Destruction of Mold Contaminated Products Was First Recommended In Bible

The Envirionmental Protection Agency estimates 30 percent of buildings in the United States are contaminated with mold neurotoxins.  Aspergillus, Fusarium and Stachybotrus molds can all produce fatal neurotoxins.  Deadly peanut allergies are caused by fungal Aflatoxins.

Florida Detox and Wellness Institute offers testing and treatment for mold neurotoxicity, which can cause disability and hundreds of symptoms, including addiction, anxiety, depression,  fatigue, irritibility, fibromyalgia, attention deficit disorders, immune suppression, headaches, including migraines, cancer and many other disorders.

We are excited to be able to offer testing for Ochratoxin, Tricothecene and Aflatoxin mold neurotoxins, in addition to genetic testing for increased sensitivity to Lymes Disease and mold neurotoxins.  Twenty four percent of the population possesses specific HLA DR DQ genetic patterns, which reduce their ability to clear mold neurotoxins over 400 percent, compared to the other seventy six percent of the population, which does not genetically clear mold neurotoxins more slowly.  This explains why only a minority of us are affected by sick building syndromes, caused by mold contamination.

Steven Sponaugle, Research Director, Florida detox and Wellness Institute

www.floridadetox.com

Leviticus, Chapter 13

47 “If any clothing is contaminated with mildew—any woolen or linen clothing, 48 any woven or knitted material of linen or wool, any leather or anything made of leather- 49 and if the contamination in the clothing, or leather, or woven or knitted material, or any leather article, is greenish or reddish, it is a spreading mildew and must be shown to the priest. 50 The priest is to examine the mildew and isolate the affected article for seven days. 51 On the seventh day he is to examine it, and if the mildew has spread in the clothing, or the woven or knitted material, or the leather, whatever its use, it is a destructive mildew; the article is unclean. 52 He must burn up the clothing, or the woven or knitted material of wool or linen, or any leather article that has the contamination in it, because the mildew is destructive; the article must be burned up.

53 “But if, when the priest examines it, the mildew has not spread in the clothing, or the woven or knitted material, or the leather article, 54 he shall order that the contaminated article be washed. Then he is to isolate it for another seven days. 55 After the affected article has been washed, the priest is to examine it, and if the mildew has not changed its appearance, even though it has not spread, it is unclean. Burn it with fire, whether the mildew has affected one side or the other. 56 If, when the priest examines it, the mildew has faded after the article has been washed, he is to tear the contaminated part out of the clothing, or the leather, or the woven or knitted material. 57 But if it reappears in the clothing, or in the woven or knitted material, or in the leather article, it is spreading, and whatever has the mildew must be burned with fire. 58 The clothing, or the woven or knitted material, or any leather article that has been washed and is rid of the mildew, must be washed again, and it will be clean.”

59 These are the regulations concerning contamination by mildew in woolen or linen clothing, woven or knitted material, or any leather article, for pronouncing them clean or unclean.

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Computer Viruses Can Load Child Pornography Onto Computers

 

AP IMPACT: Framed for child porn — by a PC virus

  • By JORDAN ROBERTSON, AP Technology Writer – Sun Nov 8, 2009 12:17PM EST
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  • San Jose Mercury News Monday 02nd November, 04:33:51 PM

Of all the sinister things that Internet viruses do, this might be the worst: They can make you an unsuspecting collector of child pornography.

Heinous pictures and videos can be deposited on computers by viruses — the malicious programs better known for swiping your credit card numbers. In this twist, it’s your reputation that’s stolen.

Pedophiles can exploit virus-infected PCs to remotely store and view their stash without fear they’ll get caught. Pranksters or someone trying to frame you can tap viruses to make it appear that you surf illegal Web sites.

Whatever the motivation, you get child porn on your computer — and might not realize it until police knock at your door.

An Associated Press investigation found cases in which innocent people have been branded as pedophiles after their co-workers or loved ones stumbled upon child porn placed on a PC through a virus. It can cost victims hundreds of thousands of dollars to prove their innocence.

Their situations are complicated by the fact that actual pedophiles often blame viruses — a defense rightfully viewed with skepticism by law enforcement.

“It’s an example of the old `dog ate my homework’ excuse,” says Phil Malone, director of the Cyberlaw Clinic at Harvard’s Berkman Center for Internet & Society. “The problem is, sometimes the dog does eat your homework.”

The AP’s investigation included interviewing people who had been found with child porn on their computers. The AP reviewed court records and spoke to prosecutors, police and computer examiners.

One case involved Michael Fiola, a former investigator with the Massachusetts agency that oversees workers’ compensation.

In 2007, Fiola’s bosses became suspicious after the Internet bill for his state-issued laptop showed that he used 4 1/2 times more data than his colleagues. A technician found child porn in the PC folder that stores images viewed online.

Fiola was fired and charged with possession of child pornography, which carries up to five years in prison. He endured death threats, his car tires were slashed and he was shunned by friends.

Fiola and his wife fought the case, spending $250,000 on legal fees. They liquidated their savings, took a second mortgage and sold their car.

An inspection for his defense revealed the laptop was severely infected. It was programmed to visit as many as 40 child porn sites per minute — an inhuman feat. While Fiola and his wife were out to dinner one night, someone logged on to the computer and porn flowed in for an hour and a half.

Prosecutors performed another test and confirmed the defense findings. The charge was dropped — 11 months after it was filed.

The Fiolas say they have health problems from the stress of the case. They say they’ve talked to dozens of lawyers but can’t get one to sue the state, because of a cap on the amount they can recover.

“It ruined my life, my wife’s life and my family’s life,” he says.

The Massachusetts attorney general’s office, which charged Fiola, declined interview requests.

At any moment, about 20 million of the estimated 1 billion Internet-connected PCs worldwide are infected with viruses that could give hackers full control, according to security software maker F-Secure Corp. Computers often get infected when people open e-mail attachments from unknown sources or visit a malicious Web page.

Pedophiles can tap viruses in several ways. The simplest is to force someone else’s computer to surf child porn sites, collecting images along the way. Or a computer can be made into a warehouse for pictures and videos that can be viewed remotely when the PC is online.

“They’re kind of like locusts that descend on a cornfield: They eat up everything in sight and they move on to the next cornfield,” says Eric Goldman, academic director of the High Tech Law Institute at Santa Clara University. Goldman has represented Web companies that discovered child pornographers were abusing their legitimate services.

But pedophiles need not be involved: Child porn can land on a computer in a sick prank or an attempt to frame the PC’s owner.

In the first publicly known cases of individuals being victimized, two men in the United Kingdom were cleared in 2003 after viruses were shown to have been responsible for the child porn on their PCs.

In one case, an infected e-mail or pop-up ad poisoned a defense contractor’s PC and downloaded the offensive pictures.

In the other, a virus changed the home page on a man’s Web browser to display child porn, a discovery made by his 7-year-old daughter. The man spent more than a week in jail and three months in a halfway house, and lost custody of his daughter.

Chris Watts, a computer examiner in Britain, says he helped clear a hotel manager whose co-workers found child porn on the PC they shared with him.

Watts found that while surfing the Internet for ways to play computer games without paying for them, the manager had visited a site for pirated software. It redirected visitors to child porn sites if they were inactive for a certain period.

In all these cases, the central evidence wasn’t in dispute: Pornography was on a computer. But proving how it got there was difficult.

Tami Loehrs, who inspected Fiola’s computer, recalls a case in Arizona in which a computer was so “extensively infected” that it would be “virtually impossible” to prove what an indictment alleged: that a 16-year-old who used the PC had uploaded child pornography to a Yahoo group.

Prosecutors dropped the charge and let the boy plead guilty to a separate crime that kept him out of jail, though they say they did it only because of his age and lack of a criminal record.

Many prosecutors say blaming a computer virus for child porn is a new version of an old ploy.

“We call it the SODDI defense: Some Other Dude Did It,” says James Anderson, a federal prosecutor in Wyoming.

However, forensic examiners say it would be hard for a pedophile to get away with his crime by using a bogus virus defense.

“I personally would feel more comfortable investing my retirement in the lottery before trying to defend myself with that,” says forensics specialist Jeff Fischbach.

Even careful child porn collectors tend to leave incriminating e-mails, DVDs or other clues. Virus defenses are no match for such evidence, says Damon King, trial attorney for the U.S. Justice Department’s Child Exploitation and Obscenity Section.

But while the virus defense does not appear to be letting real pedophiles out of trouble, there have been cases in which forensic examiners insist that legitimate claims did not get completely aired.

Loehrs points to Ned Solon of Casper, Wyo., who is serving six years for child porn found in a folder used by a file-sharing program on his computer.

Solon admits he used the program to download video games and adult porn — but not child porn. So what could explain that material?

Loehrs testified that Solon’s antivirus software wasn’t working properly and appeared to have shut off for long stretches, a sign of an infection. She found no evidence the five child porn videos on Solon’s computer had been viewed or downloaded fully. The porn was in a folder the file-sharing program labeled as “incomplete” because the downloads were canceled or generated an error.

This defense was curtailed, however, when Loehrs ended her investigation in a dispute with the judge over her fees. Computer exams can cost tens of thousands of dollars. Defendants can ask the courts to pay, but sometimes judges balk at the price. Although Loehrs stopped working for Solon, she argues he is innocent.

“I don’t think it was him, I really don’t,” Loehrs says. “There was too much evidence that it wasn’t him.”

The prosecution’s forensics expert, Randy Huff, maintains that Solon’s antivirus software was working properly. And he says he ran other antivirus programs on the computer and didn’t find an infection — although security experts say antivirus scans frequently miss things.

“He actually had a very clean computer compared to some of the other cases I do,” Huff says.

The jury took two hours to convict Solon.

“Everybody feels they’re innocent in prison. Nobody believes me because that’s what everybody says,” says Solon, whose case is being appealed. “All I know is I did not do it. I never put the stuff on there. I never saw the stuff on there. I can only hope that someday the truth will come out.”

But can it? It can be impossible to tell with certainty how a file got onto a PC.

“Computers are not to be trusted,” says Jeremiah Grossman, founder of WhiteHat Security Inc. He describes it as “painfully simple” to get a computer to download something the owner doesn’t want — whether it’s a program that displays ads or one that stores illegal pictures.

It’s possible, Grossman says, that more illicit material is waiting to be discovered.

“Just because it’s there doesn’t mean the person intended for it to be there — whatever it is, child porn included.”

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Vitamin D supplementation reduces insulin resistance

British Journal of Nutrition Cambridge University Press
Copyright © The Authors 2009
doi:10.1017/S0007114509992017

Full Papers

 

Human and Clinical Nutrition

Vitamin D supplementation reduces insulin resistance in South Asian women living in New Zealand who are insulin resistant and vitamin D deficient – a randomised, placebo-controlled trial


Pamela R. von Hursta1 c1, Welma Stonehousea1 and Jane Coada2

 

a1 Institute of Food, Nutrition and Human Health, Massey University, Private Bag 102 904, North Shore Mail Centre, Auckland, New Zealand
a2 Institute of Food, Nutrition and Human Health, Massey University, Palmerston North, New Zealand

Abstract

Low serum 25-hydroxyvitamin D (25(OH)D) has been shown to correlate with increased risk of type 2 diabetes. Small, observational studies suggest an action for vitamin D in improving insulin sensitivity and/or insulin secretion. The objective of the present study was to investigate the effect of improved vitamin D status on insulin resistance (IR), utilising randomised, controlled, double-blind intervention administering 100 μg (4000 IU) vitamin D3 (n 42) or placebo (n 39) daily for 6 months to South Asian women, aged 23–68 years, living in Auckland, New Zealand. Subjects were insulin resistant – homeostasis model assessment 1 (HOMA1)>1·93 and had serum 25(OH)D concentration < 50 nmol/l. Exclusion criteria included diabetes medication and vitamin D supplementation >25 μg (1000 IU)/d. The HOMA2 computer model was used to calculate outcomes. Median (25th, 75th percentiles) serum 25(OH)D3 increased significantly from 21 (11, 40) to 75 (55, 84) nmol/l with supplementation. Significant improvements were seen in insulin sensitivity and IR (P = 0·003 and 0·02, respectively), and fasting insulin decreased (P = 0·02) with supplementation compared with placebo. There was no change in C-peptide with supplementation. IR was most improved when endpoint serum 25(OH)D reached ≥ 80 nmol/l. Secondary outcome variables (lipid profile and high sensitivity C-reactive protein) were not affected by supplementation. In conclusion, improving vitamin D status in insulin resistant women resulted in improved IR and sensitivity, but no change in insulin secretion. Optimal vitamin D concentrations for reducing IR were shown to be 80–119 nmol/l, providing further evidence for an increase in the recommended adequate levels. Registered Trial No. ACTRN12607000642482.

(Received June 04 2009)

(Revised August 06 2009)

(Accepted August 11 2009)

Key Words:Vitamin D; Type 2 diabetes; Insulin resistance

Correspondence:

c1 Corresponding author: Pamela R. von Hurst, fax +64 9 443 9640, email p.r.vonhurst@massey.ac.nz

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What To Do if You are Forced to Take Swine Flu Shot

By Dr. Russell Blaylock, M.D. October 2009 “By 1853, Parliament began passing laws to make the untested vaccine compulsory throughout the British Empire. Other countries of Europe followed suit. Once the economic implications of compulsory vaccinations were realized, few dared to disagree. Then, as now, the media were controlled by the vaccine manufacturers and the government, who stood to make huge money from the sale of these spurious vaccines…” Tim O’Shea, D.C. What is in the Regular Flu Shot? Egg proteins, including avian contaminant viruses Gelatin, known to cause allergic reactions and anaphylaxis are usually associated with sensitivity to egg or gelatin Polysorbate 80 (Tween80™), which can cause severe allergic reactions, including anaphylaxis Formaldehyde: a known carcinogen Triton X100: a strong detergent Sucrose (table sugar) Resin, known to cause allergic reactions Gentamycin, an antibiotic Thimerosal: mercury is still in multidose vials Analysis of material by the Centers for Disease Control and Prevention by Dr. Russell Blaylock. (September 5, 2009) Critical Observations: Doctor visits for flu are down from the level in April Total flu hospitalizations are similar or lower than for seasonal flu (yearly flu) The number of death secondary to flu and pneumonia is unchanged from yearly rate Only two states are reporting widespread infections — Georgia and Alaska. Other states report only regional or sporadic activity, meaning it’s not very contagious. There is no evidence that the virus has mutated at all anywhere in the world The virus remains susceptible to the drugs Tamiflu and Relenza. Only 43,771 cases have been reported in the United States. Because of poor reporting the CDC estimates that true numbers indicate that one million have been infected. Many people did not get sick enough to go to a doctor. Likewise, not all people are tested who go to a doctor. Of these 5,011 have been hospitalized and 302 have died. Death Rates From the H1N1 Flu If we use the 43,771 figure and 302 deaths that means the death rate is 0.6 percent, an extremely low death rate for any flu. The percentage of hospitalized patients who died was 6 percent, again a very low incidence of death. Since the CDC estimates that one million have been infected, we must recalculate death rates. Using this more accurate figure, the death rate is in truth 0.03 percent, which means 99.97percent will not die from this flu. Your chances of dying are incredibly low. Age and Death Rates We hear a lot about the unusual age distribution with this virus, especially as regards death rates, with the young being more affected than, as with seasonal flu, the elderly (90% of deaths are usually among those greater than 65 years old). The risks of becoming infected are as follows: Ages 5 to 24 y/o——–26.7 per 100,000 (0.027%) Ages 0 to 4 y/o ———22.9 per 100,000 (0.023%) Ages 25 to 49———–6.97 per 100,000 (0.0069%) Ages 50 to 64 y/o——3.9 per 100,000 (0.0039) Over 65 y/o————-1.3 per 1000,000 (0.00013%) And the risk of needing to be hospitalized are: Ages 0 to 4 y/o———0.0045% Ages 5 to 24 y/o——–0.0021% Ages 25 to 45 y/o——0.0011% Over 65 y/o————-0.0017% This indicates that for all age groups, the risk of being hospitalized are far less than 1 percent and well over 99 percent of people will not need hospitalization. This explains why this infection is being downplayed by the virologists themselves, the ones who know most about the dangers of viruses. The distributions of death also vary considerably by age. Below is the distribution of deaths according to age. Ages 25-49 y/o———41% Ages 50 to 64 y/o—–24% Ages 5 to 24 y/o——16% Over age 65 y/o——- 9% Ages 0 to 4 y/o——– 2% So, we see that the greatest death rates in the extremely small fraction that die are between ages 25 to 49 and 65 percent are between ages 25 to 64. The least likely to die are babies up to age 4 years, yet they are targeted for vaccination and as we see from the above data, children below age 2 years get absolutely no protection from the flu vaccines. Analysis of the New Government Projections to the Media If we analyzed it according to the worst case scenario released by the government we see far lower figures than being projected: They say 150 million Americans will be infected. That is 150 X as many as now infected, and represents a much larger figure than now estimated with a 6 to 6.5 percent of a localized population. For the United States itself with a population slightly over 300 million, their figures indicate a 50 percent infection rate. There is nothing to indicate such a high infectivity rate from the past 7 months of analysis. It should also be appreciated that the infections will not occur all at once, but will slowly evolve, as we have seen thus far, meaning that at any one time a much smaller amount of Americans will be infected — which also reduces the numbers who will require hospitalizations at any one time, and who will need ICU care. As far as the number that will need hospitalization, the government now says there will be 1.8 million people hospitalized, of which 300,000 may need ICU treatment. If we use the existing data we see that the numbers are quite different. At the time the data was taken, 303 people out of one million infected died and 5,011 needed hospitalization. This means a projected hospitalization incidence of 750,000 and a death rate of 45,000 deaths. Remember, this is using their data applied to the outrageously high figure of 50% of the population being infected — that is, 150 million people. If the infection rate is 6 percent, as all the studies have shown thus far, we see much smaller numbers. Instead of 150 million infected we see 18 million infected. Using these more realistic figures we can estimate a hospitalization rate of 90,000 and a projected death incidence of 5436. Again, it is important to keep in mind that the infections will be evolving and not all at once as both sets of figures seem to imply. If we spread this over several months and waves of the infection, we see that at any one time the hospitalizations will be a much smaller number, as will the deaths. Thus far, there have been nationwide 2,000 hospitalizations a month and 99 deaths a month. Certainly the hospitals in the United States can handle the increase. In the United States we have 5,759 hospitals containing 955,000 beds and 70,000 ICU beds. Most hospitalized people will not require intensive care. Most are suffering from dehydration and only required IV fluid infusion. It should also be appreciated that most pediatric deaths and elderly deaths will occur early in the epidemic because the chronically ill and immune suppressed will become infected early. Therefore one would expect the deaths to rise initially and then fall as the infection spreads as we see from this graph: In this chart we see that the hospitalization rates are actually lower for the swine flu than in previous seasons. In this graph we see that the hospitalization rates were either lower or barely above the seasonal flu admissions in the previous two years. We can see from the CDC’s own data that the hospitalization rates and death rates are no higher, in fact they are significantly lower, than the previous two to three flu seasons. It is obvious that the government is using “scare tactics” to promote vaccine use in the United States and that the pharmaceutical makers of vaccines are in bed with these officials. The public should be outraged. Why Do Some Die From Such a Mild Virus? As stated by the virologists, this virus is no more a danger than the seasonal virus that visits each year and actually seems to be much weaker. One may also note from the CDC’s own data, the previous nonsense about 36,000 dying from the seasonal flu every year is pure fiction. We have had a little over 400 deaths nationwide over the past 5 months, nowhere near the 36,000 figure screamed from the airwaves and our TV sets, yet the public is in a state of panic. So, why are some dying from this virus? What is little understood by the general public is that the only reason people die from the flu is that they have either an immune suppressing chronic illness, such as diabetes, direct immune dysfunction, dietary deficiencies of critical immune-supporting nutrients, chronic pulmonary disease, heart disease or cancer. Smoking powerfully suppresses immunity as well as damages lungs, and we know that smokers are much more likely to suffer complications and die than non-smokers. Excess dietary omega-6 fats (corn, safflower, sunflower, soybean, peanut and canola oils) also severely weaken immunity. The EPA component of omega-3 oils also powerfully suppresses immunity. A study by the CDC found that 32 percent of children dying from H1N1 flu had asthma, when the incidence of asthma in the general population was 8 percent. Two thirds of the children who died had neurological disorders, such as seizures and cerebral palsy. So, the vast majority of children who are dying have one of a number of chronic health conditions, yet the media gives us the impression that perfectly healthy children are dying. A recent study of why so many died during the 1918 flu pandemic found that most of the deaths were secondary to bacterial pneumonia and not the flu virus itself. In 1918 hospitals had little to offer a sick patient — there were no antibiotics, other than sulfur drugs, no IV fluids and no respirators — all they could offer was a warm bed and aspirin. It was also disclosed that the number of flu-related deaths among children was lower this year than the previous two years. What are the Virologists Saying? Virologists are scientists who study viruses — their classification, their genetics, methods of spread and their ability to cause disease. No one knows more about this virus than the virologists. The British science magazine, The New Scientist, recently polled 60 virologists to get their opinion. These are the results of specific questions: Will the virulent version of the virus appear? Extremely likely—————–none Likely—————————-5 A 50/50 chance—————– 14 Possible————————– 38 Not at all————————–3 What the virologists are doing personally Stock Tamiflu or Relinza—————–14 Stock above plus antibiotics————- 6 Stock food, water and power source—-5 Get pneumococcal vaccine—————3 Nothing———————————— 30 Hand washing, mask, etc————— 3 Notice there was no mention of taking the swine flu vaccine. Behind the push to vaccinate the entire population are the pharmaceutical makers of the vaccines, who are working in conjunction with the government to make the vaccine mandatory. Homeland security and FEMA are pushing for forced vaccinations and the medical experts, virologists and epidemiologists are calling for calm and resorting to voluntary vaccination only. The former have links with the vaccine manufacturers via political contacts. A great deal of money will be made by the manufacturers, should forced vaccinations be mandated. Will This Vaccine Be Tested? According to Anthony Fauci, director of the National Institutes of Allergy and Infectious Diseases, 5 tests are planned. It is not clear as to the use of the squalene adjuvants, ASO3 and MF-59. Because of concerns raised, the FDA is now hedging. Independent studies of squalene used as a vaccine adjuvant indicates that it is associated with a very high incidence of autoimmune diseases, such as an MS-like neurological syndrome, rheumatoid joint disease and especially Lupus. The developer of MF-59 is Chiron pharmaceuticals, which was purchased by Novartis pharmaceutical company, who will be the main supplier of the swine flu vaccine for the world. According to Dr. Fauci, testing in both children and adults will be without this adjuvant and he admits that we have no data on the safety in children.(See Nature Vol 460/30 July 2009, p 562 for the interview.) There are 5 tests scheduled for safety before mass vaccinations will resume. I looked up on clinicaltrials.gov the actual studies being done. It is instructive to note that the only studies actually being done do not contain any adjuvant (the immune booster) either for babies or adults. Yet, when the mass vaccinations begin, the vaccines will have adjuvant added, possibly squalene. The real irony here is that this is the same bait and switch game they played in the 1976 swine flu vaccine disaster. They tested one vaccine and gave a different one during the mass vaccinations. Here we go again. Over 500 people were paralyzed with Guillain Barre disorder. The incidence was much higher, because it was not a reportable disease. And over 300 people died, which is also a very low figure. Dr. Fauci admits that they have no idea what will happen when they mix the three viruses from the vaccines together or when they are given sequentially. When he was asked if the results of the studies would be reviewed by the health authorities, he answered, “yes, except for those done by the Novartis company.” He justified this secrecy by saying that Norvartis had a very advanced testing system, which was done “in-house” — that is, in secrecy. It is also important to appreciate that this vaccine has been fast-tracked, meaning that many of the usual safety precautions used to prevent contamination of the vaccines will be overlooked by the regulatory agencies. According to a number of studies, vaccine contamination is widespread, with vaccines containing pestivirus, mycoplasma, viral fragments, DNA fragments and bacterial components, all of which can produce chronic systemic disorders, cancer, neurologic diseases and even slow brain degeneration. – - – The Following was composed by Dr. Russell Blaylock as a method to reduce autoimmune reactions to the flu vaccines only. Do not use this if you have the flu itself. These are just general observations and not medical advice. You should work with your doctor for a specific program.

 Treatment for Toxic Vaccine Exposure

Place a cold compress on the site of the injection immediately after the injection and continue this as often as possible for at least two days. If symptoms of fever, irritability, fatigue or flu-like symptoms reoccur — continue the cold compresses until they abate. A cold shower or bath will also help. Take fish oils — I recommend the Norwegian fish oil made by Carlson Labs — it has the correct balance of EPA and DHA to reduce the cytokine storm. The dose is one tablespoon a day — if severe symptoms develop — two tablespoons a day until well and then switch to one tablespoon a day. Children — one teaspoon a day. Curcumin, quercetin, ferulic acid and ellagic acid as a mixture — the first two must be mixed with extravirgin olive in one teaspoon. Take the mix three times a day (500 mg of each) Vitamin E (natural form) 400 IU a day (high in gamma-E) Vitamin C 1000 mg four times a day Astaxanthin 4 mg a day Zinc 20 mg a day for one week then 5 mg a day Avoid all immune stimulating supplements (mushroom extracts, whey protein) except beta-glucan — it has been shown to reduce inflammation, microglial activation and has a reduced risk of aggravating autoimmunity, while increasing antiviral cellular immunity. Take a multivitamin/mineral daily (one without iron — Extend Core) Magnesium citrate/malate 500 mg of elemental magnesium two capsules three times a day Vitamin D3: All Children — 5000 IU a day for two weeks after vaccine then 2000 IU a day thereafter Adults — 20,000 IU a day after vaccine for two weeks then 10,000 IU a day thereafter Take 500 mg to 1000 mg of calcium citrate a day for adults and 250 mg a day for children under age 12 years. Avoid all mercury-containing seafood Avoid omega-6 oils (corn, safflower, sunflower, soybean, canola and peanut oils) Blenderize parsley and celery and drink 8 ounces twice a day Take Jatoba tea extract (add 20 drops in on cup of tea) one day before the vaccine and the twice a day thereafter. (you can get it at http://www.iherb.com/Amazon-Therapeutics-Jatoba-1-oz-30-ml/14429?at=0) It is inexpensive. Dr. Russell Blaylock (www.russellblaylockmd.com)

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Curcumin Stimulates Immune Cells To Clear Alzheimers Plaque

October 05, 2006
Curcumin Stimulates Immune Cells To Clear Alzheimers PlaqueCurcumin is a compound found in turmeric spice which is used in curries. While only done in cell culture the use of curcumin enhanced the performance of immune system macrophage cells to take up beta amyloid plaques.

UCLA/VA researchers found that curcumin — a chemical found in curry and turmeric — may help the immune system clear the brain of amyloid beta, which form the plaques found in Alzheimer’s disease.

Published in the Oct. 9 issue of the Journal of Alzheimer’s Disease, the early laboratory findings may lead to a new approach in treating Alzheimer’s disease by enhancing the natural function of the immune system using curcumin, known for its anti-inflammatory and anti-oxidant properties.

Using blood samples from six Alzheimer’s disease patients and three healthy control patients, the researchers isolated cells called macrophages, which are the immune system’s PacMen that travel through the brain and body, gobbling up waste products, including amyloid beta.

The team treated the macrophages with a drug derived from curcumin for 24 hours in a cell culture and then introduced amyloid beta. Treated macrophages from three out of six Alzheimer’s disease patients showed improved uptake or ingestion of the waste product compared to the patients’ macrophages not treated with curcumin. Macrophages from the healthy controls, which were already effectively clearing amyloid beta, showed no change when curcumin was added.

It only helped in cells from half the patients.

“Curcumin improved ingestion of amyloid beta by immune cells in 50 percent of patients with Alzheimer’s disease. These initial findings demonstrate that curcumin may help boost the immune system of specific Alzheimer’s disease patients,” said Dr. Milan Fiala, study author and a researcher with the David Geffen School of Medicine at UCLA and the VA Greater Los Angeles Health Care System. “We are hopeful that these positive results in a test tube may translate to clinical use, but more studies need to be done before curcumin can be recommended.”

Older immune systems might be less able to clear the plaque junk that accumulates in the brains of those with Alzheimer’s.

The patients ranged in age from 65 to 84. Fiala noted that the patients whose immune cells responded were younger and had higher scores on a Mini-Mental State Examination suggesting that curcumin may help those with less advanced dementia. Some of the patients may have already had additional curcumin in their systems due to participation in another UCLA study, which may have impacted findings.

Rejuvenation of the immune system will probably lower the incidence of Alzheimer’s and might also reduce the incidence of other diseases caused at least in part by the accumulation of misfolded proteins and other junk. Check out some evidence that immune system aging leads to Alzheimer’s: Immune System Deficiencies May Lead To Alzheimer’s Disease

Also see my post Alzheimers Curable With Insulin Receptor Drug? for another approach that might help. Then there’s the stoner approach to protection from Alzheimer’s: THC Blocks Alzheimer’s Plaque Formation

By Randall Parker at 2006 October 05 09:15 PM  Brain Disorder Repair

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Boost Natural Killer Cells to Prevent Swine Flu


TARPON SPRINGS, FL 5/05/09/PRNEWSWIRE

Healthy immune systems increase protection from viruses, including the H1N1 swine flu.  Herbal and nutritional supplements can dramatically increase protection from swine flu by increasing levels of  Natural Killer Cells, which destroy viruses, without attacking healthy body cells.

Drastic measures including closing schools, canceling graduation ceremonies and airline flights are being used to slow spread of the H1N1 swine flu virus. Governmental authorities recommend increased hand washing and avoiding handshakes, which did not prevent previous influenza epidemics from killing millions of people, in 1918.

Rick Sponaugle, MD, Medical Director of Florida Detox and Wellness Institute, recommends increasing levels of Natural Killer Cell white blood cells, to prevent infection with swine flu and other viruses.  Natural Killer Cells protect us from viruses, during new infections, while other white blood cells attempt to produce antibodies against new viruses.  Research proves over the counter herbal and nutritional supplements can increase Natural Killer Cell levels.

Dr. Sponaugle reported, “We have measured 60 percent increases in Natural Killer Cells, using over the counter formulas containing naturally occurring inositol phosphates.  The 60 percent Natural Killer Cell increase is consistent with results published in scientific studies.”  Since Inositol phosphates occur naturally in the body, there is essentially no risk of allergic reaction.

AHCC, is an immune booster extracted from mushrooms which increased Natural Killer Cell levels, 200 to 300 percent, in published studies.  Florida Detox and Wellness Institute   increased Natural Killer Cell levels in one severely immune suppressed patient, from 3 per milliliter to 150 per milliliter.

Intravenous Vitamin C can also increase Natural Killer Cells.  Natural Killer Cell count increased from 38 to 464 in a Lymes Disease, after he received intravenous Vitamin C, at Florida Detox and Wellness Institute.

Natural Killer Cell levels tend to decrease with age. Patients with chronic fatigue syndrome, fibromyalgia, Lymes Disease, Babesia, or HIV are more likely to have lower Natural Killer Cell levels.  Herpes Simplex, Human Herpes 6, Epstein Barr and Cytomegalus viruses also suppress immunity.

Dr. Sponaugle also recommends reducing sugar consumption, to increase immunity.  Studies reveal consuming 100 grams of sugar reduced immunity for over five hours.  Researchers measured activity of neutrophils, white blood cells which engulf and destroy bacteria and other harmful microorganisms.  Neutrophil activity was reduced over 45 percent, two hours, after sugar consumption.   Am. J. Clin. Nutr., 30:613, 1977  Am. J. Clin. Nutr., 26:180, 1973.

Excessive sugar consumption causes chronic immune suppression, in  many Americans.  The average American consumes 125 grams of sucrose sugar daily, in addition to 50 grams of other refined sugars daily.  A typical 12 ounce cola drink contains ten teaspoons or 41 grams of sugar.  A Milky Way candy bar contains 35 grams of sugar. Many herbal teas and energy drinks are sweetened with high fructose corn syrup, which is essentially a refined sugar. Estimates indicate twenty percent of Americans consume over 75 grams of high fructose corn syrup daily.  Since different parts of the immune system work together, through chemical messenger systems, increasing neutrophil activity can enhance Natural Killer Cell activity.

Florida Detox and Wellness Institute has perfected scientifically advanced,  compassionate, detoxification techniques for alcohol, Xanax, Klonopin, methadone, Vicodin, Oxycontin, Percocet, Norco, Fentanyl, heroin and other opiate drugs.  Florida Detox and Wellness Institute has treated over 5,000 patients for chemical dependency. We have proven patients self-medicate underactive and overactive brain regions with food, drugs and alcohol to feel more normal. When brain chemistry and hormonal imbalance is correctly diagnosed and treated, brain craving for excess food, drugs and alcohol stops.

For more information see www.floridadetox.com or call Florida Detox at 1-888-775-2770.

Comments (2)

Vaccine Thimerosal Levels Sufficient to Completely Impair Methionine Synthase

This article indicates Thimerosal levels contained in vaccinations can completely eliminate methionine synthase activity.

Fall Defeat Autism Now!TM 2003 Conference *** Portland, Oregon *** October 3-5, 2003

Effects of Mercury on Methionine Synthase: Implications for Disordered Methylation in Autism

Richard Deth, PhD and Mostafa Waly, PhD
Northeastern University, Boston, MA 02115

Methionine synthase carries out the vitamin B12-dependent methylation of homocysteine, using a methyl group from 5-methyltetrahydrofolate (5-methylTHF). In doing so it provides a crucial link between two important metabolic systems, the single-carbon folate pathway and the methionine cycle (Fig. 1, right). Recently our laboratory discovered that methionine synthase is also required for dopamine-stimulated methylation of membrane phospholipids, a unique signaling activity of the D4 dopamine receptor (1-3). In the latter case, a homocysteine residue in the D4 receptor, generated by donation of a methyl group to the phosphatidylethanolamine (PE), is re-methylated to methionine, with 5-methylTHF again serving as a co-factor (Fig. 1, left). Thus methionine synthase also links dopaminergic neurotransmission to metabolism.

Figure 1. Pathways of single-carbon metabolism. The folate pathway (middle) supplies formate-derived single-carbon groups for purine and thymidine synthesis and methyl groups (as 5-methylTHF) to methionine synthase (Met Syn). The methionine cycle (lower right) provides S-adenosylmethionine (SAM), the methyl donor for many methylation reactions. MET313 in the D4 receptor also serves as a donor of methyl groups for methylation of the phospholipid phosphatidylethanolamine (PE).

Sufficient methylation of homocysteine is essential not only to supplement the diet-derived supply of methionine, but also to maintain a low level of homocysteine and its precursor, S-adenosylmethionine (SAH), which otherwise inhibits methylation reactions by competing with the methyl donor S-adenosylmethionine (SAM). Increased methionine synthase activity can therefore promote methylation by lowering SAH, while impaired activity will impede methylation.  In addition, THF released by methionine synthase is needed for other folate-dependent reactions, avoiding a “methyl-folate trap”.

D4 receptor-mediated phospholipid methylation (PLM) can be very robust, up to 50 methylations/receptor/sec, increasing the spacing between phospholipid headgroups and altering the fluid properties of the membrane in the region surrounding the receptor. The activity of membrane proteins located near the D4 receptor can be modulated by PLM and this “solid-state signaling” mechanism has been implicated in the molecular mechanism of attention (4). Proline-rich segments present in the cytoplasmic portion of the receptor in all species allow it to serve as a docking site for signaling proteins that become targets for PLM-based modulation. In humans and other primates, the D4 receptor possesses anywhere from 2 to 11 additional proline-rich repeat segments (Fig. 2), and a higher number of repeats (i.e. seven) brings an increased risk of attention-deficit hyperactivity disorder (ADHD) (5). Thus methionine synthase activity is important for normal attention while a decrease in its activity may contribute to ADHD.

Figure 2. Structural features of the D4 dopamine receptor. Methionine 313 serves as donor of methyl groups to the headgroups of surrounding phospholipids. Proline-rich segments allow other proteins to bind to the D4 receptor.

Methionine Synthase is Regulated by IGF-1 and Dopamine

Recently our laboratory has showed that the enzymatic activity of methionine synthase in human neuroblastoma cells is increased by stimulation of either D4 dopamine receptors or insulin-like growth factor-1 (IGF-1) receptors (6). In intact cells, this stimulation is evident as an increase in the rate of folate-dependent phospholipid methylation (Fig. 3), while pretreatment of cells with IGF-1 or dopamine or their combination increased the enzyme activity of methionine synthase by more than five-fold (Table 1).

Figure 3. Dose-dependent stimulation of folate-dependent phospholipid methylation (PLM) by IGF-I in SY5Y neuroblastoma cells.

Further investigation revealed that stimulation of methionine synthase by dopamine and IGF-1 involves activation of the PI3-kinase signaling pathway. Via different mechanisms, D4 and IGF-1 receptor activation leads to increased phosphorylation of plasma membrane inositol phospholipids by PI3-kinase. Numerous studies have shown that activation of this pathway by IGF-1 promotes cell survival while activation by other growth factors (e.g. nerve growth factor) leads to cellular differentiation. Moreover, interference with the methionine cycle blocks the ability of nerve growth factor to induce differentiation (7). Inhibition of PI3-kinase not only blocked stimulation of methionine synthase by dopamine and IGF-1, but also reduced enzyme activity to zero (Table 1), indicating an absolute dependence on PI3-kinase in the human neuroblastoma cells we used. This is the first report that extracellular signaling molecules can regulate methionine synthase.

By increasing methionine synthase activity, IGF and dopamine will decrease the levels of both homocysteine and SAH, increasing the SAM to SAH ratio and thereby promoting methylation reactions. Methylation of DNA leads to the formation of nucleosomes (stable complexes of DNA and histones), causing gene silencing. We measured global DNA methylation after a 6-hour treatment with IGF-1 or dopamine and found increases of 101% and 71% respectively, which were blocked by an inhibitor of PI3-kinase (6). Furthermore, PI3-kinase inhibition decreased methylation of the cyclin D2 gene, and increased its transcription. Together these observations indicate that PI3-kinase-dependent activation of methionine synthase provides a mechanism by which IGF-1 and dopamine can regulate gene expression via changes in DNA methylation.

Neurodevelopmental Toxins Inhibit Methionine Synthase

Environmental exposure to heavy metals, such as lead and mercury, causes neurotoxicity and leads to developmental disorders. It has been proposed that the recent dramatic rise in the incidence of autism is linked to the increased number of required vaccinations containing the ethylmercury derivative thimerosal (8,9). Since developmental disorders such as Rett syndrome and fragile-X syndrome include a crucial role for DNA methylation, we investigated the effects of various metal ions on methionine synthase activity and folate-dependent PLM.

As shown in Table 1, treatment of neuroblastoma cells with mercury (1 mM) or thimerosal (10 nM) for 60 min caused a complete loss of measurable methionine synthase activity, while lead significantly reduced enzyme activity. Ethanol, a well-recognized neurodevelopmental toxin, also eliminated activity at a concentration of 0.1%. Folate-dependent PLM studies (Fig. 4) showed that mercury and lead produced dose-dependent inhibition with a threshold near 1 nM, while thimerosal was at least 10-fold more potent. It is notable that a single dose of thimerosal-containing vaccine produces blood levels between 10 and 100 nM (10). These results clearly demonstrate the ability of neurodevelopmental toxins and thimerosal to inhibit PI3-kinase-dependent methionine synthase activity. Additional studies indicated that heavy metal-induced inhibition is likely caused by competition with Cu2+, which is required for PI3-kinase activity (6). In contrast, ethanol acts by interfering with IGF-1 receptor activation.  EMPHASIS ADDED

table 1

Table 1 Effect of IGF-1, dopamine and neurodevelopmental toxins on methionine synthase activity. IGF-1 and dopamine increase activity by 2.3- and 2.8-fold respectively. The PI3-kinase inhibitor wortmannin reduces activity to undetectable levels and blocks stimulation.The neurodevelopmental toxins ethanol, mercury, lead and thimerosal either inhibit or eliminate methionine synthase activity.

Figure 4. Inhibition of folate-dependent PLM by mercury, lead and thimerosal. Mercury and lead exhibit a threshold near 1 nM for inhibition of IGF-1-stimulated PLM (Left panel). Thimerosal inhibits both basal PLM and stimulation by either IGF-1 or dopamine at concentrations of 0.1 nM and higher (Right panel).

Implications for Autism

It has been proposed that the recent dramatic increase in the incidence of autism is due to neurodevelopmental effects of thimerosal, associated with an increase in the number of required vaccines containing this preservative (8,9). However, this proposal has met with considerable skepticism, since there was no evidence that thimerosal could produce adverse effects on a relevant biochemical process at the concentrations produced by vaccination. A single vaccination produces blood levels between 10 and 100 nM (10). Our findings clearly demonstrate that thimerosal inhibits PI3-kinase-dependent methionine synthase at concentrations well below these levels, raising the possibility that this inhibition might contribute to the pathology of autism.

Several important questions arise: 1. How might lower methionine synthase activity account for the symptoms of autism? 2. What are the risk factor(s) for developing autism?

As noted above, methionine synthase has two substrates: the homocysteine state of the D4 dopamine receptor and homocysteine itself. Reduced activity will therefore decrease D4 receptor-mediated PLM and increase homocysteine levels. Since D4 receptor-mediated PLM appears to be important for the molecular mechanism of attention (4), its impairment could lead to a reduced capacity for attention, which is a primary symptom of autism. Indeed, autism shares several features with ADHD, including a 3-4-fold higher prevalence in males vs. females and both conditions have shown a markedly higher incidence over the past several decades. Reduced activity of methionine synthase, caused by exposure to heavy metals and/or thimerosal, could therefore impair the molecular mechanism of attention, leading to symptoms of autism. ADHD may represent a milder form of autism, associated with moderate inhibition of D4 receptor-mediated PLM.

Since SAH hydrolase (Ado HCYase in Fig. 1) is reversible, a failure of methionine synthase to efficiently convert homocysteine to methionine will lead to increased formation of SAH, to an extent dependent upon the prevailing concentration of adenosine. SAH inhibits methylation reactions, and decreased methionine synthase activity could therefore reduce DNA methylation, resulting in altered patterns of gene expression and impaired development. More specifically, heavy metals and thimerosal may interfere with the ability of growth factors like IGF-1 to promote development by impairing their control over methionine synthase.

The risk of developing autism in response to heavy metal or thimerosal exposure may depend upon genetically-transmitted risk factors that interact with methylation events. For example, previous studies showed that adenosine deaminase (ADA) activity is reduced in autistic individuals (11), associated with increased prevalence of a polymorphism in the ADA gene that reduces enzyme activity (12). As illustrated in Fig. 1, reduced ADA activity will cause elevated adenosine levels that will synergize with impaired methionine synthase activity to produce higher levels of SAH, yielding greater inhibition of methylation reactions. Increased synthesis of adenosine due to elevated 5’-nucleotidase activity has also been reported in autism (13). Mutations in the adenosylsuccinate lyase (ASL) gene are a rare cause of autism (14). These mutations divert single-carbon groups toward de novo purine synthesis and limit the availability of 5-methylTHF. Moreover, increased purine synthesis is common in autism (15). Lower availability of 5-methylTHF will synergize with the inhibitory effects of metals and thimerosal. These examples serve to illustrate how genetic and metabolic abnormalities can predispose to autism. Any impairment in the ability to excrete or detoxify heavy metals will also impose a further increased risk (16).

Summary

Our studies provide new insights into the control of methylation reactions by dopamine and by growth factors that increase PI3-kinase. By increasing methionine synthase activity and accelerating the conversion of homocysteine to methionine, they can lower SAH levels and promote methylation reactions. Neurodevelopmental toxins and thimerosal interfere with PI3-kinase-dependent methionine synthase, resulting in impaired methylation, including DNA methylation that is essential for normal development. D4 receptor-dependent PLM is an essential component of the molecular mechanism of attention, and reduced methionine synthase activity will therefore lead to impairments in attention and in attention-related learning. ADHD may reflect a milder degree of impairment in these same mechanisms. Since thimerosal has largely, but not completely, been eliminated from vaccines in the U.S., it will be of particular interest to observe whether the incidence of autism decreases during the next 3-5 years. Finally, we hope that these findings may point the way toward the discovery of new therapeutic approaches for the treatment of autism as well as new diagnostic tests that could identify individuals at high risk of developing autism in response to thimerosal or heavy metal exposure.

References

  1. Sharma, A., Kramer, M.L., Wick, P.F., Liu, D., Chari, S., Shim, S., Tan, W., Ouellette, D., Nagata, M., DuRand, C.J. et al. (1999) Mol. Psychiatry 4, 235-46.
  2. Zhao, R., Chen, Y., Tan, W., Waly, M., Sharma, A., Stover, P., Rosowsky, A., Malewicz, B., & Deth, R.C. (2001) J. Neurochem. 78, 788-96.
  3. Sharma, A., Waly, M., & Deth, R.C. (2001) Eur. J. Pharmacol. 427, 83-90.
  4. LaHoste, G.J., Swanson, J.M., Wigal, S.B., Glabe, C., Wigal, T., King, N., & Kennedy, J.L. (1996) Mol. Psychiatry 1, 121-4.
  5. Deth, R.C. (2003) in Molecular Origins of Human Attention, (Kluwer Academic Publishers, Boston).
  6. Waly, M., Olteanu, H., Banerjee, R., Choi, S.-W., Mason, J., Parker, B., Sukumar, S., Shim, S., Sharma, A., Benzecry, J., Power-Charnitsky, V.-A., & Deth, R.C. (Submitted)  Molec. Psychiatry.
  7. Cimato, T.R., Ettinger, M.J., Zhou, X.& Aletta, J.M. (1997) J. Cell Biol. 138,1089-103.
  8. Bernard, S., Enayati, A., Roger, H., Binstock, T., & Redwood, L. (2002) Mol. Psychiatry 7, S42-3.
  9. Geier, M.R. & Geier, D.A. (2003) J. Am. Phys. Surg. 8, 6-11.
  10. Stajich, G.V., Lopez, G.P., Harry, S.W., & Sexson, W.R. (2000) J. Pediatr. 136, 679-81.
  11. Stubbs, G., Litt, M., Lis, E., Jackson, R., Voth, W., Lindberg, A., Litt, R. (1982) J. Am. Acad. Child Psychiatry 21, 71-4.
  12. Persico, A.M., Militerni, R., Bravaccio, C., Schneider, C., Melmed, R., Trillo, S., Montecchi, F., Palermo, M.T., Pascucci, T., Puglisi-Allegra, S. et al. (2002) Am. J. Med. Genet. 96, 784-90.
  13. Page, T., Yu, A., Fontanesi, J., Nyhan, W.L. (1997) Proc. Natl. Acad. Sci. U S A 94, 11601-6.
  14. Stone, R.L., Aimi, J., Barshop, B.A., Jaeken, J., Van den Berghe, G., Zalkin, H., & Dixon, J.E. (1992) Nat. Genet. 1, 59-63.
  15. Page, T., & Coleman, M. (1998) Adv. Exp. Med. Biol. 431, 793-6.
  16. Blaxill, M. F. & Haley, B.E. (2003) Int. J. Toxicol. 22,

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Comments (1)

Thimerosal Containing Vaccinations Linked to Autism

Journal of Toxicology and Environmental Health, Part A, 70: 837–851, 2007
Copyright © Taylor & Francis Group, LLC
ISSN: 1528-7394 print / 1087-2620 online
DOI: 10.1080/15287390701212141
837

UTEH A Case Series of Children with Apparent Mercury Toxic
Encephalopathies Manifesting with Clinical Symptoms of
Regressive Autistic Disorders
Autistic Disorders David A. Geier
Institute of Chronic Illnesses, Inc., Silver Spring, Maryland, USA
Mark R. Geier
Genetic Centers of America, Silver Spring, Maryland, USA

Impairments in social relatedness and communication, repetitive
behaviors, and stereotypic abnormal movement patterns characterize
autism spectrum disorders (ASDs). It is clear that while
genetic factors are important to the pathogenesis of ASDs, mercury
exposure can induce immune, sensory, neurological, motor, and
behavioral dysfunctions similar to traits defining or associated with
ASDs. The Institutional Review Board of the Institute for Chronic
Illnesses (Office for Human Research Protections, U.S. Department
of Health and Human Services, IRB number IRB00005375)
approved the present study. A case series of nine patients who presented
to the Genetic Centers of America for a genetic/developmental
evaluation are discussed. Eight of nine patients (one patient was
found to have an ASD due to Rett’s syndrome) (a) had regressive
ASDs; (b) had elevated levels of androgens; (c) excreted significant
amounts of mercury post chelation challenge; (d) had biochemical
evidence of decreased function in their glutathione pathways; (e)
had no known significant mercury exposure except from Thimerosal-
containing vaccines/Rho(D)-immune globulin preparations;
and (f) had alternate causes for their regressive ASDs ruled out.
There was a significant dose-response relationship between the
severity of the regressive ASDs observed and the total mercury dose
children received from Thimerosal-containing vaccines/Rho (D)-
immune globulin preparations. Based upon differential diagnoses, 8
of 9 patients examined were exposed to significant mercury from
Thimerosal-containing biologic/vaccine preparations during their
fetal/infant developmental periods, and subsequently, between 12
and 24 mo of age, these previously normally developing children
suffered mercury toxic encephalopathies that manifested with
clinical symptoms consistent with regressive ASDs. Evidence for
mercury intoxication should be considered in the differential diagnosis
as contributing to some regressive ASDs.
Autism is a neurodevelopmental syndrome characterized
by impairments in social relatedness and communication, repetitive
behaviors, and stereotypic abnormal movement patterns
(California Department of Developmental Services, 2003). While
genetic factors are recognized as being important in the pathogenesis
of autistic disorders, the role for environmental factors has
received considerable attention. Researchers have previously
reported that exposure to mercury can produce immune, sensory,
neurological, motor, and behavioral dysfunctions similar to traits
defining or associated with autistic disorders, and these similarities
extend to neuroanatomy, neurotransmitters, and biochemistry
(Bernard et al., 2001, 2002; Blaxill et al., 2004; Redwood et al.,
2001). Furthermore, recent research observing children’s communicative,
social, affective and repetitive behaviors and toy play
coded from videotapes of the toddlers’ first and second birthday
parties revealed there are children with regressive autistic disorders
that manifest between the ages of 12 and 24 mo (Werner &
Dawson, 2005), a temporal period concurrent with exposure of
these children to mercury from Thimerosal-containing biologics/
vaccines in the U.S. standard immunization schedule.

Journal of Toxicology and Environmental Health, Part A, 70: 837–851, 2007
Copyright © Taylor & Francis Group, LLC
ISSN: 1528-7394 print / 1087-2620 online
DOI: 10.1080/15287390701212141
837
UTEH A Case Series of Children with Apparent Mercury Toxic
Encephalopathies Manifesting with Clinical Symptoms of
Regressive Autistic Disorders
Autistic Disorders David A. Geier
Institute of Chronic Illnesses, Inc., Silver Spring, Maryland, USA
Mark R. Geier
Genetic Centers of America, Silver Spring, Maryland, USA
Impairments in social relatedness and communication, repetitive
behaviors, and stereotypic abnormal movement patterns characterize
autism spectrum disorders (ASDs). It is clear that while
genetic factors are important to the pathogenesis of ASDs, mercury
exposure can induce immune, sensory, neurological, motor, and
behavioral dysfunctions similar to traits defining or associated with
ASDs. The Institutional Review Board of the Institute for Chronic
Illnesses (Office for Human Research Protections, U.S. Department
of Health and Human Services, IRB number IRB00005375)
approved the present study. A case series of nine patients who presented
to the Genetic Centers of America for a genetic/developmental
evaluation are discussed. Eight of nine patients (one patient was
found to have an ASD due to Rett’s syndrome) (a) had regressive
ASDs; (b) had elevated levels of androgens; (c) excreted significant
amounts of mercury post chelation challenge; (d) had biochemical
evidence of decreased function in their glutathione pathways; (e)
had no known significant mercury exposure except from Thimerosal-
containing vaccines/Rho(D)-immune globulin preparations;
and (f) had alternate causes for their regressive ASDs ruled out.
There was a significant dose-response relationship between the
severity of the regressive ASDs observed and the total mercury dose
children received from Thimerosal-containing vaccines/Rho (D)-
immune globulin preparations. Based upon differential diagnoses, 8
of 9 patients examined were exposed to significant mercury from
Thimerosal-containing biologic/vaccine preparations during their
fetal/infant developmental periods, and subsequently, between 12
and 24 mo of age, these previously normally developing children
suffered mercury toxic encephalopathies that manifested with
clinical symptoms consistent with regressive ASDs. Evidence for
mercury intoxication should be considered in the differential diagnosis
as contributing to some regressive ASDs.
Autism is a neurodevelopmental syndrome characterized
by impairments in social relatedness and communication, repetitive
behaviors, and stereotypic abnormal movement patterns
(California Department of Developmental Services, 2003). While
genetic factors are recognized as being important in the pathogenesis
of autistic disorders, the role for environmental factors has
received considerable attention. Researchers have previously
reported that exposure to mercury can produce immune, sensory,
neurological, motor, and behavioral dysfunctions similar to traits
defining or associated with autistic disorders, and these similarities
extend to neuroanatomy, neurotransmitters, and biochemistry
(Bernard et al., 2001, 2002; Blaxill et al., 2004; Redwood et al.,
2001). Furthermore, recent research observing children’s communicative,
social, affective and repetitive behaviors and toy play
coded from videotapes of the toddlers’ first and second birthday
parties revealed there are children with regressive autistic disorders
that manifest between the ages of 12 and 24 mo (Werner &
Dawson, 2005), a temporal period concurrent with exposure of
these children to mercury from Thimerosal-containing biologics/
vaccines in the U.S. standard immunization schedule.

Entire article may be viewed at  http://www.generationrescue.org/pdf/encephalopathies.pdf

Comments (1)

Obese Six Times More Likely to Die or Be Admitted to ICU

In addition, one of the more powerful risk factors for being admitted to the ICU and of dying is obesity.

Turns out obese people are admitted 6x more often than those of normal weight. And obesity plays a significant role in the risk to children and pregnant women as well, something that has never been discussed by the media, the CDC or the public health officials.

According to Dr. Blaylock, one study found that 32.7% of those admitted to the ICU had asthma or other chronic pulmonary disease, far higher than the general population. Obesity is also associated with a high incidence of insulin resistance and metabolic syndrome, both of which would increase your risk of having a serious infection, even to mild viruses.

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Co-Occuring Bacterial Infections in 36 Childhood Swine Flu Deaths

Common Links in Swine Flu Deaths…
Posted by: Dr. Mercola
October 31 2009 | 84,414 views

 

staphylococcus aureusA recent study by the Centers for Disease Control and Prevention (CDC) found that of the 36 children who died from H1N1 from April to August, six had no chronic health conditions. But all of them had a co-occurring bacterial infection.

The most common co-occurring infection that causes flu-related deaths is staphylococcus aureus. A third of the population carries it, most in their nose or on their skin.

The flu causes upper respiratory damage, which allows the staph to make its way into the lungs.

Sources:

Dr. Mercola''s Comments
Dr. Mercola’s Comments:

 

This is exactly what I was referring to in Wednesday’s special swine flu alert. If you missed it, I urge you to take a moment to review it now. It received over 80,000 views within hours of being published.

In it, I discussed the prevailing propaganda being streamed through popularTV programslike 60-Minutes.

60-Minutes’ Story Also Highlighted Bacterial Infection as Flu Tragedy

Their segment, which aired last Sunday, did ask some hard questions to the Assistant Surgeon General. But they didn’t ask why CDC officials persist in telling the public that this H1N1 strain of influenza is quite dangerous when the experience of those in the southern hemisphere (which just finished their flu season) is in direct conflict with what the CDC is telling the American people.

And, just like most of the mainstream media, 60-Minutes did not ask some of the most essential questions that need to be answered if you are to understand what is really going on with this “pandemic.”

The issue of coexisting bacterial infections is one of those questions that need to be looked at more closely.

Their segment followed the story of a young high school football player who was infected with the H1N1 virus, received some form of medication for his flu symptoms, and then quickly developed a life-threatening staph infection in his lungs.

However, no questions were asked about what type of medication he received, even though it was clear that, after recovering slightly, he then quickly deteriorated after receiving the medication.

There was also no mention of whether the teen had already been vaccinated for seasonal or H1N1 influenza, either recently or in the past years.

A Canadian preliminary study is provocative in that it suggests that those who have gotten seasonal influenza vaccine in the past may be at greater risk for getting H1N1 and having complications.

The National Vaccine Information Center (NVIC) is calling for a comparison of vaccinated vs. unvaccinated individuals for all health outcomes, and I believe it would be prudent to do so.

After all, in order for anyone to make an informed decision about vaccines, you need to have certain facts at hand, not conjecture stating that something is “believed to be safe” even though it has never been studied!

Why Aren’t These Important Questions Being Asked?

So far 81 children have died from H1N1 in the US. The death of any child is tragic. However, using these deaths to potentially harm countless others who are not naturally at risk may be even worse.

Here are some of the questions that need honest answers, as they may paint an entirely different picture than what we are currently told by health officials and the media.

How many pediatric deaths occurred in children who:

  • Were positively lab confirmed as H1N1?
  • Had underlying chronic immune and brain dysfunction?
  • Were fully vaccinated according to CDC recommendations?
  • Had received influenza vaccine this year?
  • Had received seasonal influenza vaccine in previous years?
  • Received Tamiflu or another anti-viral prior to death?
  • Had a coinciding bacterial infection with H1N1?
  • Were never vaccinated – totally unvaccinated?

With only 81 sets of medical records to review, someone ought to be able to compile these statistics.

So far we know that, of the 36 children who died from H1N1 between April and August of this year, 30 had some form of chronic health condition, and all of them had a co-occurring bacterial infection.

Clearly, having a robust, well-functioning immune system is the best way to ensure your body’s innate ability to fight off this mild flu virus, and not succumb to secondary infections such as staphylococcus aureus.

I’d also like to know how many flu deaths might be attributed to antibiotic-resistant staph infections.

According to the Star Tribune, the most common co-occurring infection that causes flu-related deaths is staphylococcus aureus, which is commonly found on your skin and in your nose. About a third of the population carries it.

Unfortunately, methicillin-resistant staphylococcus aureus, also known as MRSA, has become a serious public health problem, one that is getting progressively worse and actually exacts a greater death toll than “modern plagues” like AIDS.

Needless to say, we already know the reason for the ever increasing threat of MRSA – over use of antibiotics, both in medicine and conventional farming practices. It’s an entirely man-made problem, the answer to which is exercising RESTRAINT in the use of antibiotics, so that they can actually work when someone’s life is really on the line…

It could be of great value to have more facts about each of these H1N1 flu deaths.

But the fact still remains that flu vaccines will nearly always decrease your overall immune function, not enhance it!

Obese at Six Times Higher Risk from H1N1 Complications

Most authorities agree that the H1N1 variant virus is quite mild. The vast majority of people (99.99%) are having very brief and mild illnesses from this virus. And yet, some people do die from it – some die each and every flu season. But who, and why?

Unfortunately, the media is not giving you the answers to these questions.

I will publish an excellent review, and a two-hour audio interview with Dr. Russell Blaylock on this issue on Tuesday, so please stay tuned! Because as he will explain in greater detail, 100 percent of those who have died had underlying health problems before they were infected.

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