Tony Pantalleresco Radio Show notes – Month October 2014

Tony Pantallaresco

Welcome to Tony Pantalleresco Radio Show notes – Month October 2014

We hope you enjoy these show notes. As always there is so much information it will make your head spin.

Enjoy ….

Show of the Month October 4 2014

Rosemary – Rosmarinus Officinalis
New mosquito-borne virus spreads in Latin America
Mycotoxin present in many types of food deteriorates neuroregeneration
How to make silver citrate
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Rosemary – Rosmarinus Officinalis

Family: Lamiaceae
1 Part Used-2 Abstracts of Published Research on Rosemary – Rosmarinus Officinalis-3 Oligo-elements-4 Vitamins and Minerals-5 Phytochemical Constituents-6 Plant Stem Cell Therapy Indications-6.1 Neurology & Nervous System-6.2 Cardio Vascular System-6.3 Hematology Oncology-6.4 Immunology-6.5 Infectious Disease-6.6 Pulmonary System-6.7 GI – Digestive – Hepatology-6.8 Musculoskeletal System-6.9 Ob Gyn/Reproductive System-6.10 Uro Genital System-6.11 Endocrine System-6.12 Dermatology-6.13 Opthalmology-6.14 Environmental Medicine

Part Used: Young Shoots

NOTE: These indications are only for use with embryonic plant stem cell tissues. Adult plants do not have the same constituents, actions or applications in most cases.

The Rosmarinus officinalis is a woody, perennial herb that is native to the Mediterranean region. Its Latin name, ros-marinus, meaning “dew of the sea,” is presumed to be linked to the plant’s preference to grow near the sea. The Rosmarinus officinalis has gray, scaly bark and grows about 6 feet tall with a spread of 4 to 5 feet. The pungent fragrance exuded by its needle-like leaves is reminiscent of pine. About an inch long, the leaves are evergreen on top and grayish-white underneath. Clusters of delicate, sea-blue flowers blossom in spring and last throughout the summer in warm, humid environments. Common uses include dye, essential oil, ground cover, hair, hedges, incense, insect repellent.

Drug Interaction:

Doxorubicin In a laboratory study, rosemary extract increased the effectiveness of doxorubicin in treating human breast cancer cells. Meanwhile, those taking doxorubicin should consult with a healthcare practitioner before taking rosemary.

Most evidence for rosemary’s medicinal uses comes from clinical experience rather than from scientific studies. However, recent laboratory studies have shown that rosemary slows the growth of a number of bacteria such as E. coli and S. aureus that are involved in food spoilage, and may actually perform better than some commercially used food preservatives.

Alopecia One traditional use of rosemary has been to try to stimulate hair growth. In one study of 86 people with alopecia areata (a disease of unknown cause characterized by significant hair loss, generally in patches), those who massaged their scalps with rosemary and other essential oils (including lavender, thyme, and cedar wood) every day for 7 months experienced significant hair re-growth compared to those who massaged their scalps without the essential oils. It is not entirely clear from this study whether rosemary (or a combination of rosemary and the other essential oils) was responsible for the beneficial effects.

Cancer Both laboratory and animal studies suggest that rosemary’s antioxidant properties may have activity against colon, breast, stomach, lung, and skin cancer cells. However, much more research in this area, including trials involving people, must be conducted before conclusions can be drawn about the value of rosemary for cancer. Carnosol is a naturally occurring phytopolyphenol found in rosemary. Carnosol functions as an antioxidant and anticarcinogenic. In the present study, we compared the antioxidant activity of carnosol and other compounds extracted from rosemary. Carnosol showed potent antioxidative activity in -diphenyl-ß-picrylhydrazyl (DPPH) free radicals scavenge and DNA protection from Fenton reaction. High concentrations of nitric oxide (NO) are produced by inducible NO synthase (iNOS) in inflammation and multiple stages of carcinogenesis.

Rosemary’s Effect on Insulin Levels

Al-Hader, A.A., Z.A. Hasan, and M.B. Aqel. “Hyperglycemic and Insulin Release Inhibitory Effects of Rosmarinus officinalis,” Journal of Ethnopharmacology. Vol 43 1994: An aqueous extract prepared from leaves of rosemary (Rosmarinus officinalis) is widely used in Jordan as a folk remedy for abdominal colic. It has been suggested that rosemary’s volatile oil causes smooth muscle relaxation by inhibiting the increase in cytosolic free calcium concentrations; in turn, a raised cytosolic free calcium level is known to be a trigger for pancreatic insulin release. With this information in consideration, the present study was conducted, using normal and diabetic rabbits, to determine the potential effects of rosemary oil on insulin release and blood glucose levels. It was found that administration of the oil produced a significant change in plasma glucose and serum insulin levels in the normal rabbits, and a significant hyperglycemic effect in the diabetic rabbits. No effect on the fasting plasma glucose levels in normal rabbits was observed. Based on these results, the authors conclude that the volatile oil of rosemary leaves (young shoots) has significant hyperglycemic and insulin release inhibitory effects.

Other Uses:
Dye; Essential; Ground cover; Hair; Hedge; Incense; Repellent.

Abstracts of Published Research on Rosemary – Rosmarinus Officinalis:

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1. J Food Prot. 2009 Aug;72(8):1744-52
In vitro antimicrobial and antioxidant activity of commercial rosemary extract formulations. Klancnik A, Guzej B, Kolar MH, Abramovic H, Mozina SS.

2. J Food Prot. 2009 May;72(5):1107-11
Inhibitory effect of commercial green tea and rosemary leaf powders on the growth of foodborne pathogens in laboratory media and oriental-style rice cakes. Lee SY, Gwon SY, Kim SJ, Moon BK.

3. Prog Neuropsychopharmacol Biol Psychiatry. 2009 Jun 15;33(4):642-50. Epub 2009 Mar 13.
Antidepressant-like effect of the extract of Rosmarinus officinalis in mice: involvement of the monoaminergic system.Machado DG, Bettio LE, Cunha MP, Capra JC, Dalmarco JB, Pizzolatti MG, Rodrigues AL.

4. Lett Appl Microbiol. 2009 Apr;48(4):440-6. Epub 2009 Feb 2.
The antimicrobial activity of four commercial essential oils in combination with conventional antimicrobials. van Vuuren SF, Suliman S, Viljoen AM.

5. J Med Food. 2008 Dec;11(4):741-6.
Anti-inflammatory and antinociceptive effects of Rosmarinus officinalis L. essential oil in experimental animal models.Takaki I, Bersani-Amado LE, Vendruscolo A, Sartoretto SM, Diniz SP, Bersani-Amado CA, Cuman RK.

6. Harefuah. 2008 Oct;147(10):783-8, 838.
The treatment of respiratory ailments with essential oils of some aromatic medicinal plants. Rakover Y, Ben-Arye E, Goldstein LH.

7. J Nutr. 2008 Nov;138(11):2098-105.
Rosmarinic acid antagonizes activator protein-1-dependent activation of cyclooxygenase-2 expression in human cancer and nonmalignant cell lines. Scheckel KA, Degner SC, Romagnolo DF.

8. Neuroreport. 2008 Aug 27;19(13):1301-4.
Beneficial effects of carnosic acid on dieldrin-induced dopaminergic neuronal cell death. Park JA, Kim S, Lee SY, Kim CS, Kim do K, Kim SJ, Chun HS.

9. Int J Food Sci Nutr. 2008 Nov-Dec;59(7-8):691-8.
Chemical composition and antifungal activity of rosemary (Rosmarinus officinalis L.) oil from Turkey. Ozcan MM, Chalchat JC.

Oligo-elements:

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B, Cu, Fe, K, Mg, Mn, Na, P, Se, Si, Zn.

Vitamins and Minerals:

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B-1, B-2, B-3, C, Calcium.

Phytochemical Constituents:

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1,8-Cineole, 13-O-Acetyloleanolic-Acid, Acetic-Acid, Alpha-Amyrin, Alpha-Humulene, Alpha-Phellandrene, Alpha-Pinene, Alpha-Selinene, Alpha-Terpinene, Alpha-Terpineol, Alpha-Thujone, Apigenin, AR-Curcumene, Ascorbic-Acid, Benzyl-Alcohol, Beta-Amyrin, Beta-Carotene, Beta-Elemene, Beta-Phellandrene, Beta-Pinene, Beta-Sitosterol, Beta-Thujone, Betulin, Betulinic-Acid, Borneol, Bornyl-Acetate, Caffeic-Acid, Camphene, Camphor, Carnosic-Acid, Carnosol, Carvacrol, Carvone, Caryophyllene, Caryophyllene-Oxide, Chlorogenic-Acid, Delta-3-Carene, Delta-Cadinene, Diosmetin, Diosmin, Dipentene, Elemol, Ethanol, Eugenol-Methyl-Ether, Fenchone, Fiber, Gamma-Terpinene, Genkwanin, Geraniol, Glycolic-Acid, Hesperidin, Hispidulin, Hispiduloside, Isoborneol, Isobornyl-Acetate, Isobutyl-Acetate, Isopulegol, Isorosmanol, Labiatic-Acid, Limonene, Luteolin, Luteolin-3′-O-(3-O-Acetyl)-Beta-D-Glucuronide,Luteolin-3′-O-(4-O-Acetyl)-Beta-D Glucuronide, Luteolin-7-Glucoside, Methyl-Eugenol, Myrcene, Myrtenol, Neo-Chlorogenic-Acid, Nepetin, Nepetrin, Octanoic-Acid, Oleanolic-Acid, P-Cymene, Pectin, Piperitenone, Rosmadial, Rsomanol, Rosmaridiphenol, Rosmarinic-Acid, Rosmariquinone, Sabinene, Safrole, Salicylates, Sinensetin, Squalene, Styrene, Tannin, Terpinen-4-OL, Terpinolene, Thymol, Toluene, Trans-Anethole, Trans-Carveol, Trans-Pinocarveol, Ursolic-Acid, Verbenone, Zingiberine
Diterpenes such as picrosalvin (= carnosol), carnosolic acid, rosmariquinone and salicylates.

Miscellaneous; rosmaricine, the triterpenes ursolic acid, oleanolic acid & derivatives.

Carnosol is a naturally occurring phytopolyphenol found in rosemary. Carnosol functions as antioxidant and anticarcinogenic. In the present study, we compared the antioxidant activity of carnosol and other compounds extracted from rosemary. Carnosol showed potent antioxidative activity in, -diphenyl-ß-picrylhydrazyl (DPPH) free radicals scavenge and DNA protection from Fenton reaction. High concentrations of nitric oxide (NO) are produced by inducible NO synthase (iNOS) in inflammation and multiple stages of carcinogenesis.

Studies have shown Rosemary to be as effective as the synthetic preservatives BHA and BHT.

Several laboratory studies suggest that rosemary contains compounds that prevent carcinogenic chemicals from binding to and inducing mutations in DNA.

The compounds epigallocatechin gallate (EGCG) and carnosol are known to be anti-inflammatory and cancer preventive.

Therefore, we studied their effect on the generation of peroxynitrite radicals and nitrite. They inhibited lipopolysaccharide (LPS) and interferon-gamma (IFN gamma) induced nitrite production by mouse peritoneal cells by more than 50% at 2.5-10 microM. Cell viability assays verified that the inhibition was not due to general cellular toxicity.

Rosemary seems to have also anti-cancer properties. Researchers at Rutgers University have demonstrated that rosemary oil can prevent the development of tumors in animals. When applied externally, rosemary oil reduced the risk of skin cancer and when taken internally it reduced the incidence of colon and lung cancer. Plant Stem Cell Therapy Indications: The Greatest Liver Agent!

Neurology & Nervous System:

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‘P’ Balances Nervous Equilibrium euphoric action, Improves Memory, Neuro vegetative dystonia. Rosemary may prevent the breakdown of acetylcholine, a chemical that allows neurons within the brain to communicate with each other. Neuroprotective carnosic acid activates a novel signaling pathway that protects brain cells from free radical damage, seen in stroke and other neurodegenerative conditions such as Parkinson’s and Alzheimer’s diseases. Carnosic acid to promote the production of Nerve Growth Factor. Cerebral artery ischemia/reperfusion. Carnosic acid reduces cytokine-induced adhesion molecules expression and monocyte adhesion to endothelial cells. Carnosic acid, may shield the brain from free radicals, lowering the risk of strokes and neurodegenerative diseases like Alzheimer’s and Lou Gehrig’s. For this purpose you will have to use 10 to 20 drops 3 x a day.

Carnosic acid has two therapeutic properties that make it a vital neuroprotective agent:

1. It protects against the narrowing of the left and right middle cerebral arteries – two of the major arteries carrying blood to the brain. Narrowing of these arteries with age is a common and important factor contributing to the development of neurodegenerative diseases.

2. Carnosic acid increases the body’s production of the antioxidant, glutathione. Glutathione is one of the most important antioxidants that help to protect the brain against free radical damage.

Also the antiplatelet activity of carnosic acid is mediated by the inhibition of cytosolic calcium mobilization and that carnosic acid has the potential of being developed as a novel antiplatelet agent.

CA activates the Keap1/Nrf2 transcriptional pathway by binding to specific (Kelch-like ECH-associated protein 1, also known as KEAP1, is a human gene) Keap1 cysteine residues, thus protecting neurons from oxidative stress and excitotoxicity. In cerebrocortical cultures, CA-biotin accumulates in non-neuronal cells at low concentrations and in neurons at higher concentrations. It was presented evidence that both the neuronal and non-neuronal distribution of CA may contribute to its neuroprotective effect. Furthermore, CA translocates into the brain, increases the level of reduced glutathione in vivo, and protects the brain against middle cerebral artery ischemia/reperfusion, suggesting that CA mayrepresent a new type of neuroprotective electrophilic compound.

References: Journal of Neurochemistry, Volume 104, Number 4, February 2008 , pp. 1116-1131(16).

Cardio Vascular System:

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‘P’ Reduces Cholesterol LDL and Triglycerides due to the rosmarinic acid and carnosic acid which assists the liver in breaking down lipids. Atherosclerosis, Improves Circulation of the extremities. Reduces the level of urea and uric acid. General detoxification by being an anti oxidant. Balances the Ionic and Mineral equilibrium. Normalizes the Vagus response A study found that depressed patients with VNS improved over time in terms of remission and response and also improved in their ability to function. It protects against the narrowing of the left and right middle cerebral arteries – two of the major arteries carrying blood to the brain. Carnosic acid prevents the migration of human aortic smooth muscle cells by inhibiting the activation and expression of matrix metalloproteinase-9 and NF-kB activation may be due to its antioxidant and antiinflammatory properties. Carnosic acid, a new class of lipid absorption inhibitor lowers triglycerides, its effectiveness in inhibiting LDL (low density lipoprotein). Carnosic Acid is the starting element of a process known as the “Carnosic Acid Cascade” of chemical reactions in the body where free radicals are quenched. Carnosic acid is transformed into carnosol; carnosol into rosmanol; and rosmanol into galdosol. With each of these transformations, free radicals are quenched. Its containment of this multi-step process that makes Rosemary young shoots one of the most potent antioxidants found in nature.

A study showed that carnosic acid effectively inhibited the TNF-a-induced migration of HASMC. The levels of ROS production, MMP-9 activation and expression, and nuclear translocation of NF-kB p50 and p65 were also all reduced by CA pretreatment. The present results led us to conclude that CA inhibits TNF-a-induced nuclear translocation of p50 and p65, thereby suppressing the activation and protein expression of MMP-9, resulting in decreased HASMC migration. Thus, CA may play an important role in the prevention of atherosclerosis.

References: British Journal of Nutrition (2008), 100, 731–738.

Elemol (sesquiterpene) a γ-lactone and not a δ-lactone as previously assumed: Antiacetylcholinesterase, Anticheilitic, Anticoronary, Antidementia, Antidepressant, Antigingivitic, Antiglossitic, Antigout, Antiinfertility, Antimetaplastic, Antimyelotoxic, Antineuropathic, Antiperiodontal, Antiplaque, Antipolyp, Antipsychotic, Antiulcer, Cancer-Preventive, Hematopoietic, Immunostimulant, Uricosuric, Xanthine-Oxidase-Inhibitor. Effect of elemol,, on the tracheal smooth muscle.

Fenchone (monoterpene and a Ketone): Antialzheimeran; Anticholinesterase; Counterirritant; Perfumery; Secretolytic.
Carnosic acid reduces cytokine-induced adhesion molecules expression and monocyte adhesion to endothelial cells.
References: European journal of nutrition 48(2):101-6, 2009 March.

Rosmariquinone (RQ), an ortho-quinone diterpenoid: act as a hydrogen-donating antioxidant.

Hematology Oncology:

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‘P’ Increases RBCs, Anticoagulant. Reduced the incidence of skin, colon and lung cancer. Anti-Cancer. Induces Apoptosis in Human Leukemia Cells through Caspase Activation and Poly (ADP-ribose) Polymerase Cleavage.

Immunology:

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‘P’ Increases WBC, Allergies associated with liver problems. Eye-related symptoms associated with seasonal allergies. Rosmarinic acid (suggested as a treatment for septic shock, since it suppresses the endotoxin-induced activation of complement). Rosmarinic Acid Induces p56lck-Dependent Apoptosis in Jurkat and Peripheral T Cells via Mitochondrial Pathway Independent from Fas/Fas Ligand Interaction 1.

Rosmarinic acid

has been shown to kill allergy-activated T cells and neutrophils during allergic reactions without affecting the T cells or neutrophils in their resting state. Using traditional antihistamines in allergic reactions, on the other hand, is somewhat analogous to turning off a fire alarm without putting out the fire. Antihistamines do nothing to lower the number of excess immune cells once they are formed. High levels of immune cells in their active form can lead to other dangers, such as free radical damage to normal tissues and to circulating proteins like HDL. They are many different types of Luteolins in Rosemary which inhibits antigen-specific proliferation and interferon-gamma production by murine and human autoimmune T cells. Flavonoids such as luteolin and apigenin are inhibitors of interleukin-4 and interleukin-13 production by activated human basophils.

Infectious Disease:

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‘P’ Contains 44 Antibacterial phytochemicals, 26 Antiviral and 12 Antiherpetic phytochemicals. Effective against: H-Pylori, Bacillus cereus, Staphylococcus aureus, Vibrio parahaemolyticus.

Pulmonary System:

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‘P’ Respiratory Decompensation. Advanced Tuberculosis. Antiasthmatic; Acute Asthma; Allergic Rhinitis; Chronic Bronchitis. In another study, researchers showed that rosmarinic acid inhibited lung injury from diesel exhaust particles, and outlined the exact steps by which rosmarinic acid brings about the cell death of activated T cells. The study also showed that the accumulation of neutrophils in human lung disease is directly related to the localized elevation of the cytokine IL-8, which supports the theory that IL-8 plays a central role in the pathogenesis of acute lung injury.

GI – Digestive – Hepatology:

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‘P’ Intestinal Decompensation, Epithelial action on colon mucosa intestinal smooth muscle relaxant. Crohn’s Disease & Colitis, Diverticulosis, Celiac Disease, Hepatic Function: Hepato Protective 63%. Liver Insufficiency, Biliary Dyskinesia. Cholelithiasis, Liver & Gallbladder major detoxifier, Gallbladder antispasmodic action in Chronic Cholecystitis. Antiacetylcholinesterase, Hepatitis A, B & C. Maintains good liver function in patients on birth control pills and implants. Protects against damage of Excess fat consumption. Carnosol and carnosic acid have been suggested to account for over 90% of the antioxidant properties of rosemary extract. Carnosic acid increases the body’s production of the antioxidant, glutathione. Fenchone components have a secretolytic effect on the respiratory tract. Also help to relieve smooth muscle spasms in the bowel.

Keap1 regulates both cytoplasmic-nuclear shuttling and degradation of Nrf2 in response to electrophiles. Transcription factor Nrf2 regulates the expression of a set of detoxifying and anti-oxidant enzyme genes. Several lines of evidence suggest that electrophiles and reactive oxygen species liberate Nrf2 from its cytoplasmic repressor Keap1 and provoke the accumulation of Nrf2 in the nucleus.

Piperitenone (monoterpene ketone): Antiacetylcholinesterase; Intestinal smooth muscle relaxant.

Musculoskeletal System:

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‘P’ Contains 33 Antiinflammatory phytochemicals, 21 Analgesic and 8 COX-2-Inhibitor phytochemicals. α-thujone (pain killing) effect, comparable to codeine.

Ob Gyn/Reproductive System:

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‘A’ Frigidity, Dysmenorrhea.

Uro Genital System:

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‘A’ Prostate Congestion. Reduces the level of urea and uric acid.

Endocrine System:

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‘A’ Adrenal Insufficiency, Gonad Senescence, (Potential for diabetes as from the latest research). Andropause, Impotency, sexual anomaly functional, Dysendocrinia. Anti-TSH action of rosmarinic acids for Hyperthyroidism.

Dermatology:

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‘A’ Skin regenerative and wound healing, displays its main activity in the dermis,Rosmarinic Acid is a potent Antioxidant it inhibits the activity of Elastase (an Enzyme that catalyzes the breakdown of Elastin). verbenone phytochemical especially useful for treating chronic skin conditions, dermatitis, eczema and psoriasis. Acne prone skin may respond favorably to the renewing effects of Rosemary verbenone, as well as to its action to fight infection and promote glandular balance and function. Its skin nourishing action makes it ideal for dry and mature skin. Alopecia, Oily Hair, Skin, Scalp conditions, and Dandruff. Antiscar.

Opthalmology:

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A Hispiduloside, Nepetrin and Sinensetin (flavonoids): Anticataract. Rosmarinic acid particularly inhibited the eye-related symptomsassociated with seasonal allergies.

Environmental Medicine:

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‘A’ as a treatment for septic shock, since it suppresses the endotoxin-induced activation of complement. Rosmarinic acid inhibits lung injury from diesel exhaust particles, and outlined the exact steps by which rosmarinic acid brings about the cell death of activated T cells. The accumulation of neutrophils in human lung disease is directly related to the localized elevation of the cytokine IL-8, which supports the theory that IL-8 plays a central role in the pathogenesis of acute lung injury.

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New mosquito-borne virus spreads in Latin America
SANTO DOMINGO, Dominican Republic — An excruciating mosquito-borne illness that arrived less than a year ago in the Americas is raging across the region, leaping from the Caribbean to the Central and South American mainland, and infecting more than 1 million people. Some cases have already emerged in the United States.–[F1] While the disease, called chikungunya, is usually not fatal, the epidemic has overwhelmed hospitals, cut economic productivity and caused its sufferers days of pain and misery. And the count of victims is soaring.–In El Salvador, health officials report nearly 30,000 suspected cases, up from 2,300 at the beginning of August, and hospitals are filled with people with the telltale signs of the illness, including joint pain so severe it can be hard to walk.–“The pain is unbelievable,” said Catalino Castillo, a 39-year-old seeking treatment at a San Salvador hospital. “It’s been 10 days and it won’t let up.”–Venezuelan officials reported at least 1,700 cases as of Friday, and the number is expected to rise. Neighboring Colombia has around 4,800 cases but the health ministry projects there will be nearly 700,000 by early 2015. Brazil has now recorded its first locally transmitted cases, which are distinct from those involving people who contracted the virus while traveling in an infected area.–Hardest hit has been the Dominican Republic, with half the cases reported in the Americas. According to the Pan American Health Organization, chikungunya has spread to at least two dozen countries and territories across the Western Hemisphere since the first case was registered in French St. Martin in late 2013.–There have been a few locally transmitted cases in the U.S., all in Florida, and it has the potential to spread farther[F2] , experts say, but Central and South America are particularly vulnerable. The chief factors are the prevalence of the main vector for the virus, the aedes aegypti mosquito, and the lack of immunity in a population that hasn’t been hit with chikungunya in modern medical history, said Scott C. Weaver, director of the Institute for Human Infections and Immunity at the University of Texas Medical Branch.–“There are going to be some very large populations at risk down there, much larger than the Caribbean[F3] ,” Weaver said.—Chikungunya is a word that comes from the Makonde language of Tanzania in eastern Africa and translates roughly as “that which bends up,” in reference to the severe arthritis-like ache in joints that causes sufferers to contort with pain. It’s usually accompanied by a spiking fever and headache. There have been only 113 deaths linked to the region’s outbreak, according to the most recent data, but chikungunya can be crippling.–Herman Slater, a 60-year-old gardener in Jamaica’s capital of Kingston, said he was laid out for almost two weeks this month with unimaginable joint pain, hammer-pounding headaches and fevers that came in waves.–“I tell you, I was surprised by how painful it was. It was taking me five minutes to get out of bed, and then I could hardly even walk,” Slater said. “My hands were so bad I couldn’t open a bottle, couldn’t comb my hair. Every night I was wet from sweat.”–In acute cases, pain can last for months. Joanna Rivas, who works as a maid in the Dominican capital of Santo Domingo, said she has had joint pain since May, and her 12-year-old daughter’s case is so severe the girl can’t hold her pen at school. Both have been taking the pain reliever acetaminophen, the main treatment for chikungunya, which has no cure or vaccine.–Besides the suffering, chikungunya has caused economic damage with the cost of providing treatment and controlling mosquitoes and by absenteeism from work. A study by the Universidad Eugenio María de Hostos in the Dominican Republic found nearly 13 percent of businesses said they had people miss work because of chikungunya in June.–Authorities throughout the region have been spraying pesticide and encouraging people to remove water containers where mosquitoes can breed. Oxitec, a British company that has tested genetically modified aedys aegypti to combat dengue in Brazil, Cayman Islands and Panama, says it has received a surge of interest since the start of the outbreak[F4] .–Chikungunya, which has been known for decades in parts of Africa and Asia[F5] , is transmitted when a mosquito bites an infected person and then feeds on someone else. It may have found fertile ground in Latin America and the Caribbean because many people are outside in the daytime, when aedes aegypti bite, or lack adequate screens on their windows.–In an article in the New England Journal of Medicine, Dr. Erin Staples of the U.S. Centers for Disease Control and Prevention said access to air conditioning to keep mosquitoes at bay might also be a factor. During an outbreak of mosquito-borne dengue in 1999 along the Texas-Mexico border, aedes aegypti were three times as abundant on the U.S. side but the number of people infected with dengue was twice as high on the Mexican side.[F6] -Conditions vary widely in the region. Haiti, where many people live in flimsy shacks with little protection from mosquitoes, has been hit hard. In Venezuela, air conditioning is widespread but the country has a shortage of insect repellent and pesticide sprayers due to the country’s economic problems.–Staples said past outbreaks have been known to affect around 30 per cent of a population, so there is room for the epidemic to grow, although it’s too early to accurately project how many will get sick or whether chikungunya will become endemic to the region like dengue.–The good news is that people seem to acquire immunity to all major strains.–“We do believe [F7] currently that if someone is unfortunate enough to get infected, they should not be infected again,” Staples said.

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Mycotoxin present in many types of food deteriorates neuroregeneration
Date:

September 19, 2014

Source:

Asociación RUVID

The research, carried out in the Faculty of Health Sciences of CEU Cardenal Herrera University, in cooperation with the University of Valencia, was published in the Journal of Applied Toxicology. This is one of the first articles worldwide to research the effect of Ochratoxin A on the subventricular zone of the brain, which in the adult mammalian brain is where neurogenesis primarily occurs.–Researchers at the Institute for Biomedical Sciences at CEU-UCH, in cooperation with colleagues of University of Valencia, showed through in vitro as well as in vivo experiments on lab animals the potential negative effect on neuroregeneration caused by Ochratoxine A, a mycotoxine found in many types of food, especially cereals and their derivatives. The study showed that Ochratoxine A deteriorates the formation of new neurons in the brain, a process called neurogenesis that, in particular, takes place in the subventricular zone, which in the adult brain is the largest of the neurogenic zones.–CEU-UCH professors José Miguel Soria, head of the research group ‘Strategies in Neuroprotection and Neuroreparation’ at the CEU-UCH Faculty of Health Sciences, and María Ángeles García Esparza, a member of the group, monitored the research, which was published in the Journal of Applied Toxicology. The authors further show that Ochratoxin Acan accumulate in the brain, where it causes increased cellular decay in the neurogenic zones, which in turn affects the production of neural stem cells. As neural stem cells regenerate neural populations, a decreased production of these could be a crucial factor in neurodegenerative diseases.–Story Source–The above story is based on materials provided by Asociación RUVID. Note: Materials may be edited for content and length.–Journal Reference-Sara Paradells, Brenda Rocamonde, Cristina Llinares, Vicente Herranz-Pérez, Misericordia Jimenez, Jose Manuel Garcia-Verdugo, Ivan Zipancic, Jose Miguel Soria, Mª Angeles Garcia-Esparza. Neurotoxic effects of ochratoxin-A on the subventricular zone of adult mouse brain. Journal of Applied Toxicology, July 2014 DOI: 10.13140/2.1.1347.1362

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How to make silver citrate
Norton, Steve Thu, 21 Jan 2010 13:45:10 -0800

Richard,

Marshall has already provided some excellent information. I do make and
use silver citrate. I think it has a place but I also believe that EIS
does as well. I think that EIS is best in some applications and that
silver citrate has benefits in others. Remember that what you read on
web sites is biased towards the sellers products and the information may
not be accurate. I do not think that one can state that in general that
EIS or silver citrate is better than the other but maybe in certain uses
one is better than the other. Below are some repeats of information I
have posted below on silver citrate. They may be of help.

– Steve N

_______________________________________________________

I know of three versions of silver citrate on the market. One is called
Sliver 100 and is made by Opti-Silver:

http://www.silver100.com/productinfo.pdf

It is made using silver oxide as the ionic silver source. The silver
oxide is mixed with citric acid and tripotassium citrate to create SC.
According to the manufacturer: “While the patent covers a broad range of
substances, the company has chosen to use citrate as the complexing
agent, and potassium as the counter-ion for maximum stability” While I
don’t make this version, I would guess that you could add tripotassium
citrate to standard SC if you are interested in potassium as the
counter-ion. A patent related to the product is at:

http://www.silver100.com/USPatent.PDF

A second silver citrate supplier is Pure Bioscience who sells SC for
both internal use and as a disinfectant under the Biocide and Axenohl
labels. They sell the SC in concentrations of up to 2400 ppm. I have
seen other SC sellers that appear to buy the concentrate, dilute it to
20 ppm and sell it under their private label. Pure Bioscience refers to
their SC as silver dihydrogen citrate, but it is simply SC made same the
same way as EIS but using a citric acid solution instead of distilled
water. Here is an article regarding their disinfectant spray:

http://cr.pennnet.com/display_article/310415/15/ARCHI/none/TOPST/1/MRSA-

infection-eradicated-for-14-months-With-SDC-disinfectant-in-Tulsa-County
-Jail/

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Show of the Month October 10 2014

Turmeric compound boosts regeneration of brain stem cells
Copper Power- Copper in medicine- Incorporation of copper into chitosan scaffolds promotes bone regeneration-

A Brief History of The Health Support Uses of Copper– Ancient Uses of Copper-

19th Century Copper-20th Century Copper– Copper in the 21st Century- Copper sulphate as a fish disease treatment

Disinfectant and method of making

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Turmeric compound boosts regeneration of brain stem cells
Date:

September 25, 2014

Source:

BioMed Central

A bioactive compound found in turmeric promotes stem cell proliferation and differentiation in the brain, reveals new research published today in the open access journal Stem Cell Research & Therapy. The findings suggest aromatic turmerone could be a future drug candidate for treating neurological disorders, such as stroke and Alzheimer’s disease.–The study looked at the effects of aromatic (ar-) turmerone on endogenous neutral stem cells (NSC), which are stem cells found within adult brains. NSC differentiate into neurons, and play an important role in self-repair and recovery of brain function in neurodegenerative diseases. Previous studies of ar-turmerone have shown that the compound can block activation of microglia cells. When activated, these cells cause neuroinflammation, which is associated with different neurological disorders. However, ar-turmerone’s impact on the brain’s capacity to self-repair was unknown.—Researchers from the Institute of Neuroscience and Medicine in Jülich, Germany, studied the effects of ar-turmerone on NSC proliferation and differentiation both in vitro and in vivo. Rat fetal NSC were cultured and grown in six different concentrations of ar-turmerone over a 72 hour period. At certain concentrations, ar-turmerone was shown to increase NSC proliferation by up to 80%, without having any impact on cell death. The cell differentiation process also accelerated in ar-turmerone-treated cells compared to untreated control cells.–To test the effects of ar-turmerone on NSC in vivo, the researchers injected adult rats with ar-turmerone. Using PET imaging and a tracer to detect proliferating cells, they found that the subventricular zone (SVZ) was wider, and the hippocampus expanded, in the brains of rats injected with ar-turmerone than in control animals. The SVZ and hippocampus are the two sites in adult mammalian brains where neurogenesis, the growth of neurons, is known to occur.–Lead author of the study, Adele Rueger, said: “While several substances have been described to promote stem cell proliferation in the brain, fewer drugs additionally promote the differentiation of stem cells into neurons, which constitutes a major goal in regenerative medicine. Our findings on aromatic turmerone take us one step closer to achieving this goal.”—Ar-turmerone is the lesser-studied of two major bioactive compounds found in turmeric. The other compound is curcumin, which is well known for its anti-inflammatory and neuroprotective properties.–Story Source–The above story is based on materials provided by BioMed Central. Journal Reference Joerg Hucklenbroich, Rebecca Klein, Bernd Neumaier, Rudolf Graf, Gereon Fink, Michael Schroeter, Maria Rueger. Aromatic-turmerone induces neural stem cell proliferation in vitro and in vivo. Stem Cell Research & Therapy, 2014; 5 (4): 100 DOI: 10.1186/scrt500

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Copper Power
Copper in medicine- homeostasis, chelation therapy and antitumor drug design.
Wang T1, Guo Z.

Author information
Abstract
As one of the most important essential transition metals, copper is involved in a variety of biological processes such as embryo development, connective tissue formation, temperature control and nerve cell function. It is also related to severe diseases such as Wilson’s and Menkes diseases and some neurological disorders. Novel components of copper homeostasis include copper-transporting P-type ATPases, Menkes and Wilson proteins, and copper chaperones in humans have been identified and characterized at the molecular level. These findings have paved the way towards better understanding of the role of copper deficiency or copper toxicity in physiological and pathological conditions. Therefore, organic compounds that can interfere with copper homeostasis may find therapeutic application in copper-dependent diseases. The antitumor activity of copper complexes was reported several decades ago, and many new complexes have demonstrated great antitumor potential. Copper complexes may have relatively lower side effects than platinum-based drugs, and are suggested to be able to overcome inherited or acquired resistance of cisplatin. In this overview, the most recent advances in copper homeostasis, copper-related chelation therapy and design of copper-based antitumor complexes will be summarized.

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Incorporation of copper into chitosan scaffolds promotes bone regeneration in rat calvarial defects.
D’Mello S1, Elangovan S, Hong L, Ross RD, Sumner DR, Salem AK.

Author information
Abstract
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

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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.

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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.

Dosages

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)

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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

Abstract

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.

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[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

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HOME

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

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Human genetic research uncovers how omega-6 fatty acids lower bad cholesterol
Date:

October 16, 2014

Source:

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 “http://www.eurekalert.org/pub_releases/2014-10/cp-hgr100814.php” \t “_blank” materials provided by  HYPERLINK “http://www.cellpress.com” \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 “http://dx.doi.org/10.1016/j.cmet.2014.09.004″ \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—

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Olive oil more stable and healthful than seed oils for frying food
Date:

October 22, 2014

Source:

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 “http://www.acs.org/content/acs/en/pressroom/presspacs/2014/acs-presspac-october-22-2014/olive-oil-more-stable-and-healthful-than-seed-oils-for-frying-food.html” \t “_blank” materials provided by  HYPERLINK “http://www.acs.org” \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 “http://dx.doi.org/10.1021/jf503146f” \t “_blank” 10.1021/jf503146f

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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.
 HYPERLINK “http://www.ncbi.nlm.nih.gov/pubmed/9152513″ \t “_blank” http://www.ncbi.nlm.nih.gov/pubmed/9152513

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 “http://drsircus.com/books/e-book/selenium-medicine/” \t “_blank” http://drsircus.com/books/e-book/selenium-medicine/ Using Glutathione and Selenium to Treat Viral Infections  HYPERLINK “http://drsircus.com/medicine/glutathione-selenium-viral-infections” \t “_blank” http://drsircus.com/medicine/glutathione…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 “http://www.holistic-online.com/Remedies/Biot/biot_anthrax-selenium-6-nat-rem.htm” \t “_blank” http://www.holistic-online.com/Remedies/…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 Abstract 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. Acknowledgments 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 References 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- 205. 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 “http://orthomolecular.emlnk6.com/lt.php?s=915ac1de175031fe3825bd4ab478a726&i=8A12A1A94″ \t “_blank” http://www.cancertherapies.org .) References: 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 “http://orthomolecular.emlnk6.com/lt.php?s=915ac1de175031fe3825bd4ab478a726&i=8A12A1A95″ \t “_blank” http://orthomolecular.org/library/jom/1977/pdf/1977-v06n04-p300.pdf 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 “http://orthomolecular.emlnk6.com/lt.php?s=915ac1de175031fe3825bd4ab478a726&i=8A12A1A96″ \t “_blank” http://vitamincfoundation.org/stone/ . 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 Orthomolecular medicine uses safe, effective nutritional therapy to fight illness. For more information:  HYPERLINK “http://orthomolecular.emlnk6.com/lt.php?s=915ac1de175031fe3825bd4ab478a726&i=8A12A1A88″ \t “_blank” http://www.orthomolecular.org Find a Doctor To locate an orthomolecular physician near you:  HYPERLINK “http://orthomolecular.emlnk6.com/lt.php?s=915ac1de175031fe3825bd4ab478a726&i=8A12A1A89″ \t “_blank” http://orthomolecular.org/resources/omns/v06n09.shtml The peer-reviewed Orthomolecular Medicine News Service is a non-profit and non-commercial informational resource. Editorial Review Board: Ian Brighthope, M.D. (Australia) Ralph K. Campbell, M.D. (USA) Carolyn Dean, M.D., N.D. (USA) Damien Downing, M.D. (United Kingdom) Michael Ellis, M.D. (Australia) Martin P. Gallagher, M.D., D.C. (USA) Michael Gonzalez, D.Sc., Ph.D. (Puerto Rico) William B. Grant, Ph.D. (USA) Michael Janson, M.D. (USA) Robert E. Jenkins, D.C. (USA) Bo H. Jonsson, M.D., Ph.D. (Sweden) Peter H. Lauda, M.D. (Austria) Thomas Levy, M.D., J.D. (USA) Stuart Lindsey, Pharm.D. (USA) Jorge R. Miranda-Massari, Pharm.D. (Puerto Rico) Karin Munsterhjelm-Ahumada, M.D. (Finland) Erik Paterson, M.D. (Canada) W. Todd Penberthy, Ph.D. (USA) Gert E. Schuitemaker, Ph.D. (Netherlands) Robert G. Smith, Ph.D. (USA) Jagan Nathan Vamanan, M.D. (India) Atsuo Yanagisawa, M.D., Ph.D. (Japan) Andrew W. Saul, Ph.D. (USA), Editor and contact person. Email:  HYPERLINK “mailto:omns@orthomolecular.org” \t “_blank” omns@orthomolecular.org This is a comments-only address; OMNS is unable to respond to individual reader emails. However, readers are encouraged to write in with their viewpoints. Reader comments become the property of OMNS and may or may not be used for publication. ************************************************************************ Parkinson’s disease can migrate from gut to brain Parkinson’s disease may start in the gut Parkinson’s disease is strongly linked to the degeneration of the brain’s movement center. In the last decade, the question of where the disease begins has led researchers to a different part of the human anatomy. In 2003, the German neuropathologist Heiko Braak presented a theory suggesting that the disease begins in the gut and spreads to the brain. The idea has since, despite vocal critics, gained a lot of ground. Researchers at Lund University in Sweden now present the first direct evidence that the disease can actually migrate from the gut to the brain.—The so-called Braak’s hypothesis proposes that the disease process begins in the digestive tract and in the brain’s center of smell. The theory is supported by the fact that symptoms associated with digestion and smell occur very early on in the disease.–Researchers at Lund University have previously mapped the spread of Parkinson’s in the brain. The disease progression is believed to be driven by a misfolded protein that clumps together and “infects” neighboring cells. Professor Jia-Yi Li’s research team has now been able to track this process further, from the gut to the brain in rat models. The experiment shows how the toxic protein, alpha-synuclein, is transported from one cell to another before ultimately reaching the brain’s movement center, giving rise to the characteristic movement disorders in Parkinson’s disease.—“We have now been able to prove that the disease process actually can travel from the peripheral nervous system to the central nervous system, in this case from the wall of the gut to the brain. In the longer term, this may give us new therapeutic targets to try to slow or stop the disease at an earlier stage”, says Professor Jia-Yi Li, research group leader for Neural Plasticity and Repair at Lund University.–The research team will now carry out further studies in which the mechanisms behind the transport of the harmful protein will be examined in detail. The current study suggests that the protein is transferred during nerve cell communication. It is at this point of interaction that the researchers want to intervene in order to put a stop to the further spread of the disease. **************************************************************************** Altering gut bacteria might mitigate lupus, study suggests Date: October 20, 2014 Source: American Society for Microbiology Lactobacillus species, commonly seen in yogurt cultures, correlate, in the guts of mouse models, with mitigation of lupus symptoms, while Lachnospiraceae, a type of Clostridia, correlate with worsening, according to research published ahead of print in Applied and Environmental Microbiology. “Our results suggest that the same investigation shold be performed in human subjects with lupus,” says principal investigator Xin Luo of Virginia Tech, Blacksburg, VA.–In the study, the investigators first showed that mouse models of lupus had higher levels of Lachnospiraceae (a type of Clostridia), and lower Lactobacillus than control mice. They also compared male and female mice, and found that the differences were present only in females. These results suggest that the gut bacteria may contribute to lupus, a disease which is nine times as prevalent in women as in men, says first author Husen Zhang.–They also monitored the gut microbiota over time in both lupus and control mice, and found that in the former, Clostridia increased in both early and late stages of the disease.–In further experiments, the investigators treated the symptoms in the lupus mice with either retinoic acid alone or vitamin A plus retinoic acid. The latter worsened the symptoms — surprisingly, Luo says, because it had been expected to reduce them — and in those mice, Clostridia increased, while Lactobacillus declined. Retinoic acid alone improved the symptoms, with opposite population changes in the gut bacteria.–The research suggests, but does not prove that altering the gut microbiota could mitigate lupus. Nonetheless, Luo suggests that people with lupus should eat Lactobacillus-containing probiotics, such as live culture yogurts, to reduce lupus flares. More generally, “The use of probiotics, prebiotics, and antibiotics has the potential to alter microbiota dysbiosis, which in turn could improve lupus symptoms,” says co-principal investigator Husen Zhang. Ultimately, says Luo, fecal transplant might prove valuable as a treatment for lupus.–“We were inspired in part to perform this research by a study on type 1 diabetes, which found that that disease is dependent on gut microbiota,” says Zhang. “Like type 1 diabetes, lupus is an autoimmune disease that is even more prevalent [than type 1 diabetes] in women.”–Story Source-The above story is based on materials provided by American Society for Microbiology. Note: Materials may be -edited for content and length.–Journal Reference- H. Zhang, X. Liao, J. B. Sparks, X. M. Luo. Dynamics of gut microbiota in autoimmune lupus. Applied and Environmental Microbiology, 2014; DOI: 10.1128/AEM.02676-14 TOP B ——————————————————————————– [F1]There is no such thing as good and bad cholesterol but what maybe happening is the omega 6 either through an antioxidant or anti inflammatory profiles maybe protecting the proteins in the cholesterol from causing oxidative damage to the fats [F2]So with Omega 6’s your getting an anti inflammatory due to the lipoxin conversion—this is why rubbing peanut oil on arthritic points seems to have a anti inflammatory effect on pain and reduces the inflammation of the area **************************************************************************** TOP C HOME Show of the Month October 25 2014 Fight against Alzheimer’s disease- New research on walnuts Exposure to aluminum may impact on male fertility, research suggests Why Are the Farmers Depressed and Suicidal Anti Virals—Uses ************************************************************************** Fight against Alzheimer’s disease- New research on walnuts Date:October 21, 2014 –Source:IOS Press BV A new animal study published in the Journal of Alzheimer’s Disease indicates that a diet including walnuts may have a beneficial effect in reducing the risk, delaying the onset, slowing the progression of, or preventing Alzheimer’s disease.—-Research led by Abha Chauhan, PhD, head of the Developmental Neuroscience Laboratory at the New York State Institute for Basic Research in Developmental Disabilities (IBR), found significant improvement in learning skills, memory, reducing anxiety, and motor development in mice fed a walnut-enriched diet.-The researchers suggest that the high antioxidant content of walnuts (3.7 mmol/ounce) may have been a contributing factor in protecting the mouse brain from the degeneration typically seen in Alzheimer’s disease. Oxidative stress and inflammation are prominent features in this disease, which affects more than five million Americans.–“These findings are very promising and help lay the groundwork for future human studies on walnuts and Alzheimer’s disease — a disease for which there is no known cure[F1] ,” said lead researcher Dr. Abha Chauhan, PhD. “Our study adds to the growing body of research that demonstrates the protective effects of walnuts on cognitive functioning.”–The research group examined the effects of dietary supplementation on mice with 6 percent or 9 percent walnuts, which are equivalent to 1 ounce and 1.5 ounces per day, respectively, of walnuts in humans. This research stemmed from a previous cell culture study led by Dr. Chauhan that highlighted the protective effects of walnut extract against the oxidative damage caused by amyloid beta protein. This protein is the major component of amyloid plaques that form in the brains of those with Alzheimer’s disease.—Someone in the United States develops Alzheimer’s disease every 67 seconds, and the number of Americans with Alzheimer’s disease and other dementias are expected to rapidly escalate in coming years as the baby boom generation ages. By 2050, the number of people age 65 and older with Alzheimer’s disease may nearly triple, from five million to as many as 16 million, emphasizing the importance of determining ways to prevent, slow or stop the disease. Estimated total payments in 2014 for all individuals with Alzheimer’s disease and other dementias are $214 billion.–Walnuts have other nutritional benefits as they contain numerous vitamins and minerals and are the only nut that contains a significant source of alpha-linolenic acid (ALA) (2.5 grams per ounce), an omega-3 fatty acid with heart and brain-health benefits. The researchers also suggest that ALA may have played a role in improving the behavioral symptoms seen in the study.–Story Source-The above story is based on materials provided by IOS Press BV. Note: Materials may be edited for content and length. –Journal Reference- Abha Chauhan, PhD et al. Dietary Supplementation of Walnuts Improves Memory Deficits and Learning Skills in Transgenic Mouse Model of Alzheimer’s Disease. Journal of Alzheimer’s Disease, Volume 42, Number 4 / 2014 DOI: 10.3233/JAD-140675 ********************************************************************* Exposure to aluminum may impact on male fertility, research suggests Date: October 21, 2014 Source: Keele University Aluminium symbol from the periodic table. Human exposure to aluminum has increased significantly in recent times, experts say. The observation of “significant contamination of male semen by aluminum must implicate aluminum as a potential contributor to these changes in reproductive fertility.” New research from scientists in the UK and France suggests that human exposure to aluminum may be a significant factor in falling sperm counts and reduced male fertility. Fluorescence microscopy using an aluminum-specific stain confirmed the presence of aluminum in semen and showed aluminum inside individual sperm. And the team of scientists, at the universities of Lyon and Saint-Etienne in France and Keele in the UK, found that the higher the aluminum, the lower sperm count. The research, led by Professor Christopher Exley, a leading authority on human exposure to aluminum at Keele, and Professor Michele Cottier, a specialist in cytology and histology at Saint-Etienne, measured the aluminum content of semen from 62 donors at a French clinic. Professor Exley said: “There has been a significant decline in male fertility, including sperm count, throughout the developed world over the past several decades and previous research has linked this to environmental factors such as endocrine disruptors. [F2] “Human exposure to aluminum has increased significantly over the same time period and our observation of significant contamination of male semen by aluminum must implicate aluminum as a potential contributor to these changes in reproductive fertility.” The mean aluminum content for all 62 donors was found to be very high at 339 ppb [F3] with the aluminum content of semen from several donors being in excess of 500 ppb. A statistically significant inverse relationship was found between the aluminum content of semen and the sperm count. Higher aluminum resulted in a lower sperm count. Story Source-The above story is based on materials provided by Keele University. Note-Materials may be edited for content and length. Journal Reference-J.P. Klein, M. Mold, L. Mery, M. Cottier, C. Exley. Aluminium content of human semen: implications for semen quality. Reproductive Toxicology, 2014; DOI: 10.1016/j.reprotox.2014.10.001 ************************************************************************* Why Are the Farmers Depressed and Suicidal? Is the same thing that’s destroying the bees also crippling our farmers?–When Ginnie Peters’ farmer husband took his own life after a sudden mood shift, she really hit the nail on the head when she said: These chemicals that farmers use, look what they do to an insect. It ruins their nervous system. What is it doing to the farmer? No one can deny that farming is drastically different than it was in the 1950s, and today it requires extra demand, complete expertise and the stress of uncertainty. Most farmers don’t go into it for high profits. The EPA, however, has long denied that the pesticide exposure they experience is directly tied to psychological symptoms, mental illness, behavioral changes and higher rates of suicide. Even though those are the very symptoms caused by such exposure, and the results of the EPA’s own studies, decades and decades ago, have arrived at the very same conclusion. Farmers serve our country too – has our government left these unsuspecting service men in a dangerous lurch, the same as military people who come back with mystery illnesses? Lorann Stallones, an epidemiologist and psychology professor at Colorado State University says: For years there was a high level of denial in the farming community that mental illness exists, period. But there’s been a shift – partly because there’s more people talking about being mentally incapacitated. Scientific American has recently reported: Some research suggests that the chemicals that farmers and their workers spread on fields may alter some of these brain chemicals.–Peters and his wife were among 89,000 farmers and other pesticide applicators in Iowa and North Carolina who have participated in the Agricultural Health Study led by the National Institute of Environmental Health Sciences. –Last month, epidemiologist Freya Kamel and her colleagues reported that among 19,000 studied, those who used two classes of pesticides and seven individual pesticides were more likely to have been diagnosed with depression. Those who used organochlorine insecticides were up to 90 percent more likely to have been diagnosed with depression than those who hadn’t used them. For fumigants, the increased risk was up to 80 percent.–The authors who wrote in the journal Environmental Health Perspectives say: Our study supports a positive association between depression and occupational pesticide use among applicators… and suggests several specific pesticides that deserve further investigation in animal studies and other human populations, While previous studies have only asked participants once about their depression – this one asked twice – once years back and again in 2010. It also included a large pool of farmers, meaning that people couldn’t really dismiss the study later for saying it was too small for consequence. The group came to the same conclusions when they studied the group between 1993 – 1997. Startlingly: Farmers with the highest number of lifetime exposure days to pesticides were 50 percent more likely to later have a depression diagnosis. Of course, after all these years, no one’s brave enough to say the P-word – Proof. Even though they show that psychological issues in rats is possible with exposure. For instance: tests on rats show altered brain cells, neurotransmitters and production of a protective acid. All important aspects of the complexity of brain and hormone health.[F4] Last year, it became glaringly apparent to researchers that French farmers were twice as likely to seek treatment for depression than those who don’t use herbicides. The rate increases with the increase of years using herbicides. –These are not just acute high exposures, either, like chemical companies like to ‘claim and blame.’ Many past studies have shown that chronic low exposure leads to problems that aren’t obviously until years later. Stallones, who wasn’t part of the main study says “but the association [with depression] held true for those that didn’t report poisoning.”–When there were larger dose poisonings in a short period, the rate of Colorado farmers risk for depression doubled in the next few years and North Carolina and Iowa farmers were 2.5 times more likely in the same situation. –Other health problems linked to depression are also linked to pesticide exposure. From Scientific American: For instance, Dr. Beate Ritz, a neurologist and professor at the University of California, Los Angeles, found that Californians exposed to pesticides are more likely to have Parkinson’s disease. One effect of the neurological disease, characterized by a lack of the chemical dopamine, is depression. […] Several studies have linked suicide to pesticide use. In Brazil, workers that used more pesticides were more likely to commit suicide, and in China, a World Health Organization survey of 9,800 people in the rural Zhejiang province revealed that those who stored pesticides in their homes had more than double the risk of having suicidal thoughts. Wendy Ringgenberg, an assistant professor at the University of Iowa, combed through 19 years of national data and reported that farmers and farm workers were 3.6 times more likely to die of suicide than other professions. However, the study did not examine the causes of suicide. Interestingly, some of the pesticides linked to depression and suicide in the study are not supposed to be in use[F5] . Chemical company giants like Monsanto, Bayer Cropscience and Syngenta say that their products were not included in the study and won’t comment on the bigger picture of brain health and long-term pesticide use. Also left from the study were the newer class of pesticides – neonicotinoids, which are implicated for mass bee die-off as they kill the nervous system of exposed insects. Ginnie Peters’ husband was using neonicotinoids – his father had chronic depression as well. Peters was exposed to organophosphates by doing his own crop spraying. Peters had chronic insomnia too. Ginnie is trying to bring awareness about suicide in farmers, linked to exposure to pesticides. I don’t have ability to do the science, but I have my gut, and what happened to Matt, it had to be the chemicals. What the researchers of new studies aren’t saying, or do not know, is that this supposed phenomenon has gone on, vastly under the radar for a long, long time. If you are interested in going down this dark rabbit hole, there are a couple rare and out-of-print books to help start connecting dots. Brain Fog by the late Bruce Haney, who himself was one such horticulturist with depression and behavioral changes that he noticed in his friendly competitors too. He tried desperately to get the attention of Congress in the 1990s and nursed many farmers and servicemen back to health. He cited all the notable EPA studies that knew the psychological connection, but which never led to any thoughtful halt on chemical approval. Then there is Environmental and Chemical Toxins and Psychiatric Illness by James S. Brown Jr., M.D. The symptomology and research is vast – the title aptly describes every piece of information found therein. If you are interested in the effects of chemical exposure on your own health, then please check out Our Chemical Lives and the Hijacking of our DNA: A Probe Into What’s Probably Making Us Sick. ************************************************************************** Anti Virals—Uses Allium sativum, apple juice, Andrographis paniculata,  HYPERLINK “http://www.healthline.com/natstandardcontent/arabinoxylan” arabinoxylan, astragalus,  HYPERLINK “http://www.healthline.com/adamcontent/avian-influenza” avian flu,  HYPERLINK “http://www.healthline.com/adamcontent/avian-influenza” bird flu,  HYPERLINK “http://www.healthline.com/natstandardcontent/cats-claw” cat’s claw,  HYPERLINK “http://www.healthline.com/natstandardcontent/clove” cloves,  HYPERLINK “http://www.healthline.com/goldcontent/co-enzyme-q10″ coenzyme Q10,  HYPERLINK “http://www.healthline.com/natstandardcontent/cranberry” cranberry,  HYPERLINK “http://www.healthline.com/goldcontent/echinacea” echinacea, Echinacea  HYPERLINK “http://www.healthline.com/adamcontent/purpura” purpura,  HYPERLINK “http://www.healthline.com/natstandardcontent/elder” elderberry, forsythia, Forsythia suspense, honeysuckle,  HYPERLINK “http://www.healthline.com/goldcontent/garlic” garlic, ginger, ginseng,  HYPERLINK “http://www.healthline.com/galecontent/licorice” Glycyrrhiza glabra, grape seed extract (GSE),  HYPERLINK “http://www.healthline.com/natstandardcontent/green-tea” green tea, infection, influenza, Isatis tinctora,  HYPERLINK “http://www.healthline.com/galecontent/lemon-balm” lemon balm, leptotaenia, Leptotaenia dissecta Nutt.,  HYPERLINK “http://www.healthline.com/galecontent/licorice” licorice, Lonicera japonica,  HYPERLINK “http://www.healthline.com/natstandardcontent/mullein” mullein,  HYPERLINK “http://www.healthline.com/goldcontent/acetylcysteine” N-acetyl-cysteine, Olea europea, olive leaf,  HYPERLINK “http://www.healthline.com/natstandardcontent/propolis” propolis,  HYPERLINK “http://www.healthline.com/natstandardcontent/reishi-mushroom” reishi,  HYPERLINK “http://www.healthline.com/natstandardcontent/resveratrol” resveratrol, Sambucas nigra L.,  HYPERLINK “http://www.healthline.com/galecontent/schisandra” schizandra, Schizandra chinensis, scullcap, shiitake,  HYPERLINK “http://www.healthline.com/natstandardcontent/ginseng” Siberian ginseng, St. John’s wort,  HYPERLINK “http://www.healthline.com/goldcontent/vitamin-e” vitamin e. Evidence of antiviral activity of selected herbals: Andrographis paniculata : The leaves of Andrographis paniculata, an annual herb, have been used widely as part of Indian  HYPERLINK “http://www.healthline.com/galecontent/folk-medicine” folk medicine and  HYPERLINK “http://www.healthline.com/galecontent/ayurvedic-medicine-1″ Ayurveda for centuries. The Chinese and Thai herbal medicine systems have also incorporated this herb, valued mostly for its “bitter” properties as a treatment for  HYPERLINK “http://www.healthline.com/galecontent/digestive-disorders” digestive problems and a variety of febrile illnesses. More recently, this herb, in its standardized extract form, has become popular in Scandinavia as a remedy for  HYPERLINK “http://www.healthline.com/galecontent/acute-respiratory-diseases” upper respiratory infection ( HYPERLINK “http://www.healthline.com/galecontent/acute-respiratory-diseases” URI) and  HYPERLINK “http://www.healthline.com/adamcontent/flu” influenza. For example, a 300 milligram Kan Jang tablet containing 4% andrographolides has been recommended to be taken four times daily for cold treatment (for a total daily dose of 48 milligrams andrographolides). Lower doses have been evaluated for respiratory infection prevention; for example, a single 200-300 milligram standardized tablet taken daily. Use appears to be safe for up to two weeks. Higher doses may be unsafe, leading to significant side effects. Kulichenko et al. carried out two randomized parallel-group trials of the SHA-10 extract of  HYPERLINK “http://www.healthline.com/galecontent/andrographis” andrographis (Kan Jang, Swedish Herbal Institute) in adults diagnosed with influenza. Both studies found significant improvements in reduction of duration of influenza symptoms (1-2.5 days sooner, depending on particular symptom, p< 0.01). Although the study suffers from a poorly described randomization procedure and a lack of a standardized outcome measure for symptoms, it does seem to provide preliminary evidence that andrographis extract may be effective not only for standard URI treatment but also specifically for influenza treatment. Apple juice: Freshly prepared apple juice has appreciable antiviral activity, but the activity may decline more readily than that of commercial juice in response to heat and storage. : Astragalus is an extremely versatile herb which may act as an immune strengthener. It is a commonly used herb in  HYPERLINK “http://www.healthline.com/galecontent/traditional-chinese-medicine” traditional Chinese medicine and is used as a component of many immune-supporting formulas, whether prepared as a sliced and boiled herb in food preparations, in extracts, or in capsules. The IL-2 inducing activity of the triterpene saponins found in astragalus might be the mechanism involved in the immunomodulatory and anticancer effects of astragalus species. : Echinacea may boost the immune defenses in various ways. It contains three compounds with specific antiviral activity: caffeic acid, chicoric acid, and echinacin. It strengthens the body’s local defenses by use of a substance, echinacein, that deactivates germs’ tissue-dissolving  HYPERLINK “http://www.healthline.com/adamcontent/enzyme” enzyme. This prevents germs from spreading and infecting other body tissues. In one study, echinacea stimulated production of white blood cells and phagocytes, and increased macrophage germ-killing activity. A University of Munich study demonstrated that echinacea boosted production of infection-fighting T-lymphocytes up to 30% more than standard immune-supportive drugs. In Germany echinacea is used to treat  HYPERLINK “http://www.healthline.com/adamcontent/flu” flu,  HYPERLINK “http://www.healthline.com/adamcontent/common-cold” colds,  HYPERLINK “http://www.healthline.com/adamcontent/bronchitis” bronchitis,  HYPERLINK “http://www.healthline.com/adamcontent/tonsillitis” tonsillitis,  HYPERLINK “http://www.healthline.com/adamcontent/otitis” ear infections and  HYPERLINK “http://www.healthline.com/adamcontent/pertussis” whooping cough. Root extracts of echinacea are believed to boost  HYPERLINK “http://www.healthline.com/galecontent/interferons-1″ interferon levels, vital to the body’s defenses. :  HYPERLINK “http://www.healthline.com/natstandardcontent/elder” Elderberry has been used has been used as a remedy for flu, cough, colds, and upper respiratory infections for over 2500 years. Recent studies demonstrate black elderberry’s effectiveness against all strains of influenza virus. A constituent present in black elderberry (with actions similar to neuraminidase inhibitors  HYPERLINK “http://www.healthline.com/goldcontent/oseltamivir” oseltamivir and  HYPERLINK “http://www.healthline.com/goldcontent/zanamivir” zanamivir) prevents the spread of virions from infected cells to new cells. Black elderberry is most effective in either a syrup form or in lozenges. Forsythia ( Forsythia suspensa ): Forsythia is a traditional Chinese herb used for treating colds, flu, and other viruses. It is often mixed with honeysuckle and sometimes  HYPERLINK “http://www.healthline.com/galecontent/lemon-balm” lemon balm and/or ginger as a tea. :  HYPERLINK “http://www.healthline.com/goldcontent/garlic” Garlic may possess antiviral activity. Experts claim it is most effective in its natural form, and they recommend juicing and drinking several  HYPERLINK “http://www.healthline.com/natstandardcontent/clove” cloves as needed. Garlic capsules are available and are preferred by those who find the taste of fresh garlic unpleasant. Experts recommend taking 2 capsules daily for prevention of infection. Garlic contains several antimicrobial compounds including allicin, reportedly one of nature’s strongest broad-spectrum  HYPERLINK “http://www.healthline.com/galecontent/antibiotics-3″ antibiotics. Studies have shown that garlic inhibits the growth of many types of bacteria, including  HYPERLINK “http://www.healthline.com/natstandardcontent/alt-probiotics-1″ Bacillus, Brucella, Citrobacter, E. Coli, Hafnia, Klebsiella, Salmonella typhi, Shigella, Vibrio cholerae, and various forms of Staphylococcus and Streptococcus. Further studies are needed before any firm recommendations can be made. Grape seed extract (GSE): GSE is a general antimicrobial agent with specific antiviral properties. It is best known for its application against Candida albicans, an organism responsible for  HYPERLINK “http://www.healthline.com/galecontent/fungal-infections-1″ fungal infections. Although not proven by scientific research, it may be effective against a long list of other microorganisms as well, including  HYPERLINK “http://www.healthline.com/adamcontent/herpes-simplex” herpes simplex type 1 virus, and influenza A virus. GSE may be used in liquid concentrate form or in capsules. GSE may be taken internally, in minute doses such as 2 to 4 drops twice daily diluted in at least 4 ounces of carrot, orange, pineapple or grapefruit juice. : Certain constituents called catechins found in  HYPERLINK “http://www.healthline.com/natstandardcontent/green-tea” green tea have been studied for their ability to inhibit influenza virus replication and their direct virucidal effects. One study evaluated polyphenolic compound catechins ((-)-epigallocatechin gallate (EGCG), (-)-epicatechin gallate (ECG) and (-)-epigallocatechin (EGC)) from green tea for their ability to inhibit influenza virus replication in cell culture and for potential direct virucidal effect. Among the test compounds, the EGCG and ECG were found to be potent inhibitors of influenza virus replication. It has been suggested that the antiviral effect of catechins on influenza virus is mediated not only by specific interaction with HA, but via alteration of the physical properties of the viral membrane. Honeysuckle ( Lonicera japonica ) is often used in China to treat bacterial and viral conditions. It is taken as a liquid from flower extracts or as a tea. Isatidis ( Isatis tinctora ): This herb is one of the best-known traditional Chinese medicine antiviral herbs. Isatidis may be a remedy for any virus but appears to be especially good for hepatitis, because it helps reduce both swelling and  HYPERLINK “http://www.healthline.com/adamcontent/hepatitis” liver inflammation. Isatidis is mild and can be used in children or those who do not tolerate heat well. Isatidis may also be a good anti-bacterial agent. Leptotaenia ( Leptotaenia dissecta Nutt.): Available in both capsules or as a liquid extract, leptotaenia is an herb known to be useful in treating  HYPERLINK “http://www.healthline.com/adamcontent/pneumonia” pneumonia, flu, colds, and bronchitis, as well as viruses such as Herpes simplex I and II and  HYPERLINK “http://www.healthline.com/adamcontent/hepatitis-c” hepatitis C. :  HYPERLINK “http://www.healthline.com/galecontent/licorice” Licorice root has been used to prevent and remedy infections, fevers and inflammation. It has broad antimicrobial activity against viruses, bacteria, yeast and fungi. Licorice contains at least eight antiviral and 25  HYPERLINK “http://www.healthline.com/galecontent/antifungal-therapy” antifungal substances. Licorice also possesses antiviral compounds that promote interferon release. By itself, licorice is a dynamic herb that should only be used for short periods of time. Olive leaf ( Olea europea ): This herb has general antimicrobial and antiviral properties. It usually comes in powder form in capsules.  HYPERLINK “http://www.healthline.com/galecontent/schisandra” Schizandra ( Schizandra chinensis ): This herb has been used in traditional Chinese medicine as an antiviral herb, specifically in cases of viral hepatitis. Schizandra may be taken in capsule form or the dried berries may be found in herb shops. : Hypericin, a constituent of St. John’s wort, has been extensively studied as an antiviral. While hypericin has been shown to be effective in inactivating enveloped viruses, such as  HYPERLINK “http://www.healthline.com/adamcontent/hepatitis-b” hepatitis B and C, and  HYPERLINK “http://www.healthline.com/adamcontent/acute-cytomegalovirus-cmv-infection” cytomegalovirus, it has not been effective against non-enveloped viruses, such as  HYPERLINK “http://www.healthline.com/adamcontent/hepatitis-a” hepatitis A, or  HYPERLINK “http://www.healthline.com/adamcontent/fifth-disease” parvovirus B-19. :  HYPERLINK “http://www.healthline.com/goldcontent/vitamin-e” Vitamin E is a commonly encountered  HYPERLINK “http://www.healthline.com/adamcontent/safety-and-vitamins” nutritional supplement with  HYPERLINK “http://www.healthline.com/galecontent/antioxidants” antioxidant properties. Based on animal study, vitamin E may reduce PGE2 production, which in turn leads to enhancement of Th1 cytokines. N-Dimethylglycine- Studies also show DMG: Provides useful building blocks for the biosynthesis of vitamins, hormones, neurotransmitters, antibodies, nucleic acids, and other metabolically active molecules Supports all aspects of immune response by acting as an anti-viral, anti-bacterial, and anti-fungal agent Promotes cardiovascular functions by supporting normal triglyceride and cholesterol levels, reducing angina, improving circulation, and decreasing elevated homocysteine levels Improves oxygenation, thus reducing fatigue and increasing energy for improved physical and mental performance Supports neurological function and mental clarity by acting as a precursor to the amino acids that are building blocks for neurotransmitters Acts as an antioxidant against free radicals Supports detoxification and enhances liver function, particularly Phase II detoxification (the phase that excretes converted toxic metabolites) DMG has anti-tumor properties, modulates the immune system, and helps protect DNA. · Recommended Ranges for Use of DMG to be taken daily in divided doses: General Use & Anti-Aging 125-500 mg Sports Practice & Fitness 375-1,000 mg Endurance Sports 1,000-2,500 mg Immune Response (Prevention) 375-750 mg Compromised Immune Response 750-1,200 mg Cardiovascular & Circulatory Problems 375-1,000 mg Diabetics & Hypoglycemics 375-1,000 mg Autism, ADD, & Seizures 375-1,000 mg Autoimmune Diseases (Lupus) 750-1,000 mg Chronic Fatigue, Fibromyalgia 1,000-1,500 mg Liver Detoxification 750-1,000 mg Respiratory Dysfunction (Asthma/Allergies) 750-1,000 mg Stress 250-750 mg Hydrogen Peroxide 3% Virus inactivation by hydrogen peroxide]. [Article in Russian]  HYPERLINK “http://www.ncbi.nlm.nih.gov/pubmed?term=Mentel%27%20R%5BAuthor%5D&cauthor=true&cauthor_uid=203115″ Mentel’ R,  HYPERLINK “http://www.ncbi.nlm.nih.gov/pubmed?term=Shirrmakher%20R%5BAuthor%5D&cauthor=true&cauthor_uid=203115″ Shirrmakher R,  HYPERLINK “http://www.ncbi.nlm.nih.gov/pubmed?term=Kevich%20A%5BAuthor%5D&cauthor=true&cauthor_uid=203115″ Kevich A,  HYPERLINK “http://www.ncbi.nlm.nih.gov/pubmed?term=Dre%C4%ADzin%20RS%5BAuthor%5D&cauthor=true&cauthor_uid=203115″ Dreĭzin RS,  HYPERLINK “http://www.ncbi.nlm.nih.gov/pubmed?term=Shmidt%20I%5BAuthor%5D&cauthor=true&cauthor_uid=203115″ Shmidt I. Abstract The effect of H2O2 on adenovirus types 3 and 6, adenoassociated virus type 4, rhinoviruses 1A, 1B, and type 7, myxoviruses, influenza A and B, respiratory syncytial virus, strain Long, and coronavirus strain 229E was studied in vitro, using different H2O2 concentration and timec of exposure. H2O2 in a 3 percent concentration inactivated all the viruses under study within 1–30 min. Coronavirus and influenza viruses were found to be most sensitive. Reoviruses, adenoviruses and adenoassociated virus were relatively stable. H2O2 is a convenient means for virus inactivation. Selenium- Recent work with selenium has demonstrated that a deficiency in this trace mineral will lead to increased viral pathogenesis. Selenium-deficient animals infected with a viral pathogen demonstrate immune dysfunction, including altered chemokine and cytokine expression patterns. A benign coxsackievirus infection of selenium-deficient mice leads to the development of myocarditis and further experiments demonstrated that the change in virulence was due to point mutations in the viral genome. Thus, replication in a selenium-deficient host led to a normally benign virus acquiring virulence due to viral mutations. A deficiency in selenium is also associated with disease progression in HIV-infected individuals and with hepatitis C virus-induced liver cancers. It appears that adequate levels of selenium help to protect the host against viral infection.—– Coincidentally, I began to study Ebola less than a month before the 1995 outbreak in Kikwit, Zaire that brought this virus so drastically into the public consciousness. I did so because of a poster presentation I had seen that spring in Santa Fe, at a meeting of the International Society for Antiviral Research. A Russian group presented a world map showing the geographic areas where various hemorrhagic viral diseases tended to occur, and I was struck by the fact that the area shown for the filoviruses Ebola and Marburg matched a region in Africa that I suspected might be a low-selenium region. What we found was striking: several gene regions in Ebola contained large numbers of UGA codons, up to 17 in one segment. We later published a paper showing that it might be possible for Ebola to synthesize selenoproteins from these gene regions, and proposed a mechanism whereby this might induce artificial selenium deficiency and contribute to the blood clotting characteristic of Ebola pathology.During the revisions to the final draft of that paper, we learned of a 1993 paper in a Chinese journal that reported the use of selenium to treat an Ebola-like hemorrhagic fever, with remarkable results. Luckily, the English translation of the abstract was available. Using the very high oral dose of 2 mg selenium per day as sodium selenite, for only 9 days, the death rate fell from 100% (untreated) to 37% (treated) in the very severe cases, and from 22% to zero in the less severe cases. Apparently there were about 80 people involved in this outbreak. Dr. Hou of the Chinese Academy of Medical Sciences, the author of this study, has since told me that he thinks more lives could have been saved if he had been permitted to give the selenite by injection, because in many of the more severly affected there is so much organ damage due to internal bleeding that they may have been unable to fully absorb or retain the oral dose of selenium. All in all, this is the closest thing to a curative result in the treatment of hemorrhagic fever that I have ever heard of. TOP C ——————————————————————————– [F1]So this would indicate there are cures —they just don’t know them [F2]Soy—Pesticides—herbicides and fluoride and a host of of other nano paricles like nano silver and titanium dioxide [F3]339 ppb-500pb == nano sized which would by pass the blood barrier of the testicals [F4]Now imagine the farmer and field hands having these exposures and then you as a consumer eating these chemicals that may not wash out —and then you wonder what is going on with anti anxiety and anti depressing drugs—which only masked the symptoms and further cause imbalances in brain chemistry [F5]Funny how that is always the case—not supposed to be used— and is out there —makes you wonder about the double standard