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Clinical Features Associated With Hypocalcemia
Neuromuscular irritability
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Neurological signs and symptoms
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Mental status
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Ectodermal changes
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Smooth muscle involvement
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Ophthalmologic manifestations
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Cardiac
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Charlie's Restoration Giveaway #2 (Entire Home EMF Mitigation & Protection Along With Personal Protection) - Click Here To Enter
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Dear Carnivore Dieters, A Muscle Meat Only Diet is Extremely Healing Because it is a Low "vitamin A" Diet. This is Why it Works so Well...
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Sickle Cell Disease and Phenylketonuria (PKU): You May Have the Genes, But Your Diet Determines Your Symptoms
Sickle cell trait is much more common among Africans in Africa than among African-Americans. But sickle cell anemia is more common here. How can that be? The answer is very simple – EPIGENETI…
acountrydoctorwrites.blog
Thiocyanate Rich Foods
Thiocyanate Rich Foods Foods rich in Potassium Thiocyanate/Dioscovite – helps prevent sickling Staples: African yams (...
journeytohealthsca.blogspot.com
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‘America’s Other Drug Problem’ — Overprescribing
Another name for overprescribing medications is “polypharmacy.” The issue has been snowballing in the last decade as Big Pharma continues to develop new drugs. The stated intent is the hope of lengthening life through chemistry, but the goal is growing revenue.
childrenshealthdefense.org
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9 Signs of Folate Deficiency & How to Reverse It - Dr. Axe
A folate deficiency is serious, as folate is needed for copying and synthesizing DNA, producing new cells, and supporting nerve and immune functions.
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Time to assume that health research is fraudulent until proven otherwise? - The BMJ
Health research is based on trust. Health professionals and journal editors reading the results of a clinical trial assume that the trial happened and that the results were honestly reported. [...]More...
blogs.bmj.com
From the article
As he described in a webinar last week, Ian Roberts, professor of epidemiology at the London School of Hygiene & Tropical Medicine, began to have doubts about the honest reporting of trials after a colleague asked if he knew that his systematic review showing the mannitol halved death from head injury was based on trials that had never happened. He didn’t, but he set about investigating the trials and confirmed that they hadn’t ever happened. They all had a lead author who purported to come from an institution that didn’t exist and who killed himself a few years later. The trials were all published in prestigious neurosurgery journals and had multiple co-authors. None of the co-authors had contributed patients to the trials, and some didn’t know that they were co-authors until after the trials were published. When Roberts contacted one of the journals the editor responded that “I wouldn’t trust the data.” Why, Roberts wondered, did he publish the trial? None of the trials have been retracted.
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Drug-induced immune hemolytic anemia: MedlinePlus Medical Encyclopedia
Drug-induced immune hemolytic anemia is a blood disorder that occurs when a medicine triggers the body's defense (immune) system to attack its own red blood cells. This causes red blood cells to break
Drug-induced immune hemolytic anemia is a blood disorder that occurs when a medicine triggers the body's defense (immune) system to attack its own red blood cells. This causes red blood cells to break down earlier than normal, a process called hemolysis.
Anemia is a condition in which the body does not have enough healthy red blood cells. Red blood cells provide oxygen to body tissues.
Normally, red blood cells last for about 120 days in the body. In hemolytic anemia, red blood cells in the blood are destroyed earlier than normal.
In some cases, a drug can cause the immune system to mistake your own red blood cells for foreign substances. The body responds by making antibodies to attack the body's own red blood cells. The antibodies attach to red blood cells and cause them to break down too early.
Drugs that can cause this type of hemolytic anemia include:
- Cephalosporins (a class of antibiotics), most common cause
- Dapsone
- Levodopa
- Levofloxacin
- Methyldopa
- Nitrofurantoin
- Nonsteroidal anti-inflammatory drugs (NSAIDs)
- Penicillin and its derivatives
- Phenazopyridine (Pyridium)
- Quinidine
Nitrofurantoin and glucose-6-phosphate dehydrogenase deficiency: a safety review - PubMed
Nitrofurantoin, a broad-spectrum antibiotic available since 1953, is used widely for the treatment of urinary tract infections as it often retains activity against drug-resistant uropathogens. It is contraindicated in pregnant women at term, and in neonates. Like trimethoprim/sulfamethoxazole...
pubmed.ncbi.nlm.nih.gov
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VITAMIN DEPENDENCY
by Andrew W. Saul
"Man is a food-dependent creature. If you don't feed him, he will die. If you feed him improperly, part of him will die." (Emanuel Cheraskin, MD, DMD)
Dependency is a fact of life. The human body is dependent on food, water, sleep, and oxygen. Additionally, its internal chemistry is absolutely dependent on vitamins. Without adequate vitamin intake, the body will sicken; virtually any prolonged vitamin deficiency is fatal. Surely this constitutes a dependency in the generally accepted sense of the word.
Nutrient deficiency of long standing may create an exaggerated need for the missing nutrient, a need not met by dietary intakes or even by low-dose supplementation. Recently (1), Robert P. Heaney, M.D., used the term "long latency deficiency diseases" to describe illnesses that fit this description. He writes:
"(I)nadequate intakes of many nutrients are now recognized as contributing to several of the major chronic diseases that affect the populations of the industrialized nations. Often taking many years to manifest themselves, these disease outcomes should be thought of as long-latency deficiency diseases. . . (I)nadequate intakes of specific nutrients may produce more than one disease, may produce diseases by more than one mechanism, and may require several years for the consequent morbidity to be sufficiently evident to be clinically recognizable as "disease." Because the intakes required to prevent many of the long-latency disorders are higher than those required to prevent the respective index diseases, recommendations based solely on preventing the index diseases are no longer biologically defensible."
There are at least two key concepts presented here:
The first is, "Inadequate intakes of specific nutrients may produce more than one disease." This exactly supports Dr. William Kaufman's statements to this effect 55 years ago, when he wrote that, in considering "different clinical entities one cannot exclude the possibility that they may be caused by the same etiologic agent, acting in different ways. For example, in experimental animals, it has been shown that the lack of a single essential nutrient can produce a variety of dissimilar clinical disorders in different individuals of the same species. . . (O)ne might not suspect that the same etiologic factor, lack of a specific essential nutrient, was responsible for each of the various clinical syndromes of the same tissue deficiency disease which is permitted to develop at different rates in different individuals of the same species." (2)
While amyotrophic lateral sclerosis, progressive muscular atrophy, progressive bulbar palsy, and primary lateral sclerosis are not all the same illness, they and the other neuromuscular diseases may have a common basis: unacknowledged, untreated long-term vitamin dependency. Therefore, each may respond to an orthomolecular approach such as that successfully used by Dr. Frederick R. Klenner (3) for multiple sclerosis and myasthenia gravis, half a century ago.
The second key point Dr. Heaney makes is that vitamin "intakes required to prevent many of the long-latency disorders are higher than those required to prevent the respective index diseases." This confirms Dr. Abram Hoffer's observations to this effect some 40 years ago, when he treated prisoners of war presenting severe, protracted nutrient deficiencies.
Dr. Hoffer wrote (4) that when released, after as much as 44 months of captivity, "only 75 percent had survived. They had lost about one-third of their body weight. In camp they suffered from classical scurvy, beriberi, pellagra, many infections, and from protein and calorie deficiency. They were rehabilitated in hospitals and were given doses of vitamins that were then considered high. Since then these Hong Kong veterans have suffered from a variety of physical and psychiatric conditions." However, "the history of a small sample, about 12, is much different, for they have been taking nicotinic acid (niacin) 3 grams per day. These 12 have recovered and remain well as long as they take this quantity of vitamin regularly.
"About 35 years ago (in the 1930s and 1940s) it was reported that some chronic pellagrins required at least 600 milligrams per day of vitamin B3 to prevent the return of pellagra symptoms. This was astonishing then and unexplainable since pellagra as a nicotinic acid deficiency disease should have yielded to vitamin (small) doses. Today the concept of vitamin-dependency disease has developed. It is based upon the realization that there is a much wider range of need for nutrients than was believed to be true then.
"A person is said to be vitamin dependent if his requirements for that vitamin are much greater (perhaps 100-fold greater or more) than is the average need for any population. The optimum need is that quantity which maintains the subject in good health, not that quantity which barely keeps him free of pellagra. From this point of view the Hong Kong veterans have become vitamin B-3 dependent as a result of severe and prolonged malnutrition. It is likely that any population similarly deprived of essential nutrients for a long period of time will develop one or more dependency conditions."
Thirty years ago, in another paper (5), Dr. Hoffer made this statement:
"The newer concept of vitamin-dependent disease changes the emphasis from simply dietary manipulation to consideration of the endogenous needs of the organism. It comes within the field of orthomolecular disease. . . The borderline between vitamin deficiency and vitamin-dependency conditions is merely a quantitative one when one considers prevention and cure." (p. 251)
The differentiation between deficiency and dependency is dose. Every patient that was ever helped by high-dose nutrient therapy lends support to the concept of vitamin dependency. By the same token, symptoms resulting from inappropriate and abrupt termination of large doses of nutrients provide equally good evidence for vitamin dependency. While deprivation of low doses of vitamin C causes scurvy, abrupt termination of high maintenance doses may cause its own set of problems. Called "rebound scurvy," this includes classical scorbutic symptoms, as well as a predictable relapse of illness that had already responded to high-dose therapy.
Writes Robert F. Cathcart, M.D.:
"There is a certain dependency on ascorbic acid that a patient acquires over a long period of time when he takes large maintenance doses. Apparently, certain metabolic reactions are facilitated by large amounts of ascorbate and if the substance is suddenly withdrawn, certain problems result such as a cold, return of allergy, fatigue, etc. Mostly, these problems are a return of problems the patient had before taking the ascorbic acid. Patients have by this time become so adjusted to feeling better that they refuse to go without ascorbic acid. Patients do not seem to acquire this dependency in the short time they take doses to bowel tolerance to treat an acute disease. Maintenance doses of 4 grams per day do not seem to create a noticeable dependency. The majority of patients who take over 10-15 grams of ascorbic acid per day probably have certain metabolic needs for ascorbate which exceed the universal human species need. Patients with chronic allergies often take large maintenance doses.
"The major problem feared by patients benefiting from these large maintenance doses of ascorbic acid is that they may be forced into a position where their body is deprived of ascorbate during a period of great stress such as emergency hospitalization. Physicians should recognize the consequences of suddenly withdrawing ascorbate under these circumstances and be prepared to meet these increased metabolic needs for ascorbate in even an unconscious patient. These consequences of ascorbate depletion which may include shock, heart attack, phlebitis, pneumonia, allergic reactions, increased susceptibility to infection, etc., may be averted only by ascorbate. Patients unable to take large oral doses should be given intravenous ascorbate. All hospitals should have supplies of large amounts of ascorbate for intravenous use to meet this need." (6)
This need is especially serious for the cancer patient, whose exceptionally positive response to mega-ascorbate therapy, and dramatically negative response to ascorbate deprivation, is the very picture of vitamin dependency. Linus Pauling colleague Ewan Cameron, M.D., wrote:
"Ascorbate, however administered, is rapidly excreted in the urine, so that administration should be continuous or at very frequent intervals. Furthermore, exposure to high circulating levels of ascorbate induces over-activity of certain hepatic enzymes concerned with its degradation and metabolism. These enzymes persist for some time after sudden cessation of high intakes, resulting in depletion of circulating levels of ascorbate to well below normal unsupplemented values. This is known as the rebound effect. It causes a sharp decrease in immunocompetence and must be avoided in the cancer patient. Clinical experience has shown that the best responses are observed when vitamin C is administered intravenously, so insuring a high plasma level. However, because long-term continuous intravenous administration is impractical, we recommend an initial intravenous course of ten days duration, followed by continuous maintenance oral regimen." (7)
In short, the body only misses what it needs. That is dependency.
The destructive consequences of alcohol and other negative drug dependencies are taught in elementary schools. At the same time, the consequences of ignoring our positive nutrient dependencies go largely undiscussed even in medical journals. Vitamin dependencies induced by genetics, diet, drugs, or illness are most often regarded as medical curiosities. The Hoffer-Osmond discovery that schizophrenics, forming about one or two percent of the population, are dependent on multi-gram doses of niacin, remains a psychiatric heresy. The Irwin Stone-Linus Pauling idea of population-wide, genetically-based hypoascorbemia has received negative attention, when it has received any attention at all. Yet, writes Dr. Emanuel Cheraskin, "hypovitaminosis C is a very real and common, probably epidemic, problem which clearly has not been properly viewed and surely not adequately reported." (8)
This is not a total surprise. It took decades for medical acknowledgement that biotin and vitamin E are actually essential to health.
Simple cause-and-effect micronutrient deficiency, a doctrine long enamored of by the dietetic profession, is not always sufficient to explain persistent physician reports of megavitamin cures of a number of diseases outside the classically accepted few. Perhaps it is a law of orthomolecular therapy that the reason one nutrient can cure so many different illnesses is because a deficiency of one nutrient can cause many different illnesses.
And if nutrient deficiency is basically about inadequate intake, then dependency is essentially about heightened need. As a dry sponge soaks up more milk, so a sick body generally takes up higher vitamin doses. The quantity of a nutritional supplement that cures an illness indicates the patient's degree of deficiency. It is therefore not a megadose of the vitamin, but rather a megadeficiency of the nutrient that we are dealing with. Orthomolecular practitioners know that with therapeutic nutrition, you don't take the amount that you believe ought to work; rather, you take the amount that gets results. The first rule of building a brick wall is that you have got to have enough bricks. A sick body has exaggeratedly high needs for many vitamins. We can either meet that need, or else suffer unnecessarily.
Until the medical professions fully embrace orthomolecular treatment, "medicine" might well be said to be "the experimental study of what happens when poisonous chemicals are placed into malnourished human bodies."
(Editorial published in the Journal of Orthomolecular Medicine, 2004. Vol. 19 No. 2, p. 67-70. Reprinted with permission.)
This article is also available in German at dependency
References:
1. Heaney RP: Long-latency deficiency disease: insights from calcium and vitamin D. Am J Clin Nutr. 2003; Nov; 78(5):912-9.
2. Kaufman W: The common form of joint dysfunction: Its incidence and treatment. Brattleboro, VT: E. L. Hildreth and Co. 1949; Chapter 5. DoctorYourself.com - Megavitamin Arthritis Treatment, Part 5
3. Smith L: Vitamin C as a Fundamental Medicine: Abstracts of Dr. Frederick R. Klenner, M.D.'s Published and Unpublished Work. Tacoma, WA: Life Sciences Press. 1988. Renamed in 1991: Clinical Guide to the Use of Vitamin C: The Clinical Experiences of Frederick R. Klenner, M.D. https://www.seanet.com/~alexs/ascorbate/198x/smith-lh-clinical_guide_1988.htm
4. Hoffer A: Editorial. J. Orthomolecular Psychiatry. 1974; Vol 3, No 1, p. 34-36.
5. Hoffer A: Mechanism of Action of Nicotinic Acid and Nicotinamide in the Treatment of Schizophrenia. In: Hawkins D and Pauling L: Orthomolecular Psychiatry: Treatment of Schizophrenia. San Francisco: W.H. Freeman. 1973; p. 202-262.
6. Cathcart RF: Vitamin C, titration to bowel tolerance, anascorbemia, and acute induced scurvy." Medical Hypothesis. 1981; 7:1359-1376. How to Determine Vitamin C Dosage
7. Cameron E: Protocol for the use of vitamin C in the treatment of cancer. Medical Hypotheses. 1991; 36:190-194. Also: Cameron E: Protocol for the use of intravenous vitamin C in the treatment of cancer. Palo Alto, California: Linus Pauling Institute of Science and Medicine. Undated, c.1986.
8. Cheraskin E: Vitamin C and fatigue. J. Orthomolecular Medicine, 9:1, p 39-45, First Quarter, 1994.
Andrew Saul is the author of the books FIRE YOUR DOCTOR! How to be Independently Healthy (reader reviews at Reviews of Fire Your Doctor by Andrew W. Saul ) and DOCTOR YOURSELF: Natural Healing that Works. (reviewed at The DOCTOR YOURSELF book )
by Andrew W. Saul
"Man is a food-dependent creature. If you don't feed him, he will die. If you feed him improperly, part of him will die." (Emanuel Cheraskin, MD, DMD)
Dependency is a fact of life. The human body is dependent on food, water, sleep, and oxygen. Additionally, its internal chemistry is absolutely dependent on vitamins. Without adequate vitamin intake, the body will sicken; virtually any prolonged vitamin deficiency is fatal. Surely this constitutes a dependency in the generally accepted sense of the word.
Nutrient deficiency of long standing may create an exaggerated need for the missing nutrient, a need not met by dietary intakes or even by low-dose supplementation. Recently (1), Robert P. Heaney, M.D., used the term "long latency deficiency diseases" to describe illnesses that fit this description. He writes:
"(I)nadequate intakes of many nutrients are now recognized as contributing to several of the major chronic diseases that affect the populations of the industrialized nations. Often taking many years to manifest themselves, these disease outcomes should be thought of as long-latency deficiency diseases. . . (I)nadequate intakes of specific nutrients may produce more than one disease, may produce diseases by more than one mechanism, and may require several years for the consequent morbidity to be sufficiently evident to be clinically recognizable as "disease." Because the intakes required to prevent many of the long-latency disorders are higher than those required to prevent the respective index diseases, recommendations based solely on preventing the index diseases are no longer biologically defensible."
There are at least two key concepts presented here:
The first is, "Inadequate intakes of specific nutrients may produce more than one disease." This exactly supports Dr. William Kaufman's statements to this effect 55 years ago, when he wrote that, in considering "different clinical entities one cannot exclude the possibility that they may be caused by the same etiologic agent, acting in different ways. For example, in experimental animals, it has been shown that the lack of a single essential nutrient can produce a variety of dissimilar clinical disorders in different individuals of the same species. . . (O)ne might not suspect that the same etiologic factor, lack of a specific essential nutrient, was responsible for each of the various clinical syndromes of the same tissue deficiency disease which is permitted to develop at different rates in different individuals of the same species." (2)
While amyotrophic lateral sclerosis, progressive muscular atrophy, progressive bulbar palsy, and primary lateral sclerosis are not all the same illness, they and the other neuromuscular diseases may have a common basis: unacknowledged, untreated long-term vitamin dependency. Therefore, each may respond to an orthomolecular approach such as that successfully used by Dr. Frederick R. Klenner (3) for multiple sclerosis and myasthenia gravis, half a century ago.
The second key point Dr. Heaney makes is that vitamin "intakes required to prevent many of the long-latency disorders are higher than those required to prevent the respective index diseases." This confirms Dr. Abram Hoffer's observations to this effect some 40 years ago, when he treated prisoners of war presenting severe, protracted nutrient deficiencies.
Dr. Hoffer wrote (4) that when released, after as much as 44 months of captivity, "only 75 percent had survived. They had lost about one-third of their body weight. In camp they suffered from classical scurvy, beriberi, pellagra, many infections, and from protein and calorie deficiency. They were rehabilitated in hospitals and were given doses of vitamins that were then considered high. Since then these Hong Kong veterans have suffered from a variety of physical and psychiatric conditions." However, "the history of a small sample, about 12, is much different, for they have been taking nicotinic acid (niacin) 3 grams per day. These 12 have recovered and remain well as long as they take this quantity of vitamin regularly.
"About 35 years ago (in the 1930s and 1940s) it was reported that some chronic pellagrins required at least 600 milligrams per day of vitamin B3 to prevent the return of pellagra symptoms. This was astonishing then and unexplainable since pellagra as a nicotinic acid deficiency disease should have yielded to vitamin (small) doses. Today the concept of vitamin-dependency disease has developed. It is based upon the realization that there is a much wider range of need for nutrients than was believed to be true then.
"A person is said to be vitamin dependent if his requirements for that vitamin are much greater (perhaps 100-fold greater or more) than is the average need for any population. The optimum need is that quantity which maintains the subject in good health, not that quantity which barely keeps him free of pellagra. From this point of view the Hong Kong veterans have become vitamin B-3 dependent as a result of severe and prolonged malnutrition. It is likely that any population similarly deprived of essential nutrients for a long period of time will develop one or more dependency conditions."
Thirty years ago, in another paper (5), Dr. Hoffer made this statement:
"The newer concept of vitamin-dependent disease changes the emphasis from simply dietary manipulation to consideration of the endogenous needs of the organism. It comes within the field of orthomolecular disease. . . The borderline between vitamin deficiency and vitamin-dependency conditions is merely a quantitative one when one considers prevention and cure." (p. 251)
The differentiation between deficiency and dependency is dose. Every patient that was ever helped by high-dose nutrient therapy lends support to the concept of vitamin dependency. By the same token, symptoms resulting from inappropriate and abrupt termination of large doses of nutrients provide equally good evidence for vitamin dependency. While deprivation of low doses of vitamin C causes scurvy, abrupt termination of high maintenance doses may cause its own set of problems. Called "rebound scurvy," this includes classical scorbutic symptoms, as well as a predictable relapse of illness that had already responded to high-dose therapy.
Writes Robert F. Cathcart, M.D.:
"There is a certain dependency on ascorbic acid that a patient acquires over a long period of time when he takes large maintenance doses. Apparently, certain metabolic reactions are facilitated by large amounts of ascorbate and if the substance is suddenly withdrawn, certain problems result such as a cold, return of allergy, fatigue, etc. Mostly, these problems are a return of problems the patient had before taking the ascorbic acid. Patients have by this time become so adjusted to feeling better that they refuse to go without ascorbic acid. Patients do not seem to acquire this dependency in the short time they take doses to bowel tolerance to treat an acute disease. Maintenance doses of 4 grams per day do not seem to create a noticeable dependency. The majority of patients who take over 10-15 grams of ascorbic acid per day probably have certain metabolic needs for ascorbate which exceed the universal human species need. Patients with chronic allergies often take large maintenance doses.
"The major problem feared by patients benefiting from these large maintenance doses of ascorbic acid is that they may be forced into a position where their body is deprived of ascorbate during a period of great stress such as emergency hospitalization. Physicians should recognize the consequences of suddenly withdrawing ascorbate under these circumstances and be prepared to meet these increased metabolic needs for ascorbate in even an unconscious patient. These consequences of ascorbate depletion which may include shock, heart attack, phlebitis, pneumonia, allergic reactions, increased susceptibility to infection, etc., may be averted only by ascorbate. Patients unable to take large oral doses should be given intravenous ascorbate. All hospitals should have supplies of large amounts of ascorbate for intravenous use to meet this need." (6)
This need is especially serious for the cancer patient, whose exceptionally positive response to mega-ascorbate therapy, and dramatically negative response to ascorbate deprivation, is the very picture of vitamin dependency. Linus Pauling colleague Ewan Cameron, M.D., wrote:
"Ascorbate, however administered, is rapidly excreted in the urine, so that administration should be continuous or at very frequent intervals. Furthermore, exposure to high circulating levels of ascorbate induces over-activity of certain hepatic enzymes concerned with its degradation and metabolism. These enzymes persist for some time after sudden cessation of high intakes, resulting in depletion of circulating levels of ascorbate to well below normal unsupplemented values. This is known as the rebound effect. It causes a sharp decrease in immunocompetence and must be avoided in the cancer patient. Clinical experience has shown that the best responses are observed when vitamin C is administered intravenously, so insuring a high plasma level. However, because long-term continuous intravenous administration is impractical, we recommend an initial intravenous course of ten days duration, followed by continuous maintenance oral regimen." (7)
In short, the body only misses what it needs. That is dependency.
The destructive consequences of alcohol and other negative drug dependencies are taught in elementary schools. At the same time, the consequences of ignoring our positive nutrient dependencies go largely undiscussed even in medical journals. Vitamin dependencies induced by genetics, diet, drugs, or illness are most often regarded as medical curiosities. The Hoffer-Osmond discovery that schizophrenics, forming about one or two percent of the population, are dependent on multi-gram doses of niacin, remains a psychiatric heresy. The Irwin Stone-Linus Pauling idea of population-wide, genetically-based hypoascorbemia has received negative attention, when it has received any attention at all. Yet, writes Dr. Emanuel Cheraskin, "hypovitaminosis C is a very real and common, probably epidemic, problem which clearly has not been properly viewed and surely not adequately reported." (8)
This is not a total surprise. It took decades for medical acknowledgement that biotin and vitamin E are actually essential to health.
Simple cause-and-effect micronutrient deficiency, a doctrine long enamored of by the dietetic profession, is not always sufficient to explain persistent physician reports of megavitamin cures of a number of diseases outside the classically accepted few. Perhaps it is a law of orthomolecular therapy that the reason one nutrient can cure so many different illnesses is because a deficiency of one nutrient can cause many different illnesses.
And if nutrient deficiency is basically about inadequate intake, then dependency is essentially about heightened need. As a dry sponge soaks up more milk, so a sick body generally takes up higher vitamin doses. The quantity of a nutritional supplement that cures an illness indicates the patient's degree of deficiency. It is therefore not a megadose of the vitamin, but rather a megadeficiency of the nutrient that we are dealing with. Orthomolecular practitioners know that with therapeutic nutrition, you don't take the amount that you believe ought to work; rather, you take the amount that gets results. The first rule of building a brick wall is that you have got to have enough bricks. A sick body has exaggeratedly high needs for many vitamins. We can either meet that need, or else suffer unnecessarily.
Until the medical professions fully embrace orthomolecular treatment, "medicine" might well be said to be "the experimental study of what happens when poisonous chemicals are placed into malnourished human bodies."
(Editorial published in the Journal of Orthomolecular Medicine, 2004. Vol. 19 No. 2, p. 67-70. Reprinted with permission.)
This article is also available in German at dependency
References:
1. Heaney RP: Long-latency deficiency disease: insights from calcium and vitamin D. Am J Clin Nutr. 2003; Nov; 78(5):912-9.
2. Kaufman W: The common form of joint dysfunction: Its incidence and treatment. Brattleboro, VT: E. L. Hildreth and Co. 1949; Chapter 5. DoctorYourself.com - Megavitamin Arthritis Treatment, Part 5
3. Smith L: Vitamin C as a Fundamental Medicine: Abstracts of Dr. Frederick R. Klenner, M.D.'s Published and Unpublished Work. Tacoma, WA: Life Sciences Press. 1988. Renamed in 1991: Clinical Guide to the Use of Vitamin C: The Clinical Experiences of Frederick R. Klenner, M.D. https://www.seanet.com/~alexs/ascorbate/198x/smith-lh-clinical_guide_1988.htm
4. Hoffer A: Editorial. J. Orthomolecular Psychiatry. 1974; Vol 3, No 1, p. 34-36.
5. Hoffer A: Mechanism of Action of Nicotinic Acid and Nicotinamide in the Treatment of Schizophrenia. In: Hawkins D and Pauling L: Orthomolecular Psychiatry: Treatment of Schizophrenia. San Francisco: W.H. Freeman. 1973; p. 202-262.
6. Cathcart RF: Vitamin C, titration to bowel tolerance, anascorbemia, and acute induced scurvy." Medical Hypothesis. 1981; 7:1359-1376. How to Determine Vitamin C Dosage
7. Cameron E: Protocol for the use of vitamin C in the treatment of cancer. Medical Hypotheses. 1991; 36:190-194. Also: Cameron E: Protocol for the use of intravenous vitamin C in the treatment of cancer. Palo Alto, California: Linus Pauling Institute of Science and Medicine. Undated, c.1986.
8. Cheraskin E: Vitamin C and fatigue. J. Orthomolecular Medicine, 9:1, p 39-45, First Quarter, 1994.
Andrew Saul is the author of the books FIRE YOUR DOCTOR! How to be Independently Healthy (reader reviews at Reviews of Fire Your Doctor by Andrew W. Saul ) and DOCTOR YOURSELF: Natural Healing that Works. (reviewed at The DOCTOR YOURSELF book )
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Role of Mercury Toxicity in Hypertension, Cardiovascular Disease, and Stroke
J Clin Hypertens (Greenwich). 2011;13:621–627. ©2011 Wiley Periodicals, Inc.Mercury has a high affinity for sulfhydryl groups, inactivating numerous enzymatic reactions, amino acids, and sulfur‐containing antioxidants (N‐acetyl‐L‐cysteine, ...
www.ncbi.nlm.nih.gov
Absract: Mercury has a high affinity for sulfhydryl groups, inactivating numerous enzymatic reactions, amino acids, and sulfur‐containing antioxidants (N‐acetyl‐L‐cysteine, alpha‐lipoic acid, L‐glutathione), with subsequent decreased oxidant defense and increased oxidative stress. Mercury binds to metallothionein and substitute for zinc, copper, and other trace metals, reducing the effectiveness of metalloenzymes. Mercury induces mitochondrial dysfunction with reduction in adenosine triphosphate, depletion of glutathione, and increased lipid peroxidation. Increased oxidative stress and reduced oxidative defense are common. Selenium and fish containing omega‐3 fatty acids antagonize mercury toxicity. The overall vascular effects of mercury include increased oxidative stress and inflammation, reduced oxidative defense, thrombosis, vascular smooth muscle dysfunction, endothelial dysfunction, dyslipidemia, and immune and mitochondrial dysfunction. The clinical consequences of mercury toxicity include hypertension, coronary heart disease, myocardial infarction, cardiac arrhythmias, reduced heart rate variability, increased carotid intima‐media thickness and carotid artery obstruction, cerebrovascular accident, generalized atherosclerosis, and renal dysfunction, insufficiency, and proteinuria. Pathological, biochemical, and functional medicine correlations are significant and logical. Mercury diminishes the protective effect of fish and omega‐3 fatty acids. Mercury inactivates catecholaminei‐0‐methyl transferase, which increases serum and urinary epinephrine, norepinephrine, and dopamine. This effect will increase blood pressure and may be a clinical clue to mercury‐induced heavy metal toxicity. Mercury toxicity should be evaluated in any patient with hypertension, coronary heart disease, cerebral vascular disease, cerebrovascular accident, or other vascular disease. Specific testing for acute and chronic toxicity and total body burden using hair, toenail, urine, and serum should be performed.
Severe elemental mercury poisoning managed with selenium and N-acetylcysteine administration
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More Thoughts on Thiamine Deficiency - Hormones Matter
I am reporting actual cases of thiamine deficiency that are a sampling of hundreds of similar cases that I encountered over the years.
www.hormonesmatter.com
David PS
Member
The Adderall Shortage is Causing Mass Chaos for Patients, Doctors and Pharmacies
“My life is turned upside down. My ability to deliver both at work and in my personal life the way I’m used to is compromised.”
www.vice.com
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A 2010 article by Dr. Hyman - Worth reading
www.huffpost.com
How to Rid Your Body of Mercury and Other Heavy Metals: A 3-Step Plan to Recover Your Health
I will provide you with a clear, three-step plan to help you detoxify from mercury and other heavy metals and recover your health. I have used this plan successfully and safely with patients over the last 10 years.
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Burning Feet Syndrome - A Review
( Attached ) This review includes treatment suggestions but it does not list vaccine adverse events as a cause of the condition. See the articles below for evidence of vaccine indused neuropathy.
pubmed.ncbi.nlm.nih.gov
www.ncbi.nlm.nih.gov
www.ncbi.nlm.nih.gov
www.truthforhealth.org
( Attached ) This review includes treatment suggestions but it does not list vaccine adverse events as a cause of the condition. See the articles below for evidence of vaccine indused neuropathy.
Postvaccinal inflammatory neuropathy: peripheral nerve biopsy in 3 cases - PubMed
Autoimmune inflammatory polyneuropathy (PN) can be triggered by vaccination. We report 3 such cases. A 36-year-old female nurse presented 15 days after a hepatitis B vaccination (HBV) with acute sensory disturbances in the lower limbs. She had severe ataxia but no weakness. Cerebrospinal fluid...
pubmed.ncbi.nlm.nih.gov
Spectrum of neurological complications following COVID-19 vaccination
COVID-19 vaccines have brought us a ray of hope to effectively fight against deadly pandemic of COVID-19 and hope to save lives. Many vaccines have been granted emergency use authorizations by many countries. Post-authorization, a wide spectrum of neurological ...
www.ncbi.nlm.nih.gov
Post COVID‐19 vaccine small fiber neuropathy
www.ncbi.nlm.nih.gov
Vaccine Injury Resources - Truth for Health Foundation
Vaccine Injury Treatment Guide: Your Roadmap to Recovery A comprehensive guide for COVID vaccine injury self treatment. DOWNLOAD Recommended Vaccine Injury Laboratory Tests A list of laboratory tests provided by Truth For Health Foundation designed to provide answers to anyone who suspects or...
www.truthforhealth.org
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Dr Jennifer Daniels - Iodine, Gelatin, Water, Rice, Cholesterol and Other Great things for The Body
View: https://www.bitchute.com/video/0loEDMYDI73s/
April 2022. Dr Daniels is 65 years old!!!
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FDA confirms Adderall shortage in the US
The FDA has confirmed a nationwide shortage of Adderall.
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Taurine for fluoride and mercury toxicity
pubmed.ncbi.nlm.nih.gov
pubmed.ncbi.nlm.nih.gov
Neuroprotective influence of taurine on fluoride-induced biochemical and behavioral deficits in rats - PubMed
Epidemiological and experimental studies have demonstrated that excessive exposure to fluoride induced neurodevelopmental toxicity both in humans and animals. Taurine is a free intracellular β-amino acid with antioxidant and neuroprotective properties. The present study investigated the...
pubmed.ncbi.nlm.nih.gov
Hepatoprotective effects of taurine against mercury induced toxicity in rats - PubMed
An attempt has been made to study the influence of taurine on mercury intoxicated rats. The animals were treated with sublethal dose of mercuric chloride (2 mg/kg body wt.) for 30 days. During the mercury treatment, the level ofAspartate transaminase(AST), Alanine transaminase (ALT) and Alkaline...
pubmed.ncbi.nlm.nih.gov
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Searchable database for psychiatric drugs side effects
This database was put together by the group that published the study on how anti-psychotic drugs are mostly useless for the symptoms of the disease they are prescribed for and also create a state of learned hopelessness. For a horror-story, do a search for any of the SSRI drugs and look at the...
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Serotonin Syndrome
Serotonin syndrome is a potentially life-threatening syndrome that is precipitated by the use of serotonergic drugs and overactivation of both the peripheral and central postsynaptic 5HT-1A and, most notably, 5HT-2A receptors. This syndrome consists of ...
www.ncbi.nlm.nih.gov
Symptomatology Triad Associated With Serotonin Syndrome
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Taurine and Sepsis
pubmed.ncbi.nlm.nih.gov
pubmed.ncbi.nlm.nih.gov
www.ncbi.nlm.nih.gov
Mechanism of taurine reducing inflammation and organ injury in sepsis mice - PubMed
The fundamental basis for the pathogenesis of sepsis is an inflammatory imbalance, which is considered to be the main target for treatment. Taurine is an intracellular free amino acid that has anti-inflammatory and antioxidant effects. To investigate the protective mechanism of taurine in...
pubmed.ncbi.nlm.nih.gov
Protective effect of taurine on sepsis‑induced lung injury via inhibiting the p38/MAPK signaling pathway - PubMed
Sepsis, a leading cause of acute lung injury (ALI), is characterized by an overwhelming systemic inflammatory response and widespread organ injury, particularly in the lungs. Taurine, an intracellular free amino acid, has been used for the treatment of various diseases, including lung injury...
pubmed.ncbi.nlm.nih.gov
Taurine Administration Ablates Sepsis Induced Diaphragm Weakness
Infection induced diaphragm weakness is a major contributor to death and prolonged mechanical ventilation in critically ill patients. Infection induced muscle dysfunction is associated with activation of muscle proteolytic enzymes, and taurine is known ...
www.ncbi.nlm.nih.gov
EMF Mitigation - Flush Niacin - Big 5 Minerals
