|02-06-2012, 08:11 PM||#421|
Join Date: May 2012
Another blessing of gay semen worship.
you really think all these celebrities got Lyme disease from camping out in the woods?
This would also explain the coverup, they don't want you to know homosexuals are spreading it.
Just look at the wiki article, they admit the bacteria that causes it are in semen, but deny that it's spread through semen. That's like saying AIDS can't be spread through sexual contact, which is what they really would love to say, because they want everyone to get AIDS and die.
Last edited by angelsaredemons; 02-06-2012 at 08:17 PM.
|02-06-2012, 08:16 PM||#422|
Join Date: Jan 2010
Location: in the abyss of reality.
no i do not think they got it from just camping in the woods.
Considering most LLMD believe 90% of the population of the world how one gets Lyme is kinda blurred now and so many are being born with it too.
|05-06-2012, 05:30 PM||#423|
Join Date: Feb 2007
Louis Kuhne - Forgetten Genius Healer
Louis Kuhne was a 19th Century German naturopath who was far ahead of his time. He ran a large healing center and had worldwide renown. (In fact, his work was very appreciated in India and his book New Science of Healing was Gandhi's favorite health book.) He thought that the success of his work would lead to new advances in medicine, that it would eventually win over the world and end the barbaric practices of "modern" medicine.. He would be shocked to see that that the medical establishment has instead entrenched itself in a more and more fragmented view of the human body. Kuhne's theory is that:
"...the love that you withhold is the pain that you carry...Let imagination create a world of unconditional responsibility." (from LFA - "The Is-ness")
|05-06-2012, 05:37 PM||#424|
Join Date: Feb 2007
Facial Diagnosis - Our Body Speaks
Read Kuhne's Facial Diagnosis (1897):
"...the love that you withhold is the pain that you carry...Let imagination create a world of unconditional responsibility." (from LFA - "The Is-ness")
|07-06-2012, 07:50 PM||#425|
Join Date: Jan 2010
Location: in the abyss of reality.
Lyme disease not so rare in Texas, study says
HOUSTON (FOX 26) -
Lyme Disease in the Lone Star State is believed to be rare but a study by an area scientist seems to be proving otherwise. Dr. Maria Esteve-Gassent is a Research Professor at Texas A & M University. She's been studying ticks and Lyme Disease for seven years. Now Dr. Esteve-Gassent and her students are collecting ticks from all over Texas. "We go personally out there and we hunt ticks," says Dr. Esteve-Gassent. They're testing the ticks for Lyme Disease. From Houston to Sugar Land to Austin and Dallas, to name a few, they have found ticks that have tested positive for Lyme Disease.
Dr. Esteve-Gassent says she tested about 300 of the itty bitty biting bugs so far. About a quarter of the ticks found here in Texas have Lyme. Although Lyme in the Lone Star State is said to be rare. "Most doctors will say there's no Lyme Disease in Texas. Hopefully this will change at some point," says Dr. Esteve-Gassent. She started the study months ago because she says there are so many questions about lyme in Texas and so few answers. One thing we do know, if you find a tick on your skin you're advised to carefully remove it with tweezers making sure to remove the mouth of the embedded bug from your skin and then see a doctor immediately. "The good thing about Lyme Disease it's curable if you catch it within the first week or so," she says.
You usually pick up ticks in wooded areas and they stay attached to your skin for several days. Dr. Esteve-Gassent suggests you spray Off bug repellent with Deet before going out. "It will repel ticks. So use it. Every time you go outdoors spray it on your kids, on yourself, on your clothes. Wear long sleeves and pants," says Dr. Esteve-Gassent and she says check your children and yourself when you go back indoors. "I would check behind the ears, nape of neck, under the arms, bend of the arms, bend of knees, back of thighs, waist area," she advises.
If Lyme is not caught early the disease can be debilitating with severe pain and even heart and brain problems. Dr. Gassent is also accepting ticks.
So if you find one in your yard and you would like it tested you can seal it in a container submerged in rubbing alcohol and mail it to her at Dr. Maria Esteve Gassent, Phd
Texas A&M University College of Veterinary Sciences
VMS 215 College Station, TX 77843-4467
Dr. Esteve-Gassent will present her findings at a microbiology conference in California this month. Also, once her study is complete the results will be featured in a medical journal.
|07-06-2012, 07:51 PM||#426|
Join Date: Jan 2010
Location: in the abyss of reality.
Risk Maps Are Not Accurate for the South in 2012
The paper, “Human Risk of Infection with Borrelia burgdorferi, the Lyme Disease Agent, in Eastern United States”1 designates most of Virginia and the entire south below and west of Virginia as a low risk area for Lyme disease. The authors state, “The absence of infected host-seeking nymphs in most southern states suggests reported cases may be mostly misdiagnosis or travel.” Because their 6- to 8-year-old data are in contrast to recent data from Virginia, West Virginia, North Carolina, and Florida,2–5 I am concerned that harm to southern patients and public health efforts could occur if medical professionals used this work to aid in diagnosis and consideration of risk as the authors suggest they do.
Although bites from Ixodes scapularis ticks and Lyme disease are not as common as in the northeast, they do occur. North Carolina declared a central county (Wake) endemic for Lyme disease in 20106 and a growing number of other counties have had one local case meeting state and Centers for Disease Control and Prevention (CDC) standards. As of 2011, Virginia had declared about two-thirds of their counties endemic for Lyme disease including at least seven in the far west and five along the Virginia-North Carolina border.2
By the authors' own description their methods for collecting I. scapularis ticks including seasonality and drags were not suitable for the south, although acknowledging that these ticks are widespread in the region. Thus, following their sampling criteria based on northern methods, they collected only 1 tick each in Alabama and Georgia (in 2004), five in North Carolina (in 2005 and 2006), and 2 in South Carolina (2004 and 2005). Other states in the deep south were not sampled for this paper (see supplemental materials online)1,7,8; these few numbers cannot be expected to produce reliable results for the density of infected ticks. The sparse number of ticks collected was attributed to different host-seeking behavior from northern climes. These different behaviors are used to explain the lower likelihood of humans being bitten in the south. Although there is some merit to this argument, such assumptions may need further exploration now that there is evidence of emerging disease in the south and widespread I. scapularis tick populations.9
Tick populations are dynamic. Studies have found significant variation in abundance and activity patterns among years and habitats.10,11 Generalizing from short-term or spatially limited studies, as this study1 did for southern regions, is not recommended. As stated by Schulze and others, “Failure to recognize the biases in … sampling techniques can potentially lead to incorrect conclusions that can have significant public health consequences.”12 For example, in contrast to the Yale data, a 2006 study conducted by Smith and others in Chatham County, North Carolina collected 3,446 ticks of which 15 were nymphal I. scapularis. Forty percent of these were positive for B. burgdorferi sensu lato.3
The authors state their maps (which show zero risk of infected ticks and low risk for Lyme disease for all of the south below Virginia except an emerging coastal area in North Carolina) may be used to make personal protection decisions, to plan efficient allocation of public health resources, and to assist the medical community in considering diagnosis and treatment decisions. Global models and out-of-date data for Lyme disease demand cautious interpretation when it comes to public health recommendations and individual diagnosis and treatment decisions. Evidence-based medicine's need for up-to-date local data supersedes the use of the Yale Lyme disease risk maps.
©The American Society of Tropical Medicine and Hygiene
This is an Open Access article distributed under the terms and of the American Society of Tropical Medicine and Hygiene's Re-use License which permits unrestricted non-commercial use, distribution, and reproduction in any medium, provided the original work is properly cited.
, 2012. Human risk of infection with Borrelia burgdorferi, the Lyme disease agent, in eastern United States. Am J Trop Med Hyg86: 320– 327.
Abstract/FREE Full Text
Department of Health, Commonwealth of Virginia
, 2011. Available at: http://www.vdh.state.va.us/clinician...%20Disease.pdf. Accessed February 27, 2012.
, 2010. Bacterial pathogens in ixodid ticks from a Piedmont County in North Carolina: prevalence of rickettsial organisms. Vector Borne Zoonotic Dis10: 939– 952.
CrossRefMedlineWeb of Science
West Virginia Tickborne Disease Surveillance Summary
, 2000–2010. Available at: http://www.dhhr.wv.gov/oeps/disease/...%20Summary.pdf. Accessed March 5, 2012.
Florida Department of Health, Bureau of Environmental Public Health Medicine. Lyme Disease
. Available at: http://www.myfloridaeh.com/medicine/...me_disease.htm. Accessed March 5, 2012.
, 2010. Lyme disease found in Wake. Available at: http://www.newsobserver.com/2010/03/...d-in-wake.html. Accessed March 6, 2012.
, 2010. Field and climate-based model for predicting the density of host-seeking nymphal Ixodes scapularis, an important vector of tick-borne disease agents in the eastern United States. Glob Ecol Biogeogr19: 504– 14.
Web of Science
, 2006. Spatiotemporal patterns of host-seeking Ixodes scapularis nymphs (Acari: Ixodidae) in the United States. J Med Entomol43: 166– 176.
CrossRefMedlineWeb of Science
National Center for Emerging and Zoonotic Infection Diseases
. Available at: http://www.cdc.gov/ticks/geographic_...ml#blacklegged. Accessed November 7, 2011.
, 1996. Temporal and spatial dynamics of Ixodes scapularis (Acari: Ixodidae) in a rural landscape. J Med Entomol33: 90– 95.
MedlineWeb of Science
, 2000. Population size and drag sampling efficiency for the blacklegged tick (Acari: Ixodidae). J Med Entomol37: 357– 363.
, 1997. Biases associated with several sampling methods used to estimate abundance of Ixodes scapularis and Amblyomma americanum (Acari: Ixodidae). J Med Entomol34: 615– 623.
MedlineWeb of Science
|07-06-2012, 07:56 PM||#427|
Join Date: Jan 2010
Location: in the abyss of reality.
Increase In Deer Tick Population Sweeping Across O
POWELL, Ohio - An insect expert was traveling the state to warn counties and veterinarians about an increase in deer ticks, 10TV’s Kristyn Hartman reported on Monday.
Fifteen years ago, deer ticks were unheard of in Ohio. Now 26 counties, including Franklin and Delaware, are on the watch list
The black legged deer tick, which can be as small as a poppy seed, can carry Lyme disease.
If bites are diagnosed early, the illness can be easily treated with antibiotics. If missed, it can mean years of misery, Hartman reported.
Paige Caulley said that she discovered that first hand.
"We think I was bit when I was really, really young," said Caulley, 27.
Caulley grew up in Connecticut, where Lyme disease was more common. She said that she knew many classmates who had gotten the illness.
The Powell resident said that she has suffered from health problems throughout her life but never associated them with Lyme disease.
Caulley said that the problems grew worse after her daughter was born 18 months ago.
"I had a family doctor who just told me I need to start exercising. And that I need to see a therapist. And that it was all in my head. And I was in so much pain that I could barely walk," Caulley said.
Caulley looked to many doctors for help before finding a specialist in New York.
Now, Caulley makes monthly trips to New York, takes a variety of pills and gives herself a daily intravenous drip of antibiotics. Her medical bills exceed $50,000.
Glen Needham, an entomologist at the Ohio State University, who works with the state health department, travels the state warning county health departments and veterinarians that ticks are on the march across Ohio.
"We've gone from what we believe were no counties with black legged ticks, to two counties, to 26 counties," he said.
Hunters brought deer heads to the state lab for tick checks. In one year, numbers ballooned from 29 ticks to 1,800, Hartman reported.
“Dogs will be kind of canary in the cave for us.” Needham said. "So we think dogs may get Lyme Disease first in the state. And that may alert us to where some of these hot spots are," Needham said.
The infection is first identified by a bull’s-eye rash that many people may not notice.
Those infected could have a few days of flu-like symptoms, then feel better. But the disease does not go away. It could spread into the heart, the joints, and the nervous system.
Caulley thought that is what happened to her. Now she faces four more months of an IV antibiotic and a struggle to feel well, but a struggle that she thought was worth it, Hartman reported.
"I'm like 50 percent better," Caulley said.
Needham says Lyme disease may be difficult to diagnose, because patients experience a variety of symptoms. To cut the risk of getting sick, he said people should spray skin and clothes with an insecticide containing DEET.
Watch 10TV News and fresh 10TV.com for more information.
©2012 by 10TV.com. All rights reserved. This material may not be published, broadcast, rewritten or redistributed.
|07-06-2012, 10:42 PM||#428|
Join Date: Jan 2010
Location: in the abyss of reality.
US Observer FDA blocks healthy options
The Food and Drug Administration (FDA) takes its regulation job seriously, seemingly targeting anyone who won't or can't play ball in its high-dollar industry-giants-only club. Unfortunately for Americans, it seems to have forgotten its edict to promote public health.
Of the products that pass the FDA's “evaluation,” how many cause serious illness or death? LOTS. NutraSweet (Aspartame) comes to mind, as does saccharin, many vaccines, and a great many "food safe" additives the FDA has stamped with their approval. Just watch T.V. and pay attention to the amount of commercials asking people to call an attorney if they have taken any number of “FDA Approved” drugs/products that have caused serious illness or death. It is clear, just because the FDA evaluates a product or drug as safe, doesn't mean that it is.
So, when a product comes along that actually does have health benefit, the FDA appears to descend upon it in hopes to squash it from existence. Are they merely protecting the interests of the corporate giants and pharmaceutical behemoths that seek to keep us reliant upon dosages of their products? For the average American citizen, the answer seems pretty clear. "I don't trust the government, especially the FDA. The American people are sicker now and more apt to be on some prescription drug than any other time in history. How is this good? They [the FDA] keep attacking natural alternatives like raw cow and goat milk, plant extracts, home gardens and supplements that have proven positive results," says one such citizen who is disillusioned with what they call "the bull the FDA is feeding us."
One exciting and reportedly "miraculous" health product is Master Mineral Solution - commonly called MMS or Cleansing Water. It is made with sodium chlorite and citric acid to chemically generate the mineral, chlorine dioxide (NaClO2).
According to the Environmental Protection Agency (EPA), who used Chlorine Dioxide to decontaminate office buildings and mail after the anthrax attacks in 2001, Chlorine Dioxide has:
“...been used since the early 1900s.
In 1967, the U.S. Environmental Protection Agency (EPA) initially registered liquid chlorine dioxide as a disinfectant and sanitizer for specific uses, such as animal farms, bottling plants, food processing, handling, and storage plants. It also included other uses, including:
• bleaching pulp and paper
• bleaching textiles
• washing fruit and vegetables
• disinfecting flume water
• disinfecting meat and poultry
• disinfecting food processing equipment
• sanitizing water
• controlling odors
• treating medical wastes
• treating municipal water”
The EPA also says: “Chlorine dioxide kills microorganisms by disrupting transport of nutrients across the cell wall. Chlorine dioxide smells somewhat like chlorine bleach. Chlorine dioxide should not be confused with chlorine gas. They are two distinct chemicals that react differently and produce by-products that have little in common.”
According to many testimonials of individuals using MMS, it has successfully treated cancer, the flu, infections, serious burns, arthritis, arteriosclerosis, stroke, asthma, Lyme disease, diabetes, hepatitis (all strains), leukemia, Lou Gehrig’s disease, HIV, AIDS, Herpes, spider bites, and malaria. It has also been reported that it successfully treats autism.
Basic logic would dictate that if it didn't work, or it caused adverse reactions, there wouldn't be so many who openly and fervently support MMS. There are sites all over the internet touting personal experiences with MMS. Groups on Facebook and even YouTube channels have been dedicated to its benefits. It has literally been used by millions around the globe.
Instead of looking into MMS's potential for the people's common health, the FDA has chosen to strike out at the claims of its benefits. They are doing this primarily because of the amount of positive personal experiences. You see, MMS has not been "evaluated". As such, it is potentially harmful in the eyes of the FDA, and they have even issued an alert on its use. But then again, growing your own garden (and sharing food), or milking your own cows is now dangerous too, at least according to the FDA. Do a search on the internet and see how the FDA is attacking these common practices which have been around since the dawn of time! In fact, it appears that any personal medicinal and food choice is being criminalized at an alarming rate. Soon, we will only be able to eat what they tell us; grow what Monsanto provides us; supplement and medicate ourselves with only the "best" unnatural chemicals created in the labs of the corporate partners to the FDA.
Who would you trust? A cancer survivor who found life in a natural product, or a government agency that tells you to take products that it deems are safe that actually make you ill? Hmmm... tough question.
Currently, the FDA is targeting individuals involved in the distribution of MMS and the US~Observer is stepping forward to shield them and expose the FDA for what it is; a scheme, with no constitutional authority to exist. It seems designed to keep some people wealthy while the rest of us are programmed into thinking they are there to help. Look for more specifics coming soon...
If you would like to know more about MMS go to www.genesis2church.org or www.jimhumble.biz.
Read the letter sent by Jim Humble to MMS users and supporters!
And, read more MMS news here...
Here is more information regarding the FDA and some of its evaluated drugs:
The FDA's homicide victims
Coumadin = Rat Poison
Chemotherapy = Agent Orange or Mustard Gas
http://www.usobserver.com/archive/ma...rgeted.htmMore to be added soon...
|08-06-2012, 01:38 AM||#429|
Join Date: Jan 2010
Location: in the abyss of reality.
What is the real reason why lyme is covered up
There are an extraordinary number of citizens being diagnosed with Multiple Sclerosis, Lupus, ALS, Chronic Fatigue Syndrome, Alzheimers, Bipolar Depression, Fibromyalgia, Parkinson's...and the list goes on. I do not believe that this epidemic of diseases is naturally occurring. More and more disease labels are being invented for conditions that may be variations of only several causes. Each person may present with a slightly different symptom complex according to genetic factors, past bodily insults, or what coinfections one may harbor. Many independent researchers feel that these so called separate diseases, have common infectious causes.
"Infections are often misdiagnosed or not even sought - and because of this, infections often are either untreated or are inappropriately treated." Prof. G.H. Cassell 37th ICAAC, Toronto, 1997 JAMA 1997; 278:2051- 2052
Dr. Garth Nicolson, President of The Institute for Molecular Medicine, and Joyce Riley of The American Gulf War Veterans Assoc., among others, feel that Gulf War Illness is spreading to the general public and is being divided up into separate disease labels such as those listed above. Many patients with these disease labels are sending their blood to be tested at The Institute for Molecular Medicine and The Bowen Lab, are finding they are infected with mycoplasma and or the Lyme Disease organism. The Bowen Lab specializes in testing for the cyst form of the Lyme organism and for Erlichiosis and Babesiosis (other tick-borne infections). Mycoplasma and the cyst form of the Lyme spirochete are being found in much of the chronic illness population. Mycoplasma Fermentens Incognitus, one of the most common strains being isolated, is patented by the U.S. Army and Army pathologist Dr. Lo. Lo,Shyh-Ching-Pathogenic mycoplasma - U.S. Patent 5,242,820 issued Sept.7 1993
"Now if Saddam Hussein had wanted to kill our soldiers, he would have just outright killed them with mustard or cyanide, right?" reasons Captain Joyce Riley. That wasn't the plan," she continues. "The plan was to give a country a disease that they would bring back to their families. What better way to give a country a disease than to give it to the military, who move all over the country.?"
Unfortunately, the amount of media coverage needed to raise enough awareness to start curbing this illness is no where to be found. "You don't hear about this on the evening news," said Captain Riley. "You are not being told about this. Dan Rather doesn't tell you about it, does he? No. And so you think that if it isn't on the nightly news it must not be true, right? If a tree falls in the forest and Dan Rather doesn't cover it, does it still make a noise? Think about it."
It doesn't take too much thinking to realize why the government and press remains hush-hush about Gulf War Illness. If for no other reasons, the U.S.
Government, namely the Department of Defense, wants to minimize public awareness regarding this issue, to cover the fact that The United States sold to Iraq, before and during the war, many of the biological and chemical agents that were used against our troops.
Gulf War Illness ( mycoplasma ) is known to be treatable with antibiotics. The Army even published a paper to this effect. Ask yourself, why then is the government preventing Gulf War Veterans from being treated? They are even denying that biologicals play a role in GWI. The Army's mycoplasma patent clearly states that " mycoplasma fermentens incognitus will be found in patients who have been diagnosed as having AIDS or ARC, Chronic Fatigue Syndrome, Kibuchi's Disease, autoimmune diseases such as Collagen Vascular Disease and Lupus and chronic debilitating diseases such as Alzheimer's Disease."
In other words the Army knows what segments of the population are infected with this pathogen and they know antibiotics are an effective treatment. I asked a Red Cross pathologist if the government advised the Red Cross to screen the blood supply for this pathogenic organism. He turned bright red and told me that no, they were not told to screen the blood supply for this organism. What is the real reason why the mycoplasma and lyme epidemics are being covered up? Is there a connection between the lyme spirochete and mycoplasma fermentens? The cyst form of lyme looks like a mycoplasma. There is a possibility that genetic engineering is playing a role here. Parts of one organism can now be isolated and inserted into other organisms. This could be one explanation for so many emerging diseases with such similar sets of symptoms. Designer diseases have come into vogue. This tampering with nature makes diagnoses and treatment much more difficult, which many times is the desired goal, especially for biowarfare purposes. I just want to add that it is legal to test biological and chemical agents on the American public without their knowledge or consent ( U.S. CODE, Sec. 50 ).
I would like to list here just some of the symptoms common to Lyme Disease,Chronic Fatigue Syndrome/Fibromyalgia, Multiple Sclerosis, and mycoplasma infection ( Gulf War Illness).
Insomnia, vision changes, headaches, shakes, chills, fevers, numbness, burning, tingling, electric shock feelings, neck pain, muscle and joint pain, jerking and twitching of limbs and muscles, restless leg syndrome, spasms, cramps, fatigue, eye problems, muscle weakness, balance problems, abnormal anxiety and depression, acid reflux, etc. For more extensive lists of symptoms caused by mycoplasma and Lyme disease, please visit.... http://www.immed.org/signsympt.htm , www.lymenet.org and www.wildernetwork.org
It is very important to note that any one person will not have every single symptom. Everyone's symptoms differ in intensity, the number of symptoms you have and what organ systems are affected. This often determines the diagnoses people end up with. It's crucial to be able to recognize the same general symptom complex which is common to these illnesses. This commonality suggests a similar infectious cause....especially when antibiotics are effective.....especially when identical antibiotics are effective....such as in Lyme and GWI. I've mentioned in previous articles that most of these chronic diseases supposedly have no known definitive tests, causes or cures....only symptomatic treatments. How convenient and profitable!
We must not blindly accept the claims of the huge corporate charity organizations. We are constantly being told that we need to donate more and more money to various charities so they can find causes and cures for all these diseases. If anyone knows of significant causes or cures that have been discovered lately, maybe they could share them with me. I can't seem to think of any. In fact, it appears that many times, what may be true causes for M.S. and other diseases, are being intentionally covered up. If we are going to donate money to these large charity organizations, then we need to be involved. We need to demand that specific organisms be looked at in relation to Multiple Sclerosis and other disease labels. If these organizations do not respond then we need to withdraw our support and encourage others to do the same. We should be supporting private researchers of our choice....but in order to do that responsibly, it would be wise to do a little research on our own so that we can determine which researchers have honest and caring motives. Believe me, they are out there!
Charity organizations bring in millions and millions of dollars each year.
Do we know where any of it really goes? Just think about it....keeping people sick can be very lucrative. Some charity organizations have been instrumental in intimidating and or closing down certain private labs which were discovering treatable causes for specific diseases. We must also ask ourselves why so many microbiologists have recently died so mysteriously.
The main message here is that we need to start playing a larger role in our own health care. Investigate and don't believe everything you are told by government health agencies or charity organizations. One of the biggest problems is that many doctors are controlled by corporations and do believe what they are told. How can we expect doctors to treat us effectively when perhaps they have been given the wrong basic information to begin with?
Only a couple of labs currently test for mycoplasma fermentens. Most antibody tests for lyme are very inaccurate. Those labs which are finding these organisms in much of the population, are being harassed, intimidated and shut down...under false pretenses. Does this sound right to you?
Last but not least, we need to stand up for our veterans. Many are sick and dying. They are being intentionally ignored by our government. Why would a government intentionally weaken their military by forcing vaccines that are known to be experimental and contaminated, selling biologicals to a country that is supposedly a potential enemy, and then not treating the sick veterans when the U.S. Army knows very well what they are infected with. I can only come to the conclusion that our country is being weakened from within and that it is intentional.
I'd like to share a quote by Matt Tietjen from the "Spare Change" newspaper in Boston....."Let us refrain from engaging in the sort of blind patriotism that only romanticizes involvement in the military, encouraging today's youth to enlist and become vulnerable to the same circumstances that have devastated the lives of many veterans. The United States of America is a great country in many ways, and this is because of the sacrifices made by it's citizens for more than two centuries. In this light, the non treatment of Gulf War Veterans is a criminal offense on the part of the government. Unless our previous generations died in vain, we live in a democracy. This makes the government accountable to us; it's not the other way around. We should show our patriotism this year by not only respecting our veteran's service but also their right to life, liberty and the pursuit of happiness. When these rights are taken away from those who once fought for us, true patriotism can only be exercised with an American flag waving freely in one hand and a protest sign lodged firmly in the other."
Real patriotism requires that we stand up and demand curative treatment for our sick and dying veterans. Anyone can wave a flag and sing a patriotic song.
Gulf War Illness is not a psychiatric disease caused by stress. Does the government really expect us to believe that stress caused all the birth defects in children born to Veterans? Or that stress caused their doctors to become ill from treating Veterans? What about all the family members who also came down with Gulf War Illness? Now it appears to be running rampant through the general population. It's rather sad that we had to reach this state of affairs before standing up for what's right. It's time to take a good look at what going on and change our priorities. Let's hope it's not too late.
For mycoplasma testing - www.immed.org - Also lots of info, in general, concerning how mycoplasma relates to different diseases.
For accurate Lyme Disease testing, I feel that www.bowen.org is a good place to start.
|08-06-2012, 01:49 PM||#431|
Join Date: Jan 2010
Location: in the abyss of reality.
Dr Trevor Marshall How the Microbiome causes Autoi
At the 2012 International Congress on Autoimmunity, in Granada, Spain, Prof Trevor Marshall delivered this plenary lecture -- explaining how the Human Microbiome causes Human Immune dysfunction, including many autoimmune diseases.
|09-06-2012, 08:14 PM||#432|
Join Date: Jan 2010
Location: in the abyss of reality.
First report of human babesiosis in Australia
A 56-year-old man with serious hepatic, renal and bony injuries was transferred to Canberra Hospital in mid November 2010 following a motor vehicle accident. His medical history included type 1 diabetes mellitus, excessive alcohol and prescription medicine use, depression, hypertension and hypercholesterolaemia. He had no history of injecting drug use. He had been living on the south coast of New South Wales with his son.
During the first 4 months of his admission he required surgery, prolonged broad-spectrum antibiotic therapy and total parenteral nutrition. He developed worsening cholestatic liver function, moderate-to-severe thrombocytopenia and fluctuating anaemia. By late March 2011, he was pancytopenic with worsening anaemia due to intravascular haemolysis, lymphopenia and severe thrombocytopenia, and required ongoing blood product transfusions. The result of an HIV test was negative.
In early April, the patient was transferred to the intensive care unit because of respiratory and haemodynamic deterioration. On 10 April, intraerythrocytic parasites were incidentally identified during routine examination of blood films taken that morning. Ring-form parasites, initially thought to be a Plasmodium species, were confirmed on thick and thin films. Results of immunochromatographic tests were negative for Plasmodium falciparum; however, intravenous artesunate and primaquine therapy for presumed severe malaria was commenced. Broad-spectrum antibiotic therapy was continued. After 48 hours without clinical improvement, the parasitaemia level had increased from 1.7% to 2.6% infected red blood cells. Re-examination of the blood films and recognition that the organisms did not produce hemozoin led to the presumptive diagnosis of babesiosis infection. This was confirmed by Australian and overseas experts who viewed electronic files of the slides. The patient was then given intravenous quinine (600 mg 8-hourly) and clindamycin (600 mg 6-hourly) for babesiosis. Azithromycin and tigecycline were also added to provide additonal broad-spectrum antimicrobial cover, but clinical deterioration continued, and the levels of parasitaemia, anaemia and thrombocytopenia did not improve. He developed multiorgan failure and required haemodialysis. The parasitaemia peaked at 5.1% infected red blood cells despite ongoing blood transfusions (including 18 units of packed red cells over 8 days). As his condition was too unstable for him to undergo total red cell exchange, an exchange of 500 mL of blood was performed on 16 April. He did not recover from the multiorgan failure, and severe thrombocytopenia contributed to acute gastrointestinal bleeding. On 18 April — 5 days after commencing specific antibabesiosis therapy — he suffered a fatal asystolic arrest.
Following the patient’s death, a retrospective study of the blood films taken during his hospital admission was undertaken. Ring-form parasites were detected in very low numbers back to the end of the first week of March 2011, coinciding with the development of severe thrombocytopenia.
Initially, the multiple blood products that the patient received during his admission were thought to be the likely cause of his babesiosis. But blood films stored by his local pathology service and taken between September and November 2010 (ie, before his hospital admission) revealed pre-existence of the intraerythrocytic parasite and hyposplenic features. As the patient had not received blood products before his hospital admission in November 2010, the parasitaemia could not have been transfusion related. He had reported being bitten by ticks, but had been too sick to qualify this further. Due to general ill health, he had not worked or left the local area for many years. His only overseas travel had been to New Zealand almost 40 years earlier, a country with no known human babesiosis. It thus seemed unlikely that the babesiosis was acquired from overseas.
The patient had lived on the south coast of New South Wales for over 30 years — on a small farm with two horses and two Staffordshire bull terriers for 25 years, and then at a house in a small town with his son and a new Staffordshire bull terrier (acquired from within Australia) for 8 years. The new Staffordshire bull terrier was their only pet and was still living at their south coast home in mid 2011. Both his son (who was asymptomatic) and his Staffordshire bull terrier underwent testing for babesiosis; the results were negative.
To identify the organism and further elucidate its source, blood samples and films from the patient were examined at the Centers for Disease Control and Prevention (CDC) in Atlanta, United States, and at the School of Veterinary and Biomedical Sciences, Murdoch University, Western Australia. Both laboratories agreed that the morphological characteristics of the parasites in the blood films were consistent with a small Babesia. Intraerythrocytic organisms were mostly single and measured 1.5–2.5 m in size but were highly polymorphic; pyriform and ovoid forms predominated, bizarre amoeboid forms were also common, and an occasional tetrad (Maltese cross form) was noted (Box 1). Immunofluorescent antibody testing for Babesia microti was performed by the CDC on serum samples from the patient (positive result, with titre of 1 : 256) and his son (negative result).
Complete sequencing of the 18S ribosomal RNA gene (18S rDNA) and partial sequencing of the β-tubulin gene (both amplified by polymerase chain reaction) confirmed that the organism in the patient’s blood was B. microti. At the CDC, a nested PCR that specifically amplifies a 154-base-pair fragment from the B. microti 18S rDNA was initially used to confirm the presence of B. microti in the patient’s blood. In addition, sequencing of a 1767-base-pair fragment amplified with primers Crypto FL (5'-AACCTGGTTGATCCTGCCAGTAGTCAT-3') and Crypto RN (5'-GAATGATCCTTCCGCAGGTTCACCTAC-3'), was performed to strengthen the PCR findings.1 The 18S rDNA sequence obtained was 100% similar to the GenBank entry AY693840 obtained from a B. microti isolate 18S rDNA gene. At Murdoch University, two nested sets of universal piroplasm 18S rDNA primers were used, one of which has been published.2 The patient’s son’s blood was used as a negative control. The consensus sequence was 100% homologous to known human-derived Babesia species isolates. In addition, five novel primer sets designed during this study were used to obtain a partial β-tubulin gene fragment (791 base pairs), which confirmed the presence of B. microti in the patient’s blood and showed 100% homology with North American isolates (eg, GenBank entries AB083377 and AY144722). A phylogenetic tree for this locus (produced using the maximum likelihood method) revealed clustering with isolates of B. microti obtained from the tick species Ixodes scapularis (formerly known as Ixodes dammini), humans and voles in North America.
To our knowledge, this is the first report of a human case of babesiosis in Australia, which we believe was locally acquired.
Human babesiosis is an emerging tick-borne zoonosis. The first human case was reported in Croatia in 1957.3 In 1968, Babesia divergens was identified as the cause of human babesiosis in Europe; this was soon followed by the discovery of human cases of B. microti infection in the US.4 More recently, human cases of babesiosis have emerged from Asia, Africa and South America.5-8
Since B. microti has never been detected in Australia before, its discovery as the cause of infection in this patient, who had no significant history of travel, raises intriguing questions about its natural hosts and epidemiology on this continent. Traditionally, B. microti is considered to have a Holarctic distribution, associated with a variety of small mammalian hosts (rodents, including voles, and shrews), and is transmitted by several Ixodes tick species present throughout the northern hemisphere, with humans becoming infected as accidental hosts. Recent phylogenetic analyses based on complete sequences of the genes encoding 18S ribosomal RNA, β-tubulin and the η subunit of the chaperonin-containing t-complex polypeptide 1 suggest that B. microti represents a genetically diverse species complex that comprises several geographically distinct clusters located in North America, Eurasia and Japan, and is closely related to “Babesia microti-like” species isolated from an ever-expanding range of feral and domesticated mammal hosts.9
In Australia, babesiosis is a well documented disease of cattle (Babesia bigemina and Babesia bovis) and dogs (Babesia canis, Babesia vogeli and Babesia gibsoni), and babesiosis tick vectors have been imported to the continent since European settlement.10,11 Australia also has a diverse variety of native Ixodes ticks, including Ixodes holocyclus (responsible for tick paralysis), and a few Babesia and Theileria species have been described morphologically in native marsupial hosts (but not B. microti).12 Unfortunately, a paucity of molecular studies means that the taxonomy and phylogenetic relationships of the endemic piroplasms (intraerythrocytic tick parasites, including Babesia and Theileria) are not well understood.
Based on phylogenetic analysis, the isolate from this patient was most closely related to North American strains of B. microti, so it is unlikely that the piroplasm described here originated from a native Australian mammal, but not impossible. In the absence of transfusion or injecting drug history, the patient must have become infected following a tick bite. Two scenarios seem probable. The patient might have been bitten by an imported tick (contained within clothing or luggage that had recently arrived from an endemic country), but no history suggested such contact. Alternatively, a local tick might have transmitted an autochthonous infection, presumably originating from one or more species of introduced rodent.
The natural history of this patient’s infection is notable. Babesia ring forms were detectable on routine blood films taken while he was an outpatient — 7 months before he died. At that time, he was asymptomatic and neither anaemic nor thrombocytopenic, but 6 months later the babesiosis became symptomatic and severe. The parasitaemia of 5.1% around the time of his death was likely to have been an underestimate of the true figure as it would have been diluted by the multiple blood products that he was receiving at the time. Asymptomatic parasitaemia is well described in babesiosis, both in the setting of primary infection and following treatment of symptomatic infection.4 It is unclear what transformed this patient’s chronic asymptomatic infection into a severe symptomatic infection that probably contributed to his death. He did have risk factors for severe babesiosis: hyposplenism, liver impairment and his age;4 however, these were present when the infection was asymptomatic months earlier. It is possible that his chronic hospitalisation, and general deconditioning from the long admission, resulted in significant immunosuppression.
Severe babesiosis from B. microti is a serious condition with a case fatality rate of 5%–10%.13 Indeed, this patient’s condition did not improve despite his receiving recommended therapy once the diagnosis of babesiosis was made. Even the artesunate that he received for suspected malaria (immediately before the diagnosis) has been shown to have activity against B. microti in animal models.14
Although the animal host for B. microti is yet to be identified in Australia, the proximity of ticks, other wildlife and human populations along Australia’s eastern seaboard means that further cases may be encountered. Clinicians working in Australia should therefore be aware of the signs and symptoms of babesiosis and how to diagnose it (Box 2). Further investigation into the piroplasms of native mammals, introduced rodents and their ticks is necessary to identify the source of this infection. As transfusion-related babesiosis is well recognised in other countries,15 this case may have future implications for the screening of blood products in Australia.
|09-06-2012, 08:16 PM||#433|
Join Date: Jan 2010
Location: in the abyss of reality.
|10-06-2012, 09:17 PM||#434|
Join Date: Jan 2010
Location: in the abyss of reality.
Beyond Lyme lies the tuth
Controversy rages over very existence of chronic infection
Sunday, May 12, 2002
BY CAROL ANN CAMPBELL
They talk of breathtaking pain. Their hands shake, and, sometimes, their faces go numb. Fatigue can send them to bed. Some sleep 12 hours each day and can no longer concentrate. Others can no longer walk. They have left jobs as lawyers, nurses and managers.
These people say they have chronic Lyme infection.
Some Lyme disease experts say they do not.
Twenty five years after its discovery, Lyme disease, a tick-borne illness that can cause fever, headache, joint pain and neurological problems, remains steeped in controversy even as research hits record levels. Conflicting science has created two camps that fiercely push their views in one of modern medicine's most enduring disputes.
Leading scientists are stepping into the fray. Columbia University in New York is opening a chronic Lyme disease research center. The National Institutes of Health will spend more than $39 million on research this year, nearly double the amount spent just five years ago.
New discoveries further muddle the Lyme landscape. Researchers are finding new tick-borne illnesses, even a new strain of Lyme, that complicate treatment and, perhaps, explain why some people with Lyme disease do not seem to get well.
Patient organizations, meanwhile, are gaining political and financial strength. They are funding their own research and lobbying state and local governments to demand that the illness be taken seriously.
"Attention is finally being paid to this disease," said Pat Smith, president of the Lyme Disease Association, based in Ocean County.
But after thousands of research studies and years of debate, physicians still disagree on whether Lyme disease is easily cured with a short course of antibiotics, or whether long-term infection can cause debilitating disease.
"I honestly don't feel a lot of these people have Lyme disease. I'm not sure a majority have Lyme disease," said David L. Weld, director of the American Lyme Disease Foundation, a Westchester County, N.Y., group whose scientific advisers are skeptical about the existence of chronic Lyme infection.
The stakes are high. On the line are insurance coverage, research grants and professional reputations. Lawsuits are being filed by patients who say their Lyme disease worsened because doctors did not diagnose it and treat them.
"Expect more lawsuits," said Smith.
Just about all physicians agree that Lyme disease, if caught and treated early, usually can be cured with four to six weeks of antibiotics. The disease is transmitted by ticks, and some patients experience the characteristic "bull's-eye" rash after a tick bite. Many never recall being bitten.
Most physicians also agree that a subset of patients go on to develop chronic pain and fatigue and, sometimes, serious neurological problems.
The question is why.
"No one is saying these people are not sick. They experience a level of pain that is comparable to that of a brain tumor or cancer," said Phillip Baker, a microbiologist who oversees Lyme research for the National Institute of Allergy and Infectious Disease.
"The question is whether the problems are due to a persistent infection, or to something else," he said.
Patient advocates and some doctors say they believe that the Lyme bacteria, called a spirochete because of its spiral shape, can burrow deep in the body and survive the standard four to six weeks of antibiotic treatment. Patient advocates say they believe the Lyme bacteria remains alive in some people's bodies, wreaking havoc. Some patients may need aggressive antibiotic treatment for months, even years.
Another camp, many of them academic experts, says something else is going on. These scientists say they believe a round of antibiotics will almost always completely kill the Lyme bacteria. They suspect some post-Lyme syndrome may cause problems in a small percentage of patients, and that some of the people who say they have chronic Lyme disease actually have some other illness. Further antibiotics, they say, are useless.
On the pro-infection side are doctors like Steven Phillips, an internist in Ridgefield, Conn. He published a 1998 study in the journal Infection that showed he was able to detect the Lyme bacteria in patients who had undergone six weeks of antibiotic treatment.
"This has been done over and over again. It's not just me. I don't understand why the controversy still exists," Phillips said.
At Jersey Shore Medical Center in Neptune, Martin D. Fried, director of pediatric gastroenterology and nutrition, has detected the spirochete in the gastrointestinal tracts of children who have undergone lengthy antibiotic treatments.
"I've had kids on months and months of antibiotics and done a scope (a microscopic examination of the intestine) and still found the infection," Fried said. He suspects Lyme if a child with abdominal problems also has joint pains and, perhaps, some sudden psychiatric disturbance such as panic attacks or anxiety. Some complain of blurred vision.
"I've been able to show it (the Lyme organism) is there," Fried said. "But I have not been able to prove what symptoms the organism is responsible for."
His colleagues are skeptical, he acknowledged.
"I go to meetings and they look at me and laugh," he said. "But I ask my patients a lot of questions and try to see the whole picture. I had a kid diagnosed with irritable bowel syndrome. I said, 'Have you ever had a rash?' The mother shows me a perfect bull's-eye rash."
A 1996 article in the journal Infection reported the presence of the bacteria in the urine of Lyme patients with arthritis, including many who had undergone intensive antibiotic treatment. Lyme advocates cite other studies, and say the very existence of some 200 support groups and thousands of angry patients underscores the failure of short-term Lyme treatment.
The other camp says the Lyme bacteria is killed with four to six weeks of antibiotics. Doctors in this camp argue that research showing that the spirochete can survive standard antibiotics are mostly small studies published in minor journals. They point instead to a 2001 National Institutes of Health study of 129 chronic Lyme patients. Half got 90 days of antibiotics; half got a placebo. Yet outcomes were the same for both groups. The study showed a powerful placebo effect.
"There is a problem that needs to be identified. But it's clear from the study that more antibiotics are not the answer," said Leonard Sigal, director of the Lyme Disease Center at the University of Medicine and Dentistry of New Jersey -- Robert Wood Johnson Medical School in New Brunswick. He said in rare patients a post-Lyme syndrome may spark an unusual autoimmune response, or that, perhaps, the original Lyme infection has caused some kind of permanent damage.
"My heart goes out to these people," he said. "But I would like to be very sure that, yes, this is due to Lyme. It's possible these people had Lyme, were cured, and now something else is going on."
The dispute leaves sick patients angry and unsure where to go for treatment they believe can make their lives livable again. Many are angry at doctors such as Sigal. Lyme activists have picketed his appearances at conferences and attacked him on the Internet and in Lyme support groups.
Sigal, who has researched Lyme disease for 21 years, says he has simply not seen good scientific evidence of post-Lyme infection and that he does not know the source of the anger against him.
"Why don't you ask the people using my name in vain?" he responded, angrily. "If I don't think somebody has Lyme, I will tell them. ... This nonsense has been going on for years," he said.
The number of Lyme cases in the United States has reached record levels, according to the latest figures from the U.S. Centers for Disease Control and Prevention in Atlanta. The agency reported 17,730 cases in 2000, an 8 percent increase from the year before. In New Jersey, the numbers jumped dramatically -- from 1,719 in 1999 to 2,459 in 2000. The CDC says Lyme cases are underreported.
Experts predict an especially bad tick season this year because of the mild winter.
The scientific debate rages on as patients crowd the offices of so-called Lyme-friendly doctors. One is Andrea Gaito, whose Basking Ridge office is tucked inside an elegant Colonial house. One recent morning Karen Simnor, a mother of four from Middletown, told Gaito about numbness, headaches, blurry vision and memory loss.
"As soon as I stop the antibiotics, I relapse," she said.
Also here is John Holly, a 55-year-old from Barnegat who said he quit his job as a linesman for an electric utility after he developed arthritis related to Lyme disease. Kevin Danyi of Bethlehem, Pa., said he woke up one morning and one side of his face was numb. The 40-year-old estates and trusts lawyer said his memory began to fail. He now shakes and his gait is unsteady. He has tested positive for Bartonella henselae, another tick-borne disease.
"My memory is shot," Danyi said. His 8-year-old daughter Elisabeth tested positive for Lyme disease and has been out of school since January.
Patients say they have gone from doctor to doctor seeking help. Kathy Whitney, a 43-year-old from Dumont, visited four infectious disease doctors after she began to lose her memory two years ago. She started falling down. She needed painkillers to get out of bed to drive her children to school. She could no longer work in her job as transportation coordinator for a company in Bergen County.
She tested positive for Lyme but no one, she said, would treat her. Brain abnormalities showed up on an MRI and doctors told her she had multiple sclerosis. Eventually she came to Gaito, who ordered a new round of tests. One recent day Gaito reviewed Whitney's charts.
Then she tossed them down on an examining table.
"This is a perfect example of how crazy this all is," she said, exasperated. "Here this woman has a spinal tap that shows Lyme. And a test from Stony Brook University comes back positive. She has all the neurological symptoms of Lyme. And doctors are telling her she doesn't have Lyme."
Gaito said Whitney has no biological markers for multiple sclerosis. She prescribed antibiotic treatment.
"Could you call my other doctor?" Whitney asked. "She doesn't think I have Lyme."
Gaito, who is president of the International Lyme and Associated Diseases Society, said the NIH study did not treat people long enough to make a difference. She is now studying the cervical tissue of women with Lyme disease. She also noticed that three of her patients developed multiple myeloma, a serious cancer, and she is now exploring links between the two diseases.
Further complicating the issue are other tick-borne illnesses, such as babesiosis and ehrlichiosis. These diseases can interfere with the treatment of Lyme disease. The New Jersey Department of Health and Senior Services tested 500 ticks in the state and preliminary results found that 30 percent were infected with at least one of the pathogens, the disease-causing agents. But additional tests failed to confirm the original findings and state officials consider the study flawed. They may attempt a second study with new laboratory equipment.
A Hunterdon County doctor, Eugene Eskow, identified another potential tick-borne pathogen, Bartonella henselae. The pathogen is related to cat-scratch fever. Eskow published his work last year in the Archives of Neurology.
Weld of the American Lyme Disease Foundation said "another fly in the ointment" emerged recently with the discovery of another strain of Lyme.
"There is a possibility that this new spirochete may be either working in cohorts with the Lyme bacteria or on its own, causing a lot of the late term cases," he said.
Patient advocacy groups, like the Lyme Disease Association, have been gaining political and financial strength. They are pushing for better health insurance coverage of long-term intravenous treatment, which can cost thousands of dollars each month.
Insurance companies generally cover the standard four to six weeks of antibiotic therapy after an initial diagnosis of Lyme disease. Obtaining long-term therapy, even if prescribed by a doctor, is far more difficult. Companies for the most part refuse to pay, though some leave the door open for exceptions.
"There are varying medical opinions of what long-term treatment means," said Annette Catino, CEO of QualCare Inc. of Piscataway. "We will get second and third opinions. These cases go on forever and there is no valid medical research that substantiates that long-term treatment. So it's not universally covered."
A policy statement by Horizon Blue Cross Blue Shield of New Jersey says the company covers 28 days of intravenous antibiotics with the "possibility" of extended treatment if symptoms exist along with objective evidence of Lyme infection.
AmeriHealth New Jersey, a subsidiary of Independence Blue Cross and Blue Shield of Pennsylvania, does not approve long-term intravenous antibiotic treatment for Lyme disease. "Our policy is based on the best medical evidence of the existing medical literature," said spokesman Butch Ward.
Brendan Peppard, director of research for the New Jersey Association of Health Plans, said companies have been influenced by the large NIH study.
"Long-term treatment is not effective at reducing or eliminating symptoms," he said. He said long-term antibiotic treatment has its own potential complications, such as serious infection.
The Lyme Disease Association also has handed out $1 million in research grants in the past decade. The group recently gave $80,000 to Steven Schutzer, a researcher at UMDNJ who is looking into the genetic makeup of Lyme disease.
Smith addresses state legislatures and state advisory boards from Rhode Island to New Jersey to California. She said government money goes mostly to basic research.
"We want research into chronic Lyme disease," said Smith, who has two daughters who have been treated for the illness.
Her organization, along with the Greenwich Lyme Disease Task Force, donated $675,000 in March to create a chronic Lyme disease research center at Columbia University. The Lyme Disease Association and its five affiliates are now trying to raise an additional $2.4 million for the center.
The Columbia center is directed by Brian Fallon, a psychiatrist who has a $4.7 million grant by the National Institutes of Health to study how Lyme disease affects the brain. Fallon became interested in Lyme disease when previously healthy patients began seeing him for anxiety, depression and memory loss. Some could no longer remember simple words. One of his published studies describes a telephone operator who could no longer transfer calls.
"I began thinking they were physically ill and began learning about Lyme disease," he said. He said brain scans show decreased blood flow to parts of their brains. Diagnosis of the disease is complex. Symptoms mimic those of other diseases. Tests are not definitive.
"The truth is that Lyme is a common illness that if caught early can be easily treated," Fallon said. "But when caught later it can result in a disorder that's harder to treat and can result in anything from mild to severe psychiatric, neurological and rheumatological problems."
Baker of the NIH said new technology may provide answers someday. He does not believe, he said, that evidence points to persistent infection, but the explanation cannot be excluded entirely. He said scientists are working on super-sensitive tests and genetic analyses. Baker wonders if a tiny amount of undetectable Lyme bacteria may produce a dangerous toxin.
He doubts the hypothesis.
"But one never knows," he said. "In this disease a lot of people think their views are correct and everyone else is wrong. I'm trying to keep an open mind."
Next Article: A new strategy in the war on Lyme disease.
Copyright 2002 New Jersey Online. All Rights Reserved.
|12-06-2012, 04:12 PM||#435|
Join Date: Jan 2010
Location: in the abyss of reality.
Why I let my husband die
On a hot sticky day in July 2003, Jill Anderson was driving home across the North Yorkshire moors with some groceries when something told her to put her foot down. Hurrying back, she dumped her shopping bags in the kitchen and ran upstairs, where her husband Paul was sitting on the bed. "What's wrong? Has anything happened?" she said.
"I'm sorry," said Paul. "I've taken enough this time."
He slumped on to the bed, falling into a deep sleep. By next morning, he was dead.
Nine years later, Jill is sitting in a cafe in sunny
Bristol reliving that day, her marriage to "the love of her life", her arrest on charges of manslaughter – and what it was like being in a relationship with the threat of suicide constantly hanging over it.
Jill met Paul in September 1992. She was 37, and had been single for much of her late 20s and early 30s. "I'd been on countless dates, but they were never people I wanted to spend much time with, or felt comfortable with," she says. Paul was different. "I felt secure with him, felt I could say or do anything and he would accept me.
"I knew very quickly he was the one I'd been waiting for. I didn't think I'd ever meet anyone, and suddenly there he was, and it was lovely. He made life magical."
[Related article: 'How my husband's suicide inspired me']
They married two and a half years later. But three days before the wedding, Paul picked up a flu-like virus. Weeks passed, then months, and he didn't get any better. He started to feel weak, and spent periods in bed. Doctors did tests, but told him there was nothing wrong, and sent him home with
some aspirin. Undeterred, the couple spent hours researching Paul's symptoms online, and soon self-diagnosed chronic fatigue syndrome, or myalgic encephalitis, usually known as ME.
CFS is persistent exhaustion that doesn't go away with sleep or rest. There is no cure, but treatment can ease the symptoms, the most common of which is muscle pain. Paul was unlucky: he was one of around 25% of sufferers with severe symptoms that were compounded by health problems since he was very young, including arthritis. CFS's physical symptoms can lead to emotional and psychological problems, too, born out of frustration, and from the fact that often the medical profession doesn't take the condition seriously.
"From our wedding day on, Paul's health was up and down, but always on a downward curve," says Jill.
Shortly after they married, they moved from London to Yorkshire, for some quiet. Paul was a linguist and they had started a translation agency, which was thriving. It meant they could work from home so didn't need to live in the city. On the day they moved in, Paul "was full of beans, putting up shelves, building a dining table and bench. We were so happy, we thought he was finally on the mend. But it was the adrenalin of moving because after that he crashed."
It wasn't until three years later that a consultant finally accepted there was something wrong with Paul. He was given pain relief drugs and encouraged to seek psychological help, which he didn't do. "He was open-minded about [therapy] and would have had some if he thought it would get results," says Jill. "But he had some homeopathic treatment and fishing was a form of therapy for him."
Jill watched as her husband gradually lost his health. In the early days, he was still well enough to take a gentle stroll in the countryside. "We would do five miles, then it was four, three, two, one, until he could only walk 100 yards before he was too tired to go on," she says. His pain increased, and by the time he died, he was virtually bedridden. The business, reliant on Paul's translating, didn't survive and they were declared bankrupt.
She became his carer. "Looking after Paul, as well as trying to keep the business ticking over before it went under, was a full-time job," she says. "It got to the point when I didn't have time to even cut my own toenails."
Did it occur to her to ask for some help? "I should have done, but I wanted to do it on my own. We both thought we were coping. I was in contact with support groups, but we never had anyone come in to relieve me. Paul would get terribly upset if I even called a helpline, as he didn't want to be a burden to me. He was constantly looking for ways to make my life easier, like setting up online shopping."
A year before he died, Paul gave up his beloved fishing. He had started to get less movement in his upper back, and the pain was becoming vicious. It was around this time that he made his first suicide attempt. He left Jill a note:
"To my darling Jill, I love you more than I could ever say. I'm so sorry. I just can't stand the pain any more. Thank you for everything you have done for me. Please try to have the best life you can. I love you for ever. Your loving Paul."
Jill got him quickly to Harrogate district hospital, where they saved his life. "I understood why he wanted to die, as he was in so much pain," she says, quietly. "But it terrified me. I loved being with him and didn't want him to go."
Paul made a second suicide attempt shortly after that, this time taking a combination of pills. Again, she called an ambulance and he was rushed to hospital. From that point on, he was contemplating suicide on a regular basis – on the third occasion, a few months before he died, attaching a hosepipe to the car exhaust.
"I watched him go into the garage," says Jill. "I waited five minutes then followed him in there. I pulled the hosepipe out of the car window, and he shouted 'I want to die!' I said, you can't – and gave him a list of all the reasons to stay alive."
During those months, as suicide became part of the language of their relationship, how did she cope? "I don't know. I just saved him and then we'd carry on as if nothing had happened."
Did they ever talk about it? "Just to the extent that I would tell him how much I didn't want him to die. I became dedicated to saving his life – clean sheets, neck pillows, his favourite foods, anything I could think of to alleviate his suffering in the hope that he would make some sort of recovery, and wouldn't want to [kill himself]."
It was in the final six months of Paul's life that the couple realised his illness was serious. "Before then, neither of us wanted to admit he was terminal, that he was never going to get better. I lived on hope and couldn't accept he wouldn't recover. I kept thinking, what if he'd not gone out that day [when he caught the virus] and got soaked, or what if we'd moved to Devon and given him some sea air? But Paul would always say that nothing would have made any difference."
The day Paul died, he and Jill had started, finally, to fill out a detailed, 60-page form that would allow them to claim disability allowance. It was something Paul had been putting off for months. Jill now believes it was the trigger for his suicide – and it was this realisation that made her rush home that hot July day. "The form meant Paul had finally accepted that he was never going to get better," she says. "He failed on every question. It sounds stupid, but I think we were both stunned [by the realisation]."
When Jill found him, after returning home from her shopping trip, she hoped – despite what he told
her – that he had not taken enough pills to kill himself. But this time, she didn't call for an ambulance. "I felt defeated. I had to accept that he didn't want to go on. I didn't want to see him pumped full of drugs again, forced to stay alive when he didn't want to be."
Instead, she left him sleeping, and lay down beside him. At 9:30am the following morning, Paul took his last breath. She called her doctor at 11am. "I wanted a few more hours with him," she writes in her memoir. "It was selfish but these moments were all I had left of him. I felt a strange euphoria; there was no physical pain in this place any more."
Later that day, the police arrived to take a statement – standard procedure. And Jill's story could have ended there, with the sad but peaceful death of her husband, an end to his suffering, and the beginning of a slow grieving process. But on 30 July 2003, nearly two weeks after Paul's death, Jill was arrested for assisted suicide and manslaughter.
She was questioned for three days – about Paul's illness, their marriage, his suicide attempts, and her actions on the day he died. She told them she didn't know why she hadn't called for an ambulance when she found him, but regretted not doing so. In September 2004, she was charged with manslaughter. The charge of assisted suicide was dropped because the police couldn't find any evidence that Jill had assisted Paul in taking his own life. She gave up her passport and had to report weekly to the police station. "It was awful. They turned my life upside down. My solicitor kept telling me, they are clutching at straws, they'll drop the charges."
They didn't. The case came to trial – by jury – on 20 April 2005. Much was made of Paul's history of hypochondria, and the fact that he had rejected psychiatric treatment.
Jill was found not guilty. Today, she believes hers was a test case, the result having serious implications for the emotive assisted suicide and right-to-die debates. Does she ever wish she'd never confessed to finding him before he died, and thereby implicating herself? After all, his previous attempts to take his own life were surely proof enough of his intentions. "No. And they would have found out anyway."
The day Jill was arrested, she told the police: "I have to live with this for the rest of my life." I ask her why, when she was so convinced that her actions were right, she said that as it suggests she blames herself for what happened.
"I was Paul's carer, and the duty of any carer is to look after someone and make sure nothing happens to them," she says. "So in that way, I failed. Because of all the media attention, and the trial, I've been made to feel guilty. But deep inside, I know I did the right thing for him. I knew he didn't want to live with such pain, feel suicidal – or try to take his own life and end up in a coma, a vegetable – permanently paralysed."
As the trial ended, Jill's grief began. "I started grieving as soon as he died, but it's been such a strange, traumatic process that sometimes I think it was only [after the trial] that I really started to come to terms with it all," she says. "And grief is not a one-off thing, it comes in waves, like acts in a play. There are certain points in your life – the trial, moving house, writing this book – that propel you forward."
Today, Jill lives in Devon, where she had planned to live with Paul. Despite her occasional sweet smile, she carries a heavy sadness about her. "Life is reasonable," she says. "But it's awful being without him. I hate being on my own. He's completely irreplaceable."
Has writing the book been cathartic? "No, it's been like rubbing salt in the wounds." She smiles. "But ultimately, I hope it will be."
Jill Anderson's memoir, Unbroken Trust: The Forbidden Goodbye of a Husband's Suicide, is published by Simon & Schuster), £12.99. To order a copy for £10.39, including free UK p&P, go to guardian.co.uk/bookshop or call 0330 333 6846
guardian.co.uk © Guardian News and Media 2012
|14-06-2012, 08:04 PM||#436|
Join Date: Jan 2010
Location: in the abyss of reality.
Some maladies are thought to be "autoimmune," that is, one's immune system supposedly goes wacky and starts attacking its own body. I think this can happen, but only in rare instances, and perhaps only in transplant cases (which is where it is really attacking a foreign body.)
The way "autoimmune" disorders are typically diagnosed is a blood panel is drawn and immune system disorder is seen based on excessive counts of one or more immune factors, which is typical of many infections. Then, smears and cultures, antigen and antibody tests, biopsies, and other diagnostics are run, but nothing is seen. Disregarding the fact that only a tiny fraction of bacteria, parasites, toxins, fungi, or other pathogens are tested for that could be causing an inflammatory condition such as this, it is assumed that the immune system is attacking the body. The immune system is pretty sophisticated and sensitive. A lot more sophisticated than the current diagnostic capabilities of conventional medicine. It compares DNA or protein coatings of pathogens against its own. If it does not get a match, it puts out a call to arms.
A first line response of the body to infection (especially bacterial and parasitic) is inflammation. Inflammation "calls" immune cells to the scene to combat the invader. I think it is the height of folly to believe that testing for a tiny fraction of possible pathogens and not finding anything is a better barometer of infection than a body's typical response to infection.
In recent years, conventional medicine has found or suspected that there are many disorders actually caused by pathogens, and sometimes common ones, that were not suspected before. Some cases of cirulation dysfunction, heart disease, Parkinson's, lupus, MS, and other illnesses are now suspected to be caused by chlamydia, rather common bacteria that appears to get out of control in some people. Inflammatory bowel diseases like IBS are now known to some researchers to be often caused by giardia. Same with Lyme disease and spirochete bacteria. Mycoplasmas are now being investigated as being the cause of other chronic disorders, but there are no conventional medical tests which detect them. (Update: there was recently advertised a clinic in California which tests blood samples for 4 types of mycoplasma using a pioneer method.)
Parasites like worms can cause a myriad of problems throughout the body, especially if they "escape" the intestinal tract. The typical test for parasites in the US is a fecal swab. If it comes up negative, the patient is declared to be free of parasites, although this test probably is less than 1% accurate in detecting active parasitic infection in the body. See the article called "Conventional Diagnosis of Parasites" on this web site for more information.
Look how long it took for the establishment to acknowledge that heliobacter pylori is the usual cause of gastric ulcers, even though the fact was proven over thirty years ago. Even in 2000, some MDs are still prescribing acid blockers. Conventional researchers have found chlamydia trachomatis, yersinia enterocolitica, shigella, y. pseudotuberculosis, and ureaplasma urealyticum as the cause of some inflammatory disease. As far as I know, these bacteria are not typically tested for when attempting to diagnose an "autoimmune" disease. Even then, one of the most sophisticated conventional diagnostics for bacteria, the ALISA antibody test, is only about 30% accurate. It even says right on the results that it shouldn't be used as a diagnostic test.
Lupus, MS, rheumatoid arthritis, scleroderma, and many other inflammatory disorders are now being treated by a handful of forward-thinking doctors with low dose long term antibiotics. See http://rheumatic.org/ They claim great success in most cases, although progress can be slow (probably because they are using low dose instead of high doses of antibiotics). This treatment is based on the work of Thomas McPherson Brown, MD. Don't hold one's breath for effective therapy for these disorders to be prescribed by conventional doctors anytime soon, though.
The normal prescription for inflammatory disorders are strong antiinflammatories like steroids. These can certainly decrease symptoms but since they are covering up the problem and doing nothing to treat it, make it worse in the long run. A more ridiculous prescription for treating a pathogen-induced illness is a drug which decreases immune function. Since there are less immune cells to "call to arms" there is less inflammation. I can think of no better way to allow a pathogen to overrun and destroy tissue more quickly.
Many who are familiar with complementary health measures for "autoimmune" disorders will note that good treatments for many of them are herbs that should, according to conventional medicine, make the disorder worse. Echinacea, cat's claw (uncaria tometosa), goldenseal, pau d'arco, to name a few, are some of the better herbal immune stimulators. Yet they are often found valuable in rheumatoid arthritis, lupus, IBS, circulation dysfunction, heart disease, Parkinson's, scleroderma, and many other disorders, when taken in sufficient dosage. Since they are generally antiinflammatory and antibacterial, they are often appropriate treatments since they provide some palliation while addressing the cause.
Another consideration in inflammatory disorders is organ function. There must be sufficient cleansing capacity to be able to fight inflammatory disorders since "trash" like metabolic byproducts in the tissues inhibits immune function and may provide more food for bacteria, fungi, or parasites. It is therefore necessary to ensure the lymphs, kidneys, liver, and colon are working well. Whether an herbal or conventional antibiotic regimen will be used, cleaning the organs is a valuable exercise.
Parasites can sometimes cause inflammation directly and can greatly increase histamine response to bacteria or other pathogens, and allergens or other toxins. As one conventional medicine study determined when the correlation between schistosoma mansoni (blood flukes) and lupus and rheumatoid arthritis was studied: "Antibodies against nuclear material in s. mansoni are probably a consequence of heavy disturbance of the immune system in this chronic infection with great permanent antigen load. It is a matter of discussion, whether production of these antibodies is induced by nuclear material from the host or from the parasite." This parasite is easy to detect since it produces a well known antigen in the blood. Yet, how often is the test run when trying to find the cause of rheumatoid arthritis or SLE?
The "Conventional Diagnosis of Parasites" article describes the expensive and time-consuming methods that must be used to rule out parasite involvement. I think it easier, and certainly cheaper and less time consuming, to merely treat for parasites, since most of the herbs used are also beneficial against bacteria and fungi and without side effects. The liver, kidneys, and lymphs should be clean before attempting to deparasitize since it may strain these organs.
Toxins absorbed or ingested into the body can also wreak havoc on the immune system. Some of the toxins produced by pathogens can be tested for, but are probably not tested in over 99.9% of cases when they could be suspect. Toxic metals, solvents, and other poisons are tested for even less, although it is known that excessive amounts of toxic metals like mercury in the tissues can cause immune system dysfunction. So can aspartame, which causes symptoms indistinguishable from MS in some cases and can cause blood sugar problems when used long term (probably when there are insufficient vitamins (like B6) and minerals which help to detoxify the wood alcohol (major pancreas toxin) and phenylalinine (brain and nervous system toxin when used to excess)). It can take up to 18 months of completely avoiding toxins like aspartame and mercury before they are reduced to neglible levels in body tissues.
White cells will usually "attack" a toxin which is in the tissue, trying to remove it, assuming the immune system is not completely exhausted from fighting pathogens and toxins, which can happen in some cases. Not suspecting or attempting to diagnose a toxin, one might think the immune system was attacking the body's tissues, when it is really doing what it should - attempting to remove the offending substance. Avoiding ingestion and absorption of toxins is the best regimen. Any Hulda Clark book, or the Toxin Avoidance section, gives details.
Any problems in the dental area must be addressed for success in fighting infections coming from the mouth. Toxic dental materials can be a direct problem, as can dental bacteria and their toxins which can infect root canals and other areas of the mouth. Bob's Dental Awareness website discusses these problems. An excerpt from the site:
"The new and latest scientific research implicating toxic compounds emitted by mercury amalgam fillings and root canal teeth anaerobic bacteria show definite links to systemic diseases such as CFS, fibromyalgia, ALS, MS, lupus, multichemical senstivity, Parkinson's, endocarditis, and more. Research by notable scientists at leading Universities has unveiled a lack of knowledge within organized dentistry about the hazards of todays dental procedures and a complete lack of concern over the patient's well being. Research and clinical trials have indicated that the toxins excreted by anaerobic bacteria may be the cause of the onset of as much as 85% of the systemic diseases in this country alone. It is a proven and accepted fact that these dental induced toxins inhibit or destroy key enzymes needed for cell reproduction and energy conversion. These toxins also destroy key cellular proteins in the cerebral spinal fluid which allows these and other toxins to destroy nerves and mutate other cellular tissues. This website is designed to get you in touch with the facts with hyperlinks to the National Medical Library, websites of noted research scientists and my personal research into these dental induced problems."
Other problems with chronic disease can be caused by slow elimination. Many disorders are greatly exacerbated if there is not sufficient elimination. If the colon is not kept clean, toxins are reabsorbed before they are eliminated. Slow elimination also provides an ideal breeding ground for pathogens, adding more toxins and the increased risk of them crossing the intestinal barrier.
To combat autoimmune disorders, I would use cleansing and antiseptic regimens.
|14-06-2012, 08:05 PM||#437|
Join Date: Jan 2010
Location: in the abyss of reality.
Parasitic worms and inflammatory diseases
The debate on whether infection precipitates or prevents autoimmunity remains a contentious one. Recently the suggestion that some unknown microbe can be at the origin of some chronic inflammatory diseases has been countered by accumulating evidence that decreasing infection rates might have an important role to play in the rising prevalence of autoimmune disorders. The ‘Hygiene Hypothesis’ was initially postulated to explain the inverse correlation between the incidence of infections and the rise of allergic diseases, particularly in the developed world. Latterly, the Hygiene Hypothesis has been extended to also incorporate autoimmune diseases in general. Amongst the various infectious agents, a particular emphasis has been put on the interaction between parasitic worms and humans. Worm parasites have co-evolved with the mammalian immune system for many millions of years and during this time, they have developed extremely effective strategies to modulate and evade host defences and so maintain their evolutionary fitness. It is therefore reasonable to conclude that the human immune system has been shaped by its relationship with parasitic worms and this may be a necessary requirement for maintaining our immunological health. Fully understanding this relationship may lead to novel and effective treatments for a host of deleterious inflammatory reactions.
The last three decades have witnessed a dramatic increase in the incidence of autoimmune inflammatory diseases in developed countries, including type 1 diabetes (T1D), multiple sclerosis (MS), rheumatoid arthritis (RA), and Crohn's disease, to name but a few (1,2). Autoimmune disease is characterized by an immune-mediated attack on a target organ that it is no longer recognized by the immune system as self. Autoimmune pathology can be caused by both antibody and cell-mediated components. Predisposition to autoimmunity is under polygenic control, but studies on identical (monozygotic) twins demonstrate that environmental factors might be equally important (3,4). The rising trend in autoimmune diseases looks set to continue and the projected incidences over the next 30 years are potentially catastrophic. The countries that have seen the most pronounced rise in autoimmunity have over the same period seen tremendous improvements in sanitation and socioeconomic status. Moreover, the steady migration from rural to urban areas has dramatically reduced childhood exposure to infectious organisms. Rapid anthropogenic transformation of the environment and life style has not allowed time for the human immune system to adjust to these changes. The very characteristics of the immune system that had previously been so advantageous for combating infections might now be the principal contributing factor for the increasing prevalence of autoimmune disease. Improvements in living conditions and the reduced exposure to childhood infections in particular, have been suggested to contribute to the increase in atopy and autoimmunity (5). This so-called Hygiene Hypothesis has, in recent years, attracted interest and controversy in equal measure. Epidemiological data from the World Health Organization (WHO) largely support the hypothesis, indicating that autoimmune inflammatory diseases like T1D and MS are extremely rare in most African and Asian populations, yet increase conspicuously when these same populations migrate to a modern setting (6,7). In this piece we will review the evidence for the Hygiene Hypothesis particularly with regard to parasitic worm (helminth) infections and consider any potential therapeutic avenues that it may prescribe.
INFECTIOUS DISEASE, AUTOIMMUNITY, AND THE HYGIENE HYPOTHESIS
The Hygiene Hypothesis suggests that parasites and microbes have been important for shaping and tuning the evolution of the human immune system (8). According to this hypothesis, the immune system is in a state of preparedness, primed to repel the pathogen assaults that characterized the lot of humanity for most of its existence. In developed countries industrialization has strongly contributed to human migration from rural areas to the cities. One of the consequences of resettlement has been the removal of people from the pathogen-replete ecosystems in which their immune systems had adapted since prehistory. Sanitation, and access to clean food and water became a common life standard for most individuals in the developed world. Additionally, following the Second World War the use of antibiotics became commonplace, dramatically altering exposure to bacterial pathogens. The fact that infections were no longer prevalent has led to the emergence of autoimmune inflammatory diseases. This suggests that parasites, if not actually preventing autoimmunity per se, at least divert the immune system to the more productive cause of limiting tissue pathology. Parasites themselves wield an astonishing array of mechanisms to evade the ravages of the host's immune system and in so doing ameliorate the more self-destructive aspects of a response.
Industrialized countries are indeed experiencing an increase in autoimmune diseases. A very different picture is present in developing countries. Because of limited economic resources, health aid organizations tend to focus more on the three so-called ‘Big Killer Diseases’; HIV, malaria and tuberculosis. As a consequence, six neglected infectious diseases with low mortality rates such as filariasis, leprosy, onchocerciasis, schistosomiasis, soil-transmitted helminths, and trachoma, are still widespread yet autoimmune inflammatory diseases are virtually absent (WHO and International Diabetes Federation databases) (see Figure 1). Loss of parasite colonization in those individuals living in developed countries has had a unique impact on our immune response and, together with genetic predisposition, is probably the pre-eminent factor contributing to the development of autoimmune disease (9–12).
T1D occurs equally among males and females and is more common in whites than in non-whites. Data from the IDF (International Diabetes Federation) database indicate that T1D is rare in most African and Asian populations. Conversely, some northern European (Finland and Sweden) and northern American countries, have high rates of T1D. Over a million people worldwide have MS and this incidence also appears to be increasing. Onset of symptoms typically occurs between the ages of 15 and 40 years, with a peak incidence in people in their 20s and 30s, and women are affected twice as often as men. MS occurs worldwide but is most common in Caucasian people of northern European origin. It is extremely rare among Asians and Africans (13). Crohn's disease also occurs most frequently among North Europeans and North Americans. Although the disorder can begin at any age, its onset principally occurs between 15 and 30 years of age. There appears to be a familial aggregation of patients with Crohn's disease such that 20–30% of patients with Crohn's disease have a family history of inflammatory bowel disease.
T1D AS AN EXAMPLE OF AN INFLAMMATORY AUTOIMMUNE DISEASE
T1D is an autoimmune condition characterized by a progressive cellular infiltration of the pancreas resulting in the destruction of insulin-producing cells. Since insulin regulates glucose uptake into cells from the circulation, its deficiency is responsible for glucose accumulation in the blood and ensuing cell starvation (hyperglycaemia, coma, etc.). T1D was considered a death sentence until the early 1920s, when pancreatic extracts were used to correct hyperglycaemia (14). This discovery led to the availability of an effective treatment – insulin injections – and the first clinical patient was treated in 1922. Despite the substantial technological improvement for monitoring glycaemia, relatively little progress has been made in terms of therapy; to date, insulin injection remains the only dependable treatment.
T1D is an autoimmune polygenic disorder, with numerous gene loci contributing to susceptibility. Historically, the first genes associated with T1D were the Human Leukocyte Antigens (HLA) on chromosome 6, in particular the DR and DQ class II regions (15,16). There remains controversy about the relative contributions of DR and DQ on T1D susceptibility with some studies supporting a stronger association for the DQ locus and a secondary role for DR (17). Recently, other genes outside the HLA complex have been associated with predisposition to T1D, including cytotoxic T lymphocyte associated antigen 4 (CTLA-4) and lymphoid tyrosine phosphatase (PTPN22) (18).
As mentioned above, genetic components affect the propensity for T1D but the environment appears to play a fundamental role in regulating the onset of the disease. Many different intercepting factors must be taken into account. Within the Caucasian population the incidence of T1D varies between nations. For example Scandinavian countries have the highest incidence of T1D in Europe, whereas relatively under-developed countries like Albania and Romania have some of the lowest (see Table 1). However, these statistics need to be considered in the context of genetics, i.e. the relatively limited genetic diversity seen in Scandinavia (particularly Finland) overlaying and possibly synergizing with the effects of a hygienic environment. Interestingly in Europe, countries with a more agriculture-based economy have lower incidences of T1D (19). This suggests that exposure of the population to a diet containing fewer processed foods and more direct contact with animal-transmitted pathogens such as Salmonella could be a relevant factor in preventing T1D. The North–South gradient also seems to play a role in diabetes incidence. Indeed in Southern European countries the lower socio-economic status and higher temperatures might predispose the inhabitants to infections and contribute to the lower frequency of T1D. Two of the largest islands in the Mediterranean, Sicily and Sardinia, present an interesting contrast in T1D incidence and the effects of genetics. These islands are located at similar latitudes and bio-geographical zones, yet Sicily has a low incidence of T1D whereas Sardinia has one of the highest in the world, indicative of a strong genetic modifier (20). If we look now at countries outside Europe (and/or North America) we can see that the inverse correlation between poverty and T1D is even more pronounced. Poor sanitation and prevalence of infections seem to protect the inhabitants of developing countries from autoimmune diabetes (see Table 1). A good example is the interdependence between access to clean water, and diseases such as T1D (Figure 1). Indeed many parasitic diseases such as Schistosomiasis require a freshwater environment for transmission. Overall these considerations strongly suggest that the continuous improvement in sanitation and living standards in developed countries is a key factor for the increase of T1D.
According to the IDF database the global incidence of T1D in children and adolescents is increasing, with an estimated overall annual rate of about 3%. Before the 1920s childhood diabetes, although uncommon, was rapid and fatal, therefore it could be argued that the introduction of insulin treatment contributed to a subtle increase in the frequency of T1D susceptibility genes. That said, the dramatic rise of T1D in children under 14 years of age in developed countries cannot be explained by genetic factors alone. The T1D epidemic observed over the last 50 years in Western Europe and North America is predicted to plateau. For example, Norway showed no increase over the last decade (21). The high T1D-incidence areas (with the exception of Finland) in Europe appear to have reached a plateau, but the overall trend is still rising in ex-Eastern Bloc countries and in the Middle East, particularly in Kuwait (22–24). Since changes in the environment seem to play a more significant role, predications are that childhood diabetes will not increase exponentially in the high incidence areas but will rather take place in those countries that are gradually seeing an improvement in their living standards and hygiene. For instance, the projections for diabetes incidence in the year 2025 predict a sharp increment in diabetes in the Middle East, South America, Mexico, and South Ea
ANIMAL MODELS OF HUMAN AUTOIMMUNE DISEASE: THE NOD MOUSE AND SCHISTOSOMA MANSONI INFECTION
Since the 1970s the NOD (Non-Obese Diabetic) mouse has provided a good model for the study of T1D. Initially generated in Japan by Makino and co-workers, the NOD mouse has became one of the most popular models to study T1D (25). NOD mice spontaneously develop T1D, with features similar to the human disease. NOD T1D is under polygenic control and, much like the human disease, associates with particular Class II major histocompatibility (MHC) polymorphisms (26). The pancreas of NOD mice become infiltrated with mononuclear cells around 6 weeks of age, with cells appearing chiefly around the islets and pancreatic ducts. By 8–12 weeks of age the infiltrate progresses to the islets, causing destruction of the β cell mass. Pathology is primarily cell-mediated, with dendritic cells (DC), macrophages (MΦ) and B cells responsible for the initiation of the autoimmune process by presentation of pancreatic antigen and secretion of inflammatory mediators (27,28). Subsequently, CD8+ and CD4+ T cells enter the pancreas, infiltrate the islet area and β cell destruction arises through a Th1-mediated immune response (29) (Figure 2). After 12 weeks of age the clinical signs of disease start to manifest with polydypsia and glycosuria and by the age of 30 weeks 80–100% of female mice are diabetic. NOD mice show a distinct gender difference with female NOD mice developing T1D at a much higher incidence than the males (10–20%). There are variations between colonies and the conditions under which NOD mice are kept appear to greatly influence the rate and frequency of onset of diabetes. It rapidly became clear that NOD mice kept under germ-free conditions developed diabetes at a much faster rate and higher incidence than mice kept under conventional conditions (30). This observation, made independently in many different laboratories, provoked immunologists to consider the possibility that infection and/or exposure to microbial products was responsible for the reduction of T1D incidence in some animal colonies. Experiments designed to test this hypothesis and elucidate the mechanisms of T1D prevention, revealed that infections triggering both Th1- and Th2-like responses could delay or abolish autoimmune pathology in NOD mice (see Table 3).
st Asia (see Table 2).
The NOD mouse appears to be a good model for testing the predictions of the Hygiene Hypothesis, therefore we have used it to study the effects of bacterial and helminth infection on the onset of T1D. Schistosoma mansoni infection, or even exposure to antigens derived from this helminth, results in long-lasting prevention of diabetes characterized by a strong Th2 response (31,32). S. mansoni protection appears to stem largely from a shift to a non-pathological Th2 response, although there is also evidence for the generation of immunosuppressive regulatory cells (Treg) (32). Essentially similar results have been observed using two other species of helminth, Heligmosomoides polygyrus and Trichinella spiralis (C. Lawrence, unpublished data). Similarly, infection of NOD mice with live attenuated Salmonella bacteria induces a long-lasting protection from T1D (35). Prevention of a Th1-mediated autoimmune disease such as T1D by infection with a classic Th1-stimulating pathogen appears rather paradoxical. Potentially a generalized Salmonella-induced IFN-γ release may mediate suppression through its effects on the innate immune system, particularly DC, but the mechanism awaits full characterization (our unpublished observations). At any rate, the invocation of a simple Th1 to Th2 shift is unable to explain all the immunomodulatory effects of microbial infection that lead to prevention of T1D, and may instead require a more complex paradigm incorporating, for example, the action of Treg.
HELMINTH MODULATION OF THE IMMUNE SYSTEM
Amongst the various infectious agents, helminth parasites are regarded as master manipulators of the host immune system, often inducing a long-lasting asymptomatic form of infection (37,38). Parasitic worms can establish and reproduce in mammalian hosts, switching off the inflammatory immune response and inducing a tolerant response to parasite antigens. Following encounter with S. mansoni antigens, profound changes are observed in the innate immune system of the host, including modification of DC, MΦ, and NKT cells, phenotype and cytokine secretion (39,40). S. mansoni antigens can induce the secretion of regulatory cytokines from these cells as well as B1 B cells (41), resulting in the expansion of Th2 and Treg populations that might be responsible for maintaining self-tolerance (42–45) (see Figure 3). DC and MΦ are fundamental to directing immune responses along either a tolerating or activating pathway, therefore it is not surprising that helminths have evolved strategies targeting receptors on these cells. Toll like receptors (TLRs) and C-type lectin receptors (CLRs), broadly expressed on DCs and MΦs, are the main parasite targets for evading immuno-surveillance (46). More specifically, glycosylated molecules (expressed and secreted by S. mansoni) bind to the CLR and antagonize a TLR pro-inflammatory pathway (47). Numerous studies have shown that S. mansoni products induce IL-10 production by DCs and have a direct anti-inflammatory effect on DCs by controlling TLR ligand-induced DC maturation (48). S. mansoni has also been shown to induce alternatively activated MΦ, which secrete small amounts of inflammatory mediators and inhibit T cell proliferation (49).
The influence of helminth products on the innate immune system is not just restricted to DCs. Depending on the nature of the pathogen, NKT cells can direct the immune response in an appropriate direction by secreting a wide variety of pro- and anti-inflammatory cytokines (50). Schistosomes are rich in glycosylated molecules, which heavily decorate their integument or are actively secreted, and glycolipids presented by CD1d (a non-classical MHC molecule) on antigen presenting cells (APCs) may thus be able to activate regulatory NKT cells (51).
One of the most obvious and well-documented responses to S. mansoni is the Th2 dominance in the T cell population. Any initial Th1 response to the parasite is quickly redirected to a state of quiescence (52). The cytokine environment is fundamental for this purpose: large amounts of IL-4, IL-5 and IL-13 are secreted from the T cell pool, reinforcing not just T cell polarization, but also the anti-inflammatory loop on DC and MΦ (32). The parasite is also capable of containing the side-effects of such a strong Th2 response, inducing the secretion of IL-10 and TGF-β by other T cell subtypes (53,54). For example, animals and humans infected or exposed to S. mansoni antigens do not automatically develop allergies at a higher incidence (see Figure 3). The de novo induction and/or the expansion/recruitment of Treg almost certainly underlies the ability of many parasites to both evade a sterilizing immune response and also suppress both Th1 and Th2 arms of the adaptive immune system (55,56).
|20-06-2012, 12:38 AM||#438|
Join Date: May 2012
google 'Rheumatoid arthritis AND mycoplasma", the symptoms of Lyme disease are the same as those caused by mycoplasmas.
they probably engineered it not have a cell wall, since that's how antibiotics work.
Last edited by angelsaredemons; 20-06-2012 at 12:40 AM.
|21-06-2012, 07:56 PM||#439|
Join Date: Jan 2010
Location: in the abyss of reality.
Foxes, not deerkey to rise in Lyme disease, study
Increases in the deer population have been blamed for the explosion of Lyme disease cases in recent years, but changes in the numbers of foxes and coyotes - and what they eat - may actually be responsible, according to a study published Monday.
This could have implications for how wildlife is managed, and shed light on the complex ecosystems underlying the rise of Lyme and other tick-borne diseases.
Wisconsin saw a 280% jump in Lyme disease cases in the decade from 1997 to 2007, with a total of 2,376 cases statewide just last year. Other states in the Midwest and the East Coast have seen even greater increases. The bacterial infection that starts with a distinctive bull's-eye rash can require extensive antibiotic treatment and may lead to arthritic and nervous system complications.
But what do small predators such as foxes and coyotes have to do with a disease spread by the deer tick?
The answer lies not only in the life cycle of the Lyme bacterium, Borrelia burgdorferi, but also in the ecological changes of all the animals with which it comes in contact. Normally, small mammals get infected by the bacteria, ticks get infected by feeding on the mammals, and then ticks feed and lay their eggs on deer. Foxes disrupt the chain by feeding on the small mammals.
"It was thought that deer were the only game in town for ticks," said Taal Levi, lead author of the new study and a research fellow at the Cary Institute of Ecosystem Studies in New York.
Foxes have hunting habits that are different from those of coyotes: They will kill many small mammals at once, stashing the kill for later. Coyotes, on the other hand, especially those that have crossbred with wolves, will eat deer, rabbits, or even foxes, and are not efficient predators of small mammals the way foxes are. As coyotes have expanded in numbers and range, the new study suggests, they interfere with the important role served by foxes: to suppress Lyme disease rodent hosts, especially around human habitation.
Start with small mammals
The chain of events that leads to Lyme disease starts small, with a larval tick biting, say, a white-footed mouse that carries Borrelia bacteria. The tick matures into a nymph that can infect other animals each time it feeds. The life cycle of the tick typically ends with deer, on which they prefer to feed and lay their eggs. The unlucky outdoorsman or hunter may intrude at any stage and be bitten. Hunting, it turns out, was key to understanding the spread of Lyme.
Using harvest records from 1982 to the present, the researchers tracked the number of deer, coyotes and foxes in Wisconsin, Minnesota, Pennsylvania and Virginia. In all four states, coyote hunter harvests were up over the 30-year period, while fox harvests decreased.
Incidence of Lyme disease over the same time period mirrored the rise of coyotes and the decline of foxes. Deer abundance and Lyme cases were not related in Wisconsin, debunking the common belief that more deer equals more Lyme, according to the study, which was published in the Proceedings of the National Academy of Sciences.
There also was no consistent increase in Lyme with deer numbers in the other states. In fact, an area with a high fox population in western New York was notably devoid of Lyme.
A new picture was emerging, where Lyme appeared to be more closely associated with changes in predators rather than deer. Local survey data from the Wisconsin Department of Natural Resources helped to corroborate the hunter data. Deer observations were stable, even somewhat declining, from 1999 to 2009. The initial emergence of Lyme in the state may be linked to a deer boom in the 1980s and '90s. In the past 15 years, however, deer have waned while Lyme has continued its relentless spread. This more recent burst in Lyme prevalence appears to be linked to the statewide rise of coyotes and fall in foxes. Foxes don't build dens where coyotes are present, and they may even be killed by coyotes. As a result, the small animals that host infected ticks are left to multiply freely.
Infectious disease emerging from altered predator-prey dynamics is nothing new; Levi points to bubonic plague and hantavirus as diseases whose spread also depends heavily on rodents and other common prey species. For Lyme research, shifting the focus from deer alone to the ecosystem underlying the disease has been challenging, says Levi, and perhaps overdue.
Jennifer Coburn, Borrelia researcher at the Medical College of Wisconsin, agrees: "These ideas fill an important hole in our knowledge of why Lyme disease is continuing to emerge. It's not all accounted for by deer, who are dead-end hosts (for the bacteria)."
Tracking wildlife numbers
As the prevalence of other tick-borne pathogens increases, tracking wildlife numbers and transmission patterns may become even more important. Bacteria such as Anaplasma, and parasites like Babesia, are also spread by deer ticks. Last August, a new species of Ehrlichia bacteria was found in ticks in Wisconsin and Minnesota. While Borrelia, the bacteria that cause Lyme, can infect someone 36 hours after being bitten, Anaplasma can be transmitted from tick to human much more quickly. To stay on the safe side, Coburn advises meticulous tick checks every evening when returning from the outdoors.
Based on their research, Levi and colleagues suggest a deer reduction strategy be combined with efforts to rehabilitate the red fox, to reduce tick abundance and ultimately to stall the spread of Lyme disease. In fact, this may be already happening organically, as wolves recover and cougars move eastward. These top predators may control the coyote population, thus helping foxes recover.
Adrian Wydeven, an ecologist with the DNR, said wolf predation can also contain the spread of chronic wasting disease in deer, but he believes implementing the new study's strategy of predator manipulation on a large scale would be very difficult.
Wisconsin already has proactive management of these animals in place, according to David Drake, wildlife specialist at the University of Wisconsin-Madison. The No. 1 goal of the harvest strategies is to ensure healthy populations of these species, with the aim of minimizing crop damage and threats to property from deer and predators.
Human diseases don't figure high on the priority list: "I would not structure a deer season with the sole idea of reducing Lyme disease," said Drake.
Rather, he views Lyme and other tick-borne maladies as a controllable public health concern, just not through wildlife management. The onus is on the individual, not the DNR, to manage ticks and, he said, "the public is aware enough of tick (avoidance) strategies." Plus, "dogs and cats can bring ticks into the house, and you have a lot more interaction with your pets than with deer."
Tick prevention tips
Use bug repellents containing DEET.
Wear long pants tucked into socks and long-sleeved shirts when walking in the woods or grassy areas.
Check skin and clothes for ticks after being in the woods.
Remove tick by grasping it as close to skin as possible with tweezers and gently pulling until it releases grip. Clean bite with antiseptic.
If you live near woods, remove brush and litter and put wood chips or gravel path between your yard and the woods as a buffer zone to minimize tick exposure.
- CDC, Wisconsin Department of Health Services
|21-06-2012, 08:30 PM||#440|
Join Date: Jan 2010
Location: in the abyss of reality.
Thanks for the link to wikipedia.
I feel bacterial and mycoplasma infections is the root cause to nearly all human disease's As we all know these infections can be easily treated and cured and big pharma and tptb know this and we are all distracted by looking at each disease as a seperate issue people are in complete denial that perhaps M.S is actually caused by an infection or that Rheumatoid arthritis could be caused by an infection it's like all these are some sort of disease that a cure is being sort after but never quite being reached.
The charities a not much better either they prevent cures being found and are so petrified that if people are actually cured they will have to shut down they will loose their golden cash cow.