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Wednesday 31 October 2018

TSO for Autism with Allergies? Published after 5 years - Also Ponstan again


As we know, things often do not move fast in the world of medical research, at least when it comes to autism.
Back in 2014 I wrote some posts about a novel immuno-modulatory therapy, based on TSO, a harmless gut parasite, developed for autism by one parent. He then shared it with Eric Hollander at The Albert Einstein College of Medicine. Then a small biotech company called Coronado, tried to develop TSO to treat a variety of inflammatory conditions, including autism.

A pilot trial in autism was funded by the Simons Foundation and Coronado.
Coronado did not achieve the desired results in their ulcerative colitis TSO trials, so their share price took a dive and they later changed their name to Fortress Biotech. It looks like they have given up on TSO.
The autism Dad, Stewart Johnson, who originally came up with the idea has not updated his TSO website since 2011.


I do wonder if he continues to give TSO to his son. The good thing is that he fully documented his son's treatment, shared it with a leading autism researcher and has left the information in the public domain.    
The research data from the pilot trial has finally been published.


OBJECTIVES:

Inflammatory mechanisms are implicated in the etiology of Autism Spectrum Disorder (ASD), and use of the immunomodulator Trichuris Suis Ova (TSO) is a novel treatment approach. This pilot study determined the effect sizes for TSO vs. placebo on repetitive behaviors, irritability and global functioning in adults with ASD.

METHODS:

A 28-week double-blind, randomized two-period crossover study of TSO vs. placebo in 10 ASD adults, ages 17 to 35, was completed, with a 4-week washout between each 12-week period at Montefiore Medical Center, Albert Einstein College of Medicine. Subjects with ASD, history of seasonal, medication or food allergies, Y-BOCS ≥ 6 and IQ ≥70 received 2500 TSO ova or matching placebo every two weeks of each 12-week period.

RESULTS:

Large effect sizes for improvement in repetitive behaviors (d = 1.0), restricted interests (d = 0.82), rigidity (d = 0.79), and irritability (d = 0.78) were observed after 12 weeks of treatment. No changes were observed in the social-communication domain. Differences between treatment groups did not reach statistical significance. TSO had only minimal, non-serious side effects.

CONCLUSIONS: 

This proof-of-concept study demonstrates the feasibility of TSO for the treatment of ASD, including a favorable safety profile, and moderate to large effect sizes for reducing repetitive behaviors and irritability.


some excerpts:-

Autism spectrum disorder (ASD) is a neurodevelopmental disorder characterized by marked deficits in two core symptom domains: social-communication, and repetitive behaviors and restricted interests. Current literature supports a link between neuroinflammation, imbalanced immune responses, and ASD. Characteristic cytokine profiles of Th2 anti-inflammatory and Th1 proinflammatory cytokine responses have been reported in ASD. Additionally, some individuals with ASD demonstrate an amelioration of symptoms during fever episodes. This suggests a role for immune-inflammatory factors, as fever is a cardinal symptom of infectious and inflammatory processes, and induces the secretion of pro-inflammatory cytokines which are part of an autoregulatory loop. Early in neurodevelopment, microglia play a protective role in promoting neurogenesis, suppressing inflammation and eliminating inhibitory synapses. Pro-inflammatory cytokines are known to activate microglia, which in turn secretes cytokines that participate in the inflammation process. There is evidence for neuroglial activation and neuroinflammation in the cerebral cortex, cerebellum and white matter of individuals with ASD, which relates to an increase of glial-derived cytokines. Additionally, viral infection during pregnancy correlates with increased frequency of ASD in offspring. This is modeled in rodents subjected to maternal immune activation (MIA), which results in autism-like behavioral abnormalities in their offspring.

Both T helper 17 (TH17) cells and the effector cytokine interleukin-17a (IL-17a), are present in mothers who have MIA-induced behavioral abnormalities in their offspring. In this animal model of MIA, the abnormal autistic-like behavior in offspring is prevented by maternal treatment with an anti-inflammatory cytokine IL-6 antibody. Additionally, recent studies suggest that therapeutic targeting of TH17 cells in susceptible pregnant mothers may reduce the likelihood of bearing children with inflammation-induced ASD-like phenotypes. In sum, due to the inflammatory mechanisms implicated in the development and symptomatology of ASD, immunomodulatory interventions should be explored as an experimental therapeutics’ pathway.

The study of helminth worms, such as Trichuris Suis Ova (TSO), for the treatment of autoimmune disorders emerged from the “hygiene hypothesis”. This hypothesis states that stimulation of the immune system by infectious agents, such as microbes that stimulate normal immune responses, is protective against the development of inflammatory diseases, and that due to a rise in hygiene in urban settings there are less protective microbes in humans. This subsequently leads to an increase in autoimmune inflammatory disorders, including multiple sclerosis, inflammatory bowel disease, asthma, allergic rhinitis and possibly ASD. The interaction of the developing immune system with microorganisms, including helminths, may be an important component of normal immune system maturation. TSO has been studied in clinical trials of other immune-inflammatory disorders such as allergies, inflammatory bowel disease, ulcerative colitis, Crohn’s disease, and multiple sclerosis with mixed results. This is the first such study in ASD or any neurodevelopmental disorder.  

The porcine whipworm TSO is proposed to work through multiple mechanisms, including interference with antigen presentation, cell proliferation and activation, antibody production, and modulation of dendritic cells. In addition to the induction of regulatory cells, TSO may modify the cytokine profiles released by the local inflammatory cells. Helminths, including TSO, are well known to induce tolerance in their hosts via differential modulation of increased anti-inflammatory Th2 cytokine (IL-4, IL-5, IL-10, IL-13) and decreased pro-inflammatory Th1 and Th17 cytokine (IL-1, IL-12, IFN-γ, TNF-α, IL-6) responses. Th2 cell induction leads to strong IgE, mast cell and eosinophil response, while cytokines IL-4 and IL-13 trigger intestinal mucous secretion, enhance smooth muscle contractibility, and stimulate fluid secretion in the intestinal lumen. Additional studies have shown that a similar exposure to TSO results in the augmentation of the anti-inflammatory Th2 response, a dampening of the toll-like receptor (TLR)-induced proinflammatory Th1 and Th17 responses, and an increased presence of myeloid and plasmacytoid dendritic cells, which are antigen producing cells that stimulate T-cells.

Our subjects were part of an ASD subgroup, and were high functioning adults, as defined by an IQ greater than 70, with a history of seasonal, medication, or food allergies, and/or a family history of autoimmune illness. Thus, results may not be generalizable to a larger more heterogeneous ASD population.

This study suggests that immune-modulating agents could be a useful therapeutic approach to address certain domains in individuals with ASD. Those that will benefit the most are likely to have marked restricted and repetitive behaviors and irritability. Future studies are needed to replicate these preliminary findings in larger samples, and effect sizes support future trials with 25 subjects per group in a parallel design study. Alternatively, they could be completed in a younger population, stratified for higher baseline severity, and using other immunomodulatory agents.  

Conclusions 

This trial provided key data necessary for planning further definitive studies of TSO in the ASD population. TSO was observed to improve symptoms in the restricted and repetitive patterns of behavior domain of ASD. These symptoms map onto the positive valence systems and cognitive systems of the NIMH Research Domain Criteria (RDoc) matrix, which provides an integrative research framework for the study of mental disorders. Specifically, the Approach Motivation, Habit and Cognitive Control constructs of the matrix are targeted by TSO. Future trials should continue to integrate the RDoc framework, and be conducted in more homogeneous syndromal forms of ASD with marked immune and microglial abnormalities. 

Acknowledgements:

This work was supported by the Simons Foundation under Grant number 206808, and by Coronado Biosciences. Coronado Biosciences also provided both TSO and the matching placebo. This data was presented at the International Meeting for Autism Research (2015, Poster 20516), and the American College of Neuropsychopharmacology Conference (2013, Panel and Poster T177).  


My posts related to parasites and autism are below. The role of the ion channel Kv1.3 is interesting.


                            

Personalized Medicine
The problem with personalized medicine, like Stewart Johnson and the TSO treatment for his son, is that it may be just too personalized to apply to most other people.  As a result, investing money in the many possible autism treatments is a highly risky business. Many potential autism treatments like, Arbaclofen, are stumbled upon by accident or in a n=1 trial. 
Our reader Knut Wittkowski has got backing for his mefenamic acid-based therapy to halt the progress of autism to severe and non-verbal.
He made a deal with Q BioMed and the drug is now called QBM-001.  The idea was to modify the already existing painkiller Ponstan (which is OTC in many countries) so that it had reduced side effects and most importantly can be patented.


The treatment window during which the child is sensitive to the effects of the drug is proposed to be 12-24 months.
Q BioMed want to submit an orphan drug application in 2019. The problem with that is that autism is now very common and it is hard to see how an autism drug for children up to 2 years of age would qualify. You cannot really tell at 12 months if someone is going to have mild or severe autism, so you would have to give it to everyone with a diagnosis.
Orphan drugs are for rare conditions and have stronger/longer patent protection to allow drug developers to get their money back. 
Nonetheless, good luck to Knut. 
The original post on Ponstan and Knut’s work.


Ponstan is widely available outside of the US. It is particularly good at lowering temperature in children during fevers.

Sensitive periods and treatment windows are the topics of a forthcoming post. We did earlier look at critical periods, which are key times during the development of the brain.  It is important to know when these are, because you need to have your therapy in place at these times. Sensitive periods are the time periods when a therapy can be effective. Correcting some defects is only possible within these critical windows and this needs to be understood by those planning clinical trials.

Knut is a rare researcher who has fully grasped this.









Wednesday 24 October 2018

Choose your Statin with Care in FXS, NF1 and idiopathic Autism


There are several old posts in this blog about the potential to treat some autism using statins; this has nothing to do with their ability to lower cholesterol. 

Statins are broadly anti-inflammatory but certain statins do some other particularly clever things. This led me to use Atorvastatin and Fragile-X researchers to use Lovastatin.


Fragile X is suggested by an elongated face and big/protruding ears; 
other features include MR/ID and autism.

I was recently forwarded a Scottish study showing why Simvastatin does not work in Fragile X syndrome, but Lovastatin does.
Fragile X mental retardation protein (FMR1) acts to regulate translation of specific mRNAs through its binding of eIF4E (see chart below). In people with Fragile X, they lack the FMR1 protein. Boys are worse affected than girls, because females have a second X chromosome and so a "spare" copy of the gene.


         Simvastatin does not reduce ERK1/2 or mTORC1 activation in the Fmr1-/y hippocampus.

So  ? = Does NOT inhibit

The researchers in Scotland did not test Atorvastatin in their Fragile X study.
The key is to reduce Ras. In the above graphic it questions does Simvastatin inhibit RAS and Rheb.

RASopathies have been covered in this blog. Too much of the Ras protein is a common feature of much ID/MR. Investigating RAS took me to PAK1 inhibitors and the experimental drug FRAX486. This drug was actually developed to treat Fragile X; it is now owned by Roche. At least one person is using FRAX486 to treat autism.
You might wonder why the researchers do not just try Lovastatin in humans with Fragile X.  Unfortunately, Lovastatin was never approved as a drug in Scotland, or indeed many other countries.  Some researchers just assumed they could substitute Simvastatin, which on paper looks a very similar drug and one that crosses the blood brain barrier better than Lovastatin.



The cholesterol-lowering drug lovastatin corrects neurological phenotypes in animal models of fragile X syndrome (FX), a commonly identified genetic cause of autism and intellectual disability. The therapeutic efficacy of lovastatin is being tested in clinical trials for FX, however the structurally similar drug simvastatin has been proposed as an alternative due to an increased potency and brain penetrance. Here, we perform a side-by-side comparison of the effects of lovastatin and simvastatin treatment on two core phenotypes in the Fmr1-/y mouse model. We find that while lovastatin normalizes excessive hippocampal protein synthesis and reduces audiogenic seizures (AGS) in the Fmr1-/y mouse, simvastatin does not correct either phenotype. These results caution against the assumption that simvastatin is a valid alternative to lovastatin for the treatment of FX.  

Although we propose the beneficial effect of lovastatin stems from the inhibition of ERK1/2-driven protein synthesis, it is important to note that statins are capable of affecting several biochemical pathways. Beyond the canonical impact on cholesterol biosynthesis, statins also decrease isoprenoid intermediates including farnesyl and geranylgeranyl pyrophosphates that regulate membrane association for many proteins including the small GTPases Ras, Rho and Rac [18, 46, 48, 49]. The increase in protein synthesis seen with simvastatin could be linked to altered posttranslational modification of these or other proteins. Indeed, although we see no change in mTORC1-p70S6K signaling, other studies have shown an activation of the PI3 kinase pathway that could be contributing to this effect [32]. However, our comparison of lovastatin and simvastatin shows that there is a clear difference in the correction of pathology in the Fmr1-/y model, suggesting that the impact on ERK1/2 is an important factor in terms of pharmacological treatment for FX.  There are many reasons why statins would be an attractive option for treating neurodevelopmental disorders such as FX. They are widely prescribed worldwide for the treatment of hypercholesterolemia and coronary heart disease [50], and safely used for longterm treatment in children and adults [46]. However, our study suggests that care should be taken when considering which statin should be trialed for the treatment of FX and other disorders of excess Ras. Although the effect of different statins on cholesterol synthesis has been well documented, the differential impact on Ras-ERK1/2 signaling is not well established. We show here that, contrary to lovastatin, simvastatin fails to inhibit the RasERK1/2 pathway in the Fmr1-/y hippocampus, exacerbates the already elevated protein synthesis phenotype, and does not correct the AGS phenotype. These results are significant for considering future clinical trials with lovastatin or simvastatin for FX or other disorders of excess Ras. Indeed, clinical trials using simvastatin for the treatment of NF1 have shown little promise, while trials with lovastatin show an improvement in cognitive deficits [28-30]. We suggest that simvastatin could be similarly ineffective in FX and may not be a suitable substitute for lovastatin in further clinical trials.


Conclusion
If you are treating Fragile X, best to start with Lovastatin and see if it helps.  In theory it might also help NF1 (Neurofibromatosis Type 1).

It looks to me that Atorvastatin also inhibits the relevant pathway and does much more besides that (PTEN, BCL2 etc)

What is Roche doing with FRAX486?




Wednesday 17 October 2018

Autism as a Hierarchy of Impairments


A French Pyramid, worth visiting

Today’s post is not full of complex science.
I am reminded from time to time that I am supposed to be writing a book about translating autism science into practical therapy. To even partially do justice to all the science, things have to get a little complicated, at which point it will inevitably lose many readers.
What is much easier to achieve is to explain what autism is, and is not, and what, if anything, you might want to do about it.
I think you can consider autism as a hierarchy of impairments that together define a particular person’s “autism”.  For example, epilepsy is not just a comorbidity of someone’s autism, it is an integral part of it, and very much so biologically.
All of this is a simplification, but I think it does actually help represent what is currently diagnosed as autism.




Most people diagnosed today with autism are at the lower end of the pyramid/hierarchy, they have impaired social and communication skills to some degree and some of the issues in the level above, maybe some anxiety or ADD or ADHD.
People with severe autism rise through the levels to the summit, perhaps escaping from some elements.
When you then add prevalence to this hierarchy of impairments, you get the graphic below.
Really severe autism is thankfully rare. This was the old autism defined under the diagnostic regime of DSM3.  DSM is an abbreviation of the Diagnostic and Statistical Manual of Mental Disorders, published by the American Psychiatric Association.
In 1994 DSM version 4 introduced Asperger’s as an extension of autism.
We are currently on DSM5 which dropped the term Asperger’s opting for three levels of severity.  Severe autism is called level 3 and mild autism is level 1.  So, a genuine little professor type of Asperger’s would be level 1. Some people are getting diagnosed at intermediate points like 1.5.
Given the fact that the underlying biology is actually extremely complex, involving many hundreds of affected genes, it is perfectly possible to have a person with impaired social skills, who has a high IQ, no physical impairments, but self-injures.





  

Having identified where a person fits in this autism hierarchy, it is then time to see what are the likely consequences.
Having understood the consequences, you can then make plans to mitigate them.









In the case of the person with Asperger’s (DSM5 level 1) there may be very few issues that need to be addressed; but if you ignore the fact they may spend their school years being bullied and feeling excluded, they may fall victim to the 9 times elevated risk of suicide.
Ignoring what appear as minor quirky issues may have major consequences later.
At the summit of the pyramid the big dangers are seizures, self-injury and early death, but not from suicide.
Aggression and self-injury have to be brought under control during childhood, because in adulthood society does not tolerate it.  In most countries there is a lack of appropriate places to house adults with such behaviours and then bad things will inevitably happen.
Some people’s physical impairments fade away, some people never have any, but for some others such issues remain lifelong.
Cognitive dysfunction is part and parcel of DSM3 autism, what now is called Level 3 autism, under DSM5. As we have seen in this blog, some aspects of cognition can be improved using biology.

Personalized Medicine?
When deciding whether to treat a 2 or 3-year-old with autism using personalized medicine it is very important to understand the consequences. If the young child has severe autism (DSM3, or DSM5 level 3) then you know what the likely outcome will be if the child remains untreated. We know that 10-15% of these cases will dramatically improve without any intervention, but 85% will not. Intensive ABA interventions will accelerate skill acquisition in many cases, but it does not address the biological dysfunctions. The end result is a shortened lifespan (on average 40 years), much of it likely in an institution of one kind or another.  This you compare against the risk and cost of personalized medicine.
If you have a 3-year-old with mild autism (DSM5 level 1), the biological issues are quite mild and you will likely achieve great things with simple steps like teaching social skills and finding the right schools (small class sizes and no bullying). If you have very mild autism you may well find the positives outweigh the impairments associated with autism. Great attention to detail, perseverance, reliability and perhaps a high IQ may not make you cool at school, but are highly valued in the "right" workplace.

Not surprisingly, it is mild autism (DSM5 level 1) that gets most of media attention these days. At some point perhaps they will add DSM5 level 0.5 to include even mildly quirky people, but the next target for diagnosis appears to be adult females who could fit DSM5 level 1, but who slipped through the net.  Expect prevalence to continue to increase.







Wednesday 10 October 2018

Ketone Therapy in Autism (Summary of Parts 1-6)




Open the above file via Google Drive, so it is big enough to read. Click the link below. You can also take links from it to the relevant blog post.

https://drive.google.com/file/d/1Jl_JMUrX7suXz0n_yJPCLPinrvdddBhI/view?usp=sharing

In the mini series of posts on ketones and autism we have come across a long list of effects that will benefit certain groups of people.



1.     Change in gut Bacteria


2.     Ketones as a brain fuel    


3.     Niacin Receptor HCA2/ GPR109A

4.     NAD sparing

5.     CtBP Activation by reducing NADH/NAD+ ratio

6.     NLRP3 Inflammasome inhibition

7.     Class 1 HDAC inhibition

8.     Increase BDNF

9.     Ramification of Microglia

10.PKA activation

11.PPAR gamma activation
It was interesting that the beneficial effect of the Ketogenic Diet in epilepsy is driven by changes the high fat diet makes to the bacteria in your gut and seems to have nothing really to do with ketones. Well it took a hundred years to figure that one out.
In the case of Alzheimer’s, you can see that more than one effect is potentially beneficial. People with Alzheimer’s do have low glucose uptake to the brain, but they also have elevated inflammatory cytokine IL-1B.
In Huntington’s it is the HDAC inhibition effect that seems to be what helps.  This brings us back to HDAC inhibition as a potentially transformative therapy with long lasting effects. It appears that the small number of people who achieve long lasting benefit from short term use of sulforaphane or EGCG may have experienced HDAC inhibition changing the expression of up to 200 genes.  In the case of sulforaphane from broccoli, some people have gut bacteria that produces large amounts of the enzyme myrosinase, which means they convert very much more of the glucoraphanin in broccoli to sulforaphane (an HDAC inhibitor).
It does look like a low dose of a potent HDAC inhibiting cancer drug is what is needed by certain single gene autisms and perhaps some idiopathic autism. This was covered in a dedicated post where we saw the long-lasting benefit of short-term use of Romidepsin. Vorinostat, a very similar drug, but which is taken orally, should be trialled in Shank 3, Pitt Hopkins and Kabuki, to see if the same transformative long-lasting effect can be reproduced.
In Multiple Sclerosis (MS) the effect on Niacin receptor HCA2/GPR109A should help a lot, but so should PKA activation.
In mitochondrial disease it was suggested that increased ketosis will help conserve NAD, which may be deficient. Also, using ketones as an alternative brain fuel may bypass problems that occur when glucose is supposed to be the fuel and thereby boost brain function. The most important effect is likely to be activation of PPAR gamma by C10, which increases the number of mitochondria and boosts the enzyme complex 1.
Many of the people with autism and an overactive immune system stand to benefit from activating CtBP, inhibiting the NLRP3 inflammasome, or activating HCA2/GPR109A.
I think there should be clinical trials using a potent HCA2 activator in autism comorbid with immune over-activation. 
We can see that some people who respond to BHB, experience an immune rebound on cessation, so this helps narrow down the likely beneficial mode of action.  In this immune sub-group, the idea to using other activators of HCA2/GPR109A would seem worthwhile. 

PPAR gamma activation should help those with mitochondrial dysfunction, but this effect is produced only by C10, not BHB or C8. For C10 you eat a ketogenic diet or add it as a supplement (e.g. cheaper MCT oil, or coconut oil).

As recently highlighted by our reader Agnieszka, perhaps the fever effect in autism can be explained by short-term ketosis. Fever is known to sometimes raise the level of ketones, particularly in children (it is called non-diabetic ketosis).  So if your child's autism improves during, or just after fever, test the level of ketones in their urine.


Conclusion

We may have shown the benefits of a high fat ketogenic diet, but there are very many different fats and they do not all produce the same effects.

There are many saturated fatty acids, they are numbered based on how many Carbon atoms they have.

So, C8, known as Caprylic acid has the formula  C8H16O2

Eating C8 looks to be a great way to increase the level of ketones in your blood.

Eating C10 should be good for people with mitochondrial dysfunction and people with diabetes.

Your food contains many other saturated fatty acids and your gut bacteria produce even more.


Common Name Systematic Name Structural Formula Lipid Numbers
Propionic acid Propanoic acid CH3CH2COOH C3:0
Butyric acid Butanoic acid CH3(CH2)2COOH C4:0
Valeric acid Pentanoic acid CH3(CH2)3COOH C5:0
Caproic acid Hexanoic acid CH3(CH2)4COOH C6:0
Enanthic acid Heptanoic acid CH3(CH2)5COOH C7:0
Caprylic acid Octanoic acid CH3(CH2)6COOH C8:0
Pelargonic acid Nonanoic acid CH3(CH2)7COOH C9:0
Capric acid Decanoic acid CH3(CH2)8COOH C10:0
Undecylic acid Undecanoic acid CH3(CH2)9COOH C11:0
Lauric acid Dodecanoic acid CH3(CH2)10COOH C12:0
Tridecylic acid Tridecanoic acid CH3(CH2)11COOH C13:0
Myristic acid Tetradecanoic acid CH3(CH2)12COOH C14:0
Pentadecylic acid Pentadecanoic acid CH3(CH2)13COOH C15:0
Palmitic acid Hexadecanoic acid CH3(CH2)14COOH C16:0
Margaric acid Heptadecanoic acid CH3(CH2)15COOH C17:0
Stearic acid Octadecanoic acid CH3(CH2)16COOH C18:0
Nonadecylic acid Nonadecanoic acid CH3(CH2)17COOH C19:0
Arachidic acid Eicosanoic acid CH3(CH2)18COOH C20:0

C4, familiar as Butyric acid, helps maintain the integrity of the intestinal barrier and the blood brain barrier.  Butyric acid, or butyrate, is also an HDAC inhibitor and it seems that in animal models, and some humans, a small amount can be beneficial but large amounts can have a negative effect. A small amount in humans seems to be about 500 mg a day.  There are earlier posts is this blog on butyrate.

C3, familiar as Propionic acid, is bad for you and too much propionic acid will by itself cause autistic behaviours. NAC counters the effect of propionic acid in mouse models.

All those people eating coconut oil are consuming a 99% mixture of fatty acids with 1% phytosterols.

Phytosterols like β-SitosterolStigmasterolAvenasterol and Campesterol likely explain why coconut oil actually reduces "bad" cholesterol, rather than increasing it, as predicted by the American Heart Association and others. This counters the negative effect of the Palmitic acid (C16).

Lauric acid (C12) is thought to increase HDL ("good") cholesterol and may have a beneficial effect on acne.

Myristic acid (C14) is also thought to increase HDL ("good") cholesterol.

Palmitic acid (C16) raises LDL ("bad") cholesterol and large amounts have other negative effects.

Oleic acid is also found in olive oil and is seen as a fat with beneficial effects.



Fatty acid content of coconut oil
Type of fatty acid pct
Caprylic saturated C8
7%
Decanoic saturated C10
8%
Lauric saturated C12
48%
Myristic saturated C14
16%
Palmitic saturated C16
9.5%
Oleic monounsaturated C18:1
6.5%
Other
5%
black: Saturated; grey: Monounsaturated; blue: Polyunsaturated


So the only "bad" part of coconut oil is the Palmitic acid (C16).

As for MCT oil, what is in that?


In pharmaceutical MCT oil, like the one sold by Nestle, the contents are:-


Shorter than C8      1%
C8 (Octanoic)      54%
C10 (Decanoic)   41%
Longer than C10    4%

What is the effect of those fatty acids with more than 10 carbon atoms?  Nobody likely knows.



Cooking with MCT Oil? 

This is what Nestle has in mind for dinner.


Mct Spaghetti With Meat Sauce






4 Tbsp. MCT Oil® (Medium Chain Triglycerides)
1 lb. very lean ground veal or beef
1 tsp. salt
1/2 tsp. pepper
1/4 cup chopped onion
3 Tbsp. chopped green pepper
1 cup MCT Tomato Sauce (see recipe on site)
2 cups cooked spaghetti

Heat MCT Oil; add veal, salt and pepper.
Cook until meat is brown.
Add onion, green pepper, and tomato sauce. Cook for 30 minutes over low heat.
Add cooked spaghetti, stir and serve.