Common features in those with autism include: raised blood or serum lactate, regional disturbances in glucose uptake in the brain, particularly in the cortex, and reduced brain levels of high-energy phosphate compounds. This is another curiosity of autism. Actually, children’s diets are overloaded with phosphate, and that is one reason for hyperactivity. Children are at increased risk to other conditions that result from excessive phosphate intake. These include: infant colic, sleep disturbances, eczema, allergies, and asthma. Avoidance of phosphates in sodas, processed meats, and baked goods has often been found to be effective against these conditions.
These observations would suggest a mitochondrial energy disorder in the brain. Mitochondrial dysfunction may result from any of the following four imbalances:
1. Impairment of mitochondrial fatty acid oxidation due to carnitine deficiency. Carnitine pumps fatty acids into the mitochondria. With the help of vitamins B6, C, and niacin, the body produces carnitine from the amino acids lysine and methionine found in high quality protein. Adequate amounts are not thus formed so some carnitine must come from muscle and organ meats in the diet for it is not found in vegetables. Obviously, a low protein or a vegetarian diet would likely create a deficiency of this vital nutrient, and impair the mitochondrial function causing a loss of energy and a build up of triglycerides and fatty acids in the blood and cells.
The Cincinnati Children’s
Cellular energy production itself produces free radicals that can damage cell structures, including the mitochondria, and ultimately lead to various diseases if the body’s natural antioxidant capacity is inadequate. Acylcarnitine and lipoic acid are both endogenous (naturally present in the body) antioxidants that have been shown to restore the mitochondrial function and reduce free radical damage. (Hagen TM et al., 1998; Lyckesfeldt J et al., 1998). Together with coenzyme Q10 and NADH, they work to maintain the function of the mitochondria.
It should be noted that not only fatty acids are needed, but glucose must be able to enter the mitochondria to produce energy needed by the cell and by the muscles. Just as L-carnitine pumps in fatty acids, Alpha Lipoic Acid pumps in glucose, thus, its supplementation tends to overcome syndrome X, where the cells are resistant to glucose. This resistance produces unnaturally-high, blood levels of insulin and sugar.
Since the amino acid L–carnitine is frequently lacking
in the autistic, this could predispose to heart problems and a lack of
energy. The primary function of carnitine is to escort fatty acids into the
mitochondrial furnace where the fat is burned to fuel ATP for energy. In
this action, it reduces blood levels of triglycerides and cholesterol
dramatically and aids weight loss. It boosts energy levels for those
suffering from elevated blood sugar levels and kidney insufficiency. This
reduces fatigue. Tests by Dr. Carl Pepine at the
L-carnitine (500 mg capsules twice daily on an empty stomach, or with a carbohydrate snack) reduced ketone, triglyceride (up to 40%), and cholesterol (up to 21%) levels, and increased HDL levels (up to 15%). Acetyl-L-carnitine is equally effective with one added benefit. It decreased oxidative damage to the brain that was not observed with L-carnitine. The suggested use is 200 mg three times a day, increasing after one week to 400 mg three times daily, to improve brain energy levels. Basic L-carnitine may draw moisture and become unstable, and it is not the most bioavailable. While the citrate, lactate, and tartrate are good forms, the most effective form is L-carnitine fumarate. It is up to 9% more bioavailable. Carnitine will conserve calcium, magnesium, and potassium, and may reduce heart arrhythmias and fatigue—which will reduce risk of heart attack.
Due to increased fat burning, carnitine supplementation creates a significant need for caloric increase. If none is supplied there will likely be weight loss. It also generates increased free radicals that can severely damage cells unless additional antioxidants are supplied—particularly vitamins C and E and selenium. Additionally, lower than normal levels of certain essential fatty acids, such as cholesterol (needed as the precursor to many hormones) and triglycerides (a large proportion of the blood’s fatty substances) can be exacerbated by supplemental carnitine. One Mother says, “We lost our seizure control, and did not regain it until calories had been upped significantly...Please, everyone, let’s consider very carefully the premise that carnitine supplementation creates a significant need for caloric increase.” The level of fatty acids in the autistic child is an important factor because the endocrine system and its hormones, the brain and its neurotransmitters, the myelin sheath, and all the immune system components are derived from lipids (fats).
However, mitochondria cannot metabolize very-long-chain fatty acids (VLCFA) which many autistic have accumulated; so, if carnitine pumps additional ones into the cell, they can accumulate in the cells where they have toxic effects. Adrenoleukodystrophy (ALD) is a rare, fatal, degenerative disease caused by a build up of very-long-chain, fatty acids (c22 to c28) that destroys the myelin (protective sheath) of the nerves (remember Lorenzo’s Oil? It’s a preparation of 20% erucic and 80% oleic acids that might be useful to the autist with accumulated VLCFA). It helps to normalize these fatty acids. Canola oil is a very-long-chain fatty acid (c22) that should be avoided. Inability to handle VLCFAs is almost universally true in autistic children, but is also seen in Alzheimer’s patients, chronic fatigue, and cardiovascular disease. The accumulation of VLCFAs inside the cell membrane represents defects in peroxisomal, beta-oxidation that is likely the result of hypothyroidism and a high-starch (high insulin) diet. 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 (that is, the Phase I liver enzymes are sluggish). These can be safely enhanced with Milk Thistle, Bistort, Royal Jelly, Sheep Sorrel, and Ginger, but other herbs that enhance Phase I are usually, potentially, liver toxic. Elevation of DHA is not particularly disturbing unless Omega-6 fatty acids (particularly Arachidonic Acid) are suppressed (both EPA and DHA in excess suppress them). In some cases, the VLCFA DHA is reduced. In that case, supplementation of DHA has proven most helpful in relieving many symptoms of VLCFA disease.
Carnitine supplementation holds great promise, and it must be supplemented when Depakote™ is being used, but I think there are some things we must guard against. Additional carnitine will pump more fatty acids into the mitochondria to produce additional energy. It would help to know, from a previous blood test, that the triglycerides and cholesterol were normal or elevated. When using carnitine, to avoid creating a deficiency in fatty acids, we must supplement with Evening Primrose and cod-liver oils as outlined elsewhere in this paper, and ensure the child is getting enough calories for his size and activity. The wild card is the VLCFAs. To determine their status run the Red Blood Cell Lipid test. Symptoms of fatty acid deficiency would tend to be thirst, dry skin and hair, brittle nails, excess urination, dandruff, eczema, and rough skin. If these symptoms, or low triglyceride/cholesterol levels, or excess VLCFAs were present, I would not supplement manganese, selenium, vitamin B2, and carnitine until these problems were being corrected. As I understand it, carnitine could lower the fatty acids and blood fats adversely, and could overload the cell with VLCFAs that it cannot burn. Look to the thyroid, do the iodine test, and if indicated, support the thyroid.
Autoimmune presentation may be depicted by this elevation of VLCFAs, vaccenic acid, Mead acid, EPA and DHA due to upregulation of nitric oxide synthase and nitric oxide. Status of the immune system is viewed primarily through the balance and sufficiency of EFAs of both the Omega 6 and Omega 3 series. Immune function is highly dependent upon the AA cascade. Although many disorders are indeed inflammatory in nature, depicting elevation of AA, many more disorders are a result of depleted AA stores (as in Chronic Fatigue Syndrome, Crohn’s Disease, Rheumatoid Arthritis, Lupus, and metal toxicity) and consequently the body fails to mount an appropriate immune response.
2. A second cause of mitochondrial energy disorder is inflammation associated with the release of excess nitric oxide as mentioned above. The Far Infrared Sauna, the herb Ginkgo Biloba, and DHEA selectively increase the release of nitric oxide synthase, the enzyme that reacts with arginine to produce nitric oxide (NO). It is reported that one week on this sauna showed a 40-fold increase of this enzyme in the endothelial cells of the aorta! This may be great for reducing blood pressure, but these should be avoided in this instance because excess NO can cause uncoupling of oxidative phosphorylation as well as inhibiting the Krebs cycle enzyme, aconitase. This will result in organic acidemias, and low mitochondrial energy production. Lactic acidosis and a carnitine deficiency in autistic patients suggest excessive nitric acid production in mitochondria (Lombard, 1998, Chigani, et al, 1999), and mercury may be a participant. Methyl mercury accumulates in the mitochondria, where it inhibits several mitochondrial enzymes, reduces ATP production and Ca2+ (calcium) buffering capacity, and disrupts mitochondrial respiration and oxidative phosphorylation (Atchison & Hare, 1994; Rajanna and Hobson, 1985; Faro et al., 1998). The behavior associated with excess NO production in the autist is maniacal laughter. NO is a gas that lasts only a few seconds. Thus, a large serving of Arginine tends to spike NO and shortly lose its effect. If Arginine is supplemented, use only the time-released type (Perfusia-SR by Thorne Research, Inc.) in order to maintain a more constant, low-level of NO.
Neurological problems are among the most common and serious of mercury poisoning, and include memory loss, moodiness, depression, anger and sudden bursts of anger/rage, self-effacement, suicidal thoughts, lack of strength/force to resolve doubts or resist obsessions or compulsions. Mercury causes decreased lithium levels, which is a factor in neurological diseases such as depression and Alzheimer’s. Lithium protects brain cells against excess glutamate induced excitability and calcium influx, and low levels cause abnormal brain cell balance and neurological disturbances. Medical texts on neurology point out that chronic mercurialism is often misdiagnosed as dementia or neurosis or functional psychosis.
Mercury, at extremely low levels, interferes with formation of tubulin, producing neurofibrillary tangles in the brain similar to those observed in Alzheimer’s patients with high levels of mercury in the brain. Mercury and the induced neurofibrillary tangles appear to produce a functional zinc deficiency in the AD sufferers, as well as causing reduced lithium levels. Mercury binds to hemoglobin in the red blood cell, and will reduce the amount of oxygen that can be carried in the blood—a major cause of Fatigue. Mercury, at a level of 1 part per ten million, will actively destroy the membrane of red blood cells. Mercury binds with cell membranes interfering with sodium and potassium enzyme functions, causing excess membrane permeability, especially in terms of the blood-brain barrier. Less than 1 ppm mercury in the blood stream can impair the blood-brain barrier. Mercury also blocks the immune function of magnesium and zinc. Exposure to mercury vapor causes decreased zinc and methionine availability, depresses rates of methylation (a bodily process of converting inorganic forms to organic forms, part of the detoxifying process), and increases free radicals—all factors in increased susceptibility to chronic disease and to cancer. Mercury, especially organic mercury, causes accumulation of calcium into the cells, therefore, one does not want to take much calcium, and one wants to have a high ratio of magnesium to calcium, that is, keep magnesium up and calcium down to reduce the accumulative effects. Mercury also blocks the metabolic action of manganese, allowing an increased production of NO and the entry of calcium ions into cell. Mercury, then, is excitotoxic in its action.
Magnesium and manganese are the doorkeepers regulating the proper amount of calcium entering the cell. Mercury, if excreted in the urine, pulls out magnesium from the body, thus increasing the manganese relative to magnesium levels. Rarely is mercury excreted, and most commonly it migrates to the brain where it can drive both brain toxicity and increases in manganese. In either case, increases in manganese relative to magnesium may increase measles viral mutations. Shifts in magnesium to manganese cations in the body can significantly enhance viral mutation rates by 6-10-fold.
The significance of this in your child’s life may be seen in the following: A group measured mercury levels in 15 preterm and 5 term infants before and after Hep B vaccination. According to the group, after-vaccination mercury levels in both preterm and term infants showed a significant increase. Mercury levels in the preterm infants were three times higher than in the term infants, and this was statistically significant, according to the team—Dr. Gregory V. Stajich from Mercer University, Atlanta, Georgia.
A recent study demonstrates that oral administration of N-acetylcysteine (NAC), a widely available and largely nontoxic amino acid derivative, produces a profound acceleration of urinary methyl mercury excretion in mice. Mice that received NAC in the drinking water (10 mg/ml) starting at 48 hr after methyl mercury administration excreted from 47 to 54% of the 203 Hg in urine over the subsequent 48 hr, as compared to 4-10% excretion in control animals. When NAC was given from the time of methyl mercury administration, it was even more effective at enhancing urinary methyl mercury excretion, and at lowering tissue mercury levels. In contrast, excretion of inorganic mercury was not affected by oral NAC administration. Three other nontoxic elements that readily bond to mercury rendering it less toxic and more easily excretable are Oxygen, Sulfur, and Selenium. When eating fish, take 50 mcg of selenium and a capsule of NAC and enjoy! Selenium binds strongly to Mercury, cadmium, and arsenic depleting the stores of this trace element that is needed for cellular health. Latest research shows a conclusive connection between reduced levels of selenium and increased risk of cancers.
A lack of selenium also adversely affects the conversion of T4 thyroid hormone to T3. Stress also reduces the conversion of T4 to the more active T3. Additionally, when the liver can no longer listen to insulin, conversion of T4 to T3 is hindered. However, it is the transformation within the cells that counts, and a lack of glutathione (universal in ASD, said to be at 1/3 normal) not only hinders the conversion, but also reduces uptake of T3 into cells. Researchers found that, in non-diabetic, non-fasting, healthy individuals, T4 to T3 conversion was 36%, but in those fasting, this dropped to 18%. In diabetic, non-fasting individuals conversion of T4 to T3 was 12% (Nutrition and Healing, July 2004)! Both cadmium and mercury inhibit the conversion of thyroxine (T4) to active T3, but high arsenic (that binds selenium) or low copper enhances it (perhaps by increasing the above conversion rates), leading to high T3 readings. Those doing DMSA have confirmed this. When selenium was depleted, T3 increased. In people who are hyperinsulinemic with a thyroid hormone that comes back totally normal, it is important to measure their T3. Just as often as not, their free T3 will be low, but get their insulin down and it comes back up. Hyperinsulinemia also causes the excretion of calcium and magnesium in the urine. People with hyperinsulinemia (insulin resistance) can take all the calcium and magnesium they want by mouth, and it will largely go out in their urine. Magnesium chloride oil/gel are available to rub on (inquire), and Epsom salts baths can supply needed magnesium sulfate working around this problem.
Paradoxically, in a Chinese study, researchers found that selenium and vitamin E deficiency reduced blood levels of T3 by more than one-third! Vitamin E was thought to protect the T4/T3 conversion process. Nothing is simple when it comes to the hormonal system! All myelination is controlled by T3. Free T3 regulates serotonin and melatonin metabolism. T3 controls serotonin uptake, binding to its receptors, so if there are serotonin problems, look to the thyroid. Arsenic causes T4 to convert to too much T3, which can cause Edema of the Septum Pellucidum and ensuing aggression. Thus, when arsenic poisoned, one may have to watch selenium levels greatly. To efficiently convert T4 to the active form T3, you need a specific ratio of zinc to copper of about 8:1. If you have had hair analysis and or fecal testing or blood tests you may know what your ratio is. If not, I would suggest finding out. Zinc deficiency decreases concentrations of triiodothyronine (T3) and free thyroxine (fT4) in serum by approximately 30%. Most of the zinc is cellular with only a small amount in the blood plasma. Blood tests, therefore, are a poor indicator of systemic zinc status. Mercury (in amalgam, and thimerosal in vaccines) will also cause hypothyroidism by interfering with selenoenzymes (Watanabe et al, 1999), and mercury competes and really messes up zinc absorption/utilization creating all kinds of effects throughout the body.
3. Defects in respiratory chain enzymes produce mitochondrial energy
disorders: Pyruvate Dehydrogenase or mitochondrial respiratory chain
defects, that is, NAD, NADH, Coenzyme Q10, and cytochrome oxidase
deficiency. Although we find a variety of autistic phenotypes to have
associated mitochondrial abnormalities, the most common is nonspecific PDD,
typically of a form that manifests language and cognitive regression or
stagnation during the second year. Most surprising among multiplex families
is that the biochemical and clinical markers of mitochondrial disease often
segregate in an autosomal-dominant manner (that is, genetically induced).
Although no molecular lesion has yet been found in the autosomal dominant
families, the biochemical findings are most consistent with abnormal
mitochondrial Complex I activity (that is NAD/NADH activity—WSL). Early and
careful evaluation of autistic children for these more subtle mitochondrial
disturbances may rescue them from more severe brain injury (Kelley, Richard,
Kennedy Krieger Institute,
4. Excess glutamate exposure, a common and increasing source being MSG, flavor enhancers, and protein substitutes. Generally, autistic children show low glutamine, high glutamate readings. Plasma levels of glutamic acid and aspartic acid are elevated even as levels of glutamine and asparagine were low (Moreno-Fuenmayor et al, 1996). Mercury inhibits the uptake of glutamate, with consequent elevation of glutamate levels in the extracellular space (O’Carroll et al, 1995). Thimerosal enhances extracellular free arachidonate and reduces glutamate uptake (Volterra et al, 1992) causing an excitotoxic situation. Cells that are without oxygen may release excessive glutamate, exacerbating the situation. Low oxygen is common in autistics. Excessive glutamate is implicated in epileptiform activities (Scheyer, 1998; Chapman et al, 1996). Children’s forming brains are four times more sensitive to neuro-excitotoxins. The lower the energy production of the cell, the more susceptible it is to excitotoxicity. Low magnesium levels (common in “our” children) can double free-radical production and magnify their toxicity! The generation of increased levels of free radicals within the cell can activate the p53 tumor-suppressor gene triggering apoptosis (cell suicide). Excess glutamate can kill neurons by necrosis (by allowing excess calcium into the cells) as well. Magnesium is the calcium regulator. Elevated plasma glutamate lowers cellular GSH by inhibiting cystine uptake.
Additionally, high glutamate levels result in the depletion of glutathione. Streptococcal infection is also more likely to be an issue in individuals with high glutamate levels, as glutamate is related to virulence in streptococci. Streptococcus flourishes in a high glutamate, low glutathione environment. Thus, the combined effects of changes in gut flora and depleted glutathione lay the groundwork for leaky gut.
Additionally, high levels of insulin inhibit an enzyme in the cell wall responsible for helping to regulate proper intracellular calcium balance. Since the interstitial fluid outside the cell usually contains a thousand-times higher concentration of calcium than is normally present within the cell, this excess insulin response to our improper (high carbohydrate) diet simply opens the calcium floodgates into the cell by inhibiting this membrane enzyme. Mercury, and especially organic mercury, causes accumulation of calcium into the cells, therefore, one does not want to take much calcium, at least one wants to have a high ratio of Mg/Ca, that is, keep magnesium up and calcium down to reduce the accumulative effects—and supplement manganese. Otherwise, excessive calcium will enter the cells, impairing metabolism, producing cross-linkages and premature aging, and eventually producing dangerous arterial spasms. Manganese is a natural chelating agent when taken in the food supply or as a supplement. Manganese and magnesium will do everything a calcium channel blocker will do, but more naturally and effectively. There will be no excessive intracellular infiltration by calcium transporting through the cell membrane as long as manganese and magnesium, and possibly zinc, are present. Manganese works in a similar way to magnesium’s characteristic of displacing calcium ions. One of the keys to mercury’s effects on health may be its ability to block the functioning of manganese, a key mineral required for physiological reactions. Potassium helps restore electrical balance in heart cells while limiting the amount of calcium that can enter those cells. New studies in humans and in the laboratory show that PCBs and mercury interact to cause harm at lower thresholds than either substance acting alone.
Though forced to remove MSG, baby formula today frequently utilizes caseinate that contains a high enough level of glutamate to endanger a newborn’s brain! These excitotoxic additives are hidden under the terms hydrolyzed vegetable protein, protein isolate, protein extracts, caseinate, and natural flavorings! Another damaging excitotoxin is Aspartame™ that has increased exponentially in all our foods. Some of the many aspartame toxicity symptoms reported include seizures, headaches, memory loss, tremors, convulsions, vision loss, nausea, dizziness, confusion, depression, irritability, anxiety attacks, personality changes, heart palpitations, chest pains, skin diseases, loss of blood sugar control, arthritic symptoms, weight gain (in some cases), fluid retention, and excessive thirst or urination. The phenylalanine in aspartame lowers the seizure threshold and depletes serotonin. Lowered serotonin triggers manic depression, panic attacks, anxiety, rage, mood swings, suicidal tendencies, etc. Clearly, regular exposure to a toxic substance such as formaldehyde may worsen, or in some cases contribute to the development of chronic diseases. Other excitotoxins include fluoride, aluminum, iron overload, and organophosphate pesticides and herbicides.
We have spoken of the need for supplemental iron, but we need to be aware of iron overload. Hemochromatosis is a disease in which the body absorbs too much iron from the normal diet or supplements. Over many years, the excess iron builds up in the joints, liver, pancreas, pituitary gland, heart, and other organs causing serious organ damage. It can cause a bronzing of the skin. Untreated, the disease can lead to arthritis, cirrhosis, diabetes, impotence, sterility, hypothyroidism, heart disease, or liver cancer. Hemochromatosis patients often have “sore tongues”, and sore “swallowing mechanisms”, which may explain food problems, speech problems, and the like.
About one in 200 Americans have hemochromatosis and one in 10 are carriers for the disease. Typically, symptoms first appear in men between the ages of 30 and 50 years and in women who are past menopause. “The most common symptoms are fatigue, abdominal pains (which may also indicate an iron deficiency—WSL) and joint pains,” says Virgil Fairbanks, M.D. Iron overload as seen in hereditary hemochromatosis patients enhances suppressor T-cell (CD8) numbers and activity, decreases the proliferative capacity, numbers, and activity of helper T cells (CD4) with increases in CD8/CD4 ratios, impairs the generation of cytotoxic T cells, and alters immunoglobulin secretion when compared to treated hereditary hemochromatosis patients or controls. Its treatment is to avoid iron supplements and give blood regularly.
This same build up of excess iron may have nothing to do with genetic, excess absorption, but with mal-utilization of iron. When copper is deficient, the body can’t use iron so it accumulates and causes free radical damage. The disease is also called siderosis, which is characterized by a gray pallor to the skin from iron accumulation in the tissue. One study concluded “The frequency of thyroid disorders in men with hemochromatosis is about 80 times that of men in the general population.” What this likely means is that when men become copper deficient, they accumulate iron and become hyperthyroid. Iron, copper, manganese, and zinc work as a four-horse team. When one slacks the traces, it affects the pull of the others. Too much of one will deplete the others. So, when supplementing zinc, we have spoken of the need to balance with copper, but it is just as vital to supplement with iron, or at least keep track of iron stores. Manganese must be kept track of too. Anemia, possibly with high copper, is often the first sign of hypothyroidism.
It would appear that the pathology of autism is one of immune dysregulation, with associated food intolerance, and opportunistic infection that triggers excessive production of the inflammatory cytokines and nitric oxide leading eventually to neural mitochondrial inhibition. Dr. Rosemary Waring tells us that the excess cytokines reduces available sulfates also.
One of the better qualities of sulfur is its ability to be fairly well absorbed and utilized via oral administration. The safe administration of sulfur can be achieved orally with these sulfur-bearing substances: methylsufonylmethane (MSM), garlic, methionine, alpha lipoic acid, biotin, thiamin, bromelain, and in small doses, N-acetylcysteine. The problem is, these may not oxidize to sulfate. In that instance, one can supplement sulfates orally as glucosamine and chondroitin sulfate (these may be contraindicated where cholesterol levels are high—check with your doctor), and by Epsom salts baths. Sulfates are normally poorly absorbed orally (max 20%), but taking them with bromelain will enhance absorption significantly. One can also enhance absorption and speed effectiveness of glucosamine by 4 or 5 times by taking it with some essential fatty acids.
Remember that glucosamine is often manufactured from shellfish, so if sensitive to shellfish it could be a problem. Kirkman Labs offers a Magnesium sulfate cream for transdermal application. Before supplementing with sulfate, one should address the issues of dysbiosis and leaky gut in order to break the cycles of chronic inflammation. All of the aforementioned sulfur supplements are safe when used as directed on the product. Nevertheless, long time use may suppress serum chloride indicating that the child should be permitted to salt his foods to taste. MSM, Epsom salts baths, glucosamine and chondroitin sulfate, glutathione, Cysteine, Alpha lipoic acid, methionine, copper, and other forms of sulfur also deplete molybdenum, and it should be supplemented when using these nutrients. Molybdenum is an essential, trace element. It helps regulate iron stores in the body, and is a key component of at least three enzymes: xanthine oxidase, aldehyde oxidase, and sulfite oxidase. These enzymes are involved with carbohydrate metabolism, fat oxidation, urine metabolism, and toxic sulfite and aldehyde metabolism. Molybdenum deficiencies are associated with esophageal cancer, sexual impotence, and tooth decay. “Garlic suppresses the enzyme cyclooxygenase needed for beta oxidation of Long-Chain Fatty Acids”—Patricia Kane. If your fatty acid test shows this to be a problem, eliminate garlic and garlic salt.
Sulfate is a ubiquitous substance that has biochemical significance in every cell of the body. When its quantity, quality, or varieties were in any way compromised, the effects manifest in a pervasive manner in all systems of the body. Sulfate deficiencies, like no other single metabolic agent, has the potential to effect a degenerative cascade of dysfunction that significantly disrupts and alters digestive, immune, circulatory, detoxification, endocrine, and neurological functions. Sulfate deficiencies have been reported in people with migraine, rheumatoid arthritis, jaundice, and other allergic conditions all of which are anecdotally reported as common in the families of people with autism.
The satellite familial incidences and chromosomal loci proximities of Bi-polar and Unipolar Depression, Alzheimer’s Disease, Parkinson’s Disease, schizophrenia, Lou Gehrig’s Disease, Down’s Syndrome, Mental Retardation, Epilepsy, Homocystinuria, blood-sugar disorders, alcohol/chemical dependency, and Crohn’s Disease/Ulcerative Colitis/Irritable Bowel in regards to Autism is pointing to some possible commonalties in etiology that cannot be ignored. The transport mechanism that should transfer iron into the blood is defective in persons with Crohn’s Disease. The body’s natural response to an inflammation/infection is decreasing the iron transport from the intestines into the blood. This is done because bacteria need iron for growth. However, when the inflammation is INSIDE the intestines, this defense mechanism works contra productive causing iron build-up in the intestines. This reactive iron can damage the intestine. Therapies that utilize sulfate have been very successful with many of these disorders and strongly suggest that it may play a pivotal role in the etiology of these disorders as well.
Additionally, TNF is an important part of the inflammation process that your body uses to attack foreign substances. What is really interesting is, it is a known fact that all Crohn’s patients have a very high level of TNF. Actually, the most potent, recently-released, FDA-approved drug for Crohn’s, Remicade™, eliminates TNF, and it has been shown to have a marked beneficial effect on Crohn’s. See several, natural ways to eliminate excess TNF in the following pages and skip the side effects.
Elevated serotonin is found in: psychosis or schizophrenia, mood disorders, organic-brain disease, mental retardation, autism, and Alzheimer’s; while low levels of the metabolism of serotonin (which also produces high serotonin) are found in those with depression, anxiety, suicide, violence, arson, substance abuse, insomnia, violent nightmares, impulsive behavior, reckless driving, exhibitionism, hostility, argumentative behavior, etc. Phenol-sulfotransferase (PST) liver enzymes (Phase II) metabolize serotonin. These require sulfate to perform their function.
Mitochondrial malfunction is widespread in Autism. Nutrients that may improve the mitochondrial function include magnesium, Coenzyme Q10, acetyl-L-carnitine, N-acetylcysteine, vitamins B1, B2, niacin/niacinamide, folic acid, NAD (Nicotinamide Adenine Dinucleotide) or NADH (ENADA™), alpha-ketoglutarate, and antioxidants such as vitamins E and C, alpha lipoic acid, manganese, and selenium. Supplementation of glutathione has improved skill with numbers and fine motor skills. Oral glutathione is significantly assimilated, and of benefit to the gut according to research found by Dr. McGinnis. Take it with some vitamin C that will improve its assimilation by up to 20%. Kirkman Labs has a lotion for transdermal application that may enhance the systemic levels significantly. Where possible, help the body produce its own supply by using supplements mentioned elsewhere in this paper. Supplementing glutathione, particularly with high-dose-IV Glutathione, depletes NADH, and it must be supplemented.
It should be noted that acetyl-L-carnitine provides an acetyl group to aid in formation of the neurotransmitter acetylcholine and, in fact, has neurotransmitter properties much like acetylcholine. Acetyl-L-0 is an antioxidant that increases mitochondrial energy production in the brain, stabilizes the cell membrane, increases cholinergic transmission in the brain (helps memory), and chelates iron. It is shown to reverse hippocampal and prefrontal loss of neurons associated with aging and significantly reduces Lipofuscin pigment accumulation in the brain. It reduces receptor loss associated with aging and improves learning and memory in aged animals and humans. It is shown to defend brain cells against lipid peroxidation, and it increases both glutathione and CoQ10 concentrations. In addition, it can increase the inhibitory neurotransmitter GABA (Blaylock: Excitotoxins).