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The Neurogenic Diet in the Treatment of
Neuro-degenerative Disorders
Basic proposal for clinical studies concerning MSA and Parkinson’s Disease
John Grinstein Ph.D.
Biochemistry Research Institute UK
uk@br13.com
Introduction
Diet is defined as a prescribed course of eating and drinking in which the amount and kind of food, as well as the times at which it is to be taken, are regulated for therapeutic purposes. But the term “diet” originally embraced a wider spectrum of factors, including all the main daily activities of an individual, or everything which determines his/her lifestyle. The word diet, originates from the Greek word diaita, which means a way of life.
The Nutritional Medicine Research in the UK have assigned the name “Neurogenic Diet,” to a nutritional programme and a life environment aiming to induce the generation of new neurons in the central nervous system and the repair of damaged neurons in the human brain. Research on Neurogenesis has been progressing since the 1960s and achieved a breakthrough in 1998 with publications by Gerard Kemperman of The Salk Institute, La Jolla CA, stating that neurogenesis, in the human brain, can be induced under enriched living environmental conditions.
The field of Neurogenesis is an encouraging one, because of its implications in developing new strategies to treat Neuro-degenerative disorders such as MSA, Shy-Drager Syndrome, Alzheimer’s disease, Multiple Sclerosis and Parkinson’s disease.
Neurogenesis research, published in mainstream journals of medicine and neuroscience worldwide in the last five years, has substantiated the observations confirming the appearance of new neurons in the adult human brain. These results, based on brain-imaging and radio-labelling of neuronal DNA nucleotides, have provided a conclusive demonstration.
These discoveries now undermine or invalidate the previous neuroscientists’ dogma that the adult human brain cannot generate new neurons.
The Neurogenic Diet aims to widen the spectrum of presently known enriched living environmental conditions to induce neurogenesis, with specific dietary intervention programmes.
We have demonstrated that, in Parkinson’s disease and in Shy Drager Syndrome, dietary interventions of at least one year’s duration can result in the regression of the condition in 33% of patients. A lessening in disability has been detected in 42% of patients on the diet for 3 months.
Our study aims to demonstrate that these dietary intervention improvements are due to the activation and repair of damaged neurons, in areas of the brain, affected in Parkinson’s disease and Shy Drager Syndrome. The Neurogenic Diet consists mainly of a regime that approaches neuronal regeneration through the gradual introduction of six distinctive stages, as follows:
1.- Revision and Adjustment of Medication
2.- Primary Dietary Intervention
3.- Secondary Dietary Intervention
4.- Determination of Etiological Factors
5.- Glial Cells Regenerative Factor [GCRF]
6.- Physical Activity and Neurogenesis
The Neurogenic Diet
STAGE 1
Revision and Adjustment of Medication.
This first stage is designed to create the groundwork, with the appropriate physiological conditions, to allow the release of any form of blockade on neuronal receptors in the affected areas of the brain and peripheral nervous system. These obstructions can be caused by chemical disturbances due to inappropriate drug dosages or adverse interactions between any two prescribed medications.
Parkinson’s Disease symptoms:
Tremor
Rigidity
Bradykinesia (slowness)
Mask-like facies
The above symptoms are observed in patients at the initial stages of Parkinson’s disease and in patients who have not been on any form of prescribed medication for a period of over five years, following the onset of the disease.
Dopamine Antagonists are chemicals which interfere with the interaction of dopamine and its specific receptor. Most antidepressants, pain killers and sleeping pills, exert their effect by blocking dopamine receptors. Therefore, its long term use can cause Parkinsonism.
Symptoms that develop as a result of the adverse effects of anti-Parkinsonian medication:
Dyskinesias
On-off effect
Disorders of balance
Muscular pain, cramp
Depression
Salivation
Respiratory disturbance
Dryness of mouth
Constipation
Hypotension
Orthostatic hypotension
Dysphagia
Sleep disruption
Urinary retention
Hallucinations
Urinary tract infections
Lung pleural fibrosis
Falling asleep while active
Fulminant liver failure
Onset of confusion
The above symptoms affect patients with Parkinson’s disease who have been on anti-Parkinsonian medication for a period of one year or more. These adverse effects have been widely reported in the medical literature in the last two decades.
The Neurogenic Diet
STAGE 2
Primary Dietary Intervention.
This stage introduces a specific dietary programme aiming to enhance the response to medication by facilitating transport and absorption of the prescribed drugs. As a result, a reduction in the dosages of prescribed medications is possible. This will consequently translate into a reduction in adverse reactions or side effects for the patient. As a result there is an increase in dopaminergic activity that can be demonstrated in studies utilizing PET Scans.
The Neurogenic Diet
STAGE 3
Secondary Dietary Intervention.
This includes a diet that will provide the nutritional precursors necessary for the brain’s own synthesis of neurotrophins.
Neurotrophins or neurotrophic factors, are protein molecules secreted by brain glial cells, (cells adjacent to neurons). These factors are secreted to provide essential nutrients and repair substances to the adjacent neurons.
A defect in the synthesis of any of these neurotrophins will inevitably cause a neurological problem. Presently, there are 26 human neurotrophic brain factors that have been isolated from brain tissue, characterized and their amino acid sequences identified.
These neurotrophic factors are quite simply, a chain of 200 to 400 amino acids. There are in nature, 20 basic amino acids and each of them repeats in different sequential order, in each of these neurotrophic factors. All 20 of these different amino acids are found originally in all foods in varying concentrations. As an example, one of the 20 amino acids is Glutamic Acid. There are 4 grams of glutamic acid in 100 grams of almonds, but only 0.001 grams of glutamic acid in 100 grams of spinach. If a patient has a deficiency in the absorption, synthesis or transport of glutamic acid, neurotrophins will not be synthesized in the brain in the necessary amounts. As a consequence of a deficiency of neurotrophins in the brain, a dysfunction in the maintenance and repair systems of neurons in the brain will occur. In this basic example, it will be obvious that a dietary recommendation should include a higher level of rich glutamic acid foodstuffs (like almonds) in the diet, but not of low glutamic acid (spinach).
Special emphasis has to be placed on providing all dietary precursors for the synthesis of Glial Cell Derived Neurotrophic Factor (GDNF), because it has been demonstrated that GDNF is essential for the nutrition, maintenance and repair of dopaminergic neurons.
Nutrients in the circulatory system, originating from ingested food, reach capillary blood vessels, cross the capillary membrane, [blood brain barrier,] and go into the neuroglial cells. These nutrients are used to synthesize molecules like GDNF, which is secreted towards adjacent dopaminergic neurons. 
GDNF interacts with specific GDNF Receptors in dopaminergic neurons. As a result of this interaction, specific membrane neuronal ion channels are activated. This precipitates a cascade of biochemical reactions, resulting in protective events and the transport of nutrients into dopaminergic neurons.
The Neurogenic Diet
STAGE 4
Determination of the Etiological Factors.
To enable an enriched living environment to induce neurogenesis effectively, the etiological factors, (those which may have caused the disease), should be investigated thoroughly. We have created a library with research results on more than 500 chemical substances known to induce Parkinsonism, Multiple Sclerosis and Shy Drager Syndrome. If the patient maintains direct contact with the causative agent, the disease will continue to progress in an accelerated manner. However, avoiding further connection with the causative agent, will help to stop the progression of the disease. In some instances, avoiding contact with a mild causative agent, has shown the gradual disappearance of all symptoms.
References on PD and MSA etiology
Anna Philip A,; Jankovic, Kirkpatrick, Joel B. Multiple System Atrophy The Putative Causative Role of Environmental Toxins. Archives of Neurology Jan, 1999.
Pezzoli G, Strada O, Silani V, et al. Clinical and pathological features in hydrocarbon-induced parkinsonism. Ann Neurol. 1996;40:922-925.
Tanner CM, Langston JW. Do environmental toxins cause Parkinson’s disease? a critical review. Neurology. 1990;40(suppl 3):17-30.
Rajput AH, Uitti RJ, Stern W, et al. Geography, drinking water chemistry, pesticides and herbicides and the etiology of Parkinson’s disease. Can J Neurol Sci. 1987;14:414-418.
Tanner CM, Chen B, Wang WZ, et al. Environmental factors in the etiology of Parkinson’s disease. Can J Neurol Sci. 1987;14:419-423.
Tanner CM, Chen B, Wang W, et al. Environmental factors and Parkinson’s disease: a case-control study in China. Neurology. 1989;39:660-664.
Koller W, Vetere-Overfield B, Gray C, et al. Environmental risk factors in Parkinson’s disease. Neurology. 1990;40:1218-1221.
Golbe LI, Farrell TM, Davis PH. Follow-up study of early life protective and risk factors in PD. Mov Disord. 1990;5:66-70.
Tanner CM, Grabler P, Goetz CG. Occupation and the risk of Parkinson’s disease: a case-control study of young-onset versus old-onset patients. [abstract]. Neurology. 1990;40(suppl 1):422.
Melamed E, Lavy S. Parkinsonism associated with chronic inhalation of carbon tetrachloride. [letter]. Lancet. 1977;1:1015.
McCrank E, Rabheru K. Four cases of progressive supranuclear palsy in patients exposed to organic solvents. Can J Psychiatry. 1989;34:934-935.
Gorell JM; Johnson CC; Rybicki BA; Peterson E. Occupational exposure to manganese, copper, lead, iron, mercury and zinc and the risk of Parkinson’s disease. Neurotoxicology Apr-Jun 1999, 20 (2-3) p239-4..
The Neurogenic Diet
STAGE 5
Glial Cells and GCRF
Fruit and vegetables are well known for their cancer prevention properties. More than 360 epidemiological and clinical studies, undertaken world-wide, have concluded that populations consuming large amounts of fruit and vegetables have a lower predisposition to develop cancer.
Glial Cell Regenerative Factor (GCRF) is an extract produced from selected organic fruit and vegetables. Preliminary clinical studies on the use of GCRF have shown an immediate effect in the regression of two forms of brain tumour: Medulloblastoma and Glioblastoma. The sources of GCRF, being purely fruit and vegetables, allow GCRF to penetrate the blood brain barrier easily and provide the basic substances required for Glial Cell DNA repair.
Molecular biologists have identified more than 700 anti-tumour and cancer preventive substances present in fruit and vegetables.
In conjunction with a diet, rich in the specifically required fruit and vegetables, GCRF actively helps the healing process of glial cells in the brain. Abnormal functionality of glial cells, the source for the biosynthesis of neurotrophins, reduces the self healing capacity of the brain.
GCRF molecular components are purely organic substances, present in fruit and vegetables, and therefore not rejected in their passage through the blood brain barrier. Innovative molecules, or large polypeptides, cannot cross the blood brain barrier. For this reason, GDNF, a protein, cannot be used by itself as a brain therapy. With its 211 amino acid chain, it is not able to penetrate brain blood vessels. GCRF, is able instead, to provide the precursors for GDNF biosynthesis in glial cells. These precursors, mainly organic molecules from food sources, are all recognized as essential brain nutrients.
Therefore, they easily penetrate the blood brain barrier and are transported into glial cells, where GCRF is broken down into essential amino acids, ions and other molecular components, required to synth
esize GDNF. GDNF is then secreted from glial cells into adjacent dopaminergic neurons, mainly, into neurons of the substantia nigra. Increased secretion of GDNF has been reported to induce an essential neuronal trophic effect. [trophic = nourishment]
The Neurogenic Diet
STAGE 6
Physical Activity and Neurogenesis.
The only effective methods to enhance neurogenesis, demonstrated so far by neuroscientists, are physical exercise and learning. To allow these crucial steps to be effective, as a neuro-regenerative healing therapy, the previous stages have to be accomplished successfully.
To illustrate the above, a farmer, exposed to a particular herbicide known to cause Parkinsonism, will not achieve any benefit from a neuro-regenerative exercise programme against Parkinson’s disease, as long as he continues to inhale that particular herbicide.
As an additional example, a patient using the drug reserpine, as a therapy for his depression, will be continuously aggravating his Parkinsonism and no exercise programme will produce any improvement in him. Reserpine is known to induce Parkinsonism in both humans and animals.
Once successful stages 1 to 5 of the Neurogenic Diet have been achieved, a final stage, with an individually designed exercise scheme, will produce a successful enhancement of the process of neurogenesis.
Each exercise scheme must be designed specifically for each individual patient, taking into consideration his/her physical capabilities, age and general clinical condition.
The number of new, dentate gyrus hippocampus neurons, in mice that have unlimited access to wheels and running, ended up more than twice as many as those in mice living in standard cages.
The number of new dentate girus hippocampus neurons in mice, living in standard cages and laboratory conditions, was regarded as the standard for mice in control conditions.
CLINICAL USE OF OTHER DIETARY INTERVENTIONS IN THE TREATMENT OF SPECIFIC HUMAN DISORDERS.
Alkaline-ash diet. A diet consisting mainly of fruit, vegetables and milk with minimal amounts of meat, fish, eggs, cheese, and cereals, which, when catabolized, leave an alkaline residue to be excreted in the urine.
Bland diet. A regular diet omitting foods that mechanically or chemically irritate the gastrointestinal tract.
Challenge diet. A diet in which one or more specific substances are included for the purpose of determining whether an abnormal reaction occurs.
Diabetic diet. A dietary adjustment for patients with diabetes mellitus intended to decrease the need for insulin or oral diabetic agents.
Elimination diet. A diet designed to detect which ingredient of the food causes allergic manifestations in the patient.
Giordano-Giovannetti diet. A diet designed for patients with renal failure; it provides small amounts of protein, primarily as essential amino acids, along with alpha-keto derivatives of amino acids.
Gluten-free diet. For the treatment of Celiac disease or gluten-sensitive enteropathy, This involves elimination of all wheat, rye, barley and oat gluten from the diet.
High-calorie diet. A diet containing upward of 4,000 calories per day.
High-fiber diet. A diet high in the non digestible part of plants, which is fiber. Soluble fiber delays absorption of glucose, which helps to control blood sugar in diabetes mellitus, and delays absorption of lipids, which helps to control hyperlipidemia.
Kempner diet. A diet of rice, fruit and sugar, plus vitamin and iron supplements, devised by Kempner to treat hypertension. In 2,000 calories, the diet contains 5 gm or less of fat, about 20 gm of protein, and not more than 150 mg of sodium.
Ketogenic diet. Demonstrated in several recent clinical trials to be an effective tool to treat Petit Mal Epilepsy in children. It consists of a high-fat, low-carbohydrate, and normal protein diet causing ketosis.
Low purine diet. A diet low in precursors of purines (such as tissues rich in cells with abundant nuclei, as in liver, glandular meats, etc.) to minimize formation of uric acid. Useful in treatment of patients with gout or urate-containing renal calculi.
Low residue diet. A diet that leaves minimal unabsorbed components in the intestine, to minimize functional stress on the colon.
Low salt diet. A diet with restricted amounts of sodium chloride, necessary in the treatment of some cases of hypertension, heart failure, and other syndromes characterized by fluid retention and/or edema formation.
Meulengracht's diet. A feeding program for patients with peptic ulcer disease, containing a relatively full diet, free of acidic or highly seasoned food.
Minot-Murphy diet. The use of large amounts of raw liver in the treatment of pernicious anemia. First successes in the treatment of this disease occurred with this diet and led to development of liver extract for treatment.
Ornish prevention diets. Relaxed versions of the Ornish reversal diet, which is designed to prevent coronary artery disease. These diets reduce dietary fat in proportion to blood cholesterol level.
Ornish reversal diet. A diet designed by Dean Ornish, who has evidence that it will reverse coronary artery disease. It consists of 10% of calories from fat (mostly polyunsaturated or monounsaturated, with 5 mg cholesterol per day), 70 to 75% from carbohydrates
Smooth diet. A diet containing little roughage; used primarily in diseases of the colon.
2a. Research on Neurogenesis
Script and slides from the documentary:
“Original Home Video Clips Showing the Genuine Personal Experiences of Parkinson’s Disease and MSA Sufferers.”
2b. RG40 Organic Vegetable Extract
Protocol for Studies on MSA and Parkinson’s Disease
2c. The Neurogenic Diet in the Treatment of Neuro-degenerative Disorders
Basic proposal for clinical studies concerning MSA and Parkinson’s Disease.
Research Abstracts & Publications
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”THE ORIGIN OF THE SPECIES”.
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