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Friday 15 June 2018

Raising Expectations?


Monty, aged 14 with ASD, has finished his year-end assessments in his first year at high school.  Monty has classic autism, which we can also call a type of Strictly Defined Autism (SDA), or what autism used to be under DSM3, before the diagnosis was extended in 1994 to include Asperger’s at the clever end and PDD-NOS in the middle.  From that point onwards, autism means entirely different things to different people.
For the last 6 years Monty has moved up each year with his neurotypical peers, who are two years his junior.  During those years I used to go to the parent teacher meetings at school and explain that if Monty could not keep up, it would be just fine to hold him back another year, for example if he came at the bottom of the class in most subjects. We held him back two academic years, 6 years ago, in the “big reset” and I assumed this would likely need to be repeated, since people with SDA cannot acquire skills as fast as typical people.
This blog is really all about using biology to try and have someone with SDA keep up with typical peers, or switch from SDA to something more Asperger’s-like.  This did look like an impossible task at the age of 9.
Can people aged 9 with SDA “catch up” academically with NT peers?  Remarkably, it does seem to be possible.
This year’s report card is nearly all As.
Big brother has just graduated from the same school and he is as amazed as me that Monty, the one with autism, now gets better grades than so many of the others. “What is the matter with the rest of them?”, he asks, “why can’t they beat him, he has autism”. 
The big difference is that Monty pays attention in class, has two great part-time assistants, does his homework and does academic work in the school holidays and he has his personalized PolyPill.
One teacher commented that if the others worked as hard as Monty, they would also be getting As.
Monty now comes home with another A* and his Assistant asks why we are surprised. Monty’s original school assistant from 3 to 8 years old, and so pre-PolyPill, never had such moments.

Conclusion
It is getting rather repetitive writing about Monty’s success in mainstream school – but what happens in the long run is what most parents really want to know. 
Since we all like a good story and a happy ending, most popular accounts of autism are not representative.
“The Reason I Jump” was written by the non-verbal Japanese, 13-year-old, Naoki Higashida, with help from his mother and then translated into English and other languages.  Most people loved this uplifting book, but some parents of non-verbal kids with autism clearly hate it, either because they do not believe he actually wrote much of it, or because it suggests that inside the head of the non-verbal child with severe autism is a literary genius.
The very detailed personal autism story is the one about Noah Greenfeld, now in his 50s. This man with severe regressive autism was the subject of 3 books written by his father in Noah’s youth and one by his brother decades later, so you can learn how things ended up, if you were left in any doubt.
Josh Greenfeld, Noah’s father, once described to the TV news show, 60 Minutes, the process he went through in his thinking about Noah.
“At first, you just hoped he’d be normal,” he said. “Then you just hoped he could talk. And then you just hoped he could communicate a little more or understand. And then, finally, you reached the point where you just hope he can be well fed, well taken care of — be happy, not feel pain. You become very, very basic.”

So, while it is very thorough story, going from failed use of ABA, to all kinds of institutions and numerous doctors, in essence nothing helped.
In his brother’s book there is a whole section about Noah recovering and adopting a “normal” life, but this turns out to be a trick the author is playing. This clearly upset many parents who bought the book, but not the literary reviewer at the New York Times.  
Even Noah’s Japanese mother, Fumiko Kometani, wrote a book, Passover, that includes him, for which she won a Japanese literary award, but the New York Times regarded it as anti-Semitic. Noah’s father was Jewish and the book is a Japanese perspective of living in the United States. 



A Place for Noah (1978)
''A Place for Noah'' (1978) picked up the account in August 1971, and focused on the family's six-year quest to find a school or day-care center where Noah could be educated or trained. On a deeper level, it is also about the family's struggle to keep a place for Noah in their hearts as well as their home. ''I can never kill the dream that is my son,'' Mr. Greenfeld wrote in January 1977.


The sweetest recent moment for the Greenfelds came in February 1986, in Tokyo, where Foumiko was presented with the Akutagawa Award, Japan's most important literary prize. As Mr. Greenfeld described it, ''It's as if there were a single Pulitzer Prize, and it came with a black belt.''
Is this a happy ending? ''With Noah, there is no ending,'' said Mr. Greenfeld, noting that Noah could not understand, or share in, his mother's triumph. ''With Noah, you think of the old Pearl Buck line - a continuing sadness that never ends.''

This is the book that won the Akutagawa Award in Japan but appears to have been loathed in the United States. 

This is the sibling's view of growing up in the upturned world of severe autism.

Noah Greenfeld, the subject of several well-received books by his father, Josh, was “probably the most famous autistic child in America.” Or so claims the journalist Karl Taro Greenfeld, Noah’s older brother. His new memoir supplies plenty of anecdotes to prove his point — a “60 Minutes” crew moves into the Greenfeld house; Karl’s juvenilia about Noah “ends up” in The New York Times and Esquire. Yet for Karl, living in a family that was “one of the public accounts of autism” was shaming. He became “locally famous,” as he puts it, “for nothing more than having a retard brother.”






One interesting point highlighted in the above short video is that Noah's brother wanted people to know what an autistic adult looks like, since he believes there will soon be many more. He is right, but his "autism" is not the one that most people will encounter. The SDA type of autism affects about 0.3% of the population, but Noah is at the severe end of SDA, so maybe 0.1% of the population. Soon in the US, the very flaky CDC figures will inevitably tell us that 2% of the population have "autism". Of those people with "autism", only 1 in 20 will look like Noah. One reason the CDC figures are misleading is that they apparently include "educational autism" (school diagnosed) as well as medical autism (diagnosed by some kind of doctor/psychiatrist). 

An Asperger blogger’s review of the books: -


Raising Expectations?
Coming back to the tittle of this blog post, for parents of children with Strictly Defined Autism (SDA), DSM3 type autism, or just call it severe autism, I think the experience of Josh Greenfeld, Noah’s dad, is pretty typical, albeit that Noah is at the severe end of DSM3 autism. This kind of autism is not something nice and does not end well. Noah's Dad gave up calling it autism in the end, he preferred to call it brain damage.
The fact that Josh lived to 90 years old and his son is still alive is remarkable and I see that as a success; but Noah never defeated autism.  It was not however what Josh wanted. In his words:-  "A fellow parent who had a developmentally disabled - I don't know what word to use anymore - child (told me) that we're the only parents in the world who somehow wish and pray fervently for our offspring to pre-decease us. And there's truth in that. Because if he's gone, then it's easier for us to go psychologically."
ABA did not work for Noah, at all. As his big brother summed it up “Noah flunked Lovaas” and Noah was treated by the man himself.
From reading this blog, you might imagine that Noah likely has severe regressive autism, caused by mitochondrial disease. What he likely needed was the mito cocktail developed by Dr Kelly, at Johns Hopkins, and quite possibly C7 (Triheptanoin), BHB (beta-hydroxybutyrate) and C8 (caprylic acid).  Even that might not have helped, but it is always better to at least try.  
I suppose I started my autism experience with realistic expectations a decade ago and so I get to keep raising them. ABA did help, we can say that “Monty graduated Lovaas”, but it was nowhere near enough.  If you want more, you have to treat the underlying biology.

PS  
I have not read any books like those in today's post, just reviews of them this week for this post. They are not my cup of tea.

I did read a lot of books on ABA  (not my cup of tea either, but necessary) and a little about neuropsychology (actually a good read). The neuroscience books (heavy going) are out of date by the time they are published and everything you could want to know is there in journals on the internet, for free, one way or another.



38 comments:

  1. Peter, can you explain why you mention treatments such as quite possibly C7 (Triheptanoin), BHB (beta-hydroxybutyrate) and C8 (caprylic acid). Are those for mito issues or something else? Thanks! MH

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    1. MH, these will be covered in future posts, but C7 in large amounts and BHB and C8 even in small amounts look very interesting to treat mito issues. BHB and C8 in small amounts seem to help about 1 in 5 of broader autism. This all relates to ketones, which seem to have multiple, seemingly unrelated, benefits. It appears that you can have most of these benefits without fundamentally altering your diet.

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  2. Here is some very interesting research concerning NKCC1 and the finding that at least half the water in the brain (or water for CSF production) does not happen via osmosis as is currently believed, but rather via NKCC1 acting as a water co-locating transporter:

    Press Release:

    https://www.sciencedaily.com/releases/2018/06/180614213715.htm

    Paper:

    https://www.nature.com/articles/s41467-018-04677-9

    With respect to Bumetanide, these findings are really, really huge. It is also very interesting to see how intranasal vasopressin is now being looked at very strongly for improving socialization aspects of autism, especially in males, while also pointing out vasopressin is also known as anti-diuretic hormone in the periphery. In the hypothalamus, oxytocin releasing neurons and vasopressin releasing neurons are in two different nuclei in a salt and pepper like distribution. Not to get off on too much of a tangent, but while there have been some studies on intracranial pressure and autism, I have seen nothing too terribly interesting here, so maybe it should be looked at more closely in this regard.

    Now for those who don't want to read the study, both furosemide (blocks both NKCC1 and KCC2) and bumetanide (blocks NKCC1) were used to block the rise of CSF in the choroid plexus.

    It is also worth noting that in macrocephaly, the ventricles (which CSF drains out of) are compressed due to there not being enough space in the skull for the enlarged brain. This of course can cause increases in intracranial pressure. This makes me wonder if it would make sense for there to be a study concerning the large head autism phenotype and the potential benefits of a more aggressive use of Bumetanide in reducing intracranial pressure than the 1mg or 2mg per day doses used in the handful of studies that have looked at Bumetanide and autism. Of course, there are risks with any diuretic and this kind of research would require significant medical supervision but in light of this research mentioned above, this I feel is a big question that needs to be answered soon.

    All kinds of bad things happen to brain function from chronic intracranial pressure, so it is reasonable to ask if interventions that simply reduce intracranial pressure in those with autism who have compromised ventricles could significantly improve symptoms for those with autism who also have large heads.

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  3. Roger, I have not carried out many lab tests. I was lucky in that the first drug I tried (bumetanide) worked. If that works certain other drugs may well also work.

    It is really a case of informed trial and error. Most of my core PolyPill, I found very early on, the only recent addition is Agmatine (thanks to Tyler). I think something else will be added, perhaps relating to ketones.

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  4. Peter, there are some things that I would think would be part of your polypill. For example, cinnamon? Or cocoa flavanols? Or sytrinol? Can you elaborate? Congrats to Monty and you for continued successes. MH

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    1. MH, many things do help a little, but at some point there is a limit to what is practical; this limit is going to vary from person to person. I do think cinnamon has a benefit, you need a teaspoon a day. High flavanol cocoa is also a good choice but you need a teaspoon of that. Sytrinol also helps, but only for a few days and then the effect is lost.

      If someone made a highly concentrated product that included broccoli sprouts, cinnamon and cocoa, that tasted OK I would buy it.

      I think you need to rank therapies out of 10, for both short term and long term effect and then choose based on availability, price and practicality.

      For Monty Bumetanide scores 10 and it cost me 25 cents a day, I have found some 1s and 2s that I do not use.

      There is a drug I wrote quite a lot about called Telmisartan, an angiotensin receptor blocker, it has a wide range of metabolic effects that might correct some variances found in autism. It did have an effect in Monty, it made him want to sing, which is nice, but it is not enough to warrant taking it.

      The PDE4 inhibitor Daxas should also help, and I think it does a little, but it does have some GI side effects including nausea.

      I wrote a lot about PAK1 inhibitors. Our reader who started her company to develop autism drugs found a potent experimental PAK1 inhibitor helps a lot, but the only product generally available is an expensive bee propolis. It might help a little, but $30 for a tiny bottle is a lot to pay because you need a lot of it.

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    2. Funny that you mention Sytrinol and other statins in the past, it shows that Im somewhat the oposite with things.

      For example HMB (yes the anticatabolic food supplement) increases my mood and increase HMG-coA activity (statin do the oposite?) and is suspected to increase cholesterol synthesis.

      Getting bumetanide soon, I expect end of next week I will have it. How fast would you say the effects should be noticable Peter?

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    3. Aspie1983, it is very variable how long it takes to see a benefit from bumetanide. I would say about 2 weeks is typical, but it can be longer.

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  5. Forgot to add, I seem to be a responder to agmatine, it does the same as you mentioned it does to your son (increases playing). I seem to have less approach anxiety in social situations.

    Please note Im also still on biogaia gastrus. That being said I tried 2000mg agmatine earlier today and I had a wave of anxiety coming over me for about 30mins (which started about an hour after intake), doses of 500-1000mg do not seem to give me anxiety at all.

    This is the first time Ive tried 2000mg though, I will try it some other day see if it does the same.

    Good day to all

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  6. Hi Peter, I was intrigued by the review of C7, BHB Salts and Caprylic Acid. Parenthetically, caprylic acid is often prescribed by DAN/MAP doctors to address dysbiosis. Your discussion includes it for different, apparently metabolic, reasons. While BHB Salts are a big commercial success with people who follow the Keto diet and want to achieve effects of ketosis extraneously, apparently C7 is not available commercially that I can find. I am wondering if you know places in the world where it can be obtained? - Thanks - Mira

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    1. Mira, it seems to be difficult to obtain C7 outside of a clinical trial. You need large amounts of it.

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  7. Tyler, thanks for the science daily post on inflow/outflow of liquid from the brain and intracranial pressure. It is helpful to show that to doctors who are concerned about the bumetanide use. On the other point, vasopressin, what is your view on the balovaptan trials, which focus on vasopressin in the opposite way, namely to block the receptors. We have reached out to the team at Yale doing the 'Aviation' study which is the only one I know of accepting children under 18 to the balovaptan trial, to request participation. I will report on that as we find out more. Thanks, Mira

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    1. I know nothing about balovaptan, though I assume it is the Vasopressin 1A antagonist I have read about before. This strange contradiction between studies showing benefits to vasopressin inhalation as well as V1A antagonists I suppose will probably be addressed sooner or later.

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  8. Peter - Just wanted to say congrats to Monty on his academic accomplishments this year!
    (Also, wondering if your ketone investigation might include the nutraceutical oxaloacetate - brand name Benegene, among others?)

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    1. Lattegirl, Oxaloacetate has numerous effects, but they do not really relate to ketosis, they relate to insulin signalling, your mitochondria (via PGC1) and inflammation.

      https://www.ncbi.nlm.nih.gov/core/lw/2.0/html/tileshop_pmc/tileshop_pmc_inline.html?title=Click%20on%20image%20to%20zoom&p=PMC3&id=4271074_ddu37108.jpg

      Oxaloacetate inhibits mitochondrial complex 2, which for some people could be very bad.

      Although sold as a supplement, you can see that oxaloacetate really should be considered a drug. It might well be good for some people, but might harm others.

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  9. Here is some more research showing trehalose excelling at reducing inflammation and cleaning out cellular waste via autophagy induction:

    Press Release:

    https://www.sciencedaily.com/releases/2018/06/180620125941.htm

    Paper:

    https://www.tandfonline.com/doi/abs/10.1080/15548627.2018.1474313

    I have posted plenty of stuff on trehalose before (my son gets 50g per day), but this research is novel in that it quantifies how much trehalose manages to cross the blood brain barrier, whereas most previous research dealt with its positive autophagy inducing effects in peripheral organs like the liver.

    Mice were given trehalose in their drinking water (it is important to note mice lack trehalase in the gut which breaks down trehalose into two glucose sugars while humans have significantly more of this enzyme), but in spite of this fact, there are studies showing a high dose of trehalose (100g in one Alzheimer's study) overwhelms the trehalase enzyme and increases trehalose levels in the blood (trehalase is also in the blood and liver so the half-life is presumed to be short).

    The main problem with oral trehalase is that even though it is broken down slowly into glucose, every 5g of trehalose is 20 calories as each gram is 4 calories, so 100 grams of trehalose is 400 calories (roughly that of a non-diet soda). There is also some recent research linking it to C. Difficile infections as it is a recently popular ingredient for sweetening and preserving meat and apparently some C. Difficile strains like trehalose. The evidence is not that strong, plus the fact that there are many things that can lead to an environment for C. Difficile to thrive, so I feel it is a safe intervention for addressing a dysfunction (autophagy) that seems to pop up all the time in autism studies that look at the topic. I have now used it myself for years and have never had anything resembling gut problems whatsoever. I have no idea if it has improved my circulatory system or helped keep my neurons healthy, but I have had no negative effects from trehalose so far.

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  10. Peter, how come you never wrote (much) about carbonic anhydrase inhibition (CAI)?
    CAI has an important role in treating neuropathic pain and seems to connect many of the interventions we use. This paper, which you probably have read or maybe even linked to, mentions for example CAI as acetazolamide, celecoxib (COX-2), topiramate and sulfonamides more generally.

    "Carbonic anhydrase inhibition and the management of neuropathic pain"
    https://www.ncbi.nlm.nih.gov/m/pubmed/27211329/

    Not a fruitful avenue? Or just a less important or even coincidental connection? I just wanted to know if you've been down this road before.

    /Ling

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    1. Ling, neuropathic pain has the same over-expression of NKCC1 and under-expression of KCC2 as bumetanide-responsive autism. It is possible to target the AE3 exchanger as a means of lowering intracellular chloride as an alternative to blocking NKCC1. This is why I wrote some posts about Diamox/acetazolamide. However, CAI drugs cause GI side effects in many people, making them unsuitable for long term use.

      If they develop a drug with no side effects for neuropathic pain, it would be logical to then trial it on Autism, Down Syndrome, Fragile-X etc.

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    2. Thanks for letting me know what your take on this avenue is. Saves me a couple of research hours... :)

      /Ling

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  11. A new study elucidates how a high fiber diet, as well as acetate may be linked to being protective of obesity, type 2 diabetes, and metabolic syndrome which are overrepresented in the autistic population:

    Press Release:

    https://www.sciencedaily.com/releases/2018/06/180621172437.htm

    Paper:

    https://www.sciencedirect.com/science/article/pii/S1550413118303796

    The study was done on fruit flies, but other studies have linked dietary acetate and/or a high-fiber diet to being protective in obesity, type II diabetes, and other cardiovascular problems:

    http://circ.ahajournals.org/content/135/10/964

    Even though I don't believe a high-fiber diet acetate intervention is going to eliminate the core symptoms of autism and I am unaware of any autism studies looking into the matter, it might ameliorate some health problems that can exacerbate other health problems related to autism. Plus, having your child die from heart failure due to obesity/metabolic syndrome in their 40's is not something I think any parent wants for their child.

    Acetate supplementation is not without risks as I have read before that high levels (rather than normal levels which might be corrected by supplementation if levels are already low), is linked with some cancers.

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    1. Tyler I have said this before about acetate, but people tended to just ignore it when I spoke about simple apple cider vinegar with the exception of one woman from greece on this blog.

      Anyway a lot of care needs to be taken ACV as it cause severe throat burns.

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    2. Well you can always just use ACV in food such as on a salad. I have never noticed it having any burning sensation myself, but getting my son to drink vinegar I don't think is ever gonna happen unless it was seriously watered down and sweetened. ACV has been used from the time of the Romans and perhaps before as a general health tonic, so maybe the acetate qualities are what give ACV it's legendary appeal, especially since soldiers on the march are most likely going to be eating foods that don't spoil easy and that means milled grains that are low in fiber, and smoked and salted game.

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  12. Congratulations for Monty and all who are involved in his success!

    For my son it was his first year in primary school and now it is clear to me that using biology you can raise educational potential in a child with SDA to the levels not expected before.
    And this may turn out challenging for eduational system. In case of my son, he needs personalized eduaction as much as personalized medicine.

    Trying to develop "ketogenic diet for the jellybeans addicted" I've been using BHB for more than 2 months now with clear cognitive impact (bumetanide-like) as well as exceptional mood and affection.
    Peter, can you share where you found that ketone bodies/C8 help 1 in 5 of autism?

    Last thing in my year-end report: CACNA1A variant was found on WES in my son, but I don't know more details and testing is still in progress.

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    1. The study I was thinking of was:

      A modified ketogenic gluten-free diet with MCT improves behavior in children with autism spectrum disorder
      https://www.sciencedirect.com/science/article/abs/pii/S0031938418300507

      50% of the small sample (15 children) are responders. It said 40% were super-responders.

      I think you need the supplemental data. I had assumed super-responders were 40% of the 50% (ie 20%), but it is not clear from the text.

      The above trial was based on the diet, not the BHB supplement.

      I try BHB after the summer allergy season. Then I will put all the studies together and write about it.

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    2. Fortunately P/Q-type calcium channels are also blocked by cheap L-type channel blockers. Some common anti-epileptic drugs also block P/Q channels, perhaps some people with autism on these AEDs might be better off on a regular calcium channel blocker.

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    3. Agnieszka, I guess you've already found this page on CACNA1A, but I post it anyway since it was good and maybe somebody else will find it interesting too:
      http://epilepsygenetics.net/2015/09/11/cacna1a-this-is-what-you-need-to-know-in-2015/

      Also, I am very excited and happy to hear that you've found a treatment with such a big positive impact on your son, but also that it is with a compound that I've never heard of!
      I look forward both to read more of the "jellybean-version" of the ketogenic diet, and of course any Epiphany-post on the subject.
      I have a lot of questions like:
      Is this related to calorie restriction or not?
      Is this all about energy and ATP?
      What is your son eating nowadays - I thought you did gluten and dairy free and maybe also sugar free and histamine free and now maybe ketogenic too... What is left? :-o

      All the best,
      /Ling

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    4. Thanks Peter for explaining.

      There are anecdotal reports about unexpected seasonal allergies improvement on KD and this can explain it:

      https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4190937/

      "Fasting mitigates immediate hypersensitivity: a pivotal role of endogenous D-beta-hydroxybutyrate"

      "The results of the present study demonstrates that fasting suppress hypersensitivity reaction, and indicate that increased level of D-beta-hydroxybutyrate by fasting plays an important role, via the stabilization of mast cells, in suppression of hypersensitivity reaction."

      Unfortunately data on ketogenic diet, BHB, MCT etc in ASD is still scarce.

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    5. Ling, BHB (or "exogenous ketones") seems popular for weight loss in the US and also among self-hackers, body builders etc. This does not mean it is known among European neurologists, even experts on ketogenic diet.

      I like this review on BHB, written by an enthusiast (=manufacturer):
      https://www.perfectketo.com/what-is-betahydroxybutyrate-or-bhb/

      BHB seems to do more than optimizing energy issues:
      https://www.ncbi.nlm.nih.gov/pubmed/25193333
      "β-hydroxybutyrate: much more than a metabolite."

      BHB is HDACs and anti-inflammatory via blocking NLRP3 inflammasome (=downregulating pro-inflammatory IL-1beta).

      Exogenous ketones, MCT and dietary interventions were discussed here a while ago - search for Tyler's and RG's comments.

      I tried to find a way to mimic KD without significant dietary restrictions with the hope that in autism one does not need so deep ketosis as to control seizures. These papers seem to confirm it:

      https://link.springer.com/content/pdf/10.1007%2Fs11011-018-0219-1.pdf
      http://journals.sagepub.com/doi/abs/10.1177/08830738030180020501

      They report positive effects with relatively low BHB blood levels.

      My son eats a lot and I would say eating is his hobby ;-) This is one of the reasons I found going full ketogenic diet difficult. I couldn't see any significant impact of histamine-rich foods so I assume he's not histamine intolerant. I wouldn't dare to experiment with calorie restriction or intermittent fasting in a child, especially prone to migraines. Sugar-free diet... I tried for one day - this does not go in line with my son's hobby ;-)

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    6. Agnieszka, the good news is that the UCLA study that found the mode of action of the KD in epilepsy (those 2 bacteria) has already produced a medical start up called Bloom Sciences. They are developing a medical food, which they think will take a couple of years and "Bloom is also considering how the microbiome benefits of the ketogenic diet could be helpful in other neurological conditions, including autism, depression, and Parkinson’s disease.

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    7. Peter, this is interesting. I wonder if 'KD-related' microbiome manipulations will be enough in autism as it was found in epilepsy.

      Ling, I've copied wrong link in the earlier comment. This is the paper I mean:
      https://www.sciencedirect.com/science/article/abs/pii/S0031938418300507
      - instead of the old one by Prof. Evangeliou (which is also interesting, especially that it is about intermittent KD).

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    8. Thanks for all the explaining and all the links! I don't think we'll ever see the end of this stream of treatment possibilities.

      /Ling

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    9. Take a look at Fig 6F on page 8 of

      The Gut Microbiota Mediates the Anti-Seizure Effects of the Ketogenic Diet
      DOI: https://doi.org/10.1016/j.cell.2018.04.027

      there is a profound change in the hippocampal GABA/Glutamate ratio with the KD, or the 2 bacteria. This is going to affect autism. It shifts from 0.4 to 1.5.

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    10. Shame I cant imagine seeing myself living without carbs, intense cravings for sugar (atleast at the start of the diet?) for sure.

      Also what about cortisol levels, as far as I know carbs are a great surpressor of cortisol. Couldnt keto lead to sleep problems or aggression or other cortisol related problems? Or does the gaba/glutamate balancing that the diet does offset these behaviors?

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    11. Aspie, sugar craving may decrease on KD and it is not that relevant while using exogenous ketones.

      Peter, if so, is there any way to influence microbiome to achieve similar results now, not waiting for Bloom Sciences product?

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    12. Agnieszka, there is a lot written on these 2 types of bacteria, like here:=

      Strategies to promote abundance of Akkermansia muciniphila, an emerging probiotics in the gut, evidence from dietary intervention studies
      https://www.sciencedirect.com/science/article/pii/S1756464617301627

      Perhaps you have found a simpler way using BHB. The advantage of BHB is that you will have more effects than just changing gut bacteria.

      The great news is that you found a great benefit from BHB, even though you cannot be sure why.

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  13. Agnieszka the KD seems promising, but I have my doubt if the full benefits can be mimiced by exogenous ketones such as BHB. After all glucose deprivation is critical in the KD, not to mention the effects that low carb intake will also have on the on the microbiome (they love carbs in the gut).

    That it is not to say that BHB supplementation does not have benefits of its own though and possibly (partially) mimicing a ketogenic diet.

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    1. Aspie1983, there is US government funding to try to develop the KD in a pill. It does look like ketones as a fuel is only a small part of the benefit of the KD, so for many people a KD pill would be all they need.

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    2. Hope so,

      Attempting to trick the body with a pill the body pretty much always comes with a compensatory mechanism in the long run, dont forget the ultimate goal of the body is the maintain homeostasis and its pretty damn good at that.

      Would like to add that (atleast for myself), coconutoil (and thus MCT's) does seem to give me more mental capacity.

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