Damping Down Diabetes

PrevalenceSRxA’s Word on Health was very excited to learn of some amazing new research coming out of UC San Francisco.  Scientists there have identified a new way to manipulate the immune system and keep it from attacking the body’s own molecules in autoimmune diseases such as type 1 diabetes, rheumatoid arthritis and multiple sclerosis.

More than 100 different autoimmune diseases have been discovered and they disproportionately affect women.  Of the 50 million Americans living and coping with autoimmune disease  more than 75% are women.  Autoimmune diseases are one of the top 10 leading causes of death of women under the age of 65 and are responsible for more than $100 billion in direct health care costs annually.   Crohn’s disease, ulcerative colitis, lupus, multiple sclerosis, rheumatoid arthritis, psoriasis and scleroderma by themselves account for > $50 billion.

eTACBut now, researchers, led by immunologist Mark Anderson, MD, PhD, a professor with the UCSF Diabetes Center, have discovered a type of immune cell called an extrathymic Aire-expressing cell (eTAC), which puts a damper on immune responses.  eTAC’s are a type of  dendritic cell – which make up less than 3% of the cells in the immune system. And, eTAC cells themselves account for a small fraction of all dendritic cells. eTACs reside in lymph nodes and spleen in both humans and mice.

In this study, Anderson’s team determined that eTAC’s can counteract the overactive immune response in autoimmune diseases and, in a mouse model of diabetes, can be manipulated to stop the destruction of the pancreas.

By displaying “self” molecules to T cells that target them, and permanently turning off these T cells, eTACs help the immune system tolerate the molecules naturally present within us.  “The mouse model we are working with involves using T cells that normally attack the islet cells of the pancreas, specifically by recognizing a molecule called chromagranin A that is present on islet cells,” Anderson said. “But if the eTACs can get to the T cells first and display chromagranin A, they can prevent T cells from attacking the islets.”

mouse diabetesAnderson aims to exploit eTACs therapeutically by finding out how to grow them in large numbers outside the body. “We need to figure out how to grow a lot of these cells, to load them up with whatever molecule it is that we want to induce tolerance to, and then to load them back into a patient,” he said. “Such a strategy could help selectively shut down an unwanted immune response, such as the anti-islet immune response in type 1 diabetes.”

Dendritic cells work with T cells a bit like a sheriff working with a bloodhound.  But instead of presenting an article of clothing, dendritic cells present a specific molecule. If the molecule displayed by the dendritic cell matches the one the T cell was born to target, then that T cell would be activated to expand its numbers and to attack cells or tissues where the molecule is present.

When the interaction is between eTACs and T cells, however, the targeted T cell instead is turned off forever, and never seeks its molecular prey.

Diabetes wordcloudGiven that the prevalence and incidence of and type 1 diabetes and other autoimmune diseases, such as Crohn’s, lupus and celiac disease are on the rise, this new research is extremely important, both from a public health and economic perspective.  With as many as three million Americans having type one diabetes and the incidence growing by more than 3% per year a cure is desperately needed.

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You Can Teach an Old Drug New Tricks

Drug discovery is a laborious process.

From initial discovery of a promising target to the final medication becoming available, is an expensive, and lengthy process. At present, the costs of bringing a single new drug to market is around $1.2 billion, an amount that doubles every five years.

Aside from the cost, it takes, on average, 12 years for an experimental drug to progress from bench through FDA approval to market.

Annually, North American and European pharmaceutical industries invest more than $40 billion to identify and develop new drugs. Even so, for every 5,000 compounds that enter pre-clinical testing, only five, on average, are tested in human trials, and only one of these five receives approval for therapeutic use.

So, it’s hardly surprising that many pharmaceutical companies are choosing to take a closer look at old drugs. Last week, SRxA’s Word on Health brought you news of a host of potential new uses for aspirin.

And aspirin is not alone.  Old drugs often get a surprising second shot at life. In the past few weeks, the news has buzzed about the skin cancer drug – bexarotene – that may cure Alzheimer’s; a common antimalarial drug – hydroxychloroquine – that may help to destroy cancerand, a leukemia drug that inhibits the Ebola virus.

Then, of course, there’s the personal favorite of many women – Latisse.  Originally developed as a glaucoma treatment , it was found to have the desirable side effect of making eyelashes fuller and longer and is now FDA approved for this purpose.

Testing drugs already approved for one use to see if they can treat other conditions, can reduce time and money. Since these known drugs have already undergone toxicology and safety testing, the clinical development program can be streamlined.

Sometimes it’s pure serendipity.

Take Viagra for example. Although these days it’s the stuff of pharmaceutical industry legend , in the early 1990s, it was just a chest pain drug that wasn’t performing very well in clinical trials. So how did the little blue pill go from heart to crotch?  Pfizer was ready to call it quits when they decided to look into one unexpected but common side effect: long-lasting erections. Then came the drug patent and the rest is history.

The discovery that lithium could be used to treat manic episodes in bipolar patients was equally fortuitous. In 1949, Australian psychiatrist John Cade was injecting guinea pigs with urine extracts from schizophrenia patients to try and isolate a compound that caused mental illness. By accident he happened to use a compound with lithium – which at the time was used as a treatment for gout, as the control. Although he didn’t find the compound that caused mental illness, he did find one that treated it!

Back in 2010 we reported on the repurposing of thalidomide. Although the drug caused serious birth defects when it was launched in the 1960’s as a morning sickness pill it has since been found to be useful in reducing severe and frequent bleeding in patients with  hemorrhagic telangiectasia (HHT); in the treatment of patients with newly diagnosed multiple myeloma when taken  in combination with dexamethasone; and for the acute treatment of the cutaneous manifestations of moderate to severe erythema nodosum leprosum

The National Institutes of Health (NIH) recently established The Learning Collaborative (TLC) to study how to more easily repurpose known drugs to treat rare forms of blood cancers.

TLC is a dedicated collaboration between the NIH Chemical Genomics Center (NCGC) and its Therapeutics for Rare and Neglected Diseases (TRND) program, The Leukemia & Lymphoma Society (LLS), and Kansas University Cancer Center (KUCC) to discover and develop new drug therapies for rare blood cancers. TLC is creating a pipeline of new therapies to treat leukemia from both the discovery of new treatments as well as identifying new uses for approved and abandoned drugs.  For example, Auranofin, a drug originally used for rheumatoid arthritis, is now in clinical trials for treating chronic lymphocytic leukemia.

Word on Health will continue to follow the drug recycling trend and bring you news as it breaks. In the meantime if you have noticed any beneficial side effects from the medicines you’re taking, we’d love to know.

There’s a Shot for That

On May 14, 1796 Edward Jenner injected fluid from the cowpox blisters on the hands of dairymaid Sarah Nelmes, into James Phipps, an 8-year-old boy.  Jenner hoped the fluid from the cowpox lesion would somehow inoculate the boy against the smallpox scourge which at the time was killing over 400,000 Europeans a year. His hunch proved correct.

Today vaccines save 3 million lives per year worldwide. By training the human immune system to recognize and ward off dangerous pathogens, vaccines can protect against disease for decades, or even for a lifetime. Preventive vaccines work by introducing harmless microbial chemical markers, known as antigens, which resemble the markers on living microbes. The antigens train the immune system to recognize and destroy those microbes should they ever appear in the body. By injecting cowpox antigens into Phipps bloodstream, Jenner primed his immune system to attack the similar smallpox virus.

Now, medical scientists are taking Jenner’s ideas in a whole new direction. By exploiting a growing understanding of the immune system they are developing therapeutic vaccines targeting established diseases rather than trying to prevent them.

Last spring, the FDA approved Provenge, a personalized immunotherapy that activates a patient’s own immune cells to target and attack advanced prostate cancer. To make the Provenge prostate cancer vaccine, biochemists at Seattle’s Dendreon Corporation extract a sample of a patient’s own immune cells and bathe them in a chemical soup of prostate cancer antigens that are chemically linked to a cytokine that screams, “Attack this!”.  The activated immune cells are then injected back into the patient’s body to spread the call to arms.

While Provenge was the first of the new generation of therapeutic vaccines, it’s certainly not the last. BCC Research has identified 113 therapeutic vaccines in development, many of which are already in human trials. They even go so far as to estimate that the market for therapeutic vaccines will have an annual growth rate of 115% and reach an estimated $2.9 billion in 2014.

Other cancer vaccines are among the front runners. With a near-endless supply of patients willing to undergo novel treatments, cancer researchers have been among the most aggressive in experimenting with therapeutic vaccination. The Cancer Vaccine Collaborative is working on treatments that target multiple cancer antigens, which should trigger a more aggressive immune response and increase the odds of defeating tumors. All of which is good news for the 1.5 million Americans diagnosed with cancer each year.

While cancers cause a proliferation of diseased cells, some autoimmune diseases, cause the cells of the immune system to turn against healthy tissues. In diabetes, for example, the immune system attacks insulin-making pancreatic beta cells.

In multiple sclerosis, it’s the myelin sheaths that are designed to protect the nerves that come under attack.

Autoimmune vaccines hold the promise of shutting down these attacks. One promising approach boosts T-regulatory cells, a subgroup of the white blood cells. At the University of Calgary’s Diabetes Research Centre in Alberta, immunologist Pere Santamaria has attached a cocktail of antigens from pancreatic beta cells to synthetic iron oxide nanoparticles. This stimulates the development of T-regulatory cells into killer T cells that destroy the immune cells which cause the serial killer like autoimmune attack.

Santamaria’s team recently tested his vaccine in diabetes-prone mice. It restored normal blood sugar and insulin levels in animals that already had diabetes and prevented or slowed its onset in young mice that had not yet developed the disease. The team is now readying the vaccine for human trials and is designing related vaccines to treat other autoimmune diseases, including multiple sclerosis, rheumatoid arthritis, and inflammatory bowel disease.

If effective, such therapeutic vaccines could help the three million Americans with type 1 diabetes and the 400,000 people diagnosed with multiple sclerosis. Vaccines against dust mites and asthma are also in the works.

Some of the new therapeutic vaccines are actually designed to attack the body, albeit in a selective way. A new experimental heart-disease vaccine takes aim at unwanted biochemicals within the body, specifically low-density lipoprotein (LDL), better known as bad cholesterol. When large quantities of LDL cholesterol circulate through the bloodstream, it can be deposited on artery walls, leading to a buildup of plaque and triggering inflammation. Anti-cholesterol vaccines encourage the immune system to attack LDL and remove plaques. Scientists have also discovered that the vaccine lowers blood pressure and protects against the rupture of aneurysms, at least in mice.

Clinical trials in humans are expected to start later this year and if successful could help to prevent the 800,000+ deaths per year from cardiovascular disease.

Even more people could be helped by an anti-obesity vaccine. Nearly 75 million adults are classified as obese in the United States. Researchers are working on a vaccine that targets ghrelin – a gastrointestinal hormone that appears to stimulate appetite.

Others, are looking at vaccines to prevent addiction to cocaine, methamphetamines, opiates and nicotine.

It is too soon to know how and when these vaccines will come to market or how effective they will be, but it’s clear that therapeutic vaccines are coming and will be used against a host of the most prevailing public health issues of the 21st century.

T-A T-A to A-T?

SRxA’s Word on Health is delighted to share news that could change the lives of the 500 or so children and families in the US, dealing with a rare and deadly disease.  The breakthrough, announced this week in the online edition of Nature Medicine, suggests that scientists may have found a way to prevent and possibly reverse the most debilitating symptoms of ataxia telangiectasia (A-T) a rare, progressive childhood degenerative disease that leaves children, unable to walk, and in a wheelchair before they reach adolescence.

As regular readers of this blog know, A-T is a cause close to our hearts, and the courage of these children and their families inspire us daily.

Karl Herrup, chair of the Department of Cell Biology and Neuroscience and his colleagues at Rutgers have discovered why this genetic disease attacks certain parts of the brain, including those that control movement coordination, equilibrium, muscle tone and speech.

When the team examined the brain tissue of young adults who died from A-T, they found a protein (HDAC4) in the nucleus of the nerve cell instead of in the cytoplasm where it belongs. When HDAC4 is in the cytoplasm it helps to prevent nerve cell degeneration; however, when it gets into the nucleus it attacks histones – the small proteins that coat and protect the DNA.

What we found is a double-edged sword,” said Herrup. “While the HDAC4 protein protected a neuron’s function when it was in the cytoplasm, it was lethal in the nucleus.”

To prove this point, Rutgers’ scientists analyzed mice, genetically engineered with the defective protein found in children with A-T, as well as wild mice. The animals were tested on a rotating rod to measure their motor coordination. While the normal mice were able to stay on the rod without any problems for five to six minutes, the mutant mice fell off within 15 to 20 seconds.

However, after being treated with trichostation A (TSA), a chemical compound that inhibits the ability of HDAC4 to modify proteins, they found that the mutant mice were able to stay on the rotating rod without falling off – almost as long as the normal mice.

Although the behavioral symptoms and brain cell loss in the engineered mice are not as severe as in humans, all of the biochemical signs of cell stress were reversed and the motor skills improved dramatically in the mice treated with TSA. This outcome proves that brain cell function could be restored.

Neurological degeneration is not the only life-threatening effect associated with A-T. The disease, which occurs in an estimated 1 in 40,000 births, causes the immune system to break down and leaves children extremely susceptible to cancers such as leukemia or lymphoma. There is no known cure and most die in their teens or early 20s.

Herrup says although this discovery does not address all of the related medical conditions associated with the disease, saving existing brain cells and restoring life-altering neurological functions would make a tremendous improvement in the lives of these children.

 “We can never replace cells that are lost,” said Herrup. “But what these mouse studies indicate is that we can take the cells that remain in the brains of these children and make them work better. This could improve the quality of life for these kids by unimaginable amounts.”

A-T families are cautiously excited by the news. The A-T Children’s Project facebook page notes “This is certainly hopeful news, and we look forward to the results from further studies.”

We certainly do. A cure cannot come soon enough.

Hope for hard-to-match kidney patients

The first (unsuccessful) human-to-human kidney transplant took place 75 years ago.  Some 16 years later, the first successful human transplant took place. Now, according to the United Network for Organ Sharing (UNOS), there are currently 111,714 people in the US awaiting organ transplantation.  Approximately 20,000 of these are so called “hard-to-match” kidney transplant patients.

In other words, their immune systems will reject most kidneys because of antibodies circulating in their blood that react to proteins known as human leukocyte antigens (HLA). These proteins are found on most cells and are used by the immune system to recognize what is foreign to the body.

In HLA-sensitized patients, the body has been exposed to foreign HLA in the past, either through pregnancy, blood transfusion or previous kidney transplant. As such, it immediately recognizes most donor organs as unfamiliar. And, unless these antibodies can be removed, they will result in severe antibody mediated rejection (AMR) and early loss of the transplanted organ.

Apart from the scarcity of donor kidneys, the biggest barrier to kidney transplant is the percentage (nearly 1:3) of patients on the waiting list whose immune systems make them likely to reject most kidneys available to them. Highly HLA-sensitized patients are very difficult to match with less than 7% receiving transplants each year.

SRxA’s Word on Health was therefore interested to hear of a new study from Johns Hopkins which showed that desensitizing such patients with a combination of therapeutic plasmapheresis and intravenous immunoglobulin (IVIG) doubled their chance of survival eight years after transplant surgery, as compared with those who stay on dialysis awaiting compatible organs.

Additionally, the protocol enabled a dramatic 98% transplant rate rather than the traditional 7%.

The results of this study should be a game changer for health care decision makers, including insurance companies, Medicare and transplant centers,” said lead investigator Robert A. Montgomery, M.D., D. Phil. “There’s a dramatic survival benefit, so people should take note. If this were a cancer drug that doubled chances of survival, people would be lined up out the door to get it. It’s really extraordinary to go from 30 percent survival to 80 percent survival after eight years.”

Widespread use of the pre-surgery protocol developed at Johns Hopkins could potentially lead to 3,000 more kidney transplants from living donors each year. The protocol uses plasmapheresis to remove the HLA from the blood before the transplant, then the patient receives low-dose intravenous immune globulin (a human plasma protein) to replace the problematic antibodies and prevent their return. This process is performed every other day for several days before transplant and then for up to 10 days following the surgery.

Although the protocol has great benefit in living donor transplants, it cannot be used in patients receiving cadaver organs – where time is of the essence,  because several days of plasmapheresis and IVIG are needed before surgery can take place.

Additionally, the patient will still to take the same anti-rejection drugs as all other organ transplantation patients.

The desensitization protocol also makes kidney transplants more expensive, However, the cost savings when compared to remaining on dialysis are enormous. Better still, the patient no longer has to endure the difficulties of dialysis, a process that takes about five hours a day, three days a week, and which often makes the tasks of daily life from working to caring for children nearly impossible.

“This treatment increases survival, ensures a better lifestyle and saves the health care system money,” says Montgomery. “There aren’t many things like that.”

Let’s hope healthcare insurers are reading this and taking note.

Worming our way towards a Cure for M.S.?

Hot on the heels of our recent fecal transplant posting, SRxA’s Word on Health brings you news that might once again trigger your yuck factor.

According to an article in last week’s Wall Street Journal, help may be at hand, or maybe we should say “stomach” for people with multiple sclerosis – as the help is courtesy of  none other than parasitic worms.

Early safety studies conducted in the US suggest that the eggs of pig whipworms have anti-inflammatory properties that can reduce the size of brain lesions in MS patients. A similar trial is now under way in Denmark. And in Britain, academics at the University of Nottingham are studying the potential health benefits of hookworms.

If these trials prove successful, treatment with parasitic worms, or more correctly, helminthic therapy, could provide a simple, cheap, and controllable treatment for the debilitating condition, which affects 2.5 million people world-wide.

Multiple sclerosis is an inflammatory disease of the brain and spinal cord, in which an overactive immune system attacks the nerve fibers responsible for sending signals to the rest of the body. Its symptoms include impaired vision, muscle weakness and spasm, fatigue, memory loss and depression. Although a number of medications can slow the disease’s progression, many of them have unpleasant side effects including hair loss, muscle aches, sleeplessness and flu-like symptoms.

Interest in helminthic therapy surged in 2007 with the publication of an Argentina study which showed that the progression of multiple sclerosis was much slower in patients who carried parasitic worms in their intestines than in those who didn’t. Another recently published study in the Multiple Sclerosis Journal suggested that pig whipworm is effective in treating MS symptoms.

The results are quite promising,” says John Fleming, a professor of neurology at the University of Wisconsin School of Medicine and Public Health, who led the study.

Five patients took part in the Phase 1 trial. All were newly diagnosed with relapsing-remitting MS, a form of the disease in which new symptoms can appear and old ones resurface or worsen. Whipworm eggs were taken from disease-free pigs and grown in a clean laboratory environment. Every two weeks over the course of three months, the patients in the study drank 2,500 of the eggs mixed into a sports drink. The eggs hatched in the patient’s intestines and were killed by the immune system after about a week.  Patients who took part said the liquid was salty but didn’t taste or smell unpleasant.

During the study, patients underwent MRI scans, which tracked the number of new brain lesions that developed before, during and after they ingested the worm eggs.

What makes us optimistic is that brain lesions in four out of the five patients decreased over the course of the study and then rebounded after it finished,” says Dr. Fleming. While the pattern shown by the MRIs is encouraging, he adds, larger and longer studies will be needed before any definite conclusions are possible.

Researchers say the Wisconsin study’s findings could mean that the immune system’s over-response to the brain tissue was lessened by anti-inflammatory effects from the worms, and this could offer an alternative approach to treating MS.

The theory behind helmintic therapy is known as “the hygiene hypothesis.” This argues that developed countries such as the U.S., Europe and Japan have higher incidences of allergies and autoimmune diseases because the population has little or no exposure to parasites or infections. In developing countries, where people are exposed to low-level infections or infestations, the rates of such diseases are much lower.  Essentially, the proponents of this therapy argue, our immune system is created to be in balance with the worm’s influence on us.  Naturally, our body wants to fight the foreign nematode invaders, but the worms don’t like that and they’ve actually evolved to suppress our immune response to their presence.  That means that without them our immune system over-reacts to things that in its ancestral setting it would have ignored

We spoke to a friend of ours who has MS and asked, would you intentionally swallow worms if it would help control your disease? After some initial hesitation, she gave the idea the thumbs up.  “Although it sounds gross, it’s probably no worse than injecting myself every day with chemicals that I really know nothing about and which leave me looking like a pin cushion” she told us.

What about you?

Time to get a little dirty?

Rising levels of allergic asthma and eczema have scientists wondering if there is such a thing as being “too clean”.

“We see auto-immune diseases like asthma and eczema increasing rapidly in North American children, but we don’t see the same effect in children in the developing world,” says Dr. B. Brett Finlay, a professor in the Michael Smith Laboratories at the University of British Columbia.

This has led Finlay to embark on a new project called the Impact of the Microbiota on Immune Development and Disease.  Researchers will look at the role of intestinal microbiota (normal bacteria that live in our gut) on immune development and disease, including asthma and eczema.

This makes a lot of sense.  The gastrointestinal tract is  afterall the primary site of interaction between the host immune system and microorganisms, both symbiotic and pathogenic.

Some of our everyday habits such bleaching countertops or giving antibiotics to young children may be killing off good bacteria along with the bad bacteria.  This so-called ‘hygiene hypothesis’ claims that our desire to be ultra-clean may mean that kids aren’t getting the bacteria they need to have strong immune systems later in life.

Finlay has assembled a team to study and identify the various types of microorganisms that live in the gut. They will also track the health development of young children enrolled in the Canadian Healthy Infant Longitudinal Development Study (CHILD) in order to both better understand the role microbiota plays in the immune system, and development of autoimmune disease.

The goal will be to gain a genetic understanding of the bacteria that lives in and on the human body, specifically those found orally, on the skin, the gut, nasal/lung and vaginally.

Previous studies in humans have suggested that immunological dysregulation is the cause of many non-infectious diseases such as autoimmunity, allergy and cancer.  Gut microbes are thought to  play a role in preventing diseases such as obesity inflammatory bowel disease and type -1 diabetes.

Word on Health, will be following this story closely.  In the meantime we’re thinking a little less housework might not be a bad thing!

Columbus Day Musings

Those of us lucky enough to have vacation to mark Columbus Day may have time to think about the explorer who is widely credited with having discovered and colonized the Americas.  Here at Word on Health, we’ve been wondering which of the many nasty medieval diseases did Christopher Columbus suffer from?

According to most historians it wasn’t the usual suspects: plague, dysentery, typhoid or ergotism.

Until recently, most attributed his death, at the age of 55 to complications of gout.  However, new evidence from Dr. Antonio Rodriguez Cuartero, a professor at the University of Granada, paints a different picture.  After studying Columbus’ family history, personal diaries and the letters penned by Columbus’ son, the professor contends that all signs point to Reiter’s syndrome.

All sources seem to agree that during his later years, Columbus became increasingly incapacitated by pain in his joints, painful urination and bleeding from his eye.  One cannot blame the leech-applying physicians of his day, for attributing these symptoms to gout.  More than 500 years later we still don’t know much about Reiter’s syndrome, or “reactive arthritis’ as it is also known.

Some people think that it involves the immune system, which is “reacting” to the presence of bacterial infections in the genital, urinary or gastrointestinal systems, but the exact cause remains unknown.

Complications of Reiter’s include aortic insufficiency, left-sided heart failure, pulmonary edema and endocarditis, which may give further credibility to Cuartero’s theory that Columbus died of a heart attack.

Whatever the reason, we say Rest in Peace Christopher & Happy Columbus Day to all our readers!

Unlocking the Mystery of Autoimmune Disease

A key feature of the immune system is its ability to discriminate between self and non-self.

When the mechanisms that prevent the immune system from attacking itself break down, it can result in autoimmune disorders such as multiple sclerosis, rheumatoid arthritis, Crohn’s disease and diabetes.

Now researchers at Columbia University Medical Center claim they have not only found out why people with autoimmune diseases attack their own tissues and organs, but also how to correct the problem.

According to a study just published in The Journal of Clinical Investigation scientists have identified a defect in the T cell regulatory pathway which normally controls autoreactive T cells.  The majority of people with Type 1 diabetes who were tested were found to have a defect in CD8+ T cells that impacted their recognition of a common target structure known as HLA-E/Hsp60sp. More importantly, researchers were able to successfully correct the defect in-vitro.

For decades, autoimmune diseases have been treated by reducing overall immune response. That’s been effective in extending life spans, but has been hard on the quality of life for many of those patients,” said lead researcher Hong Jiang, M.D. Ph.D.

Current therapies for treating autoimmune disease include steroids, which systemically suppress the immune system, resulting in multiple side effects, including weight gain and increased susceptibility to infections.  Therapies based on this new research are designed to selectively suppress immune responses to self-antigens without damaging the body’s normal anti-infection and anti-tumor responses.

This research is significant. The Columbia University scientists believe that this greater understanding of the defect could eventually lead to prevention of autoimmune diseases altogether.

SRxA’s Word on Health is keeping everything crossed.

Lady Gaga Knows Her Autoimmune Quotient – Do You Know Yours?

Over the last two weeks the Web has been abuzz with questions about Lady Gaga’s health. Turns out, we are informed, that she has a family history of lupus and has tested borderline positive for the disease.

The Lady Gaga story underlines an important message for millions of other Americans who have a history of autoimmune disease in their families. According to Virginia Ladd, President and Executive Director of the American Autoimmune Related Diseases Association (AARDA) “Lupus is one of more than 100 autoimmune diseases and these diseases cluster in families.  Having a family member with lupus could mean you are at increased risk for lupus and other autoimmune diseases.

That’s why it’s important, just as Lady Gaga has done, to know your family history, to inform your doctors, and take proactive steps to ensure your future health.

Evidence suggests that people need to take responsibility for their own autoimmune health. An AARDA study of autoimmune patients found that the average time for diagnosis of a serious autoimmune disease is 4.6 years. During that period, the patient typically has seen 4.8 doctors; and 46% of the patients were told initially that they were too concerned about their health or that they were chronic complainers.

One of the factors that makes getting a correct autoimmune disease diagnosis so difficult is that symptoms can vary widely, notably from one disease to another, but even within the same disease. The medical community’s lack of knowledge of autoimmune disease compounds the problem. Even though these diseases share a genetic background and tend to run in families, most health questionnaires at doctors’ offices do not ask whether there is a family history of autoimmune disease.

AARDA has devised an eight-step plan to help people increase their awareness of autoimmune diseases and calculate their Autoimmune Quotient (AQ):

1. Understand that autoimmune disease constitutes a major U.S. health crisis affecting 50 million Americans.

2. Get educated about the 100+ autoimmune diseases.

3. Be aware that autoimmune diseases target women 75% more often than men.

4. Know that autoimmune diseases run in families.

5. Do your own family medical history and inform your physician if you find that you have a history of autoimmune disease.

6. Keep a “symptoms” list if you believe you may have an autoimmune
disease.

7. Realize that getting an autoimmune disease diagnosis is often
challenging.

8. Hold the power to protect your family’s future health and well-being
in your hands – be proactive about your health.

To find out more about autoimmune diseases, or how to calculate your AQ, visit the AARDA Web Site.