Cause of Alzheimer's & Breast & Prostate Cancers

Floyd’s Herbivore Feeding Deterrents (Thorns) Hypothesis on Cause of Alzheimer’s Disease And Others Diseases Paul Ewald, professor of biology and author of the book, Plague Time, The New Germ Theory of Disease, wrote, “Cancer, heart attacks, stroke, Alzheimer’s disease, and infertility are like the acts of an anonymous vandal”. In his book, Excitotoxins, The Taste that Kills, Russell L. Blaylock, M.D. notes that a multitude of seemingly unrelated diseases, such as strokes, heart attacks, arthritis, brain injury, migraine headaches, and cancer are associated with excitotoxins such as glutamate, calcium and cell death. Dr. Blaylock writes, “It appears that several of the excitotoxins, including glutamate and aspartate, work by opening calcium channels, at least on certain subtypes of receptors”. My theory or hypothesis is that the influx of calcium into the cell is not the cause of the cell death, but is in response to the threat of toxicity posed by that “anonymous vandal” that Paul Ewald writes about. This so-called “vandal” or “vandals”, in my opinion, are agents of Nature that are there to enforce Nature’s balance. Nature employes the use of phenolic compounds (I call them “thorns”) in plants as feeding deterrents to herbivores. These compounds can be grouped in three major groups: alkaloids, terpenoids, and phenolic compounds (mostly phenylpropanoids). The oxidation of these thorns creates a significant risk for our bodies by the release of excessive free radicals. Alkaloids (poisons), are synthesized principally from amino acids. These nitrogen-containing compounds protect plants from a variety of herbivorous animals, and many possess pharmacologically important activity. Our immune system’s defenses were not designed to overcome these deterrents over the long run. Consequently, as we learn to avoid them, or reduce the activity of our enzymes that oxidize them, the better off we are at consuming those plants. Dr. Blaylock lists the amino acids glutamate, aspartate and cysteine as excitotoxins that are found in nature. Phenolic compounds are widely distributed in the plant kingdom. Wheat appears to be well protected by Nature as it is quite high in alkaloids. Dr. Blaylock wrote, under the topic of, A Cascade of Destruction: The Free Radicals, that, “Once this cascade of destruction is triggered by the influx of calcium, the whole process proceeds with the explosiveness of a nuclear chain reaction”. I think that the process is initiated when our enzymes act on the inhibitors. I see this as nature’s way of enforcing its Balance of Nature by using agents such as “thorns” or inhibitors. Others have said that the redox process inside the cell is likened to a severe thunderstorm. When our bodies try to oxidize the “thorns” they become emboldened – just the opposite of what you would expect. Many of nature’s inhibitors come into the body via the diet and end up in VLDL cholesterol. The cholesterol remnants apparently containing these “thorns” are eventually transferred to LDL cholesterol. APOE is essential for the normal catabolism of triglyceride-rich lipoprotein constituents. As herbivores, including man, attempt to metabolize these “thorns” in the lipoproteins, excessive damage to the tissues ensue. Consequently, as a process of adaptation to the “thorns” in the diet, the body has mutated and produced two additional forms or alleles of the APO-E gene. Notice the difference in the different gene products. The APO-E2 does not bind tightly to its cell surface receptor and the “thorns” have difficulty getting into the cells. However, a consequence of the APO-E2 mutation is the build-up is a terminal disease called hyperlipoproteinemia. APO-E3 is the most common form of the allele and is probably the wild-type. That leaves APO-E4. Let’s see what kind of a change it offers in response to the “toxins” in the triglyceride-rich lipoprotein constituents. APO-E4 can bind to its receptor but binds to cholesterol to a lesser degree than APO-E3. As a result, people with APO-E4 allele often have high levels of cholesterol in their blood. So, the alternate APO-E alleles E2 and E4 result in less affinity of either the receptor or cholesterol itself. This lesser affinity for cholesterol on the part of APO-E4 is largely responsible for the familial or late onset form of Alzheimer’s disease.

The Race Gene

The Race Gene Race is about a difference in degree; not a difference in kind. The difference in degree is related to the strength or activity of the enzymes or factors that control the expression of the genes that control the enzymes. Response to Stress Race is about different levels of immune response and consequentially the body’s immune response to stress. The Reason for Different Races Our bodies must adapt to the staples in our diet. This is the reason, in my opinion, for the different races. In other words, a rice-based diet will produce a different set of physical characteristics than a diet based on wheat. Melanocytes are the cells that produce melanin which is a pigment in the skin, eyes, and hair. It is not the number of melanocytes in our skin that determine whether one is lighter or darker in skin color. More importantly, it is the level of activity of the melanocytes. The enzyme, tyrosinase is responsible for the level of activity in the melanocytes. Consequently, the greater the activity of tyrosinase, the darker the skin color. Tyrosinase (monophenol monooxygenase) is an enzyme that catalyses the oxidation of phenols, and, as such, catalyzes the production of melanin and other pigments from tyrosine by oxidation. Complete lack of the enzyme produces albinism. Nature employed the use of phenolic compounds (I call them thorns) in plants as feeding deterrents to herbivores. These compounds can be grouped in three major groups: alkaloids, terpenoids, and phenolic compounds (mostly phenylpropanoids). The oxidation of these thorns creates a significant risk for our bodies by the release of free radicals. Our immune system’s defenses were not designed to overcome these deterrents. Consequently, as we learn to avoid them, or reduce the activity of the enzymes that oxidize them, the better off we are eating those plants. Now, wheat is high in alkaloids. Caucasians are more adapted to eating a wheat-based diet that other cultures or races. Therefore, the thorns in the western diet do not pose as great a risk for Caucasians as they do for African-Americans. Some races, such as the black race, more frequently express the melanin-producing genes, thereby conferring a greater concentration of skin melanin. On the other hand, other races such as the white race, less frequently express melanin-producing genes, thereby conferring a lesser amount of skin melanin. – Wikipedia. The Melanocortin-1 receptor (Mc1r) is one of the key proteins in regulating hair and skin colour. Mc1r functions at the surface of specialist pigment producing cells (called melanocytes) to regulate melanogenesis in mammals. Mutations of the Mc1r gene can either create a receptor that constantly signals, even when not stimulated, or can lower the receptor’s activity. Alleles for constitutively active Mc1r are inherited dominantly and result in a black coat colour, while alleles for dysfunctional Mc1r are recessive and result in a light coat color. Both eumelanin and pheomelanin are found in human skin and hair, but eumelanin is the most abundant melanin in humans, as well as the form most likely to be deficient in albinism. Eumelanin is found in hair and skin, and colors hair from brown to black. In humans, it is more abundant in peoples with dark skin. There are two types of eumelanin, which are distinguished from each other by their pattern of polymer bonds. The 2 types are black eumelanin and brown eumelanin. Pheomelanin is also found in hair and skin and is more abundant in fair-skinned humans. Pheomelanin also may become cancerous when exposed to the ultraviolet rays of the sun. Chemically, pheomelanin differs from eumelanin in that its oligomer structure incorporates the amino acid L-cysteine, as well as DHI (cross-linked 5,6-dihydroxyindole and DHICA 5,6-dihydroxyindole-2-carboxylic acid units. Neuromelanin is the dark pigment present in pigment bearing neurons of four deep brain nuclei: the substantia nigra (in Latin, literally “black substance”), the locus ceruleus (“blue spot”), the dorsal motor nucleus of the vagus nerve (cranial nerve X), and the median raphe nucleus of the pons. Both the substantia nigra and locus ceruleus can be easily identified grossly at the time of autopsy due to their dark pigmentation. In humans, these nuclei are not pigmented at the time of birth, but develop pigment during maturation to adulthood. Although the functional nature of neuromelanin is unknown in the brain, it may be a byproduct of the synthesis of monoamine neurotransmitters for which the pigmented neurons are the only source. The loss of pigmented neurons from specific neuclei are seen in a variety of neurodegenerative diseases. In Parkinson’s disease there is massive loss of dopamine producing pigmented neurons in the substantia nigra. A common finding in advanced Alzheimer’s disease is almost complete loss of the norepinepphine producing pigmented neurons of the locus ceruleus. Neuromelanin has been detected in primates and in carnivores such as cats and dogs. Persons with Parkinson’s disease, a disorder that affects neuromotor functioning, have been shown to have decreased neuromelanin in the substantia nigra as consequence of diminished dopamine synthesis. While no correlation between race and the level of neuromelanin in the substantia nigra has been observed, the significantly lower incidence of Parkinson’s in blacks than in whites has “prompt[ed] some to suggest that cutaneous melanin might somehow serve to protect the neuromelanin in substantia nigra from external toxins.”[9] http://www.seniorpsychiatry.com/pages/articles/lewy.html) . A decreased molecular weight or a decrease in the degree of polymerization of ocular melanin has been proposed to turn the normally anti-oxidant polymer into a pro-oxidant. In its pro-oxidant state, melanin has been suggested to be involved in the causation and progression of macular degeneration and melanoma. Melanin and human adaptation Melnocytes insert granules of melanin into specialized cellular vesicles called melanosomes. These are then transferred into the other skin cells of the human epidermis. The melanosomes in each recipient cell accumulate atop the cell nucleus, where they protect the nuclear DNA from mutations caused by the ionizing radiation of the sun’s ultraviolet rays. In 1995 a landmark study demonstrated that over 80% of humans with red hair or fair skin have a dysfunctional variant of the Mc1r gene [1] (http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=Abstract&list_uids=7581459&qu . (Check). “This discovery provoked interest in determining why there is an unusual prevelance of red hair and pale skin in some northern European populations, specifically Scotland and Ireland. The Out-of-Africa model proposes that modern humans originated in Africa and migrated north to populate Europe and Asia. It is most likely that these migrants had an active Mc1r variant and, accordingly, darker hair and skin (as displayed by indigenous Africans today).” This article from Wikipedia goes on to say that, “Concordant with the migration north, the selective pressure maintaining dark skin decreased as radiation from the sun became less intense. Thus variations in Mc1r began to appear in the human population, resulting in the paler skin and red hair of some Europeans. Studies find no evidence for positive selection driving these changes. Instead, the absence of high levels of solar radiation in northern Europe relaxed the selective pressure on active Mc1r, allowing the gene to mutate into dysfunctional variants without reproductive penalty, then propagate by genetic drift. [10].” I think otherwise. I think that a lowered immune response to stress of Northern Europeans is also reflected in a lower expression of the Mc1r gene. I think that the same stressors that are present in today’s Western diet are responsible in part or whole for the white race. See the graph listed below. Our immunity is our basic survival mechanism and over the years it has been responsibly for the survival of the species. There are numerous things in the environment and in the diet, such as bacteria, toxins and viruses that can potentially harm the body. Consequently, our bodies must be able to distinguish between “self” and “non-self”. Dr. Peter J. D’Adamo notes in his book, Live Right For Your Type, that, “Our blood type antigen is a powerful marker of self to our immune system. It is a guardian at nature’s gate, allowing access to friends and preventing entry to foes.” When man began farming and animal husbandry that brought about a dramatic change in his diet. Consumption of the agricultural diet introduced new challenges to the immune system. As such, the appearance of Blood Group A, a new ABO Blood Type, resulted from man’s new diet. Along with this new blood type came an alteration in its immune function. Instead of having antibodies against Type A antigens as the existing blood type B had, this new Type A blood had antibodies against Type B antigens, a complete opposite of Type B blood. What caused this flip in the antibodies? My take on this is that Type B people were accustomed to eating herbaceous materials such as leafy greens and full of the sugar glucose, whereas, the new farming diet incorporated more starch and protein than primarily glucose. The immune system, regardless of blood type, recognizes Type O as “self”. Some of the Type O antigens are converted to either Type A or Type B antigens resulting in Type A and Type B blood types. An enzyme exists in mineralocorticoid target tissues to prevent over stimulation by glucocorticoids. That enzyme, 11-beta hydroxysteroid dehydrogenenase type II (Protein:HSD11B2), catalyzes the deactivation of glucocorticoids to 11-dehydro metabolites. Licorice is known to be an inhibitor of this enzyme and chronic consumption can result in a condition known as pseudohyperaldosteronism. There should be a link between licorice consumption and diabetes. Sugar and salt is a leitmotif of Swedish cooking according to Mark Kurlansky, author of Salt – A World History. The Swedish word for it is sockersaltad. One of the most infamous uses of sockersaltad in Scandinavia is salt lakrits, salted licorice candy. The Dutch are also afflicted with the same craving along with other Scandinavian countries. By the consumption of sockersaltad, the glucocorticoids are or should be stimulated. This should increase the incidences of diabetes. In 1984 Borch-Johnson et al in Norway and Sweden first suggested there was an inverse correlation between type 1 and duration of breast feeding. This was not supported in 3 subsequent studies but in 1999 Elliott looked at the incidence of type 1 diabetes in children from 10 different countries which suggested that a consumption of specific milk proteins (beta-casein A and B) correlated with type 1 diabetes incidence. Different breeds of cows produce varying amounts of these proteins which produce a peptide called beta-casomorphin-7 which has immune suppressing activity. As the body gets burned by oxidizing phenols such as tyrosine, the tissues get burned. As such, the body, in a process of healing itself, cuts back on some enzyme in the pathway. As the enzyme tyrosinase becomes less effective, there is less activity in melanin. The mutation is in the receptor Mc1r. PHENOL is a poisonous caustic compound: a poisonous caustic crystalline compound obtained from coal, wood tar, or benzene, used in the manufacture of resins, dyes, and pharmaceuticals and as an antiseptic and disinfectant.

Floyd’s Herbivore Feeding Deterrents (Thorns) Hypothesis on Cause of Alzheimer’s Disease And Others Diseases

Floyd’s Herbivore Feeding Deterrents (Thorns) Hypothesis on Cause of Alzheimer’s Disease And Others Diseases Paul Ewald, professor of biology and author of the book, Plague Time, The New Germ Theory of Disease, wrote, “Cancer, heart attacks, stroke, Alzheimer’s disease, and infertility are like the acts of an anonymous vandal”. In his book, Excitotoxins, The Taste that Kills, Russell L. Blaylock, M.D. notes that a multitude of seemingly unrelated diseases, such as strokes, heart attacks, arthritis, brain injury, migraine headaches, and cancer are associated with excitotoxins such as glutamate, calcium and cell death. Dr. Blaylock writes, “It appears that several of the excitotoxins, including glutamate and aspartate, work by opening calcium channels, at least on certain subtypes of receptors”. My theory or hypothesis is that the influx of calcium into the cell is not the cause of the cell death, but is in response to the threat of toxicity posed by that “anonymous vandal” that Paul Ewald writes about. This so-called “vandal” or “vandals”, in my opinion, are agents of Nature that are there to enforce Nature’s balance. Nature employes the use of phenolic compounds (I call them “thorns”) in plants as feeding deterrents to herbivores. These compounds can be grouped in three major groups: alkaloids, terpenoids, and phenolic compounds (mostly phenylpropanoids). The oxidation of these thorns creates a significant risk for our bodies by the release of excessive free radicals. Alkaloids (poisons), are synthesized principally from amino acids. These nitrogen-containing compounds protect plants from a variety of herbivorous animals, and many possess pharmacologically important activity. Our immune system’s defenses were not designed to overcome these deterrents over the long run. Consequently, as we learn to avoid them, or reduce the activity of our enzymes that oxidize them, the better off we are at consuming those plants. Dr. Blaylock lists the amino acids glutamate, aspartate and cysteine as excitotoxins that are found in nature. Phenolic compounds are widely distributed in the plant kingdom. Wheat appears to be well protected by Nature as it is quite high in alkaloids. Dr. Blaylock wrote, under the topic of, A Cascade of Destruction: The Free Radicals, that, “Once this cascade of destruction is triggered by the influx of calcium, the whole process proceeds with the explosiveness of a nuclear chain reaction”. I think that the process is initiated when our enzymes act on the inhibitors. I see this as nature’s way of enforcing its Balance of Nature by using agents such as “thorns” or inhibitors. Others have said that the redox process inside the cell is likened to a severe thunderstorm. When our bodies try to oxidize the “thorns” they become emboldened – just the opposite of what you would expect. Many of nature’s inhibitors come into the body via the diet and end up in VLDL cholesterol. The cholesterol remnants apparently containing these “thorns” are eventually transferred to LDL cholesterol. APOE is essential for the normal catabolism of triglyceride-rich lipoprotein constituents. As herbivores, including man, attempt to metabolize these “thorns” in the lipoproteins, excessive damage to the tissues ensue. Consequently, as a process of adaptation to the “thorns” in the diet, the body has mutated and produced two additional forms or alleles of the APO-E gene. Notice the difference in the different gene products. The APO-E2 does not bind tightly to its cell surface receptor and the “thorns” have difficulty getting into the cells. However, a consequence of the APO-E2 mutation is the build-up is a terminal disease called hyperlipoproteinemia. APO-E3 is the most common form of the allele and is probably the wild-type. That leaves APO-E4. Let’s see what kind of a change it offers in response to the “toxins” in the triglyceride-rich lipoprotein constituents. APO-E4 can bind to its receptor but binds to cholesterol to a lesser degree than APO-E3. As a result, people with APO-E4 allele often have high levels of cholesterol in their blood. So, the alternate APO-E alleles E2 and E4 result in less affinity of either the receptor or cholesterol itself. This lesser affinity for cholesterol on the part of APO-E4 is largely responsible for the familial or late onset form of Alzheimer’s disease.