Improving nutrition by use of HCl and an enzyme
supplement, and by judicious supplementation of amino acids and other
nutrients, relieves bowel problems and overcomes infection. Taurine, like
carnitine, is synthesized from methionine and cysteine. It, too, is found
only in animal products. A deficiency in intake of these three amino acids,
or a metabolic defect in metabolizing these sulfur-amino acids may lead to a
deficiency of taurine creating numerous symptoms, including poor digestion
of fat. Taurine deficiency is seen in Parkinson’s Disease, anxiety, Candida,
AIDS, cardiac insufficiency, hypertension, impaired vision, cholesterol-gall
stones, convulsions, depression, and kidney failure. Inborn errors of
taurine metabolism have been described, with low-blood taurine resulting in
early signs of depression, lethargy, fatigability, sleep disturbances,
progressive weight loss, and depth perception impairment. Taurine is a major
part of the GTF- Factor needed to process carbohydrates, it being a
metabolite of cysteine. A lack of exposure to full-spectrum light of the sun
may lead to a reduced concentration of the neurotransmitter taurine in the
pineal and pituitary glands, and probably accounts for seasonal affective
disorder (SAD). Vitamin A, D, and E deficiency and stress causes a spill of
taurine into the urine. These kids are highly stressed, and are typically
lacking these nutrients. Since many live without benefit of daily sun, this
is a serious problem, compounding “autism” symptoms. SAD has been
scientifically correlated to a lack of sunlight -- and decreased serotonin.
(This is why modern antidepressant drugs called SSRIs -- like Prozac, Paxil
and Zoloft – “selective serotonin reuptake inhibitors” are often
prescribed.) A study published in the British Medical Journal Lancet in 2002
measured blood levels of serotonin, finding that production of serotonin by
the brain was directly related to the duration of bright sunlight.
Additionally, “Understanding how circadian rhythm works has many practical
applications,” said Sancar, a member of the
Characterized by feelings of sadness and depression, symptoms of these mood disorders also include irritability, fatigue, excessive eating, food cravings, oversleeping, social withdrawal, and loss of interest in sex. Symptoms of “winter blues” are milder than those of full-blown SAD; so, many people suffer from it and don’t even realize it!
Dr. Martel references a large body of research evidence indicating that the cool-white fluorescent bulbs, (and incandescent are nearly as bad) found in virtually all classrooms, cause increased stress, hyperactivity, anxiety, fatigue, irritability, attention problems, and poor-learning performance. A part of this relates to the electro-magnetic frequencies (EMF) given off by the transformers, and the 60-cycle flickering of the lights. Demand full-spectrum lamps that correct these errors. Please insure your home and office are equipped with proper lighting. See www.Mercola.com.
The cellular-level, enzymatic effects of mercury binding with proteins include blockage of sulfur-oxidation processes, and a lack of several neurotransmitter amino acids which are significant factors in many autistics. A supplement of molybdenum enhances sulfite oxidase activity and helps convert potentially harmful sulfites into sulfates, but copper and sulfur suppress this action. For 36%, supplemental molybdenum reduced urinary sulfite loss and improved symptoms, one of which is wheezing. This improved enzyme activity enhances detoxification of the very-toxic, cyanide ions improving oxidative phosphorylation and cellular oxidation increasing ATP (energy molecule). By supplementing Moly and vitamin B6 and avoiding sulphites one may become cough free, and asthma, irritable bowel, eczema, headaches, and behaviour problems all improve.
A deficiency of molybdenum would likely be associated with abnormally low levels of uric acid in the blood and excess sulfate in the urine. Supplementing molybdenum (which is depleted by supplemental sulfur) at 100 mcg three times a day for adults, or the amino acid L-taurine (500 mg daily, shortly reducing to 100 mg), will improve the function of the liver, producing better quality bile (darkening of the stool), protecting against gallstones, and improving the digestion of fats. Taurine is vital in preventing cataracts. It spares potassium, magnesium, and calcium in the heart, preventing arrhythmias, aids in detoxifying the body, and serves with GABA and glycine as inhibitory neurotransmitters in the brain. It promotes the proper regulation of blood sugar in those who may be insulin insufficient. Taurine is relatively inert, has a half-life of about 5 days, and can remain as a free amino acid. Vitamin B6 is essential to its formation. It is considered to be conditionally essential for human infants and children. In other words, many don’t have enough unless supplemented.
A deficiency of taurine or GABA in relation to serotonin and dopamine may lead to convulsions; so, in the nervous system, adequate presence of taurine stabilizes cell membranes, which raises the seizure threshold and helps treat epileptic seizures. Its anti-convulsant effect is long lasting, and can be confirmed both clinically and by repeat EEG’s (electro-encephalograms). It strengthens neutrophils (white blood cells/part of immune system) in their ability to kill bacteria. I’ll pick up the taurine thread eight paragraphs later.
Glycine is the major inhibitory neurotransmitter in the brain stem and spinal cord, where it participates in a variety of motor and sensory functions. Glycine is also present in the forebrain, where it has recently been shown to function as a co-agonist at the N-methyl-D-aspartate (NMDA) subtype of glutamate receptors (it stimulates their function). In the latter context, glycine promotes the actions of glutamate, the major excitatory neurotransmitter. Thus, glycine subserves both inhibitory and excitatory functions within the CNS. Blockage of the glutamate receptors could cause reduced pain, tunnel vision, inability to shift attention, auditory problems, repetitive behaviors, dilated pupils, and language problems. The reason is that it controls pruning of brain cells during development, modulates pain, and modulates dopamine and serotonin. Nevertheless, suppression of the NMDA by dissociative anesthetic has temporarily evoked speech and improved behavior in the Autistic (Stubbs at 1994 ASA Conference)
The NMDA receptor, when activated, opens the calcium channel and allows calcium and sodium into the cell, displacing potassium. This excites or fires the cell. It is activated mainly to amplify the effect of glutamate during periods of especially intense excitation. If this channel is not closed, it keeps firing, creating overactivity of that circuit and whatever it controls (cramps and spasms in muscles, stimming, etc.) even to destruction of the neuron. People of any age with depleted levels of reduced glutathione are especially vulnerable to the free-radical damage associated with glutamate excitotoxicity. Glutamate excitotoxicity damages or destroys some neurons, leading to deficiencies in memory and learning; on the other hand, excess of GABA can lead to lethargy. At the same time, excess ammonia, not detoxified through sufficient glutamine synthesis by the glia, leads to further neural damage. “There is evidence that depletion of reduced glutathione makes neurons more susceptible to excitotoxicity, and that intact mitochondrial function is essential for neuronal resistance to excitotoxic attack. It is believed, for example, that reduced levels of the energy currency of the cell (ATP) that accompanies loss of mitochondrial function causes depolarization of neuronal membrane, which exposes NMDA receptors to excessive levels of glutamate. The resulting neurohormonal cascade leads, in many cases, to the death of neurons in the brain, and in the central and peripheral nervous systems.”—LEF Magazine, March 1996.
Most of the excitatory neurons of the cerebral cortex and hypothalamus have glutamate as their primary transmitter. One type of glutaminergic neuron accumulates zinc within vesicles at axon terminals and releases it into the synapse upon firing. The precise roles of zinc in synaptic function are not known, although its presence is certain, and there are zinc-binding sites on one subset of glutamate receptors called the NMDA (N-methyl-D-aspartate) receptor where it is said to lock the calcium channel tightly. Zinc, copper, and magnesium all appear to play important modulatory roles in controlling the NMDA receptor, which has been implicated in various forms of cortical plasticity, including learning. Zinc and magnesium are known to play a role in neuroprotection. It is possible, then, that decreased levels of some minerals in the brain may produce abnormal NMDA mediated plasticity and subsequent abnormalities in behavior. Since the blockade of NMDA receptors in the cerebral cortex enhances the release of dopamine from lower brain regions, reduced glutamate transmission could be the ultimate cause of excessive dopamine activity in the brains of both autistic and schizophrenic patients. Additionally, (according to Dr. Russell Blaylock, MD) magnesium deficiency doubles the production of free radicals in both epithelial cells and neurons dramatically increasing excitotoxicity! Low magnesium lowers cellular glutathione levels and increases excitotoxic, neuronal death. High glutamate levels have been shown to deplete cellular glutathione. Glutathione has been shown to down-regulate the excitotoxic NMDA receptor, thus blocking excitotoxicity. Hypomagnesmia also inhibits GABA responses, which would increase cortical excitability. Though having adequate magnesium protects against excess calcium entering the cell, when there is a lack of ATP energy due to Krebs cycle (mitochondrial) problems, or simply a lack of glucose from hypoglycemia, the magnesium block is removed and calcium pours into the cell! Autistic children have a high incidence of hypoglycemia, which increases their risk of seizures and excitotoxicity.
High levels of another NMDA-receptor-blocking agent, kynurenic acid (a tryptophan metabolite that requires vitamin B6 for its further metabolism), are found in the spinal fluid of patients with AIDS dementia, and are frequently seen in autism. The amino acid glycine indirectly activates NMDA receptors, and may reduce apathy, withdrawal, and cognitive impairment in schizophrenic patients. Strychnine poisoning results in muscular contractions and tetany as a result of glycinergic disinhibition and resulting overexcitation. Other a- and b-amino acids, including b-alanine and taurine, also activate glycine receptors, but with lower potency.
The enzyme kynureninase, which breaks down kynurenine, requires magnesium and pyridoxal phosphate (P5P), and its activity is decreased in a vitamin B6 or magnesium deficiency (Shibata, 1991). Increased serum kynurenine has been found in Tourette’s Syndrome (TS) (Dursun, 1994; Rickards, 1996). Kynurenine promotes vasoconstriction, reducing blood flow, via noradrenaline release (Rudzite, 1991). Anxiety can be produced by increased kynurenine (Orlikov, 1991), which can be related to magnesium deficiency (Shibata, 1991). An increased release of catecholamines is found in magnesium deficiency (Gunther, 1989). Enhanced stress responsivity of TS patients undergoing lumbar puncture was shown by their significantly high ACTH secretion and their significantly high norepinephrine excretion as compared to normal controls; and reported a higher level of anxiety before and during the procedure than the controls (Chappell, 1994). A heightened reactivity of the hypothalamic-pituitary-adrenal (HPA) axis and related noradrenergic sympathetic systems is suggested in TS (Chappell, 1994; Leckman, 1995).
Kynurenine markedly increases tics in animals when injected peripherally (Handley, 1977). L-Kynurenine interacts with GABA receptors in vitro, displacing GABA, and induces convulsions in vivo in rats (Pinelli, 1985). L-Kynurenine sulfate induces locomotor excitement (continuous rotation in rats around a longitudinal axis in one or another direction) and potentiates the convulsant effect of caffeine (Lapin, 1982). A lack of the neurotransmitter GABA has been implicated in a number of psychiatric and neurologic disorders (McGeer, 1989). The main support for GABA involvement in TS comes from drug studies that have shown in some patients the suppression of tics with the use of the GABA agonist clonazapam (Goetz, 1992; Hewlett, 1993). GABA modulates dopamine concentrations in the nucleus accumbens and corpus striatum (Dewey, 1997).
When the human brain becomes inflamed, cells called macrophages (glial cells) respond by releasing a neurotoxin called quinolinic acid, a metabolite of kynurenic acid. This toxin is also elevated in Parkinson’s Disease, MS, ALS, and is responsible for the dementia that occurs in AIDS patients. What quinolinic acid does is stimulate neurons to repeatedly depolarize after the manner of glutamate. This eventually causes the neurons to demyelinate and die. People with elevated quinolinic acid have short-term memory problems. Lithium protects against neuronal injury when quinolinic acid is injected into the striatum, a process often used as an animal model of Huntington’s disease.
If the stool is light tan or gray in color, taurine and/or glycine supplementation will restore normal bile and improve fat digestion. Taurine excess may be seen when vitamin B6 or zinc is deficient in Rheumatoid Arthritis and liver disease. In fact, taurine in serum rises with low serum zinc, and results in low taurine levels in the brain, increasing the possibility of seizures. Taurine levels, whether high or low, indicate further lab work is needed. For example, if Taurine levels are low, and the clinical picture is suggestive of candidiasis, one should test for Candida through comprehensive stool analysis and/or anti-Candida antibodies. If Candida is found, supplement Taurine. If Taurine levels are high, zinc and vitamin B6 levels are probably low, and should be tested. P5P, the active form of vitamin B6, is necessary for many amino acid reactions to take place.
Taurine’s function and effectiveness are controlled by vitamin B6 and zinc. Zinc and vitamin B6 are almost universally deficient, and they are lost due to diarrhea. Considering the atrocious diet, and an inflamed gut, why wouldn’t an autistic need to supplement vitamin B6 and zinc, and possibly taurine? Always balance with copper in a 1-to-8, copper/zinc ratio, unless you know a high copper condition exists, or your child is hyper to copper, and monitor that ratio lest you create a copper anemia that will be made worse if you treat it with iron. An overactive thyroid can create a copper anemia also since copper gets used up in de-activating thyroid hormones.
Be careful with taurine for it tends to shut down the
E1 Prostaglandins. Omega-6s (particularly GLA), when properly balanced with
Omega 3s (particularly EPA), give rise to the E1 series of anti-inflammatory
prostaglandins. When this balance is not present, arachidonic acid is
produced excessively creating the inflammatory E2s. Elevated PgE2 suppresses
immunity. The B-vitamins help convert essential fatty acids (EFA) into the
prostaglandin (PG) tissue regulators. It turns out that, through
hydrogenation, milling, and selection of w3-poor, Southern foods, we have
also been systematically depleting, by as much as 90%, a newly discovered
trace, Nordic EFA (w3) that is the sole precursor of the PG3 prostaglandins,
of special importance to primates. This shortage of fatty acids has occurred
even as a concurrent fiber deficiency increases body demand for EFAs. Since
substrate EFA is processed by many B-vitamin catalysts, an EFA deficiency
will mimic a panhypovitaminosis B, that is, a mixture of substrate beriberi
and substrate pellagra resembling vitamin deficiency beriberi and pellagra
but exhibiting as even more diverse endemic disease. Excess, unconverted
Omega 6 tends to cancer, whereas adequate Omega 3 inhibits cancer. A good
balance between Omega 6 and Omega 3 is being shown to be preventive of many
forms of cancer. Supplementation with cod-liver oil for up to 12 weeks may
be necessary to see this shift from PgE2 to PgE1, however, vitamin E in
succinate form enhances both cellular and humoral immunities, and induces
macrophages to produce elevated levels of IL-1 and/or to down-regulate PgE2
synthesis. It also shields the immune cells from the toxic effects of
chemotherapy and radiation therapy. A small shot of insulin, according to
recent research, makes chemotherapy more efficient at targeting cancer cells
directly, and reduces side effects. These eicosanoids serve as a
communication “wiring” for the body, communicating information from cellular
DNA. Injections of succinate by doctors at