Reply To: Scripts 2014

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    The objective of this study was to investigate the effects of a copper loaded chitosan scaffold on bone regeneration in critical-sized calvarial defects in rats. Chitosan scaffolds and copper-chitosan scaffolds were fabricated and characterized by scanning electron microscopy (SEM). Chitosan and copper-chitosan scaffolds were implanted into 5 mm diameter critical-sized calvarial defects in Fisher 344 male rats. Empty defects (no scaffolds) were included as a control. After 4 weeks, the rats were sacrificed for microcomputed tomography (micro-CT) and histological analysis of new bone tissue development. Microscopy images revealed the uniformly porous structure of chitosan and copper-chitosan scaffolds. Significant bone regeneration was noted in the defects treated with copper-chitosan scaffolds when evaluated using micro-CT and histological analysis, when compared with other groups tested. On analysis of the micro-CT scans, an eleven-fold and a two-fold increase in the new bone volume/total volume (BV/TV) % was found in defects treated with the copper-chitosan scaffolds, when compared to empty defects and chitosan scaffolds, respectively. This study demonstrated the suitability of copper-crosslinked chitosan scaffolds for bone tissue engineering and provides the first evidence that inclusion of copper ions in scaffolds can enhance tissue regeneration. © 2014 Wiley Periodicals, Inc. J Biomed Mater Res Part B: Appl Biomater, 2014
    A Brief History of The Health Support Uses of Copper
    Throughout history, healers have understood the value of copper in obtaining and maintaining optimum health. Whether topically applied or ingested, many forms of copper and copper compounds (such as copper carbonate, copper silicate, copper oxide, copper sulfate, copper chloride, etc.) were used throughout history for the treatment of disease. Copper has been used for medicinal purposes as far back as ancient Egypt, Greece and Rome as well as in the ancient Aztec civilization.
    Ancient Uses of Copper
    An ancient Egyptian medical text, known as the Smith Papyrus (circa 2400 B.C.), mentions using copper as a sterilization agent for drinking water and wounds. Another ancient text, known as the Ebers papyrus (circa 1500 B.C.) mentions the use of copper for headaches, “trembling of the limbs,” burns, and itching. The island of Cyprus provided a readily available supply of copper to Greece and is known to have provided much of the copper needed for the empires of ancient Phoenicia and Rome as well. It has also been documented that Israel’s Timna Valley provided copper for the Pharaohs.
    Hippocrates (circa 400 B.C.), known as the father of modern medicine (and for whom the doctor’s Hippocratic oath was named) mentions copper as a treatment for leg ulcers associated from varicose veins. The Greeks also sprinkled a powder of copper oxide and copper sulfate on open wounds and treated wounds with a mixture of honey and red copper oxide.
    In the first century A.D., the book De Materia Medica by Dioscorides, describes using verdigris (which they made by exposing metallic copper to vinegar steam to form copper acetate) in combination with copper sulfate as a remedy for bloodshot eyes, inflamed eyes, “fat in the eyes”, and cataracts.
    Evidence from the time of Roman physician Aulus Cornelius Celsus (14 to 37 A.D.), tells us that copper and its derivatives were firmly established as important drugs. In his book, De Medicina, Celsus details numerous uses for copper, along with specific instructions for the preparation of the particular form of copper recommended for each disease or condition. Among his specific directions are a copper oxide mixture made with raisin wine, saffron and myrrh for the treatment of venereal disease and a copper mixture made with rose oil for chronic ulcers.
    Pliny (23 to 79 A.D.) described a number of remedies involving copper. Black copper oxide with honey was used to kill intestinal worms and purge the stomach. In diluted form, nose drops were used to “clear the head”; eardrops relieved ear discomfort and infection, and taken by mouth it relieved mouth sores and ulcers. Diluted copper mixtures were also used for “eye roughness,” “eye pain and mistiness.”
    The ancient Aztec civilization also used copper for medical purposes, including gargling with a copper mixture for sore throats. In ancient India and Persia, copper was used to treat lung diseases. Copper compounds such as malachite and copper oxide were used on boils and other skin conditions. Copper acetate and copper oxide were used for eye infections. Evidence also shows us that nomadic Mongolian tribes used copper sulfate, taken by mouth, to treat venereal ulcers.
    19th Century Copper
    The first recorded observation of copper’s role in the immune system in modern times was published in 1867 when it was reported that, during the cholera epidemics in Paris of 1832, 1849 and 1852, copper workers were immune to cholera.
    In 1885, the French physician, Luton, reported using copper acetate in his practice to treat arthritic patients. For external application he made a salve of hog’s lard and 30% neutral copper acetate. For internal treatment, he used pills containing 10 mg. of copper acetate.
    In 1895, in a published review of the pharmacological actions of copper compounds, copper arsenate was reported to treat acute and chronic diarrhea as well as dysentery and cholera. An organic complex of copper developed by Bayer was shown to have curative powers in the treatment of tuberculosis. Copper treatment for tuberculosis continued until the 1940s.
    20th Century Copper
    As early as 1912, patients in Germany were treated for facial epithelioma with a mixture of copper chloride and lecithin, suggesting that copper compounds might assist anti-cancer activity.
    Recent work with mice in the U.S. has shown that treatment of solid tumors with non-toxic doses of various organic complexes of copper markedly decreased tumor growth and metastasis and thus increased survival rate. These copper complexes did not kill cancer cells but caused them to revert to normal cells. Based on work in the treatment of cancers using copper complexes, researchers have found that these same complexes may prevent or retard the development of cancers in mice under conditions where cancers are expected to be induced.
    First observed in rats in 1936, numerous studies have drawn attention to the relationship between copper deficiency and heart disease, which effect has now been traced to both a deficiency in copper and an imbalance in the copper-to-zinc ratio in the body.
    In 1939, the German physician, Werner Hangarter, noticed that Finnish copper miners were unaffected by arthritis as long as they worked in the mining industry. This observation led Finnish medical researchers plus the Germans, Hangarter and Lübke, to successfully use a mixture of copper chloride and sodium salicylate to treat patients suffering from rheumatic fever, rheumatoid arthritis, neck and back problems, and sciatica.
    A Manual of Pharmacology and its Applications to Therapeutics and Toxicology, published by W. B. Saunders Company in 1957 recommends the use of 0.5 gram of copper sulfate, dissolved in a glass of water, in a single dose, or three doses of 0.25 gram fifteen minutes apart, to induce vomiting. Interestingly, Pliny (23 – 79 A.D.) also mentions using copper for just this purpose.
    Copper aspirinate has been shown not only to be more effective in the treatment of rheumatoid arthritis than aspirin alone, but it has been shown to prevent or even cure the ulceration of the stomach often associated with aspirin therapy. More than 140 copper complexes of non-steroidal anti-inflammatory agents (aspirin and ibuprofen, for example) have been shown to be more active than their parent compounds.
    It has been demonstrated that copper complexes such as copper aspirinate and copper tryptophanate, markedly increase healing rate of ulcers and wounds. For example, copper complexes heal gastric ulcers five days sooner than other reagents. Further, it has been shown that, whereas non-steroidal anti-inflammatory drugs, such as ibuprofen and enefenamic acid suppress wound healing, copper complexes of these drugs promote normal wound healing while at the same time retaining anti-inflammatory activity.
    With reports of seizures in animals and humans who had significant and prolonged copper deficiencies in their diets, researches postulated that copper plays a role in the prevention of seizures. Research uncovered that organic compounds which are not themselves anti-convulsants, exhibit anticonvulsant activity when combined with copper. Further, it was found that copper complexes of all anti-epileptic drugs are more effective and less toxic than their parent drugs.
    The 1973 work by Dr. L.M. Klevay at the U.S. Department of Agriculture, Human Nutrition Research Center pointed to a relationship between copper and cholesterol. In subsequent work, published in 1975, Dr. Klevay theorized that a metabolic imbalance between zinc and copper — with more emphasis on copper deficiency than zinc excess – is a major contributing factor in coronary heart disease.
    Subsequent work by other investigators has shown that copper complexes also can have a valuable role in the minimization of damage to the aorta and heart muscle as oxygenated blood reperfuses into tissues following myocardial infarction. This action is based on the anti-inflammatory action of copper complexes.
    It has been speculated that the reason that the heart attack rate in France is lower than in the rest of Europe is because of the significant consumption by the French of red wine, which has a higher copper content than white wine because it is prepared with the skin of the grape intact.
    Copper’s role in the immune system has recently been supported by observations that individuals suffering from Menke’s disease (an inherited disease in which there is defective copper absorption and metabolism) generally die of immune system-related phenomena and other infections. Further, animals deficient in copper have been shown to have increased susceptibility to bacterial pathogens such as salmonella and listeria. This kind of evidence has led researchers to suggest that copper compounds not only can cure various conditions, but can aid in the prevention of disease.
    Copper in the 21st Century
    Copper jewelry worn directly on skin has been used for a hundred years or more as a remedy for many ailments, including arthritis. Now, copper bracelets to ease joint and arthritis pain are ubiquitous in health food stores, and health magazines and catalogues.
    With the understanding that copper deficiency can result in gray hair, skin wrinkles, crow’s feet, varicose veins and saggy skin, copper has recently been touted as a “Fountain of Youth” for its ability to improve the elastic fiber in skin, increase skin flexibility, and act as an anti-wrinkle treatment. It has even been said to be able to return gray hair back to its natural color.
    As modern researches continue to investigate the role of copper in the functioning of the human body, the efficacy of copper as a trace element critical to human health and wellness is slowly but surely being discovered . . . or, shall we say, rediscovered, since the incredible healing properties of copper have been understood and used throughout human history.
    Copper sulphate as a fish disease treatment
    Copper sulphate (sulfate) can be used to treat a range of parasites affecting marine aquarium fish. Protozoan parasites such as Crytocaryon (marine Ich), Trichodina, Amyloodium (marine velvet disease) as well as monogenean flukes – Dactylogyrus (gill flukes) and Gyrodactylus (skin fluke). It is not recommended for treating freshwater fish.
    Using copper
    Copper is active against many marine protozoan and monogenean parasites, but its use can be complicated. Copper is easily de-activated because it reacts with calcareous material often found in marine aquariums, i.e. coral and limestone, to form insoluble copper carbonate.
    The solubility of copper is highly dependent on pH. As pH increases above 7, copper precipitates out of solution – 100x increase for every one-unit increase in pH. The danger is that should the pH of the tank drop, that is become more acidic, then the level of ‘free’ copper can quickly rise to toxic levels as the precipitated copper is re-dissolved. In addition, organic matter also binds up copper.
    When treating parasite disease, the free copper level must be maintained between 0.15 – 0.20 mg/litre. If the concentration drops below this range it will not kill the parasites. If it rises above this level then it will kill the fish! Copper will also adversely affect invertebrates. Because of these complications it is advised never to treat the community tank but instead treat affected fish in a separate hospital tank.
    A stock solution is prepared using 1 gram of copper sulphate (CuSO4.5H2O) to 250 mls distilled water. This solution now contains 1 mg copper per millilitre. The initial dose is 0.15 mg copper per litre. Therefore if the tank contains say 200 litres then the dose required will be 200 x 0.15 mgs copper = 30 grams = 30 mls of stock solution.
    The copper level of the tank should be measured immediately and thereafter twice daily using a test-kit that measures in increments of at least 0.05 mg/litre. If the residual copper level in the tank drops below 0.15 mg/litre – then add additional doses of 0/05 mg/ litre of the stock solution until the optimum level is restored. Using the same example 200 x 0.05 mgs copper = 10 mgs copper = 10 mls stock solution
    Copper can easily be removed by activated carbon– Charcoal
    Useful conversions are:
    ppm = mg/litre i.e. 5 ppm = 5 mg / litre
    mg / litre x 3.785 = mg / gall (US) i.e 5 mg / litre = 18.9 mg / gall (US)
    mg/ litre x 4.546 = mg / gall (UK) i.e 5 mg / litre = 22.7 mg / gall (UK)
    To convert imperial gallons to US gallons multiply by 1.2
    Other useful figures:
    1 ounce = 28.35 grams
    1% solution =
    10 ml per litre
    10 gram per litre
    38 gram per gall (US)
    45 gram per gall (UK)
    Disinfectant and method of making
    The process of making a disinfectant comprises electrolytically generating silver ions in a solution of citric acid and water to form an aqueous solution of silver citrate. Preferably, the solution of citric acid and water comprises a solution of approximately 5.0% to 10% citric acid in water by volume. A potential difference of 12 volts to 50 volts provides a flow of silver ions in the range of 0.1 amperes to 0.5 amperes per square inch. A more fuller explanation of the content of the solution within the ion chamber 170 will be described in greater detail hereinafter
    The silver and citric acid formulations were prepared using 100/100 silver:silver electrodes. The electrodes were immersed in 1.0, 5.0 and 10% citric acid solutions and a current was applied for approximately two hours. The solutions were stored for 24 hours to allow for precipitation. The solutions were filtered using #2 Whatman filter paper. The final pH was adjusted to 6.0 with sodium carbonate and sodium bicarbonate
    US 6197814 B1
    A non-toxic environmentally friendly aqueous disinfectant is disclosed for specific use as prevention against contamination by potentially pathogenic bacteria and virus. The aqueous disinfectant is formulated by electrolytically generating silver ions in water in combination with a citric acid. The aqueous disinfectant may include a suitable alcohol and/or a detergent. The aqueous disinfectant has been shown to be very effective at eliminating standard indicator organisms such as staphylococcus aureus, samonella cholerasuis and Pseudomonas aeruginosa.
    TOP A
    [F1]More then likely made in a lab in Canada and the USA—since they deal with this type of technology by bioengineering the insects to attack and disable people
    [F2]Limited exposure—
    [F3]INTERESTING COMMENT you have to wonder with this statement —if they know something no one else knows— is it going to spread because they spread it— why would the bug not die off or subside??? See these are the things that make one go hmm
    [F4]Another part of this —makes one go hmmm — gm organism—to fight another type of gm organism—hmmm did we just step into a different time line where people are being victoms of genetically engineered warfare??makes you wonder
    [F5]Africa and asia and now it iis finding fertile ground in latin America—hmm that is a huge huge flight from that part of the planet to the latin American countries
    [F6]SO the US mosquitos did not have the pathogen and the Mexican side did??good genetic engineering and a good double blind study—this is what it appears to me..
    [F7]Does sound encouraging
    TOP B
    Show of the Month October 18 2014
    “And those who were seen dancing were thought to be insane by those who could not hear the music.”
    Human genetic research uncovers how omega-6 fatty acids lower bad cholesterol
    Olive oil more stable and healthful than seed oils for frying food
    Has selenium loading as part treatment/prevention of Ebola been suppressed since 1995
    Addiction Therapy for Drugs, Alcohol, Caffeine, and Sugar
    Parkinson’s disease can migrate from gut to brain
    Altering gut bacteria might mitigate lupus
    Human genetic research uncovers how omega-6 fatty acids lower bad cholesterol
    October 16, 2014
    Cell Press
    Supplementing the diet with omega-6 polyunsaturated fatty acids has beneficial effects on heart health by lowering “bad” LDL cholesterol and raising “good” HDL cholesterol,[F1] but the underlying mechanisms involved are poorly understood. Now research based on the genetic information from over 100,000 individuals of European ancestry has uncovered a gene that affects blood cholesterol levels through the generation of a compound from omega-6 polyunsaturated fatty acids, called lipoxins. The study, publishing online October 16 in the Cell Press journal Cell Metabolism, also provides additional evidence that aspirin assists in preventing heart attacks by promoting lipoxin production. These insights could change the way doctors care for patients at increased risk for heart disease.—“Our findings could help pave the way for novel therapeutic approaches to prevent cardiovascular disease and its associated clinical sequelae, including heart attacks and stroke,” says senior author Dr. Ivan Tancevski, of the Innsbruck Medical University, in Austria.–In assessing the genetic information from the study participants of European descent, Dr. Tancevski and his colleagues identified one gene, called Alox5, that codes for an enzyme that generates lipoxins from omega-6 polyunsaturated fatty acids to help the body get rid of bad cholesterol. Lipoxins have anti-inflammatory properties.—The team found that aspirin, which is widely used to prevent heart attacks and stroke, also acts on this pathway. In experiments conducted in mice, aspirin stimulated production of lipoxins that then promoted the transport of excess cholesterol to the liver, where it is excreted through bile. Treating mice that had atherosclerotic plaques in their blood vessels with aspirin even caused the plaques to regress[F2]. “Aspirin is known to prevent cardiovascular disease due to its antithrombotic and anti-inflammatory effects. We now identified a third mechanism by which aspirin may confer protection,” says Dr. Tancevski.–The researchers went a step further in generating and testing chemically modified lipoxins mimetics that were even more effective at lowering LDL cholesterol, suggesting that new lipoxin-based specific drugs could provide greater benefits for patients.–Story Source–The above story is based on HYPERLINK “” \t “_blank” materials provided by HYPERLINK “” \t “_blank” Cell Press. Note: Materials may be edited for content and length.–Journal Reference-Ivan Tancevski et al. The Arachidonic Acid Metabolome Serves as a Conserved Regulator of Cholesterol Metabolism. Cell Metabolism, 2014; DOI: HYPERLINK “” \t “_blank” 10.1016/j.cmet.2014.09.004
    Good sources of Omega 6 – Almond oil-peanut oil-sesame seed oil ( unroasted) sunflower oil—evening primrose oil—wheat germ oil—
    Olive oil more stable and healthful than seed oils for frying food
    October 22, 2014
    American Chemical Society
    Frying is one of the world’s most popular ways to prepare food — think fried chicken and french fries. Even candy bars and whole turkeys have joined the list. But before dunking your favorite food in a vat of just any old oil, consider using olive. Scientists report in ACS’ Journal of Agricultural and Food Chemistry that olive oil withstands the heat of the fryer or pan better than several seed oils to yield more healthful food.–Mohamed Bouaziz and colleagues note that different oils have a range of physical, chemical and nutritional properties that can degrade oil quality when heated. Some of these changes can lead to the formation of new compounds that are potentially toxic. By-products of heating oil can also lower the nutritional value of the food being fried. Bouaziz’s team wanted to find out which cooking oil can maintain its quality under high heat and repeated use.–The researchers deep- and pan-fried raw potato pieces in four different refined oils — olive, corn, soybean and sunflower — and reused the oil 10 times. They found that olive oil was the most stable oil for deep-frying at 320 and 374 degrees Fahrenheit, while sunflower oil degraded the fastest when pan-fried at 356 degrees. They conclude that for frying foods, olive oil maintains quality and nutrition better than seed oils.–The authors acknowledge funding from the Ministère de l’Enseignement Supérieur et de la Recherche Scientifique and the Ministère de l’Agriculture, Tunisia.
    Story Source–The above story is based on HYPERLINK “” \t “_blank” materials provided by HYPERLINK “” \t “_blank” American Chemical Society. Note: Materials may be edited for content and length.-Journal Reference–Akram Zribi, Hazem Jabeur, Felix Aladedunye, Ahmed Rebai, Bertrand Matthäus, Mohamed Bouaziz. Monitoring of Quality and Stability Characteristics and Fatty Acid Compositions of Refined Olive and Seed Oils during Repeated Pan- and Deep-Frying Using GC, FT-NIRS, and Chemometrics. Journal of Agricultural and Food Chemistry, 2014; 62 (42): 10357 DOI: HYPERLINK “” \t “_blank” 10.1021/jf503146f
    Has selenium loading as part treatment/prevention of Ebola been suppressed since 1995?
    (There are ONLY three articles in Pubmed for Selenium & Ebola)
    Computational genomic analysis of hemorrhagic fever viruses. Viral selenoproteins as a potential factor in pathogenesis – 1997
    A number of distinct viruses are known as hemorrhagic fever viruses based on a shared ability to induce hemorrhage by poorly understood mechanisms, typically involving the formation of blood clots (“disseminated intravascular coagulation”). It is well documented that selenium plays a significant role in the regulation of blood clotting via its effects on the thromboxane/prostacyclin ratio, and effects on the complement system.
    Selenium has an anticlotting effect, whereas selenium deficiency has a proclotting or thrombotic effect. It is also well documented that extreme dietary selenium deficiency, which is almost never seen in humans, has been associated with hemorrhagic effects in animals.
    Thus, the possibility that viral selenoprotein synthesis might contribute to hemorrhagic symptoms merits further consideration. Computational genomic analysis of certain hemorrhagic fever viruses reveals the presence of potential protein coding regions (PPCRs) containing large numbers of in-frame UGA codons, particularly in the -1 reading frame. In some cases, these clusterings of UGA codons are very unlikely to have arisen by chance, suggesting that these UGAs may have some function other than being a stop codon, such as encoding selenocysteine.
    For this to be possible, a downstream selenocysteine insertion element (SECIS) is required. Ebola Zaire, the most notorious hemorrhagic fever virus, has a PCR with 17 UGA codons, and several potential SECIS elements can be identified in the viral genome. One potential viral selenoprotein may contain up to 16 selenium atoms per molecule. Biosynthesis of this protein could impose an unprecedented selenium demand on the host, potentially, leading to severe lipid peroxidation and cell membrane destruction, and contributing to hemorrhagic symptoms. Alternatively, even in the absence of programmed selenoprotein synthesis, it is possible that random slippage errors would lead to increased encounters with UGA codons in overlapping reading frames, and thus potentially to nonspecific depletion of SeC in the host.
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    Review: micronutrient selenium deficiency influences evolution of some viral infectious
    Recently emerged viral infectious diseases (VIDs) include HIV/AIDS, influenzas H5N1 and 2009 H1N1, SARS, and Ebola hemorrhagic fevers. Earlier research determined metabolic oxidative stress in hosts deficient in antioxidant selenium (Se) (<1 μMol Se/L of blood) induces both impaired human host immunocompetence and rapidly mutated benign variants of RNA viruses to virulence. These viral mutations are consistent, rather than stochastic, and long-lived. When Se-deficient virus-infected hosts were supplemented with dietary Se, viral mutation rates diminished and immunocompetence improved. Herein is described the role of micronutrient Se deficiency on the evolution of some contemporary RNA viruses and their subsequent VIDs. Distinguishing cellular and biomolecular evidence for several VIDs suggests that environmental conditions conducive to chronic dietary Se deprivation could be monitored for bioindicators of incipient viral virulence and subsequent pathogenesis.
    Selenium Medicine: And the Rising Tide of Mercury
    HYPERLINK “; \t “_blank”
    Using Glutathione and Selenium to Treat Viral Infections
    HYPERLINK “; \t “_blank”…infections
    Selenium Deficiency and Ebola Virus
    During the spring of 1995 Ebola virus created havoc in the African nation of Zaire. Researchers studying the ebola virus found many similarities between it and the HIV virus. For example, like HIV, Ebola has the potential to create several proteins requiring selenium. However, in the case of Ebola, the selenium content appears much higher than in HIV. It could be as much as ten times higher. (17)
    According to Dr. Taylor, the Ebola virus behaves very much like HIV. When selenium levels in infected cells drop, Ebola reproduces and aggressively searches for cells with more selenium, spreading the infection throughout the body. The population of Zaire was found to be deficient in selenium (may be because the soil in this country is deficient in selenium.) This may partially explain why both HIV virus and Ebola virus are rampant in Zaire. Normal immune defenses against the virus is handicapped by selenium deficiency.
    Selenium Reduces Bacterial Blood Poisoning
    When selenium was used in large dosages with other antioxidants such as vitamins C and E it was found to reduce the hospital-induced sepsis (bacterial blood poisoning) and acute respiratory distress syndrome by 50 percent. (18)
    HYPERLINK “; \t “_blank”…at-rem.htm
    Theoretical Evidence that the Ebola Virus Zaire Strain May Be Selenium-Dependent: A Factor in Pathogenesis and Viral Outbreaks?
    Ethan Will Taylor1 and Chandra Sekar Ramanathan
    A theoretical analysis of the genomic structure of the Ebola virus Zaire strain reveals the existence of several open reading frames (ORFs) containing large numbers of inframe UGA codons. This clustering of UGA codons is very unlikely to have arisen by chance, and raises the possibility that these ORFs may encode selenoproteins, since, in addition to its usual role as a stop codon, UGA can under certain conditions encode selenocysteine. The other major requirement for selenocysteine insertion at UGA codons appears to be met in this case, due to the presence of selenocysteine insertion sequences (SECIS) in stable stem-loop structures in the appropriate Ebola Zaire mRNAs. Specifically, there is a SECIS in the 3’untranslated region of the nucleoprotein mRNA, where the largest potential selenoproteins are encoded, one of which may contain up to 16 selenium atoms per molecule. The expression of this hypothetical protein could impose an unprecedented selenium demand upon the host, potentially leading to severe lipid peroxidation and cell membrane destruction. This could also contribute to the characteristic hemorrhaging caused by intravascular blood clotting, due to the thrombotic effect of Se deficiency. The possibility that this gene might contribute to the extreme pathogenicity of the Zaire strain of Ebola virus by this mechanism is also consistent with the observation that this potential selenoprotein gene is not present in the Ebola Reston strain, which was not pathogenic in humans. ———It has long been apparent that an increased susceptibility to infectious diseases is common in malnourished human populations. This has traditionally been viewed as simply a consequence of the fact that the immune system must be maintained by adequate nutrition in order to function optimally. Only recently has data begun to accumulate in support of the idea that nutritional factors may sometimes have a direct effect on pathogens, and that passage through nutritionally deficient hosts may facilitate evolutionary changes in infectious agents. In this communication, we present theoretical molecular evidence that the highly pathogenic Zaire strain of the Ebola virus may be dependent on the trace mineral selenium (Se), due to the presence in the Ebola genome of several open reading frames (ORFs) containing clusters of up to 17 inframe UGA codons, which potentially encode the rare amino acid selenocysteine (SeC). We will argue that, by analogy to other known examples, this raises the possibility that Se deficiency in host populations may actually foster viral replication, possibly triggering outbreaks and perhaps even facilitating the emergence of more virulent viral strains. —-This concept is not unprecedented: a classical example of a nutrient effect on viral replication is the well documented induction of endogenous retrovirus expression in cells cultured in arginine-deficient media (recently reviewed by Becker1). Note that arginine is an essential component of many viral proteins. Thus, paradoxically, in this case viral replication appears to be triggered by a deficiency of something the virus requires. This would most likely involve some sort of repressor type of mechanism. Based on the data that we will review here, we suggest that, for some viruses, an analogous situation may exist in the case of Se. —-Aside from the nonspecific protection that can be achieved in vivo by a nutritional boost in immune function, specific antiviral effects have been claimed for various antioxidant nutrients, and Se in particular. A surprising range of in vitro and in vivo antiviral activities has been reported for various simple Se compounds, including inhibition of hepatitis B in humans, influenza virus in culture, and retroviruses like the mouse mammary tumor virus and bovine leukemia virus (reviewed by Schrauzer and Sacher2 and by Taylor et al.3). Recent work has also demonstrated the in vitro activity of Se compounds against the human immunodeficiency virus, HIV-1.4,5 —The most compelling data pertain to Keshan disease, a classical Se-deficiency disease manifested as a non-obstructive cardiomyopathy. Chinese investigators suspected an infectious agent might be a cofactor, and eventually isolated coxsackievirus from the hearts of Keshan disease victims; the combination of the virus and Se deficiency produced cardiomyopathy in mice.6 Recently, Beck and coworkers have shown that in Se-deficient mice, even a normally nonvirulent strain of coxsackievirus B3 can produce myocarditis similar to that seen in Keshan disease7 (and references therein). Significantly, during passage through Se-deficient mice, the virus mutates into a more virulent strain that is pathogenic even in normal animals on Se-adequate diets. —–Along similar lines, it is of considerable interest that Ziegler has pointed out a correlation between high rates of endemic Kaposi’s sarcoma (KS) in African subsistence farmers and geographic regions in Africa where the soils are of volcanic origin.8 These include regions surrounding the entire East African Rift Valley and the Nigeria-Cameroon border. It is widely documented that low Se levels in plants and Se deficiency syndromes of livestock are common in areas with soils of volcanic origin: the Rift Valley is a typical example. Furthermore, Se deficiency in humans has been specifically documented in northern Zaire (e.g.9). Since recent evidence strongly suggests that KS involves a novel herpes virus, this association of KS in Africa with low Se areas suggests a possible analogy to Keshan disease and coxsackievirus. Significantly, we have also found very large ORFs with start codons and up to 11 in-frame UGA codons in herpesviruses like cytomegalovirus and Epstein Barr virus (reported at 8th ICAR, Taylor et al.5), suggesting that some herpesviruses may also be “Se-dependent”.—Rather than being indirect (e.g. involving a nonspecific antioxidant effect), the possibility that some antiviral effects of Se might involve virally-encoded selenoproteins has apparently not been considered until very recently.3,5 Even though first demonstrated about ten years ago, it has still has not become widely appreciated that SeC can be encoded by the UGA codon, which usually serves as a stop codon in the genetic code. Conventional analyses of potential protein coding regions in genes still do not usually discriminate UGA from the other two stop codons, and thus they fail to reveal that proteins might be encoded in regions containing UGA codons. Such regions are routinely assumed to be inactive due to the presence of stop codons, which is probably true in the vast majority of cases, because efficient SeC incorporation is only possible when the mRNA contains a cis-acting signal known as a SeC insertion sequence.10 However, as shown in Figure 2, such consensus SeC insertion sequences capable of forming the required characteristic stem-loop RNA structures are present in several Ebola mRNAs that also encode UGA-rich ORFs. —We recently reported a similar potential for selenoproteins to be encoded in HIV-13,5,11 and in coxsackievirus B3,11 in regions overlapping known genes. In both cases, the link between Se deficiency and the associated viral diseases (AIDS and viral myocarditis, respectively) is strongly supported by an extensive body of literature (reviewed in2,3,7,12). –In the Ebola virus genome (Zaire strain), there are several ORFs with highly significant clusters of inframe UGA codons. Overlapping the major nucleoprotein (NP) gene, there are two ORFs in the -1 reading frame, containing 17 and 11 UGA codons, respectively (Figure 1). The first ORF has excellent potential to be expressed by a ribosomal frameshift from the NP coding region, due to the presence of an “ideal” heptameric shift sequence and an RNA pseudoknot (PK) 8 bases downstream (Figure 3A). This frameshift site comes very near the beginning of the ORF, and could permit the formation of a fusion protein consisting of the N-terminal 314 residues of NP fused to a 181 residue C-terminal module potentially containing 16 SeC residues, encoded in the -1
    Potential Selenoprotein Genes in Ebola Virus
    Figure 1. UGA-rich open reading frames (ORFs) overlapping the Ebola Zaire nucleoprotein (NP) coding region. The figure shows a schematic of the three reading frames for a portion of the NP gene, with stop codons shown as vertical lines. The dotted lines are UGA stop codons, which can potentially encode selenocysteine. There are two UGA-rich ORFs -1 to the main NP reading frame, ORF1 with 17 and ORF2 with 11 inframe UGA codons. Neither ORF1 or ORF2 has a start codon. ORF1 could be expressed as an NP fusion protein containing a selenoprotein module, by means of a frameshift at either one of two potential -1 frameshift sites, shown with an arrow symbol as A and B. These frameshift sites are shown in detail in Figure 3. ORF2 is less likely to be a functional gene, because it could only be expressed from an edited or spliced NP mRNA, and splicing has never been demonstrated in filoviruses (see text). However, there is a complete splice acceptor (SA) site at the very beginning of the ORF, and several potential upstream splice donor sites (not shown). The only other requirement for selenoprotein synthesis, a selenocysteine insertion sequence (SECIS) in the required stem-loop structure, is present in the 3’-untranslated region of the NP mRNA (Figure 2A). (Figure produced using the beta version of the gene finder program, developed in collaboration with Dr. Dan Everett, University of Georgia).
    Figure 2. Schematic RNA secondary structures predicted for selenocysteine insertion sequences (AUG…AAA…UGA) in the Ebola virus RNA with potential to form the required stemloop structures.10 A: In the 3′-untranslated region of the nucleoprotein mRNA, bases 2758-2836 in GenBank #L11365; E = – 10.1 kcal/mole. B: At the 3′ end of the vp35 mRNA, bases 4094-4160; E = – 13.4 kcal/mole. C: At the 3′ end of the vp30 mRNA, bases 9029-9087; E = – 9.4 kcal/mole. Note that the computed stability of these structures is comparable to that determined by Sanchez et al.19 for the 5′-end stem-loop structures in the Ebola mRNAs (average E = -13.3 kcal/mole, range = -7.6 to -20). All base pairs (shown as ladder rungs) are Watson-Crick except those marked by a slash, which are GU base pairs. These structures were predicted using the Zuker FOLD program20 as implemented in the GCG software package (Program Manual for the Wisconsin Package, Ver. 8, September 1994, Genetics Computer Group, 575 Science Drive, Madison, WI 53711).
    Figure 3. Potential -1 frameshift sites near the beginning of the major UGA-rich ORF in the Ebola Zaire nucleoprotein (NP) coding region, consisting of slippery sequences (underlined) and potential RNA pseudoknots. The location of these sites are indicated by A and B in Figure 1. Codonanticodon interactions of the P- and A-site tRNAs are shown schematically both before (below sequence) and after slippage (above sequence). A: An “ideal” (XXXYYYZ) heptameric -1 frameshift sequence beginning at position 1405 in GenBank #L11365, located 8 nucleotides upstream from a potential pseudoknot. The A-C bulge shown in the major stem probably forms a hydrogen bonded purine-pyrimidine A:C base pair, as these have been observed in some experimental RNA stem structures. The ORF in the -1 reading frame has a total of 17 in-frame UGA codons, 16 of which are downstream from this frameshift site. B: A second near-ideal frameshift site and potential pseudoknot in the NP coding region beginning at position 1582, 178 bases downstream from that shown in A. This could produce a shift into the same ORF with 17 UGA codons, but the potential selenoprotein module would contain only 11 SeC residues (Figure 1).
    frame (bases 1411 to 1953 in GenBank PKs are mere “artifacts”, the chance of the #L11365; subsequent numbering refers to next 16 stop codons following shift site A in the same sequence). Slightly downstream the “blocked” -1 reading frame (Figure 1) all there is a second near-ideal frameshift site being UGA could be estimated as (1/3)16, or and potential PK, also in the NP coding less than one in 43 million. Thus, the high region beginning at position 1582 (Figure significance of this clustering of UGA 3B). This could provide a “second chance” codons, combined with the presence of the to express the selenoprotein module, when-frameshift signals and the distinctive SeC ever the first frameshift failed. This second insertion sequence in the 3′-untranslated resite follows the sixth UGA codon in the gion of the Ebola NP mRNA, argues over-ORF, so a frameshift here would yield a whelmingly that this must be the gene of an potential selenoprotein module with only actual selenoprotein. However, one cannot 11 SeC residues. These redundant frameshift completely rule out the possibility that it sites could provide for either an increased could be a vestigial gene that may have only probability of translating the selenoprotein recently become inactive. module, or for two alternate forms of the NP A second UGA-rich ORF overlapping the fusion protein. Ebola NP gene, encoded between bases 2212
    Because there are three different stop and 2598, contains 11 UGA codons over 129 codons (UGA, UAA and UAG), if this is not residues (ORF2 in Figure 1). This ORF a real gene and the potential shift sites and lacks a start codon, but could be expressed
    Potential Selenoprotein Genes in Ebola Virus
    from an edited or spliced RNA. There is a definite splice acceptor site very near the beginning of the ORF, a CAGA sequence preceded by a pyrimidine rich sequence and an upstream “CURAY” sequence (CUGAC). There are various potential splice donors in the large NP mRNA that could bring this region inframe to the main NP ORF or the upstream selenoprotein ORF with 16 UGAs. Since there are no reports of Ebola replication and transcription in the nuclei of infected cells, this ORF and the associated potential splice sites may be mere artifacts. However, Borna disease virus provides a precedent for nuclear replication/transcription and RNA splicing of a negative non-segmented single stranded RNA virus.13 Thus, we cannot rule out the possibility that splicing of this Ebola mRNA could occur,
    e.g. in the unknown “reservoir” species that is the natural host for Ebola virus. Furthermore, RNA editing can also bring such an “out of frame” ORF into frame, and RNA editing is known to occur in a number of viruses, including Ebola Zaire.
    There are several additional potential selenoprotein ORFs overlapping the first 6 genes of Ebola virus, including the vp24, vp30, vp35 and vp40 regions, all of which have potential SeC insertion sequences in their mRNAs (shown for vp30 and vp35 in Figure 2). Because the sequence has not yet been released, we are unable to report on the polymerase coding region, where we have consistently found potential overlapping selenoprotein genes in a number of other viruses. On the Ebola minus strand genomic RNA there are also potential SeC insertion sequences and several UGA-rich ORFs (up to 9 UGAs), some with start codons, and some potentially expressed from spliced genomic RNAs. On both plus and minus strands, some of these potential genes have start codons in the context of Kozak-like sequences, suggesting they may be programmed to bind ribosomes and initiate protein synthesis. All these data will be presented in detail in a subsequent publication.
    If viruses like HIV-1, coxsackievirus B3 and Ebola do encode selenoproteins, why does all the evidence suggest that dietary Se inhibits viral replication, whereas Se deficiency triggers replication? Why would Se not “feed” the virus? The answer must lie in how viruses use Se.
    As discussed previously,3 due to the inefficiency of frameshifting and SeC insertion mechanisms, these hypothetical viral selenoproteins could only be formed in very small amounts. Thus, in most cases they are not likely to be major structural proteins; some might have regulatory roles, acting in the midphase of the life cycle, and might not even be packaged in virions. If even one such selenoprotein were involved in negative feedback on replication (a repressor type function), decreased levels of that protein would provide the virus a way to respond to low Se levels by leaving the cell in search of a new host. By such a mechanism, the virus could satisfy a basal dependence on Se by escaping from a cell where Se levels had become dangerously low.
    Since Se is an essential antioxidant, critical as a component of glutathione peroxidase in blood cells and liver cells (the very cell types that Ebola and many other viruses prefer to infect), very low Se levels are potentially associated with oxidative stress, lipid peroxidation and cell death. Thus, viral survival might be enhanced by the stimulation of replication under low Se conditions.
    At the same time, host/viral competition for a limited amount of Se – particularly in a malnourished host – could significantly contribute to pathogenesis. This could be particularly acute with Ebola virus, due to the unprecedented high Se requirement implicit in the ORF with 16 UGA codons.
    Dietary Se is also known to have immunopotentiating effects (reviewed in12). Thus, in addition to any direct effects exerted via (hypothetical) viral selenoproteins, Se deficiency can also weaken the immune system’s ability to fight viral infection, permitting increased replication, rapid mutation, and facilitating the emergence of more virulent strains, as Beck et al. suggest in the case of coxsackievirus.7
    Given the unique dependence of selenoprotein genes upon a trace nutrient whose availability varies widely in geographical areas and host populations, the presence and activity of such genes would very likely be strain specific, as we suggested for coxsackievirus.11 This could help explain why some viral strains can be very virulent, even when significant subsets of indigenous populations have antibodies to a similar, presumably much less virulent viral strain, which appears to be true even for filoviruses.14,15
    Certainly, prolonged Se deficiency in a host population could eventually lead to the inactivation and loss of any viral seleno-protein genes. Whether that loss would lead to more virulent strains, or whether those strains might undergo a compensatory attenuation by passage through the host population, would be difficult to predict.
    However, in the case of Ebola virus, there is some reason to think that the presence of a gene with an exceptionally high Se demand could be a factor in the pathogenicity of specific viral strains. This is supported by the striking observation that in the Ebola Reston strain, which was devoid of pathogenicity in the 3 humans that were infected, there is no equivalent to the major potential selenoprotein gene overlapping the NP gene in Ebola Zaire (ORF1 in Figure 1). In the Ebola Reston NP mRNA, the UGA-rich ORFs are disrupted by non-UGA stop codons, there are fewer UGA codons, no analogous frameshift sites or PKs, and no SECIS element in the 3′-UTR. Thus there is no way that this potential selenoprotein gene could be expressed in Ebola Reston. This is a definite major difference at the gene level between these strains, which have previously been considered to be very close genetically. This potential NP-associated selenoprotein gene is also absent in Marburg virus, which also has a lower mortality rate than Ebola Zaire.
    Since the hypothetical selenoprotein overlapping the Ebola Zaire NP gene could only be expressed as an NP fusion protein, it is possible that it could be formed as an NP variant comprising as much as a few percent of the total NP present in virions (more likely a fraction of a percent), in which case it might be possible to detect selenium in Ebola Zaire virions. This percentage would be expected to decrease in late infections if cellular stores of SeC became depleted. In regard to the possible function of such a viral selenoprotein, it is tempting to speculate that it might provide some type of antioxidant protection to the Ebola virions in a rapidly degenerating cellular environment.
    Ebola is classified as a “hemorrhagic fever” virus, and produces the characteristic hemorrhaging due to the formation of blood clots (“disseminated intravascular coagulation”), leading to the obstruction and rupture of small blood capillaries. For this reason, counterintuitively, the anticoagulant drug heparin has been used to reduce the bleeding in Ebola patients.
    It is very well documented that Se plays a significant role in the regulation of blood clotting via its effects on the thromboxane/ prostacyclin ratio. Se has an anti-clotting effect, whereas Se deficiency has a pro-clotting or thrombotic effect.16 Se deficiency has been associated with thrombosis and even hemorrhaging, which has been documented in a number of animals with severe Se deficiency (often artificially induced), but is almost never seen in humans, probably because such an extreme Se deficiency is rarely attained due to the diversity of human diets.
    Thus, the possibility that a rapid depletion of Se due to the formation of viral selenoproteins could be a factor contributing to the severity of the hemorrhagic symptoms is mechanistically very feasible. Our analysis suggests that severe Ebola infections could produce an artificial and extreme Se depletion, resulting in extensive cellular damage due to lipid peroxidation, combined with enhanced thrombosis. This could also contribute to the associated immune deficiency that has been observed in Ebola infections.
    To our knowledge, indicators of Se status and lipid peroxidation have never been examined in Ebola patients. However, Se has apparently been used with great success by the Chinese in the palliative treatment of an infectious hemorrhagic fever.17 Although this did not involve Ebola virus, there are a number of different hemorrhagic fever viruses, and they may share common mechanisms. This example provides yet another reason to expect that pharmacological doses of Se may also have some benefit in Ebola infections.
    In the light of the extensive data on the antiviral effects of Se, the association between coxsackievirus and Keshan disease, and the geographic correlation for KS proposed by Ziegler, it is certainly intriguing that a number of emerging viruses have emanated from these same regions of Africa, that are potentially low in Se. By providing compelling theoretical evidence for the existence of selenoprotein genes in a number of viruses, now including Ebola virus, we have attempted to provide a unifying theoretical model to explain some of these disparate observations.
    Taken as a whole, these observations and theoretical findings suggest the basis for a new paradigm in antiviral chemotherapy: the use of nutritional factors to alter the dynamics of the virus-host interaction so as to reestablish a balance in which the natural host defenses can be more effective. In essence, this is the fundamental concept of orthomolecular medicine, so perhaps this is not such a “new” paradigm after all. What is new and exciting is that this simple concept may be more widely applicable, to more virulent viral diseases, and a broader range of vitamins and minerals – in this case Se -than previously thought possible.
    Finally, because SO2 reacts with Se compounds in soil, making it more difficult for plants to absorb, it has long been suspected that fossil fuel burning and acid rain may be contributing to a gradual decrease of Se in the food chain.18 Thus, like deforestation in jungles and rain forests, the resulting alterations in global Se cycling and distribution may be yet another example of how human activity possibly contributes to the emergence of new viral diseases. Ultimately, it is only a deeper understanding of the impact of these human activities on both microbes and their hosts that will empower us to rectify the resulting imbalances in our shared ecosystem.
    The authors would like to thank Dr. Anthony Sanchez of the Centers for Disease Control and Prevention, Atlanta, GA, for providing the sequence of the Ebola Reston nucleoprotein gene, as well as other unpublished sequences. We are also grateful to Dr. Gerhard Schrauzer of the University of California, San Diego, for making us aware of the previous use of Se to treat an Asian epidemic hemorrhagic fever.17
    Potential Selenoprotein Genes in Ebola Virus
    Becker Y. (1995) Endogenous retroviruses in the human genome – a point of view. Virus Genes 9:211-218.
    Schrauzer G.N., Sacher J. (1994) Selenium in the maintenance and therapy of HIV-infected patients. Chem-Biol Interact 91:199-
    Taylor E.W., Ramanathan C.S., Jalluri R.K., Nadimpalli R.G. (1994) A basis for new approaches to the chemotherapy of AIDS: novel genes in HIV-1 potentially encode selenoproteins expressed by ribosomal frameshifting and termination suppression. J Med Chem 37:2637-2654.
    Sappey C., Legrand-Poels S., Best-Belpomme M., Favier A., Rentier B., Piette J. (1994) Stimulation of glutathione peroxidase activity decreases HIV type 1 activation after oxidative stress. AIDS Res Human Retrovir 10:1451-1461.
    Taylor E.W., Ramanathan C.S., Nadimpalli R.G., Schinazi R.F. (1995) Do some viruses encode selenoproteins? Evaluation of the theory in the light of current theoretical, experimental and clinical data. Antiviral Res 26:A271-86.
    Bai J., Wu S., Ge K., Deng X., Su C. (1980) The combined effect of selenium deficiency and viral infection on the myocardium of mice. Acta Acad Med Sin 2:29-31.
    Beck M.A., Shi Q., Morris V.C., Levander
    O.A. (1995) Rapid genomic evolution of a non-virulent Coxsackievirus B3 in selenium-deficient mice results in selection of identical virulent isolates. Nature Med 1:433-436.
    Ziegler J.L. (1993) Endemic Kaposi’s sarcoma in Africa and local volcanic soils. Lancet 342:1348-1351.
    Vanderpas J.B., Contempre B., Duale N.L., Goossens W., Bebe N., Thorpe R., Ntambue K.,Dumont J., Thilly C.H., Diplock A.T. (1990) Iodine and selenium deficiency associated with cretinism in northern Zaire. Am J Clin Nutr 52:1083-1086.
    10.Berry M.J., Larsen P.R. (1993) Recognition of UGA as a selenocysteine codon in eukaryotes: a review of recent progress. Biochem Soc Trans 21:827-32.
    11.Taylor E.W., Ramanathan C.S., Nadimpalli
    R.G. (1995) A general approach to predicting potential new genes in nucleic acid sequences: application to the human immunodeficiency virus. In: Proceedings of the First World Congress on Computational Biomedicine, Public Health and Biotechnology. Austin, TX: World Scientific, Tokyo, in press.
    12.Taylor E.W. (1995) Selenium and cellular immunity: evidence that selenoproteins may be encoded in the +1 reading frame overlapping the human CD4, CD8 and HLA-DR genes. Biol Trace Elem Res 49:85-95.
    13.Cubitt B., Oldstone C., Valcarcel J., de la Torre J.C. (1994) RNA splicing contributes to the generation of mature mRNAs of Borna disease virus, a non-segmented negative strand RNA virus. Virus Res 34:69-79.
    14.Johnson E.D., Gonzales J.P., Georges A. (1993) Filovirus activity among selected ethnic groups inhabiting the tropical forest of equatorial Africa. Trans R Soc Trop Med Hyg 87:536-538.
    15.Becker S., Feldmann H., Will C., Slenczka
    W. (1992) Evidence for occurrence of filovirus antibodies in humans and imported monkies: do subclinical filovirus infections occur worldwide? Med Microbiol Immunol Berl 181:43-55.
    16.Meydani M. (1992) Modulation of the platelet thromboxane A2 and aortic prostacyclin synthesis by dietary selenium and vitamin E.
    BiolTrace Elem Res 33:79-86.
    17.Hou J.C., Jang Z.F., He, Z.F. (1993) Inhibitory effect of selenite on complement activation and its clinical significance. Chung Hua I Hsueh Tsa Chih 73:645-646.
    18.Frost D.V. (1987) Why the level of selenium in the food chain appears to be decreasing. In:Selenium in Biology and Medicine, G.F. Combs, Jr., J.E. Spallholz, O.A. Levander,
    J.E. Oldfield, Eds. AVI Van Nostrand, New York. Part A, pp. 534-547.
    19.Sanchez A., Kiley M.P., Holloway B.P., Aupern D.D. (1993) Sequence analysis of the Ebola virus genome: organization, genetic elements, and comparison with the genome of Marburg virus. Virus Res 29:215-240.
    20. Zuker M., Steigler P. (1981) Optimal computer folding of large RNA sequences using thermodynamics and auxillary information. Nucl Acids Res 9:133-148.
    Addiction Therapy for Drugs, Alcohol, Caffeine, and Sugar
    by Reagan Houston
    (OMNS Oct 21, 2014) In 1977, Alfred Libby and Irwin Stone (1, 2) realized that addiction is both a disease and poor nutrition. Having lost their appetite, addicts are deficient in vitamin C, other vitamins, minerals, and protein. Genetics and certainly bad lifestyle may have contributed to the disease, but conventional medical therapy is almost useless until their nutrition is restored. In one test, very high doses of vitamin C gave a temporary cure to 30 out of 30 drug addicts. Vitamin C was observed to be an easy, quick, and painless remedy. Ewan Cameron (3) treated cancer patients on heavy doses of opiate-type painkillers. When vitamin C stopped the pain for five cancer patients, the patients wanted no morphine. Importantly, they had no withdrawal symptoms. Stone suggested that ascorbate mimics morphine and probably fits into the opiate receptor sites.
    Libby and Stone’s Protocol for Drug Addicts:
    Work with your physician and stop intake of all drugs or Methadone.
    Dissolve 25 to 85 grams (25,000-85,000 milligrams) of sodium ascorbate powder in milk and have the patient drink it during the day.
    Adjust ascorbate dose up or down according to the estimated drug intake. Continued to adjust dose to almost cause loose stools.
    Give multivitamins, a mineral tablet, and vitamin E and protein powder. Doses were widely variable and adjusted for each patient.
    The vitamin C was started as soon as possible in many divided doses through the day. Other items were also given in divided doses.
    Continued full dose for 4 to 6 days and then slowly decreased the vitamin C down to 10,000 to 30,000 mg/day. Continued the lower doses indefinitely or as needed.
    What Happened to Patients after Starting Vitamin C?
    One incoherent patient received 30,000 mg of vitamin C. In 45 minutes he could hold a normal conversation.
    After 12 to 24 hours, appetite started to return, mental alertness and visual acuity were improved.
    Patient was often amazed that treatment worked without another narcotic.
    After 2 or 3 days, patient felt fine, and he or she could sleep.
    One patient took 45,000 mg of sodium ascorbate in milk. Five hours later, he took a heavy dose of heroin but felt no drug effect. Remarkably, vitamin C had stopped the desire for drugs. (1)
    To repeat: Libby and Stone demonstrated a simple but effective method of temporarily curing 30 out of 30 drug addicts regardless of the type of drug. Their cure is temporary since patients could be followed for only about 30 days. This did not give time to evaluate and treat the basic causes of the addictions. However, treatment for basic causes can proceed with greater expectation of success since the patients have become properly nourished.
    (Reagan Houston, MS, PE (Professional Chemical Engineer), age 91, takes his vitamins. His daily exercise usually includes three flights of stairs in about 50 seconds. His web site is HYPERLINK “; \t “_blank” .)
    1. Libby AF and Stone I. The Hypoascorbemia-Kwashiorkor approach to drug addiction: a pilot study. Orthomolecular Psychiatry. 1977; 6(4): 300-308. Read the complete article at HYPERLINK “; \t “_blank” or Google: “Libby Stone drug addiction 1977.”
    2. Stone I. The Healing Factor: Vitamin C against Disease. 1972, New York. Free full text at HYPERLINK “; \t “_blank” .
    3. Cameron E & Baird GM. Ascorbic acid and dependence on opiates in patients with advanced disseminated cancer. J International Research Communication. 1973; 1(6):33.
    Nutritional Medicine is Orthomolecular Medicine
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