Heal Your Gut to Reverse Autoimmune Disease

Heal Your Gut to Reverse Autoimmune Disease

Source: GreenMedInfo.com
Ali Le Vere, B.S., B.S.
June 13, 2017

Health Begins In the Gut.  From a clinical standpoint, insofar as functional medicine is concerned, whether you present with rheumatoid arthritis, multiple sclerosis, ulcerative colitis, or systemic lupus erythematosus—the fundamental objective is the same: heal the gut.

Hippocrates understood the inextricably intertwined relationship between the systemic health of the organism and the nine-meter tube from mouth to anus when he famously uttered, “All disease begins in the gut” over two thousand years ago. The ancient Greek physician also illuminated his understanding of the therapeutic role of nutrition when he championed holistic medicine with his proclamation, “Let food be thy medicine and medicine be thy food”.

After all, covering an average surface area of thirty-two square meters, the size of half a badminton court, the gut represents the second largest interface between the external environment and the internal biochemical milieu of the body (Helander & Fandriks, 2014). Over sixty tons of food will pass through our gastrointestinal tract in our lifetime.

Why is gut health so paramount in prevention and treatment of autoimmune disease? If you are a savvy consumer of holistic health information, you probably already know how important our microbiome—the collection of one hundred trillion commensal bacteria that inhabit our colon, plus their genetic material—is to our health. Although the widely cited 10:1 ratio has been revised, researchers estimate that we have at least as many bacterial cells as human cells, which has led some scientists like Stanford’s Dr. Justin Sonnenberg to hypothesize that humans may merely be elaborate vessels designed for the propagation of bacterial colonies (Sender, Fuchs, & Milo, 2016).

At any single moment, two to six pounds of bacteria resides within us. Even more awe-inspiring is that a single person contains 3.8×10^13 bacteria (38,000,000,000,000 colony forming units)—a number representing more than all the stars in the galaxy (Sender, Fuchs, & Milo, 2016).

Following the advent of germ theory and the discovery of vaccinations, scientists were under the impression that all bacteria were bad bugs, and speculated that specific microbes were the causative agents behind particular disease entities. This led to the reductionist, pill-for-every-ill therapies that predominate in Western medicine, as well as to the maligning of all bacteria as organisms to be feared and eradicated. Thus the age of antibiotics, triclosan-laden anti-bacterial soaps, hand sanitizer, chemical cleaners, and the “there’s a shot for that” mentality was inaugurated.

Ironically, it is rumored that on his deathbed, Louis Pasteur, the father of immunization and pasteurization himself, admitted that it is the terrain—the gut ecology and biochemical milieu—that matters, rather than the infecting pathogen (Tracey, 2017). In other words, our bodies, like plants, are more susceptible to pests, or infection, when our ecosystem is in a state of disharmony—when our microbial soil is depleted and our micronutrient status is compromised.

The magic bullet approach initially introduced by Pasteur, however, was misguided, and has the potential to produce dire consequences for immune health. In fact, the hygiene hypothesis, embraced by many scientists, purports that the reason that autoimmune diseases and atopic disorders (eczema, allergies, asthma) are epidemic in the Western world while virtually absent from developing nations is the hyper-sanitized, antibiotic-ridden society in which we live, which has decimated our gut microflora and thus obliterated their beneficial effects on our immune systems (after all, 70% of our immune system resides within our gut) (Vighi et al., 2008).

According to the hygiene hypothesis, the immune system acquires self-tolerance, or the ability to distinguish self from stranger and safety from danger, and thus prevent overreactions against our own tissue, based on repeated infectious exposures (Eschler, Hasham, & Tomer, 2011). Further, “Some pathogens have the potential to prevent or abrogate rather than induce an autoimmune process,” such that annihilating them with antibiotics results in improper maturation of the immune system and a tendency towards autoimmune reactions (Christen, 2014).

However, antibiotics are not only harmful in that they prevent infections from instructing development of the immune system. They also disrupt the finely tuned symphony of actions orchestrated by our microbiota, or those friendly bugs that inhabit our gut. The microbiota serve innumerable roles, including competing for attachment sites with potentially pathogenic microbes, reducing their virulence, inhibiting the effects of bacterial toxins, and generating anti-microbial substances such as bacteriocidins and hydrogen peroxide that can selectively suppress pathogenic bacteria and fungi (Corr et al., 2009; Castagliuolo et al., 1999).

Our gut microbes also promote the de-conjugation and detoxification of proliferative, carcinogenic estrogen species and other exogenous toxins, reducing their enterohepatic recirculation (Gorbach, 1984). Commensal bacteria likewise aid in nutrient extraction and assimilation, as the secondary bile acids and short-chain fatty acids they produce from fermentation of indigestible carbohydrates lead to liberation of compounds like peptide YY from cells, which decreases intestinal transit, encourages satiety, maximizes nutrient absorption, and increases energy harvested from food (Boulange et al., 2016).

Critically, gut bacteria reinforce the intestinal barrier, preventing metabolic endotoxemia, a process which contributes to metabolic syndrome, non-alcoholic fatty liver disease (NAFLD), coronary heart disease, stroke, and polycystic ovarian syndrome (PCOS) (Neves et al., 2013; Lindheim et al., 2017). The products of microbial fermentation of prebiotic carbohydrates also increase insulin sensitivity and improve glucose balance, which prevents the pathologic insulin resistance, oxidative stress, and endothelial dysfunction that lead to diabetes and cardiovascular disease (Boulange et al., 2016).

The maintenance of the intestinal lining by the microbiota similarly prevents autoimmune disease. For instance, a decrease in bifidobacteria populations leads to intestinal hyperpermeability, or leaky gut, which in turn leads to the translocation of metabolic byproducts, food antigens, bacteria, and lipopolysaccharide (also known as LPS, an immunogenic cell wall component from Gram-negative bacteria) across the gut barrier into systemic circulation (Rapin & Wiernsperger, 2010). This activates the mesenteric lymph nodes and gut-associated lymphoid tissue (GALT) and instigates a downstream inflammatory cascade.

Medications Compromise Gut Barrier Integrity

A single course of antibiotics can lead to perturbations in microbiota lasting up to 16 months on average, or 18 to 24 months for Clindamycin and up to four years following triple therapy for Helicobacter pylori (Hawrelak & Myers, 2004; Jernberg et al., 2010; Cotter et al., 2012). Even worse, novel molecular analysis techniques using 16S rRNA have demonstrated that antibiotic-resistant microbes are present up to four years post-antibiotic (Jernberg et al., 2010; Cotter et al., 2012).

Other commonly used medicinal agents, non-steroidal anti-inflammatory drugs (NSAIDs) such as Motrin, Ibuprofen, and Naproxen, increase concentrations of gram-negative bacteria, which produce lipopolysacchide (LPS), the endotoxin that can traverse the gut barrier and generate a milieu favoring insulin resistance, type 2 diabetes, NAFLD, PCOS, coronary heart disease and stroke (Marlicz et al., 2014).

In addition to inducing gastrointestinal ulcers, increasing risk of myocardial infarction by a third, and doubling risk of congestive heart failure, NSAIDs have also been demonstrated to decrease concentrations of bifidobacteria and lactobacilli—beneficial commensal flora populations in our gut (Bhala et al., 2013; Montenegro et al., 2014). Because bifidobacteria are responsible for butyrate production, the short chain fatty acid that heals and seals the gut lining, a decrease in bifidobacteria can perpetuate leaky gut syndrome.

What’s more, acid-blocking drugs, or proton pump inhibitors (PPIs) such as Prilosec and Nexium, used for gastroesophageal reflux disease (GERD), are associated with a decrease in small bowel beneficial bifidobacteria and a significant decline in microbial diversity within seven days of beginning therapy (Seto et al., 2014; Wallace et al., 2011). PPIs have likewise been shown to increase the risk of small intestinal bacterial overgrowth (SIBO) and the potentially fatal infection, Clostridium difficile (Lo & Chan, 2013; Janarthanan et al., 2012).

With antibiotics in particular, however, there is evidence of localized permanent extinction—in other words, some species of microorganisms never recover post-antibiotic, and cannot be “reinoculated” unless you undergo the arduous and expensive process of fecal microbiota transplant (FMT).

Furthermore, even food preparation and processing can influence intestinal permeability. When food is browned or caramelized as part of the Maillard reaction, reducing sugars spontaneously react with lipids, nucleic acids, and aminopeptides, creating advanced glycation end products (AGEs) in a process that generates free radicals, inflammation, and ensuing intestinal permeability (Vlassara & Uribarri, 2004; Bengmark, 2007).

The Leaky Gut – Autoimmune Connection

The intestinal barrier is a mucosal surface wherein epithelial cells known as enterocytes are separated by tight junction proteins, desmosomes, and adherens junctions that function as architectural scaffolding and selective gates, opening and closing to allow fluid and nutrients to be absorbed and waste products to be excreted (Groschwitz & Hogan, 2009). According to Turner (2009), epithelial cells “establish a barrier between sometimes hostile external environments and the internal milieu” (p. 799). This barrier is critical because “The mucosa is directly exposed to the external environment and taxed with antigenic loads…at far greater quantities on a daily basis than the systemic immune system sees in a lifetime” (Mayer, 2003).

Tight junctions, regulated by a molecule called zonulin, as well as by conformational changes in the proteins occludin and claudin, are dynamic intercellular structures that modulate the trafficking or passage of macromolecules from the intestinal lumen to the submucosa and into systemic circulation (Fasano, 2012). According to Rapin and Wiernsperger (2010), “Tight junctions play a major role in regulating the paracellular passage of luminal elements” (p. 635).

Under normal circumstances, solutes exceeding a certain size, or molecular radius, are prohibited from absorption across the gut barrier by competent tight junctions (Fasano, 2012). However, when insults such as gluten, dysbiosis, pathogens, toxins, over-exercising, chemotherapy, radiation, and medications such as NSAIDs and steroids disrupt the tight junctions, microbial products and intact food proteins that have not been degraded into their constituent parts translocate across the paracellular space into the body (Fasano, 2012).

Macrophages embedded in the GALT are part of the innate immune system, or the non-specific, first line of defense against infection (Fasano, 2011; Yu & Yang, 2009). These cells, along with dendritic cells, recognize the incoming undigested food particles, toxic agents, and bacterial components as foreign invaders, and present them to cells of the adaptive immune system called T and B lymphocytes, leading to clonal expansion (proliferation or multiplication of specific subsets of T and B cells) and recruitment of more pro-inflammatory immune cells to the gut through a process called leukocyte homing.

The release of inflammatory cytokines, or intercellular signaling molecules such as interleukin-1 (IL-1), interleukin-2 (IL-6), and tumor necrosis factor alpha (TNF-α) at the site of immune activation causes other immune cells migrating throughout the lymphatic vessels of the body to express more cell adhesion molecules (CAMs). CAMS enable white blood cells to stick to and roll along blood vessels and extravasate, or navigate across, the blood vessels made leaky by histamine and other local vasodilators, into the inflamed intestinal tissue. Cytokines contribute to this vicious process of leaky gut syndrome, as they also play a prominent role in compromising tight junction integrity (Watson, Duckworth, Guan, & Montrose, 2009). This culminates in a massive inflammatory response that can become systemic and lead to autoimmunity.

When the amino acid sequence is homologous between the target antigen, such as gluten, against which the immune system is mounting a response, and tissue proteins, such as the thyroid tissue, a case of mistaken identity occurs, and the immune response can become directed against self tissues, manifesting as autoimmune disease (Hashimoto’s thyroiditis in this instance). Summarized by Suzuki (2013), “Disruption of the intestinal tight junction barrier, followed by permeation of luminal noxious molecules, induces a perturbation of the mucosal immune system and inflammation, and can act as a trigger for the development of intestinal and systemic diseases” (p. 631).

A protein called zonulin is responsible for induction of tolerance and orchestration of immune responses by modulating intercellular tight junctions in the gastrointestinal epithelium in a rapid, reversible, and reproducible fashion (Fasano, 2011). Zonulin evolved as an adaptive mechanism to flush out microorganisms as part of the innate immune response against bacterial colonization of the small intestine (Fasano, 2011).

Specific gliadin-permeating peptides can initiate intestinal permeability via MyD88-dependent release of zonulin, which causes conformational changes in tight junction architecture and cytoskeletal assembly that leads to paracellular entry of gliadin (a gluten sub-fraction) into the intestinal submucosa (Thomas, Fasano, & Vogel, 2006). Signaling through the CXCR3-mediated, MyD88-dependent pathway generates a Th1-dominant, pro-inflammatory cytokine milieu that recruits mononuclear cells into the submucosa (Fasano, 2011). After gliadin infiltrates the lamina propria, the barrier function can be further disrupted by the persistence of inflammatory mediators such as TNF-α and interferon-gamma (IFN-γ) (Fasano, 2011).

In those individuals predisposed to celiac disease, gliadin is presented by HLA-DQ and HLA-DR major histocompatibility complex (MHC) molecules, leading to abrogation of oral tolerance and a transition to a Th1/Th17 response (Fasano, 2011). Dendritic cells home to pancreatic and mesenteric lymph nodes and present gliadin, leading to “migration of CD4−CD8−γδ and CD4−CD8+ αβ T cells to the target organ (gut and/or pancreas) where they cause inflammation” (Fasano, 2011). This results in the interaction between T cells and antigen-presenting cells, producing the adaptive immune response that causes profound villous atrophy in celiac disease (Fasano, 2011). Celiac disease patients have higher concentrations of serum zonulin during the acute phase of disease compared with their healthy counterparts, and also have over-expressed CXCR3, the intestinal receptor for gliadin (Fasano, 2011).

However, even in healthy individuals, biopsies reveal a transient zonulin release upon gluten ingestion accompanied by an increase in intestinal permeability that does not reach the level observed in celiac disease (Drago et al., 2006). The authors of the in vitro study state, “Based on our results, we concluded that gliadin activates zonulin signaling irrespective of the genetic expression of autoimmunity, leading to increased intestinal permeability to macromolecules” (Drago et al., 2006, p. 408). Furthermore, when intestinal biopsies were examined from celiac patients with active disease, celiac patients in remission, non-celiac gluten-sensitive patients, and non-celiac controls, intestinal permeability was found to occur after gliadin exposure in all individuals (Hollon et al., 2015).

The same mechanism is implicated in all autoimmune diseases—leaky gut leading to molecular mimicry and/or the bystander effect—biochemical processes that could be characterized as “friendly fire” that are responsible for the resultant tissue damage and symptom expression (Fasano, 2012). Thus, compromised gut integrity, or dysfunctional intestinal permeability, is a precursor and essential trigger for all autoimmune disease, including celiac disease, type 1 diabetes, rheumatoid arthritis, multiple sclerosis, Crohn’s disease, ulcerative colitis, and ankylosing spondylitis, and can also appear in allergic syndromes such as asthma (Fasano, 2012; Drago et al., 2006; Westall, 2007; Edwards, 2008; Yacyshyn & Meddings, 1995; Martinez-Gonzalez et al., 1994; Schmitz et al., 1999; Hijazi et al., 2004).

Moreover, intestinal permeability, as assessed by a lactulose-mannitol test, may predispose a patient to the development of food reactions, as increased intestinal permeability is associated with food allergy (Laudat et al., 1994; Andre, 1986). However, food allergy itself may inflict “mucosal damage caused by local hypersensitivity reactions to food antigens,” creating a pattern in which an individual becomes sensitive to more and more foods (Tatsuno, 1989).

An Ounce of Prevention is Worth a Pound of Cure

For people resistant to dietary and lifestyle modifications to resolve intestinal permeability, I will share that I am a living testament to the consequences of dysfunctional intestinal permeability, which leads to a domino scenario where autoimmune conditions are developed one after another. This scenario is far from uncommon, as a fourth of patients with autoimmune disease tend to develop additional autoimmune diseases, leading to multiple autoimmune syndrome. It is often cited that an individual is three times as likely to develop another autoimmune disease after acquiring one (Cojocaru, Cojocaru, & Silosi, 2010). Hence, my mission is to save others from the heartache I have endured as a consequence of these devastating chronic illnesses.

The succession of autoimmune diseases I developed due to a confluence of environmental triggers, genetic susceptibilities, and compromised gut barrier speak to the importance of preserving tight junction integrity and acting as a guardian of your gut epithelium. The gravity of leaky gut syndrome is illustrated by Brandtzaeg (2013), who states, “Increased epithelial permeability for antigens is a crucial primary or secondary event in the pathogenesis of several disorders” (p. 67).

In my case, a multitude of factors converged to produce autoimmunity—intestinal hyper-permeability, dysbiosis, food sensitivities, mitochondrial dysfunction, genetic polymorphisms, histamine intolerance, mycotoxins, adrenal dysfunction, heavy metal toxicity, micronutrient deficiencies, hormonal imbalances, and a host of recalcitrant and stealth infections. Reversing an autoimmune disease is magnitudes of order more complex than preventing one, which is why educating the public at large about how intestinal permeability serves as a prelude to autoimmunity is of the utmost importance.

However, if you go to a conventional physician complaining of a leaky gut, your concerns are likely to be dismissed and more often than not, you will leave with a recommendation to spend less time on the internet—or even worse, your symptoms will be branded psychosomatic and your doctor will label you a hypochondriac, as almost half of autoimmune patients experience in the subclinical stages of their disease (AARDA, 2017).

Despite the litany of peer-reviewed studies in the scientific literature on pathologic paracellular intestinal hyper-permeability, the biomedical establishment is by and large ignorant to this condition and its implications. Ironically, although Western medicine relegates leaky gut syndrome to the realm of fanciful fairy tales, the pharmaceutical industry is actively investigating drugs to reverse it (Kato et al., 2017). Only when there is a financial incentive and a pharmaceutical approach developed for a disorder is it anointed with legitimacy in the eyes of the allopathic physician.

If health is your objective, however, restoration of gut barrier integrity should be prioritized, since, “The autoimmune process can be arrested if the interplay between genes and environmental triggers is preventing by re-establishing intestinal barrier function” (Fasano & Shea-Donohue, 2005). Because gluten is pivotally implicated in intestinal hyper-permeability, its exclusion from the diet, along with an oligoantigenic elimination-provocation diet, should be a first line of treatment in any patient on the autoimmune spectrum.

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Moms Speak Out About Genetically Modified Foods [GMOs]

Source: InstituteForResponsibleTechnology
November 23, 2016

No mother ever knowingly risks her child’s health. Hear what these mothers have to say about their experience with genetically modified foods.

Mumps outbreak in Long Island likely caused by vaccine-resistant virus; majority of those affected were immunized

Mumps outbreak

Source: NaturalNews.com
Isabelle Z.
August 6, 2016

Long Beach has been hit with a mumps outbreak that is vaccine-resistant. According to health officials in the Long Island town, almost two dozen individuals are believed to have contracted the virus, with four confirmed cases and at least 14 suspected ones.

All of the cases involve people in their 20s, and the outbreak is being attributed to a new vaccine-resistant strain of the virus. In fact, most of those who have contracted mumps in this case have been vaccinated against it. Despite this, officials are actually urging people who have been in contact with those who are infected to get a mumps booster shot! If this strain of the virus is vaccine-resistant, and those who have been vaccinated are getting it anyway, why should people get yet another vaccine?

It’s also worth noting that none of the people currently affected are seriously ill. The symptoms of mumps tend to be mild, and include swollen cheeks, a headache, body aches and low-grade fever. There is no treatment, and it usually clears up on its own in just a few days.

Mumps is, however, highly contagious. It can be transmitted through the transfer of saliva, sneezing or coughing. As beach season continues in full swing, some Long Beach restaurants are even supplying diners with plastic cups as a means of stemming the outbreak. People who have symptoms of the illness are being advised to stay home for five days to avoid spreading it.

Controversy over mumps component of MMR vaccine

As some Natural News readers may recall, two Merck scientists filed a False Claims Act complaint back in 2010 saying that the Big Pharma firm knowingly falsified mumps vaccine data in order to come up with an efficacy rate of 95 percent. They achieved this by spiking the blood test involved with antibodies taken from animals.

This not only allowed them to earn hundreds of millions of dollars from the U.S. government, but also helped them crush the competition and monopolize the vaccine market.

The complainants said that Merck never tested the vaccine against actual mumps viruses out in the real world, and alleged that senior management was aware of this and allowed it to happen. That’s why it’s so important to seek out studies that are free from industry collusion.

Mumps outbreaks becoming fairly common among the vaccinated

Mumps outbreaks seem to be occurring a lot lately. Earlier this year, for example, the illness broke out at Harvard and a handful of other Boston colleges. More than three quarters of those afflicted had been vaccinated.

Dozens of university students in Illinois came down with mumps last year, despite the majority of them having previously been administered two rounds of the MMR vaccine. Do you spot a trend here?

It’s important to note that not only does the MMR vaccine not actually prevent mumps, but it might actually be responsible for spreading it. That’s because the injection contains a weakened version of the live virus, which causes an infection in the body. It can then be “shed” to other people, such as those who have not been vaccinated, or those who have compromised immune systems. That’s why it makes absolutely no sense that authorities are urging people who have been exposed to get yet another vaccine.

Of course, there are other reasons people might want to avoid the vaccine besides the fact that it doesn’t protect against mumps. The MMR vaccine has been linked to a number of harmful effects, including neurological damage, autism, developmental delays, seizure disorders, asthma and autoimmune dysfunction, to name just a few.

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This Is The Most Damaging Thing To Your Body

Source: iHealthTube.com
August 3, 2016

So many things are posing a challenge to our health on a daily basis. Naturopath Ann Boroch discusses what she calls the ‘body breaker’, and possibly most damaging thing to our health. Find out how it affects all of us to varying degrees and what we can do to keep it under control or at least reduce its effects on our health. The more you know that this is the most damaging thing to your body, the more you can help yourself.

The Average Flu Shot Left This 9-Year-Old Girl Paralyzed And Non-Verbal

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Source: NaturalBlaze.com
Brianna Acuesta
July 9, 2016

A 9-year-old girl from Tampa, Florida went in for a flu shot one day, just as millions of Americans do every year, not knowing that her life would be forever changed because of it.

The girl, Marysue Grivna, was an active 9-year-old that loved to play outside, help out in the kitchen, and could speak two languages.

Just six days after she went in for a flu shot, Marysue succumbed to a rare autoimmune disorder brought on by the shot in which the body attacks itself by targeting protective covers around nerve fibers. When the coverings are destroyed, it leaves the brain and spinal cord vulnerable to damage, sometimes leading to loss of vision and paralysis.

This is exactly what happened to Marysue just days after receiving the vaccine. She experienced paralysis one morning and was not able to speak or get out of bed, despite being fully conscious with her eyes open.

Her mother said this about that fateful morning:

“The look on her face was like ‘Help me,’ like she was scared but she couldn’t respond to me,” Carla recalled.

By the time she reached the ICU at St. Joseph’s Hospital, Marysue had already experienced two seizures.

She spent the next three months hospitalized and underwent several tests to determine what the cause of her illness was. The doctors sent samples of her blood and urine to the Center for Disease Control and infectious disease specialists ran tests as well. All involved essentially told Marysue’s parents to say goodbye to their only child.

Continue Reading At: NaturalBlaze.com

Microbial Diversity & Weight Gain

Source: DavidPerlmutterMD
Dr. David Perlmutter
June 20, 2016

A new study in laboratory animals inoculated with human gut microbes shows how desperately important dietary prebiotic fiber is, in terms of maintaining microbial diversity. Low levels of prebiotic fiber lead to loss of diversity, which, in humans, is associated with a variety of diseases, including diabetes and autoimmune conditions. The study further demonstrates that while introduction of prebiotic fiber does restore the diversity to some degree, subsequent generations of these laboratory animals are less able to recover their diversity, with some species of gut organisms actually becoming extinct.

Find the study here: http://www.drperlmutter.com/study/die…

Big Pharma’s Dirty Little Secret: Vaccine-Induced AutoImmune Disease Injury

This article is copyrighted by GreenMedInfo LLC, 2016
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Big Pharma’s Dirty Little Secret: Do Bleeding Calves, Narcolepsy and Infertility Have the Same Mechanism for Vaccine Injury?
Source: GreenMedInfo.com
Celeste McGovern
May 29, 2016

Nasal flu vaccine left  energetic and happy 10-year-old Bobby Hunter with disease that makes him afraid to smile (photo credit: Daily Express)

Scientists reveal how a hyperactivated immune system can unleash disease

Bobby Hunter was 10 years old when his mother noticed her usually energetic boy was struggling to stay awake and he looked exhausted all the time. Then he began collapsing. Eventually Bobby was diagnosed with narcolepsy, a lifelong incurable condition where victims suddenly drop into deep dream sleep, sometimes a dozen times a day or more. It can be accompanied by bizarre and terrifying symptoms: waking hallucinations of demons, insomnia, sleep paralysis and a sudden loss of muscle control or cataplexy often triggered by strong emotions. Bobby now has to be accompanied everywhere he goes in case he falls unconscious; he’ll never bathe or drive or cross a street alone. But his case is particularly cruel. Now, he is a child who is afraid to smile or laugh because it might trigger an attack.

Bobby’s mother Amanda is adamant he first became ill after he received the nasal flu vaccine at his school. But could such a small thing cause such a devastating disorder?

Narcolepsy Nightmare Explained

This month at the 10th Autoimmunity Congress in Leipzig, Germany a leading pharmaceutical researcher presented his international team’s findings suggesting that vaccination could indeed have the “unexpected” effect of inducing crippling narcolepsy, an autoimmune disease.

Sohail Ahmed, lead author of a ground breaking paper published last summer in Science Translational Medicine explained how the now-retracted Pandemrix vaccine was implicated in a narcolepsy epidemic of more than 1,300 children in several European countries and spates of cases linked to other vaccines for the 2009 swine flu pandemic that never materialized.

It turns out,  part of the influenza nucleoprotein in the swine flu vaccine looked (molecularly) just like a receptor for a neurotransmitter in the brain called orexin that regulates the sleep/wake cycle, explained, Ahmed former global head of clinical sciences at Novartis and later GlaxoSmithKline who is currently with Roche Pharmaceuticals.

When the vaccine was injected with an adjuvant to ramp up the immune response, the immune system went into overdrive. Something  — maybe chemical ingredients in the vaccine, maybe inflammation  –  breached the blood brain barrier and the immune system targeting the vaccine virus also locked in on the receptors in the brain sleep centre. Narcoleptic patients’ own immune system then destroyed a hub of 70,000 or so orexin-producing cells in their brains before their hosts started knocking out. The autoimmune reaction can’t be turned off because the immune system is programmed to relentlessly attack anything it perceives as a foreign invader. It’s a case of mistaken identity and in immunology it’s called a “cross-reaction.”

But could other vaccines still in circulation that contain the H1N1 virus trigger narcolepsy too? Could the same mechanism cause kids like Bobby Hunter to get narcolepsy from the nasal flu vaccine?

Both Ahmed and immunologist Maria Teresa Arango at Leipzig confirmed that it could indeed. Bobby probably carries the HLA-DQB1*0602 genetic marker that leaves him at a higher risk of getting narcolepsy. But so does 20% of the US population. For pharmaceutical industry dependents like Ahmed, so long as cases like Bobby’s are not epidemic as they were with Pandemrix, they are collateral damage the pharmaceutical industry is willing continue to keep flu vaccines rolling.

But what if other vaccine proteins are acting in more unexpected ways, contributing to other autoimmune diseases?

Arango said such cross-reactivity could be the underlying mechanism for widely varied and unexpected documented vaccine adverse autoimmune events affecting other parts of the brain or body. She pointed to the work of Dr. Darja Kanduc.

Massive Peptide Sharing, Massive Autoimmunity?

Kanduc is a biochemist at the University of Bari in Italy who presented her findings in Leipzig at a one-day symposium on vaccine safety sponsored by the Children’s Medical Safety Research Institute. Bari has been looking for molecular similarities between microbial and human proteins and found that a massive, unexpected “peptide sharing” exists between human proteins and microbe proteins.

Where overlap (“peptide sharing”) occurs between a foreign protein and human protein, they have a same identical amino acid sequence (for example, SLVDTYR).  An immune response launched against SLVDTYR might hit A (the microbial protein) and also B (the human protein). In immunology terms, this is a cross-reaction between A and B — in the same way Ahmed’s team illustrated vaccine-induced narcolepsy.

Normally such cross-reactions do not occur, explains Kanduc. “In fact, the human immune system has been ‘educated’ to ignore foreign proteins and avoid cross-reactions in order not to harm the similar human ‘self’ proteins.” In immunology, this is called immunotolerance. Our immune system does not press the panic button and launch an attack on every foreign viral protein it encounters.

Tolerance Lost

Our natural immunotolerance has proved a big problem for vaccine manufacturers over the years. Simply injecting a viral or bacterial particle into our bodies does not trigger the immune storm they want. Our bodies aren’t designed to encounter pathogens via intramuscular injection, after all. Our immune system refuses to attack the injected pathogen since that would mean also attacking the look-alike human proteins. It would rather not go to war than risk the home casualties.

Imagine the immune system as a border guard. If a guard at the Canada-US border pulled every vehicle that drove up to his checkpoint aside, emptied the suitcases, called in the sniffer dogs, strip-searched the occupants and called for the SWAT team, things would get ugly pretty fast. Most of the time, border guards are alert but passive. Our immune system is the same way with foreign proteins.

So vaccine manufacturers pepper vaccines with adjuvants — crude extracts of mycobacteria, toxins such as mercury, aluminum salts, or mineral oils to force the reluctant immune system to go into attack mode – from passive border guard to hypervigilant nutter pulling a gun on a granny.  Celebrated Yale immunologist Charles Janeway called this “immunologist’s dirty little secret” underlying vaccination.

 “Adjuvants expand, potentiate, and increase immune responses,” explains Kanduc. “Such hyperactivation has a price: the loss of specificity. The hyper-stimulated immune system does not discriminate any more between foreign proteins and self-proteins…Adjuvants render the immune system blind. Human proteins that share peptide sequences will be attacked.”

Kanduc likens immunotolerance to a protective wall. “The dam is demolished by the adjuvants and the cross-reactivity flood can crush and alter human proteins.” This might also cause numerous cross-reactions, manifested as a wide variety of autoimmune attacks.

Can vaccines induce genetic disease?

Kanduc looked for peptide sharing between a single influenza A H5N1 protein and human proteins. She found that the viral protein shares 70 peptides with the human host — proteins involved in basic cell functions including proliferation, neurodevelopment, and differentiation.

Among the human proteins that could be on the firing range: reelin, a protein involved in neuron layering, neurexins, proteins that connect neurons,  syndrome 10 protein for Bardet-Biedl syndrome, a transcription factor for Williams Syndrome (a rare genetic neurodevelopmental disorder), a protein associated with amyotrophic lateral sclerosis, and so on.

When these human proteins are altered, as for example by genetic mutations, neurological disorders such as epilepsy, obesity, dystonia, amyotrophic lateral sclerosis, Sudden Infant Death Syndrome and demyelinating diseases like multiple sclerosis occur, says Kanduc.

 “The same spectrum of diseases might occur if these human proteins are attacked and altered by cross-reactions following an expanded and indiscriminate immune response induced by an adjuvant vaccine,” she adds.

With such “massive overlap” of proteins, the potential for vaccines to induce all sorts of autoimmune diseases is possible; it explains why such diverse autoimmune phenomena have been documented in the medical literature with respect to vaccination, from neurological disorders to skin afflictions to impaired fertility.

“The type of autoimmune phenomenon and disease that is eventually established will depend on the molecules and organs attacked,” explains Kanduc. “For example, attacks against myelin may evoke demyelinating diseases [such as multiple sclerosis] whereas immune reactions against proteins involved in behaviour  and /or cognition may cause autism and behaviour disorders.”

Autoimmune Infertility?

Such autoimmunity may be the mechanism underlying cases of premature menopause and infertility in adolescent girls following injection with the vaccine against HPV, described in Leipzig by an Australian GP. Deirdre Little, a general practitioner in South Bellingen, first published a case study of her 16-year-old patient who developed premature ovarian insufficiency (POI) following HPV vaccination. Since then Little has encountered six more post-HPV cases of sterility in adolescents in her practice – though primary ovarian insufficiency is almost unheard of  — normally affecting one in 100,000 girls under age 20.

Continue Reading at: GreenMedInfo.com

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Celeste McGovern is a Canadian freelance journalist in the UK.

© [May 29] GreenMedInfo LLC. This work is reproduced and distributed with the permission of GreenMedInfo LLC. Want to learn more from GreenMedInfo? Sign up for the newsletter here http://www.greenmedinfo.com/greenmed/newsletter.