Food Causing Dementia, Parkinson’s
Due to heat, new substances originate in especially proteinous prepared foods. Part of these substances are mutagenic or toxic. And some of these can also bind to neurotransmitter-receptors and -transporters in the brain. Because of the mutagenic properties of these substances, neurotransmitter-receptors and/or -transporters are destroyed. Depending on what kind of neurotransmitter is destroyed, different brain diseases can be caused, like dementia, Parkinson’s and schizophrenia.
To stop progress of, or prevent brain diseases, consume as little prepared food (proteinous prepared food in particular). Consume as much fruits (there are about 6000 different fruits), and some fresh raw animal food regularly (like sashimi or fresh raw egg yolk). Combined, these foods contain all nutrients you need.
When we are old, we are supposed to be wiser, and advise the younger.
When we are old, we are not supposed to wear a diaper and forget our grandchildren’s names.
The brain processes signals; signals from the eyes, ears, skin, etc. These signals are transmitted in the brain by messengers or neurotransmitters. These neurotransmitters can only function if there is something they can deliver the messages to, i.e. receptors.
In brain-diseases production or secretion of one or more neurotransmitters is malfunctioning, or receptors have been destroyed. Depending on which
neurotransmitter-system is failing, a brain-disease is caused.
In Parkinson’s dopamine- (1) and/or serotonine-receptors are deficient. (2) In dementia acetylcholine-metabolism is impaired. And in schizophrenia in general too little dopamine (3) and/or serotonine (4) reach the receptors.
What causes brain-diseases?
Substances destroying receptors, or structurally impairing production or secretion of neurotransmitters cause brain diseases.
Prepared food, and proteinous prepared food in particular always contains such substances. Due to the influence of heat, in all foods that are cooked, steamed, baked, grilled etc., new substances originate, like beta-carbolines, pyridines, quinolines and other heterocyclic amines.
– Some of these substances are directly toxic to the brain. (5)
Mostly, these substances only become toxic (or more toxic) through being partly
decomposed in the body (6), by enzymes (7) or by oxidation. (8)
Sometimes these substances are toxic because they decrease, sometimes irreversibly (9), neurotransmitter levels (10). Some of these substances are only toxic to a single type of neurotransmitter receptors, like dopamine receptors. (11)
– To function, receptors are not just susceptible to neurotransmitters made by the
body, but also to substances that look alike, disturbing the normal influence of
neurotransmitters. That’s why drugs fighting the symptoms of brain-diseases
temporarily can have some effects. Many beta-carbolines, for example, stimulate secretion of acetylcholine. Eventually this may lead to exhaustion of the acetylcholine-system, and dementia.
– Neurotransmitter-transporters can also be ”occupied” by substances that look like neurotransmitters. Certain beta-carbolines and quinolines for example, can ”occupy” dopamine-transporters, which can also cause Parkinson’s. (12) Because when dopamine receptors are occupied, dopamine accumulates, and more likely oxidizes.
– Also, many beta-carbolines locally stimulate secretion of glutamate (a neurotransmitter), by stimulating secretion of acetylcholine (13), like amphetamines and cocaine do.
(14) Secretion of too much glutamate locally damages the brain (15), by stimulating secretion of radicals. (16)
Glutamate also stimulates secretion and decomposition of dopamine (17), causing exhaustion, and eventually death of dopamine-receptors (18). Dopamine receptors are deficient in Parkinson’s. Logically, this can lead to schizophrenia too. (19) (like cocaine can (20)) It just takes a little time. That’s why ‘non-environmental’ schizophrenia mostly is not ‘discovered’ before the age of 15 to 25.
In only 10 to 20% of patients Alzheimer’s is inherited.
So, what about the rest?
Acetylcholine is needed to think. In Alzheimer’s acetylcholine metabolism is impaired, causing severe memory lapses. At the onset of Alzheimers acetylcholine deficiency remains unnoticed, due to increased activity of remaining receptors. In advanced Alzheimer’s remaining receptors cannot compensate the loss of receptors anymore. (21)
Acetylcholine receptors can be killed by inactive substances that occupy receptors and look similar to neurotransmitters. (22) In Alzheimer’s, receptors are occupied by a plague of damaged proteins and -fats (23) and brain fluids contain higher levels of these substances. (24) In Alzheimer’s, the body tries to eliminate those substances by increasing the level of ‘cleaners’. (25) Some of those cleaners can however also damage brain-neurons. (26)
Acetylcholine deficiency in Alzheimer’s is not caused by a genetic failure that causes enzymes to decompose acetylcholine too fast; in Alzheimer’s, activity of acetylcholine-decomposing enzymes is not increased, but even decreased 24% (18% in Parkinson’s)(27). This indicates that production / secretion of acetylcholine is exhausted. And yet substances inhibiting this enzyme are used as anti-Alzheimer ‘drugs’ (28), just to fight symptoms. Production of acetylcholine can be exhausted through ongoing stimulation of acetylcholine-secretion by beta-carbolines from prepared food in the first place.
In Alzheimer’s even in broad daylight serotonine is transformed into melatonine, which isn’t normal. (29) Therefore, dementia (and Parkinson’s) often comes with depressions. (30) Beta-carbolines from cooked foods can impair the serotinine-melatonine metabolism.
Acetylcholine is also needed for muscle-contractions. Normally, secretion of acetylcholine is regulated by dopamine. In Parkinson’s however, dopamine-receptors have been damaged, or occupied by dietary protein-oxidation products. Therefore, in Parkinson’s muscle-contractions can not be controlled as well.
Whether you will get Parkinson’s, depends on how sensitive your receptors are. (31)
Certain heterocyclic amines and imidazoles damage dopamine molecules, causing reactive radicals to originate. (32) These radicals damage DNA (33) and kill brain cells. (34) Too much iron (34), copper or manganese (35) can also cause dopamine to oxidize.
In Parkinson’s patients radicals levels are elevated, and antioxidant levels are decreased. (36) In Parkinson’s CRF-level is decreased too. And certain pyridines that are toxic to dopamine-receptors, also decrease CRF level. (37) Those pyridines too originate from food-proteins, due to the influence of heat.
Many beta-carbolines influence the secretion and decomposition of dopamine (38). Blood-beta-carboline- (39), brainfluid-beta-carboline- (40) and/or -toxic quinoline level (41) are elevated in Parkinson’s patients.
Some schizophrenics are born that way, and others become schizophrenic in reaction to rape or other excessive psychological stress. Some just get ‘unreal’ signals from prepared food-substances.
In schizophrenics, dopamine-receptors are more sensitive. (42)
Wheat-opioid peptides can occupy dopamine-receptors, what may cause schizophrenia. In areas where people hardly consume wheat-products, schizophrenia incidence is much lower. (43)
Glutamate-deficiency can be caused by substances ”occupying” glutamate-receptors (44), and may also cause schizophrenia. (45) Certain beta-carbolines / heterocyclic amines can lower the susceptibility of GABA-receptors (46), and can therefore cause schizophrenia. (47)
Besides the afore-mentioned neurotransmitter-receptors, schizophrenia can also be caused through blockage of glycine- (48) ,N-acetyl aspartate-, phosphatidylcholine- or sphingomyeline-receptors (49).
Because the brain is the control-room of the body, blockage of neurotransmitter-receptors can cause all kinds of psychological and physical problems. Blockage of histamine-, acetylcholine- or epinephrine-neurotransmitters by anti-depressants for example, can also cause obesity, constipation and dizziness (50).
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Abstracts of most sources can be found at the National Library of Medicine
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