An Immune Disorder at the Root of Autism

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Hi : this might be the link that ties it all together...our modern society:------------------------------------------------------------------------------------------------------------------------------This phenomenon of a modern society eliminating the parasites in our systems causing an increase in diseases has been studied with crohns...more primitive cultures have no crohns...but they have parasites that keep the immune system busy working over the "worms"...they have even created studies where they introduce the parasites as a fix for crohns...I

can imagine a day where we have to take our daily dose of worms to regulate inflammation diseases... I sure hope they hurry up!!

An example of modern

cleaning methods creating new and wonderful diseases..Go ahead and grab that public bathroom door handle....you will be healthier for it! sounds like certain parasites are beneficial to a healthy system! Who Knew..." a worm a day keeps the inflammation away"======================================================== An Immune Disorder at the Root of AutismBy MOISES VELASQUEZ-MANOFFPublished: August 25, 2012FACEBOOKTWITTERGOOGLE+E-MAILSHAREPRINTSINGLE PAGEREPRINTSIN recent years, scientists have made extraordinary advances in understanding the causes of autism,

now estimated to afflict 1 in 88 children. But remarkably little of this understanding has percolated into popular awareness, which often remains fixated on vaccines.Eleanor So here’s the short of it: At least a subset of autism

— perhaps one-third, and very likely more — looks like a type of inflammatory disease. And it begins in the womb.It

starts with what scientists call immune dysregulation. Ideally, your immune system should operate like an enlightened action hero, meting out

inflammation precisely, accurately and with deadly force when necessary, but then quickly returning to a Zen-like calm. Doing so requires an optimal balance of pro- and anti-inflammatory muscle.In

autistic individuals, the immune system fails at this balancing act. Inflammatory signals dominate. Anti-inflammatory ones are inadequate. A state of chronic activation prevails. And the more skewed toward inflammation, the more acute the autistic symptoms.Nowhere

are the consequences of this dysregulation more evident than in the autistic brain. Spidery cells that help maintain neurons — called astroglia and microglia — are enlarged from chronic activation. Pro-inflammatory signaling molecules abound. Genes involved in inflammation are switched on.These

findings are important for many reasons, but perhaps the most noteworthy is that they provide evidence of an abnormal, continuing biological process. That means that there is finally a therapeutic target for a disorder defined by behavioral criteria like social impairments, difficulty communicating and repetitive behaviors.But

how to address it, and where to begin? That question has led scientists

to the womb. A population-wide study from Denmark spanning two decades of births indicates that infection during pregnancy increases the risk of autism in the child. Hospitalization for a viral infection, like the flu,

during the first trimester of pregnancy triples the odds. Bacterial infection, including of the urinary tract, during the second trimester increases chances

by 40 percent.The

lesson here isn’t necessarily that viruses and bacteria directly damage

the fetus. Rather, the mother’s attempt to repel invaders — her inflammatory response — seems at fault. Research by ,

an expert in neuroimmunity at Caltech, demonstrates this important principle. Inflaming pregnant mice artificially — without a living infective agent — prompts behavioral problems in the young. In this model, autism results from collateral damage. It’s

an unintended consequence of self-defense during pregnancy.Yet

to blame infections for the autism epidemic is folly. First, in the broadest sense, the epidemiology doesn’t jibe. Leo Kanner first described infantile autism in

1943. Diagnoses have increased tenfold, although a careful assessment suggests that the true increase in incidences is less than half that. But in that same period, viral and bacterial infections have generally declined. By many measures, we’re more infection-free than ever before in human history.Better

clues to the causes of the autism phenomenon come from parallel

“epidemics.†The prevalence of inflammatory diseases in general has increased significantly in the past 60 years. As a group, they include asthma, now estimated to affect 1 in 10 children — at least double the prevalence of 1980 — and autoimmune disorders, which afflict 1 in 20.Both are linked to autism, especially in the mother. One large Danish

study, which included nearly 700,000 births over a decade, found that a mother’s rheumatoid arthritis, a degenerative disease of the joints, elevated a child’s risk of autism by 80 percent. Herceliac disease,

an inflammatory disease prompted by proteins in wheat and other grains,

increased it 350 percent. Genetic studies tell a similar tale. Gene variants associated with autoimmune disease — genes of the immune system

— also increase the risk of

autism, especially when they occur in the mother.In some cases, scientists even see a misguided immune response in action. Mothers of autistic children often have unique antibodies that

bind to fetal brain proteins. A few years back, scientists at the MIND Institute, a research center for neurodevelopmental disorders at the University of California, , injected these antibodies into pregnant

macaques. (Control animals got antibodies from mothers of typical children.) Animals whose mothers received “autistic†antibodies displayed repetitive behavior. They had trouble socializing with

others in the troop. In this model, autism results from an attack on the developing fetus.But there are still other paths to the disorder. A mother’s diagnosis of asthma or allergiesduring the second trimester of pregnancy increases her child’s risk of autism.So does metabolic syndrome, a disorder associated with insulin resistance, obesity and,

crucially, low-grade inflammation. The theme here is maternal immune dysregulation. Earlier this year, scientists presented direct evidence of this prenatal imbalance. Amniotic fluid collected from Danish newborns who later developed autism looked mildly inflamed.Debate

swirls around the reality of the autism phenomenon, and rightly so. Diagnostic criteria have changed repeatedly, and awareness has increased. How much — if any — of the “autism epidemic†is real, how much artifact?YET when you consider that, as a whole, diseases of

immune dysregulation have increased in the past 60 years — and that these disorders are linked to autism — the question seems a little moot.

The better question is: Why are we so prone to inflammatory disorders? What has happened to the modern immune system?=========================================================== An Immune Disorder at the Root of AutismPublished: August 25, 2012FACEBOOKTWITTERGOOGLE+E-MAILSHAREPRINTSINGLE PAGEREPRINTS(Page 2 of 2)There’s

a good evolutionary answer to that query, it turns out. Scientists have

repeatedly observed that people living in environments that resemble our evolutionary past, full of microbes and parasites, don’t suffer from

inflammatory diseases as frequently as we do.Generally

speaking, autism also follows this pattern. It seems to be less prevalent in the developing world. Usually, epidemiologists fault lack of diagnosis for the apparent absence. A dearth of expertise in the disorder, the argument goes, gives a false impression of scarcity. Yet at least one Western doctor who specializes in autism has explicitly noted that, in a Cambodian population rife with parasites and acute

infections, autism was nearly nonexistent.For

autoimmune and allergic diseases linked to autism, meanwhile, the evidence is compelling. In environments that resemble the world of yore,

the immune system is much less prone to diseases of dysregulation.Generally,

the scientists working on autism and inflammation aren’t aware of this —

or if they are, they don’t let on. But Becker, a geneticist at the National Institutes of Health,

has pointed out that

asthma and autism follow similar epidemiological patterns. They’re both

more common in urban areas than rural; firstborns seem to be at greater

risk; they disproportionately afflict young boys.In

the context of allergic disease, the hygiene hypothesis — that we suffer from microbial deprivation — has long been invoked to explain these patterns. Dr. Becker argues that it should apply to autism as well. (Why the male bias? Male fetuses, it turns out, are more sensitive

to Mom’s inflammation than females.)More recently, at

Duke University has chimed in. He’s not, by training, an autism

expert. But his work focuses on the immune system and its role in biology and disease, so he’s particularly qualified to point out the following: the immune system we consider normal is actually an evolutionary aberration.Some

years back, he began comparing wild sewer rats with clean lab rats. They were, in his words, “completely different organisms.†Wild rats tightly controlled inflammation. Not so the lab rats. Why? The wild rodents were rife with parasites. Parasites are famous for limiting inflammation.Humans

also evolved with plenty of parasites. Dr. and many others think

that we’re biologically dependent on the immune suppression provided by

these hangers-on and that their removal has left us

prone to inflammation. “We were willing to put up with hay fever, even some autoimmune disease,†he told me recently. “But autism? That’s it! You’ve got to stop this insanity.â€What

does stopping the insanity entail? Fix the maternal dysregulation, and you’ve most likely prevented autism. That’s the lesson from rodent experiments. In one, Swiss scientists created a lineage of mice with a genetically reinforced anti-inflammatory signal. Then the scientists inflamed the pregnant mice. The babies emerged fine — no behavioral problems. The take-away: Control inflammation

during pregnancy, and it won’t interfere with fetal brain development.For

people, a drug that’s safe for use during pregnancy may help. A probiotic, many of which have anti-inflammatory properties, may also be of benefit. Not coincidentally, asthma researchers are arriving at similar conclusions; prevention of the lung disease will begin with the pregnant woman. Dr. has more radical ideas: pre-emptive restoration of “domesticated†parasites in everybody — worms developed solely for the purpose of correcting the wayward, postmodern immune system.Practically speaking, this seems beyond improbable. And yet, a trial is under way at the Montefiore Medical Center and the Albert Einstein College of Medicine testing a medicalized parasite called Trichuris suis in autistic adults.First used medically to treat inflammatory bowel disease, the whipworm, which is native to pigs, has anecdotally shown benefit in autistic children.And

really, if you spend enough time wading through the science, Dr. ’s idea — an ecosystem restoration project, essentially — not only

fails to seem outrageous, but also seems inevitable.Since

time immemorial, a very specific community of organisms — microbes, parasites, some viruses — has aggregated to form the human superorganism. Mounds of evidence suggest that our immune system anticipates these inputs and that, when they go missing, the organism comes unhinged.Future

doctors will need to correct the postmodern tendency toward immune dysregulation. Evolution has provided us with a road map: the original accretion pattern of the superorganism. Preventive medicine will need, by strange necessity, to emulate the patterns from deep in our past.« PREVIOUS PAGE 1 2Moises Velasquez-Manoff is the author of “An Epidemic of Absence: A New Way

of Understanding Allergies and Autoimmune Diseases.â€==============================================================----------------------------------------------------------------------------------------------------------------------------Subject: Re: Is this normal?To: erythema_nodosum_Group Date: Tuesday, August 28, 2012, 1:09 PM

Hi W,I have always thought that while we all seem to have different triggers, we must all have some sort of genetic predisposition that makes us sensitive to things that the vast majority of people shrug off with no ill effect. Only medical research is going to find out if that is true, and if so, what it is and how to "cure " it. I also think that all the related disorders like sarcoidosis and IBD and maybe even PG will be helped by a research finding a commonality that links them. If it were found that all of us shared a genetic defect the expressed itself in different ways AND EN, maybe there would be a way to repair this defect or at least keep it from expressing itself. Until that time, keeping a good attitude is probably one of the best things we can do to make the best of the cards we've been dealt...whether a mild form of EN or the more debilitating and serious PG.Thanks for that info on PG, W. And it is nice to have a

guy in the group, as it gives us a different perspective. ;-)Love, > > Subject: Is this normal?> To: erythema_nodosum_Group > Date: Monday, August 27, 2012, 1:38 PM> > > > > > > > > > > > > > > > > Â > > > > > > > I have recently suffered my first bout of EN. The severe swellings on my legs and one arm have gone down and the bruising is slowly fading. However I still feel quite unwell. My joints ache, particularly my shoulders, wrists, knees and ankles, I get pains over my eye, (although they don't last long), my skin itches and I feel very tired after a small amount of activity, despite getting a full nights sleep. Is this normal after a bout of

EN? I am beginning to feel like a real moaner so have stopped telling people how I feel and just try to get on with things but I'm not sure how long I can keep this up. I eat a good balanced diet, lots of fruit and veg and have started taking vitamin d and omega 3. I just want to know if this is normal or shoul I ask the dr for more investigations. > > Any info gladly received.> > > > Best wishes> > Sue> ======================================================> > > > > Pyoderma Gangrenosum (or PG)> This Skin Disorder Of Unknown Cause Is Related To IBD.By Amber J. Tresca, About.com GuideUpdated August 09, 2010> There are many complications that can occur with Inflammatory Bowel > Disease (IBD) including arthritis, liver disease, nutritional disorders,> anemia, and skin disorders. Skin disorders are a fairly common >

problem, and may affect up to 25 percent of people who suffer from IBD. > One type of skin disorder that may occur in IBD is pyoderma gangrenosum.> > What is pyoderma gangrenosum?> Pyoderma gangrenosum is a skin disorder that affects about 5 percent > of people with ulcerative colitis and about 1 percent of people with > Crohn's disease. Other diseases associated with pyoderma gangrenosum > include rheumatoid arthritis, myeloid blood dyscrasias, and hepatitis. > Pyoderma gangrenosum may first appear as a blister, red bump, or > pustule, and eventually forms an ulcer. The ulcers may appear alone or in a group, and are commonly found on the extremities (more frequently on the legs than on the arms).> > How does it start?> Pyoderma gangrenosum may start rapidly at the location of a previous > minor injury, such as a pinprick or cut. The surrounding skin breaks

> down, and an ulcer quickly forms. Pyoderma gangrenosum ulcers have > unique purplish-colored, indistinct edges. They also tend to be quite > painful as well as slow to heal. Doctors are unsure what causes pyoderma> gangrenosum, but theorize that it may be an autoimmune condition, as it> is related to other autoimmune disorders.> > How is pyoderma gangrenosum related to IBD?> As many as 50 percent of the cases of pyoderma gangrenosum occur in > people with one form of IBD. At times, the occurrence of these ulcers > corresponds to an active flare-up of IBD, and may respond when the > underlying IBD is treated. Other cases, however, do not appear to be > directly related to disease activity, and pyoderma gangrenosum may begin> or even worsen when the IBD is quiescent.> > How are the ulcers treated?> To confirm the diagnosis of pyoderma

gangrenosum through diagnostic > testing, a dermatologist may be consulted. The ulcers may be swabbed and> cultured to test for infections, and biopsies may be used to rule out > other causes. Because pyoderma gangrenosum is not caused by a bacterium,> antibiotics may not be effective as treatment.> > Smaller pyoderma gangrenosum ulcers may be treated with:> Compression bandagingSteroid creams or injectionsOral anti-inflammatory antibioticsDressings of silver sulphadiazine cream or hydrocolloids> > Larger ulcers that resistant treatment may require more intense therapy with:> SteroidsCyclosporinCyclophosphamideMethotrexateTacrolimus ointment> > ==============================================================> > > > Prevention> > > > > > You can't prevent pyoderma gangrenosum. If you have the

condition, try > to avoid injuring your skin. Injury or trauma to your skin can provoke > new ulcers to form. > > > > ==============================================================> Treatment> > > If you have an underlying disease associated with pyoderma gangrenosum,> treating that condition may help control the ulcers. However, other > treatments may be necessary to heal the wounds. > > > Drugs> > Your doctor may prescribe the following: > > Corticosteroids. Corticosteroids help relieve > inflammation. Usually pyoderma gangrenosum is treated with oral > corticosteroids, such as prednisone. Side effects of corticosteroids may> include increased blood pressure, weight gain with fat deposits in your> abdomen, face and back of your neck, and increased risk of infection. > In some

milder cases, a topical steroid â€" a medication you apply to your> skin â€" may be used. Side effects may include skin thinning and acne.Immunosuppressant drugs. These drugs help calm the> autoimmune response in your skin, which reduces inflammation. Because > these drugs suppress your immune system, they can place you at higher > risk of infections.Nonsteroidal anti-inflammatory medications. > Medications in the sulfone family, such as dapsone, are often used. > Milder cases might involve using minocycline, an anti-inflammatory and > antibiotic medication.Tumor necrosis factor inhibitors. Drugs such as > infliximab (Remicade), etanercept (Enbrel) and adalimumab (Humira) have > shown some success in treating pyoderma gangrenosum, especially in > people who have associated inflammatory bowel disease. Remicade is given> by infusion, and Enbrel and Humira are given as

injections. These drugs> also can make you more vulnerable to infection and to certain cancers.High-dose intravenous immunoglobulin. When > corticosteroids aren't enough to control pyoderma gangrenosum, > intravenous immunoglubulin has shown promise as a treatment.> > As your skin heals, you'll likely taper off the corticosteroids or > immunosuppressants. You can expect your skin to recover several months > after beginning therapy. Without treatment, the ulcers may widen, remain> the same or slowly heal. > > > > =========================================================> > SKIN DISORDERS COMMONLY SEEN IN IBD> ERHTHEMA NODOSUM> The name literally means “red bumps.� These tender red nodules, which> usually appear over the shins or ankles and sometimes on the arms, > occur most in people with ulcerative colitis

(2%-4%), although they may > also affect those with Crohn’s disease of the colon (1%-2%). Women are > more commonly affected than men. Erythema nodosum generally appears in > conjunction with a flare-up of IBD, but it also may occur just before a > flare-up. It tends to improve when the bowel disease is brought under > control.> > PYODERMA GANGRENOSUM> This condition is marked by pus in the skin associated with deep > ulcerations. Like erythema nodosum, pyoderma gangrenosum is most often > found on the shins or ankles but sometimes occurs on the arms, too. > Beginning as small blisters, these lesions eventually join together to > form into deep,chronic ulcers. The disorder is somewhat more common > among people with ulcerative colitis (5%) than those with Crohn’s > disease (1%). Pyoderma gangrenosum often follows a similar course to

the> pattern of the IBD itself, and may heal as the symptoms of IBD are > brought under control. Antibiotics, injections of medications into the > ulcers, and topical ointments all may be used as treatments.> > > ENTEROCUTANEOUS FISTULAS> A fistula is a small tunnel connecting two parts of the body. An > enterocutaneous fistula is an abnormal channel from the intestine to the> skinâ€"often from the rectum to the vagina, bladder, or buttocks. It also> may be a complication of surgery. This type of fistula may leak pus or > fecal matter. Fistulas are more common in Crohn’s disease than in > ulcerative colitis, affecting approximately 30% of people with Crohn’s. > Treatment depends on the location and severity of fistulas.> > > SKIN TAGS> Skin tags are fairly common in people with Crohn’s disease. They >

develop around hemorrhoid swellings in and around the anus. When the > swellings go down, the skin around them thickens and forms into small > flaps. Fecal matter may attach to skin tags, irritating the skin. > Practicing good hygiene will help reduce discomfort and calm the > irritation. Surgical removal o>