 h, plasma, erythrocytes and brain cortex samples were taken. TBI resulted in significant increase in brain cortex, erythrocytes and plasma lipid peroxidation, total oxidant status (TOS) in brain cortex, and plasma IL-1β values although brain cortex vitamin A, β-carotene, vitamin C, vitamin E, reduced glutathione (GSH) and total antioxidant status (TAS) values, and plasma vitamin E concentrations, plasma IL-4 level and brain cortex and erythrocyte glutathione peroxidase (GSH-Px) activities decreased by TBI. The lipid peroxidation and IL-1β values were decreased by NAC and Se treatments. Plasma IL-4, brain cortex GSH, TAS, vitamin C and vitamin E values were increased by NAC and Se treatments although the brain cortex vitamin A and erythrocyte GSH-Px values were increased through NAC only. In conclusion, NAC and Se caused protective effects on the TBI-induced oxidative brain injury and interleukin production by inhibiting free radical production, regulation of cytokine-dependent processes and supporting antioxidant redox system.



And now to Molybdenum 

Molybdenum (Mo) is a trace dietary element necessary for human survival.

Low soil concentration of molybdenum in a geographical band from northern China to Iran results in a general dietary molybdenum deficiency, and is associated with increased rates of esophageal cancer.  Compared to the United States, which has a greater supply of molybdenum in the soil, people living in those areas have about 16 times greater risk for esophageal cancer.
So you would not want to have molybdenum deficiency.

Four Molybdenum-dependent enzymes are known, all of them include molybdenum cofactor (Moco) in their active site: sulfite oxidase, xanthine oxidoreductase, aldehyde oxidase, and mitochondrial amidoxime reductase.

Moco cannot be taken up as a nutrient, and thus it requires to made in your body from molybdenum.

If your body cannot make enough Moco you may develop what is called molybdenum cofactor deficiency, which would ultimately kill you. It is ultra rare.

Symptoms include early seizures, low blood levels of uric acid, and high levels of sulphite, xanthine, and uric acid in urine.

When caused by a mutation in the MOCS1 gene it is called the type A variant.

Molybdenum cofactor deficiency may indeed be extremely rare, but MOCS1 is a known autism gene.  Perhaps there exists partial molybdenum cofactor deficiency, which is not rare at all?

Source:-  Identification of candidate intergenic risk loci in autism spectrum disorder

MOCOS (Molybdenum cofactor sulfurase)

Molybdenum cofactor sulfurase is an enzyme that in humans is encoded by the MOCOS gene.

MOCOS sulfurates the molybdenum cofactor of xanthine dehydrogenase (XDH) and aldehyde oxidase (AOX1), which is required for their enzymatic activities.

MOCOS is downregulated in autism and is suggested to induce increased oxidative-stress sensitivity, which would not be good.

So it looks like we need a clever way to upregulate MOCOS.

You need adequate molybdenum cofactor (Moco), for which you do need adequate molybdenum.

You need the genes MOCS1 and MOCOS to be correctly expressed.

SIRT1 activation, which is a future therapy for Alzheimer’s, is suggested to increase MOCOS, as may NRF2.

Sirtuin-activating compounds (STAC) are chemical compounds having an effect on sirtuins, a group of enzymes that use NAD+ to remove acetyl groups from proteins. They are molecules able to prevent aging related diseases like Alzheimer's, diabetes, and obesity.  There is quite a long list that includes ranges from polyphenols such as resveratrol, the flavonols fisetin, and quercetin also butein, piceatannol, isoliquiritigenin,

Fisetin is found in strawberries, cucumbers and supplements.  In normal animals, fisetin can improve memory; it also can have an effect on animals prone to Alzheimer's.

Here is the excellent French paper on MOCOS:-

With an onset under the age of 3 years, autism spectrum disorders (ASDs) are now understood as diseases arising from pre- and/or early postnatal brain developmental anomalies and/or early brain insults. To unveil the molecular mechanisms taking place during the misshaping of the developing brain, we chose to study cells that are representative of the very early stages of ontogenesis, namely stem cells. Here we report on MOlybdenum COfactor Sulfurase (MOCOS), an enzyme involved in purine metabolism, as a newly identified player in ASD. We found in adult nasal olfactory stem cells of 11 adults with ASD that MOCOS is downregulated in most of them when compared with 11 age- and gender-matched control adults without any neuropsychiatric disorders. Genetic approaches using in vivo and in vitro engineered models converge to indicate that altered expression of MOCOS results in neurotransmission and synaptic defects. Furthermore, we found that MOCOS misexpression induces increased oxidative-stress sensitivity. Our results demonstrate that altered MOCOS expression is likely to have an impact on neurodevelopment and neurotransmission, and may explain comorbid conditions, including gastrointestinal disorders. We anticipate our discovery to be a fresh starting point for the study on the roles of MOCOS in brain development and its functional implications in ASD clinical symptoms. Moreover, our study suggests the possible development of new diagnostic tests based on MOCOS expression, and paves the way for drug screening targeting MOCOS and/or the purine metabolism to ultimately develop novel treatments in ASD.  

Lately, a diminished seric expression of glutathione, glutathione peroxidase, methionine and cysteine has been highlighted in a meta-analysis from 29 studies on ASD subjects.45 Along this line, purines and purine-associated enzymes are recognized markers of oxidative stress. ROS are generated during the production of uric acid, catalyzed by xanthine oxidase and XDH.46 Conversely, uric acid is nowadays recognized as a protective factor acting as a ROS scavenger.47, 48 Interestingly, allopurinol, a xanthine oxidase inhibitor, was found efficient in reducing symptoms, especially epileptic seizures, in ASD patients displaying high levels of uric acid.49 However, in our cohort, only 3 out of 10 patients exhibited an abnormal uric acid secretion. It can therefore be postulated that still unknown other MOCOS-associated mechanisms may have a role in the unbalanced stress response observed in ASD OSCs.
Identifying and manipulating downstream effectors of MOCOS will be the next critical step to better understand its mechanisms of action. In parallel, we plan to ascertain some of its upstream regulators. For example, bioinformatic analyses revealed that the promoter region of MOCOS includes conserved binding sites for transcription factors such as GATA3 and NRF2. In addition, other putative interactors, such as the NAD-dependent deacetylase sirtuin-1 (SIRT1), may have a regulatory role on MOCOS expression. Interestingly, these three genes have been associated with ASD, fragile X syndrome, epilepsy and/or oxidative stress.54, 55, 56, 57 In conclusion, our study opens an unexplored new avenue for the study of MOCOS in ASD, and could set bases for the development of new diagnostic tools as well as the search of new therapeutics.


It looks like a little extra selenium may be in order to increase those GPx enzymes that are need to speed up aspects of the antioxidant activity of GSH.

When it comes to molybdenum, things get much more complex. You certainly do not want to be deficient in molybdenum and you do not want Molybdenum cofactor deficiency; you also do not want molybdenum cofactor Sulfurase (MOCOS) mis-expression.

It is fair to say that quite likely there is a problem related to molybdenum that affects oxidative stress in autism; but it is not yet clear what to do about it.  I rather doubt the solution is as simple as just a little extra molybdenum, but it is easy to try.

On the plus side, we see that if you have autism, epilepsy and high uric acid you are likely to benefit from allopurinol, which also seems to help in COPD.

There is nothing new about allopurinol possibly be effective in some autism, as from this 25 year old book, Diagnosis and Treatment of Autism.

Again we see that activating NRF2 looks a good idea, that applies to both autism and COPD.
One thing to note is that NRF2 activators are good for cancer prevention, but if you have a cancer you want NRF2 inhibitors.

NRF2 activators include sulforaphane (SFN), R-alphalipoic acid (ALA), resveratrol and curcumin.  SFN is by far the most potent.  Resveratrol and curcumin have a problem with bioavailability.


  1. Not to get too off-topic but here is a use of NAC that I was unaware of that came out today:

    Press Release:


    Now there are a lot of interesting things here to me, especially since one avenue of exploration I feel I have had success with is treating autism as you would treat drug addiction (this is not a novel or original idea in autism research obviously). I was also not aware of NAC's use in restoring glutamate homeostasis which this research study's hypothesis is based upon.

  2. Peter,
    How do you think Nac affects dopamine in the autistic brain?
    Could you describe it as an agonist or antagonist especially to D2 receptors?
    My son is not drug naive and was on dopamine blockers for almost a year, not to mention different kinds/dosage of antidepressants. I suspect this made his already low leves of dopamine much worse. I know how he reacts when treatment addresses to dopamine.
    Selenium, strawberries, apples, bananas, sesame, nigelia sativa, zinc, vitamin e etc. could boost dopamine naturally.
    Metformin could also be used on early abnormalities in glucose dysregulation, also involved with D2 receptors.
    Having these in mind, I made an arbitrary treatment plan, dividing things into two categories: dopamine boosters(I take it easy, don't use Ldopa or stimulants yet) and dopamine antagonists, or even modulators(?).
    In addition, although dopamine may play a role in addiction, my son behaves as if he doesn't get addicted. Lots of Asperger's are prone to addictive medications.
    Therefore I concluded that drugs for addiction are not very promising for us, probably because they can "modulate" dopamine through a mechanism that remains unclear.
    What is your thesis on dopamine in the autistic brain?
    Do you take it into cosideration while treating your son?
    What about Bumetanide or Low dose Clonazepam, could they have a direct or indirect impact on dopamine?

    1. Petra, I don't think my son has issues regarding dopamine.

      Dopamine dysfunction is suggested to explain why some people with autism are hyperactive, have tremors, motor deficits and these kinds of things.

    2. Sorry Peter if I overload your comment section but I noticed that my son responds better to Bumetanide when taken with a cup of greek coffee, at least so far.
      I found this article and would like you to see if this is relevant:
      Heartwire from Medscape
      Added to Diuretics, Low-Dose Dopamine Renoprotective in Small Acute-HF Trial
      Steve Stiles
      September 21, 2009

    3. Petra, it is interesting. Dopamine increased the diuretic blocking effect on NKCC2 the kidneys, but does it increase the effect on NKCC1 in the brain. In your son it either does, or the caffeine has a different positive effect.

      Greek coffee is so strong it really is a drug, so it is not a surprise it has some special effects.

    4. Peter, caffeine could also be connected to uric acid and nitrosative stress/peroxynitrite.

      RG, have a look at these:

      "caffeine has a chemical structure similar to that of allopurinol, a medication that treats gout by lowering uric acid"

      Is Caffeine Bad for Gout?
      by SHARON PERKINS Last Updated: Dec 23, 2010

      How caffeine combats Parkinson's and Alzheimer's

      According to Ikarian studies (Ikaria is a Greek island where the healthiest people live), they found out that Ikarians who drink 3 to 4 little cups of Greek coffee spread during the day, are even healthier than those who drink just one or two.

      Peter, maybe you consider adding Greek coffee to your "grandpa's medicine cabinet".

    5. Thank you Petra. For some reason, I can't remember what, I thought that caffeine should be avoided for my daughter. Something to do with the seizures I think. I'll look into it.

  3. Hi Peter and community,

    I'm sure many of you may have already seen this, but I found very exciting news today that I wanted to share, and discuss. The following two links provide very exciting insights into the findings from the University of Toronto / Sinai Health's Lunenfeld-Tanenbaum Research Institute about how the nSR100 protein may be the culprit in many cases of autism:

    Of course, my first reaction is, how can we increase nSR100 (also knows as SRRM4) levels. I've started to look, and have not found anything yet. Not sure that anyone has tested yet for natural substances that would impact nSR100/SRRM4 levels.

    I'll post what I found in my research, and would really appreciate any insights anyone else has. If we can find a natural / already available substance to increase nSR100/SRRM4 levels, this could make a meaningful difference to many of us.

    Thanks in advance!


    1. I read this research today as well and it does have some important takeaways. I think the better question is not what can be done to upregulate nSR100 in the brain, but what kind of hiccup, developmental or otherwise, is causing not enough nSR100 to be produced. In the paper it is suggested a multiple of factors (including many linked to syndromic ASD) can lead to this happening. The problem seems to be that the production of this protein is dysfunctional in response to neuronal activity which causes a myriad of other downstream problems to occur.

      Another paper released yesterday:

      deals with alternative splicing as well (I guess there must be some alternative splicing conference for ASD going on somewhere). One part of the paper suggests that the alternative splicing of activity-dependent neuron specific exons (not to be confused with axons) is downregulated which to me suggests that when neurons "do stuff", what happens in response to "doing stuff" is not happening which means the more hyperexcitable a neuron becomes, the bigger a problem you are going to have in maintaining neural homeostasis.

      So therapeutically, my gut tells me that for optimal cognititive functioning when a compromised ability to produce nSR100 in response to increased neural activity is present is a function of having appropriate refractory periods when learning. In other words, don't overstress your child and give them peace and quiet so if the house is noisy because of siblings or other environmental issues, try to create a fortress of solitude (a quiet room) where they can chill out or maybe do your best to soundproof and lightproof their bedroom. Some parents of ASD kids will try and reduce the noise their children hear via earmuffs, but I think that is a bad idea because the response from the auditory neurons is to become more sensitive (i.e. hyperactive). Just reduce as much unnatural noise and light (televisions/appliances) and let your kid chill out since it appears those with nsr100 deficiency have a smaller neural fuel tank and need more time to refuel then typical people who may bounce back faster. This does not mean (in my opinion) that people with nsr100 deficiency can't do cognitively demanding work, just that they can't do it for very long or else you get a lot of dysfunctionally translated proteins being produced which will undoubtedly gum up the works in neurons and need to be cleaned out via autophagy.

      Well that is my 2 cents on the subject.

    2. Hi Tyler,

      Thanks for your insights! I agree with you, it would be very helpful to know the "why" in relation to reduced nSR100 production. Is it not enough of another protein upstream of nSR100, is an epigenetic issue (i.e. nSR100 "tagged" to be turned off when it should be on), etc. By knowing the why, that may offer up other avenues for treatment.


  4. Hi Petra, Peter,

    My son does not seem to have issues with dopamine or serotonin but does seem to have an aberrant opiod biochemistry (though I know it's all connected). As a child (he still is one), he used to have that loony, silly happy kind of disposition which although dampened over the years, still finds a way to rear its mental (a middle class absurd term meaning mad) head sometimes, mostly at the most inappropriate time.

    Had been reading an old review article by Wakefield et al. (2002) where they described gut/hepatic encephalopathies, how developing brain might be affected in utero in infantile autism or endogenous opiates in regressive aurism. My son was born autistic but as also mentioned by them, if bowel clearance leads to alleviation in autistic traits (son starts giving those odd, peripheral vision expressions even if very very midly affected digestion wise) the opiod system might be involved. So essentially in my son, who has near perfect bowel health, additional liver strengthening may be one direction towards intervention. What else could I opiod antagonist? Results with naltrexone are as best inconclusive, and the u shaped response curve makes it more complex? I am ordering non pharma products to see if something works although they will only have a supportive effect? What about cognition..the neurotypical type and communication?

    Had been going through a rough patch
    (lost father) and then son came down with a bad itchy viral rash. But Petra, even with that ill health my son learnt to write a few Hindi letters (which is quite meaningless to him as English is the primary medium of instruction here). So my son is inching ahead on his snail trail. What wouldn't I give to speeden up the pace!

    I have arranged for clonazepam..Petra, could you tell me what dose to try? At least it might give me a clue about the kind of interventions I should be trying..?

    School will be off for the winters in a few days time so I can do with a little experimentation. Please suggest if you think of anything. He will be five in January.

    1. Kritika,
      Condolences on the loss of your father.
      I was just thinking...and apologize if this isn't helpful and you have already tried this product, I haven't been reading comments the past few months...but I was thinking you might want to try the Pomgenex drink mix. Peter wrote a blog post about it not too long ago and I will never give any other sulforaphane product--it was superb. My son really did well with it, mainly because it tastes good and he drank it with no problem! :) However I also gave him biotin and some herbal antifungals with it, cat's claw and pau darco alternated every 3 days. We have since transitioned off it while doing low dose ALA chelation, and I try not to give more than one candida causing ingredient at a time since his diet is not the best and he eats, drinks a lot of fruit sugars. Over time I have found with my son bioflavonoids and antioxidants are more effective with his sensory issues than pharmaceuticals.

  5. Peter, thank you for this post. Allopurinol seems like it might be a good fit here. Have you tried it?

    I did try the molybdenum for a while, it used to specifically help with tolerating sulphur rich foods like garlic, otherwise I could not see it do anything. With verapamil, my daughter's food sensitivities mostly went away, so we didn't need it anymore and stopped.

    I also used to give her selenium, again I couldn't see it do anything obvious, and I read that it should not be used without iodine, so stopped it.

    1. I have not tried Allopurinol, but I think it should help some people. Even Dr Frye gives it the thumbs up for some people in this paper:-

      Metabolic and mitochondrial disorders associated with epilepsy in children with autism spectrum disorder

      I think a small dose of selenium will do no harm, but I doubt it will do much good. But it does have some logic, particularly if you live in a low selenium area and have a restricted diet.

      Molybdenum helped one reader, but again I do not expect great things.

  6. Hi Kritika,

    I am sorry for your loss.

    For low dose clonazepam, research says 1mcg/k, but Peter says a little lower dose may do the job.
    My son is the type of Asperger's that gets agitated with benzos, so not wanting to reach to that point, I trialled 75mcg and also have 80mcg to trial. When I had 500mcg pills I could prepare the dose myself but now that I only have 2000mcg I have my pharmacist do it (100 pills for 8 euros).
    I am also aware of gut/hepatic encephalopathies and brain damage could be an issue for some autism. My son has a moderate NAFLD and keep a close eye on possible interventions. I use melatonin and vitamin e as most well tolerated and with stably positive behavioural outcome.
    I think this opioid like effect usually comes after inappropriate food. I don't press my son eat food he doesn't feel safe with and give simple dishes.
    I believe hyperactive inattentive kids, with eating/sleeping disorders may have lack of dopamine. This is well researched in ADHD. I can see my nephew, who is on rispredal, have trouble concentrate on school subjects. He used to be a very good and creative student.
    This is something that deeply hurts me.

    Wish good health to your family.

  7. Hi Petra,

    Thanks for your suggestion regarding clonazepam. The tablets I purchased have a strength of 0.25mg so will have to do some calculations. How I miss my glass pipettes and flasks.

    Petra, my son is not exactly too hyperactive..probably a little less present and involved, at least in activities which I perceive to be of use. And there is this tendency to lose track and get distracted by what could be visual stimulus or internal body based one (which often seem to be connected). He does not have an eating or sleeping disorder although eight hours continuous uninterrupted sleep in the night is enough to recharge his batteries and usually does not sleep more than this in a single go. However, it's another two hours in the afternoon so the total quanta seems fine for him. He is usually a relaxed child and as he grows, finds ways to self regulate. When I took him to his doc for the viral rash, he tried to maintain his cool by finding himself a piece of bubble wrap which he quietly burst while sitting on the examintion stool (though he did resist when doc lifted his clothes to examine him).

    Unlike your family, where male child seems to be susceptible to neurodevelopmental disorders, my son is a unique sample in ours. We do have a streak of atypical social behaviour inspite of or because of intellectual excellence running through our immediate as well as widely extended family. .. lots of genius uncles, grandpas who just got bored of the rut. So there is a mental streak or possibility of genetic susceptibility.

  8. Kritika,
    Have a look at this:

    "Vitamin A is needed for the functioning of the body’s mucous membranes. A deficiency can lead to diminished secretion of digestive juices creating digestive issues, or the drying out of the linings of the nose and throat. Most importantly, it affects the eyes, causing night blindness among other issues. It is believed that the alienated behavior of an autistic individual may be due to a damaged/under developed retina, which provides a tiny visual window where they only see colors and vague shapes. This makes it very hard for them to follow movement, especially the subtleties of facial expressions. New environments are also visually challenging, hence their desperate need for routine. A deficiency in vitamin A often leads to visual stimming, such as staring at lights/fans, repetitive blinking, rolling the eyes, or moving/flapping fingers in front of the eyes. Vitamin A supplementation with cod liver oil has proven effective in reducing these behaviors and repairing the retina. Vitamin A is a fat soluble vitamin, meaning that it gets stored in the body. Supplementing too much can have side effects, so one should be tested to determine levels."

    I'd like to test for vitamin a. I've never heard anyone in Greece tested for vitamins a or e. It's quite common to test D3, B12, folic acid these days here.
    Blood tests, of course, can only show what happens in the blood, not in the brain.

    1. Hi Petra,

      This entire piece of write up about visual issues gives me such a sense of deja vu. When my son was given an ASD diagnosis at the age of 2.8 and I prepared to extinguish his autism through drugs and supplements, vit A and cod liver oil were the first interventions I tried. After what I felt like a little improvrment, within ten days, my son responded with even more visual stimming..And I had not even given more than a regular dose. Then i read up that excess of vit A can aggravate visual sensory behaviour. He reverted back to normal, his normal, after stopping the supplements.

      Petra, my son does not have too much of stimulatory behaviour or what is called autistic mannerisms like hand flapping, rocking, spinning. Finger flipping in front of eyes is a rare occurrence, peripheral vision being the most common and which comes in phases. It's so difficult to ascertain a pattern.

      Actually, the very factor that makes supplements and drugs so potent, makes them potentially so adverse in their effect too. An orange will not cause you stomach pain but 200 mg of potassium taken as a supplement can.

      After reading Roger Kulps comment, I remembered that I was diagnosed with subclinical hypothyroidism in my first trimester and around five months into pregnancy, had developed a rash on my tummy for around three dayd, which I thought was an allergy. But recently my son broke out with a similar rash which the doc said had a viral cause. So my tummy rash could have been a viral infection. that could have been another contributing factor. I otherwise had an uneventful pregnancy, put on only a a kg or two, had perfect blood pressure and sugar levels and was active throughout, and finally had a NVD but was given pitocin and an epidural. And my Professor father got himself an autoimmune disorder by getting himself extremely upset over some mishsp. So in bits and pieces, the clues are there but what to do with it?

      Looking at the brighter side, thankfully my son seems clever enough to take care of himself. Today he cut his finger and as I fumbled about thinking what to do, he opened the drawer, took out a packet of wet wipes and gave it to me gesturing me to apply it on his finger.

    2. Petra,

      There is this vit a protocol
      ( There are for most vitamins I think), where you supplement with mega doses of the vitamin for two days and then stop. Some have reported dramatic improvements. What is your opinion?

      I am getting more and more convinced that in my son, not letting his system settle into complacency is the key..Akin to shock therapy, a biochemical shock therapy. So varying treatment regimes, rotating them, intermittent treatments. Just do not let the system doze off, lest your child wakes up after a long sleep a la Rip Van Winkle.

      A similar protocol exhists for vit d but looking at my son's healthy bone structute, vit d deficiency seems unlikely. In fact, I dnetimes wonder if too much vit d, it's supplementation now routine in infants in urban upper class medical system, could have been an additional load.

      Wondering and wondering..

    3. Hi Kritika,
      I really don't know what's the deal with antioxidants/nutrients in autism.
      In the past I used mega doses of various supplements, such as: Nac 3g, Biotin 20mg, melatonin 10mg, carnitine 2g, vitamin C 2g, cinammon 500mg, broccoli 1500mg, high B comlex and so on.
      I saw the positive responses and then the loops that some of them may have caused, I wouldn't bother with them anymore, otherwise.
      I know that autophagy doesn't work well in some people/autism and antioxidants may aggravate this issue further.
      For the time being, I only use small to moderate doses.

    4. Petra,

      I think I will give carnosine a try, since thiol antioxidants did not suit my son. Also thinking of giving liver life and cytoflora a try, along with a rotating probiotic regime. The miraculous effect of homeopathic detox medicine is making that direction of intervention not that much a fantastical thought. Thinking of doing it systematically and if it does not work, that is one less treatment option to trial. There has been a sudden boom in availability of big brands in the supplement industry in India and prices are falling drastically.

      And I was thinking, first came the Estee Lauder and Mac cosmetics, then Kentucky fried Chicken and now obviously it's i-herb.

      So this is evolution.

    5. Kritika, I can certainly recommend Cytoflora, it has been almost incredible for my son, in terms of speech improvement and it convinced me that he needs his gut "fixed", even though he never had any obvious symptoms of GI issues. LiverLife can work really well too, however, my son seems to be very sensitive to it, so I stopped for the time being. Homeopathic detox also worked well for my son. Basically, reducing the toxic load is the name of the game, BEFORE giving supps. I am now giving my son liquid Zeolite. He was super flautulent and had really stinky poops a day after taking the first drops, which shows that he had bad stuff stuck in his body (he's never been flautulent before) I support his detox with Cytoflora and strong probiotics and vitamin C. I tried loads of different supps with my son, but nothing worked and his doctor made me realise that he needs "stuff taking out before adding more stuff in", so that's what I'm doing.

    6. Thanks anonymous for the reinforcement. And your doctor put it quite eloquently..Stuff needs to be taken out before adding more stuff in. I am waiting for the bioray products I had ordered and will let you know how it turns out. I never really believed in all this but rewording Galileo ..Where reason fails us, senses must step in.

    7. Kritika, yes, go ahead and give carnosine a try. As I read it looks a very good idea.
      It must be expensive, here is about 50-60 euros, but this is not the case if it works.
      If I were you, I would start low, 250mg or less?
      As soon as we feel longer term stabilized, I may use a little carnosine because my son excludes beef from his diet, except small quantity of minced meat, which has lost nutrients comparing to whole piece.

    8. Petra, I ordered kirkmans, 200 mg , 90 tabs for INR 2,123 which is not very costly. Actually what seemed costly to me six months back does not seem so anymore. Then along with it I also ordered a zinc, selenium, vit a and e combination. The company Carn-aware, which manufactures carnosine under Dr. Chez's direction does add zinc and vit e to it but I think Chez has carried out a study where he trialled carnosine alone. It does have an effect fast on whom it is effective but many parents have reported that the dramatic changes are transient and sometimes the child ends somewhere even below the baseline.

      This is what scares me..we do not have nothing to lose but something to gain as differeing from Peter's perspective of things.

    9. Kritika, I don't know what would be the mechanism behind possible regression and I think, before giving, you should make a research to minimize chances of side effects.
      Maybe you trial it for a week, as far as I can remember you are a vegetarian, aren't you? If it makes you feel better, or even doesn't upset you, you may feel more confident.

    10. Thanks Petra,

      I will try it out as I say. What is a little carnosine,I can polish of an entire cow..holy cow..if that makes my son better.

      Regards and a merry chistmas to you.

    11. Hi Kritika,
      Thanks for your wishes and retaliate.
      I am really sorry if I offended your culture and traditions.
      I just can't help my impulsiveness..I am Greek.. what do you expect.. we are depicted as "weird" people, roasting whole animals on a spit at the back of our fact we do that at our front yards.
      I do appreciate your sense of humour, though.

  9. The day I tried the Vitamin A, my daughter was able to call out 'mummy!' and 'daddy!' to get our attention. Usually this is difficult, she will say the entire sentence, such as ' mummy, let's go', or 'daddy bring me water' etc and keep repeating it until she gets our attention. That day we were visiting friends and watching tennis together, she wanted to stretch out on the sofa, and said, ' Uncle Art, please give me blankie'. Except for scripts, she never attaches a person's name to a sentence. She will usually go in front of that person or make eye contact and say what she wants. I really should add this back in again.

  10. Peter,
    Like you,I am very interested in digging down to the root causes of syndromic autism,and connecting all the dots,like I have with myself.This gets back to your earlier post you link to about Vitamin D,hypothyroidism,and autism.I have learned so much,and had some of my most important tests,since you published this.When I first started on this long diagnostic journey,in 2009,I was fresh out of an acute case of either meningitis,or encephalitis,that dragged on for months,and a resulting regression,that was one of the three worst I had suffered in my life.My mother told me I had my first regression as an older infant after an acute case of meningitis,with pulmonary complications.I suffered many regressions from acute infection,well into adulthood.

    My autism was rediagnosed after this last regression,in 2008,and at the time,my mother was presented with papers,to put me in a residential treatment facility,which she refused to sign.For most of my life,I was verbal,but otherwise low functioning.You know that was before my folate receptor autoantibodies,and MTHFR Deficiency was found,through testing by a DAN! doctor.It took a few years,but I was able to reverse my autism,and stop getting acute infections,but I still have many chronic medical issues.

    This DAN! doctor,who pretty much only saw kids on the spectrum,tested my Vitamin D levels,and told me I had the lowest blood levels he ever saw.I had rickets/osteomalica for many years.

    Besides the MTHFR Deficiency,most of my medical issues are autoimmune,and began as a child.In 2015,I had a Whole Exome Sequencing.I found out I have a pair of pathogenic mutations,for an extremely rare primary immune deficiency,that often involves the brain and neurodevelopment as well.I know a number of parents through Facebook,whose children have both autism,and PIDs.I believe the connection between some forms of autism,and primary immune deficiency is a very under researched one.

    This also gets us back to Vitamin D,and these links I wanted to share with you.There is a direct connection to thyroid function,autoimmune disease,and Vitamin D levels.

    TSH can also be produced outside the pituitary,in T cells,B cells,splenic dendritic cells,bone marrow hematopoietic cells,intestinal epithelial cells and lymphocytes.

    Your earlier post you link to is correct,there seems to be some evidence out there of thyroiditis and autism.Mostly,it seems to go back to thyroid function,and autoimmunity during pregnancy.

    It is another area that cries out for more research.

    1. There was a research group from some children's hospital a while back that published a small, yet very compelling study on Vitamin D and DHA with autism as well as other hypotheses concerning how both Vitamin D and DHA help influence serotonin regulation. Their hypothesis (if my memory serves me correctly) was that without Vitamin D and DHA signaling, there is an imbalance in the production of two enzymes regulating serotonin in the body and brain namely TPH1 and TPH2. Excess TPH1 production would cause hyperserotonemia in the gut and in the peripheral circulation, thereby starving the brain of tryptophan for use in creating serotonin in the brain. Also, they had suggested that Vitamin D is necessary for activating the transcription of the gene that produces TPH2 in the brain and that DHA helps assist in serotonin signaling via making the serotonin receptor more fluid.

      Here is the paper if you are interested:

    2. Pretty certain everybody will have heard of this paper by now, but thought I would post a link here for convenience & as relevant to the vitamin D discussion: "Gestational vitamin D deficiency and autism-related traits: the Generation R Study" by Vinkhuyzen et al in

      Roger - love that March 2015 paper on maternal thyroid autoantibodies you posted a link to. Alexandria

  11. Tyler, I don't know how relevant this may be to things you are explaining here, but I thought I should let you know.
    My researcher doctor prescribes a kind of omega 3 fatty acids containing only high dose DHA. I just don't recall the name of the product right now, it's quite expensive, though.

    1. Well I take fish oil myself as the enzyme needed to convert Omega-3's from plant sources to DHA decreases with age and I just turned 41.

      As for therapeutic use of Vitamin D and DHA I have read many studies with respect to developmental disorders (autism/ADHD/OCD/etc.), but I have seen nothing blockbuster in terms of effect for whatever disorder they were testing Vitamin D and/or DHA. I think it is one of those things like Vitamin E where not having enough will give you health problems, but megadoses of the stuff will not cure any disease and can easily cause problems as well when used in excess.

      Of course if mom is older as many moms are these days, she may not have as much DHA in circulation as a younger mom, and the paper I posted above was specifically about treating high risk young children with Vitamin D/DHA supplementation to address serotonergic functionality.

      Also, I had posted this study before on this blog but was not sure if Roger came across this study and since he is interested in Vitamin D and autism, this study happened to be one of the bigger ones on the subject I had come across recently.

    2. Tyler, thank you very much for clarifying things for me.
      You've been really explicit here.
      My son is marginally low in vitamin D and the endocrinologist recommends low dose supplementation for a few days and then stop and start again after some time.
      Fresh fish is recommended at least once a week, hoping they can convert it to nutrients.
      As you may know, I use vitamin e 200IU/d, and recently uped the dose to 400IU/d divided into two doses during the day.
      I talked to a geneticists who tests for metabolism and told me that 400IU is quite safe a dose. She believes vitamin e is an excellent antioxidant.

  12. Here is some very interesting research that might ignite a debate earlier on this blog about whether it is better to supplement Inosine or else restrict it due to it metablolzing to uric acid (excess levels of uric acid cause gout):

    Press Release:


    This paper generally deals with autoimmunity and inflammation but specifically about an inherited autoimmune disorder called IPEX syndrome. What the researchers found were a lot of things relevant to some of the topics covered here lately.

    For one, the researchers found that IPEX syndrome bred mice had low levels of Lactobacillus species in their gut. When the researchers supplemented the mice with Lactobacillus Reuteri, the gut microbiome was "reset" and inflammation subsequently subsided in the mice, thereby increasing their survival rate. They then looked to see why L Reuteri supplementation actually reduced inflammation and found that levels of a L Reuteri metabolite named Inosine were also increased (IPEX syndrome reduces the levels of Inosine via a mutant gene). After that revelation, they then connected the dosts and found that Inosine binds to A2A receptors and as a result inhibit the production of TH1 and TH2 immunity cells. So in other words, Inosine supplementation and/or L Reuteri supplementation or even A2A agonists (as the researchers point out) might dampen down inflammation, especially in the gut and likely elsewhere in the body. One thing to note here is that in addition to a myriad of drugs being A2A antagonists, caffeine is probably the most well known one.

    I also must point out that I have supplemented Inosine with my son for several years now for other reasons I won't get into right now other than to say it is for autism, so this all might be confirmation bias on my part, but perhaps the Inosine debate should be given another look in light of this new information.

    1. Tyler, for us I think it was Biogaia gastrus that lowered uric acid by 0,4/5.
      It was 0,8 above normal means for years.
      What do you make out of it?

    2. Well high levels of uric acid are usually a symptom of something else going wrong and are a response by the body to mitochondrial stress as uric acid is a potent antioxidant. A similar mechanism happens during infection and general sickness where the body upregulates the kynurenine pathway at the expense of the serotonin pathway because one of the end products of the kynurenine is NAD+ which is depleted by oxidative stress as well (cells will do anything to keep NAD+ from getting too low because when this happens apoptosis is triggered). So chronically upregulated kynurenine metabolism is seen as bad because quinolinic acid (which is converted to NAD+ provided there is enough of the enzyme and Vitamin B6 around to process it) is excitotoxic and a potent oxidant all on its own.

      The point being is that uric acid may have been decreased not because of any direct effect of lowering it from Biogaia Gastrus, but rather the initial insult in your child driving the increased production of uric acid as an antioxidant response may have been attenuated instead (hypothetically of course).

    3. Tyler, thank you. This helps me a great deal.

      As I read, quinolinic acid, which is present in Huntington's disease, Parkinson's and such disorders, could be treated with nicotinamide ( Asperger's young male said that here), natural phenols, curcumin and licofelone, which is a drug for osteoarthritis, phase III trials.
      I use lots of curcumin spice in my son's food because it goes well with his favourite dish, chicken breasts with Tai rice. It's so much that his food becomes deep yellow.
      There may also be a possibility that vitamin e helps here.

      "α-tocopherol (Vitamin E) is also a potent antioxidant. Using a neuronal cell-based assay, glutamate-induced neuronal death was significantly attenuated in a dose-dependent manner by α-tocopherol [89]. Also, treatment with idebenone in this in vitro model resulted in complete neuroprotection in a dose-dependent manner [89]."

      Once again thank you very much.

  13. More interesting stuff on ketosis and its possible mechanism of action in an ID syndrome called Kabuki syndrome:

    A previous study where the same researcher was looking at drug options for Kabuki syndrome in basically trying to do the same thing (relaxing chromatin):

    What was interesting here is that CHD8 (a chromatin modifying gene) is one of the biggest candidate genes for autism and in many cases of autism CHD8 seems to cause a cascade of problems in early neurodevelopment. According to this paper on CHD8 and autims:

    it is suggested that CHD8 acts as a "promoter" greater than 90% of the time which essentially means that its dysfunction causes many ASD related risk genes that are regulated by CHD8 to be downregulated.

    In effect, my reading of this with respect to the first study on Kabuki syndrome is that HDAC inhibitors (like beta hydroxybutyrate which is elevated in the body when in a state of ketosis) would be the way to go with respect to attenuating a lot of the autism epigenetic abnormalities encoded in early development.

    I know that there are some commercial outfits that have been working diligently on putting out BHB supplements as a sports performance fuel, but I am not sure if they are out yet. The idea behind these supplements is to give the body and brain an extra fuel reserve that goes well beyond the glycogen stores in muscle so that athletes can have the best of both worlds in terms of anaerobic and aerobic metabolism.

    This might be a product/supplement we should keep our eyes out for as ketosis dieting is a challenge for many people and the jury is still out as to what the long-term downsides of ketosis dieting might be at the moment.

    1. Hi Tyler,

      My daughter has been on the Ketogenic/MAD diet for nearly three years. We have loosened it up somewhat in the last few months in order to add in more carbs. To compensate, we have added in MCT oil as the main source of fat to maintain ketosis. It is working well, she is able to stay in steady ketosis in spite of chips or other fun foods here and there. I run labs on her at least a couple of times a year, and so far we have not noticed any problems that can be tied to the diet.

      Anecdotally, there are many children and some adults on the diet for five plus years, and there don't appear to be any serious negative effects. Of course, almost all of them are on it for epilepsy, so the motivation to stay on is high.

    2. I will likely try this in the summer. Cooperation from the staff of the public school my son attends make trying out this intervention right now a waste of time.

      BTW, is there a specific protocol you follow or do you just follow ketogenic guidelines generally?

    3. Hi Tyler,

      RG referenced long ago here some papers by Dr Mary Newport, who treated her husbands with Alzheimer's disease with dietary ketone monoester, this way inducing hyperketonemia without strict ketogenic diet:

      “Plasma BHB levels were measured occasionally to assess KME-plasma BHB dose-response relationships. Noticeable improvements in performance (conversation, interaction) were observed at higher, post-dose BHB levels, compared to pre-dose values.”

      What do you think about this?

      Thinking about supplements increasing BHB blood level, what is your opinion on the products mentioned here: ?

      I bought some Keto Os, but was not aware that it contains cow’s milk protein that my son is allergic to, so I did not try on him.

    4. Well I have checked for BHB supplements around every 6 months or so to see if anything has changed from before when company X, Y, and Z had been making promises for a usable product. From when I first heard about ingestible ketone esters, I read thatthey are expensive to manufacture so figuring out how to make them cost effectively is the challenge here and Keto OS is definitely not cheap.

      I may end up buying some Keto OS thanks to making me aware of it to see if it is the real deal. The ingredients on the back of the package list BHB as the second ingredient, but how much you get per serving is speculative because the manufacturer can claim anything they want unless some independent lab tests their claims (which I have no idea as to whether this has occurred or not).

      Also, I looked at the other link but probably know about as much as you do from reading it and trust product reviews I read on the internet probably about as much as you do. I will likely order some anyways because the potential payoff could be big if it does as it says and my son has some undiagnosed problem with carbs (which is my suspicion in many autisms).

      I will also say that I would not try this type of product out on my child before testing it on myself (as I do with most stuff) while of course using some keto strips to see if it has any effect on my metabolism. I will let you know how it goes once I see how it effects me first.

    5. We were strict Keto for a long time, and then switched to MAD. We were supposed to start at hospital but did not because they lost their dietician suddenly and they could not easily find a replacement, and we did not want to wait.

      I started with this book, its sort of the epilepsy Keto bible, written by Dr. Kossoff who is the main neurologist behind the diet at Johns Hopkins. This is a good place to start as it fleshes out the ketogenic diet for the parents, comprehensive book, helps you understand how to start, what to watch out for including tests to be done before and during the diet. Most importantly, it brings it home that the ketogenic diet is a medical diet and to be used with care and only if neccessary.

      This is the other book that helped quite a bit:

      Dr. Peter Attia's blog is excellent, helped me a lot in understanding the process of ketosis:

      Dr. Georgia Ede's blog and her four part series on doing the diet herself is what I used to actually implement the diet.

      There are many who write about the ketogenic diet, most of them do it for weight loss, and almost all of them are grossly underinformed. caveat emptor.

    6. Hi Agnieszka,

      Peter Attia has written about exogenous ketone supplements on his blog. He ran some good experiments and you will find them on the link in my reply to Tyler.

      Branched Chain Amino Acids are also ketone suppliers, except they taste pretty awful.

      I looked at your link and its quite interesting, especially since Dr. Agostino usually recommends an ultra strict version of the ketogenic diet for cancer.

      I find that the MCT Oil itself is pretty good. I am also going to experiment with Dr. Newport's formula once my daughter's diarrhea is resolved.

    7. I looked into the box labelled "old ideas suspended due to procrastination" and found also a bottle of KetoForce lying there for a few months. This contains 11.7 g BHB per 30 ml serving and "does not taste all that pleasant on its own" according to the manufacturer. In my words: it is awful. I would think it’s impossible to get a child to swallow it, but two years ago I was sure my son would no way drink effervescent NAC, which he now uses daily.

      Trying both products on myself seems easier at the moment and I assume that commonly used urine keto strips do not detect BHB so blood testing will be needed.

      There is one thing that keeps me thinking about this way. My son used to have episodes of severe headaches with mast cell degranulation, believed to be a kind of periodic calcium channelopathy by his neurologist. The odd thing was that while he was definitely suffering then, his stimming disappeared totally, his speech and ability to perform complex tasks was exceptional. He had several tests during such episodes, but there was only one consistent finding: ketonuria. Either it was just an epiphenomenon or he benefited from ketotic state.

      Also ketonuria is common during fever and I wonder how this relates to "fever effect".

      RG, what does Dr Newport’s formula consist of? I think I read once about it on her webpage, but now can’t find.

    8. Hi Agnieszka,

      I just found this comment from you, seem to have missed it originally, so sorry for this very late reply. I have a short write up published by Mary Newport, detailing her formula, but am not able to attach it here. So, I am emailing it to Peter now, so he can put it up here for everybody to see.

    9. This paper might be relevant to the old discussion on ketogenic diet/exogenous ketones here:

      "Ketone Bodies as a Possible Adjuvant to Ketogenic Diet in PDHc Deficiency but Not in GLUT1 Deficiency"

      The number of persons included is not impressive: 5 adolescents, but I think it's the first report on BHB use in children, so 5 is better than no one. That's what they found in short:

      "To improve quality of life and compliance, we tried to replace KD partially or totally with L,D-3-hydroxybutyrate in three
      GLUT1-DS and two PDHD patients. The clinical evolution of GLUT1-DS and PDHD patients was strikingly different. In all GLUT1-DS patients, a partial replacement of KD with L,D-3-hydroxybutyrate led to clinical degradation. Conversely, a positive effect of KB administration was obvious in two PDHD patients although KD was still necessary when energetic needs increase, for example, during febrile illness periods."

      I wonder why they saw such a difference.

      My son has increased mast cell degranulation signs recently for a number of reasons. This comes with poor apetite in him and as usual after few days his stimming reduced and he speaks better for a while. As I had Keto-diastix at hand I found he is in ketonemia, the result was some +++ (8-16 mmol/l).

      Perhaps the same happens in "fever effect".

  14. Hi Petra,

    My carnosine should reach me anytime next week but I am again bogged down with doubts, the same coz of which I kept postponing carnosine trial on my son. What do you make of Panghorns contrarian view, rather warning against use of carnosine for most autism, where he basically suggests that the child might end up worse than where he started after an initial improvement. What do you about going low and slow and with breaks?

    Reply when you get the time.


  15. NOW brand "detox regulators" has NAC with Selenium and Molybdenum in handy capsules. We are considering starting Histidine along with this as it works well with Selenium to potentially have antihistamine properties amongst others.

  16. Histidine (1g a day) helps reduce pollen allergy in my son. If you buy the bulk powder it is a very cheap intervention. It is suggested to stabilize mast cells. Large doses may reduce your zinc level, so some people add a small dose of zinc, just in case. Zinc is often low in autism, for no known reason.

  17. I've seen a lot of comments on ALA (or RLA) not being good for people with hypothyroidism. I think it's about inhibition of the T3 to T4 conversion(?) If this is true, then ALA might not be suitable for all. (Just like NAC might not be suitable for people with asthma) Anyone who knows anything about this better than me?


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