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Solving the Autism Puzzle – The Fatty Acid Question and “Big, Fat Neurons”!

Neuron By Kent Heckenlively, Esq.

(Author's note - Further discussions with Dr. Kane have allowed me to significantly improve and deepen the science of this article.  Worth reading again!)

Let me be clear.  I hate the expression “autism puzzle.”  The only time I’ll have the slightest affection for it is when it’s used in a sentence such as “The autism puzzle has been solved.”

This article delves into theories which will hopefully bring that day closer.  I don’t say the theory expressed here is true.  But it's interesting.  And I believe it’s worth discussion.

In the recently published book, “Food and Nutrients in Disease Management”, ($133 on Amazon) edited by Ingrid Kohlstadt is a chapter entitled “Autistic Spectrum Disorder: Dynamic Intervention for Neuronal Membrane Stabilization” by Patricia Kane, Ph.D, Annette Cartaxo, M.D., and Richard Deth, Ph.D. In the chapter a number of interesting claims are made.  I believe they’re consistent with the experiences of many people with autism, and if verified, provide a clear picture of what has gone wrong with the disease, and more importantly, the road out of autism and other neurological disorders.

The discussion begins with evidence of neuroinflammation discovered by Dr. Andrew Zimmerman and his colleagues at Johns Hopkins in 2005.  This neuroinflammation upsets the balance between excitatory and calming neuro-transmitters, causing the glutamate system to become overexcited and GABA production to be curtailed.  This results in the development of autistic symptoms and other neurological disturbances such as seizures.

Two biomarkers of this glutatmate excitotoxicity are mitochondrial dysfunction involving 1) viral exposures which damages the mitochondrial membrane resulting in formation of swellings (dendritic beading) along the nerve dendrites and 2) the formation of lipid rafts, ceramides within the cells impairing mebrane function.  The authors assert that the appearance of dendritic beading is indicative of a damaged mitochondrial membrane, made up of fatty acids called cardiolipin, after exposure to a virus.  They have also observed that calcium disregulation is also an accompaniment to mitochondrial dysfunction, leading inevitably to oxidative stress.

The authors have examined red cell fatty acid analysis for the past 12 years through a biomedical analysis at BodyBio (Dr. Kane's company) on thousands of children with autism and other disorders with testing by the Peroxisomal Disease Laboratory of the Kennedy-Krieger Institute at Johns Hopkins University.  They have hypothesized that autism is the result of a disturbance in cellular function due to toxic insult.  Specifically, there’s a build-up of very long chain fatty acids (VLCFAs) which causes impairment in the functioning of the peroxisome.  The peroxisome is a cellular organelle responsible for critical cellular functions such as detoxification, creating cellular fatty acid structures (phospholipids), generating bile acids necessary for digestion, and breaking down very long chain fatty acids.

In discussing autism with me, Dr. Kane suggested I imagine the very long chain fatty acids as prison bars, imprisoning the cell so that these rigid structures form lipid rafts not allowing the organelles (organs within the cell like the mitochondria andperoxisome) and the cell membrane to perform its fluid, vibrating function, but rather leave it static, like a couch potato. The cell membrane is composed of 50% phospholipids, which are critical for the health and vitality of cellular function.

The cellular membrane should be viewed as something akin to a port, the skin of the cell from which the cell receives nutritents from the outside world.  If the docks aren’t in good shape then the cell can’t get the material it needs to function properly and cannot expel what it does not need.  Because of the disruption in the cell membrane, the formation of lipid rafts due to toxic insult, receptors such as the dopamine receptor that Dr. Richard Deth has written so much about relating to autism, is not embraced properly by the phospholipids, leading to distortion of the cell and the ability of the receptors like dopamine to sit properly in the membrane.  Phosphatidylcholine makes up 50% of the outer lipid membrane and is the most powerful tool we have in our arsenal to heal the mebrane, heal the brain.

The authors write, "Peroxisomal disorders are characterizes by an accumulation in tissue and body fluids of renegade fatty  acids: saturated and mono-unsaturated VLCFAs (very long chain fatty acids), odd chain fatty acids, and branched chain fatty acids, pristanic and phytanic, which are normally degraded within the peroxisome, but instead can accumulate and form lipid rafts, or ceramides, which derange cell membrane structure.  The accumulation of renegade or VLCFAs reflects blocked detoxification and methylation pathways, and may be characteristic in autism, PDD, seizure disorders, stroke, neurological disease and states of neurotoxicity."  In essence, the buildup of very long chains causes swelling or edema of the cell from the buildup of very long chain fatty acids.  Harvard autism neurologist Dr. Margaret Bauman originally found that children with autism had "big, fat neurons" while Dr. Kane discovered that children with autism had "big, fat peroxisomes" after examining the levels of very long chain fatty acids in red cell studies from Johns Hopkins.

In 1996 Dr. Kane had proposed that autism may be the aftermath of a toxic insult, a viral infection which evoked hepatic encepahlopathy, resulting in hyperammonenemia and suppression of several key enzymes, such as carbamylphosphate synthesase, glutamine synthesase and ornithine transcarbamylase.  The high levels of ammonia would cause an "increase in brain edema (water) and a deterioration in neuropsychological function." 

The ammonia would also cause abnormalities in neurotransmitters and induce injury to astrocytes which are already under oxidative stress.  For this and a number of other reasons, Kane believes the oxidative stress should be viewed as the result of a toxic event, rather than the cause of autism.  Kane asserts that because of this, treating a patient with anti-oxidants is a little like pouring water on a house after it's already burned to the ground.  She suggests "treatment should be centered on re-building membrane structure and thereby stabilizing membrane function."  This involves clearing the body of ammonia, very long chain fatty acids, and giving the cells those building blocks which they've long been denied.

Another problem which has attracted the authors’ attention is her finding of increase in the white matter in the brains of children with autism after observing the buildup of DMAs in the red cell fatty acid test from Johns Hopkins.  Normally these markers are low, showing demyelination in children with pervasive developmental delay and seizures.  In autism, there is instead a state of overmyelination.  Dr. Bauman notes in her recently updated book on autism that the most likely explanation for the increase in brain size is "the presence of abnormal myelin production."

In their work Drs. Kane and Cartaxo (a developmental pediatrician)have also noted that about one-third of the autistic children tested have low cholesterol.  Low cholesterol is yet another indicator of poor cell membrane integrity.  Because of my complete dedication to you readers I had my daughter’s blood tested by the Peroxisomal Disease Laboratory of the Kennedy-Krieger Institute of Johns Hopkins University through BodyBio for the presence of abnormal fatty acids.   (Yes, you may address me by my Native American name, “Don’t-have-a-buck” for my propensity to test all of these various theories!)

My daughter tested high for levels of very long chain fatty acids which form these lipid rafts (indicating neuroinflammation) high levels of DMAs (myelin markers, also showing neuroinflammation), and low in essential fatty acids.  In resolving these issues it’s Kane’s approach to “burn” off the very long chain fatty acids, “build” by supplementing the essential chain fatty acids necessary for proper neuron development, and “balance” the other fatty acids.  This usually involves the “intravenous administration of phosphatidylcholine (Lipostabil), folinic acid, (Leucovrin) reduced glutathione (Wellness Pharmacy) and phenylbutyrate, appropriate co-enzymes, such as vitamins and minerals, and balanced essential fatty acids (including oral supplementation with evening primrose oil, egg yolk, meat fat, sunflower oil, flax oil, high EPA fish oil, wild salmon, sardines) targeted to the patient’s individual results.”

In my discussions with Dr. Kane she was also able to relate these theories to many other therapies which have been used in autism.  Hyper-baric oxygen therapy (HBOT) for example is quite good for burning off the very long chain fatty acids she’s seen in many autistic children.  However, it will also burn off the essential fatty acids as well and can destabilize the neurons.  Therefore, as a result, those children most likely to benefit are those who already have a good balance of essential fatty acids so that they can handle the decrease. 

Dr. Kane has been using the short chain fatty acid, phenylbutarate for the past 14 years for children with seizure disorders, post stroke, brain injury, and autism.  She found that phenylbutyrate as a prescription or over the counter, burned off very long chain fatty acids, but without the complications of HBOT.  Phenylbutyrate though must be used with balanced essential fatty acids and phosphatidylcholine to keep the cells healthy.

Children with seizures are more likely to have a buildup of very long chain fatty acids, but an exceptionally low amount of total lipid content within their cells, and thus HBOT treatment may increase their seizure activity.  The high level of myelin marker DMAs (indicating brain inflammation), elevation of very long chain fatty acids (also from brain and liver inflammation) with low essential fatty acid levels from my daughter’s test also explains the failure of her stem cell treatments last year.  Her body didn’t have enough short chain fatty acids to provide the raw materials necessary for the stem cells to flourish.

In a similar vein, the ketogenic diet, which involves eating a great deal of fat, causes the body to burn off very long chain fatty acids forming lipid rafts or ceramides, but may not fully resolve the problem unless the essential fatty acids, phosphatidylcholine and butyrate are given.  This may be why approximately one-third of the children who have success on the diet have their seizures reappear after stopping the diet.  There is no need to use the severe restrictions of the ketogenic diet as Kane describes in another chapter of the book, "Food and Nutrients in Disease Management" on seizures.  Kane has a diet called the Membrane Stabilizing Diet and can be found in the Detox Book for Patients.

The question of susceptibility genes for autism has also drawn a great deal of attention from Dr. Kane, although she notes there has been a lack of consistent findings.  She observes that certain genes can lead to an increased immune reactivity that may be turned on during fetal development due to the mother's exposure to toxins or after the child is born in relation to heavy metals, chemicals, virus, toxic mold, or pesticides.  She has had several patients with gross exposure to heavey metals such as arsenic from the city’s water supply, as well as methylmercury during fetal development from the mother’s daily consumption of white albacore tuna, and massive metallic mercury exposure from a spill at the mother's dental clinic. 

One point that is often misunderstood is that heavy metals are liquid soluble and reside in cells.  It is impossible to detoxify heavy metals bound to proteins like metallothionen or within the nervous system with chemical chelators like DMSA or DMPS.  These children had gross developmental abnormalities from heavy metal posioning which were resolved through the intravenous administration of Lipostabil (phosphatidylcholine), Leucovorin (folinic acid), glutathione, and phenylbutyrate.  It is Kane's opinion that “in-born” errors of metabolism don’t present any greater challenges than those errors of metabolism which are acquired later in life.

Dr. Kane’s lipid therapy treatment has also impacted her own life.  When her son was 18 months old he had a severe stroke which left him in such a debilitated state the doctors told her she should place him in an institution.  She believes this happened as a result of her dentist putting pure mercury into a filling and covering it with amalgam.  She believes this mercury went straight into her child during her pregnancy as well as while she was breast-feeding.  She states the only medical reason a child can have a stroke before the age of 3 is due to an ornithine transcarbamylase deficiency (this enzyme detoxifies ammonia).  As the enzyme ornithine transcarbamylase is suppressed with exposure to mercury, ammonia levels rise, and the child has repeated strokes.  She was able to save her son's life by using lipid therapy and within a few months had completely recovered.  Dr. Kane went on to work with children whom everybody else had given up on, children with brain injury, intractable seizures, global development delay, and autism.

Although Dr. Kane's son completely recovered from the stroke, unfortunately, when he went away to college he was exposed to an array of neurotoxins.  He worked in an enclosed space with acrylic paint (arsenic, lead, cadmium), soldering lead/copper in his art work, and also received a meningitis vaccination required by the university (he had never been vaccinated previously).  He had not one stroke, but a series of strokes, and began exhibiting autistic symptoms.

In a panic Dr. Kane called her long-time friend Dr. Bernie Rimland and asked if he'd ever heard of adult-onset autism.  After receiving a negative answer from Dr. Rimland she went to the library desparate to find an answer.  She found a case of a brother and sister with adult-onset autism from the cluster of cases from the mercury exposure at Minamata Bay, Japan in the 1950s.  The exposure of mercury had suppressed the enzyme ornithine transcarbamylase causing an increase in ammonia and autistic symptoms.  (There's also a report in Medline of adult-onset autism in a 31 year-old man from infection by the herpes virus and Dr. Kane told me she had seen a case of West Nile dementia in a 70 year-old man that presented with autistic symptoms.)  For the second time in his life, Dr. Kane’s son started on lipid therapy and he again recovered.

In Dr. Kane’s view autism is best described as a disruption of cellular lipid metabolism.  She believes the starting point for this discussion is viral in nature, and complicated by heavy metals such as lead, mercury, or cadmium, pesticides, toxic mold exposure, chemicals, Lyme disease and other infections.  Each one of these environmental insults on its own, or in combination, can disrupt lipid metabolism.

Personally, I believe Dr. Kane’s work to be an important contribution to addressing autism.  She has presented her work at Columbia University, the NIH, Johns Hopkins, as well as many other medical institutions.  This work seems to be well-known, as I had no difficulty in getting my regular pediatrician to sign off on these tests.  After having so many tests done at labs of unknown quality it was refreshing to see this last set being sent off to Johns Hopkins.

I’ll keep you posted as to what happens next.

Kent Heckenlively is Legal Editor of Age of Autism



Did the diet work for your daughter as this was in 2009 what is your view over this diet?
I am looking into if for my son who is 5.


Many questions: Are the adverse affects of vaccines critically worse in the offsping of parents who were/are deficient in omega 3s and higher in inflamation-causing omega 6s due to the rise of hydrogenated vegetable oils (Big Ag) in 60s and 70's?

Diets Lacking Omega-3s Lead to Anxiety, Hyperactivity in Teens: Generational Omega-3 Deficiencies Have Worsening Effects Over Time
July 29, 2013 — Diets lacking omega-3 fatty acids -- found in foods like wild fish, some eggs, and grass-fed livestock -- can have worsened effects over consecutive generations, especially affecting teens, according to a University of Pittsburgh study.
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Published in Biological Psychiatry, the Pitt team found that in a rodent model second-generation deficiencies of omega-3s caused elevated states of anxiety and hyperactivity in adolescents and affected the teens' memory and cognition.
"We have always assumed that stress at this age is the main environmental insult that contributes to developing these conditions in at-risk individuals but this study indicates that nutrition is a big factor, too," said Bita Moghaddam, lead author of the paper and professor of neuroscience in the Kenneth P. Dietrich School of Arts and Sciences. "We found that this dietary deficiency can compromise the behavioral health of adolescents, not only because their diet is deficient but because their parents' diet was deficient as well. This is of particular concern because adolescence is a very vulnerable time for developing psychiatric disorders including schizophrenia and addiction."Diets lacking omega-3 fatty acids -- found in foods like wild fish, eggs, and grass-fed livestock -- can have worsened effects over consecutive generations, especially affecting teens, according to a University of Pittsburgh study.
Performing experiments in rats in Moghaddam's laboratory, the research team examined a "second generation" of omega-3-deficient diets, mimicking present-day adolescents. Parents of many of today's teens were born in the 1960s and 1970s, a time period in which omega-3-deficient oils like corn and soy oil became prevalent, and farm animals moved from eating grass to grain. Since omega-3s are present in grass and algae, much of today's grain-fed cattle contain less of these essential fatty acids.
The Pitt team administered a set of behavioral tasks to study the learning and memory, decision making, anxiety, and hyperactivity of both adults and adolescents. Although subjects appeared to be in general good physical health, there were behavioral deficiencies in adolescents that were more pronounced in second-generation subjects with omega-3 deficiencies. Overall, these adolescents were more anxious and hyperactive, learned at a slower rate, and had impaired problem-solving abilities.
"Our study shows that, while the omega-3 deficiency influences the behavior of both adults and adolescents, the nature of this influence is different between the age groups," said Moghaddam. "We observed changes in areas of the brain responsible for decision making and habit formation."
The team is now exploring epigenetics as a potential cause. This is a process in which environmental events influence genetic information. Likewise, the team is exploring markers of inflammation in the brain since omega-3 deficiencies causes an increase of omega-6 fats, which are proinflammatory molecules in the brain and other tissues.
"It's remarkable that a relatively common dietary change can have generational effects," said Moghaddam. "It indicates that our diet does not merely affect us in the short-term but also can affect our offspring."
Other Pitt researchers involved in the study include Gonzalo Torres (ENGR '81), associate professor of neurobiology, and, from the Moghaddam laboratory: Corina Bondi, postdoctoral fellow; Jody Tock, laboratory technician; and Nelson Totah (A&S '12G), now a postdoctoral fellow at Max Planck Institute for Biological Cybernetics. The team also included, from the National Institutes of Health, Stanley Rapoport, senior investigator and chief of the brain physiology and metabolism unit; Ameer Taha, visiting fellow; and Yewon Cheon, program coordinator.


Kent, just following up to see if you had done any of the therapy with your daughter. This article plus reading everything I could get my hands on pointed me in the direction of the BodyBio testing. It will be done before Christmas. I hope it will help to explain why other treatments have not helped much in our fight over the last three years. Thanks for your great article and sharing.

mike pescatore

Essential fatty acids added to infant formula?Is it safe to add DHA/ARA to formula?Seems that everybody is aboard the DHA train although researchers have yet to determine its exact function.Will alter lipid rafts and displace critical signaling proteins.Suppresses inflammatory and immune system function.Increases prion formation.Accellerates neuronal necrosis and apoptosis in late stages of alzheimers.Peroxidizes with iron supplement to form f-4 neuroprostanes.Added to 12x the amount of iron found in breast milk.Disrupts protein palmitoylation.Affects gender differently.Fuel to initiate oxidative stress and mitochondrial dysfunction.Lets add a structurally different source to infant formula.Esterified in all three positions.Lets increase the amounts of DHA and ARA in a one size fits all fashion for the first time in human history and feed it to our infants during critical stages of neurodevelopment.Alter cholesterol levels through its statin-like effects.Sounds like "Generally Regarded As Safe" to me.If these supplements are capable of having an effect on brain and eye development,shouldn't we know exactly how and at what risk?If the human body needed to synthesize more than what evolution provided us with the enzymes to do so,they would truly be classified as essential.Nobody knows what amount is deficient or excessive.Everybody just knows that they are essential.Better brain and eye development should be common with today's children after seven years of supplementation.Instead the opposite results are becoming apparent.I guess that I just don't understand.When has it become acceptable to add supplements to infant formula with little understanding of their cellular mechanics?Lets shift the focus from BPA bottles to what they actually contain.Lets examine the sole source of nutrition that infants are consuming.Above all,lets know that this nutrition is safe and not just "Generally Regarded As Safe".
Check out my website at

Benedetta Stilwell

Your article I can not get out of my head. Have you looked at what are some of the newer treatments are for Kawasaki's treatments. They are using blood thinners on those that have developed aneurism and those that do not respond to IVIG they are using steroids and even chemo type shots!

I don't know about your child but my children constantly ran temperatures growing up and the ped constantly said - oh don't worry it is a virus. But I knew it was not. I know this sounds weird but I could tell you the diffence in a fever that actually involed a pathogen and one that was this inflammatory disease (virus)

Benedetta Stilwell

OH and I forgot the L-Carnitine.
And if it was not so expensive it would be Co-Enzyme Q 10 too
Anything else I left out? B12 Maybe???

List is kinda of long.

Benedetta Stilwell

Thanks Maria; Okay vitamin E should also be given from what I understand in your last article .

So, that is vit C
Vit. E
fish oil or flax seed oil and from what I understand the fish oil tablet holds twice as much omega 3 than the fax seed oil
Vit. B6
low power asprin
folic acid
and his seziure medicine Keppra

for my daughter I added ginger and turmeric
they claim it is anti inflammatory and since she is always about to throw the ginger could not hurt.

All this along with a low glycemic diet or an Atkins diet. Eat plenty of fish fried up in olive oil (omega 6)

And a club to make sure my three stays on a low carb diet!

María Luján

A recent manuscript
Altern Ther Health Med. 2009 Jul-Aug;15(4):34-43.
Syndrome of allergy, apraxia, and malabsorption: characterization of a neurodevelopmental phenotype that responds to omega 3 and vitamin E supplementation.Morris CR, Agin MC.
Department of Emergency Medicine, Children's Hospital & Research Center Oakland, California, USA.

OBJECTIVE: Verbal apraxia is a neurologically based motor planning speech disorder of unknown etiology common in autism spectrum disorders. Vitamin E deficiency causes symptoms that overlap those of verbal apraxia. Polyunsaturated fatty acids in the cell membrane are vulnerable to lipid peroxidation and early destruction if vitamin E is not readily available, potentially leading to neurological sequelae. Inflammation of the gastrointestinal (GI) tract and malabsorption of nutrients such as vitamin E and carnitine may contribute to neurological abnormalities. The goal of this investigation was to characterize symptoms and metabolic anomalies of a subset of children with verbal apraxia who may respond to nutritional interventions. DESIGN AND PATIENTS: A total of 187 children with verbal apraxia received vitamin E + polyunsaturated fatty acid supplementation. A celiac panel, fat-soluble vitamin test, and carnitine level were obtained in patients having blood analyzed. RESULTS: A common clinical phenotype of male predominance, autism, sensory issues, low muscle tone, coordination difficulties, food allergy, and GI symptoms emerged. In all, 181 families (97%) reported dramatic improvements in a number of areas including speech, imitation, coordination, eye contact, behavior, sensory issues, and development of pain sensation. Plasma vitamin E levels varied in children tested; however, pretreatment levels did not reflect clinical response. Low carnitine (20/26), high antigliadin antibodies (15/21), gluten-sensitivity HLA alleles (10/10), and zinc (2/2) and vitamin D deficiencies (4/7) were common abnormalities. Fat malabsorption was identified in 8 of 11 boys screened. CONCLUSION: We characterize a novel apraxia phenotype that responds to polyunsaturated fatty acids and vitamin E. The association ofcarnitine deficiency, gluten sensitivity/food allergy, and fat malabsorption with the apraxia phenotype suggests that a comprehensive metabolic workup is warranted. Appropriate screening may identify a subgroup of children with a previously unrecognized syndrome of allergy, apraxia, and malabsorption who are responsive to nutritional interventions in addition to traditional speech and occupational therapy. Controlled trials in apraxia and autism spectrum disorders are warranted.



Could you provide the contact information (phone number or website) for the lab in order to arrange for the testing. I am not clear who to contact and can't seem to find it.




I am so glad that Pat Kane is getting some recognition for the work she has been doing with kids for the past twenty years. Seven years ago, I read an article that she wrote and found a Doctor of Chinese Medicine in my area(CA) that was working with her to run the Fatty Acid Tests on my son who had recently been diagnosed with regressive autism. He had acidosis, high ammonia, imbalanced fatty acids and Klebisella and clostridia difficle in his stool. Under her care and a nutrient dense diet, he lost his diagnosis within 8 months and continued to recover until he became pretty NT after 2 years of treatment. At that time, she was not doing IV and she recovered him through bicarbs, butyrate and fatty acids like phoscol. He did not have any other therapy during this time. He continued to do well until a severe mold exposure stalled his development and we had to retrace our steps to recover him again. This time, we have used functional homeopathy as well to strengthen his immune system and we feel this should prevent any future problems.

I highly recommend her.


I have several thoughts in relationship to this great article. I just keep going over it.

Lorenzo’s oil is so true. I have recently been following a yahoo site for apraxia run by the Cherab Foundation and headed by Lisa Geng.

This organization has funded some interesting anecdotal studies of children with apraxia. They experimented with omega 3,6, 9 ratios and came to the conclusion that certain ratios work better than others.

We started my grandson of ProEFA by Nordic Naturals about 2 months ago and just recently added ProEPA and he is doing remarkable things. He had been on other fish oils, but they did not produce any noticeable affect. He is 3 ½ and was not really progressing even though we had done many treatments with DAN doctor. But wow with this particular ratio of omegas in two month he has started requesting by signs and has a much longer attention span, many verbal approximations, calmer, eye contact, pointing the list goes on an on.

I also wanted to add to the comments made about celiac disease. There was a large donation of blood made to the Mayo Clinic that was gathered at Warren Air force Base in from 1948 till 1954. The Mayo Clinic decided to test this large group for celiac. Guess what? Celiac is 4.5 times more common than 50 years ago.

Whatever I am going to start looking right away into lipid therapy.

No apologies

CM-- very interesting information, thank you. The 7 year-old child in the Depakote (VPA) case study developed unambiguous autism. He had been entirely NT. When the VPA was stopped, some of the autistic symptoms diminished but the dementia remained.

US govt. attorneys in the Omnibus attempted to use Depakote as an example of environmental cause as "evidence" that autism could not be environmentally-induced past prenatal stages or very early infancy, therefore (they hoped to reason) vaccines at 1 year or 18 months could not induce it. This case study of the seven year-old (and I'm sure others) stand in the face of that argument if anyone would bother to pursue information on it. Point being, if Depakote can induce autism later in childhood, so would substances with similar damage-pathways be able to do so later in childhood. Much later, apparently.

From the studies you mentioned coupled with the information from this article, it appears that thimerosal and other vaccine components combined may certainly have "similar damage pathways" to Depakote.

I'm hoping that, at some point, some of the science on our side will grab hold of the government's and mainstream science's admission of Depakote as a known cause and yank on it until all the similarities are made obvious, then attack with deductive reasoning. It seems possible that a big part of the key to autism's cause is somewhere in this overlap.

Kent Heckenlively


I want to be sure you have the most complete information possible so here is the low-down on the fatty acids test. Also, just wanted to note I got an e-mail from Dr. Richard Deth about a recently published medical article confirming much of Dr. Kane's phospholipid theories, as well as the work of Dr. Jill James. (I guess you know what my next article will be about!)

Here's the information on the fatty acids test:

The BodyBio red cell fatty acid test that is run through Johns Hopkins is a dual run (they run the test twice!) which is a 9 hour process. The laboratory is a research laboratory (not a commercial lab) and the gold standard in the world for fatty acid analysis. Once the red cell fatty analysis is complete it is run through the biomedical analysis written by Dr. Patricia Kane at BodyBio and NeuroLipid Research Foundation that matches the data to the medical literature and guides researchers and clinicians in treatment for their patients. The BodyBio fatty acid test gives information on the renegade fatty acids (very long chain fatty acids that make up lipid rafts and are the aftermath of neuroinflammation), myelin markers, essential fatty acids, saturated fatty acids, total lipid content, trans fatty acids, branched chains, odd chains, 85 fatty acids are analyzed overall. The fatty acid test is $420, however, because it is a university research laboratory and no other laboratory is able to do the analysis in the US some insurance companies will cover the cost (not Kaiser, HMOs or Medicaid, but Blue Cross Blue Shield, etc might if ordered by the child's pediatrician).

All the best,
Kent Heckenlively


Viral and heavy metals, gee, who has been saying that all along? THE PARENTS!!

I guess it wasn't such a good idea to give me a postnatal rubella shot as I was breastfeeding and give my son a hep b full of mercury (in 1999) the day he was BORN. My poor little guy, how he suffers from having a mother who trusted these idiots. I wonder do any of these doctors feel guilty for destroying so many chidren? I doubt it.

Benedetta Stilwell

Oh and by the way what really suprised me about celiac disease is that it is more common that once thought. IT IS 1 out of 139, not everyone expresses it in the same way or with equal severity.

Benedetta Stilwell

I give my son one or two vitamin D's a day along with vit C. Since we started, it has cut down those days when he stays in bed with a sinus infection or feeling bad to almost zero.

Many Familys have put their children with autism on gluetin and cassien free diets. There is something going on here too. Perhaps the American diet is yet another insult on an already stressed mitochondria and the right fatty acids.

A recent article on "Celiac Disease" by Alessio Fasano in "Scientic American" in the August edition

This article said that celiac disease will provide a valuable model for understanding autoimmune disorders. "Symptoms driven by local disruptions of nutrient absorption." Disruption of iron absortion, anemia, poor folate uptake, system of osteoporosis, joint pain, chronic fatigue, short stature (not so for some out our children with autism), skin lesions, epilepsy, dementia, schizophrenia and seizure.

They have discovered that celiac disease has three things that lead to an autoimmune disorder such as: 1) An enviromental factor which is the hard to digest gluten (but for autism it is a sharp needle full of vaccine) 2.) a genetic component 3.) a leaky gut (yes they actually found an enzyme that unzips the glue that holds together the lining of the small intestines and it is made by our own bodies as well as some bacteria) with autism the leaky gut could be instead a sharp needle filled with a vaccine!

Kotesh P

Genova Diagnostics offering Red Blood Cell Fatty Acid test and they accept insurance. I think this is equal to JH University Test as they also test Red Blood Cell. Here is the link.


is it correct to say that the type of fatty acid test that should be done for our autistic kids is called GPL essential fatty acid test or is it called something else. Please advise so I can have this test done.
Thank you


Kent - I am sooooo excited. This makes so much sense for my child and I have spent the last day and a half (and late into the night on this one). Now to figure out which Fatty Acid Disorder. This is ten times more serious than I thought (my son's constant hypoglycemia).

Start digging... and you never know what you may find... This is even more complicated than I thought.

Fatty Oxidation Disorder (there are TONS)
I'm listening to the videos right now (but first I had to sign up for their newsletter)





OMG!!! I am so sick of "psychiatrists" saying asd is "behavioural" and giving psychiatric drugs.


Wow! It sounds like she's really on to something.

"They have also observed that calcium disregulation is also an accompaniment to mitochondrial dysfunction, leading inevitably to oxidative stress."
-Since adequate levels of vitamin D are necessary for proper absorption of calcium, would a vitamin D deficiency cause calcium disregulation? I've read that vitamin D deficiency can cause hypotonia, which can be a symptom of mitochondrial disease.

To add on to Gatogorra's points about Valproic Acid already being a known cause of autism...
Dr. Kane mentioned "hepatic encepahlopathy, resulting in hyperammonenemia" may be a contributing factor.

"Valproate levels within the normal range are capable of causing hyperammonemia and ensuing encephalopathy"

Also, Valproic Acid DOES alter fatty acid metabolism:
"Valproic acid alters fatty-acid metabolism, impairs beta-oxidation (a mitochondrial process), and disrupts the urea cycle. This leads to hyperammonemia, among other metabolic derangements, and, ultimately, end-organ effects (hepatitis, pancreatitis, hemodynamic compromise) may be the result of severe toxicity due to these impaired metabolic processes.

Through several mechanisms, valproic acid depletes carnitine levels resulting in decreased transport of fatty acids and their accumulation in the cytoplasm. This process may result in development of fatty liver"

And the following study reports that after being on VPA for 1-2 years, patients have a high chance of developing cognitive decline:

One case in this study,
"Described an ll-year-old girl with symptomatic localization related epilepsy and normal intelligence that developed reversible mental deterioration and pseudoatrophic brain changes while receiving valproate (VPA). After 2 years and 6 months on VPA the girl insidiously developed mental deterioration (loss of 18 IQ points and drop in age-adjusted PM score from the 95th to the 50th percentile) associated with MRI-documented pseudoatrophy
of the brain."
"These signs and symptoms improved after discontinuation of valproate."


This turned out to be another aspect of vaccine injury which overlaps with Depakote-- Valproate does appear to effect peroxisome function and lipid metabolism like I'd been wondering aloud in an earlier comment. In the study below, investigators believe this may explain the "positive" (seizure-reducing) effects of the drug, though they don't go on to investigate whether this may also explain the negative effects of the drug (such as causing autism and dementia). If this were true (if disabling peroxisomes led to both terrible side effects but also seizure-reduction) this would not be unusual, since most of the negative side effects of psychoactive drugs are actually simply an extension of their *primary* effects.

"Neuronal Peroxisome Proliferator-Activated Receptor γ Signaling: Regulation by Mood-Stabilizer Valproate"

Abstract: Valproate (Depakote) remains an effective medication for the prevention and treatment of seizures in epilepsy and of mood symptoms in bipolar disorder. Both of these disorders are severe and debilitating, and both warrant further medication options as well as a better understanding of the side effects associated with their current treatments. Although a number of molecular and cellular processes have been found to be altered by valproate, the medication’s therapeutic mechanism has not been fully elucidated. In this paper, peroxisome proliferator-activated receptor (PPAR) signaling was examined to determine valproate’s effects on this transcriptional regulatory system in neuronal tissue. PPAR signaling has been found to affect a number of biochemical processes, including lipid metabolism, cellular differentiation, insulin sensitivity, and cell survival. When primary neuronal cultures were treated with valproate, a significant decrease in PPARγ signaling was observed. This effect was demonstrated through a change in nuclear quantities of PPARγ receptor and decreased DNA binding of the receptor. Valproate also caused gene expression changes and a change to the peroxisome biochemistry consistent with a decrease of PPARγ signaling. These biochemical changes may have functional consequences for either valproate’s therapeutic mechanism or for its neurological side effects and merit further investigation".

Again, this may only bolster the vaccine-cause theory if any of these parallels turn out to be similar enough.

rick everett

I find the comments on ammonia to be interesting.
One thing to be considered is the stomach dwelling bacterium helicobacter pylori. HP is the only creature able to withstand the strong gastric acids. It does so by, first, burrowing into the stomach wall, and second, releasing a small cloud of urease (sp?) to neutralize it.
The byproduct of this process is ammonia. Ordinarily it is dealt with by the liver but when overloaded, the liver shunts the toxin laden blood back into the system. If this is accompanied by inflammation the BBB and gut barrier can be compromised with a net result of ammonia in the brain.


Please, I hope soemone can answer this. My son is 5 and has been on omega 3 6 9 and for well over a year. If I order the GPL test, should'nt his levels of EFA's all be fine? I am really wanting to try HBOT and stem cell therapy,specifically together. Theis article actually tells me ways to find out if these therapies will help, I just want to make sure I am understanding which test to get. Is the EFA test the only test I would need to do? Thank you so much.


This is really riveting. For those of us who started to suspect that autism had more than a metaphoric connection to adrenoleukodystrophy (ALD-- the basis for Lorenzo's oil), this provides some more evidence. And since the body is finite, why wouldn't induced errors of metabolism mimic inborn errors in many ways?

Kent-- maybe at some point you could ask Dr. Kane about the connection between Depakote, thimerosal and certain vaccine strain viruses. There's a paper in the "files" section on EOH entitled "Chemo Brain" (scanned in three parts) which might be of interest because it bolsters many of the discussions listed here and Depakote has the distinction of already having been conceded as an actual cause of autism by the US government and mainstream medicine. Obviously Depakote-induced autism is *not* a competing theory to vaccine-induced autism. Exposure to Depakote isn't ubiquitous enough to explain the epidemic. Instead, I think the Depakote argument bolsters the vaccine cause theory, particularly from some of the angles you've mentioned in this post. I believe the Depakote discussion could act as a wedge to forcing concessions that vaccines, with their almost identical modes of destruction in some places to the substance now admitted to cause ASD, are suspect.

When I met Dr. Deth at David Kirby's presentation last year, I asked him about the overlaps between certain specific areas of vaccine-induced damage and that caused by Depakote, which even govt. attorneys in the Omnibus admitted could cause autism (their claim was that only prenatal exposure or exposure soon after could do this, though this isn't true). Among some of the overlaps, such as cytokine damage, glutatmate excitotoxicity, and tubulin disruption-- some of which induces alzheimer's typeII astrocytosis, Depakote also induces hyperammonenemia and mitochondrial dysfunction in several ways. This is the reason that Depakote is now only given with acetyl L-carnitine, because it causes carnitine depletion, but replacing carnitine is only a bandaid remedy considering all the other forms of damage the drug induces.

I asked Dr. Deth if he thought that this overlap of specific damage might, in some ways, serve to prove that thimerosal and certain other vaccine components were the culprits in autism. He seemed surprised that the case study I was referring to involved a seven year old boy who regressed into autism as a result of Depakote treatment for post-chemotherapy seizures, a case of the drug exacerbating and compounding the damage already caused by chemotherapy drugs (induced susceptibility, induced disease; not inborn susceptibility or inborn disease).

I have no idea how or if Depakote also induces errors in lipid metabolism but it wouldn't be surprising.

Benedetta Stilwell

I may be wrong but looking on the internet the information I get is that omega 3 comes from fish oil, omega 6 is olive oil, and omega 9 comes from beef,pork,chicken -meat other than fish.


Thanks once again, Kent, for being the intrepid explorer-journalist for us all. Love the sentence "It is her opinion that “inborn” errors of metabolism don’t present any greater challenges than those errors of metabolism which are acquired later in life." This segues very nicely with Denis Noble's book on systems biology that I am reading now, The Music of Life: Biology Beyond Genes. It seems like more and more that downward causation is the place to start -- the interaction and feedback from environment, body, system, organ, cell down to gene via epigenetics/gene expression. Hence you see new articles coming out looking at oxidative stress in inborn errors of metabolism(i.e., PMID 19604711, 19223582), with an eye to "new" therapies for those with "inborn errors"(which seem like old hat to us biomed folk). Our genes, our toxic and microbial exposures, our accidents and encounters are not our fate. The life and growth of an organism is a process, not a given we must resign ourselves to. Thanks for constantly helping parents to think through the many and intricate processes that make up the life and development of our children.

Holly M.

I used Effalex too on both kids. Was it recommeded in Leo Galland's book SUPERIMMUNITY for Kids? BTW, that is a great book. I think I used 3 bottles worth on 2 kids. I didn't see anything + or - and didn't re-order because I was afraid of mercury in the tuna oil.


What an excellent post! It isn't easy getting through such technical material but well worth it. This is extremely interesting information.

There are still many places, not to mention lots of pregnancy/baby books, where you will find the tired old line that cholesterol and saturated fats are bad for your health. The planet-sized heap of nutritional misinformation funded by the processed food industry and big pharma has plunged us into a dark ages of fearful food superstitions, not to mention disease and death.

But just as in the real Dark Ages, there are bright lights pointing the way in the darkness. Thank you for the effort that went into creating this post!


Kent I found this article so enjoyable on so many fronts. For one, I have read everything I could on Patricia Kane but never details on her child and connection to Autism.
Her lipid therapy advice has served us well.
Today I started teaching my son cursive, a feat that 3 years ago would have been impossible.
He has been taking high dose Phosphacholine (8K daily) ever since his OT wanted to give up and teach him keyboarding skills due to severe hypotonia. While recovering well in speech, this ghastly defect was holding him back in every area of life. He couldn't even open a lunch snack or color with a crayon.
I resorted to experimenting with phosphalipids when I researched Patricia Kane their connection to improving fine motor skills and ADHD.
The result was incredible as we began to dose up.(Studies show it non-toxic up to 40K) Spontaneously my son began to draw pages and pages of material and writing made a turn around too. The OT and teachers were blown away!
I also found that Phosphalipids like PC and PS worked well with mito support and excellently when high dosed before HBOT.
Much later we invested in an ION panel and I was stunned to see how high my son's lipid peroxide level was in the 94th percentile. He really needed the membrane repair and as we address strengthening it the gains continue to abound.
Fortunately our DAN doctor has been excellent about addressing this and integrating Patricia Kane's ideas into our treatment plan.
It's great stuff!


Lipid Detox Thetapy:

Roger Kulp

Dr. Kahler's talk must have been something. Too bad they didn't upload a video. This is one of the better leads I have gotten. From this, and running a lot of this stuff through Google, I can see I probably have more than one of the lesser seen IEMs.

Are the more serious IEMs, that involve wasting, lipodystrophy, cardiac problems, etc. seen spectrum wide?

One more "comorbid condition" neurodiversity will dare not speak of.

Dan E. Burns, Ph.D.

Exciting stuff, Kent. Thanks. Everybody: would anyone care to comment on the "Lorenzo's Oil" connection? How is that like and unlike the "burn, build, and balance" approach that Kent alludes to in his article?

Maurine Meleck

Kent, As usual your writings are always very informative. Thanks for this article. Of course I pulled out my grandson's ammonia lvels from a test done 3 years ago and recalled that it was at the 99th percentile-so again I am very disturbed. What exactly is lipid therapy?? Still confused as where to go with this. Assuming one does mito testing and it proves positive---is the special diet the next move?


10 years ago, a mom I met on one of my discussion groups mentioned a product called Effalex, Essential Fatty acids,which was an elixer composed of omega 3-6-9. The omega 3 from tuna, the omega 6 from evening primrose oil, and omega 9 from borage oil. She told me of the amazing improvement in her son, like a miracle had happened. I was eager to get some of it. I was able to find a bottle at Walmart. I gave my autistic son a single dose one evening and the next day he was a new child. He was speaking in sentences instead of single word echolalia, he got on his trike and rode it like a pro instead of dragging it around by the handlebars, he started initiating play with other children instead of playing alone in an isolated corner. Tantrums stopped abruptly. He toilet trained overnight. Self injury and stimming stopped. His self limited diet (white junk food) gave way to craving salmon and vegetables. His strange fears vanished. Even his fear of Jello vanished. (he'd scream in terror just looking at it! now he eats it!! The list goes on. His shocking instant almost-cure prompted phone calls from the teachers, principal and bus driver, asking what happened to effect such instant gains.. I continued dosing for a week, and the gains continued however not quite as dramatic as day one. After a week there seemed to be no more dramatic gains but I was satisfied with the amazing and miraculous changes!
It has been 10 years and there was no regression after I stopped giving him the product. The word quickly spread and more anecdotal stories were posted of similar miracles. But just as quickly, the product disappeared from shelves in America. I have not heard if the FDA sanctioned the company that made it, but there has got to be a reason why this product disappeared from shelves. I imagine they were bullied into pulling out of this market. You can find it online, in England. I would like to know why this product disappeared like this. Dr Kane actually posted about the product too and slammed it as unproven and unscientific and admonished it was dangerous to be playing with long chain fatty acids. Then she invited patients to her own clinic for testing, and if I recall, were invited to buy her products. I did not go there.
Today my son is almost indistinguishable from NT teens. He is social and outgoing attending regular high school, with only special-ed math, his weak subject. I only wish other parents could find this product and give it a try, if only for a week.

Heidi N

I can agree with everything but she left out pleomorphic bacteria. Sorry, but too many have reported recovering from only treating pleomorphic bacteria. I do feel all the rest of what she said is correct, but left out that pleomorphic bacteria makes one susceptible to stock-piling the pathogens and toxins.

More evidence for the meta/mito connection has a list of disorders which may affect the brain as an organ in the body.

María Luján

There are some sources on pediatric inborn errors of metabolism
Here is a link of a presentation from a recent National Metabolic Conference


For me? Two donuts and a croissant. Yum!


What constitutes "lipid therapy"??

Roger Kulp

A couple of questions that would relate directly to me

1)Has anybody published a listing of errors or defects in metabolism that occur in autism ? Especially non-mitochondrial ones.If so, where could I find such a list,and especially the clinical presentations of each?

2)What happens when you have both metabolic defects,as well autistic bowel disease growing up ? Has this been documented much ?

I would assume in such cases,things like lifelong malnutrition,with failure to thrive,and issues with sexual development would not be unexpected.

How about lipodystrphy,which I do have.

Kotesh P

It appears that Essential Fatty Acid Test from Johns Hopkins is same as GPL Essential Fatty Acid Test.

Here is the link for GPL test.


María Luján

Hi I have found some animations (free, from educational sites) on beta oxidation of fatty acids- some more clear than others.
Let me know if there is someone interested and if it is possible, I wil post here.

Benedetta Stilwell

MCT oil can cause vomiting and the runs.

To do the ketogenic diet it would take the help of a trained dietician with the weight of John Hopkin's behind the dieticain because the diet is a mathamatical nightmare (well to me anyway), and it is rough they even watch how much water is allowed to be consumed!

John Hopkins University just this year came out with their studies and said the same effects that were shown with the ketogenic diet could also be obtained with Atkins 15 carbs a day or Low glycemic diet 40 or 60 carbs a day, if the food was the right food???? However, this would allow little ones important nutients such as vit C into their diet.

But L-carnitine being low in children with autism? Yeah, I already thought so, but why is it that way since it is our own bodies that makes it? Why isn't the body making the right amounts? L-carnitine is found at the highest amounts in beef and the ultimate meat is lamb. Also I buy the stuff in pill form. A few little pills in a bottle for 10 dollars. The neurologists said as high as 500 mg a day is what is needed.

That is about all I know, and it is not much. That and the fact that my blueberries did not bear this year? Don't know why about that either but berries of all kinds are excellant for the low glycemic diet.

I am going ot go back and read the stuff about the Autistic blood and Dr. Kanes website. Thanks for that.


I had to write to express how grateful I am to read about how two Ph.D.'s and an M.D. advocate the use of diet, nutrition and supplements to treat "the result of a toxic event" caused by our Western medicine.

My wife and I are happy we found your page. Thank you.


My brain hurts! This is a lot of technical stuff for us high-school chemistry biomed parents to digest, but, wow, thank you! So much of this makes sense and helps explain why many of the biomed treatments we've used with our son have helped, or at least partially helped.
The "myelin sheaths" on ends of neurons reminded me of Guillian-Barre Syndrome, which my grandmother died from. Is it possible there is some genetic connection or predisposition there? And is this also related to Alzhiemer's? And what could be the effect throwing large quantities of antibiotics into this mix (my son's 18-month old bloodstream, I mean)?

Geez, my head is spinning.

We're about to start MCT Oil at the suggestion of our son's DAN doctor. Does anyone have any more experience/info on MCT Oil? He is also doing the hyperbaric chamber, cranio-sacral therapy, and glutathione supplements. Anyone else seen results from this mix?

Holly M.

Shortly after my daughter's 4-month old shots she screamed constantly and never slept. I thought she was hungry and gave her cereal. When her diaper reeked of ammonia I called the cereal company's 800# and asked if this was normal. Within days her seizures started. I found Mary Megson's ?? work on Cod Liver Oil and started her on that. Her seizures stopped after 10 weeks. She still got autism but hasn't seized in 8 years. At age 2 she did high pressure HBOT and made huge gains. At that time she had lots of CLO other supplements and some chelation under her belt. She's nearly recovered today.

María Luján

About impact of xenobiotics in fatty acid beta oxidation
Chem Res Toxicol. 2009 Apr;22(4):699-707.
Serum metabolomics reveals irreversible inhibition of fatty acid beta-oxidation through the suppression of PPARalpha activation as a contributing mechanism of acetaminophen-induced hepatotoxicity.Chen C, Krausz KW, Shah YM, Idle JR, Gonzalez FJ.
Laboratory of Metabolism, Center for Cancer Research, National Cancer Institute, National Institutes of Health, Bethesda, Maryland 20892, USA.

Metabolic bioactivation, glutathione depletion, and covalent binding are the early hallmark events after acetaminophen (APAP) overdose. However, the subsequent metabolic consequences contributing to APAP-induced hepatic necrosis and apoptosis have not been fully elucidated. In this study, serum metabolomes of control and APAP-treated wild-type and Cyp2e1-null mice were examined by liquid chromatography-mass spectrometry (LC-MS) and multivariate data analysis. A dose-response study showed that the accumulation of long-chain acylcarnitines in serum contributes to the separation of wild-type mice undergoing APAP-induced hepatotoxicity from other mouse groups in a multivariate model. This observation, in conjunction with the increase of triglycerides and free fatty acids in the serum of APAP-treated wild-type mice, suggested that APAP treatment can disrupt fatty acid beta-oxidation. A time-course study further indicated that both wild-type and Cyp2e1-null mice had their serum acylcarnitine levels markedly elevated within the early hours of APAP treatment. While remaining high in wild-type mice, serum acylcarnitine levels gradually returned to normal in Cyp2e1-null mice at the end of the 24 h treatment. Distinct from serum aminotransferase activity and hepatic glutathione levels, the pattern of serum acylcarnitine accumulation suggested that acylcarnitines can function as complementary biomarkers for monitoring the APAP-induced hepatotoxicity. An essential role for peroxisome proliferator-activated receptor alpha (PPARalpha) in the regulation of serum acylcarnitine levels was established by comparing the metabolomic responses of wild-type and Ppara-null mice to a fasting challenge. The upregulation of PPARalpha activity following APAP treatment was transient in wild-type mice but was much more prolonged in Cyp2e1-null mice. Overall, serum metabolomics of APAP-induced hepatotoxicity revealed that the CYP2E1-mediated metabolic activation and oxidative stress following APAP treatment can cause irreversible inhibition of fatty acid oxidation, potentially through suppression of PPARalpha-regulated pathways

J Toxicol Sci. 2009;34 Suppl 2:SP217-22. Links
Children's toxicology from bench to bed--Liver injury (1): Drug-induced metabolic disturbance--toxicity of 5-FU for pyrimidine metabolic disorders and pivalic acid for carnitine metabolism.Ito T.
Nagoya City University, Graduate School of Medical Sciences, Department of Neonatology and Pediatrics, Aichi, Japan.

Congenital disorders of metabolism show a wide spectrum of symptoms as a consequence of impairment of a certain metabolic pathway by mutated enzymes resulting in abnormal accumulation of enzyme substrates, deficiency of expected products, and abnormal burden to collateral metabolic pathways, etc. However, in some occasions, depending on which pathway up to what degree of disturbance, it can be asymptomatic until a certain kind of burden is placed on to the patient. Enzyme deficiency involved in pyrimidine degradation, such as Dihydropyrimidine dehydrogenase (DPD) and Dihydropyrimidinase (DHP), has been reported with convulsion or autism as symptoms, but many asymptomatic cases are also reported. However, when the patients are treated with 5-fluorouracil, a pyrimidine analogue anticancer drug, lethal side-effects can be seen even in asymptomatic patients. Some oral cephem antibiotics have pivalic acid side chain to increase absorption rate at intestine. These antibiotics degrade into active antibiotics and pivalic acid at the intestinal wall. This pivalic acid is carnitine-conjugated and excreted into urine. Carnitine acts as a carrier of long chain fatty acid to mitochondria and to beta-oxidation, thus an important molecule for energy production by beta-oxidation and maintenance of mitochondrial function. Because of this, long term administration of such antibiotics could induce depletion of carnitine from the body and lead to low ketotic hypoglycemia, convulsion and consciousness disturbance. This paper reports some possible serious side effects closely linked to drug metabolism.
Trends Mol Med. 2009 Jul;15(7):293-302. Epub 2009 Jun 26. Links
Organelle interplay in peroxisomal disorders.Thoms S, Grønborg S, Gärtner J.
Department of Pediatrics and Pediatric Neurology, Georg August University Göttingen, Robert-Koch-Strasse 40, 37075 Göttingen, Germany. [email protected]

Peroxisomes are no longer regarded as autonomous organelles because evidence for their interplay with other cellular organelles is emerging. Peroxisomes interact with mitochondria in several metabolic pathways, including beta-oxidation of fatty acids and the metabolism of reactive oxygen species. Both organelles are in close contact with the endoplasmic reticulum (ER) and share several proteins, including organelle fission factors. Today, the study of peroxisome biogenesis disorders mainly focuses on metabolic defects such as accumulation of very long chain fatty acids or plasmalogen deficiency. In addition to metabolic dysregulation, mitochondria and ER abnormalities have also been observed. Whether these contribute to disease pathology is not yet known, but recent findings suggest that this possibility should be considered. Here, we discuss the potential involvement of organelle interplay in peroxisomal disorders.

María Luján

J Inherit Metab Dis. 1999 Jun;22(4):428-41. Links
Defects in activation and transport of fatty acids.Brivet M, Boutron A, Slama A, Costa C, Thuillier L, Demaugre F, Rabier D, Saudubray JM, Bonnefont JP.
Department of Biochemistry, AP-HP Hôpital de Bicêtre, France.

The oxidation of long-chain fatty acids in mitochondria plays an important role in energy production, especially in skeletal muscle, heart and liver. Long-chain fatty acids, activated to their CoA esters in the cytosol, are shuttled across the barrier of the inner mitochondrial membrane by the carnitine cycle. This pathway includes four steps, mediated by a plasma membrane carnitine transporter, two carnitine palmitoyltransferases (CPT I and CPT II) and a carnitine-acylcarnitine translocase. Defects in activation and uptake of fatty acids affect these four steps: CPT II deficiency leads to either exercise-induced rhabdomyolysis in adults or hepatocardiomuscular symptoms in neonates and children. The three other disorders of the carnitine cycle have an early onset. Hepatic CPT I deficiency is characterized by recurrent episodes of Reye-like syndrome, whereas severe muscular and cardiac signs are associated with episodes of fasting hypoglycaemia in defects of carnitine transport and translocase. Convenient metabolic investigations for reaching the diagnosis of carnitine cycle disorders are determination of plasma free and total carnitine concentrations, determination of plasma acylcarnitine profile by tandem mass spectrometry and in vitro fatty acid oxidation studies, particularly in fresh lymphocytes. Application of the tools of molecular biology has greatly aided the understanding of the carnitine palmitoyltransferase enzyme system and confirmed the existence of different related genetic diseases. Mutation analysis of CPT II defects has given some clues for correlation of genotype and phenotype. The first molecular analyses of hepatic CPT I and translocase deficiencies were recently reported.

J Inherit Metab Dis. 2009 Apr 28.
Treatment recommendations in long-chain fatty acid oxidation defects: consensus from a workshop.Spiekerkoetter U, Lindner M, Santer R, Grotzke M, Baumgartner MR, Boehles H, Das A, Haase C, Hennermann JB, Karall D, de Klerk H, Knerr I, Koch HG, Plecko B, Röschinger W, Schwab KO, Scheible D, Wijburg FA, Zschocke J, Mayatepek E, Wendel U.
Department of General Pediatrics, University Children's Hospital, Moorenstr. 5, 40225, Düsseldorf, Germany, [email protected].

Published data on treatment of fatty acid oxidation defects are scarce. Treatment recommendations have been developed on the basis of observations in 75 patients with long-chain fatty acid oxidation defects from 18 metabolic centres in Central Europe. Recommendations are based on expert practice and are suggested to be the basis for further multicentre prospective studies and the development of approved treatment guidelines. Considering that disease complications and prognosis differ between different disorders of long-chain fatty acid oxidation and also depend on the severity of the underlying enzyme deficiency, treatment recommendations have to be disease-specific and depend on individual disease severity. Disorders of the mitochondrial trifunctional protein are associated with the most severe clinical picture and require a strict fat-reduced and fat-modified (medium-chain triglyceride-supplemented) diet. Many patients still suffer acute life-threatening events or long-term neuropathic symptoms despite adequate treatment, and newborn screening has not significantly changed the prognosis for these severe phenotypes. Very long-chain acyl-CoA dehydrogenase deficiency recognized in neonatal screening, in contrast, frequently has a less severe disease course and dietary restrictions in many patients may be loosened. On the basis of the collected data, recommendations are given with regard to the fat and carbohydrate content of the diet, the maximal length of fasting periods and the use of l-carnitine in long-chain fatty acid oxidation defects.
and there is a Cochrane review on carnitine

Cochrane Database Syst Rev. 2009 Apr 15;(2):CD006659.
Carnitine supplementation for inborn errors of metabolism.Nasser M, Javaheri H, Fedorowicz Z, Noorani Z.
Department of Health Information, Institute for Quality and Efficiency in Health care, Dillenburger Street, 27, D-51105, Köln, Germany, D-51105.

BACKGROUND: Inborn errors of metabolism are genetic conditions which can lead to abnormalities in the synthesis and metabolism of proteins, carbohydrates, or fats. It has been proposed that in some instances carnitine supplementation should be provided to infants with a suspected metabolic disease as an interim measure, particularly whilst awaiting test results. Carnitine supplementation is used in the treatment of primary carnitine deficiency, and also where the deficiency is a secondary complication of several inborn errors of metabolism, such as organic acidaemias and fatty acid oxidation defects in children and adults. OBJECTIVES: To assess the effectiveness and safety of carnitine supplementation in the treatment of inborn errors of metabolism. SEARCH STRATEGY: We searched the Cystic Fibrosis and Genetic Disorders Group's Inborn Errors of Metabolism Trials Register, the Cochrane Central Register of Controlled Trials (The Cochrane Library 2007, Issue 4) and MEDLINE via Ovid (1950 to July week 4 2007), LILACS (15/05/2008) and Iranmedex (15/05/2008) and also the reference lists of retrieved articles.Date of most recent search of the Group's Inborn Errors of Metabolism Register: 27 October 2008. SELECTION CRITERIA: Randomised controlled trials and quasi-randomised controlled trials comparing carnitine supplementation (in different dose, frequency, or duration) versus placebo in children and adults diagnosed with an inborn error of metabolism. DATA COLLECTION AND ANALYSIS: Two authors independently screened and assessed the eligibility of the identified trials. MAIN RESULTS: No trials were included in the review. AUTHORS' CONCLUSIONS: There are no published or ongoing randomised controlled clinical trials relevant to this review question. Therefore, in the absence of any high level evidence, clinicians should base their decisions on clinical experience and in conjunction with preferences of the individual where appropriate. This does not mean that carnitine is ineffective or should not be used in any inborn error of metabolism. However, given the lack of evidence both on the effectiveness and safety of carnitine and on the necessary dose and frequency to be prescribed, the current prescribing practice should continue to be observed and monitored with care until further evidence is available. Methodologically sound trials, reported according to the Consolidated Standards of Reporting Trials (CONSORT) statement, are required. It should be considered whether placebo-controlled trials in potentially lethal diseases, e.g. carnitine transporter disorder or glutaric aciduria type I, are ethical.

María Luján

I have found this research of fatty acids and ketogenic diet
Epilepsia. 2008 Nov;49 Suppl 8:117-9.Links
UCP-mediated free fatty acid uncoupling of isolated cortical mitochondria from fasted animals: correlations to dietary modulations.Davis LM, Rho JM, Sullivan PG.
Spinal Cord and Brain Injury Research Center, University of Kentucky, Lexington, Kentucky, USA.

Uncoupling proteins (UCP) translocate protons from the mitochondrial intermembrane space to the matrix, thereby "uncoupling" electron transport from the production of ATP. It has been shown that these proteins are highly expressed in animals maintained on the ketogenic diet (KD). Although the exact mechanism remains unclear, it is known that these proteins are activated within a protective antireactive oxygen species (ROS) mechanism by free fatty acids (FFA). In our current studies, mitochondrial samples were probed for the presence of UCP2, which is the most ubiquitously expressed UCP isoform. We found that both traumatic brain injury and fasting upregulated the expression of UCP2, with a synergistic upregulation in fasted injured animals. We then used mitochondria from fasted naive animals to screen a number of FFA for their activation of uncoupling as well as their ability to reduce ROS. We found that arachidonic acid (AA), docosahexaenoic acid (DHA), eicosapentaenoic acid (EPA), palmitoleic acid, myristic acid, and butyric acid increased mitochondrial uncoupling when added after oligomycin. These FFA, along with oleic acid, also reduced ROS in mitochondria incubated with oligomycin. In order to correlate our data to KD and fasting, both of which have been shown to be neuroprotective after neurologic insult, we determined the serum levels of FFA in KD and fasted animals using gas chromatography/mass spectroscopy. We also determined brain and cerebrospinal fluid (CSF) FFA levels from fasted animals.

and about uncoupling proteins
J Bioenerg Biomembr. 1999 Oct;31(5):457-66. Links
Fatty acid interaction with mitochondrial uncoupling proteins.Jezek P.
Institute of Physiology, Department of Membrane Transport Biophysics, Academy of Sciences of the Czech Republic, Prague. [email protected]

The phenomena of fatty acid interaction with mitochondrial integral membrane proteins, namely uncoupling proteins (UCPs), are reviewed to emphasize the fatty acid cycling mechanism that has been suggested to explain the UCP function. Fatty acid-induced uncoupling is suggested to serve in bioenergetic systems, to set the optimum efficiency, and to tune the degree of coupling of oxidative phosphorylation. Fatty acid interaction with the "classic" uncoupling protein (UCP1) from mitochondria of thermogenic brown adipose tissue (BAT) is well known. UCP1 is considered to mediate purine nucleotide-sensitive uniport of monovalent unipolar anions, including anionic fatty acids. The return of protonated fatty acid leads to H+ uniport and uncoupling. Experiments supporting this mechanism are also reviewed for plant uncoupling mitochondrial protein (PUMP) and ADP/ATP carrier. The fatty acid cycling mechanism is predicted, as well for the recently discovered uncoupling proteins, UCP2 and UCP3.

Postepy Biochem. 2008;54(2):188-97.Links
[Uncoupling proteins in modulation of mitochondrial functions--therapeutic prospects][Article in Polish]

Woyda-Płoszczyca A, Jarmuszkiewicz W.
Instytut Biologii Molekularnej i Biotechnologii, Uniwersytet im. Adama Mickiewicza w Poznaniu.

Enormous interest in mitochondrial uncoupling proteins (UCPs) is caused by relevant impact of these energy-dissipating systems on cellular energy transduction. A key role of UCPs in regulation of mitochondrial metabolism is supported by existence of their different isoforms in various mammalian tissues. Recent studies have shown that UCPs have an important part in pathogenesis of various disorders, such as obesity, type-2 diabetes, cachexia, aging or tumor. The obscure roles of UCPs in normal physiology and their emerging role in pathophysiology, provide exciting potential for further investigation. However, neither the exact physiological nor biochemical roles of UCP homologues are well understood. Therefore, providing mechanistic explanation of their functions in cellular physiology may be the basis for potential farmacological targeting of UCPs in future on clinical scale.
Curr Diabetes Rev. 2006 Aug;2(3):271-83. Links
Uncoupling proteins: role in insulin resistance and insulin insufficiency.Chan CB, Harper ME.
Department of Biomedical Sciences, University of Prince Edward Island, Charlottetown, Canada. [email protected]

Uncoupling proteins (UCPs) are modulators of mitochondrial metabolism that have been implicated in the development of both insulin resistance and insulin insufficiency, the two major pathophysiological events associated with type 2 diabetes. UCP2 mRNA is expressed in a wide range of tissues; however UCP2 protein expression is restricted to fewer tissues, including the endocrine pancreas, spleen, stomach, brain and the lung. To date, its role in the pathophysiology of diabetes has been most strongly associated with impaired glucose-stimulated insulin secretion from the beta-cell, particularly after its induction by free fatty acids. The physiological role of UCP2 remains controversial, but it may act as a downstream signal transducer of superoxide. UCP3 mRNA and protein are expressed in relatively few tissues, predominantly skeletal muscle, brown adipose tissue and heart. Increased expression of UCP3 in skeletal muscle is associated with protection from diet-induced insulin resistance in mice. In patients with type 2 diabetes UCP3 protein in muscle is reduced by 50% compared to healthy controls. The primary physiological role of the novel UCPs does not appear to be protection against positive energy balance and obesity; this is based largely on findings from studies of UCP2 and UCP3 knockout mice and from observed increases in UCP3 expression with fasting. The mechanism(s) of action of UCP2 and UCP3 are poorly understood. However, findings support roles for UCP2 and UCP3 as modifiers of fatty acid metabolism and in mitigating damage from reactive oxygen species.

Now, the fatty acid metabolism is linked to mitochondrial function AND insulin defficiency/ resistence...
AND this is one of the studies on carnitine/ammonia testing in ASD

J Autism Dev Disord. 2004 Dec;34(6):615-23. Links
Relative carnitine deficiency in autism.Filipek PA, Juranek J, Nguyen MT, Cummings C, Gargus JJ.
Department of Pediatrics, College of Medicine, University of California, Irvine, CA, USA.

A random retrospective chart review was conducted to document serum carnitine levels on 100 children with autism. Concurrently drawn serum pyruvate, lactate, ammonia, and alanine levels were also available in many of these children. Values of free and total carnitine (p < 0.001), and pyruvate (p = 0.006) were significantly reduced while ammonia and alanine levels were considerably elevated (p < 0.001) in our autistic subjects. The relative carnitine deficiency in these patients, accompanied by slight elevations in lactate and significant elevations in alanine and ammonia levels, is suggestive of mild mitochondrial dysfunction. It is hypothesized that a mitochondrial defect may be the origin of the carnitine deficiency in these autistic children.

and also there are more studies conditions- treatable- related to beta oxidation of fatty acidsRev Neurol (Paris). 2009 Jul 8. [Epub ahead of print] Links
[Multiple acyl-CoA dehydrogenase deficiency (MADD): A curable cause of genetic muscular lipidosis.][Article in French]

Maillart E, Acquaviva-Bourdain C, Rigal O, Brivet M, Jardel C, Lombès A, Eymard B, Vianey-Saban C, Laforêt P.
Centre de référence de pathologie neuromusculaire Paris-Est, groupe hospitalier Pitié-Salpêtrière, Assistance publique-Hôpitaux de Paris, Paris, France.

INTRODUCTION: Multiple acyl-CoA dehydrogenase deficiency (MADD) is a rare genetic disease involving fatty acid oxidation. It is due to the deficiency of one of the two electron transporters: electron transfer flavoprotein (ETF) or electron transfer flavoprotein ubiquinone oxydoreductase (ETF-QO). Symptoms begin more often in childhood or in young adulthood with a multisystemic disease with encephalopathy or muscular weakness. CASE REPORTS: We report here two adult cases with ETF-QO deficiency, confirmed by mutation analysis (ETFDH gene), revealed by a muscular weakness associated with muscle lipidosis. One of our patients presented an acute encephalopathy with vomiting ten years before the onset of muscular symptoms. The second patient exhibited a slowly progressive pelvic girdle muscle weakness. Diagnosis was established by characteristic abnormalities of acylcarnitine profile by tandem mass spectrometry. For both patients, a dramatic clinical improvement was observed under treatment with riboflavine and L-carnitine. CONCLUSION: Since it is a treatable disorder, this diagnosis must be considered by performing an acylcarnitine profile in all patients presenting with an unexplained muscular weakness.

The beta oxidation disorders are complicated
Postepy Hig Med Dosw (Online). 2009 Jun 8;63:266-77.
An overview of beta-oxidation disorders.Moczulski D, Majak I, Mamczur D.
Katedra Medycyny Wewnetrznej, Uniwersytet Medyczny w Łodzi, Łódź.

Fatty acids (FAs) are components of cell membrane, enzymes, and hormones and are one of the most important energy sources for many organisms. There are several types of fatty-acid oxidative degradation processes in the cell, namely alpha-, beta-, and omega-oxidation, which take place in specialized cellular structures: mitochondria and peroxisomes. The best-known pathway is beta-oxidation taking place in the matrix of mitochondria. It is responsible for the degradation of straight-chain FAs. The pathway of beta-oxidation of fatty acids is comprised of at least 25 enzymes and specific transport proteins. Deficiencies in 18 of them have been demonstrated to cause disease in humans. These diseases show a wide variety of symptoms, which can be expressed at random, one at a time, or in sets, characteristic of the individual rather than the metabolic character of the disease. Disorders of beta-oxidation are believed to cause about 1-3% of unexplained sudden infant deaths (SIDS). Acute fatty liver of pregnancy (AFLP) and the syndrome of hemolysis, elevated liver enzymes, and low platelets (HELLP syndrome), which have significant neonatal and maternal morbidity and mortality, have also been associated with beta-oxidation deficiency in fetuses. This review summarizes recent observations on disorders associated with fatty-acid oxidation: deficiencies of beta-oxidation enzymes, namely VLCAD, TFP and LCHAD, MCAD, MCKAT, M/SCHAD, and SCAD, and deficiencies of the enzymes TCP I, CT, and CPT II of the carnitine cycle.

Kent Heckenlively


So many wonderful questions and observations.

In writing these articles I always walk a fine line between providing information and being seen as endorsing them. I have gotten some interesting results from tests, but can't yet tell you anything about treatment. If you want further information on testing you could go to Dr. Kane's web-site,

I do believe this theory goes along with the observations made in my article "A Tale of Autistic Blood". If you understand what's going on here, the red blood cells are being deprived of vital nutrients and minerals and becoming inflamed.

This work also goes along with the "Lorenzo's Oil" story, although when I discussed the issue with Dr. Kane, it was her opinion that the family erred by trying to make something new, rather than following the suggestions of Dr. Hugo Moser, founder of the Peroxisomal Disease Lab at Kennedy-Krieger Institute.

Testing for my daughter cost $725. The two tests I had done were the BodyBio Blood Analysis and the BodyBio Fatty Acid Analysis. With the infusions and added supplements I'm guessing it'll be a few thousand dollars.

All the best,

Mary Barclay

I have a question. Can this kind of fatty acid dysfunction be the cause of what you talked about in your article "A Tale of Autistic Blood" posted on June 3rd?

Of all the theories I've read the ideas presented here and in "A Tale of Autistic Blood" jump out at me in a profound way. In my gut I know that, for my son, the answer is in the blood. My sons' blood work looks most similar to that of an AIDS patient.

I would really like to hear exactly what test you are having done, in-regards to this particular theory.

Thank You

Benedetta Stilwell

Kent thanks for the work and research here, this is pretty difficult stuff to have to read through it, decide what might be useful and what is just junk.

Benedetta Stilwell

Reading your article I think it means that the trouble is not inside the mitochondria, but the transport system that takes stuff across the membrane into the mitochondria and then brings energy stuff back out? L-carintine has something to do with transporting stuff across.

I read something about this from research being done at Arizonia University.

There is also the MCT oil (medium chain triglyerides) that is given in the Ketogenic diet. Buy it in powder form and mix it up with water. It can be purchased probably here on the net. That might be a wild goose chase though, MCT oil probably works on the liver to cause the liver to produce more ketones, for energy instead of the regular carbs for energy. But with the MCT oil it does cause the body to go into deeper starvation (ketogenic state) though.

But could I get my three to do any of this stuff? I can't even get them to keep on the Atkins diet - we are now on a low glycemic diet. And unless they have a guarentee that it works, well I can see their point. They are going along with fasting once a month. I hope that will clear long chains, or is that just another one of my hair brain ideas?

María Luján

Hi Kent
Two very recent manuscripts are in line with the ideas of Dr Kane

Prostaglandins Leukot Essent Fatty Acids. 2009 Apr;80(4):221-7.
Plasma fatty acid profiles in autism: a case-control study.Wiest MM, German JB, Harvey DJ, Watkins SM, Hertz-Picciotto I.
Division of Epidemiology, Department of Public Health, University of California, Davis, CA 95616, USA.

Increasing evidence is mounting in support of fatty acid metabolism playing a role in neurodevelopmental disorders such as autism. In order to definitely determine whether fatty acid concentrations were associated with autism, we quantitatively measured 30 fatty acids from seven lipid classes in plasma from a large subset of subjects enrolled in the Childhood Autism Risk from Genetics and the Environment (CHARGE) study. The CHARGE study is a large, population-based case-control study on children aged 2-5 born in California. Our subset consisted of 153 children with autism and 97 developmentally normal controls. Results showed that docosahexaenoic acid (DHA, 22:6n-3) was significantly decreased in phosphatidylethanolamine. Dimethyl acetals were significantly decreased in phosphatidylethanolamine and phosphatidylcholine as well. These results are consistent with the only other study to measure dimethyl acetals in children with autism, and suggest that the function of peroxisomes and the enzymes of the peroxisome involved with fatty acid metabolism may be affected in autism.

Prostaglandins Leukot Essent Fatty Acids. 2009 Jul 14.
Novel plasma phospholipid biomarkers of autism: Mitochondrial dysfunction as a putative causative mechanism.Pastural E, Ritchie S, Lu Y, Jin W, Kavianpour A, Khine Su-Myat K, Heath D, Wood PL, Fisk M, Goodenowe DB.
Phenomenome Discoveries Inc., 204-407 Downey Road, Saskatoon, Saskatchewan, Canada S7N 4L8.

Autism is a neurological disorder that manifests as noticeable behavioral and developmental abnormalities predominantly in males between the ages of 2 and 10. Although the genetics, biochemistry and neuropathology of this disease have been extensively studied, underlying causal factors to this disease have remained elusive. Using a longitudinal trial design in which three plasma samples were collected from 15 autistic and 12 non-autistic age-matched controls over the course of 1 year, universal and unambiguous alterations in lipid metabolism were observed.
Biomarkers of fatty acid elongation and desaturation (poly-unsaturated long chain fatty acids (PUFA) and/or saturated very long chain fatty acids (VLCFA)-containing ethanolamine phospholipids) were statistically elevated in all autistic subjects.
In all 8 of the affected/non-affected sibling pairs, the affected sibling had higher levels of these biomarkers than the unaffected sibling. Exposure of neurons, astrocytes and hepatocytes in vitro to elevated extracellular glutamate levels resulted in lipid biomarker changes indistinguishable from those observed in autistic subjects. Glutamate stress also resulted in in vitro decreased levels of reduced glutathione (GSH), methionine and cysteine, in a similar way to the decreases we observed in autism plasma. Impaired mitochondrial fatty acid oxidation, elevated plasma VLCFAs, and glutamate toxicity as putative causal factors in the biochemistry, neuropathology, and gender bias in autism are discussed.
My comment: in all autistic subjects the VLCFA were elevated


"treatment should be centered on re-building membrane structure and thereby stabilizing membrane function." Absolutely. But if there is an active/replicative viral infection going on, by an enveloped virus, rebuilding the membrane function will be an uphill struggle.


Kent - again you have given me much to think about. I was taken aback when I read your article. The term "very long chain fatty acids" jumped right out at me. I have heard it before, in one of my favorite movies of all time: Lorenzo's Oil, the story of the Odone family and their search to cure their son of ALD. Augusto Odone discovered that myelin destruction in ALD was caused by an overabundance of these VLCFA's, and invented Lorenzo's Oil to correct the problem. Just last week I met a family whose 8 year old son was stricken with ALD symptoms 3 months ago. The dad told me it was too late for the oil, that children need to take it before they become symptomatic. They did not know their son was in danger, although their younger child also has the ALD gene and is on the oil. Doctors are confident that he will not become symptomatic at all. I am now going to have to read that book again to clarify the thousand questions your article has raised. Thanks again Kent, for your exhaustive search for answers. I look forward to your every post.

A. F.

Mr. Heckenlively, thank you very much for this article. I'd like to give my son's doctor this information. Is there any way you could post, for us to give to a doctor, instructions on how we can also do a test for our child, who to contact, how much it costs, etc.?
Thanks a lot.

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