Parkinson’s disease is a “disease of the mind” which affects the synapses in the brain. It is created by a person’s own subconscious mind, and it is part of a family of conditions that share similar symptoms and which are separated according to the patient’s history. These conditions may include repetitive trauma to the head (Pugilistic Parkinson’s, as in boxing), heavy metal toxicity, meningitis, or prolonged exposure to certain chemicals or medications. It can also be caused by sustained elevated levels of adrenaline, and be secondary to mimicking diseases such as Lyme disease. However, for many Parkinson patients, the real underlying cause is a miasma, which is defined as ‘noxious input’. It lies there like a trap door waiting to get sprung open. Any of the above-mentioned causes, as well as an adrenaline spike, could serve as the trigger. The miasma could be in a form of an unintentional death wish or as a result of a curse. It affects one or more genes, on one or more chromosomes.
The common notion that Parkinson’s disease results from inadequate amount of dopamine is only partly true. It addresses the effect and not the cause.
Statistically, one out of every 272 people worldwide is affected by Parkinson’s disease. It is characterized by tremors at rest, by pill-rolling movement of the fingers, muscular rigidity, postural instability, shuffling gate, freezing or being stuck in place, by a typical expressionless facial expression (‘facies’), decreased blinking, slurred or inaudible speech, drooling, depression and despite patients having the tendency to fall asleep, many are unable to have REM sleep. Many of the symptoms are side effects of the medications that are prescribed in order to control the tremors. Stress amplifies the tremors and increases the need for more medication.
The pharmaceutical approach to treating Parkinson’s disease involves the administration of synthetic dopamine such as Sinemet, Sinemet CR, Stalevo and Percopa, as well as their agonists Miraplex and Requip.
The areas in the brain that are associated with Parkinson’s disease are the cerebellum, thalamus, sub-thalamic nuclei (putamen, caudate nucleus and globus pallidus), hypothalamus, hippocampus, the motor cortices and the pars compacta of the substantia nigra, the site of dopamine production. They communicate with each other via neurotransmitters. The hypothalamus communicates with the organs outside the brain via specific hormones it secretes.
Outside of the brain, in addition to the heart, the organs that are involved with Parkinsonism and that are responsible for regulating dopamine are the thymus, adrenals and the liver. The thymus, by itself, just like the substantia nigra, cannot lead to Parkinsonism. When the heart, the thymus and the substantia nigra fail to communicate with each other (Sibling Rivalry), at the same time that the heart’s energy production is continuously low, tremors at rest will ultimately appear. An adrenaline spike can reverse the patient’s polarity, blow fuses and lead to Sibling Rivalry.
Commonly, the trigger can be traced to a frightening incident that occurred nearly twenty years prior to the appearance of the first symptom just as it is in multiple sclerosis (MS), another “disease of the mind.” Because it began so long ago, the body got used to it, and gradually the condition became an integral part of the body, like a nose or an elbow, and therefore, it became ingrained in the sub conscience. When asking a Parkinson patient or an MS patient if they wish to be rid of the disease and become well again, they are quick to respond ‘yes,’ but muscle testing as they reply contradicts their response. Consciously they say ‘yes’ but subconsciously they say ‘no.’ The point is that the non-physical (metaphysical) side of both conditions must be resolved before the physical side will respond. No recovery is possible until all the physical and metaphysical components have been fully resolved. As long as their conscious and subconscious are not reconciled, patients will make all the ‘wrong’ decisions and ‘sabotage’ their treatments, because the subconscious mind is trying to ‘preserve’ and ‘protect’ what it recognizes as ‘normal.’
With repetitive mechanical trauma, as in boxing, of the nine dopamine-producing centers in the brain, the substantia nigra is the least affected by the punches. One blow never leads to Parkinson’s disease (or syndrome). The fact that Parkinson-like tremors and other related symptoms are present, merely suggests that the repeated jarring of the brain led to a decrease in dopamine production, by turning down or shutting off dopamine production in an attempt to give the brain time to repair itself. It is not reflective of any brain damage. In most cases, it is possible to restore dopamine production, if the practitioner is able to locate the ‘switches.’ Since at this time devices that can locate these switches have not yet been developed, being skilled at muscle testing and pulsing is essential. If there is physical contact between practitioner and patient during muscle testing, it is necessary for the tester and the patient to be hydrated. Dehydration and electrolyte deficiencies can also lead to the reappearance of the tremors or their amplification.
Calcium deficiency can also cause tremors. These tremors range from mild to violent and resemble Parkinson tremors, without the pill-rolling, and are they frequently treated as such. Muscle contraction and nerve conductivity require the presence of calcium. Calcium deficiency could be nutritional or metabolic. All vegetarians or meat eaters get their calcium from their diets. Diet is the primary source of calcium for all animals. Calcium must be bound to vitamin D, which is fat-soluble, in order to be absorbed. Vegetarians should add fats to their salads, such as found in olive oil, avocado, sunflower seeds or cheese, in order to facilitate calcium absorption. The organs or glands that are associated with calcium metabolism (adrenals, parathyroid, pancreas, large and small intestines) should be checked. Once again, muscle testing and pulsing are essential. Synthetic calcium in amounts larger than 45 mg per day decreases the electrical rhythm of the heart and should be avoided.
Dopamine is one of four neurotransmitters that are also associated with insomnia. Too much dopamine results in insomnia. Too little dopamine could sometimes lead to tremors, but not always, and never by itself.
Beginning with the first signs of twilight sleep, and all during our sleeping hours, the thymus secretes a hormone, which inhibits dopamine production. Let’s call it dopamine inhibiting hormone (DIH). It is the same hormone that is associated with sleep (and insomnia, when its production decreases). It inhibits the synthesis of four neurotransmitters (I, II, III & IV) in the brain, including the production of dopamine (referred to here as Neurotransmitter I) by the substantia nigra. Three of these four neurotransmitters, (I, II and III) are associated with Parkinsonism, while the fourth neurotransmitter (IV) transmits messages from the Limbic system to the motor cortices, and is not associated with Parkinsonism. DIH does not affect dopamine production by the other eight dopamine secreting centers, which have the same chemical formula but different spatial configurations, and which transmit different messages.
The cerebellum also produces a neurotransmitter (Neurotransmitter V), whose function is inter-communication between the two sides of the cerebellum, to ensure they do not send conflicting information to the muscles. Without it the patient can lose its balance or become ‘stuck.’ Neurotransmitter V is secreted in response to messages carried by another neurotransmitter (Neurotransmitter VI) from the thalamus to the motor cortices, in response to limbic input. The putamen communicates with the motor cortices via neurotransmitter VII, with the cerebellum via neurotransmitter VIII, with the substantia nigra via neurotransmitter IX and with the limbic system via neurotransmitter X.
The synthesis of each neurotransmitter follows the genetic blueprint that is encoded on various chromosomes. Neurotransmitter I (dopamine) is encoded on chromosome 6. II is on chromosome 16. III is on 18. IV is on 4. V is on 6. VI is on 17. VII is on 14. VIII is on 6. IX is on 5 and X is on 16. A ‘glitch’ on any of these chromosomes that affects any of these neurotransmitters, be it physical or metaphysical must be corrected before Parkinson’s disease could be resolved.
From a chemical point of view, all the neurotransmitters that are associated with Parkinson’s disease are monoamines.
The hypothalamus ‘tells’ the thymus when to secrete DIH and when to stop secreting it. DIH is secreted in order to enable us to go to sleep. The hypothalamus does it by releasing a hormone that we are going to call Thymus DIH Releasing Hormone (TDIHRH), which begins breaking down after 6 hours and disappears from the blood completely after about 14 hours. We can also initiate the synthesis of this hormone by physically closing our eyes and keeping them closed, as we do when we attempt to take a nap or go to sleep. The synthesis of this hormone stops when the thalamus produces a neurotransmitter (II), which simultaneously instructs the substantia nigra to produce dopamine, and the hypothalamus, to stop secreting that hormone (TDIHRH), so that the thymus will stop secreting dopamine inhibiting hormone (DIH). The thalamus does so when we wake up or when we open our eyes. The absence of this neurotransmitter (II) is one of the causes of Parkinson’s disease. As stated earlier, this neurotransmitter is one of the four neurotransmitters that are inhibited by the presence of DIH in the brain. In addition, the hypothalamus also secretes a hormone, which we are going to call adrenal parasympathetic thymus inhibiting hormone (APTIH), which is part of a feedback loop to stop the synthesis of DIH by the thymus, when traces of this hormone are still found in the blood at the time DIH is not needed or wanted.
A summary of the neurotransmitters and hormones that are involved in the various pathways that are associated with Parkinson syndrome, as well as a ‘check list’ are provided at the end of this chapter.
During our waking hours, when we contemplate moving, the thalamus commands the substantia nigra, via Neurotransmitter III, to secrete dopamine, which transmits the message to initiate gross movement from the motor cortex to the cerebellum, where that movement is going to be toned down or refined. ‘Skill memory’ movements are initiated by the cerebellum, and do not require toning down or refinement.
One of the functions of the liver is to break down the DIH that is in the blood, as it returns from the brain. Unlike most hormones, which have a short life before they break down, DIH does not break down on its own. It is broken down by the liver when the blood, which contains DIH, flows through it. When the energy that is available to the liver decreases and remains decreased over years, the liver slows down, becomes less efficient (‘it falls behind’), and fails to remove all the DIH from the blood. DIH, which is secreted by the thymus, passes through the blood-brain barrier. When it is not removed from the blood it continues to circulate with the blood, re-entering the brain. The presence of DIH in the blood continues to inhibit dopamine-secreting cells in the substantia nigra. This leads to a decrease in dopamine production, and to ultimately ‘turning off’ some of these cells, even at a time that the thalamus commands the substantia nigra to secrete dopamine, since DIH over-rides neurotransmitter II. When the thymus synthesizes DIH continuously, it becomes fatigued, and over time it will weaken. This slowing down is also seen, in part, due to less available energy, as a result of the heart making less energy. The absence of DIH in itself is not enough to initiate dopamine production.
As long as Parkinson patients are alive, their substantia nigra never stops producing dopamine. Even the most advanced cases still produce about thirty percent. As soon as energy is restored to the brain, dopamine production increases dramatically. The production of all the other neurotransmitters that are not associated with Parkinsonism (including acetylcholine, serotonin and glutathione) will also increase, returning to normal in approximately two hours. Dopamine production is limited by the number of open or available receptors on the cell membranes in the cerebellum, which, in turn, is determined by the amount of dopamine that is in the system, regardless if it is naturally produced, synthetic dopamine that the patient is taking or a combination of the two. Synthetic dopamine has the same spatial configuration as naturally-produced dopamine, but it transfers only about 60 percent of the signal from the motor cortices to the cerebellum, so no matter how much synthetic dopamine a patient is taking, there is always a need for more. There are more dopamine receptor sites in the cerebellum that a healthy person needs. They are never all ‘occupied’ at the same time. However, in Parkinson patients that take synthetic dopamine these sites are frequently all occupied, shutting natural dopamine production down via the feed-back mechanism and making the patient dopamine-dependent (addicted). Keeping in mind that (1) despite the fact that all dopamine receptors are ‘occupied,’ the dopamine that they release into the cells transmit only 60 percent of the signal, and therefore there is a constant demand for more dopamine, and that (2) synthetic dopamine lowers heart rhythm, which lowers the energy (electricity) that is available to the brain, so dopamine remain ‘stuck’ in the receptors and is unable to get into the cells, which (3) amplifies the symptoms and (4) increases the demand for additional medication. (5) The patient becomes stuck in a loop, in which (6) the heart rhythm continues to drop, generating less electricity, until finally (7) when the energy production falls below a certain level, organs fail and the patient dies.
Pharmaceuticals that affect the motor cortices (dopamine ‘agonists’) exaggerate the movement-generating signals that are to be transmitted to the cerebellum, and with it, the need for more dopamine to carry these increased signals, thereby dramatically enhancing the dependency. These drugs can cause dyskinesia, the involuntary jerking or swaying movements. They also interfere with liver function. They decrease or stop the synthesis of four substances that serve as electrolytes, and which are indispensable for retention of the energy generated by the heart. The irony is that synthetic dopamine, like most pharmaceutical preparations, has a side effect. It (indirectly) lowers the electrical rhythm of the heart, thrusting the patient into the loop that was described in the preceding paragraph.
One major consequence of this drop in energy is the decrease in the production of endorphins. Parkinson patients cannot recover without endorphins. Dr. Bernard Bihari, a neurologist from New York City, found that we can ‘trick’ the body into making more endorphins by giving the patient very low doses of low density naltrexone (LDN). Naltrexone is a drug that was developed in the late 1960s to treat heroin overdose. A dosage of three milligrams at mid-morning should be beneficial for all Parkinson, MS and chronic depression patients, and should be taken for sixty days, or until the patient’s energy production has returned to normal. It takes at least two weeks before endorphin production resumes. In healthy patients, endorphin production is triggered by exercise (jogging), laughter and sexual climax. It should also be noted, that low-fat, low cholesterol diets and anti-cholesterol drugs impede the production of endorphins, as well as hormone production and cell division in general.
Additionally, the drop in energy is frequently associated with hypertension and type II diabetes, and the pharmaceutical drugs that are prescribed to treat these conditions decrease the heart’s energy production even more, further aggravating Parkinson symptoms. Hypertension patients who are on beta blockers must have them replaced with blood pressure medications that work through the adrenals (such as Cozaar or Norvasc) if they wish to recover.
The heart, because of its decreased energy production, is ‘responsible’ for the Parkinson facies, the drooling, the slurred and inaudible speech, shuffling gate, rigidity, inability to write, the loss of bladder control, depression and anxiety, while the motor cortices, the plugged dopamine receptors, the cerebellum and the putamen (and NOT the globus pallidus, caudate nucleus or thalamus) are responsible for the tremors. The motor cortices are the most difficult component to restore to normal function, and being of brain tissue, they heal very slowly, and they must be monitored continuously. Until all the components that are associated with the condition have been completely resolved, the tremors will remain.
The putamen is one of the sub thalamic nuclei (basal ganglia), which are part of the limbic system. It stores memory of learned (‘skill’) movements, which it sends to the cerebellum in order to execute a movement. The globus pallidus also stores ‘skill’ memory. It synthesizes Neurotransmitter VII, which carries signals from the putamen to the motor cortices. When the limbic system is involved with the tremors, patients can command (audibly or in thought) their tremors to stop.
Although the adrenals may have been the trigger in some Parkinson cases, they are not responsible for the tremors. They are, nonetheless, a component of the Parkinson syndrome. They send parasympathetic signals to the thymus to stop the synthesis of Dopamine Inhibiting Hormone (DIH), as a response to a hormone (APTIH) that is produced by the hypothalamus. Once energy to the adrenals had been restored, weak adrenals can be treated successfully with specific nutritional supplements.
As stated earlier, the cerebellum, the putamen, the motor cortices and ‘plugged’ dopamine receptors are responsible for the tremors. The first two store the memory of learned and repetitive movement. In Parkinsonism the loss of energy to the cerebellum interferes with executing learned movements such as writing, initiating movement, handling a fork, drumming and so on, which were performed before. These are easily regained by exercising these movements, after the body is balanced and the energy had been restored.
Exercises, and cardio-vascular exercises in particular, like long bike rides, speed up the heart through increased adrenaline production, which decreases the tremors in the short run, but will, in fact, aggravate the condition later. Stress and endorphin production have an inverse relationship. Stress increases adrenaline production, which in turn, inhibits endorphin production. Stress management can help reduce tremors. There are several methods that are effective: laughter, biofeedback, autosuggestion methods such as The Silva Method (“Enter the Alpha State”), music, meditation or a combination thereof.
Several hospitals are experimenting with the use of electrotherapy to treat Parkinson’s disease. Electrotherapy is a two-edged sword. While initially the treatments may lead to visible improvement, prolonged use of such therapy changes the electrochemical potentials of cell membranes, interfering with materials getting in and out of cells, permanently altering nerve perception and leading to irreversible damage. Other hospitals are conducting research with vibration therapy, a concept that was introduced by the great neurologist Dr. Jean-Martin Charcot, based on his observations that Parkinson patients showed a decrease in symptoms immediately following a long train ride. While the treatments do not decrease the shaking, they decrease the stiffness, increase stability, make walking easier and make patients sleep better and with less discomfort. This form of external sensory stimulus is received by the thalamus, which communicates it to other parts of the brain, which respond accordingly, but it does not address any of the Parkinson components. Unfortunately, the effects of the vibrations are temporary and the treatments become less effective with time.
New technology, which utilizes light energy, has shown startling results with absolutely no negative side effects. One such device, the “Parkinson Light Device,” was conceived, developed, built and patented by the author of this book and by Peter Jungen. It emits positive light energy that sweeps through all of the brain’s various tissues at a frequency, intensity and duration specific to each tissue. The electromagnetic field it creates extends only a paltry 5/16th of an inch, with an effective treating distance between 2 and 3 inches from the back of the head (no contact is made), and with a temperature increase of only 2 degrees Fahrenheit immediately next to the light source. This device reproduces certain light bands that are found in sun light, and which are absorbed by the cerebellum. In essence, the device serves as a battery charger in restoring the energy to the cerebellum.
Although it was not its intended purpose, the device also proved effective in reversing or eliminating paralysis and loss of vision caused by strokes that resulted from blood clots.
In cases where the cerebellum had little or no energy, seated Parkinson patients who were unable to stand up or walk were able to stand up on their own, walk to the bathroom and even dance. They showed remarkable improvement by the end of the first treatment. The drooling and the slurred speech stopped, and the gait returned to near normal. The facial expression became normal, and the patient was able to smile. In cases where the cerebellum was responsible for the tremors, they decreased dramatically. The effectiveness of each treatment and how frequently it has to be repeated depend on what medications the patient is on, how long the patient has been on the medications, how often the medications are taken and how skilled the practitioner is in identifying the underlying or precipitating causes. Early clinical trials showed that newly diagnosed Parkinson’s patients who have not taken any medications responded faster and in some cases became visibly asymptomatic, while those who were on medications showed improvement directly proportional to the type of medications, the amount of medications, how long they were taking them and the rate at which they were weaning themselves off the medications. As a rule, every year since the onset of the disease will require approximately one month to recover, with exception of brain tissue, and the motor cortices in particular, which are slow to heal. It should also be noted, that when the miasma is eliminated, the correction involves repairing the damaged genes. Gene repair begins with the chromosomes in the master cell in the pineal gland and it takes several weeks before all the defective nucleic acid sequences are repaired, during which time the patient will remain symptomatic. The nucleic acid that is involved with miasmas is guanine. Patients without a miasma can recover faster. Restoring the energy to the cerebellum is a pre-requisite in the treatment of Parkinson’s disease.
When a patient starts taking synthetic dopamine, the body becomes dependent on it, and it turns into an addiction. As with all addictions, weaning off can be a lengthy process, which is associated with a variety of withdrawal symptoms, none of which are pleasant. With dopamine fear, panic, stiffness, trembling and muscle cramping-type pain are not uncommon.
Synthetic dopamine must be tapered off gradually, no more than one sixteenth of the dosage at a time, so long as the gap (see below) does not exceed two percent. For about five days after decreasing the dose, the patient may experience withdrawal symptoms in the form of an increase in the tremors, stiffness, muscle tightness or crampy feeling, fear or panic, while the brain is adapting to the decrease in the presence of synthetic dopamine, and the substantia nigra picks up the synthesis of natural dopamine. These side effects could sometimes be avoided by taking specific nutritional supplements for the thymus and adrenals and waiting two weeks after beginning taking these supplements before decreasing the amount of prescribed dopamine. They should be taken for at least six weeks. When patients are on synthetic dopamine and one of its agonists (which amplify the need for dopamine), weaning off must be staggered and done in stages, decreasing the dose of the agonist before tapering off the dopamine, and switching back and forth until there is nothing left to cut.