Let’s stop and think what Secretin does to lipid (fat) metabolism. Autistic kids are universally deficient in the fatty acids. Secretin is a pro-oxidant hormone. The metabolic impact of Secretin is that it stimulates the arachidonic acid cascade (contraindicated in seizure disorders) and bicarbonate production, oxidizes or burns off (beta oxidizes) fatty acids (including both essential fats, insulating fatty acids, and very long-chain, fatty acids), increases the metabolism of bile acids, and, theoretically, may stimulate Cholecystokinin-B (CCK-B) that plays a neuromodulatory role in the regulation of GABAergic neuronal activity perhaps (theoretically) stimulating speech. When a child receives Secretin repeatedly without replenishing the lipids (fatty acids) and catalysts (vitamins and minerals), the impact could ultimately be quite negative.
On the other hand, children with autistic spectrum disorder tend to have a buildup of very-long-chain, fatty acids (VLCFA) indicative of suppressed, peroxisomal, beta-oxidation. Support for the thyroid, and supplementation of manganese, selenium, carnitine, and vitamin B2 stimulate beta-oxidation of fatty acids, but high carbohydrate meals stimulate insulin response and inhibit beta-oxidation. Characteristically, plasmalogen synthesis (any of various glycerophospholipids in which a fatty acid group is replaced by a fatty aldehyde group) and beta-oxidation of very-long-chain fatty acids are affected. It’s been found that patients with generalized, peroxisomal disorders have a profound brain deficiency of docosahexaenoic acid (DHA; 22:6 n-3) and low DHA concentrations in all tissues and in the blood (is it any wonder since DHA has only been allowed in baby formula very recently). Supplementation with docosahexaenoic acid (DHA) [22:6 (n-3)] ethyl ester (EE) (DHA-EE) normalized blood DHA values within a few weeks. Plasmalogen concentrations increased in erythrocytes in most patients and after DHA concentrations were normalized, amounts of VLCFAs decreased in plasma. Liver enzymes returned almost to normal in most cases. From a clinical viewpoint, most patients showed improvement in vision, liver function, muscle tone, and social contact. In three patients, normalization of brain myelin was detected by magnetic resonance imaging. In three others, myelination improved. In a seventh patient, myelination is progressing at a normal rate. Balancing these fatty acids can control brain performance! While characteristic alterations are varied, they classically involve elevations of AA/EPA/DHA and suppression of GLA/DGLA in autism; suppression of AA/DHA in Schizophrenia and bipolar; suppression of GLA/AA/EPA/DHA, and adrenic acid in ADHD; variable EFA instability (high or low AA/DHA) in depression; low Omega 6 (including AA) and elevated Omega 3 in Chronic fatigue syndrome. Curiously, DHA is a VLCFA.
The use of Secretin stimulates the burning off of these aberrant, excess lipids (VLCFAs) that irritate the brain (and many other systems of the body); thus, in that degree, Secretin is of immediate benefit. The administration of Secretin, DHEA, pregnenolone, or thyroid hormone stimulates the beta-oxidation (burning within the mitochondria for energy) of VLCFAs, as would nutrients (riboflavin, pyruvate, manganese) and oxidative therapies that stimulate oxidation, prostaglandin synthesis, and detoxification. Excess VLCFAs indicate a deficiency of cytochrome p450 (Phase I) liver enzymes, and pregnenolone increases Phase I activity by conserving existing Phase I enzymes. Milk thistle, Turmeric (curcurmin), ginger, Royal Jelly, Sheep Sorrel, and Pau D’ Arco enhance Phase I activity. Stimulating beta-oxidation, however, concurrently stimulates the burning off of all essential fatty acids (EFAs), as I said. These must be supplemented.
Children with ASD most often present with alkalosis, low CO2/Bicarbonate, and low oxygen. The spacy, dreamy, lack of clarity state you observe in most autistic children is often associated with a low bicarbonate and disturbed electrolyte status. Insufficient oxygen in the brain can lead to a spacy, confused, non-alert quality also. Infusions of Secretin will correct the alkalosis that most children with ASD present, ultimately impacting their hyperammonemic states that may be stabilized with the increased bicarbonate production (bicarbonate released from the pancreas plus ammonia yields urea that can be excreted). Sulfur containing amino acids become ammonia and remain ammonia without adequate folic acid, B12, zinc, and molybdenum. Excess ammonia in the blood is associated with excess lysine. Elevated, systemic levels of ammonia are toxic, and possible symptoms include: protein intolerance, headaches (migraine), fatigue, irritability, diarrhea, and nausea. These may be episodic symptoms associated with high-protein meals. Chronically elevated ammonia in the CNS can result in decreased cognitive function, confusion, slurred speech, and blurred vision. When the bloodstream is extremely acid, the kidneys use a different method and excrete ammonium ions, which contain four hydrogens, into the urine. In this instance, it may be a mistake to reduce urine ammonia levels before correcting the body pH.
“Peroxisomes are organelles within cells that are pivotal in the biotransformation of endogenous compounds in lipid metabolism such as fatty acids, steroids, prostaglandins, the formation of myelin, neurotransmission, and detoxification of exogenous compounds and xenobiotics (phenols and other compounds discussed under the section PST). VLCFAs are fatty acids with 22 or more carbons. Normally, these are oxidized down to C20 or less by p450 oxidase enzymes in the peroxisome organelles in the liver. These C20s are then shuttled by carnitine into the mitochondria for further metabolism. However, mitochondria cannot metabolize VLCFAs, so, they then accumulate in the nerve cells where they have toxic effects. This is almost universally true in autistic children, but is also seen in Alzheimer’s patients, chronic fatigue, Zellweger’s, and cardiovascular disease. The accumulation of VLCFAs [Docosahexaenoic (DHA), Docosapentaenoic w3, Behenic, Lignoceric, and Nervonic] inside the cell membrane represents defects in peroxisomal, beta-oxidation, rather than a mitochondrial disturbance. This accumulation may be used to profile the deleterious effects upon the brain, endocrine, gastrointestinal, and immune systems, as well as the cytochrome P450 liver enzyme derangement involving nitric oxide synthase (NOS) characteristic in autistic spectrum disorder due to autoimmune presentation. Therefore, the toxic aspect so often described in autism may be defined clearly through examination of Red Blood Cell lipids with elevation of VLCFAs being a reflection of blocked detoxification mechanisms”—Patricia Kane. This would indicate an inhibited Phase I pathway, probably hypothyroidism, and a lack of vitamin B2 and manganese.
Additionally, a recent study shows another disturbing aspect of this fatty acid imbalance on cell walls: Abstract: Red blood cell fatty acid compositions in a patient with autistic spectrum disorder: a characteristic abnormality in neurodevelopmental disorders? J. G. Bell, J. R. Sargent, D. R.Tocher, J. R. Dick Nutrition Group, Institute of Aquaculture, University of Stirling, Stirling UK
“Summary: The fatty acid compositions of red blood cell (RBC) phospholipids from a patient with autistic spectrum disorder had reduced percentages of highly unsaturated fatty acids (HUFA) compared to control samples. The percentage of HUFA in the RBC from the autistic patient was dramatically reduced (up to 70%) when the sample was stored for 6 weeks at (-) 20 degrees C. However, only minor HUFA reductions were recorded in control samples stored similarly, or when the autistic sample was stored at (-) 80 degrees C. A similar instability in RBC HUFA compositions upon storage at (-) 20 degrees C has been recorded in schizophrenic patients. In a number of other neurodevelopmental conditions, including ADHD and dyslexia, reduced concentrations of RBC HUFA have been recorded.
“Evidence suggests that the HUFA instability observed in a patient with ASD, and found in other neurodevelopmental disorders, may be caused by increased phospholipase activity, perhaps in conjunction with increased auto-oxidative stress. The evidence available suggests that autistic spectrum disorder involves an aberration in lipid metabolism that results in alterations in cell membrane phospholipid structure and function, and that these alterations are similar in a number of other neurodevelopmental disorders. The tryptophan metabolite, indole acroyl glycine (IAG), has been found in the urine of the majority of patients with ASD, and has also been identified in numerous other neurodevelopmental disorders. The precursor of IAG, indole acrylic acid, when added to cells in culture affects the cellular PUFA compositions and the production of PgE.”
Autism is said to often involve a demyelination of the myelin sheath of nerves, disrupting nerve transmission. Brain autoantibodies to both myelin basic protein (MBP) and neuron-axon filament protein have been found in autistic children who have about 8.3 times greater incidence of antibodies to MBP than control children. The perineuronal nets around neurons, which modulate their function, are primarily composed of chondroitin sulfate. Low sulfur would thus yield less modulation of neurons. Hepatitis B vaccine was found to inhibit sulfation chemistry for at least one week in typical people. When TNF (tumor necrosis factor) is elevated (frequently in autism), through interference with dioxygenase and sulfite oxidase, it can inhibit the conversion of cysteine to sulfate. This could be a contributing factor in PST. This can lead to decreased blood flow into the brain, a loss of Purkinje cells (often found on autopsy), alterations in neurotransmitters and neuropeptides, and possibly demyelination as found in multiple sclerosis (MS). TNF also competes with insulin at cell receptors, contributing to Insulin Resistance.
Mercury and other heavy metals (such as lead) can cause progressive myelin degeneration with the development of antibodies to myelin basic protein (MBA) and glial fibrillary acidic protein (GFAP). Recent discovery of herpes virus-6 in the damaged areas of the brains of 73% of Multiple Sclerosis sufferers is indeed disturbing. The nervous system, once the insulation is stripped, can be likened to your home with bare wires inside the walls—a dangerous situation. In the body, symptoms may be many and varied:
1) tremors, shaking, “palsy” due to malfunction of nerve transmissions
2) uncoordination in walking, writing, and other automatic physical movements
3) slurred speech
4) excessive salivation
5) deterioration of memory and thinking processes
6) blurred vision
7) difficulty urinating, incontinence
8) environmental sensitivity, allergic to smells, food, clothing, electrical equipment
9) breathing problems, short of breath
10) nervousness or nervous breakdown
11) numbness and tingling in extremities
12) heart problems/arrhythmias.
Some have found Sphingolin™ most helpful (Ecological
Formulas 800-888-4585). Vitamin B12 is often lacking, and it is essential to
sheath formation. Additionally, nervonic acid, EFAs, and
very-long-chained-fatty alcohols have clinically been shown to yield
positive outcomes. These benefit the myelin sheath, increasing perception
and response. Dr. Jeff Bradstreet, however, reports that children who took
oral, myelin-basic protein (Sphingolin™) seemed worse when they were infused
with Secretin. The Secretin burned off the fats (needed to make myelin and
prostaglandins, both the insulating fats and the very-long-chain fats). It
is a big “no no” to stimulate with peptides (Secretin) or with Sphingolin™
without fats! (Patricia Kane) If you choose to infuse, you must supplement
generously with Evening Primrose oil (EPO); and always with fatty acids, you
must supplement with the antioxidants vitamin C and vitamin E with selenium,
preferably before beginning the EPO. A failure to do so may promote
seizures, neurological disorders, and increased cancer risk due to increased
free-radical activity. Additionally, Dr. Woody McGinnis, MD,
In the case of inadequate HCl production, infusion or transdermal supply of Secretin may indeed help, but it does not fully address the most basic need—that of necessary digestion and utilization of food. The proper course for many seems not to be Secretin infusion, but a supplementing of hydrochloric acid to the degree necessary to trigger release of the Secretin so vital to proper digestion and hormonal response. In at least a minority of these children, the gut will be able to release adequate Secretin. The supply of adequate acidity to the chyme would then “Kick Start” Secretin production. One mother reports, “Since I followed your suggestion, and supplemented HCl, my son has the same responses he had to his Secretin infusion!”