Saturday, March 14, 2009

Type I Diabetes linked to a childhood virus

Many researchers and others believe there is a specific trigger for the onset of autoimmune disease. Most believe that trigger to be a virus. The hunt for that viral trigger has been going on for more than two decades. Many candidate viruses have been suggested. Here is another:

Common infant virus may trigger type 1 diabetes
Published 25.11.2008 , updated: 09.12.2008, 11:01

Human parechovirus is a harmless virus which is encountered by most infants and displays few symptoms. Suspected of triggering type 1 diabetes in susceptible people, research methods need to take this “silent” virus into consideration. This comes from findings in a study from the Norwegian Institute of Public Health.

This study was part of a long-term project at the Norwegian Institute of Public Health to investigate if environmental risk factors affect type 1 diabetes. Faecal samples and questionnaires about the health of 102 children were sent in monthly by their parents for closer study. Researchers wanted to see how common human parechovirus infections were among Norwegian infants. Existing research indicates that a related virus which only affects rodents, Ljungan virus, has been linked to the development of rodent diabetes.

Common virus

By studying stool samples from 102 infants and comparing feedback from parents about their child’s health over three years, no significant link could be found between infection episodes and typical symptoms such as coughing, sneezing, vomiting, diarrhoea or fever.

By the age of two, 86 percent of the infants had evidence of parechovirus in their faeces, and 94 percent by the age of three. Human parechovirus 1 was the most prevalent type (76 percent) followed by human parechoviruses 3 and 6 (13 percent and 9 percent respectively).

The researchers also noticed an increase in parechovirus infection between the ages of 6 and 18 months. This could be due to the loss of maternal antibodies by 6 months of age or the exposure to nursery/play groups that often begins at this age in Norway.

Most infections occurred during September to December. The 102 infants were recruited from babies born in 2004, with half from the high risk group for diabetes type 1 and the rest from a low risk group.

The “high-risk” group included babies who had been identified at birth to carry the HLA genotype conferring the highest known risk for type 1 diabetes.

The group not carrying the high-risk genotype included babies born at the same time and in the same area to the high risk babies.

The researchers conclude that most infants are infected by human parechovirus without displaying symptoms and so the total number of previous infections should be considered when looking for triggers for type 1 diabetes among those who are genetically at risk. Perhaps too few infections or infection at a too late time point could be important.


Tapia G., Cinek O., Witsø E., Kulich M., Rasmussen T., Grinde B., Rønningen K.S. Longitudinal observation of parechovirus in stool samples from Norwegian infants.(2008) J. Med. Virol. 80: 1835-1842

Tuesday, March 10, 2009

For cures now, needed changes Psoriasis Action Network

Today in my email in box I received an email from Psoriasis Action Network, a fine organization I presume. I decided to write back with what I saw as the greatest need for action in the autoimmune community. The email below speaks for itself

Dear Alyssa Brown of Psoriasis Action Network

My son has P, PsA and AS. All are related inflammatory diseases. RA, Crohn's, diabetes type I are also related and in some of our relatives on both my wife's and my side. Similar meds and research innovation that stop immune system inflammation can help these and other autoimmune inflammatory conditions.

(1) Why don't advocacy groups work together? Wouldn't our voices be more powerful?

(2) Revolutionary therapies and medication are being delayed for decades by the current FDA clinical trial process. I have read that it cost more than a billion dollars for a single drug to go through trials for a single disease. Insane! In addition it takes a decade or more from research discovery to patient bedside. Double insane!! We need research centers, perhaps twenty or so, spread across US where new research can immediately be tried on patients hero volunteers--lawsuit free with IRBs who think first of patient and LAST about protecting their institution and jobs.

(3) There are over 80 named autoimmune diseases. The FDA requires each new therapy to be tested SEPARATELY on each of the named diseases. There are many underlying similarities in these diseases, why not a clinical trial with patients from many if not all autoimmune named conditions?

(4) The expense and lengthy time requirements to bring revolutionary cures to market mean that Big Pharma wins. They get to keep peddling less effective but very profitable 'blockbuster" drugs longer before better more effective therapies come and take away their market. The time and expense also forces small companies with innovative research to sell that research to Big Pharma or enter into onerous contracts in order to bring the research to market. Imagine if the electronics industry were forced to work that way. Today we would still be using crank handle phones!

(5) Only the suffering and deaths of a tiny handful of volunteers in clinical trial count when FDA makes a call on allowing medications to market. The massive scale of suffering and death by those who get no chance at these meds is not counted.

My son has been in wheel chair for four years. He cannot get his own food or water.

Ustekinumab was shown to have "stunning results" in clinical trials TWO YEARS AGO. It still is not approved today by the FDA rhymes with DELAY. My wife and I have gone through the Abigail Alliance and contacted Centocor senior executives asking for and being repeatedly DENIED ACCESS. Under current FDA compassionate use provisions Centocor is given the final and only say. There is NO APPEAL!

The Jacob Gunvalson court case means even the federal courts refuse to help alleviate the suffering and death of helpless patients. Do something! Why aren’t we blocking traffic and marching in the streets until treatment advances are released for patient use like the AIDS folks did in the eighties. It worked for them.

Why are we such wusses? Why don’t we fight and scream and riot? We are like abused spouses who sit passively back and re- take the abuse over and over and do nothing because they are “helpless” to change the situation. No we are not helpless. AND The situation needs changing now!

Ustekinumab beat Enbrel head to head clinical trials announced last September--still no approval. Do not accept FDA DELAY. Fight the monster. My son's suffering should count. His two brushes with death should count. Patients like him should not have to beg for access that is routinely denied.

(6) Stem cell research--Prochymal is a REVOLUTIONARY advance in treatment of ALL blood and immune cell conditions. The Osiris company has found the "magical" hematopoietic stem cells that can be infused into any human being, no matter blood or MHC type, without the stem cells attacking the patient (graft versus host) or the patient's immune system attacking the stem cells. Think what that means. If healthy immune cells that give rise to healthy immune regulatory cells, virtually all patients with all immune dysfunctions could be cured. All my son needs are healthy regulatory cells to bring balance to his immune system.

Prochymal is stuck in the FDA one named disease at a time nightmare. First they used it on GvHD and stopped it!!!! GVHD kills something like 50% of all patients who experience it in less than a year of onset. Prochymal stops it.

GvHD is like having every autoimmune disease at once so if it can be stopped autoimmune disease can be stopped. Osiris tried it first on Crohn's. It stopped ALL Crohn's symptoms in as little as two weeks. Now they are trying it on diabetes type I but it should be tried for ALL AUTOIMMUNE DISEASE NOW not decades from now.

What is wrong with FDA bureaucrats who cannot understand that if we can get working regulatory cells in our bodies then these cells can with exquisite precision control our immune dysfunctions. The control will be far better and far more targeted than the massive intermediate doses of monoclonal antibodies blocking one inflammatory cytokine at a time.. First too much blocked than as time goes on too little. Exquisite LIVING control is SO MUCH BETTER!

(7) Vaccines for autoimmune, where are they. Anti-TNF alpha, anti-maladapted dendritic and T effector vaccines--lets get them approved! Let HEROES volunteer in research centers today. Stop denying access. There are also vaccines that instead of alerting body to destroy maladapted cytokines and auto-immune cells instead promote tolerance of the proteins under autoimmune attack. These vaccines act like allergy shots. An MS vaccine along these lines has shown promise. Why aren't we finding the proteins being attacked for P, and PsA and creating these tolerance vaccines?

(8) B cell depletion therapies show tremendous promise. Why is the old mouse protein, Rituxan, still the only B cell therapy on the market? Why aren’t we getting HuMax CD 20 et al approved? What is wrong with the FDA? and what is wrong with NIH and research grants to find better B cell therapies that are more targeted to only kill the active autoimmune antibody producing B cells? instead of the "good guy" B cells that stand ready to protect us from various infective illnesses that we are immune to?

I have watched my son go from the editor of his college newspaper with a huge circle of friends to a hunched over, pain wracked, helpless disabled person. These past five years have been Hell for him.

When he first exhibited symptoms of his first autoimmune disease in his senior year of college in fall of 2003, I started reading on line everything I could. I found tremendous hope there that autoimmune disease could be cured and were being cured in the lab. We expected these cures to be immediately expedited and translated into patient cures. We waited eagerly. Then we waited some more and more and more.

Still we wait even for the simplest band-aid “bridge to future” treatment like Ustekinumab. It is should have been approved in summer of 2007 on some special provisional approval that allowed access for the sickest and those willing to give up legal rights to sue. Why wasn't it? Why do we wait?

Ustekinumab is a PRIMITIVE band aid to a problem that is could soon be curable with stem cell research. But it is a very helpful band aid, so lets get approved!

Sorry to ramble. Please forward this email to anyone you think can help get my son and other patients gain faster ACCESS to revolutionary cures currently in research labs and clinical trials.


Friday, March 6, 2009

Diabetes Type I linked to a viral infection

Here is the article:

The Peninsula College of Medicine and Dentistry
New study of human pancreases links virus to cause of type 1 diabetes
Key to success is unique availability of relevant organs for research
A team of researchers from the Peninsula Medical School in the South West of England, the University of Brighton and the Department of Pathology at Glasgow Royal Infirmary, has found that a common family of viruses (enteroviruses) may play an important role in triggering the development of diabetes, particularly in children. These viruses usually cause symptoms similar to the common cold, or vomiting and diarrhoea. However, the team has now provided clear evidence that they are also found frequently in the pancreas of people who develop diabetes.

The research, which was carried out at Peninsula Medical School and funded by Juvenile Diabetes Research Foundation (JDRF), is published today, 6th March 2009, in the leading European diabetes journal, Diabetologia. It involved the detailed study of a unique collection of pancreases from 72 young people who died less than a year after the diagnosis of type 1 diabetes.

Type 1 diabetes usually starts in young people and results from the destruction of the insulin-producing beta cells in the pancreas. Patients who develop type 1 diabetes have to take multiple daily injections of insulin for the rest of their lives, and the condition affects around 300,000 people in the UK , including 20,000 children under the age of 15. There are a further estimated 440,000 cases of type 1 diabetes in children worldwide, with more than a fifth living in Europe.

It is accepted that children who develop type 1 diabetes inherit a genetic susceptibility to the disease, but studies of identical twins have shown that when one twin has the disease, the other twin will only have approximately a 40 per cent chance of developing diabetes – suggesting that factors additional to inheritance are also involved.

It has long been speculated that viruses might play a role in causing type 1 diabetes by infecting the beta cells of the pancreas. This new research, which has made use of unique source material collected in Glasgow, is the first to provide evidence supporting this theory in such a large number of pancreases from young people recently diagnosed with the disease. It has revealed that more than 60 per cent of the organs contained evidence of enteroviral infection of the beta cells. By contrast, infected beta cells were hardly ever seen in tissue samples from 50 children without the condition.

The new research suggests that enteroviral infection of the beta cells in children with a genetic disposition to type 1 diabetes may initiate a process whereby the body's immune system identifies beta cells as 'foreign' and rejects them, as it would a transplanted organ.

An extension of the study to adults with type 2 diabetes showed that a large proportion (40 per cent) of these patients also had enteroviral infection in their beta cells. This compared with only 13 percent of non-diabetic adults of the same age group. Unlike type 1 diabetes, type 2 diabetes usually starts in adults and is associated with obesity. The beta cells are not destroyed in this disease but their ability to make insulin is compromised. The way that enteroviruses might contribute to the development of type 2 diabetes has not been established but it is known from laboratory studies that an enteroviral infection of beta cells reduces their ability to release insulin. It is possible that in people who are obese (where there is a greatly increased demand for insulin secretion) a reduction of beta cell function, secondary to enteroviral infection, may be sufficient to trigger type 2 diabetes – although more research is required to confirm this.

Overall, the findings of this new study suggest that vaccination in childhood to prevent enteroviral infections of beta cells might be an attractive means to reduce the incidence of both common forms of diabetes. However, there are up to 100 different strains of enterovirus and more research will be needed to identify which particular enteroviruses are associated with the development of diabetes, and whether vaccines could be developed to prevent their spread.

Professor Noel Morgan from the Peninsula Medical School commented: "We are genuinely excited by the findings of our study. This is the first time that scientists have been able to provide such extensive evidence for the relationship between enteroviral infection of the beta cells and the development of type 1 diabetes. This is due in large part to the unique availability of such a large number of pancreases from young people who had died of type 1 diabetes soon after becoming ill. Not only did this give us access to extremely important research material, but it also underlines the importance of continued organ donation to the development of medical research in the UK. "

He added: "The next stages of research – to identify which enteroviruses are involved, how the beta-cells are changed by infection and the ultimate goal to develop an effective vaccine – will lead to findings which we hope will drastically reduce the number of people around the world who develop type 1 diabetes, and potentially type 2 diabetes as well."

Professor Adrian Bone from the University of Brighton said: "It is a real privilege to be part of this work which sheds light on how targeted beta-cell destruction may be triggered in individuals at risk of developing diabetes. Whilst experimental studies from many laboratories, including my own, have been able to document the "natural history" of the disease processes culminating in overt diabetes, the role of viral infections in initiating these events is still unproven and controversial.

"Indeed," he added, "viruses have been shown to be capable of both inducing and preventing the development of diabetes. The true importance of our present study lies in the translation of these earlier experimental findings into meaningful observations in children and young people with diabetes."

Pathologist, Dr Alan Foulis of the Royal Infirmary in Glasgow, observed: "It is 25 years since I started assembling this collection of pancreases from patients with recent onset type 1 diabetes, with the express purpose of looking for the presence of enterovirus. It is only very recently that techniques of sufficient sensitivity to detect the virus in such specimens have been developed. The success of this study is largely down to the excellent scientific collaboration we have enjoyed".

Karen Addington, Chief Executive of JDRF, said: "Type 1 diabetes is a life- threatening condition that requires a life-time of painful finger prick blood testing and insulin injections. Incidences are increasing by four per cent each year and there is currently no way to prevent it. We are proud to have funded this crucial piece of research, which helps shed light on the causes of this serious condition. JDRF passionately believes that research such as this brings us a step closer to improving treatment and eventually curing this condition."

Autoimmune process prematurely ages immune cells

Below is an article indicating that in rheumatoid arthritis, T cells age too quickly. I would think this has to do with the damage done to the immune system by being constantly switched to "overdrive". The aging can be seen in the telomere caps at the ends of the chromosomes. Researchers are looking for a way to reverse the damage to the telomere caps without causing cancer.

I think they would be better off looking for a way to stop the out of control autoimmune response as quickly as possible before the telomere damage is done.

There are four sure ways to stop autoimmune disease today and a couple other possible methods.
(1) full bone marrow transplant (gives patient new immune system but many patients die)
(2)B cell depletion--Rituxan only FDA approved medication but chance of death, however less than bone marrow transplant but autoimmune condition can recur in weeks or months
(3)bone marrow re-boot--some of patients bone marrow taken out frozen, rest of bone marrow killed, patient's frozen marrow thawed re-infused--risk of death from infection in between but no risk of gruesome death by GvHD as there is for full bone marrow transplant, also risk that frozen bone marrow may re-introduce the same autoimmune disease. No good way to separate healthy disease free patient bone marrow from autoimmune producing bone marrow.
(4)Prochymal-mixture of bone marrow pre-cursor cells from many many donors, somehow stops both GvHD and stops autoimmune disease. My belief this is the greatest hope for lifetime cures for most autoimmune patients.
Other possibilities
(5)parasites--see previous blog
(6)pregnancy--stops autoimmune for duration of pregnancy and few months after usually not always.

Here is the article about aging immune cells in Rheumatoid Arthritis patients:

Emory University
Immune cells from patients with rheumatoid arthritis have prematurely aged chromosomes

Telomeres, structures that cap the ends of cells' chromosomes, grow shorter with each round of cell division unless a specialized enzyme replenishes them. Maintaining telomeres is thought to be important for healthy aging and cancer prevention.

By this measure, T cells, or white blood cells, from patients with the autoimmune disease rheumatoid arthritis are worn out and prematurely aged, scientists at Emory University School of Medicine have discovered.

Compared with cells from healthy people, T cells from patients with rheumatoid arthritis have trouble turning on the enzyme that replenishes telomeres, they found. Reversing this defect could possibly help people prone to the disease maintain a balanced immune system.

The results are published online this week in Proceedings of the National Academy of Sciences.

In rheumatoid arthritis, T cells are chronically over-stimulated, invading the tissue of the joints and causing painful inflammation. This derangement can be seen as a result of the loss of the immune system's ability to discriminate friend from foe, says senior author Cornelia Weyand, MD, PhD, co-director of the Kathleen B. and Mason I. Lowance Center for Human Immunology at Emory University.

In childhood, new T cells are continually produced in the thymus, she says. But after about age 40, the thymus "involutes" – or shrinks and ceases to function. After that, the immune system has to make do with the pool of T cells it already has.
"What we see in rheumatoid arthritis is an aged and more restricted T cell repertoire," she says. "This biases the immune system toward autoimmunity."

Weyand, postdoctoral fellow Hiroshi Fujii, MD, PhD, and their colleagues were interested in mechanisms of T cells' premature aging, because scientists had previously observed that in rheumatoid arthritis, T cells tend to shift the molecules on their surface and function differently.

They found the answer in telomerase, the enzyme that renews telomeres and is necessary to prevent loss of genetic information after repeated cell division.
Telomerase adds short repeated DNA sequences to the ends of chromosomes to protect them. The enzyme is active in embryonic development but is usually switched off in adult cells. Many cancer cells reactivate it to enable runaway growth.

T cells are some of the very few cells in adults that can turn on telomerase when stimulated, probably because they have to divide many times and stay alive for decades.

Weyand and Fujii found that T cells from patients with rheumatoid arthritis make 40 percent less telomerase enzyme when stimulated. The cells came from 69 patients, 92 percent female, with an average age of 50, and were compared with cells from healthy people with similar demographics.

Shutting off a gene encoding part of the enzyme made normal T cells vulnerable to programmed cell death, and transferring telomerase into patients' T cells rescued them from dying.

The finding suggests that restoring defective telomerase to T cells could possibly help "reset" the immune system in rheumatoid arthritis, Weyand says.

Pharmaceutical industry researchers have been looking for drugs that could elevate or depress telomerase activity, with the goal of either prolonging life or treating cancer. However, turning on telomerase indiscriminately could lead to cancer, so any treatment would have to be targeted to the right cells, she says.
The research was funded by the National Institutes of Health and the Diane Wolf Discovery Fund.

Fujii is now an assistant professor of hematology and rheumatology at Tohoku University School of Medicine in Japan.

Reference: H. Fujii, L. Shao, I. Colmegna, J. Goronzy and C.M. Weyand. Telomerase insufficiency in rheumatoid arthritis.

The Robert W. Woodruff Health Sciences Center of Emory University is an academic health science and service center focused on missions of teaching, research, health care and public service. Its components include schools of medicine, nursing and public health; the Yerkes National Primate Research Center; the Emory Winship Cancer Institute; and Emory Healthcare, the largest, most comprehensive health system in Georgia. The Woodruff Health Sciences Center has a $2.3 billion budget, 17,000 employees, 2,300 full-time and 1,900 affiliated faculty, 4,300 students and trainees, and a $4.9 billion economic impact on metro Atlanta.

Worm Cure for Multiple Sclerosis other autoimmune

There has been a lot of research into parasitic worms as a cure for autoimmune and allergic disorders. The idea is that the worms have evolved to survive in its host by calming the host's immune system. The chemicals released by the worms mimic cytokines that push our immune systems toward tolerance. One of those cytokines is IL-10 some secretions of the worms may mimic it.

Many researchers further believe that because all humans were universally infected with these parasites from birth that some humans have lost the ability to calm down their own immune systems without the help of these parasites. Thus we see the greatly increasing rates of autoimmune conditions, asthma, and allergy in "developed" countries where most of the population no longer carries these worms but the same is not true of "third world" countries where the rate of allergy, asthma and autoimmune is stable and few in the population suffer from these conditions and all or most people in the population are infected with worms.

There is a clinic in Tijuana, Mexico, a city just a few miles south of San Diego, California, where for a few thousand dollars anyone can be infected with "clean" parasites. In this case, hookworm larva are put on the patient's arm where they burrow through the skin (slight itching sensation) enter the blood stream and eventually end up in the intestines. Many claim that their symptoms of allergy, asthma and autoimmune are greatly lessened in a couple of weeks. I cannot recommend the clinic at this time, but if you are interested here is a link to its website:

Below is a link plus the article about research in the UK to try to determine if parasitic worms can indeed turn off an autoimmune disease, in this case multiple sclerosis. Previously Dr. Joel Weinstock of formerly of the University of Iowa had successfully used pig whipworms (also an intestinal parasite) in humans as a treatment for Crohn's.

Parasitic worms may lead to treatment for multiple sclerosis

Scientists from The University of Nottingham will study the potential health benefits of parasitic worms as part of a study investigating treatments for people with the autoimmune condition multiple sclerosis (MS).

It is thought that hookworms may play a role in damping down the immune system, which is overactive in people with MS, the most disabling neurological condition in young adults.

The £400,000, three-year project funded by the MS Society, aims to determine whether infection with a small and harmless number of the worms can lead to an improvement on the severity of MS over a 12 month period.

If the trial is successful, the worms have the potential to provide a simple, cheap, natural and controllable treatment for MS.

The WIRMS (Worms for Immune Regulation in MS) study is led by Professor Cris Constantinescu and Professor David Pritchard and is a randomised, placebo controlled, phase 2 study in people with relapsing remitting MS and will be carried out at multiple centres up and down the country.

The 25 worms are microscopic and are introduced painlessly through a patch in the arm. They are then flushed out after nine months.

Professor Constantinescu, said: "People are really interested in this form of potential therapy because it's a natural treatment. It's been tested for safety and we now need to study the potential benefits and any side effects."

Jayne Spink, Director of Research at the MS Society said: "It sounds like science fiction, but it has been shown in a previous small study that people with MS who also had gut parasite infections had fewer relapses.

"Over time, parasitic worms have evolved to be able to survive an immune system attack and have been linked to a reduction in the severity of the symptoms of MS, which can be debilitating.

"If the theories can be shown to be accurate, using hookworms as a future treatment option may prove to be science fact."

MS affects more than 85,000 people in the UK and several million worldwide. Symptoms range from loss of sight and mobility, fatigue, depression and cognitive problems that often come on as attack - or relapses. There is no cure and few effective treatments.

Dorothy Sutton, 58, from Awsworth, has lived with MS for 32 years and is a Helpline volunteer for the MS Society. She said that although the treatment sounded unusual, anything that could potentially to help alleviate the symptoms of MS is a positive step.

"We have to explore every avenue of research to find treatments for MS. As long as it's safe and effective in helping the horrible symptoms, I don't think people mind where it comes from."

The Division of Clinical Neurology at The University of Nottingham's Medical School is a strong research-led unit which draws heavily on its close relationship with people with MS to inform its work.

Led by Professor Cris Constantinescu, the department features two academic and one NHS Neurology Consultants that are affiliated with the Neuroscience Directorate of Nottingham University Hospitals (NUH) NHS Trusts.

Monday, March 2, 2009

Health care reform is coming!

Health care reform is coming! Thank God! Finally! Hallelujah!

Our family pays every more every year out of pocket costs for health care for our son--over ten thousand dollars a year and rising.

Only my wife works. I am on disability retirement due to my immune dysfunction. I have no health care coverage not even Medicare because as a California teacher of a certain age no money was taken from my salary for medicared.

The money issue is a big worry. Even worse for my wife, she worries if she at age 55 has a health problem and cannot work, we will not be able to get health care for our son. Pretty evil system here in the US.

My wife and I never drank, never did drugs, never partied. Always were on the deans list and honor rolls of every education institution we attended. We did everything right. We worked all our lives including while attending college. We graduated from college in four years with outstanding grades.

I was an athlete on school teams from junior high, to high school to college. I took very good care of my health.

All the good things and good living we did were for naught, as we ended up both carrying "genetic time bombs" through no fault of our own. Now all the our good deeds do not mean that we will have health care for our son.

Good deeds: I have intervened to save three lives-- a choking victim with Heimlich, a drowning victim in a pool not my own and a victim of a violent attack by a mentally deranged stranger. My wife and I were constant volunteers at church--Church Board member, Sunday School teachers, Christian scouting directors, volunteers at church work days. We were community organizers for school bonds.

Yet good deeds do not guarantee good health. Nor do good deeds guarantee health care when you get sick. What a rotten system!

Below is a summary of our possible new health care system. Enjoy.,0,1696038.story
From the Los Angeles Times
A national healthcare reform primer
The many issues confronting President Obama as he tries to achieve insurance coverage for all Americans.
By Bob Rosenblatt

March 2, 2009

Most people with health insurance say they like what they have. They trust their doctors, and they are fearful of any change in their policy.

Many of the 47 million uninsured people in this country don't go to the doctor even if they need to because they figure they can't afford it. They skimp on medications or skip them entirely.

President Obama has said that he and Congress will make both groups happy by cutting costs for those who have coverage and by bringing quality care to those who currently have no insurance.

It's a tremendous challenge. And the goal, if accomplished, will affect every American.

On Thursday, Obama's push to expand healthcare coverage began in earnest, with the announcement of his plan to create a $634-billion fund to do just that. The amount was described as a down payment over 10 years; the final price tag would be even larger, perhaps $2 trillion or more.

The president's strategy is starkly different from the approach by the Clinton administration in 1993, when it corralled hundreds of experts and staff people to produce a detailed plan more than 1,000 pages long. The Clinton effort failed, despite Democratic majorities in both houses of Congress. Obama's approach is this: Give me a bunch of money, and we'll figure out the details later how we are going to manage this thing.

Now the wrangling truly begins -- with the administration trying to push its vision through Congress, with Democrats and Republicans trying to shape the effort to their liking and with special interests trying to affect the final outcome, whatever it may be.

The cost of covering the uninsured ultimately will depend on the number of people included, the specific benefits they receive, and the amount of financial help the taxpayers would provide. The only agreement among economists who study the issue is that the tab would be a big one:

* $200 billion to $250 billion a year, says Joe Antos of the conservative American Enterprise Institute.

* $150 billion to $175 billion a year, says Len M. Nichols of the liberal New America Foundation.

The debate over this first proposal and related, still-to-come proposals will boil down to a discussion about the powers and size of the federal government. Do we want the government to have the power to make us buy health insurance, as individuals or businesses? How much power should the government have to control costs? How much do we want to spend to provide health insurance to our fellow citizens who don't have it?

Here is a primer on the big issues to watch as the healthcare debate unfolds:

Regardless of what happens, will I be able to keep the insurance I have now?

Almost certainly. The big lesson from President Clinton's ill-fated attempt at healthcare reform in 1993 and 1994 was that people are terrified of change. They like their doctors, although they don't like insurance companies. An oft-uttered reassurance in the 2008 residential campaign was: If you like what you have, you can keep it. This will likely be a key plank in any plan offered by the Obama administration.

Further, most people get their coverage at work, and this would continue. Despite rising costs, business managers still place high value on insurance as an attractive benefit. The share of the workforce with coverage remains around 70%.

If I don't have health insurance, would I have to buy it if an agreement on reform is reached?

This is the tricky mandate issue. Advocates say you can't cover everyone unless you make everyone buy a policy.

Although nobody from the administration is using the "M" word these days -- a mandate would represent a big expansion of government authority -- many believe it is the logical way to go. So do Democratic leaders in Congress.

Before such a mandate could become law, however, Congress would have to decide the amount of financial subsidies to help people pay for their coverage. Most people without health insurance work full-time and earn less than $30,000 a year. Meanwhile, the average policy for a family of four under job-based coverage cost $12,680 last year, with the employer paying $9,325, according to figures compiled by the Kaiser Family Foundation. Coverage for an individual through work cost $4,704, with the employer paying $3,983.

A decision on a mandate would also involve intense negotiations between the government and the insurance industry over the terms and details of coverage. The industry has indicated it's willing to deliver "guaranteed issue" (nobody gets turned down) in return for a law requiring mandatory purchase of insurance.

The National Assn of Insurance Commissioners has proposed a model act for the states as a way to control costs. It says that the highest rates for any age group should be no more than 400% of the lowest rate charged to any group. This would be reduced to 300% two years after the law is passed, then to 200% after five years. That would mean a 63-year-old living in San Diego, for example, could not be charged more than double the rate paid by a 25-year-old in Santa Monica.

Price differences and subsidies are crucial. It would be meaningless to have the guaranteed right to buy health insurance if you make $30,000 a year, have high blood pressure and diabetes, and a policy would cost you $10,000.

If I have a business, would I have to buy coverage for my workers?

The answer to this question may determine the success or failure of health reform efforts.

This is the "pay or play" issue in health policy language. A company "plays" by offering coverage to its employees, or "pays" into a public fund to help cover the uninsured.

During his campaign, Obama said he favored a mandate for business. But, like the idea of a mandate for individuals, any discussion of a mandate for business was conspicuously absent from the budget document, and was never mentioned by administration officials in their briefings Thursday. They repeated over and over that the president wants every American covered by health insurance, and that he welcomes all ideas from Congress about how best to achieve the ambitious goal.

Big questions remain. If there is a mandate, which businesses should be exempt? Those with 25 or fewer workers? 10 or fewer? And what share of payroll should businesses have to contribute if they don't offer coverage?

Big companies already offer coverage and likely would continue to do so. They might favor the mandate because it levels the playing field, with all firms now in the game.

Small businesses, vociferous opponents of the Clinton plan in 1993, would be hard to persuade now to accept a mandate as they struggle with the biggest economic slump since the Great Depression.

Would there be some help for older workers who don't have coverage on the job and can't afford an individual policy?

Perhaps. One of the ideas circulating on Capitol Hill would allow people to buy into the Medicare program at age 55 or 60. (Medicare eligibility begins at 65.) Early entry would protect people who may have taken early retirement, or been laid off in their late 50s. They are old enough to have developed medical problems that make it hard to get an affordable policy. (How about Medicare for all?)

The question that would need to be resolved is how much would the government charge as a premium. Most of the cost of Medicare is borne by the taxpayers, with the beneficiaries paying only a small share. Since Medicare faces long-term financial problems, Congress might want to charge the full cost of Medicare to these new enrollees. This could range from $500 to $700 a month. (Still cheaper than what my wife and I pay out of pocket each year)

Might there be a public health insurance plan?

This idea, backed by the president, would create for the first time a public insurance plan to compete with the myriad plans offered by private-industry insurers. The plan would be designed to provide a benchmark for quality coverage, with a basic package of comprehensive benefits. The Obama health plan issued during the presidential election campaign envisioned that millions of the 47 million uninsured would move into a public plan.

How can the country pay for a reworking of its health insurance system?

There's the rub. The only thing certain is that it would cost a lot, and the debate will be vigorous over where that money should come from.

Obama has proposed a down payment of $630 billion. Most of the money would come from an increase in federal income taxes by limiting deductions for people making more than $250,000 a year.

He also wants to cut payments to Medicare HMOs, saving about $175 billion over 10 years, according to the budget plan issued Thursday. This program, known as Medicare Advantage, requires enrollees to get their hospital and doctor care within a network of providers. In return, they get extra benefits, such as dental care, which are not included in the regular Medicare program. Under regular Medicare, called fee-for-service, the beneficiary can see any doctor or hospital where Medicare payments are accepted.

Other ways to find revenue, mentioned by administration officials but not endorsed in any way, include:

* Capping the federal income tax deduction for health insurance.

Workers do not currently pay taxes on the total value of their coverage. Suppose Sarah Jones has a policy at work with premiums of $10,000 a year. She pays $2,000 and her employer pays $8,000 on her behalf. That $8,000 is not counted as income for Sarah Jones. And her employer can deduct the $8,000 as a business expense.

If this deduction were limited, the government could collect lots of money to pay for the uninsured. But it would mean higher taxes for workers who have the most expensive policies, and they won't greet that very warmly. Also, this would be a flip-flop politically for the president, since he spent millions of dollars on TV commercials during the campaign attacking the Republican presidential candidate, Sen. John McCain of Arizona, for making exactly the same proposal.

* Creating a special tax dedicated for healthcare.

This could be a special value-added tax on all goods, a kind of tax common in Europe. New taxes, however, are never popular, and especially not during a severe recession.

* Finding ways to make the system more efficient.

The president said in his budget that "healthcare costs could be reduced by a stunning 30% -- or about $700 billion a year -- without harming quality if we moved as a nation toward the proven and successful practices adopted by the lower-cost areas and hospitals."

A study of Medicare spending, for example, shows that if hospitals in L.A. used the same methods of care as hospitals in Sacramento, Medicare would have saved $468 million in 2005 on inpatient care. The Medicare patients in L.A. spent more days in hospitals, more time in the intensive care unit and were seen by more specialists. Yet despite the higher spending, patients in L.A. didn't live any longer and the quality of care was not better than in Sacramento, according to a study by the Dartmouth Institute for Health Policy and Clinical Practice.

Efficiency is one of the most popular ideas in Washington because it looks pain-free politically. After all, everybody is against waste. Except of course, when that "waste" is money you get -- or want -- for a service or product.

Currently, for example, if Drug A and Drug B are safe and effective in treating an illness, the Food and Drug Administration approves the sale of both drugs -- and Medicare and Medicaid pay for these drugs. But the House version of the stimulus bill would've allowed government programs to consider cost in deciding which drug to pay for, allowing programs to pick the cheaper one.

This was alarming to drug manufacturers and disease-specific patient-advocacy groups. Drug B might cost a lot more than Drug A, but it also might relieve pain more effectively and make life more bearable for a specific subset of the population. Neither drug makers nor these groups want the government to limit the ability of insurers and Medicare to pay for Drug B.

The Senate heard these concerns, and the final version of the stimulus bill included the word "clinical" as the standard of effectiveness that should be pursued. In other words, the programs can also emphasize how a drug works, not simply how much it costs.

What happened in the stimulus bill shows how hard it will be to create economic efficiency that slows the growth in healthcare spending.


Even in this deep recession, healthcare spending is expected to rise 5% this year, while the nation's output of goods and services (the gross domestic product) shrinks by 0.2%, according to government forecasts issued just last week.

Health reform means trying to bring insurance to those who don't have it without making the federal budget deficit even deeper, controlling the growth in health spending without denying patients what they think they need, limiting unnecessary procedures without hampering the autonomy of doctors to do what they think is best.

If Obama can figure out a way to persuade Congress to expand coverage to millions of uninsured people, while keeping those with coverage happy, it will be a feat of political magic that has eluded presidents for decades. or

Mono associated with Multiple Sclerosis

High levels of Epstein Barr viral antibodies in the blood are associated with multiple sclerosis, again!

I had a really bad case of mono in college. The only time in my life that I remember the horizon seeming to move up and down as I walked. I think the effect was caused by the very high fever. My neck was swollen up like I had the mumps.

Weird that, my now wifeof thirty three years and then fiancee did not catch mono even though she was heavily exposed. I guess not all people can get it.

Also the immune problems I have (throat and extremity swelling, flushing, syncope, anaphylaxis) were already present before the mono and seem to be no worse after the mono.

Not everyone who gets mono gets an autoimmune disease.

Not everyone who gets autoimmune has mono first. My son, who has three autoimmune diseases (psoriasis, PsA, AS) that came on suddenly in his senior year of college, never had mono.

The article linking MS to mono is below:

Epstein-Barr Virus May Be Associated with Progression of MS
Release Date: March 2, 2009

BUFFALO, N.Y. -- Epstein-Barr virus (EBV), the pathogen that causes mononucleosis, appears to play a role in the neurodegeneration that occurs in persons with multiple sclerosis, researchers at the University at Buffalo and the University of Trieste, Italy, have shown.
Multiple sclerosis (MS) is an autoimmune disease that can cause major disability. There currently is no cure.

"This study is one of the first to provide evidence that a viral agent may be related to the severity of MS disease process, as measured by MRI," said Robert Zivadinov, M.D., Ph.D., associate professor of neurology in UB's Jacobs Neurological Institute (JNI) and first author on the study.

The research appears in the Online First section of the Journal of Neurology, Neurosurgery and Psychiatry and is available at
"A growing body of experimental evidence indicates that past infection with EBV may play a role in MS," said Zivadinov, "but the relationship of EBV and the brain damage that can be seen on MRI scans had not been explored."

The study involved 135 consecutive patients diagnosed with MS at the Multiple Sclerosis Center of the University of Trieste. Evaluations of the MRI scans were carried out at the University of Trieste and at the JNI's Buffalo Neuroimaging Analysis Center (BNAC), which Zivadinov directs.
The Buffalo researchers measured total brain volume, as well as the decrease in gray matter, at baseline and three years later.

Results showed that higher levels of anti-EBV antibody measured at the beginning of the study were associated with an increased loss of gray matter and total brain volume over the three-year follow-up.

The researchers now are carrying out prospective longitudinal studies in patients who experienced a condition called "clinically isolated syndrome," a first neurologic episode that lasts at least 24 hours, and is caused by inflammation/demyelination in one or more sites in the central nervous system. If a second episode occurs, the patient is diagnosed with MS.
The study will investigate the relationship of anti-EBV antibody levels to development of gray matter atrophy, neurocognitive function and disability progression over time.

UB and Trieste researchers also are investigating interactions between environment, certain genes and EBV antibodies and the association with MRI injury in MS. A paper on this work is "in press" in the Journal of Neuroimmunology.

Marino Zorzon, M.D., from the University of Trieste, is second author on the Journal of Neurology, Neurosurgery and Psychiatry study. Murali Ramanathan, Ph.D., from the UB School of Pharmacy and Pharmaceutical Sciences and the JNI, is co-corresponding author with Zivadinov. The BNAC and JNI are located in Kaleida Health's Buffalo General Hospital.
Additional contributors to the study are Bianca Weinstock-Guttman, M.D., from UB; Maurizia Serafin, M.D., from Cattinara Hospital in Trieste; and Antonio Bosco, M.D., Ph.D., Alessio Bratina, M.D., Cosimo Maggiore, M.D., Attilio Grop, Maria Antonietta Tommasi, M.D., all from the University of Trieste, and Bhooma Srinivasaraghavan, from the BNAC.

The study was supported in part by the Consortium for International Development of the University of Trieste, Italy. The researchers also gratefully acknowledge additional support from the National Multiple Sclerosis Society and a Pediatric MS Center of Excellence Center Grant.

The University at Buffalo is a premier research-intensive public university, a flagship institution in the State University of New York system and its largest and most comprehensive campus. The School of Medicine and Biomedical Sciences is one of five schools that constitute UB's Academic Health Center. UB's more than 28,000 students pursue their academic interests through more than 300 undergraduate, graduate and professional degree programs. Founded in 1846, the University at Buffalo is a member of the Association of American Universities.

Suicide, a topic worth some discussion

Our FDA friends refuse to allow us access to life changing and life saving research developments. We live in pain and discomfort every day. What happens to us is of no importance to those in power. So depression is a normal part of the equation, especially as our end gets near. Having an "out" if things get too bad is a kind of security, a safety net, that our 'immune normal' friends cannot understand especially those who consider themselves to be religious.

I have been dead, suffocated.

I can tell you step by step how it feels. The desperate need for air does not end at any stage only gets worse and then added to by a horrible sharp pain in the center of the brain that becomes all encompassing. This pain feels like something is squeezing your brain in a giant vice. At this point you are completely deaf and blind. There is not enough oxygen for those senses to work. No part of your body is under voluntary control. More surprisingly the sense of body also disappears. There is no sensory feedback from your arms, legs or skin even on the outside of your head. You feel like you are floating someone where in the center of your brain with no connection to a body at all. Time slows down. The experience seems to last for hours and hours not the minutes it actually takes.

Suffocation is so fun, NOT.

I can assure my conservative friends that think that lethal injection of criminals is too easy because the criminals deserve worse. Our con friends do not see a twitching body or hear screams that it is a form of suffocation. They think it is a peaceful death. It is not. It is suffocation and suffocation is not fun. The screams of the criminals who die are silent but the horror and pain of the death is real.

Depression caused by our constant pain and limitations can lead to thoughts of suicide. No question. I do not recommend any method that involves suffocation. I do not recommend it at all as usually a day later things do not look so black. But having a choice of the possibility of suicide is a right we all deserve.

At the very worst times of pain, the thought that we could have an out is liberating and actually makes the pain less and the episode easier to get through. The loss of control of our lives is already so great. Why some "normal immune" folks want to deny us this, I do not understand.

February 28, 2009
Preparing to End Her Life, While Protecting Another

MULTIPLE sclerosis came into Debbie Purdy’s life about the same time as her husband, a Cuban jazz violinist named Omar Puente. “He didn’t speak English, and I didn’t speak Spanish,” she recalled. “What we had was jazz, and a dictionary.” When she received her diagnosis, one of her first thoughts was: “How do you say ‘multiple sclerosis’ in Spanish?”

That was 1995. Somehow, the couple have adjusted together to the changes in Ms. Purdy’s deteriorating body. They have adjusted as she has gone from walking with a cane to using a manual wheelchair to using an electric one. They have traded water glasses for plastic cups, installed a panic button at home in case she falls and put up a hoist to help her get in and out of bed.

But there may be a limit to the Purdy-Puente partnership, so close it feels almost symbiotic. The possibility exists that Ms. Purdy, 45, will get so sick that she no longer wants to live. Should that happen, she says, she plans to travel to an assisted suicide clinic in Switzerland and drink a lethal cocktail of drugs. As things now stand, she would have to go without her husband, she says, because helping someone die — even, say, by pushing a wheelchair onto the airplane — is illegal in Britain.

It is her choice alone, Ms. Purdy said.

“Omar’s being prepared to go to jail because he loves me and respects my choices is the same reason I wouldn’t want him to go to jail: because I love him,” she said. “I’m not even prepared to let him be interviewed by the police.”

Ms. Purdy has taken her private struggle and turned herself into the latest public face of an anguished, longstanding debate about assisted suicide in Britain. She has sued the government in an effort to force officials to provide assurance that if Mr. Puente did help her die in Switzerland, he would not be prosecuted.

Last week, her latest appeal failed when three Court of Appeal judges ruled that although they sympathized with Ms. Purdy, only Parliament could change the law. She is now considering whether to pursue the case further in the courts or to lobby for a new law.

Assisted suicide is legal in Switzerland. In recent years, about 90 Britons have killed themselves in the clinic, which is in Zurich. So far, no one back home has been prosecuted for helping them, but that does not mean it will not happen. “Many have faced police questioning and agonizing months waiting for the final decision not to prosecute,” said Ms. Purdy’s lawyer, Saimo Chahal.

Ms. Purdy explained her thinking in a recent conversation in her and Mr. Puente’s tiny house on a sloping street here in Bradford, a down-at-the-heels industrial northern city. If Ms. Purdy had not been in a wheelchair, if her hands had not been shaking, if she had not been speaking matter-of-factly about things like loss of bladder control, the painful swelling in her feet and how hard it was for her to brush her teeth, it would have been difficult to believe that she was ill at all.

She is that joyful.

SHE talked about her happiness that Barack Obama is president. She talked about how strangers actually welcome the chance to help her, because it makes them feel they have done something noble. She talked about the adventurous life she once led.

Ms. Purdy grew up in Brixton, south London, with a father who was a peripatetic inventor and a mother who stayed home to look after her and her four siblings. She went to the University of Birmingham but left when she realized how lucrative her part-time job, selling ads for the Yellow Pages, was. And thus began an era of impetuous traveling to unlikely places, like Oslo and Houston, and then talking her way into unlikely jobs, like dancing in a club in Japan, running a road-safety project for 8- to-12-year-olds in Hong Kong and working as a music journalist and travel brochure writer in Singapore, where she and Mr. Puente met.

She does not want to talk about death, but the fact is always there. She has primary progressive, rather than relaxing-remitting, multiple sclerosis, meaning that her condition is inexorably worsening. Sometimes she chokes when she swallows. She has not been upstairs in her own house in two years. She needs help cooking, cleaning and shopping.

Mr. Puente, 47, who teaches and travels the world playing music, was away but spoke by telephone later. “Debbie was the woman I chose to be my wife,” he said. “I’ve seen the whole process, from when she was a very strong woman with a wonderful big bottom and strong legs, to using a walking stick to a wheelchair. She is still articulate and enthusiastic and full of life. She doesn’t want to die.”

He does not want her to die either, and especially not alone. But, he added: “I love that woman and I don’t want her to suffer badly. Apart from everything else, she wants to control her life and make her own decisions.”

Mr. Puente is a big bear of a man, and he has a jazz musician’s sense of improvisation and possibility, a way of grasping happiness in the present. He often tells Ms. Purdy that, as her husband, it is his job to make sure her life is not unbearable.

Fifteen years ago, she lost control of her bowels for the first time. “I wanted to die,” she recalled. “I was in floods of tears and Omar sat down and said, ‘What’s wrong?’ and he laughed. And I said, ‘How can you laugh at me?’ And he said: ‘It’s your choice, either I’ll cry with you or laugh at you.’ ”

Not long ago, a team of nurses came in to install the hoist that helps Ms. Purdy in and out of bed.

“He was laughing,” Ms. Purdy said. “The nurses threw him out of the room when we were trying it out, because he was acting like it was a sex toy.”

BUT when you have a progressive disease, time moves in the wrong direction. If Ms. Purdy exhausts her options and cannot get the assurance she needs from the government, she is prepared to go to Switzerland alone, she said. But she would have to do it while she is still physically able, which would be long before she is ready to die, she said.

She has worked out all the logistics, including how to get the $6,000 the trip would cost. That does not mean she will do it; she just wants the choice.

“I don’t want to kill myself,” she said. “I don’t want to go to Switzerland and end my life early. But this is a security blanket.”

She thinks often about what she can withstand. At what point does a life slip from manageable to untenable?

“When I was 20 and jumping out of airplanes, I thought being in a wheelchair would be unbearable,” Ms. Purdy said. “But it’s not. I thought asking people for help would be horrible and unbearable.

“But what I consider dignity has changed, and what I consider unbearable and horrible has changed,” she said. “Having a stranger pick me up off my bathroom floor, that’s not undignified. What is undignified is having a stranger say that I have no control over my own life.”