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    Genetically Modified Salmon Must Be Labelled
    FDA’s proposal to label GM salmon for production outside the US is
    unenforceable, and its failure to extend labelling in the market borders on public deception[U3] Prof. Joe Cummins -This report has been submitted to the US FDA, please forward and circulate as widely as possible The Food and Drug Administration (FDA) held a public hearing regarding the labelling of food derived from AquAdvantage’s genetically modified (GM) Atlantic salmon. The purpose of the hearing was for FDA to explain the relevant legal principles for food labelling and to solicit information and views from the public. In a separate but related process, FDA held a public Veterinary Medicine Advisory Committee (VMAC) meeting and sought public input on safety and environmental impact of AquAdvantage salmon [1]. VMAC met on 19-20 September 2010, and considered comments including the advice that commercial release of AquaAdvantage salmon is too hazardous to consider in the absence of animal feeding studies [2] (AquaAdvantage Salmon Ready for Commerce? SiS 48). The VMAC committee failed to come to agreement, leaving the important issues undecided. The FDA discussion on labelling of the AquAdvantage salmon was convened on 21 Sept, but the input of comment was extended until 22 November 2010.
    Labelling issues –The labelling issues considered by FDA include the following: 1. Which facts about the AquAdvantage salmon seem most pertinent for FDA’s consideration of whether there are any “material” differences between foods from this salmon and foods from other Atlantic salmon. (Keep in mind that the use of genetic engineering does not, in and of itself, constitute a ‘‘material’’ difference under the law.)[U4]
    2. If FDA determined there are “material” differences”, how would that
    difference be described on a food labelling in a way that is truthful and not
    misleading. (Keep in mind that it is the difference in composition, or in
    functional, organoleptic (odour, taste or texture) or other material properties
    that must be described, not the underlying production process.) Information
    about changes in the attributes of the food itself, such as its nutritional
    value, functional properties (e.g., storage) or organoleptic qualities may be
    important. –When commenting on these issues, FDA requests that respondents include support for their answers with relevant data, where appropriate, and/or references to the relevant legal principles. –FDA requires labelling of GM salmon but is uncertain about GM salmon in market–In the VMAC briefing packet [3], Section 3.4 of the Environment Assessment presents information on labelling of the product, including several warning
    statements expected to appear on the product label: “fish must be reared in
    land-based, highly contained systems that prevent their release into the environment” and the “fish cannot be reared in conventional cages or net pens deployed in open bodies of water.” Presumably this may mean that the GM salmon will be labelled prior to marketing for sale as food, at which time, the labels will be removed to conceal the GM origins of the salmon to be sold as food. The introduction of transgenes and their products into the GM salmon is not considered to be a material change in Atlantic salmon even though such changes would never have appeared in natural Atlantic salmon throughout its evolutionary history.
    Flavonol quantification and stability of phenolics in fermented extracts from fresh Betula pendula leaves.
    J Pharm Biomed Anal. 2010 Oct 10;53(2):137-44–Authors: Millet A, Stintzing F, Merfort I
    An HPLC method, which allows reliable quantitation of flavonols and other phenolics in birch leaf extracts, was developed and validated. The method was applied to study the bioconversion of flavonols in fermented aqueous extracts. Almost 100% of the flavonols were converted during the 12 months observation period. The generated phenolics as well as consecutive conversion products were identified by HPLC-DAD, LC-MS and GC-MS techniques.—PMID: 20189738 [PubMed – indexed for MEDLINE]* Interesting concept here by taking in the leaves of the birch tree you can ferment the leave s and after a year would have a pretty potent pain killer as well as a immune enhancer and potentially cnacer and viral killer
    FDA warns makers of chelation treatments

    CHICAGO (Reuters) – The U.S. Food and Drug Administration is cracking down on the over-the-counter sale of so-called chelation products that claim to treat conditions such as autism, heart disease and Alzheimer’s by removing heavy metals from the body.—The FDA said on Thursday it sent warning letters to eight companies telling them their products were unapproved drugs and devices, and any claims about treating medical conditions with these products violated federal law.–“These products are dangerously misleading because they are targeted to patients with serious conditions and limited treatment options,” Deborah Autor, director of the Office of Compliance in the FDA’s Center for Drug Evaluation and Research, said in a statement.–“The FDA must take a firm stand against companies who prey on the vulnerability of patients seeking hope and relief[U5],” Autor said.—Although there are FDA-approved chelation drugs that are used in cases of heavy metal poisoning with a prescription, no chelation therapy products are approved for sale over the counter or on the Internet, the FDA said.—“What we’re telling consumers today is that any chelation therapy marketed over the counter is suspect,” Michael Levy, director of the FDA’s Division of New Drugs and Labeling Compliance, told a telephone briefing.–Serious safety issues have been linked with chelation products, which can alter the levels of certain substances in the blood.[U6] Even when used under medical supervision, these products can cause serious harm, including dehydration, kidney failure and death.–One child died while being treated for autism with an intravenous chelation product[U7], FDA officials told the briefing. And they said there are likely many cases of serious side effects because companies are not compelled to report adverse events to the agency.–Companies that got the warning letters claim that their products treat a range of diseases by removing toxic metals from the body, the agency said.—Some also claim to treat autism spectrum disorder, cardiovascular diseases, Parkinson’s disease, Alzheimer’s disease, macular degeneration — a major cause of blindness — and other serious conditions, the FDA said.–And some companies that got warning letters also make test kits and claim their products can detect heavy metals, thereby justifying the need for chelation therapy.The FDA issued the warning because agency officials said there has been an increase in claims for and the availability of these products sold directly to consumers[U8].—The FDA said companies need to act quickly to correct violations listed in the warning letters or face possible legal action, including seizure of their products.–The letters were issued to the following companies: World Health Products LLC; Hormonal Health LLC; Evenbetternow LLC; Maxam Nutraceutics/Maxam Laboratories; Cardio Renew Inc; Artery Health Institute LLC; Longevity Plus, and Dr. Rhonda Henry, a nutritionist.áSupport them!!!—My personal comment is to supprot these companies
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    [U1]Another Excuse For the State to take over your Children and regulate them and to teach them “There Way” and to violate anything that they do not see fit or that will compete for ther authority, alot of innuendo here to give off the idea that the state really cares for your offspring, But in reality they need slaves to do there bidding—If they really wanted to stop any obesity they would outlaw Mcdonalds and any other fast food franchise and eliminate all box foods that would disrupt the endocrin and digestive system and immune functions–instead these companies are allowed to sell ” Posioned Foods ” that shut down the brain or overload the brain so then there is an overwhelming compulsion to consume sugary foods which contribute to obesity
    [U2]SO if this is tehe case then the Gov’t would be libel for neglect and can be sued!!!!!!—and Should be—if the parents are feeding things to kids that are causing this issue and then the gov’t follows suit with the same type of foods under “There Guidelines” which by the way are off—then the gov’t would be involved in acting in the same irresponsible behaviour and as a result should be sued and there power base removed from any interference in matters such as these
    [U3]Interesting thought here eh!! you label a GMO Fish Outside of the USA border ( Canada as well ) and what happens—these fish wind up in a streeam or ocean where they mate–then what happens–you have the GE gene now being transferred into the wild life-making these fish the sole propriety owner ship of the Corporates who came up with this technolgy-and ten ther eis the eco system that they are now contaminating with these genes–the ocean is alot more difficult to monitor then the land( and even that is not done efficiently, Look at our Bee’s and this is just one species —no one has looked at the ant or the earthworm or if they have they have not revelaed anything as of yet
    [U4]Again this is such an oxymoron here that it is not considered a material difference under the law—Now anyone can see this is a farse at best there are laws but then there is science and in this–there would be a huge division in that anytime you are tampering with the genome( genetics) of anything there will be a change and potential anomalies that would not otherwise be present—this is to appease the people who would make a distinction or rebel to appease the resistance but nonetheless this does not change the fact that these fish are genetically altered and will cause a genetic disturbance in people as well as other fish—Look at Soy and canola–these 2 GE foods have caused all kinds of genetic anomalies in people and the land—the fish which would be more transient would spread the genetics across the oceans
    [U5]The wording as per usual is always misleading and double talk—let’s translate this in real earth language–we do not want you to have access too theses products because they will undermine our plan for eugenics—these products will pull out of the body all the chemtrail and exhaust fumes people are exposed to daily and will remove from the system the mercury in foods such as fish oils ) and other contaminats which we are unable to monitor but can indeed kill
    [U6]WHAT stupidity–anything you consume can do this–alter the blood–What I find incredible is SOY
    [U7]this again is Funny and sad that they are using this kind of scare mongering—if this actually happened at all it would have been done in the privacy of a doctors office or a Naturapth and I am not sure this would have been what killed
    [U8]NOWWW Finallly the truth —these companies are making more money then the counterpart in the pharmaceutical side
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    Show Of the Week October 25 2010
    Luteolin Inhibits Microglia and Alters Hippocampal-Dependent Spatial Working Memory in Aged Mice1,2,3
    Luteolin inhibits LPS-stimulated inducible nitric oxide synthase expression in BV-2 microglial cells
    Grape Juice but Not Orange or Grapefruit Juice Inhibits Platelet Activity in Dogs and Monkeys
    Grape juice, but not orange juice or grapefruit juice, inhibits human platelet aggregation.
    Remedy with Grape Juice Concentrate
    Salvia officinalis L.: composition and antioxidant-related activities of a crude extract and selected sub-fractions
    Distribution and biological activities of the flavonoid luteolin.–Special Note
    Luteolin Inhibits Microglia and Alters Hippocampal-Dependent Spatial Working Memory in Aged Mice1,2,3
    Saebyeol Jang4,5, Ryan N. Dilger5,6 and Rodney W. Johnson4–6*
    4 Division of Nutritional Sciences, University of Illinois, Urbana, IL 61801; 5 Integrative Immunology and Behavior Program, University of Illinois, Urbana, IL 61801; 6 Department of Animal Sciences, University of Illinois, Urbana, IL 61801
    A dysregulated overexpression of inflammatory mediators by microglia may facilitate cognitive aging and neurodegeneration. Considerable evidence suggests the flavonoid luteolin has antiinflammatory effects, but its ability to inhibit microglia, reduce inflammatory mediators, and improve hippocampal-dependent learning and memory in aged mice is unknown. In initial studies, pretreatment of BV-2 microglia with luteolin inhibited the induction of inflammatory genes and the release of inflammatory mediators after lipopolysaccharide (LPS) stimulation. Supernatants from LPS-stimulated microglia caused discernible death in Neuro.2a cells. However, treating microglia with luteolin prior to LPS reduced neuronal cell death caused by conditioned supernatants, indicating luteolin was neuroprotective. In subsequent studies, adult (3–6 mo) and aged (22–24 mo) mice were fed control or luteolin (20 mg/d)-supplemented diet for 4 wk and spatial working memory was assessed as were several inflammatory markers in the hippocampus. Aged mice fed control diet exhibited deficits in spatial working memory and expression of inflammatory markers in the hippocampus indicative of increased microglial cell activity. Luteolin consumption improved spatial working memory and restored expression of inflammatory markers in the hippocampus compared with that of young adults. Luteolin did not affect either spatial working memory or inflammatory markers in young adults. Taken together, the current findings suggest dietary luteolin enhanced spatial working memory by mitigating microglial-associated inflammation in the hippocampus. Therefore, luteolin consumption may be beneficial in preventing or treating conditions involving increased microglial cell activity and inflammation. \
    Luteolin inhibits LPS-stimulated inducible nitric oxide synthase expression in BV-2 microglial cells.
    Kim JS, Lee HJ, Lee MH, Kim J, Jin C, Ryu JH.
    College of Pharmacy, Sookmyung Women’s University, Seoul, Korea.
    Overproduction of nitric oxide (NO) by inducible nitric oxide synthase (iNOS) acts as a neurotoxic effector in the central nervous system, resulting in neurodegenerative diseases. From the alcoholic extracts of Perilla frutescens, we have purified an inhibitor of NO production in lipopolysaccharide (LPS)-activated microglia by activity-guided purification. The active compound was identified as luteolin by spectral analysis. Luteolin inhibited the NO production in LPS-activated microglia in a dose-dependent manner (IC50=6.9 microM). Luteolin also suppressed the degradation of I-kappaB-alpha, the expression of protein and mRNA of iNOS in LPS-activated microglia as observed in Western blot analysis and RT-PCR experiments. Luteolin may have beneficial effects in the treatment of neuro-inflammatory diseases through the inhibition of iNOS expression
    Grape Juice but Not Orange or Grapefruit Juice Inhibits Platelet Activity in Dogs and Monkeys (Macaca fasciularis)
    Manuscript received 15 April 1998. Initial reviews completed 13 May 1998. Revision accepted 4 August 1998.
    Hashim E. Osman, Nabil Maalej, Dhanansayan Shanmuganayagam, and John D. Folts
    University of Wisconsin Medical School Madison, WI, 53792
    Platelet aggregation (PA) contributes to both the development of atherosclerosis and acute platelet thrombus formation (APTF) followed by embolization producing cyclic flow reductions (CFR) in stenosed and damaged dog and human coronary arteries. In seven anesthetized dogs with coronary stenosis and medial damage, CFR occurred at 7 ± 3/30 min and were abolished 127 ± 18 min after gastric administration of 10 mL of purple grape juice/kg. Collagen-induced ex vivo whole blood PA decreased by 49 ± 9% after the abolishment of CFR with grape juice. Ten mL of orange juice/kg (n = 5) and 10 mLof grapefruit juice/kg (n = 5) had no significant effect on the frequency of the CFR or on ex vivo PA. In vitro studies have suggested that flavonoids bind to platelet cell membranes and thus may have an accumulative or tissue-loading effect over time. To test this we fed 5 mLof grape juice/kg to 5 cynomologous monkeys for 7 d. Collagen-induced ex vivo PA decreased by 41 ± 17% compared to control (pre-reatment) after 7 d of feeding. In the same 5 monkeys, neither 5 mL of orange juice/kg nor 5 mLof grapefruit juice/kg given orally for 7 d produced any significant change in PA. Grape juice contains the flavonoids quercetin, kaempferol and myricetin, which are known inhibitors of PA in vitro. Orange juice and grapefruit juice, while containing less quercetin than grape juice, primarily contain the flavonoids naringin, luteolin and apigenin glucoside. The flavonoids in grapes were shown in vitro to be good inhibitors of PA, whereas the flavonoids in oranges and grapefruit to be poor inhibitors of PA. The consumption of grape juice, containing these inhibitors of PA, may have some of the protection offered by red wine against the development of coronary artery disease (CAD) and acute occlusive thrombosis, whereas orange juice or grapefruit juice may be ineffective. Thus, grape juice may be a useful alternative dietary supplement to red wine without the concomitant alcohol intake.
    Grape juice, but not orange juice or grapefruit juice, inhibits human platelet aggregation.
    Keevil JG, Osman HE, Reed JD, Folts JD.
    Cardiology Section of Department of Medicine, University of Wisconsin, Madison, WI 53792, USA.
    Coronary artery disease is responsible for much mortality and morbidity around the world. Platelets are involved in atherosclerotic disease development and the reduction of platelet activity by medications reduces the incidence and severity of disease. Red wine and grapes contain polyphenolic compounds, including flavonoids, which can reduce platelet aggregation and have been associated with lower rates of cardiovascular disease. Citrus fruits contain different classes of polyphenolics that may not share the same properties. This study evaluated whether commercial grape, orange and grapefruit juices, taken daily, reduce ex vivo platelet activity. In a randomized cross-over design, ten healthy human subjects (ages 26-58 y, five of each gender) drank 5-7.5 mL/(kg. d) of purple grape juice, orange juice or grapefruit juice for 7-10 d each. Platelet aggregation (whole blood impedance aggregometry, Chronolog Model #590) at baseline was compared to results after consumption of each juice. Drinking purple grape juice for one week reduced the whole blood platelet aggregation response to 1 mg/L of collagen by 77% (from 17.9 +/- 2.3 to 4.0 +/- 6.8 ohms, P = 0.0002). Orange juice and grapefruit juice had no effect on platelet aggregation. The purple grape juice had approximately three times the total polyphenolic concentration of the citrus juices and was a potent platelet inhibitor in healthy subjects while the citrus juices showed no effect. The platelet inhibitory effect of the flavonoids in grape juice may decrease the risk of coronary thrombosis and myocardial infarction.
    Remedy with Grape Juice Concentrate—to get a good dose of this effect Go to the Wine shops where you can buy real grape concentrates with out all the sugar then you can dilute it to your level and consume this—if you cannot consume wine this maybe the next thing that maybe an alternative to you—to increase the luteolin effect add dandelion—parsley-rosemary –to the grape concentrate and blend til smooth—or for at the least 10 min high speed or til blender container feels hot—pour the fused contents into a Glass Container –date and mark and use 1 ounce several times a day—
    Salvia officinalis L.: composition and antioxidant-related activities of a crude extract and selected sub-fractions.
    Koşar M, Dorman HJ, Başer KH, Hiltunen R.
    Faculty of Pharmacy, Department of Pharmaceutical Biology, University ofHelsinki, POB 56 (Viikinkaari 5E), FIN-00014, Finland.
    The composition and antioxidant properties of a methanol: acetic acid (99:1, v/v) soluble crude extract isolated from S. officinalis L. leaves through maceration and selected fractions isolated thereof are presented in this study. The total phenol content was estimated as gallic acid equivalents, whilst qualitative-quantitative phenolic content was determined using high performance liquid chromatography with photodiode array detection. Antioxidant evaluation consisted of ferric reductive capacity and 1,1-diphenyl-2-picrylhydrazyl and hydroxyl free radical scavenging determinations. The crude extract contained hydroxybenzoic acids, hydroxycinnamic acids, flavonoids and diterpenoids, whilst caffeic acid, carnosic acid, luteolin, luteolin-7-O-glucoside and rosmarinic acid were identified from their chromatographic and spectral characteristics and quantified from their respective calibration curves. The crude extract and sub-fractions demonstrated varying degrees of efficacy in the antioxidant-related assays used, except the n-hexane fraction, which was unable to reduce iron(III) at reasonable concentrations. Although the positive controls, ascorbic acid, BHA and BHT, were more potent than the S. officinalis samples, two fractions were significantly (p < 0.05) more potent iron(III) reducing agents than pycnogenol, a proanthocyanidin-rich commercial preparation
    Flavonoids and phenolic compounds from Rosmarinus officinalis.
    Bai N, He K, Roller M, Lai CS, Shao X, Pan MH, Ho CT.
    Naturex, Inc., South Hackensack, New Jersey 07606, USA.
    A new flavonoid, 6”-O-(E)-feruloylhomoplantaginin (1), and 14 known compounds, 6”-O-(E)-feruloylnepitrin (2), 6”-O-(E)-p-coumaroylnepitrin (3), 6-methoxyluteolin 7-glucopyranoside (4), luteolin 3′-O-beta-D-glucuronide (5), luteolin 3′-O-(3”-O-acetyl)-beta-D-glucuronide (6), kaempferol (7), luteolin (8), genkwanin (9), and ladanein (10), together with 1-O-feruloyl-beta-D-glucopyranose (11), 1-O-(4-hydroxybenzoyl)-beta-D-glucopyranose (12), rosmarinic acid (13), carnosic acid (14), and carnosol (15), were isolated from the leaves of Rosmarinus officinalis . The structures were established on the basis of NMR spectroscopic methods supported by HRMS. All isolated compounds were tested for cytotoxicity in human cancer cell lines (HepG2, COLO 205, and HL-60) and for anti-inflammatory activities in lipopolysaccharide (LPS)-treated RAW 264.7 macrophage cells. Among them, compounds 14 and 15 were modestly active in the inhibition of nitrite production in macrophages, followed by compounds 8 and 5. Compounds 14 and 15 were more effective as an antiproliferative agent in HL-60 cells with IC(50) values of 1.7 and 5.5 microM, followed by compounds 8 and 7 with IC(50) of 39.6 and 82.0 microM, respectively. In addition, compounds 14 and 15 showed potent antiproliferative effects on COLO 205 cells with IC(50) values of 32.8 and 29.9 microM, respectively.
    Distribution and biological activities of the flavonoid luteolin.
    López-Lázaro M.
    Department of Pharmacology, Faculty of Pharmacy, University of Seville, Spain. C/ Profesor Garcia Gonzalez, 41011, Sevilla, Spain.
    Epidemiological evidence suggests that flavonoids may play an important role in the decreased risk of chronic diseases associated with a diet rich in plant-derived foods. Flavonoids are also common constituents of plants used in traditional medicine to treat a wide range of diseases. The purpose of this article is to summarize the distribution and biological activities of one of the most common flavonoids: luteolin. This flavonoid and its glycosides are widely distributed in the plant kingdom; they are present in many plant families and have been identified in Bryophyta, Pteridophyta, Pinophyta and Magnoliophyta. Dietary sources of luteolin include, for instance, carrots, peppers, celery, olive oil, peppermint, thyme, rosemary and oregano. Preclinical studies have shown that this flavone possesses a variety of pharmacological activities, including antioxidant, anti-inflammatory, antimicrobial and anticancer activities. The ability of luteolin to inhibit angiogenesis, to induce apoptosis, to prevent carcinogenesis in animal models, to reduce tumor growth in vivo and to sensitize tumor cells to the cytotoxic effects of some anticancer drugs suggests that this flavonoid has cancer chemopreventive and chemotherapeutic potential. Modulation of ROS levels, inhibition of topoisomerases I and II, reduction of NF-kappaB and AP-1 activity, stabilization of p53, and inhibition of PI3K, STAT3, IGF1R and HER2 are possible mechanisms involved in the biological activities of luteolin.
    Special Note—Go to and then type in herbsplusbeadworks in the search box and see how to make a green drink Extract with parsley dandelion and watercress these all have luteolin and apigenenin in them as well as other antioxidants and nutrients–This is a small investment and can be easily grown in a garden or a pot or crate or any means you have to et it going
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    Show of the Week October 29 2010
    Vitamin E –Benefits and therapeutic process
    How to Quickly Make Powdered Eggs–Comment on the Process of drying eggs
    Synergistic effects of tea polyphenols and ascorbic acid on human lung adenocarcinoma
    Bisphenol A officially declared toxic by Canada
    Divine Providence medicine Cabinet
    Vitamin E –Benefits and therapeutic process—
    Natural Alpha Tocopherol (Vitamin E) in the treatment of Cardiovascular and Renal Diseases as suggested by Drs. Wilfrid and Evan Shute and the Shute Institute for Clinical and Laboratory Medicine, London, Ontario, Canada. Use only products labeled in terms of InternatIonal Units (IU).
    Acute coronary thrombosis: 450 to 1,600 IU a day started as soon as possible and maintained.
    Older cases of coronary thrombosis: 450 to 1,600 IU if systolic pressure is under 160 Otherwise 450 IU for the first four weeks, particularly if a hypotensive agent is used concurrently.
    Acute rheumatic fever: 450 to 600 IU daily.
    Chronic rheumatic heart disease: give 90 IU daily first month, 120 IU daily second month and 150 IU daily for third month. 150 IU may be ideal dose. Occasionally more is necessary and advisable. Response will necessarily be slow.
    Anginal Syndrome: 450 to 1,600 IU if systolic pressure is under 160. Otherwise start on 150 IU for four weeks then 300 IU for four weeks, particularly if hypotensive agent is used.
    Hypertensive heart disease: 75 IU daily for four weeks, 150 IU daily for four weeks, then cautiously increase. Should be used with hypotensive agents. High doses of vitamin E have been shown to reduce high blood pressure in rats with chronic kidney failure. (Vaziri N. Hypertension, Jan 2002.)
    Thrombophlebitis and Phlebothrombosis: 600 to 1,600 IU daily.
    Thrombocytopaenic Purpura: 800 to 1,200 IU daily.
    Diabetes Mellitus: Same schedule as for cardiacs.
    Acute and Chronic Nephritis: as for cardiac patients.
    Burns, Plastic Surgery, Mazoplasia: 600 to 1,600 IU daily, using vitamin E ointment or vitamin E spray as adjunct. (Editor’s note: vitamin E may also be dripped from a thumbtack-punctured capsule.)
    The maintenance dose equals the therapeutic dose.
    Do not take iron and vitamin E at same time. If iron is indicated, separate the doses by about nine hours. -The digitalis requirement is often reduced after vitamin E takes hold, so over-digitalization should be avoided. A patient receiving vitamin E should not be digitalized by the Eggleston massive dose technique nor any of its modifications. It is usually sufficient for full digitalization to give what is ordinarily a maintenance dose of 1 1/2 grains digitalis folia or 0.1 mg digitoxin per day. By the second day the patient is often digitalized.
    Insulin dosages in diabetic cardiacs must be watched closely, for the insulin requirement may be considerably reduced very suddenly. -Hyperthyroidism is sometimes a contraindication.
    Estrogens should rarely be given at the same time as alpha tocopherol (vitamin E).
    (Editor’s note: The Shutes also recommend caution with patients who have untreated high blood pressure, a rheumatic heart, or congestive heart failure. If you are a person with these or any other preexisting medical condition, you need to WORK WITH YOUR PHYSICIAN TO DETERMINE YOUR OPTIMUM VITAMIN E LEVEL.)
    1. It reduces the oxygen requirement of tissues.
    Hove, Hickman, and Harris (1945) Arch. Biochem. 8:395.
    Telford et al (1954) Air University School of Aviation Medicine Project #21-1201-0013, Report #4, May. Randolph Field, Texas.
    2. It melts fresh clots, and prevents embolism.
    Shute, Vogelsang, Skelton and Shute (1948) Surg., Gyn. and Obst. 86:1.
    Wilson and Parry (1954) Lancet 1:486.
    3. It improves collateral circulation.
    Enria and Fererro (1951) Arch. per Ia Scienze Med. 91:23.
    Domingues and Dominguez (1953) Angiologia 5:51.
    4. It is a vasodilator.
    Shute, Vogelsang, Skelton and Shute (1948) Surg., Gyn. and Obst. 86:1.
    5. It occasionally lyses scar tissue.
    Steinberg (1948) Med. Clin. N. America 30:221, 1946.
    6. It prevents scar contraction as wounds heal.
    Shute, Vogelsang, Skelton and Shute (1948) Surg., Gyn. and Obst. 86:1.
    7. It increases low platelet counts.
    SkeIton, Shute, Skinner and Waud (1946) Science 103:762.
    8. It decreases the insulin requirement in about 1/4 of diabetics.
    Butturini (1950) Gior. di Clin. Med. 31:1.
    Tolgyes (1957) Summary 9:10.
    9. It is one of the regulators of fat and protein metabolism.
    Hickman (1948) Rec. of Chem. Progress, p.104.
    10. It stimulates muscle power.
    Percival (1951) Summary 3:55.
    11. It preserves capillary walls.
    Ames, Baxter and Griffith (1951) International Review of Vitamin Research 22:401.
    12. It prevents haemolysis of red blood cells.
    Rose and Gyorgy (1951) Fed. Proc.10:239. 1951.
    Tolgyes, S. and Shute, E. V. (1957), Alpha Tocopherol in the Management of Small Areas of Gangrene. Can. M. A. J. 76:730.
    Shute, E.V. (1957) The Prevention of Congenital Anomalies in the Human: Experiences with Alpha Tocopherol as a Prophylactic Measure. J. Ob. & Gyn. Brit. Emp. 44:390.
    Hauch, J. T. (1957) A New Treatment for Resistant Pressure Sores. Can. M.A.J. 77:125.
    Shute, E. V. (1957) Alpha Tocopherol in Cardiovascular Disease. Oxford University Med. Gaz. 9:96.
    How to Quickly Make Powdered Eggs
    Scramble your eggs in a bowl. Pour them in a saute pan and cook until done. ( an alternative would be to hard boil the eggs as well and then peel off the shell and place in bowl and mash the eggs down till the eggs are in a crumbly or crushed condition)— Drain the excess grease for a few minutes on a paper towel. Break the eggs into tiny pieces.–Spread the eggs out onto a baking sheet. Dry at 135° F for at least 10 hours.–Run the eggs through a blender until they form a fine powder. Store your powdered eggs either in a glass container or a jar with a tight lid.—you may need to add some salt as a preservative—- How to Make Powdered Eggs
    The yolks should be firm and the whites thick. Fresh eggs will sink when placed in cold water.
    Beat egg whites into a stiff meringue. Spread on a Teflon tray.
    Beat egg yolks until thick and foamy. Pour on to a separate pyrex or a nonstick material. ( some may use Teflon since it is non stick—that will be for you to determine
    Another Method —
    DRY BETWEEN 105° AND 115°.
    Dry until crisp or brittle, usually about 10-12 hours.
    Crumble, then powder eggs using a dry food/seed grinder. Combine powdered yolks and whites. For a finer powder, re-dry for a few hours then grind once again.
    áDrying Cooked Eggs: Peel hardboiled eggs and chop. Place in a pyrex or a nonstick material that is not hazardous. Yolks and whites may be dried separately or together. Dry at 105° to 115° for 8-10 hours.
    Storing Dried Eggs:
    Because of their fat content, dried eggs should be kept refrigerated. They should be kept only 3 or 4 weeks unless frozen. They will keep unrefrigerated for a week or so and are ideal for camping.—this is due to the fat if you hard boil them and then mash them down it will be with out the fats that may go rancid—and can be use stored with salt
    Using Dried Eggs:
    Generally, 1-1/2 tablespoons of dried egg powders plus an equal amount of water is equivalent to one egg. This will vary slightly depending on the size of eggs you started with. When reconstituting dried COOKED EGGS, add slightly more than half as much water as egg.
    Heavenly Scrambled Eggs
    1/4 cup dried eggs
    1/4 cup powdered milk
    2 teaspoons Butter Buds
    1/2 cup water
    Salt & pepper to taste
    Mix together all ingredients. Let stand several minutes. Cook in oiled frying pan until done.
    1 serving.
    Comment on the Process of drying eggs
    I dehydrate eggs with a Mr. Coffee dehydrator. I do 6 at a time, and use the fruit roll sheet on the top tray. I beat the eggs as if I were going to make an omlette, then freeze them in a glass jar in the freezer overnight.—When I’m ready to dry them, I let them thaw, but not warm to room temp. Freezing seems to speed up the process a little. After about 18 hours of drying, they’re dry and brittle. I powder them with an old coffee grinder, but a blender or food processor will work just as well. The egg powder goes into ziplock baggies, and in the cupboard.—I’ve used eggs that I’ve dehydrated this way for omlettes and cooking, with no problems. To rehydrate for use, I mix two measures of water for each measure of powder.—I have some eggs that were dehyrated over 5 years ago, and stored in the cupboard in a ziplock bag, that are still good to us—( Again Use some salt as a precaution to keep it preserved )—my special note
    Synergistic effects of tea polyphenols and ascorbic acid on human lung adenocarcinoma SPC-A-1 cells.
    J Zhejiang Univ Sci B. 2010 Jun;11(6):458-64
    Authors: Li W, Wu JX, Tu YY
    Tea polyphenols have been shown to have anticancer activity in many studies. In the present study, we investigated effects of theaflavin-3-3′-digallate (TF(3)), one of the major theaflavin monomers in black tea, in combination with ascorbic acid (AA), a reducing agent, and (-)-epigallocatechin-3-gallate (EGCG), the main polyphenol presented in green tea, in combination with AA on cellular viability and cell cycles of the human lung adenocarcinoma SPC-A-1 cells. The 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyl tetrazolium bromide (MTT) assay showed that the 50% inhibition concentrations (IC(50)) of TF(3), EGCG, and AA on SPC-A-1 cells were 4.78, 4.90, and 30.62 micromol/L, respectively. The inhibitory rates of TF(3) combined with AA (TF(3)+AA) and EGCG combined with AA (EGCG+AA) at a molar ratio of 1:6 on SPC-A-1 cells were 54.4% and 45.5%, respectively. Flow cytometry analysis showed that TF(3)+AA and EGCG+AA obviously increased the cell population in the G(0)/G(1) phase of the SPC-A-1 cell cycle from 53.9% to 62.8% and 60.0%, respectively. TF(3)-treated cells exhibited 65.3% of the G(0)/G(1) phase at the concentration of its IC(50). Therefore, TF(3)+AA and EGCG+AA had synergistic inhibition effects on the proliferation of SPC-A-1 cells, and significantly held SPC-A-1 cells in G(0)/G(1) phase. The results suggest that the combination of TF(3) with AA or EGCG with AA enhances their anticancer activity.–PMID: 20506578 [PubMed – indexed for MEDLINE]
    Bisphenol A officially declared toxic by Canada
    Canada became the first country in the world yesterday to declare bisphenol A (BPA) to be a toxic substance that poses risks to human health and the environment. –The announcement by the Canadian Health and Environment Ministries confirmed the chemical had formally been added Schedule 1 of the Canadian Environmental Protection Act, 1999 (CEPA 1999). —“The Government of Canada has a strong record of taking action on Bisphenol A to protect the environment and health of Canadians,” said Environment Minister Jim Prentice. “We are continuing our leadership on this issue and…working hard to monitor and manage Bisphenol A.” –BPA is an industrial chemical used to make a hard, clear plastic such as re-usable polycarbonate baby bottles. It is also used in the manufacture of epoxy resins, which act as a protective lining on the inside of metal-based food and beverage cans.
    Danger to human life or health —In the order adding BPA to the toxic register, Health Canada identified dietary intake as the primary source of human exposure. It underlined concerns regarding the link between the chemical and neurodevelopmental and behavioural effects in rodents and said it was “considered appropriate to apply a precautionary approach when characterizing risk to human health”. —“Therefore, it was concluded that bisphenol A should be considered as a substance that may be entering the environment in a quantity or concentration or under conditions that constitute or may constitute a danger in Canada to human life or health,” said the government order.
    Scientific opinions —Canada’ s announcement yesterday is the culmination of two year’s deliberations and differs markedly from the recent opinion from the European Food Safety Authority (EFSA) which dismissed scientific concerns raised recently in scores of studies – including BPA’s link with neurodevelopmental and behavioural effects. The European body said it had found no scientific evidence that would lead it to recommend altering the tolerable daily intake (TDI) of the chemical. —The Canadian position decision on BPA was also reached in the face of fierce opposition from the chemical industry. The American Chemistry Council executive director Steven Hentges yesterday said the move was “contrary to the weight of worldwide scientific evidence, unwarranted and will unnecessarily confuse and alarm the public”. —But the Canadian Government said its actions had been based on “robust and relevant scientific evidence”. It noted that Health Canada had considered both studies that were based on guidelines for good laboratory practice and those that were not because “they were considered relevant to risk characterization”. –“Our science indicated that Bisphenol A may be harmful to both human health and the environment and we were the first country to take bold action in the interest of Canadians,” said Leona Aglukkaq, Minister of Health.
    Divine Providence medicine Cabinet
    ScienceDaily (Mar. 20, 2007) — When it comes to stocking pharmacy shelves with drugs to treat human ills, God’s Creation is still is the ultimate medicinal chemist, a study scheduled for the March 23 issue of ACS’ Journal of Natural Products, a monthly publication, suggests.
    In the study, the National Cancer Institute’s David J. Newman and Gordon M. Craig conclude that only 30 percent of the critically important “new chemical entities (NCEs)” introduced between 1981 and mid-2006 were synthetic and not based on a naturally-occurring compound. NCEs are totally new drugs, never before available, rather than modified versions of existing medications sometimes termed “me-too” drugs. The remaining 70 percent of the NCEs introduced during the last 25 years were natural products — medicines obtained from sources such as plants and animals, derived from natural products or chemically designed to mimic natural products.–Natural products range from aspirin (originally obtained from the willow tree) to taxol, the anti-cancer drug discovered in the Pacific yew tree. About half of all anti-cancer drugs introduced since the 1940s are either natural products or medicines derived directly from natural products, the study notes.—The new review of natural products’ role as sources of new drugs is an expanded and updated version of reports published in 1997 and 2003. “We strongly advocate expanding, not decreasing, the exploration of Nature as a source of novel active ingredients that may serve as the leads and scaffolds for elaboration into desperately needed efficacious drugs for a multitude of disease indications,” the study concludes.–Story Source: -The above story is reprinted (with editorial adaptations by ScienceDaily staff) from materials provided by American Chemical Society, via EurekAlert!, a service of AAAS
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    Show of the Week October 31 2010
    Sodium intake and mortality in the NHANES II follow-up study
    Sodium, blood pressure, and cardiovascular disease.
    Dietary salt intake and cerebrovascular damage
    Nonhypertensive cardiac effects of a high salt diet.
    Suggestions On Salt
    Sodium intake and mortality in the NHANES II follow-up study. Department of Epidemiology and Population Health, Albert Einstein College of Medicine, Bronx, NY 10461, USA.
    Comment in: Am J Med. 2007 Jan;120(1):e5; author reply e7. –Forsch Komplementmed. 2007 Jun;14(3):184-5.
    PURPOSE: US Dietary Guidelines recommend a daily sodium intake <2300 mg, but evidence linking sodium intake to mortality outcomes is scant and inconsistent. To assess the association of sodium intake with cardiovascular disease (CVD) and all-cause mortality and the potential impact of dietary sodium intake <2300 mg, we examined data from the Second National Health and Nutrition Examination Survey (NHANES II).
    METHODS: Observational cohort study linking sodium, estimated by single 24-hour dietary recall and adjusted for calorie intake, in a community sample (n = 7154) representing 78.9 million non-institutionalized US adults (ages 30-74). Hazard ratios (HR) for CVD and all-cause mortality were calculated from multivariable adjusted Cox models accounting for the sampling design.
    RESULTS: Over mean 13.7 (range: 0.5-16.8) years follow-up, there were 1343 deaths (541 CVD). Sodium (adjusted for calories) and sodium/calorie ratio as continuous variables had independent inverse associations with CVD mortality (P = .03 and P = .008, respectively). Adjusted HR of CVD mortality for sodium <2300 mg was 1.37 (95% confidence interval [CI]: 1.03-1.81, P = .033), and 1.28 (95% CI: 1.10-1.50, P = .003) for all-cause mortality. Alternate sodium thresholds from 1900-2700 mg gave similar results. Results were consistent in the majority of subgroups examined, but no such associations were observed for those <55 years old, non-whites, or the obese.
    CONCLUSION: The inverse association of sodium to CVD mortality seen here raises questions regarding the likelihood of a survival advantage accompanying a lower sodium diet. These findings highlight the need for further study of the relation of dietary sodium to mortality outcomes.
    Sodium, blood pressure, and cardiovascular disease.
    Cohen HW, Alderman MH.
    Department of Epidemiology and Population Health, Albert Einstein College of Medicine, Bronx, New York 10461, USA.
    PURPOSE OF REVIEW: Persistent recommendations for universal restriction of dietary sodium intake are based on associations of sodium intake with blood pressure. No clinical trial data support an association of sodium intake with mortality and morbidity outcomes, however, while results of observational studies appear heterogeneous. Can these contradictory data be reconciled to inform health policy regarding sodium intake recommendations?
    RECENT FINDINGS: We reported (2006) a statistically significant (P = 0.03) association of sodium intake less than 2.3 g/day with increased cardiovascular disease mortality (hazard ratio 1.37) in a representative sample of the US adult population with an observed baseline mean sodium intake of 2.7 g/day. Others reported (2004) a significant (P < 0.01) higher stroke death among males and borderline significant (P = 0.07) for females, for highest compared with lowest sodium tertile in a community in Japan with mean intake of 5.4 g/day.
    SUMMARY: These results are consistent with earlier studies suggesting that the association of sodium with morbidity and mortality in industrial societies follows a ‘J shape’ with a direct association at high levels of average intake (over 4 g), an inverse association at lower levels (less than 2 g) and no measurable effect for the widely prevalent intakes in between.—PMID: 17556882 [PubMed – indexed for MEDLINE]
    Dietary salt intake and cerebrovascular damage.
    Perry IJ.–Department of Epidemiology and Public Health, University College Cork, Ireland.
    AIM: Diet is a major contributor to variation in the occurrence of hypertension and cardiovascular disease, including stroke, worldwide. Dietary salt intake plays a critical role in blood pressure regulation. However the question of whether high dietary salt intake increases risk of stroke, either indirectly via effects on blood pressure or directly via alternative mechanisms has received limited attention.
    DATA SYNTHESIS: Narrative review of evidence linking dietary salt intake with left ventricular hypertrophy and cardiovascular disease end-points.
    CONCLUSIONS: There is accumulating evidence that high salt intake predicts left ventricular hypertrophy, independent of other variables including body mass index and blood pressure. Data are now available from nine different studies worldwide consistent with a significant independent effect of salt intake on left ventricular hypertrophy. There is also evidence from animal experiments and ecological studies of an independent association between salt intake and risk of stroke. However, data from prospective observational studies on the relation between sodium intake and cardiovascular endpoints (including stroke) are sparse and inconsistent. Data from Alderman et al suggesting that there may be a significant inverse association between urinary sodium excretion and risk of cardiovascular disease has attracted controversy. In a number of prospective studies no association between salt intake and cardiovascular disease end-points (including stroke) has been observed. In a recent analysis from the US NHANES follow-up study, there was evidence that high salt intake is strongly and significantly associated with risk of stroke, other cardiovascular disease and all cause mortality in overweight persons, but not in those of normal weight. These findings need to be replicated. However, current data on the association between salt intake, blood pressure and left ventricular hypertrophy support public policy recommendations on the need for a moderate reduction in dietary salt intake at the population level.–PMID: 11079261 [PubMed – indexed for MEDLINE]
    Nonhypertensive cardiac effects of a high salt diet.
    Hu G, Qiao Q, Tuomilehto J.
    Diabetes and Genetic Epidemiology Unit, Department of Epidemiology and Health Promotion, National Public Health Institute, Mannerheimintie 166, FIN-00300 Helsinki, Finland.
    Dietary salt intake plays a major role in variation of blood pressure levels and cardiovascular conditions. High salt intake is associated with the occurrence of hypertension. The evidence that high salt intake increases risk of cardiovascular disease is inconsistent. Some studies indicate a significant and positive association between salt intake and risk of cardiovascular disease, whereas several other studies report that such an association may not exist and that low sodium may even be harmful. It is clear that left ventricular hypertrophy is closely related to salt intake. There is evidence indicating that high salt intake increases renal glomerular filtration rate and glomerular filtration fraction in salt-sensitive patients. The association of high salt intake, insulin resistance, and salt sensitivity, and the interaction between high salt intake, heart rate, and blood pressure are debated. —PMID: 11790286 [PubMed indexed for MEDLINE]
    Suggestions On Salt—if you are using salt and are uncertain of the negative impact -due to the programming we have been taught for a log time, then increase the potassium intake to balance this out–the ratio should be 2:1 –2 parts potassium and one part salt–as an example we would be using a half a tsp to 1 tsp of potassium here is another link to the page where you can increase the knowledge on the power of Salt–
    Here are som other tidbits on Salt
    Sodium Chloride alleviates Hyperchlorhydria (excessive Hydrochloric Acid):
    People who crave Sodium (Salt) are often found to be suffering from Adrenal Insufficiency.
    Cardiovascular System
    Sodium increases the viscosity of Blood.
    Sodium regulates osmotic Blood Pressure:
    Sodium may alleviate Hypotension (by increasing Blood Pressure).
    Sodium neutralizes Acidosis.
    Sodium is a primary Electrolyte.
    Digestive System
    Sodium alleviates Constipation.
    Sodium Sulfate alleviates Diarrhea.
    Flatulence can occur as a result of Sodium deficiency.
    Nausea can occur as a result of Sodium deficiency.
    Vomiting can occur as a result of Sodium deficiency.
    Excretory System
    Optimal Sodium levels are required for the correct function of the Kidneys.
    Sodium deficiency can cause blurred vision in the Eyes.
    Immune System
    Sodium helps to reduce Fevers.
    Optimal Sodium levels are required for the correct function of the Lymphatic System (Sodium is a component of Lymph).