Nevada homeopathic and integrative medical association 2014 conference: part 3.
I first attended one of Dr. Hinz's lectures in 2001 in Minneapolis. His main emphasis at that time was on weight loss promoted by the amino acids 5-HTP, tyrosine, and L-dopa. His early protocol worked well. Subsequently, he has broadened his scope of therapeutics to almost all neuropsychiatric conditions relating to the neurotransmitters serotonin, dopamine, norepinephrine, and epinephrine, primarily with a new intriguing emphasis on Parkinson's disease (Figure 1).
Fascinating Neuroscience Evidence
Dr. Hinz has examined over 1000 databases and helped supervise 2.8 million patient days of documented treatment from data gleaned from 1200 clinics. Although not for the fainthearted, learning Dr. Hinz's approach to managing disease is very rewarding. He is the most prolific PowerPoint composer I have ever seen. His seminars, which he presents around the country every couple of months, are necessary to attend to get an initial insight into his protocols and background science. He uses urinary serotonin and dopamine laboratory values from the DBI Laboratory to determine the sufficiency of amino acid dosing and what type of amino acid protocol should be used. Many data are presented to show that baseline levels of amino acids are not helpful for the initial therapeutic diagnosis or treatment. "Baseline testing is not reproducible from day to day."
All Manner of Psychiatric Drugs Deplete Neurotransmitters
Hinz provides data that that all SSRIs, SNRIs, tricyclic antidepressants, amphetamines, and migraine headache drugs and many environmental toxins and foods deplete neurotransmitters. This insight alone is worth the price of admission. If you don't have a reservoir of neurotransmitters, the drugs soon may become ineffective or tachyphylactic and cause a greater excretion of neurotransmitters via monoamine oxidase and catechol-O-methyltransferase, creating a deficiency of neurotransmitters in the presynaptic neuron. Of interest, he notes that the width of the synapse is 1 millionth of a centimeter and that the average neurotransmitter binding time to a postsynaptic receptor last 1 thousanth of a second.
Three Legs of the Stool
By examining several complicated feedback loops of neurogenic amino acids and sulfur-containing amino acids, Hinz makes his case for replacing these amino acids in a defined pattern that normalizes important neurotransmitter levels (Figure 2). Organic cation transporter type 2 (OCT2) occurs on a microscopic level at the entire cerebral interface with cerebrospinal fluid, on the surface of every neuron and the liver, intestines, and importantly kidney. Through passive transport, diffusion, and active transport, they deliver serotonin and dopamine to the body in a competitive inhibition manner. For example, if you give 5-HTP to manufacture serotonin, it inhibits the conversion of tyrosine to dopamine, norepinephrine, and epinephrine; and vice versa: giving only tyrosine will impede serotonin formation. They must be given together to rebuild balanced neurotransmitter levels. He assesses this by serial urinary serotonin and dopamine levels. The third leg of the stool is cysteine, a sulfur-containing amino acid. Other sulfur compounds will do, but they are much more expensive in the amounts required to rebuild thiol metabolism which is damaged in neurologic diseases.
Parkinson's Treatment and Dopamine Dominance
Most patients are treated via Hinz's three-phase system. When the urinary neurotransmitters are initially measured, they are in the high range because the kidneys are eliminating serotonin and dopamine. On replenishment with a balance of 5-HTP and tyrosine, the levels go lower as the body can now absorb them and is holding on to them. In the phase 3 measurement, the levels come again into the midrange; and most of the common anxiety, depression, insomnia, bipolar disease, migraine headaches, and multitude of other diseases respond quite well.
However, another patient type has emerged: the dopamine-dominant patient. These are Parkinson's patients, restless leg patients, and ones with addictive problems. This is another ball of wax. Hinz gives L-dopa from the Mucuna pruriens bean from South America with a 40% L-dopa content. L-dopa used to be used in Parkinson's but had to be mixed with carbidopa to control the nausea. Now he uses 5-HTP to control the nausea of L-dopa with tyrosine, cysteine, vitamin B6, calcium, and vitamin C. The doses of L-dopa needed to control Parkinson's can be quite astronomical, 10,000 to 40,000 mg per day or more to overcome the neurotoxic damage to postsynaptic neurons. There are more than 1179 known neurotoxins. The dose of L-dopa is ascertained by doing pill stops, taking the increasing doses 5 days on then 2 days off. If the symptoms get worse, patients increase the dosage; if symptoms get better, they reduce it. Needless to say, the practitioner must take Hinz's seminars and tune in to his frequent online updates and call him for interpretation of his urinary test results and unique responses from patients (marty@hinz. md.com; 877-626-2220).
Carbidopa Increases Parkinson's Death Rate by Blocking B6 Irreversibly
In a paper (containing 90 scientific references) published in Clinical Pharmacology, Hinz, Alvin Stein, and Ted Cole note that the only indication for carbidopa and benserazide is the management of L-dopa-induced nausea. (1) Both drugs irreversibly bind to and permanently deactivate pyridoxal-5'-phosphate (PLP), the active form of vitamin B6. "PLP is required for more functions and chemical reactions than any other vitamin or mineral. Over 300 enzymes and proteins require PLP to function properly. The five PLP-dependent enzymes--glutamate decarboxylase, arginine decarboxylase, histamine decarboxylase, aromatic L-amino acid decarboxylase, and sulfoalanine decarboxylase are unrivaled in the variety of reactions they catalyze." Carbidopa may induce life-threatening events, including myocardial infarction, neuroleptic malignant syndrome, agranulocytosis, hemolytic and nonhemolytic anemia, gastrointestinal bleeding, thrombocytopenia, hypokalemia, and 90 other syndromes. "Irreversible L-dopa dyskinesias do not exist; they are a function of carbidopa which has a profound ability to induce previously undocumented histamine dyskinesias."
The death rate in Parkinson's patients has increased by 328.7% between 1976 and 2011, when carbidopa was first introduced. This is an amazing revelation and should change the face of the Parkinson's patient lot.
(1.) Hinz M, Stein A, Cole T. Parkinson's disease: carbidopa, nausea, and dyskinesia. Clin Pharmacol. November 2014;2014(6):189-194.
by Michael Gerber, MD, HMD
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|Title Annotation:||Monthly Miracles|
|Article Type:||Conference news|
|Date:||Jun 1, 2015|
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