Quantum Medicine Update: Undetected HypoThyroidism and Xenobiotic Toxicity

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Quantum Medicine Update: Undetected HypoThyroidism and Xenobiotic Toxicity as Missing Links in Parkinson's and other Neurodegenerative Disorders

Do you suffer from Parkinson's Disease, Alzheimer's Disease, Multiple Sclerosis, or other neurological disorders? Migraine headaches? Do you suffer from chronic fatigue or immunosuppression? Are you feeling mentally dulled or depressed? Do you suffer from annoying tinnitus or vertigo? Digestive disturbances? Do you typically have cold hands and feet when everyone else is warm and comfortable? Are you gaining weight that no dieting seems to help? Are you losing your hair or suffering from dry skin or brittle nails? Is your cholesterol too high? Have you lost interest in sex?

If you've answered "yes" to any of the above questions, you could be suffering from a deficiency of biologically active T3 or a condition known as thyrotoxicosis, a condition whereby drugs or xenobiotics (foreign substances) interfere with normal thyroid function.

Metabolism is not a single process but rather a linking together of subsystems that regulate a wide variety of physical functions within the body. All metabolic processes require a regular supply of nutrients. If there is a deficiency, excess, an imbalance of nutrients, or an excess of accumulated pollutants, hormonal regulation may be disturbed.

The thyroid is the body's metabolic powerhouse, regulating temperature and virtually every cell in the body. Among its most important functions within the cells is to control the rate of metabolism, which can alter oxygen consumption. It accomplishes this with its two tyrosine (amino acid) molecules, each with two atoms of iodine to produce the prohormone, thyroxine or T4. However, long-term empirical observations on hundreds of patients, has revealed that xenobiotics create a deficit in the body's ability to convert T4 to the major active hormone, triiodothyronine or T3. Instead, the body tends to produce reversed T3 (rT3) which slows enzyme activity, lowers body temperature, disturbs the cellular redox potential, alters genetic transcription, and fails to function like T3 (Eur J Endocrin, 130:344-52, 1994; J Neurophysiol. 72:1, 1994; Wilson's Syndrome: The Miracle of Feeling Well, 1996) or the thyroid may simply produce inadequate amount of other hormones.

Cellular energy production is controlled by microscopic structures inside your cells, called mitochondria. Known as the cell's "powerhouse," mitochondria need ample supplies of T3 in order to burn up proper amounts of oxygen to produce an important body fuel, called ATP. Thyroid-regulated nuclear transcription in many genes results in an increase in the cell's number of proteins, enzymes, structural proteins, transport proteins, and other cellular metabolites. The thyroid gland plays a vital role in the neuroendocrine system by turning on and regulating the function of various organs and bodily processes.

The accurate assessment of thyroid function should include rT3, TSH assessment, biochemical assessment of sulfur amino acids and cofactors needed to support the trans sulfuration-sulfate pathways of the liver,(*) assessment of cellular redox potential, and functional assessments of the liver and ground regulation system (GRS). The most accurate way of assessing TSH is with highly sensitive chemoluminescent or immunoradiometric tests. A new research report reveals that TSH is dependent on iodine, selenium and zinc (J Trace Elem Med Biol 12 177-82, 1998) to function. Even when normal thyroid function is diagnosed, it's important to realize that traditional thyroid assessment is based on a cross section of so-called "normal" thyroid function and has a high degree of inaccuracy. And, in many cases, rT3 or the rT3/T3 ratio is rarely assessed.(**) Furthermore, most doctors are not generally trained to diagnose an age-related thyroid slowdown. Doctors may often dismiss signs of a slugg ish thyroid, like fatigue, muscle cramps, dry skin, hair loss, and constipation as part of the aging process.

According to some statistics, as many as 15 to 20% of women over age 60 have subclinical thyroid deficiency states that may contribute to accelerated aging and to shortening their lives (Geriatics, 1995; 50:14-15; Harvard Health Letter, 1994; 19; 2-6).

The production and secretion of T4 is dependent on healthy and harmonious neuroendocrine interactions with the pituitary, hypothalamus, and adrenal glands. For example, the pituitary gland regulates T4 production by producing a peptide hormone called TSH (thyroid stimulating hormone). Problems with the body's metabolism occur any time these hormone levels -- or the nutrient precursors needed to produce these hormones -- are deficient. One of the most common deficiency states relates to protein. Peptide deficiency states, a deficiency of the amino acids tyrosine or phenylalanine, or a deficiency of organic iodine may cause a decline in thyroid function. In addition, too much inorganic iodine, found in iodized salt, can cause the thyroid to be either over- or underactive (Lancet, 1996; 335:99-107).

Drugs taken for other conditions can block thyroid hormone production. For example, lithium, used for manic-depressive disorders, causes hypothyroidism in up to a third of long-term users (N Eng J Med, 1995; 335: 1688-94) and Cordarone (amidarone), a heart medication, can cause thyroid dysfunction (BMJ, 1996; 313: 539-44; Clin Pharm, 1993; 12:774-9).

In some people, thyroxine replacement therapy with synthetic (laboratory-made) thyroid hormone (Synthroid, Levothroid, Levothroxin) may actually accelerate neurological aging and create chronic nutritional deficiency states. Synthetic thyroid hormone (containing only T4) fails to solve the problem because the body still has to convert T4 to T3 and the other metabolites. Furthermore, T4 replacement still causes TSH values to be outside normal reference ranges in nearly half the patients receiving thyroxine therapy (Lancet, 1991: 337:171). Indeed, a lowered bone density (JAMA, 1991; 265:2688-91; Thyroid, 1994; 4;319-26) and low TSH levels have been reported in patients taking thyroxine therapy (Semin Nucl Med, 1995; 25:205-20).

Armour Thyroid and other natural thyroid preparations contain natural thyroid hormones. Whole thyroid glandulars derived from New Zealand sheep, have the exact molecular structure of human T4, T3, T2, and T1 and seem to work optimally in some individuals. Yet, the overwhelming majority of patients who take these products fail to normalize their thyroid function because they are too toxic in xenobiotics. A survey of the most popular detoxification protocols reveals incomplete detoxification caused by trapped xenobiotics in the GRS and imbalances between Phase I and Phase II liver detoxification functions. These hormone-disrupting toxins interfere with the conversion of T4 to T3 and with hormone receptor function throughout the body.

The Targeted Response Detoxification Method: Clinical Research

The widespread public concern for the detrimental health effects of worldwide pollution has been sparked by the book Our Stolen Future (Penguin, 1997). Millions of Americans are concerned about the welfare of their children and grandchildren as the planet gets more and more polluted. Already statistics reveal that man-made chemical compounds in our air, water, and food, mimic and block hormones and contribute to the 50% reduction in male sperm counts, the dramatic rise in hormone-related cancers, and neurological disorders in both adults and children. People are searching for ways to detoxify themselves of accumulated pollutants to prevent cancer and degenerative diseases and for ways to protect their unborn children (who are at risk for birth defects and developmental disorders) from the dangers of exposure to pollutants.

Xenobiotics become dangerous when the liver fails to effectively eliminate them through the biliary tract. Perfect coordination between Phase 1 and Phase II liver enzymes is necessary in order to shuttle toxins out of the body. After nearly two decades of experimentation with nutritional and homeopathic detoxification protocols, the author has developed a novel approach of increasing the operational complexity of liver and GRS detoxification. This approach augments the patterns of Phase I and II liver detoxification by utilizing a Targeted Response Detoxification Method (TRDM)(***) of supporting the biosynthesis of bile acids and trans sulfuration-sulfate pathways to encourage the excretion of xenobiotics through the liver's bile ducts while enhancing the production of glycoproteins. As stated earlier, most antioxidant/detoxification approaches fail to adequately support trans sulfuration-sulfate pathways. In these cases, it is not uncommon to find toxins causing "yang" kidney a nd skin reactions with many patients experiencing skin symptoms, urogenital disorders and other proinflammatory reactions as documented in laboratory tests that reveal high levels of oxidative stress.

Long-term clinical research on hundreds of patients with TRDM has revealed the precise ratios of nutrients and phytonutrients that seem to maximize detoxification without stressing or overloading other detoxification channels or activating proinflammatory pathways of the body. The TRDM utilizes vitamin C (calcium ascorbate), quercitin (dehydrate), selenium aspartate, Betaine, vitamin B6 (P-5-P), vitamin B2 (R-5-P), vitamin B1 (TTP), Folic acid, vitamin B12, L-Cysteine (HCL), L. Taurine, L-Methionine, Glycine, Serine, Glutathione (reduced), Inosine, CoenzymeQ10, N Acetyl Cysteine, Pine Bark Extract, Lipoic acid, Manganese (Glycinate), Zinc (Picolinate), Copper (Lysinate), Turmeric, Icelandic Sea Produce (acophyllum nodosum), Rosemary (extract), and homeopathic combinations to activate liver/GRS detoxification, maintain an optimum redox potential, and improve thyroid and neuroendocrine function. The validity of this empirical data is strengthened by hundreds of scientific papers t hat document the effects of specific nutrients on modulating detoxification and anti-inflammatory bioactivity and the fact that many of these nutrients also function as precursors and cofactors in the biochemical pathways of steroidal, peptide, and ecosanoid hormones. Most importantly, a review paper of over 60 scientific studies on the hormone-disrupting effect of xenobiotics stated: "It is clear that the endocrine system presents a number of target sites for the induction of adverse effects by environmental agents" (Journal of Endocrinology, 1997). The most important goal of TRDM is to prevent xenobiotics from interfering with the synthesis, storage/release, transport, metabolism, binding, action or elimination of natural blood-borne hormones that are responsible for the regulation of a myriad of metabolic processes.

Furthermore, the connection is clear: dioxins and PCBs have been documented to impair normal thyroid hormone-mediated events leading to permanent alterations in brain function in adulthood (Toxicol & Appl Pharm, 135, 77-88) and in children (Amer J Pub Health 77, 1294-97). A group of international experts gave a consensus statement and stressed the extreme sensitivity of the brain to chemical disruption by xenobiotics. They further indicated that these contaminants "contribute to learning disabilities, including ADHD and perhaps other neurological abnormalities." The September 1996 New England Journal of Medicine added urgency to this warning by documenting intellectual impairment in children exposed to PCBs in the womb and "deficits in general intellectual ability, short-term and long-term memory, and focused and sustained attention."

Parkinson's Disease: A Toxic Neuroendocrine System?

Researchers have determined that a mitochondrial energy crisis and oxidative stress are related to the etiology of Parkinson's disease (Advances Neurol, 1993; 60: 282-87). Oxidative stress due to environmental neurotoxins -- that also block thyroid hormones -- may be the primary cause of nigral cell death in Parkinson's disease, which, in turn, causes an uncoupling mitochondrial function (Biochem Phys 1995; 1271: 265-74).

Nicotinamide adenine dinucleotide (NADH) is one way to modulate mitochondrial energy deficits and has been reported to benefit 71% of patients with Parkinson's disease (New Trends Clin Neuropharmacol, 1991; 3/4: 75-86;Acta Neurol Scand, 1989; 129: 182-87; Ann Clin Lab Sci, 1996;26: 1-9; Acta Neurol Scand; 1993; 87:32-25). Reduced antioxidant activity has been linked to nigral cell pathogenesis of Parkinson's Disease (Neurolog Clin.;10(2) 387-403) and intervention with CoQ10 ranging from 100-250mg a day improves the function of patients with mitochondrial abnormalities (J Neurological Sci, 1989; 90: 263-72; J Neurol, 1987; 234: 62-62). Animal studies demonstrate that lipoic acid can improve cognition (Ann NY Acad Sci, 1994 717: 122-28) while N acetyl cysteine and glutathione can inhibit the production of proinflamatory cytokines (Cellular Immunol, 1992 140: 390-299).

The orthodox treatment for Parkinson's disease is the amino acid, L-Dopa and this often fails because L-Dopa needs a coenzyme called NADH to work effectively. NADH is formed from one of the B vitamins called niacin, or vitamin B3 (Biochem Med Metab Biol, 1986; 36(2): 244-51). Some Parkinsonian patients may benefit from taking niacin and/or NADH. However, a word of caution: Parkinsonian patients being treated with L-Dopa, particularly those also given benserazide or carbidopa, run a risk of developing a niacin and vitamin B6 deficiency. Niacin and B6 supplements seem to cancel out the negative effects of L-Dopa, unless it is taken with carbidopa (AMA Drug Evaluations, 5th ed, 1983, American Medical Association, Chicago, 1983). However, a common problem with conventional L-Dopa therapy is the so-called "on-off" effect, where L-Dopa works better at particular times of the day than others. These fluctuations -- linked to the consumption of proteins -- can be effectively reduced wit h predigested peptides and amino acid supplements that are taken with the evening meal (Neurology, 1989, 39: 549-52).

Other deficiencies correlated with Parkinson's disease include vitamin E (Arch Neurol, 1988; 45:1350-3); folic acid (J Neurol Neurosurg Psychiatry, 1986; 49: 920-7); and magnesium (Can J Neurol Sci, 1989, 16 (3) 310-4). Low magnesium implies cellular acidosis and reduced enzyme activity.

Excesses of manganese may lead to Parkinson's, as can too high levels of mercury or aluminum (Neuroepidem, 1989; 8(3):128-41). Copper concentrations in the cerebrospinal fluid are often significantly higher in sufferers than in the normal population and have been correlated with the severity and the rate of progression in Parkinson's cases (Lancet, 1987, ii: 238-41). (Zinc supplementation can reduce copper concentrations, while most estrogen replacement therapies raise copper).

Mineral deficiency states, especially of iron (needed to activate the enzyme that converts the amino acid L-tyrosine to L-Dopa) are found in Parkinsonian patients. In one study iron supplementation has had impressive results (J Neurol Trans, 1986;67:287-92). On the other hand, some individuals with Parkinson's disease are toxic in inorganic iron and this toxicity appears to aggravate the disease process (Can J Neurol Sci, 1990; 17(3): 28691).

Herbal treatment varies depending on each individual patient. Substantial clinical improvements in motor function were linked to Vicia faba, an extract from the fava bean that is high in a natural form of levodopa (J Neuro, Neurosurg, & Psych, 1993; 55, 725-7). Clinical success with homeopathic Atropa belladonna may help to reduce tremors in some cases. Used in the treatment of postencephalitic and post-influenzal Parkinsonism after the great influenza epidemic in the early part of this century, belladonna was reported effective (R F Weiss, Herbal Medicine, Ab Arcanum, Gothenburg, 1988). More recent research has shown that the total extract of the Belladonna root has significant benefits (Arzneimittel-Forschung, 1971, 21(4):528) while another positive study was conducted on the treatment of Parkinsonism with Bulgarian Belladonna root preparations (Zhurnal Nevropatologii Psikhiatrii Imeni S-S-Kors-akova, 1966; 66 (5):698-703). The plant Macuna pruriens is often used on patients w ith Parkinson's disease, and one study of 60 patients found it to be effective. Adverse effects, mainly affecting the gut, were very mild (Neurolog India; 25, 171-6; J Alt & Comp Med: Res on Paradigm Pract & Policy, 1995; 1 (3): 249-55).

The most impressive research on non-orthodox treatment of Parkinson's concerns the use of L-methionine. Several studies document that L-methionine is as effective as L-Dopa after three weeks in people with previously untreated Parkinson's disease (Rev Neurol [Parisl, 1982; 138 (4): 297-303). L-methionine also brought about further improvement in Parkinsonian patients who'd reached a plateau in their orthodox treatment (South Med J, 1984; 77:1577). Although L-methionine, L-cysteine, L-taurine, and glycine support liver detoxification pathways, patients with Parkinson's have a deficiency in many co-factors -- utilized in TRDM -- preventing the proper utilization of these factors and proper excretion of neurotoxins via the biliary tract system. Indeed, researchers have reported an elevated urinary excretion of cysteine and a reduced excretion of sulfate in Parkinson's and Alzheimer's disease patients as compared to controls (Neuroscience Letters, 110:216-20, 1990). Moreover, studie s have demonstrated that individuals with Parkinson's or Alzheimer's disease are toxic because of defects in sulfur detoxification processes and defects in the body's ability to produce adequate amounts of inorganic sulfate through the sulfoxidation of cysteine (Toxicol. 111:43-65, 1996). Hence, supporting Phase II liver detoxification with proper ratios of sulfur amino acids and co-factors (TRDM), can effectively reduce the load of heavy metals on the nervous system, normalize redox, and improve the delivery of nutrients to neurons. My long-term research clearly supports the findings of these researchers and indicates that restoring healthy thyroid function, modulating mitochondrial energetics, and augmenting liver and GRS detoxification protocols can be effectively accomplished with TRDM and complex homeopathic remedies that discharge harmful xenobiotics from the GRS of the body. Free radicals are "out of control" in Parkinson's disease patients mainly because of chronic long-term, toxin-induced thyroid dysfunction. Effective nutritional support of these patients may decrease runaway free radical chain reactions that sabotage neurons and cells -- the building blocks of all our organs and tissues. It appears that the ability of the body to produce natural antioxidants decreases significantly in Parkinsonian patients.

Despite an extensive body of scientific evidence reported in the book Our Stolen Future and the studies reported in this article, the bleak truth is that there continues to be no medical consensus about what causes Parkinson's disease or other neurodegenerative disorders such as ADD and ADHD. Feelings run high regarding the need for drug therapy, but the data is far from conclusive. And, despite decades of cumulative data supporting neuroendocrine disruption from xenobiotics, doctors continue to prescribe symptom-suppressing drugs, rather than correcting nutritional deficiencies and removing causative factors with effective detoxification protocols. In conclusion, the TRDM was designed to support the sulfation of steroids, lipids, peptides, neurotransmiters, thyroid hormones, while activating a detoxification of a multitude of xenobiotics. Control of liver detoxification pathways normalizes redox and has an important regulatory effect on neuroendocrine function (Human Exp Toxic ol 1:547-55, 1996). Improving sulfation results in improved intracellular communication and signal transduction through the TRDM-activation of membrane-activated sulfated glycoproteins. The complexity of cellular processes involved in hormonal communication and the central role that hormones play in many high profile diseases needs to be addressed by physicians. Seminars and workshops are being planned on Quantum Medicine and TRDM in the near future to train doctors on the myriad of effects attributed to xenobiotics while underscoring the clinical urgency and necessity of supporting the thyroid and neuroendocrine function, as both doctors and their patients struggle to survive the increasing onslaught of worldwide pollution.

(*) Great Smokies Diagnostic Laboratory, Ashville, North Carolina has laboratory protocols to assess liver detoxification functions and deficiencies of sulfur amino acids.

(**) Meridian Valley Clinical Laboratory, Kent, Washington 1-800-234-6825 assesses rT3 or the rT3/T3 ratio as well as TSH, T3 and T4 levels.

(***) Bioactive Nutritionals, Melbourne, Florida manufactures and sells the homeopathic formulations utilized in the author's clinical research. The statements made regarding the products described in this article have not been evaluated by the Food and Drug Administration. These products are not intended to treat, cure, or prevent disease.

Townsend Letter for Doctors & Patients.

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By Paul Yanick

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