New study postulates the role of dietary advanced glycation end products in the risk of Alzheimer's disease

Damaged DNA amplified by activities such as smoking

Aging impacts epigenome in human skeletal muscle

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Researchers Conclude Wireless Radiation Causes Cancer After Latest Scientific Findings Announced

National advocacy group calls on major children’s health organizations to promote safe technology in schools with the "Turn It Off 4 Kids" Initiative---PRLog Feb. 3, 2015 - The National Association for Children and Safe Technology (NACST) is taking action after two recently published studies indicate there is sufficient evidence demonstrating exposure to wireless radiation, also known as RF-EMF, causes cancer. Wireless routers and devices such as tablets, laptops, baby monitors and cell phones all emit this type of radiation.-NACST is calling on children’s health and cancer prevention organizations to make the issue of children's health and exposure to wireless radiation in educational settings an immediate priority for 2015.

The State of the Science: The Debate is Over

Professor of Oncology Lennart Hardell, MD, PhD, and Statistician Michael Carlberg of Orebro University Hospital, Sweden found a 3-fold risk with 25 or more years of cell and cordless phone use in a study published October 2014 in Pathophysiology. Very significant was the finding that people who first used mobile or cordless phones before the age of 20 had the highest risk.-Increased wireless phone use also correlated with lower survival rates for people diagnosed with the most malignant gliomas in a second study published in the International Journal of Environmental Research and Public Health by the same researchers. Hardell and Carlberg stated, “Due to the relationship with survival, the classification is strengthened.” In both studies, the authors state that RF-EMF should be regarded as a human carcinogen, “requiring urgent revision of current exposure guidelines.”--These two studies followed the July 2014 Occupational and Environmental Medicine Journal publication of the CERENAT case controlled study where French researchers found almost a 3-fold increase in brain cancer with 896 or more hours of lifetime cell phone use.--Based on the accumulation of research demonstrating the health effects from wireless radiation, Professor Olle Johansson of the Karolinska Department of Neuroscience has stated, “the debate is over” on wireless.--
“Given the established and emerging science, it only follows that students be provided a safe learning environment, free from wireless radiation,” stated an NACST spokesperson.

Scientists Call for the World Health Organization to Reclassify RF-EMF

In 2011, the WHO’s International Agency for Research on Cancer (IARC) classified RF radiation as a Class 2B, “possible human carcinogen.” Since 2011, several of the World Health Organization invited scientists have called for a reclassification to an increased risk level. The abstracts of these 2014 studies state that RF should now be regarded as a “Group 1 Human Carcinogen,”[F1] placing it in the same category as tobacco, asbestos and benzene.

NACST’s Turn It Off 4 Kids Initiative

In light of these recent scientific publications and expert warnings, NACST is reaching out to health organizations asking them to prioritize the issue of children’s health and wireless exposures in educational settings for 2015 in the following ways:

1. Call for all new school technology to be hardwired.

2. Call to replace existing wireless technology systems with hardwired systems.

3. Call for the implementation of primary prevention efforts such as educating the public about simple steps to reduce exposure, especially in regard to children and pregnant women.

4. Educate their organization’s members and audience on this issue by emails, informational web pages, updated materials, and all other means possible.

Expert Endorsements

NASCT’s Initiative has been endorsed by several prominent scientists, physicians and safety advocates including Drs. Lennart Hardell, Olle Johansson, Anthony Miller and Dariusz Leszczynski. Dr. Leszczynski was a participating scientist in the WHO IARC panel on RF-EMF and cancer, and Dr. Miller has served as Director of the Epidemiology Unit, National Cancer Institute of Canada, Toronto.--Details on NACST’s Turn It Off 4 Kids Initiative, including endorsements, are here: http://www.nacst.org/nacst-turn-it-off-4-kids.html

About NACST

The National Association for Children and Safe Technology is dedicated to raising awareness about the health impacts of wireless radiation on children as well as advancing policies that safeguard children’s health and well being.

http://www.NACST.org

http://www.prlog.org/12421346-researchers-conclude-wireless-radiation-causes-cancer-after-latest-scientific-findings-announced.html

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Evaluation of the antibacterial potential of Petroselinum crispum-Parsley and Rosmarinus officinalis[F2] against bacteria that cause urinary tract infections.

Braz J Microbiol. 2013;44(3):829-34

Authors: Petrolini FV, Lucarini R, de Souza MG, Pires RH, Cunha WR, Martins CH

Abstract
In this study we evaluated the antibacterial activity of the crude hydroalcoholic extracts, fractions, and compounds of two plant species, namely Rosmarinus officinalis and Petroselinum crispum, against the bacteria that cause urinary tract infection. The microdilution method was used for determination of the minimum inhibitory concentration (MIC) and minimum bactericidal concentration (MBC). The crude hydroalcoholic extract of R. officinalis displayed in vitro activity against Gram-positive bacteria, with satisfactory MBC for the clinical isolate S. saprophyticus. The fractions and the pure compound rosmarinic acid did not furnish promising results for Gram-negative bacteria, whereas fractions 2, 3, and 4 gave encouraging results for Gram-positive bacteria and acted as bactericide against S. epidermidis as well as E. faecalis (ATCC 29212) and its clinical isolate. R. officinalis led to promising results in the case of Gram-positive bacteria, resulting in a considerable interest in the development of reliable alternatives for the treatment of urinary infections. -PMID: 24516424 [PubMed - indexed for MEDLINE]

Recipe for this take equal parts of each and boil as a tea or make an extract or tincture by using the alcohol to pull out the components—you can use either the blender method or the soaking for this

When done would use teaspoon increments 1 tsp every 3 hours

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Chinese Hawthorn Berry

Effects of vitexin-2"-O-rhamnoside and vitexin-4"-O-glucoside on growth and oxidative stress-induced cell apoptosis of human adipose-derived stem cells.

J Pharm Pharmacol. 2014 Jul;66(7):988-97

Authors: Wei W, Ying X, Zhang W, Chen Y, Leng A, Jiang C, Liu J

Abstract
OBJECTIVES: Vitexin-2"-O-rhamnoside (VOR) and vitexin-4"-O-glucoside (VOG) are the two main flavonoid glycosides of the leaves of Cratagus pinnatifida Bge. var. major N. E. Br.[F3] that has been widely used for the treatment of cardiovascular system diseases. In this study, we simultaneously investigated the influence of VOR and VOG on human adipose-derived stem cells (hADSCs) injury induced by hydrogen peroxide (H2 O2 ) to further characterize their anti-oxidative and anti-apoptotic activity. METHODS: hADSCs were isolated, cultured in vitro and pretreated with 62.5 μm VOR or 120 μm VOG for 24 h and then exposed to 500 μm H2 O2 for an additional 4 h. KEY FINDINGS: Pretreatment of hADSCs with VOR and VOG was demonstrated to significantly ameliorate the toxicity and apoptosis effects, such as morphological distortion, nuclear condensation, decreased intracellular caspase-3 activity and percentage of cells in apoptosis/necrosis by using morphological assay, immunocytochemistry and flow cytometric evaluation[F4] . In addition, VOR and VOG caused no cytotoxic effect on hADSCs at concentrations up to 250 and 480 μm, respectively.--CONCLUSIONS: Our results indicated that both VOR and VOG contribute to the protection against H2 O2 -mediated oxidative stress damage and could be safely used for a wide range of concentrations.[F5] PMID: 24533889 [PubMed - indexed for MEDLINE]

Recipe—Percolate the leaves and or fruits of hawthorn berry---make jams---preserves---fuse in oil---and access it as needed or take daily as a tea tincture or fused with a good oil

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New study postulates the role of dietary advanced glycation end products in the risk of Alzheimer's disease

Date:

February 3, 2015

Source:

IOS Press BV

A new paper published in the Journal of Alzheimer's Disease provides evidence that cooking foods at high temperatures increases the risk of Alzheimer's disease. This study looked at the content of advanced glycation end products (AGEs) in national diets and clinical studies comparing and compared total AGEs to Alzheimer's disease rates.---AGEs are a group of compounds that are combinations of sugars and proteins and other large molecules.[F6] They can be formed in the body, and there is a large body of literature on AGEs and Alzheimer's disease. However, AGEs are also formed when food is cooked at high temperatures or aged for a long time such as in hard cheese. AGEs increase the risk of various chronic diseases through several mechanisms including increased inflammation and oxidative stress. They can also bind to the receptor for AGEs (RAGE). RAGE transports beta-amyloid proteins across the blood-brain barrier and contributes to the development of Alzheimer's disease.--Our newly published paper is the first that estimated the AGE content of diets from observational studies in various countries, which estimated the link between dietary factors and risk of Alzheimer's disease.[F7] For this purpose, the values for AGE for many types of food were taken from a study by researchers at the Mount Sinai School of Medicine in New York. They cooked 549 foods by different methods and measured the AGE content of the cooked food..--To use their findings in our study They found that the higher the cooking temperature, the higher the AGE content. For example, 100 grams of raw beef had 707 kU of AGEs, but 100 grams of roast beef had 6071 kU, we obtained information from observational studies in which diet was assessed using food frequency questionnaires or from national dietary supply values from the Food and Agriculture Organization of the United Nations. We then used either a range of cooking temperatures or methods for the observational studies or an estimate of average cooking methods and temperatures for the national dietary supply data.--In typical national diets, we found that meat made the highest contribution of AGEs, followed by vegetable oils, cheese, and fish. Foods such as cereals/grains, eggs, fruit, legumes, milk, nuts, starchy roots, and vegetables generally make low contributions to the total amount of AGEs in a diet, either because they are generally prepared at low temperatures or since they comprise smaller portions of diet[F8] s.--According to Drs. Jaime Uribarri and Weijing Cai of The Icahn School of Medicine at Mount Sinai, "This epidemiological study supports our previous findings in animals and humans of an important role for dietary AGEs in Alzheimer's disease. We found that mice kept on a diet high in AGEs, similar to Western diet, had high levels of AGEs in their brains together with deposits of amyloid-β, a component of the plaques characteristic of Alzheimer's disease, while at the same time developed declines in cognitive and motor abilities. The mice fed a low AGE diet remained free of these conditions. In addition, clinical studies have shown that subjects with higher blood AGE levels, in turn resulting from high AGE diets, are more likely to develop cognitive decline on follow up.--[F9] The findings point to an easily achievable goal that could reduce the risk of dementia through the consumption of non-AGE-rich foods, for example, foods that cooked or processed under lower heat levels and in the presence of more water, raising the importance of not just what we eat, but also how we prepare what we eat.[F10] "--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--Perrone L, Grant WB. Observational and ecological studies of dietary advanced glycation end products in national diets and Alzheimer’s disease incidence and prevalence. Journal of Alzheimer’s Disease, February 2015 DOI: 10.3233/JAD-140720

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Damaged DNA amplified by activities such as smoking

Date:

January 15, 2015

Source:

ETH Zurich

In the majority of cases, the onset of cancer is characterised by a minor change in a person's genetic material. A cell's DNA mutates in a particular area to the extent that the cell no longer divides in a controlled manner, but begins to grow uncontrollably. In many cases, this type of genetic mutation involves chemical changes to individual building blocks of DNA. These changes are induced by smoking tobacco and consuming foods such as cured meats[F11] . This is because the contents of these materials can chemically react with and change building blocks of cellular DNA, thereby creating DNA adducts. Up to now, scientists have been able to determine whether gene samples contain adducts and if so, how many. However, the procedure is laborious and finding out exactly where a building block in the genetic code has been altered into an adduct has not been possible.---Researchers from the team led by Shana Sturla, professor of Food and Nutrition Toxicology, have succeeded for the first time in amplifying gene samples containing DNA adducts while retaining references to these adducts. This type of amplification is a prerequisite for the majority of technologies used by researchers to determine a gene's DNA sequence. In the future, it may therefore be possible to expand DNA sequencing from the four basic DNA building blocks to include adducts. "The scientific community would have an important tool for making a detailed analysis of the molecular mechanisms involved in the initiation of cancer and the corresponding risk factors," says Sturla.---Artificial counterpart found---The researchers focused their efforts on a specific, typical DNA adduct, an alkylguanine called O-6-benzylguanine. They recreated an enzyme reaction in a test tube to obtain a negative copy of the genetic material -- analogous to how DNA is replicated naturally in cells. The scientists first had to find an artificial counterpart of the alkylguanine to be incorporated into the negative copy in its position -- due to the fact that nature produces molecular counterparts to the basic DNA building blocks, but not to DNA adducts. This is why replicating genes usually leads to copy errors (or mutations) when adducts are present.--The ETH researchers produced several artificial derivatives of the basic DNA building blocks in the laboratory and tested them as potential counterparts to the alkylguanine. One proved particularly suitable. The researchers were then able to produce a negative copy of a gene containing the alkylguanine.--The aim of the work carried out by Sturla and her colleagues was to demonstrate that it is feasible to amplify genes even when adducts are present. It should now be possible for researchers to find artificial counterparts to other adducts using the same method. As the ETH Professor points out, this means that altered genes could be amplified in the future and their sequences more easily ascertained. In 2010, Shana Sturla was awarded a five-year ERC Starting Grant from the European Research Council. The current project was partly financed by this award.-Story Source-The above story is based on materials provided by ETH Zurich. The original article was written by Fabio Bergamin. Note: Materials may be edited for content and length.-Journal Reference-Laura A. Wyss, Arman Nilforoushan, Fritz Eichenseher, Ursina Suter, Nina Blatter, Andreas Marx, Shana J. Sturla. Specific Incorporation of an Artificial Nucleotide Opposite a Mutagenic DNA Adduct by a DNA Polymerase. Journal of the American Chemical Society, 2015; 137 (1): 30 DOI: 10.1021/ja5100542

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Aging impacts epigenome in human skeletal muscle

Date:

November 20, 2013

Source:

Buck Institute for Research on Aging

Our epigenome is a set of chemical switches that turn parts of our genome off and on at strategic times and locations. These switches help alter the way our cells act and are impacted by environmental factors including diet, exercise and stress[F12] . Research at the Buck Institute reveals that aging also effects the epigenome in human skeletal muscle. The study, appearing on line in Aging Cell, provides a method to study sarcopenia, the degenerative loss of muscle mass that begins in middle age.---The results came from the first genome-wide DNA methylation study in disease-free individuals. DNA methylation involves the addition of a methyl group to the DNA and is involved in a particular layer of epigenetic regulation and genome maintenance. In this study researchers compared DNA methylation in samples of skeletal muscle taken from healthy young (18 -- 27 years of age) and older (68 -- 89 years of age) males. Buck faculty and lead scientist Simon Melov, PhD, said researchers looked at more than 480,000 sites throughout the genome. "We identified a suite of epigenetic markers that completely separated the younger from the older individuals -- there was a change in the epigenetic fingerprint," said Melov. "Our findings were statistically significant; the chances of that happening are infinitesimal."--Melov said scientists identified about six-thousand sites throughout the genome that were differentially methylated with age and that some of those sites are associated with genes that regulate activity at the neuromuscular junction which connects the nervous system to our muscles. "It's long been suspected that atrophy at this junction is a weak link in sarcopenia, the loss of muscle mass we get with age," said Melov. "Maybe this differential methylation causes it. We don't know."--Studying the root causes and development of sarcopenia in humans is problematic; the research would require repeated muscle biopsies taken over time, something that would be hard to collect.[F13] Melov says now that the epigenetic markers have been identified in humans, the goal would be to manipulate those sites in laboratory animals. "We would be able to observe function over time and potentially use drugs to alter the rate of DNA methylation at those sites," he said. Melov says changes in DNA methylation are very common in cancer and that the process is more tightly controlled in younger people.-Story Source-The above story is based on materials provided by Buck Institute for Research on Aging. Note: Materials may be edited for content and length.-Journal Reference-Simon Melov, PhD et al. Genome-wide DNA methylation changes with age in disease-free human skeletal muscle. Aging Cell, November 2013

TOP

[F1]This is huge---the implication here should lead to huge lawsuits and force the telecommunications industry to come up with better shielding of this radiation leaking into the brain

[F2]Parsely and Rosemary---would either water extract as a tea combo or alcohol extract for tincture

[F3]Hawthorn Berry

[F4]Plain English it stopped death

[F5]Strong as you like

[F6]This causes glycation when the sugars and proteins bind together---causing huge amounts of free radicals so when cooking proteins with carbs can cause this to happen as well

[F7]Another factor that is not considered when adding glyphosates into the foods and genetics with the sugars and proteins this to causes a chemical reaction and when adding nano silver ---the sugar makes the silver more toxic to the body----

[F8]These are not safer in the sense that they are relatively free---these are less toxic due to less consumption---but to offset the effect of AGE---things like B1 and MSM both have anti glycating effects

[F9]Again this is when High heat and proteins and carbs( sugars) are cooked together ---always remember the concept of glycation protein + sugar connected chemically when heated at high heat causes damage

[F10]This is Key

If your cooking or fusing proteins with sugars this is what will cause the issues---if your diet is relatively high in sugar then you can as well cause this effect

[F11]This is an old report ---we know today that almost anything being consumed with genetics---glyphosates –endocrine disrupting chemicals—nanoparticles—metals –phytoestrogenic foods will also cause this kind of mutation

[F12]Or environmental pollutants –Genetics—PhytoCheistry—Pesticides—Metal exposure

[F13]Unless you were harvesting people from hospitals

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Show of the Month February 14 2015

Pharma Lies To Doctors about The Medicine You are Taking

Marketable Window Dressing

Vitamin A for treating measles in children

Vitamin A may Counteract these Potentially Toxic Substances

Vitamin A supplementation for preventing morbidity and mortality in children from 6 months to 5 years of age

Vitamin A’s Immune System Health Benefits

How much sleep do we really need?

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Pharma Lies To Doctors about The Medicine You are Taking

By: Shane Ellison, MS

Following doctor’s orders has become synonymous with danger.

In my book, Over-The-Counter Natural Cures, I documented that every year, FDA- approved drugs kill twice as many people as the total number of U.S. deaths from the Vietnam War.

Death by medicine flourishes because deceit, not science, governs a doctor’s prescribing habits. --Working as a pharmaceutical chemist, I learned that the deceit comes in many forms. --Medical ghostwriting and checkbook ‘science’ are the most prominent. --Doctors rely on peer-reviewed medical journals to learn about prescription drugs. --These journals include the Lancet, British Medical Journal, New England Journal of Medicine and the Journal of the American Medical Association. --It’s assumed that these professional journals offer the hard science behind any given drug. This assumption is wrong. --Thanks to medical ghost-writing, medical journals can’t be trusted. --Medical ghostwriting is the practice of hiring Ph.D.s to crank out drug reports that hype benefits while hiding negative side effects. --Once complete, drug companies recruit doctors to put their name on the report as the authors.--These reports are then published in the above mentioned medical journals. --The carrot for this deceitful practice is money and prestige. Ghostwriters can receive up to $20,000 per report. Doctors receive prestige from having been published.--As deplorable as medical ghostwriting sounds, it is more common than you think. --Dr. Jeffrey Drazen, editor for the New England Journal of Medicine, insists that he cannot find drug review authors who do not have financial ties to drug companies. --Dr. David Healy, of the University of Wales, predicts that 50% of the journals drug review articles are written by ghostwriters hired by Big Pharma.--The editor of the British Journal of Medicine has acknowledged that medical ghostwriting has become a serious problem for his publication: “We are being hoodwinked by the drug companies. --The articles come in with doctors’ names on them and we often find some of them have little or no idea about what they have written.”--Consider the testimony from deputy editor of the Journal of the American Medical Association: --“This [journal articles] is all about bypassing science. --Medicine is becoming a sort of Cloud Cuckoo Land, where doctors don’t know what papers they can trust in the journals, and the public doesn’t want to believe.”

Confessions of Ghostwriters----

Ex-medical ghostwriter Susanna Rees stated: --“Medical writing agencies go to great lengths to disguise the fact that the papers they ghostwrite and submit to journals and conferences are ghostwritten on behalf of pharmaceutical companies and not by the named authors,’ she wrote. ‘There is a relatively high success rate for ghostwritten submissions ─ not outstanding, but consistent.”--Other ghostwriters have come forward privately:

Ghostwriter 1--“I agreed to do two reviews for a supplement to appear under the names of respected ‘authors.’ I was given an outline, references, and a list of drug-company approved phrases.-I was asked to sign an agreement stating that I would not disclose anything about the project. I was pressured to rework my drafts to position the product more favorably.”

Ghostwriter 2--“I was told exactly what the drug company expected and given explicit instructions about what to play up and what to play down.”

NSAID Popularity Courtesy of Ghostwriting not Science

To illustrate the negative impact of medical ghostwriting, we can look to commonly used non-steroidal anti-inflammatory drugs (NSAIDs). --Between 1990 and 1997, all clinical trials performed on NSAIDS such as Vioxx, Aleve, Aspirin, Motrin, and Ibuprofen, were sponsored by the drug manufacturers. --The result was that 100% of the studies showed the sponsored drug to have equal or superior efficacy when compared to other drugs. --Thus, according to studies done from 1990-1997, every NSAID drug tested during this time was superior to every other NSAID product… all at the same time! --The fallacies behind medical ghost writing on NSAIDS are exposed through injuries and deaths among users.--Approximately 107,000 patients are hospitalized every year for NSAID-related gastrointestinal complications. --Vioxx alone injured 100,000 during its rein as king of pain killers. --The risk of miscarriage for women who take the NSAID aspirin is 60 percent higher than for those who do not. --At least 16,500 NSAID-related deaths occur each year among arthritis patients. This figure is comparable to the number of deaths from the so-called acquired immunodeficiency syndrome (AIDS). In fact, NSAIDS contribute to as many deaths as multiple myeloma, asthma, and cervical cancer combined. --These statistics do not account for over-the-counter use of NSAIDS, only for arthritis patients. --We can be confident that there are considerably more deaths caused by the use of NSAIDS that go unreported. --And because few medical doctors are unaware of these statistics, NSAIDS can rightfully be considered a silent killer. --This is especially true when “experts” are paid by Big Pharma to write favorable reviews while hiding dangerous side effects.

Buying Results, Professors and Government

Other weapons of mass deception exist ─ ‘checkbook science.’ --As defined by Diana Zuckerman, Ph.D., checkbook science is research intended not to expand knowledge or to benefit humanity but instead to sell products [drugs].--It has stolen the very soul of University research, scientific method, and the patients who serve as human subjects.--Checkbook science explains why deadly drugs are approved. --Leveraging their financial power, drug companies structure the protocol designed to study whether or not a drug is safe. They choose the investigators (from academics and government institutions) and in many instances are involved in the collation, interpretation and reporting of data. Akin to medical ghostwriting, this practice allows drug companies to hide the dangers associated with drugs while highlighting benefits.5 As with medical ghostwriting, checkbook science is more common than you think. A third of academic professors have personal financial ties to drug makers. Government institutions are guilty, too. Called the “Stealth Merger” by The LA Times, top scientists at the National Institutes of Health also collect paychecks and stock options from the drug industry[F1] .-Once considered “an island of objective and pristine research, untainted by the influences of commercialization,” the National Institutes of Health has become corrupted by checkbook science. -To substantiate, we look to the following statistics from the LA Times:--Dr. Stephen I. Katz, director of the NIH’s National Institute of Arthritis and Musculoskeletal and Skin Diseases collected between $476,369 and $616, 365 in fees over a ten-year period.-------From 1997-2002, Dr. John I. Gallin, director of the NIH’s Clinical Center, received between $145,000 and $322,000 in fees and stock proceeds from the drug industry.---Dr. Richard C. Eastman is the NIH’s top diabetes researcher.-As a consultant to the drug manufacturers in 1997, he wrote to the Food and Drug Administration (FDA) defending a product without disclosing his conflict of interest. --His letter stated that the risk of liver failure from the given drug was “very minimal.” ---Six months later, a patient taking the drug in an NIH study that Eastman oversaw, Audrey LaRue Jones, suffered sudden liver failure and died--An autopsy, along with liver experts, found that the drug had caused the liver failure.---Dr. Ronald N. Germain, deputy director of a major laboratory at the National Institute of Allergy and Infectious Diseases, amassed more than $1.4 million od Big Pharma money in “consulting fees” from 1993 to 2003, plus stock options.

Jeffrey Schlom, director of the National Cancer Institute’s Laboratory of Tumor Immunology and Biology, received $331,500 in company fees over 10 years.---Jeffrey M. Trent, who became scientific director of the National Human Genome Research Institute in 1993, reported between $50,608 and $163,000 in industry consulting fees. He left the government in 2002.

Lying to Doctors is Legal

Checkbook science has been going on for more than 20 years. Known as the Bayh-Dole Act, U.S patent law was amended in 1980 to allow for these flagrant conflicts of interest. --Heart drugs introduced in the 1970‘s serve as an excellent example of how checkbook science damages the public’s health. ---By 1990, they were estimated to kill more Americans than the 58,000 killed in the Vietnam War.--This disaster could have been avoided. --Early research suggesting that these drugs were lethal would have saved thousands of lives. --Putting checkbook science to work, these risky research findings went unpublished by the pharmaceutical company that funded the research.--Children suffer, too, from checkbook science. Checkbooks science was responsible for motivating doctors to push antidepressants on this vulnerable population.[F2]

Checkbook Science Gets Antidepressant Approved for Kids!

Published research paid for by drug manufactures showed antidepressant drugs (selective serotonin reuptake inhibitors) to be safe and effective for children. --These drugs include Paxil and Prozac. -Conversely, when unpublished results were finally obtained it was discovered that depressed children taking antidepressants were twice as likely to become suicidal as children taking a placebo. --Acknowledging the deceit, the Lancet stated: “The story of research into SSRI use in childhood depression is one of confusion, manipulation, and institutional failure.”7

Drug Advertising Gets You Hooked

Hopefully the line at the pharmaceutical trough will grow shorter as the medical ghostwriting and checkbook science scandal becomes public. --Yet drug makers have an insurance policy for this ─ Direct-to-Consumer advertising. The oft repeated “ask your doctor” ensures that the herd instinctively embraces drugs, drugs, and more drugs.

Doctors Only See Positive, Not Negative, You Suffer

Understanding medical ghost-writing and checkbook science explains why medical doctors have been hypnotized into drug worship ─ they only see the positive[F3] . --It also explains why modern medicine is more deadly and lucrative than war ─ the danger has been silenced with the pen and money. -In sum, these methods of deceit ensure that doctors are not keen to the dangers of prescription drugs. --Drug companies do not take responsibility for the wanton prescription drug deceit. --Instead, victims have been made invisible – dehumanized. --They are not recognized as children or as men with a significant contribution to society.--Instead their deaths are attributed to them being sick or just too damn old[F4] . ---Those who profit from prescription drugs should hold some sort of record for demonstrating the most reckless disregard for human life.--If the deceit continues the prescription drug leviathan will silently kill more people than Napalm dropped on Vietnamese villages. Realize –research and make your own remedies—utilizing things that will not cause more problems then you already are dealing with

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Marketable Window Dressing

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Vitamin A for treating measles in children

Huiming Y¹, Chaomin W, Meng M.

Author information

Abstract

BACKGROUND:

Measles is a major cause of childhood morbidity and mortality. Vitamin A deficiency is a recognized risk factor for severe measles infections. The World Health Organization (WHO) recommends administration of an oral dose of vitamin A (200,000 international units (IU), or 100,000 IU in infants) each day for two days to children with measles when they live in areas where vitamin A deficiency may be present.

OBJECTIVES:

To determine whether vitamin A therapy, commenced after measles has been diagnosed, is beneficial in preventing mortality, pneumonia and other secondary complications in children.

SEARCH STRATEGY:

We searched the Cochrane Central Register of Controlled Trials (CENTRAL) (The Cochrane Library Issue 1, 2005), MEDLINE (1966 to March 2005), EMBASE (1980 to December 2004) and looked for unpublished studies.

SELECTION CRITERIA:

Only randomized controlled trials in which children with measles were given vitamin A or placebo along with standard treatment were considered.

DATA COLLECTION AND ANALYSIS:

Studies were assessed independently by two authors. The analysis of dichotomous outcomes was done using the StatXact software and results expressed as relative risk (RR) with 95% confidence interval (CI). Subgroup analyses were carried out for dose, formulation, age, hospitalization and pneumonia-specific mortality. Weighted mean differences (WMD) with 95% CI were calculated for continuous outcomes.

MAIN RESULTS:

There was no significant reduction in the risk of mortality in the vitamin A group when all the studies were pooled using the random-effects model (RR 0.70; 95% CI 0.42 to 1.15). Using two doses of vitamin A (200,000 IU) on consecutive days was associated with a reduction in the risk of mortality in children under the age of two years (RR 0.18; 95% CI 0.03 to 0.61) and a reduction in the risk of pneumonia-specific mortality (RR 0.33; 95% CI 0.08 to 0.92). There was no evidence that vitamin A in a single dose was associated with a reduced risk of mortality among children with measles. There was a reduction in the incidence of croup (RR 0.53; 95% CI 0.29 to 0.89) but no significant reduction in the incidence of pneumonia (RR 0.92; 95% CI 0.69 to 1.22) or diarrhoea (RR 0.80; 95% CI 0.27 to 2.34) with two doses.

AUTHORS' CONCLUSIONS:

Although we found no overall significant reduction in mortality with vitamin A therapy for children with measles there was evidence that two doses were associated with a reduced risk of mortality and pneumonia-specific mortality in children under the age of two years. There were no trials that directly compared a single dose with two doses.

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Vitamin A may Counteract these Potentially Toxic Substances

Electromagnetic Radiation

Vitamin A (large dosages of 35,000 - 100,000 IU per day) may improve the general condition of persons undergoing Radiation Therapy

: references

Vitamin A may help to prevent Radiation Therapy-induced Pneumonitis (if Vitamin A therapy is commenced prior to Radiation Therapy).

Vitamin A (especially the Retinyl Palmitate form of Vitamin A applied topically) may inhibit the ability of UV-B to cause Sunburn (i.e. topically applied Retinyl Palmitate may function as a Sunscreen). references

Environmental Toxins

Vitamin A may help to protect the body from the toxic effects of Air Pollution. references

Vitamin A may counteract some of the toxic effects of Dioxin exposure. references

Enzymes

Vitamin A (Retinol and Retinoic Acid forms) may inhibit Lipoxygenase. references

Vitamin A may inhibit Ornithine Decarboxylase. references

Hormones

Vitamin A may help to lower elevated Cortisol levels. references

Immune System Chemicals

Vitamin A may inhibit the production of excessive quantities of Tumor Necrosis Factor (TNF). references

Minerals

Vitamin A may facilitate the detoxification of Lead from the body. [more info]

Pharmaceutical Drugs

Vitamin A (administered concurrently with Methotrexate) may inhibit the damage to the Small Intestine caused by Methotrexate. references

Vitamin A (Retinol) may counteract and prevent the suppression of the Immune System that is caused by Pharmaceutical Glucocorticosteroids. references

Proteins

Vitamin A may counteract the toxicity of Amyloid-Beta Protein. references

Vitamin A may lower elevated Fibrinogen levels. references

Vitamin A may inhibit the activation of Nuclear Factor-Kappa B (NF-Kappa B). references

Recreational Drugs

Vitamin A may counteract the toxic effects of Tobacco smoking (by strengthening the Mucous Membranes of the Bronchial Tubes and Lungs): references

Vitamin A may inhibit the ability of Tobacco to cause Emphysema.

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Vitamin A supplementation for preventing morbidity and mortality in children from 6 months to 5 years of age.

Imdad A¹, Herzer K, Mayo-Wilson E, Yakoob MY, Bhutta ZA.

Author information

Abstract

BACKGROUND:

Vitamin A deficiency (VAD) is a major public health problem in low and middle income countries affecting 190 million children under 5. VAD can lead to many adverse health consequences, including death.

OBJECTIVES:

To evaluate the effect of vitamin A supplementation (VAS) for preventing morbidity and mortality in children aged 6 months to 5 years.

SEARCH STRATEGY:

We searched the Cochrane Central Register of Controlled Trials (CENTRAL 2010 Issue 2), MEDLINE (1950 to April Week 2 2010), EMBASE (1980 to 2010 Week 16), Global Health (1973 to March 2010), Latin American and Caribbean Health Sciences (LILACS), metaRegister of Controlled Trials and African Index Medicus (27 April 2010).

SELECTION CRITERIA:

Randomised controlled trials (RCTs) and cluster RCTs evaluating the effect of synthetic VAS in children aged 6 months to 5 years living in the community. We excluded studies concerned with children in hospital and children with disease or infection. We excluded studies evaluating the effects of food fortification, consumption of vitamin A rich foods or beta-carotene supplementation.

DATA COLLECTION AND ANALYSIS:

Two review authors independently assessed studies for inclusion. Data were double abstracted and discrepancies were resolved by discussion. Meta-analyses were performed for outcomes including all-cause and cause-specific mortality, disease, vision, and side-effects.

MAIN RESULTS:

43 trials involving 215,633 children were included. A meta-analysis for all-cause mortality included 17 trials comprising 194,795 children with 3536 deaths in both groups. At follow-up, there was a 24% observed reduction in the risk of all-cause mortality for Vitamin A compared with Control (Relative risk (RR) = 0.76 [95% confidence interval (CI) 0.69, 0.83]). Seven trials reported diarrhoea mortality and a 28% overall reduction for VAS (RR = 0.72 [0.57, 0.91]). There was no significant effect of VAS on cause specific mortality of measles, respiratory disease and meningitis. VAS reduced incidence of diarrhoea (RR = 0.85 [0.82, 0.87]) and measles morbidity (RR = 0.50 [0.37, 0.67]); however, there was no significant effect on incidence of respiratory disease or hospitalisations due to diarrhoea or pneumonia. There was an increased risk of vomiting within the first 48 hours of VAS (RR = 2.75 [1.81, 4.19]).

AUTHORS' CONCLUSIONS:

VAS is effective in reducing all-cause mortality by about 24% compared to no treatment. In our opinion, given the evidence that VAS causes considerable reduction in child mortality, further placebo-controlled trials of VAS in children between 6 months and 5 years of age are not required. There is a need for further studies comparing different doses and delivery mechanisms (for example, fortification).

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Vitamin A’s Immune System Health Benefits

Immune System: Ailments

Vitamin A may help to prevent most Bacterial & Viral Diseases and Vitamin A deficiency increases susceptibility to Bacterial & Viral Diseases (via numerous mechanisms that involve the Immune System): references

Vitamin A may help to prevent infections from Viruses: references

Vitamin A may be useful for the treatment of Acquired Immune Deficiency Syndrome (AIDS): references

Vitamin A may retard the onset of full-blown AIDS in persons who are infected with the HIV virus.

High Vitamin A concentrations may suppress the replication of the HIV virus in Macrophages.

Vitamin A deficiency has been correlated with increased (earlier) mortality in AIDS patients.

Vitamin A may help to increase the number of circulating Helper T-Cells in AIDS patients.

Vitamin A supplementation (during early Pregnancy) dramatically reduces the rate of vertical transmission (i.e. from mother to infant) of the HIV virus.

Vitamin A deficiency may increase the body’s susceptibility to Chickenpox infection. references

Vitamin A (50,000 - 150,000 IU per day for three to five days) may exert anti-viral effects against the Viruses that cause the Common Cold. references

Vitamin A (50,000 - 150,000 IU per day for three to five days) may exert anti-viral effects against the Viruses that cause Influenza. references

Vitamin A may deactivate the Herpes Simplex Virus Type 2. references

Vitamin A reduces the mortality rate in children infected with Measles by up to 50%. references

Vitamin A deficiency may increase the risk of (meningococcal) Meningitis. references

Vitamin A (12,500 - 25,000 IU per day) significantly reduces the severity of the Respiratory Syncytial Virus (RSV). references

Vitamin A deficiency may exacerbate the severity of Rotavirus infection. references

Vitamin A may accelerate the recovery from Shigella infections (but does not inhibit or kill Shigella species). references

Vitamin A may reduce Inflammation. references

Vitamin A (100,000 IU daily for two weeks) may improve various impairments of the function of the Immune System in Systemic Lupus Erythematosus (SLE) patients. references

Vitamin A (Retinol form) may help to prevent Malaria (by suppressing the Plasmodium falciparum Protozoa that causes Malaria). references

Immune System: Ailments: Cancer

Vitamin A may help to prevent many types of Cancer and Vitamin A therapy may suppress the further growth of the (already established) tumors involved in some types of Cancer: references

Vitamin A may may help to prevent Basal Cell Carcinoma. references

Vitamin A (40,000 IU per day) may reduce the recurrence of Bladder Cancer tumors in people with existing Bladder Cancer by up to 53%. references

Vitamin A may help to prevent Breast Cancer. references

Vitamin A may help to prevent Cervical Cancer. references

Vitamin A may help to prevent Colon Cancer. references

Vitamin A may help to prevent Endometrial Cancer. references

Vitamin A may help to prevent Esophageal Cancer. references

Vitamin A (100,000 IU per day) “may” help to treat Glioblastoma Multiforme.

The Retinyl Palmitate (300,000 IU - 1,500,000 IU per day, caution: a high dosage) form of Vitamin A may help to prevent Larynx Cancer (laryngeal cancer). references

The Retinoic Acid form of Vitamin A (administered orally) may "direct" the cancerous cells involved in Leukemia to mature and die like normal cells.

Vitamin A may help to prevent Liver Cancer. references

Vitamin A may inhibit the tumor promotion stage of Lung Cancer. references

Vitamin A may inhibit the development of the tumors associated with Mouth Cancer. references

Vitamin A may help to prevent and treat Ovarian Cancer. references

Vitamin A may help to prevent Pharynx Cancer (Pharyngeal Cancer) by strengthening the Mucous Membranes of the Pharynx. [more info]

Vitamin A may help to prevent Prostate Cancer by strengthening the Mucous Membranes of the Prostate. references

Vitamin A may prevent the initiation and/or progression of Skin Cancers by stimulating normal Cell differentiation: references

Vitamin A may inhibit the growth and metastasis of malignant Melanoma. references

The Retinol form of Vitamin A may help to prevent Squamous Cell Carcinoma. references

Stomach Cancer references

Testicle Cancer [more info]

Vitamin A may help to prevent or regress Tongue Cancer. references

Vitamin A may help to prevent carcinogens-induced Uterus Cancer. references

Supplemental Vitamin A increases the effectiveness of conventional medical treatments for Cancer (such as Surgery, Chemotherapy and Radiation Therapy).

Immune System: Underyling Mechanisms

Vitamin A may stimulate various aspects of the Immune System: references

Vitamin A may increase the effectiveness of the Cells that produce Antibodies and Vitamin A deficiency may cause impairment in the response of Antibodies to challenges by Antigens. references

Vitamin A deficiency may cause a reduction in the production of B-Lymphocytes. references

Vitamin A deficiency may cause a decline in the production of Helper T-Cells. references

Vitamin A may increase the proliferation of Lymphocytes in response to challenges by Antigens and Mitogens. references

Vitamin A may enhance the function of Macrophages. references

Vitamin A may enhance the function of Neutrophils. references

Vitamin A deficiency impairs the function of NK Lymphocytes. references

Vitamin A deficiency causes degeneration and atrophy of the Spleen. references

Vitamin A may protect and strengthen the Thymus and supplemental Vitamin A may cause the Thymus to (beneficially) double in size. references

Vitamin A may enhance the ability of the Thymus to manufacture T-Lymphocytes and Vitamin A deficiency may cause impairment of T-Lymphocyte response. references

Vitamin A may enhance the function of White Blood Cells. references

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Vitamin A for treating measles in children.

D'Souza RM¹, D'Souza R.

Author information

Update in

Cochrane Database Syst Rev. 2002;(1):CD001479.

Abstract

BACKGROUND:

Measles is a leading cause of childhood morbidity and mortality. Vitamin A deficiency is a recognised risk factor for severe measles. The World Health Organization (WHO) recommends administration of an oral dose of 200,000 IU (or 100,000 IU in infants) of vitamin A per day for two days to children with measles in areas where vitamin A deficiency may be present.

OBJECTIVES:

The purpose of this review is to determine whether vitamin A when commenced after measles has been diagnosed, is beneficial in preventing mortality, pneumonia and other complications in children.

SEARCH STRATEGY:

MEDLINE and the Cochrane Library, Issue 4, 1999 were searched.

SELECTION CRITERIA:

Only randomized controlled trials in which children with measles were given vitamin A or placebo along with standard treatment were considered.

DATA COLLECTION AND ANALYSIS:

Studies were assessed independently by two reviewers. The analysis of dichotomous outcomes was done using the StatExact software package. Sub-group analyses were done for dose, formulation, age, hospitalisation and pneumonia specific mortality. Weighted mean difference with 95% CI were calculated for continuous outcomes.

MAIN RESULTS:

The relative risks (RR) and 95% Confidence Intervals (CI) are based on the estimates from the StatExact software package. There was no significant reduction in mortality in the vitamin A group when all the studies were pooled together (RR 0.60; 95% CI 0.32 to 1.12)(Statexact estimate). There was a 64% reduction in the risk of mortality in children who were given two doses of 200,000 IU of vitamin A (RR=0.36; 95% CI 0.14 to 0.82) as compared to placebo. Two doses of water based vitamin A were associated with a 81% reduction in risk of mortality (RR=0.19; 95% CI 0.02 to 0.85) as compared to 48% seen in two doses of oil based preparation[F5] (RR=0.52; 95% CI 0.16 to 1.40). Two doses of oil and water based vitamin A were associated with a 82% reduction in the risk of mortality in children under the age of 2 years (RR=0.18; 95% CI 0.03 to 0.61) and a 67% reduction in the risk of pneumonia specific mortality (RR=0.33; 95% CI 0.08 to 0.92). There was no evidence that vitamin A in a single dose of 200,000 IU was associated with a reduced risk of mortality among children with measles (RR=0.77; 95% CI 0.34 to 1.78). Sub-groups like age, dose, formulation, hospitalisation and case fatality in the study area were highly correlated and there were not enough studies to separate out the individual effects of these factors. There was a 47% reduction in the incidence of croup (RR=0.53; 95% CI 0.29 to 0.89), while there was no significant reduction in the incidence of pneumonia (RR=0.92; 95% CI 0.69 to 1.22) or of diarrhoea (RR=0.80; 95% CI 0.27 to 2.34). Duration of diarrhoea was measured in days and there was a reduction in its duration of almost two days WMD -1.92, 95% CI -3.40 to -0.44. Only one study evaluated otitis media and found a 74% reduction in its incidence (RR=0.26, 95% CI, 0.05 to 0.92). We did not find evidence that a single dose of 200,000 IU of vitamin A per day, given in oil-based formulation in areas with low case fatality, was associated with reduced mortality among children with measles. However, there was evidence that the same dose given for two days was associated with a reduced risk of overall mortality and pneumonia specific mortality.

REVIEWER'S CONCLUSIONS:

Although we did not find evidence that a single dose of 200,000 IU of vitamin A per day was associated with reduced mortality among children with measles, there was evidence that the same dose given for two days was associated with a reduced risk of overall mortality and pneumonia specific mortality. The effect was greater in children under the age of two years. There were no trials that compared a single dose with two doses, although the precision of the estimates of trials that used a single dose were similar to the trials that used two doses.

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How much sleep do we really need?

Date:

February 11, 2015

Source:

Loyola University Health System--Loyola University Chicago Stritch School of Medicine researcher Lydia DonCarlos, PhD, is a member of an expert panel that's making new recommendations on how much sleep people need.--The panel, convened by the National Sleep Foundation, is making its recommendations based on age, ranging from newborns (who need 14 to 17 hours of sleep per day) to adults aged 65 and up (7 to 8 hours per day).--In the new guidelines, there's a wider range of what constitutes a good night's sleep. For example, the expert panel recommends that teens (ages 14 to 17) get 8 to 10 hours of sleep per night. The previous guideline had a narrower recommended range of 8.5 to 9.5 hours per night.--Dr. DonCarlos and other experts on the multidisciplinary panel examined findings from 320 studies reporting sleep duration findings for healthy individuals, effects of reduced or prolonged sleep duration and health consequences of too much or too little sleep. Results are published in Sleep Health: Journal of the National Sleep Foundation.--"The process was very rigorous," Dr. DonCarlos said. Dr. DonCarlos is a professor in the Department of Cell and Molecular Physiology of Loyola University Chicago Stritch School of Medicine.--The expert panel consists of 12 representatives, including Dr. DonCarlos, who were selected by medical organizations; and six sleep experts selected by the National Sleep Foundation. Dr. DonCarlos represents the American Association of Anatomists.--Dr. DonCarlos is a neuroendocrinologist who studies how hormones affect the structure of the brain. The section of the brain responsible for regulating hormone production is the hypothalamus. Hormones produced by the hypothalamus govern body temperature, hunger, stress responses, sex drive, circadian rhythms and sleep.--In addition to serving on the National Sleep Foundation expert panel, Dr. DonCarlos serves on the National Institutes of Health's Neuroendocrinology, Neuroimmunology, Rhythms and Sleep (NNRS) study section, which reviews applications for research grants.--"We still have a great deal to learn about the function of sleep," Dr. DonCarlos said. "We know it's restorative and important for memory consolidation. But we don't know the details of what the function of sleep is, even though it is how we spend one-third of our lives."--These are the sleep-time recommendations from the National Sleep Foundation expert panel:

Newborns (0-3 months): Sleep range narrowed to 14-17 hours each day (previously it was 12-18).

Infants (4-11 months): Sleep range widened two hours to 12-15 hours (previously it was 14-15).

Toddlers (1-2 years): Sleep range widened by one hour to 11-14 hours (previously it was 12-14).

Preschoolers (3-5): Sleep range widened by one hour to 10-13 hours (previously it was 11-13).

School age children (6-13): Sleep range widened by one hour to 9-11 hours (previously it was 10-11).

Teenagers (14-17): Sleep range widened by one hour to 8-10 hours (previously it was 8.5-9.5).

Younger adults (18-25): Sleep range is 7-9 hours (new age category).

Adults (26-64): Sleep range did not change and remains 7-9 hours.

Older adults (65+): Sleep range is 7-8 hours (new age category).

Story Source--The above story is based on materials provided by Loyola University Health System. Note: Materials may be edited for content and length.--Journal Reference--Max Hirshkowitz et al. National Sleep Foundation’s sleep time duration recommendations: methodology and results summary. Sleep Health: Journal of the National Sleep Foundation, 2015 DOI: 10.1016/j.sleh.2014.12.010

Top A

[F1]I have found personally doing research that the results or even the methods are unachievable and are misleading

[F2]Checkbook Science is what is promoting the Vaccines---nothing else—the credibility of vaccines ---cannot be found

[F3]Same with the nutriceutical side

[F4]In other words it is not the drugs but something that the person did or has had done or is not having ---the onus is on the person rather then the drug causing the issues

[F5]Water Based Vitamin A

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TOP B

HOME

Show of the Month February 21 2015

Ingredients in Vaccines

Side Effects of Vaccines

NSA hack" has been revealed

Toxic exposure is causing a pandemic of brain disorders in Life Existence—and it’s Development

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Ingredients in Vaccines---- http://www.cdc.gov/vaccines/pubs/pinkbook/downloads/appendices/B/excipient-table-2.pdf

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Side Effects of Vaccines- http://www.cdc.gov/vaccines/vac-gen/side-effects.htm

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NSA hack" has been revealed

All hard drives from all manufacturers raped wide open to the NSA from day one of manufacture SINCE 2001!--This is about the recent NSA hack discovery by Kapersky, and I have clarified what is going on and removed the confusing, misleading and obstructing content most reports have.--I have long said that there is no way to secure your computer against the NSA no matter what virus scanner you run or how you secure your system, and that Snowden was to a degree a whitewash standing as a limited hold out to prevent the real truth from being known. Kapersky just confirmed this.

Here is what happened:

A decade and a half ago, someone managed to get NSA trojans into all the hard drive manufacturers which infected all manufacturer workstations and manufacturing facilities and then wrote itself to every hard drive ever made at the 12 top manufacturers for the last 14 years AT POINT OF MANUFACTURE. When the firmware was burned in, this virus wrote itself into the firmware at point of production. Ditto for rom as well. Additionally, it wrote itself to the hard drive platters as backup. Because this virus exhibited itself as part of the root product, (which cannot be accessed by any virus scanner or read in any way) it remained totally immune to detection this entire time even when written to the hard drive platters. Kapersky finally hunted it down (most likely by taking new products and doing a linear read of hard drive platters they removed from the hard drives and put in their own custom box.)----Impossible for this bug to exist you say? Nope. Here is how: All bios chips, anything writable, and even rom, has excess capacity that goes beyond the root program. It has to have a little extra space or whatever you write to it will not fit. There are applications that can fill in this excess space with garbage to use it up and prevent writing to it in the future, but if the computer that had such an application had this NSA trojan, obviously the trojan would circumvent it and write itself in instead. This would be especially deadly with ROM chips. At any rate, ALL hard drives have this trojan, at least anything newer than the 90's.---The bug re configures the root operating parameters of anything it gets into and sets aside a permanent space for itself so re-flashing infected devices will not kill it. Kapersky determined that even all flash drives, SD cards and other memory devices which use USB also ship direct from the factory to you with this bug on them, and the manufacturers do not even know it.---Kapersky has named the organization responsible for this bug the Equation Group, and its toolbox 'the Death Star of the Malware Galaxy', and explained that the tools of its trade have hallmarks and themes similar to those of Stuxnet. Kapersky also believes that the group which wrote this particular trojan is superior to the agencies which wrote Stuxnet and Flame, and that the roots are at the NSA. Everything regarding this bug has been written with the highest possible efficiency and is of the highest professional order.

Kapersky contacted Seagate, and Seagate denied the problem. So Seagate might be a willing player in this. However, when they contacted Western Digital, Western Digital took it seriously and has started digging.---When Kapersky contacted the NSA, the NSA basically self incriminated with the following statement--"We are aware of the recently released report. We are not going to comment publicly on any allegations that the report raises, or discuss any details,". "The US. Government calls on our intelligence agencies to protect the United States, its citizens, and its allies from a wide array of serious threats - including terrorist plots from al-Qaeda, ISIL, and others; the proliferation of weapons of mass destruction; foreign aggression against ourselves and our allies; and international criminal organisations."-- According to Kaspersky, victims include state targets, governments, security developers, telecoms, aerospace and energy industries, along with the military, activists and the media. This is no doubt the real venue that got Stuxnet into Fukushima.--- Obviously if anyone out there has a chance of doing anything meaningful against the tainted vaccine war on the public, or antidepressants, or if anyone provides any hope against tyranny, they will be silenced and eliminated. THIS BUG ENSURES IT, and it is so entrenched now that there probably is no hope. The only way we are going to get over this is if we manage to stall tyranny for a couple more years, and if hard drive manufacturers get their act together. I will not hold my breath for that, this bug ensures that anyone assigned to fix this problem will be killed or eliminated day one. Heads up Russia, nothing you have is classified. Hmm, how many HDD manufacturers do I know of off the top of my head? Quantum, Maxtor, Fujitsu, Samsung, Toshiba, Western Digital, Seagate, IBM, (plus 4 more) has got to pretty much nail them all!--UPDATE: in order to hit the top 12, it has to be in the time frame between now and 2001. That fits for the Kaperski report, because there were 12 major hard drive vendors in business during that time frame, (some are gone now but their drives are still being used).

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Toxic exposure is causing a pandemic of brain disorders in Life Existence—and it’s Development

The numbers are startling. According to the US Centers for Disease Control and Prevention, about 1.8 million more children in the US were diagnosed with developmental disabilities between 2006 and 2008 than a decade earlier. During this time, the prevalence of autism climbed nearly 300%, while that of attention deficit hyperactivity disorder increased 33%. CDC figures also show that 10 to 15% of all babies born in the US have some type of neurobehavorial development disorder. Still more are affected by neurological disorders that don’t rise to the level of clinical diagnosis.--And it’s not just the US. Such impairments affect millions of children worldwide. The numbers are so large that Philippe Grandjean of the University of Southern Denmark and Harvard T.H. Chan School of Public Health and Philip Landrigan of the Icahn School of Medicine at Mount Sinai in New York—both physicians and preeminent researchers in this field—describe the situation as a “pandemic.”--While earlier and more assiduous diagnosis accounts for some of the documented increase, it doesn’t explain all of it, says Irva Hertz-Piccioto, professor of environmental and occupational health and chief of the University of California, Davis, MIND Institute. Grandjean and Landrigan credit genetic factors for 30 to 40% of the cases. But a significant and growing body of research suggests that exposure to environmental pollutants is implicated in the disturbing rise in children’s neurological disorders.[F1] --What, exactly is going on? And what can we do about it?

Chemicals and the brain

Some chemicals—lead, mercury and organophosphate pesticides, for example—have long been recognized as toxic substances that can have lasting effects on children’s neurological health, says Bruce Lanphear, health sciences professor at Simon Fraser University. While leaded paint is now banned in the US, it is still present in many homes and remains in use elsewhere around the world. Children can also be exposed to lead from paints, colorings and metals used in toys, even though these uses are prohibited by US law (remember Thomas the Tank Engine), and through contaminated soil or other environmental exposure as well as from plastics in which lead is used as a softener. Mercury exposure sources include some fish, air pollution and old mercury-containing thermometers and thermostats. While a great many efforts have gone into reducing and eliminating these exposures, concerns continue, particularly because we now recognize that adverse effects can occur at exceptionally low levels.--But scientists are also now discovering that chemical compounds common in outdoor air—including components of vehicle exhaust and fine particulate matter—as well as in indoor air and consumer products can also adversely affect brain development, including prenatally.--Chemicals in flame retardants, plastics, and personal care and other household products are among those Lanphear lists as targets of concern for their neurodevelopment effects.----Chemicals that prompt hormonal changes are increasingly suspected to have neurological effects, says Linda Birnbaum, director of the National Institute of Environmental Health Sciences and National Toxicology Program. Among the chemicals now being examined for neurological impacts that occur early in life are flame retardants known as PBDEs that have been used extensively in upholstery foams, electronics and other products; phthalates, widely used as plasticizers and in synthetic fragrances; the polycarbonate plastic ingredient bisphenol A, known commonly as BPA; perfluorinated compounds, whose applications include stain-, water- and grease-resistant coatings; and various pesticides.

Precise choreography

As Grandjean and Landrigan explain, the fetus is not well protected against environmental chemicals that can easily pass through the placenta. There’s evidence from in vitro studies, they say, that neural stem cells are very sensitive to neurotoxic substances. An infant’s brain is also vulnerable to such contaminants. At early stages of development—prenatally and during infancy—brain cells are easily damaged by industrial chemicals and other neurotoxicants. Such interference can affect how the brain develops structurally and functionally—effects that lead to lasting adverse outcomes.--“The brain is so extremely sensitive to external stimulation,” says Grandjean.--Historically, chemical neurotoxicity was examined in adults—often through cases of high levels of occupational exposure. In the past 30 to 40 years, however, scientists have begun to recognize that children and infants are far more vulnerable to chemical exposures than are adults. It has also been discovered that very low levels of exposure early in life can have profound and lasting effects. Another important discovery is that understanding how an infant or child is affected by a chemical exposure involves far more than simply calculating potential effects on a physically smaller person. Stage of development—and timing of exposure—must also be considered. Early stages of brain development involve “a very precise choreography,” explains Frederica Perera, professor of Environmental Health Sciences at Columbia University’s Mailman School of Public Health. “Any chemical that can disrupt [brain] chemistry at this stage can be very damaging,” she says.---For example, explains Deborah Kurrasch, an assistant professor at the University of Calgary’s Cumming School of Medicine who specializes in neurological research, during the early stages of brain development—when cells are becoming neurons—“timing determines destination.”--Results of Kurrasch’s latest study investigating neurodevelopmental effects of BPA illustrate what she means. In a study published in January 2015, Kurrasch and colleagues examined the effects on neurodevelopment of BPA and a common BPA substitute, bisphenol S. Specifically, they investigated how exposure to BPA and BPS—at levels comparable to those present in her community’s local drinking water supply—might affect neuron development in zebrafish at a stage comparable to the second trimester of human pregnancy, when neurons are forming and moving to the correct location in the brain.--“It’s as if they’re getting on a bus to where they need to be,” Kurrasch says. After exposure to BPA and BPS it was as if, explains Kurrasch, “twice as many neurons got on an early bus and half as many got on a late bus.” The researchers found that these exposures appeared to alter nerve development—neurogenesis—in a way that caused the fish to become hyperactive. Such an alteration, produced in this case by a “very little bit of BPA,” can cause permanent effects, Kurrasch says.--Many of the chemicals under scrutiny for their effects on brain development—BPA, phthalates, perfluorinated compounds, brominated flame retardants and various pesticides among them—appear to act by interfering with the function of hormones essential for healthy brain development. Among these are thyroid hormones, which regulate the part of the brain involved in a variety of vital functions, including reproduction, sleep, thirst, eating and puberty.--During the first trimester of pregnancy, the fetus is not making its own thyroid hormone, says Thomas Zoeller, director of the Laboratory of Molecular, Cellular and Developmental Endocrinology at the University of Massachusetts Amherst. If an environmental exposure to a substance such as a polychlorinated biphenyl or perchlorate interferes with the mother’s thyroid hormones in this period—as could happen through water pollution, for example—that could in turn affect her child at a critical stage of brain development.--Another thing to consider in the context of endocrine-disrupting chemical exposures, says Zoeller, is that a substantial portion of women of childbearing age in the US have some iodine deficiency that may be suppressing their thyroid hormones. While these deficiencies may not be prompting clinically adverse effects, they may be sufficient to impair fetal neurodevelopment. “Impacts can happen at levels far below safety standards,” says Zoeller. And there are a great many chemicals to which such women may be exposed environmentally with the potential to affect thyroid hormones, among them PBDEs, PCBs, BPA, various pesticides, perfluorinated compounds and certain phthalates.

Something in the air

One particularly concerning source of exposure to chemicals that are suspected to harm children’s brain development is air pollution, which is a complex mixture of various chemicals and particulate matter.--Perera and colleagues recently investigated the links between exposure to polycyclic aromatic hydrocarbons[F2] , a fossil fuel-related component of air pollution, and incidence of ADHD in 9-year-olds. Their study found that mothers who were exposed to high levels of PAH during pregnancy were five times more likely to have children with ADHD and to have children with more severe ADHD symptoms than those who did not have such exposure. While this study is the first to make such a connection, it joins a growing body of research pointing to links between outdoor air pollutants, including PAHs, and adverse impacts on children’s brain health and development.--Looking at air pollution’s effects on brain health is relatively new, explains Kimberly Gray, health science administrator at the National Institutes of Health. Research increasingly suggests that airborne contaminants can have subtle but significant effects on early neurological development and behavior, she says. In addition to links between prenatal PAH exposure and impaired brain function, researchers are also now investigating potential connections between black carbon, volatile organic compounds and fine particulate matter—among other components of air pollution—and impairments such as autism and lowered IQ.--In a study published in December 2014, Marc Weisskopf, Harvard T.H. Chan School of Public Health associate professor of environmental and occupational epidemiology, and colleagues looked at children whose mothers were exposed to high levels of fine particulate matter (PM2.5, particles 2.5 microns in diameter or smaller), particularly during the third trimester of pregnancy. The study, which involved more than 1,000 participants living all across the US, found that these children appeared to be twice as likely to be diagnosed with autism as children whose mothers had only low levels of such exposures. Exposure to larger particles—between 2.5 and 10 microns (what’s known as PM10)—did not appear to be associated with increasing risk for autism.----“This is very important from an epidemiological point of view” because it “places a spotlight on the mother’s exposure,” says Weisskopf. It also highlights the importance of timing and neurodevelopmental effects. Although many other factors may contribute to autism, Weisskopf explains, this study strengthens the suggestion that environmental exposures can play a role. That it appears it is the very small particles that are associated with these effects adds to what other research is finding: What might seem quantitatively small can “be quite important” when it comes to affecting brain development, Weisskopf explains.

Widespread exposure

As Grandjean and Landrigan point out, one of the disturbing recent realizations concerning environmental exposure to developmental neurotoxicants is how widespread exposure appears to be and the ubiquity of such compounds. “More neurotoxic chemicals are getting into products,” says Landrigan.--Phthalates, which are used as plasticizers—including in polyvinyl chloride plastics—and in synthetic fragrances and numerous personal care products, comprise one category of widely used chemicals that appear to have adverse impacts on brain development[F3] . Researchers at Columbia University’s Mailman School of Public Health recently found that children exposed prenatally to elevated levels of certain phthalates had IQ scores that were, on average, between 6 and 8 points lower than children with lower prenatal exposures. Children with reduced IQ scores also appeared to have trouble with working memory, perceptional reasoning and information processing speeds.--The phthalates examined in this study, known as DnBP and DiBP, are used in numerous household products, including toiletries and cosmetics, among them shampoo, nail polish, lipstick, hair styling products and soap, as well as vinyl fabrics and dryer sheets. Exposure levels associated with reduced IQ in the study are within the range that the CDC reports finding in its National Health and Nutrition Examination Survey, a nationwide ongoing biomonitoring assessment of chemical exposures. “Pretty much everybody in the US is exposed,” says study co-author Robin Whyatt, professor of environmental health sciences at Columbia University Medical Center.--While such a drop in IQ may sound small, Pam Factor-Litvak, the study’s lead author and associate professor of epidemiology at the Mailman School, notes that at the population—or classroom—level, this means fewer children at the high end of the intelligence scale and more at the less capable end. “The whole curve shifts downward,” she explains.--“Five or six IQ points may not sound like much, but it means more children requiring special education programs and fewer that are gifted,” says Maureen Swanson, Learning Disabilities Association of America’s Healthy Children Project director. “The potential economic impact is huge,” says NIEHS’s Birnbaum.

The stress factor

What prompts neurological disorders in children is “very complex,” notes Frederica Perera. Adding to the challenge of disentangling the various contributing factors is that while research on—and regulation of—chemicals typically looks at one substance at a time, people are exposed to multiple chemicals concurrently. Further adding to this complexity when it comes to brain development are social stresses that “act on the same part of the brain region,” explains University of Rochester professor of environmental medicine Deborah Cory-Slechta. She and others are finding increasing evidence that nonchemical stressors such as maternal, domestic and community distress can prompt adverse effects on early brain development, either on their own or in combination with neurotoxic chemicals.--Birnbaum says this apparent interaction between chemicals and nonchemical stressors is “very concerning and very important.”---Epidemiological studies, Cory-Slechta explains, typically correct for what are called confounding factors—other conditions that might influence the condition being measured. Many studies, she says, “are clearly not modeling what is going on in the human environment.” What she and her colleagues hope to do is “reproduce in animal studies what goes on in human communities,” particularly in communities that are most vulnerable to adverse social stressors and most exposed to chemical contaminants, including lead, pesticides and air pollution.--Lead and stress affect the same part of the brain, she says, and so can act synergistically very early in life to produce permanent changes in brain structure. These changes can result in lowered IQ, learning and behavioral problems.---Cory-Slechta’s lab is now working on replicating conditions of stress and chronic deprivation in animal models that would mirror those experienced by communities of poverty. The aim is to better understand how these effects cross the placenta and become the fetal basis of lifelong disorders. She and her colleagues are investigating, not only associations between exposures and neurodevelopment, but also the mechanisms by which effects occur.

What to do?

Assuming we want to stop harming our children’s brains, how do we proceed?

An important step is to improve our ability to determine which chemicals have neurodevelopmental effects. A rapid screening system would be ideal, says Birnbaum, because there are so many chemicals—including newly invented ones—to which people are exposed. While such a program to test large numbers of chemicals quickly using robotics has been launched by NIH, EPA and other federal agencies, there are tens of thousands that may be in use, most of which have not been fully tested for these effects.--When it comes to reducing existing exposures, some chemicals can be avoided through consumer choice. But it’s often difficult, given that many of these substances are used—like BPA on receipts—in products that don’t carry ingredient labels. Others, including air pollutants, are much harder given their ubiquity or lack of available alternatives. And, as Maureen Swanson notes, such choices are not necessarily feasible for people at all economic levels, which raises environmental justice issues.--Grandjean and Landrigan point out that the US system of chemical regulation, which lacks requirements for full premarket toxicity testing, does not do a very good job when it comes to proactive chemical safety. “Untested chemicals should not be presumed to be safe to brain development, and chemicals in existing use and all new chemicals must therefore be tested for developmental neurotoxicity,” they wrote in an article published in The Lancet.--While some sources of neurotoxicity might appear to have been adequately addressed, they have not. For example, considerable progress has been made in curtailing lead exposure through policy and public health education in the US and elsewhere. However, current understanding is that virtually any amount of lead exposure can cause damage, and harmful exposures continue—especially in countries where leaded paints and gasoline are still used . And in the US, CDC funding for lead prevention programs was dramatically reduced in 2012.--Meanwhile, children around the world—especially in less well-off countries—continue to be exposed to dangerous neurotoxicants released in industrial emissions, from waste sites and through child labor. Examples abound, and include exposures to chemicals released in electronics recycling in various locations in Asia and Africa, to lead and mercury from mining activity, to agricultural pesticides, to products contaminated with heavy metals, including food and candy.--When it comes to protecting the exquisitely sensitive developing brain, the measures currently used to assess chemical risk and set safety standards fall short, says Cory-Slechta. “It should be about primary prevention, but it’s not,” she says.

In the absence of what many environmental health advocates feel is adequate US federal regulation of chemicals, many individual US states have recently passed their own laws to protect children from harmful chemical exposures. Many address chemicals with neurotoxic effects, particularly those of heavy metals such as cadmium, lead and mercury. And even though some states are beginning to include language in their legislation to protect pregnant women from chemical hazards, this timing of exposure is left largely unaddressed.--While we now know a great deal about developmental neurotoxicants, more such exposures appear to be occurring than ever before. And there appears to be wide agreement among researchers that these exposures are taking a toll on the world’s children.

[F1]Environmental pollutants would include RF—Smart Meters—Cell phones—Haarp—NanoParticles—Smart Dust—Chemtrails—Glyphosates-an industrial waste—farm chemicals—and materials and cleaning agents –GMO’s---these are all environmental pollutants

[F2]PAHs are neutral, nonpolar molecules; they are found in fossil fuels (oil and coal) and in tar deposits, and are produced, generally, when insufficient oxygen or other factors result in incomplete combustion of organic matter-----

Crystal structure of a hexa-tert-butyl derivatized hexa-peri-hexabenzo(bc,ef,hi,kl,no,qr)coronene, reported by Klaus Müllen and co-workers.^[3] The tert-butyl groups make this compound soluble in common solvents such as hexane, in which the unsubstituted PAH is insoluble.

Polycyclic aromatic hydrocarbons are lipophilic, meaning they mix more easily with oil than water. -- PAHs are one of the most widespread organic pollutants. In addition to their presence in fossil fuels they are also formed by incomplete combustion of carbon-containing fuels such as wood, coal, diesel, fat, tobacco, and incense

[F3]Use essential oils not the synthetic fragrances

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