Persistence of Borrelia burgdorferi in Rhesus Macaques following Antibiotic Treatment of Disseminated Infection

Abstract

The persistence of symptoms in Lyme disease patients following antibiotic therapy, and their causes, continue to be a matter of intense controversy. The studies presented here explore antibiotic efficacy using nonhuman primates. Rhesus macaques were infected with B. burgdorferi and a portion received aggressive antibiotic therapy 4–6 months later. Multiple methods were utilized for detection of residual organisms, including the feeding of lab-reared ticks on monkeys (xenodiagnosis), culture, immunofluorescence and PCR. Antibody responses to the B. burgdorferi-specific C6 diagnostic peptide were measured longitudinally and declined in all treated animals. B. burgdorferi antigen, DNA and RNA were detected in the tissues of treated animals. Finally, small numbers of intact spirochetes were recovered by xenodiagnosis from treated monkeys. These results demonstrate that B. burgdorferi can withstand antibiotic treatment, administered post-dissemination, in a primate host. Though B. burgdorferi is not known to possess resistance mechanisms and is susceptible to the standard antibiotics (doxycycline, ceftriaxone) in vitro, it appears to become tolerant post-dissemination in the primate host. This finding raises important questions about the pathogenicity of antibiotic-tolerant persisters and whether or not they can contribute to symptoms post-treatment.

Citation: Embers ME, Barthold SW, Borda JT, Bowers L, Doyle L, et al. (2012) Persistence of Borrelia burgdorferi in Rhesus Macaques following Antibiotic Treatment of Disseminated Infection. PLoS ONE 7(1): e29914. doi:10.1371/journal.pone.0029914

Editor: Jean Louis Herrmann, Hopital Raymond Poincare - Universite Versailles St. Quentin, France

Received: July 22, 2011; Accepted: December 6, 2011; Published: January 11, 2012

Copyright: © 2012 Embers et al. This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.

Funding: This work was supported by NIAID grant R01-AI042352 (MTP), R01-AI26815 (SWB and EH), a TNPRC Pilot Study Grant (MEE), and NCRR grant RR00164. The funders had no role in study design, data collection and analysis, decision to publish, or preparation of the manuscript.

Competing interests: The authors have declared that no competing interests exist.

---

Introduction

Lyme borreliosis is caused by the spirochetes of the Borrelia burgdorferi sensu lato species complex. The clinical progression of Lyme borreliosis may be divided into early-localized, early-disseminated, and late stages. During the early-localized phase, the disease's most prevalent sign is an erythematous skin rash known as erythema migrans. Subsequently, patients may develop early-disseminated disease with dermatologic, rheumatologic, cardiac, and neurologic involvement. Patients with late disease present chiefly with arthritis or with neurologic manifestations [1]. The Infectious Diseases Society of America (IDSA) has issued guidelines for Lyme borreliosis therapy [2]. Signs and symptoms are usually successfully ameliorated with antimicrobial therapy. However, some patients continue to have persistent subjective complaints [3], [4] while a few patients fail to respond to antibiotic therapy, as made evident by signs of persistent infection [2], [5]. The response to treatment in patients with late manifestations is typically slower [2] and sometimes remains incomplete.

Post-treatment Lyme disease syndrome (PTLDS) is a condition that occurs in some patients after treatment for Lyme borreliosis. The cause of PTLDS is currently unknown but prolonged antibiotic therapy does not seem to be helpful [6], [7]. Objective evaluation of this phenomenon in humans is complicated by the difficulty in obtaining a patient population with confirmed Lyme borreliosis treated post-dissemination, and the vague, non-specific symptoms (fatigue, headache, memory and concentration difficulties, myalgias and arthralgias) with which PTLDS patients present. In addition, reliable procedures to determine that infection has been cleared from Lyme disease patients have not been established.

The C6 ELISA detects antibodies to a region of the B. burgdorferi VlsE lipoprotein that is immunogenic in infected individuals and common to all infectious variants tested thus far. Not only is the C6 test among the most reliable in terms of accuracy, but it is also a serologic test for Lyme disease that has been used experimentally as a predictor of treatment outcome [8]. In patients with PTLDS, anti-C6 titers were found to generally persist at a low level compared to acute patient titers [9]. To date, the experimental assessment, in animals, of antibiotic treatment effectiveness, measured by the presence or absence of spirochetes, correlated with C6 serologic test reactivity has not been reported.

Signs and symptoms of putative failure of antibiotic treatment in late disease or ineffectiveness of repeated treatment in patients with PTLDS may be formally attributed to several causes, including: 1) spirochetes that persist in the tissues, likely in small numbers, inaccessible or impervious to antibiotic; 2) inflammatory responses to residual antigens from dead organisms; or 3) autoimmune responses, possibly elicited by antigenic mimicry [10].

In an effort to gain insight into the viability of these hypotheses, we designed two experiments in which we respectively assessed the efficacy of two regimens of ceftriaxone and/or doxycycline treatment in rhesus macaques commencing at 4–7 months of infection with B. burgdorferi. Rhesus macaques were chosen because of the ability of this animal model to reproduce many of the key signs of human Lyme disease, including neuroborreliosis [11], [12], [13], [14], [15], [16], [17], [18], [19], [20], [21], [22] and because of the similarity between the available pharmacokinetics data for ceftriaxone and doxycycline in rhesus macaques and in humans [23], [24], [25], [26]. Our results confirm that spirochetes are capable of persisting in treated nonhuman primate hosts. We discuss the possible mechanisms and need for further inquiry into this phenomenon.

Results

We performed two separate experiments to assess post-treatment persistence by B. burgdorferi in nonhuman primates with treatment administered at different phases of disseminated infection. Both experiments involved infection, treatment post-dissemination, serology and detection of spirochetes in tissues. The two varied in the number of animals, B. burgdorferi strain used, time interval prior to treatment, antibiotic treatment regimen, and detection methods. The first (Experiment 1) was aimed at evaluating animals treated at the late disseminated phase of infection and the treatment regimen was chosen to correspond to the regimen used to treat human PTLDS patients in a clinical evaluation of treatment for this population [6]. The outline for Experiment 1 is depicted in Figure 1.

Download:

• PPT
  PowerPoint slide
• PNG
  larger image (620KB)
• TIFF
  original image (1.23MB)

Figure 1. Experimental design for assessment of treatment efficacy in the late, disseminated phase of infection (Experiment 1).
A) diagram of animal groups, showing inoculation (B. burgdorferi or sham) and treatment groups (treated with antibiotics or untreated); and B) the time line of the study.
doi:10.1371/journal.pone.0029914.g001

 

Full article : http://www.plosone.org/article/info:doi/10.1371/journal.pone.0029914

 

 

Is There a Cure for Autoimmune Disease?

Sun, 10 Oct 2010 18:44 CDT
Dr. Mark Hyman
drhyman.com

---

Isabel, a cute 10-year old girl from Texas who loved riding horses, walked into my office a year and a half ago with one of the most severe cases of autoimmune disease I had ever seen. Her face was swollen, her skin was inflamed, her joints were swollen, her immune system was attacking her entire body - her muscles, her skin, her joints, her blood vessels, her liver, and her white and red blood cells. Isabel couldn't squeeze her hand or make a fist. The tips of her fingers and toes were always cold from Raynaud's disease that inflammed her blood vessels. She was tired and miserable and was losing her hair. Isabel was on elephant doses of intravenous steroids every three weeks just to keep her alive, and she was taking prednisone, aspirin, acid blockers, and methotrexate, a chemotherapy drug used to shut down the immune system daily.

Despite these megadoses of medication she still wasn't getting any better, and her lab tests were still abnormal. Her doctors wanted to add another powerful immune suppressing drug (a TNF alpha blocker) to the regimen of medication she was already taking. This drug increases the risk of cancer and death from overwhelming infection, because it prevents the immune system from fighting infections normally. The inflammation slows down thus the autoimmune symptoms may abate, but you are risk for cancer and infection. Unwilling to accept this as the only course of treatment, they came to see me.

Two months after I first saw Isabel and discovered and treated the underlying causes of her inflammation - after, as she says she, "stopped eating gluten, dairy, and sugar and took some supplements" she was symptom free. In less than a year, she was completely healthy, her blood tests were normal, and she was off all her medication.

If her story is true (and it is), what are the implications for research on autoimmune disease and our approach to treating these disorders which now affect over 24 million Americans and 5 percent of the population in Western countries? These diseases include type 1 diabetes, lupus, rheumatoid arthritis, multiple sclerosis, colitis, Crohn's disease, and dozens of others, but they have one thing in common: The body attacks itself. Is there another way to treat these problems than powerful immune suppressive drugs that put patients at increased risk of infection and death?

Watch Isabel tell her story.

The Unfortunate Demise of the Case Study in Medicine

Historically medical discoveries originated from physicians' keen observation of their patients' diseases and responses to treatment. Doctors reported their findings to their colleagues or published them as case studies. Today these "case studies" are often dismissed as "anecdotes" and have become increasingly irrelevant. Instead, we now focus on randomized controlled trials as the only standard of "evidence". Sadly, this dismisses the experience of thousands of patients and physicians as they apply new scientific findings to treat difficult conditions.

Basic scientific discoveries often take decades to be translated into medical practice. Unfortunately, this prevents millions from accessing therapies that could benefit from them now. The determining factor in deciding whether to try a new approach with a patient is the risk/benefit equation. Is the treatment more likely to help than harm? How risky is the treatment? What are the side effects? How dangerous or risky is the current approach to a problem? How debilitating or life threatening is the disease being treated? These questions can guide exploration toward innovative approaches to chronic disease.

Except for treating infections with antibiotics and treating trauma, medicine today approaches most disease by suppressing, covering over, blocking, or otherwise interfering with the body's biology. We generally do not attempt to seriously address the underlying problems that lead to the disease in the first place. For example, cholesterol medications block an enzyme that produce cholesterol (among other important molecules like CoQ10), but they don't address why cholesterol may be high in the first place (factors like diet, exercise, stress, and genetics). Doctors use beta-blockers, calcium channel blockers, SSRI's (serotonin reuptake inhibitors), ACE-inhibitors, antibiotics, and anti-inflammatories. We are inhibiting, blocking, or anti-ing everything. But we don't ask one simple question:

Why is the body out of balance and how do we help it regain balance?

There is a new approach to medicine that is beginning to ask these questions.

Functional Medicine: Treating Causes, Not Symptoms

I just lectured at the Institute for Functional Medicine's basic training course for physicians. Even though the course is expensive - because unlike most other continuing medical education pharmaceutical companies do not support it - this conference was sold out. There were practitioners from 27 countries, and 24 faculty members from medical schools.

Functional medicine is a hidden movement sweeping across the globe, and it is based on a different method of diagnosing and treating disease - one that focuses on causes not symptoms, one that is based on an understanding of the dynamic way our genes interact with environment, one that goes beyond simply treating diseases based on their label. The training I lectured at teaches practitioner to understand the body as a system; to seek the causes of illness; to understand the body's basic functional systems, where they go awry, and how to restore balance; to understand the interconnections between symptoms and organs rather segregate diseases into specialties.

This approach is a fundamentally different way of solving medical problems, one that allows us to decipher the origins of illness and identify the disturbances in biology that lead to symptoms. Let's see how this approach worked for Isabel.

From Conventional Illness to Functional Health

For Isabel, the only response physicians had to her life-threatening illness was to shut down her immune system, leaving her at risk for cancer, infection, osteoporosis, muscle wasting, and psychiatric illness. But there was another way. I simply asked the question WHY. I didn't focus on WHAT the name of her disease was (mixed connective tissue disease, otherwise known as an autoimmune disease that affects the whole body), but WHY she was inflamed, WHERE this inflammation originated from, and HOW we could locate the causes and restore balance to her overactive immune system that was attacking her own body?

The immune system usually responds to some insult such as an allergen, a microbe, or a toxin, and then runs out of control. Finding and removing that trigger is essential. In a review in the New England Journal of Medicine, it was acknowledged that "even in a genetically predisposed person, some trigger, an environmental exposure, or change in the internal environment - is usually required for [autoimmunity]." (i)

When I talked to Isabel the first time, I found many potential triggers for her inflammation. She was being exposed to a toxic mold, Stachybotrys, in her house. Her mother worked in limestone pits exposing her to excessive amounts of fluoride while pregnant. Isabel had all her immunizations before 1999 when thimerosol was removed from vaccines. She also had a thimerosol-containing flu shot every year. Thimersol contains mercury and mercury is a known immune toxin. This problems was compounded by her diet which included large amounts of tuna and sushi which she loved and ate regularly (and which exposed her to even more mercury), and loads of dairy, gluten, and sugar. In the year before she got sick, she also had many courses of antibiotics.

Mold, mercury, antibiotics, sugar, dairy, gluten - all potential immune irritants.

Isabel's lab tests at her first visit with me were frightening. Her muscle enzymes and liver function tests showed severe damage. She had many autoimmune antibodies (anti-nuclear antibodies, rheumatoid factor, anti-SSA, anti-DNA, anti-RNP, lupus anticoagulant), a sign that the levels at which the body was attacking itself were extremely elevated. Other markers of inflammation were extremely high as well. Her white blood count and red blood cell count were low. Her vitamin D was also low. She had elevated levels of antibodies to gluten, which is a common cause of autoimmune disease and triggers significant intestinal inflammation. And her mercury level was extremely high in her urine after a provocation test (the only way to assess total body burden of metals). Normal is less than three. Hers was 33.

At the first visit, I simply put Isabel on an anti-inflammatory elimination diet to remove possible triggers of inflammation from food allergens. She stopped eating sugar, dairy and gluten (from wheat). I gave her a multivitamin; vitamins D, B12, and folate; fish oil; and evening primrose oil all of which are anti-inflammatory. I also gave her nystatin (a non-absorbed anti-fungal) to treat suspected yeast because of her multiple courses of antibiotics. I gave her NAC to support her liver, and told her to get off the acid blocker, the calcium channel blocker, which she used for her Raynaud's, and the intravenous steroids she had been taking.

After two months her rash was totally gone. She had no joint pain and her hair was growing back. Her autoimmune markers had dramatically improved. Her muscle enzymes, liver function, and level of inflammation were all normal.

At the second visit two months later, I added probiotics to support healthy digestive function and reduce gut inflammation. I also started her on DMSA (a chelating agent) to help bind the mercury from her tissues and cells and help her excrete it. To help her get off the prednisone I gave her herbs to support her adrenal gland function.

Seven months later, her tests were normal, including her white blood count. Her mercury came down from 33 to 16. After 11 months, her mercury was down to 11 and her gut inflammation was gone. She was off all her medications and feeling happy, normal, and was able to ride and show her horse again.

Some may dismiss this as an anecdote, or a "spontaneous remission", or claim the testing methods unconventional, or the treatments used unproven. But if there is a shimmer of a possibility that this approach works, that it can help patients recover from some of the most debilitating, devastating human diseases out there, are we not obligated to investigate further? Shouldn't we expect that scientists and physicians would be motivated into new avenues of research, that the National Institutes of Health would fund studies to test this model? And if found to be effective, shouldn't academic medical schools change their curriculum and teach this new method of practicing medicine? This is the mission of the Institute for Functional Medicine, but it needs help because it has no funding from the usual sources: government and pharma.

Isabel's experience is not rare. The approach of finding and removing triggers of disease such as hidden microbes, toxins, or allergens, and supporting the body's function with nutrients and herbs and "pro" drugs such as probiotics is more than idea that needs to be proven. It is a movement that is now being practiced by thousands of practitioners at the cutting edge of medicine. It is an approach called functional medicine that has helped tens of thousands of patients worldwide. Shouldn't this revolutionary new method of practice be expanded and made available to more patients? Isabel's story should be common. We have the knowledge and the methods. Now we just need to apply them.

To your good health,

Mark Hyman, MD

References

(i) Mackay, I. and Rosen, F. 2001. Autoimmune diseases. New Engl J Med. 345(5): 340 - 350.

About the author

Mark Hyman, MD is dedicated to identifying and addressing the root causes of chronic illness through a groundbreaking whole-systems medicine approach called Functional Medicine. He is a family physician, a four-time New York Times bestselling author, and an international leader in his field.

Scientists have discovered that Celiac Disease Can be the Root Cause of most Neurological Disorders

Healthy-Family.org
Caryn Talty
06 Nov 2007
---

We all know that celiac disease is a problem of the small intestine, but most of us are probably unaware that it could actually be the root cause of a whole host of neurological problems from brain fog, to tingling and numbness sensations in your extremities, to developmental delays and learning disorders, autoimmune disorders like multiple sclerosis and rheumatoid arthritis, movement disorders like ataxia, and even psychological issues from irritability or depression to schizophrenia. You may think these claims sound like nothing more than a bunch of smoke and screens coming from greedy alternative medicine self-help sites designed to sell you the latest vitamin and mineral supplements and get you on their own personal and highly costly gluten-free product bandwagon, but there are real scientific studies supporting these claims. In addition, there are a whole host of forums filled with people that have made recoveries from a variety of diseases and disorders by avoiding gluten.

hesitated to write this article. I sat on it actually for quite some time. The claims sound so incredulous, how could anyone actually believe this stuff? I tried to put myself back into my own shoes a little over a year ago - back before things got so crazy around our house, back before we ever stepped foot into a Whole Foods store, or went to Trader Joes for anything other than gourmet cheese or those awesome appetizers in the freezer section. That me would have read the title of this article and thought, "What an extremist nutzo." Then I would have picked up the phone and speed dialed the local pizza joint for dinner, too.

So what has happened to me since then?

In late September of last year my son received his preschool vaccinations. Within three weeks he became a real behavioral problem at school, and by six weeks we saw his first tic. By the time the Christmas holidays rolled around he was nearly impossible to take anywhere as he was an emotional time-bomb in the making and so ticcy that it was hindering his daily activities. We kept him home from preschool for a couple weeks to limit his stress, but it didn't work. Then came the insomnia. He would just lie awake blinking for hours. I used to sit in his room and choke back the tears. To comfort him I fed him more of his favorite foods: pizza, mac and cheese, Christmas cookies, etc.... How did I know that the very things I was doing were actually making his condition worse?

I visited his pediatrician, the pediatric neurologist, a naturopath, a general practitioner, an ophthalmologist. We had a CBC, titer test, EEG, eye exam, acupuncture, you name it. I even went as far as giving him a pyramid-scheme all natural remedy with no scientific basis for cure other than the sales pitch I got from the supplier. Crazy, I know. Desperate times call for desperate measures.

Then I found a forum about tics and a wonderful person by the name of Mary opened my eyes for the first time since this whole crisis began. She claimed that a Gluten-free and Casein-free diet helped cure her son. Intrigued, I ordered a white blood cell food intolerance test. Low and behold I discovered that my son was also intolerant to wheat. Is he celiac? Well, technically no. But I will say this much, he no longer has any symptoms of a chronic tic disorder now that he is gluten-free. Is he cured? I wouldn't say he is cured. I would much rather use the term "recovered". Any exposure to an offending food will trigger mild tic symptoms such as a nose twitch, and of course a bit of irritability, but the constant ticcing is definitely a thing of the past, and so are a whole host of other symptoms that we thought were just a part of his personality. In addition to going gluten and corn free (his other main intolerance), we use vitamins and minerals on a daily basis. I have done a lot of research on cerebral allergies, particularly gluten intolerance, and this is some of what I have found:

K. Mustalahti, of the Pediatric Research Centre, University of Tampere, Finland states: "Recently, a growing body of distinct neurologic conditions has been connected to untreated celiac disease, mainly in middle aged adults. These manifestations are usually chronic, such as occipital lobe epilepsy with cerebral calcifications, cerebellar ataxia, progressive leukoencephalopathy and dementia. Seven per cent of all untreated celiac disease patients are diagnosed on the basis of various neurological symptoms. Although earlier studies reported neurologic disorders in patients with classical gluten enteropathy, some recent studies report neurologic symptoms in otherwise asymptomatic celiac disease patients. The pathogenic mechanisms underlying neurological disorders remain obscure, but immunological mechanisms are implicated. In few cases neurological symptoms seem to be alleviated by gluten-free diet but mostly the disorders are permanent" (712). The current criteria for celiac disease may give the false impression that celiac disease is purely a gastrointestinal disorder with manifest small-bowel mucosal lesion" (713). Excerpts taken from: "Unusual Manifestations of Celiac Disease" Indian Journal of Pediatrics, Volume 73, August 2006. ^[1]

Recommended Reading: Cilie Yack is Under Attack. Written at the 4th grade level, this children's novel tells the story of a boy growing up in Ireland before, during, and after he is diagnosed with celiac disease.

Nathanel Zelnik, et al states, "Although in the past celiac disease was primarily considered to be a gluten enteropathy, during the past two decades, its clinical concept has been expanded, and it is now considered a multisymptom autoimmune disorder, with most of the patients being asymptomatic, oligosymptomatic, or present with extraintestinal manifestations. Among these extraintestinal manifestations, there is a growing body of publications that report neurologic conditions that are associated with celiac's disease (1672)." Zelnik et al concluded that, "the spectrum of neurologic disorders in patients with celiac's disease is wider than previously appreciated and includes, in addition to previously known entities such as cerebellar ataxia, epilepsy, or neuromuscular diseases, milder and more common problems such as migraine headache and learning disabilities, including ADHD" (1675). Excerpts taken from: "Range of Neurologic Disorders in Patients with Celiac Disease ^[2]" Pediatrics, Volume 113, June 2004.

In 2006, Dr. Bruce Roseman, M.D. et al, created a brochure entitled: Pediatric Neurology and the Many Faces of Celiac Disease ^[4]. In it he states, "We will present in our findings and show the need for all health care workers to be aware of the strong association between celiac disease and pediatric neurological problems in order to diagnose and treat children in a timely manner." Here is an excerpt about a patient who tested positive for CD and presented with a progressive 6 week history of tics much like my son did:

"Case 4: An 11 yr male with IDDM who presented with a progressive 6 week history of neck tics. Patient would extend, flex, and rotate neck abruptly lasting for approximately 30 minutes. These movements were not associated with change of mental status. On review of symptoms patient complained of chronic abdominal pain, no nausea or vomiting. Patient had no recent history of Strep infection, excessive video game exposure or sleep deprivation. Irritable Bowel Syndrome diagnosed at 5 years of age. Paternal aunt had Celiac's Disease. On physical exam patient had no focal neurological deficits. Investigation (revealed): Ig A level: <6 mg/dl; IgG: 1400 mg/dl; Anti-TTG IgA: <3, anti-gliadin Ig G: 19 U/ml, anti-gliadin Ig A, anti-reticulin Ig A and anti-endomysial: negative. Biopsy: flattening of villi."

UPDATE: In Stavanger, Norway scientists completed a one year ADHD diet study in 1996 ^[5]:

The children in the Stavanger project all followed a strict casein-free diet the first year, and the results were overwhelmingly positive, Noedland says, pointing out that 22 of the 23 families reported clear improvements in their child's behaviour and attention-span. The group set out to prove a theory by Oslo-based scientist Karl Ludvig Reichelt that a metabolic disorder making it difficult to break down certain proteins, including casein (the protein in milk that makes it possible to make cheese), could cause mental problems like Attention Deficit Hyperactivity Disorder (ADHD). A number of the children have since stopped following the diet for different reasons and some were put on medication, but after eight years six were still strictly avoiding all milk products and several had also cut out gluten, which is found in wheat, rye, barley and to some extent oats. "We see a clear difference between those who stopped and those who stayed on the diet," Noedland says.

I think my biggest initial disappointment with the medical community was the complete lack of knowledge about celiac disease and its possible neurological manifestations in children. We visited several specialists and no one ever suggested we look into dietary changes.

It wasn't until we sought help from other parents struggling with their own child's autoimmune disorders or neurological dysfunctions did we finally got the vital information we needed to make a life altering change for our son. We are on the cusp of new discoveries in neurological science as medical studies are trying to catch up with anecdotal testimonies, by testing the claims parents are making. It is my sincere hope that more and more medical professionals be made aware of the gut-brain connection and begin to look more closely at the values in trying a gluten-free diet before advancing to more serious treatments such as the use of drug therapy.

Sadly, a gluten-free diet does not always work in some cases, but it is certainly worth a try.

On a final note, I would just like to say that had it not been for lovely Mary, who took the time to console me and teach me about possibilities outside what our medical doctors understood and could offer us, my son would not have had the wonderful recovery that he had. The gluten-free diet has done so much more than diminish the tics, it has brought peace to our house, improved my son's learning abilities, his mood, his overall sense of self. So thank you Mary, wherever you are.

If you are interested in trying a Gluten-free diet to help alleviate tics, visit our new forum ^[6]!

If you would like to learn more about being gluten-free or other additional natural remedies for neurological disorders please visit the following forums:

Latitudes.org ^[7](An alternative treatment forum for Autism Spectrum Disorders and Tourette Syndrome)

Brain Talk.net ^[8]

MDJunction.com ^[9] (A gluten-free casein-free Autism support group)

Gluten Free and Beyond.org ^[10] in association with The Gluten File ^[11], is a website about diseases related to gluten sensitivity.

Ataxia.org ^[12] has a special thread in their toast forum that discusses Celiac ataxia.

You can also download and print this Gluten Syndrome/Celiac Symptom Circle ^[13] for your convenience.

Update: View and forward the link to Dr. Ford's two new educational You Tube videos [14] about the Gluten Syndrome.

Article printed from Healthy-Family.org: http://healthy-family.org

URLs in this post:

[1] "Unusual Manifestations of Celiac Disease" Indian Journal of Pediatrics, Volume 73, August 2006.: http://medind.nic.in/icb/t06/i8/icbt06i8p711.pdf
[2] Range of Neurologic Disorders in Patients with Celiac Disease: http://pediatrics.aappublications.org/cgi/content/full/113/6/1672
[3] Article continues on next page...: http://healthy-family.org/caryn/289/scientists-have-discovered-that-celiac-disease-can-be-the-root-cause-of-most-neurological-disorders/2
[4] Pediatric Neurology and the Many Faces of Celiac Disease: http://healthy-family.org/caryn/289/scientists-have-discovered-that-celiac-disease-can-be-the-root-cause-of-most-neurological-disorders/pediatric-neurology-and-the-many-faces-of-celiac-disease
[5] Norway scientists completed a one year ADHD diet study in 1996: http://www.int.iol.co.za/index.php?set_id=1&click_id=117&art_id=nw20080224092424476C121112
[6] our new forum: http://healthy-family.org/forum/
[7] Latitudes.org : http://www.latitudes.org/
[8] Brain Talk.net : http://brain.hastypastry.net/forums/
[9] MDJunction.com: http://www.mdjunction.com/forums/autism-discussions
[10] Gluten Free and Beyond.org: http://glutenfreeandbeyond.org/forum/index.php
[11] The Gluten File: http://jccglutenfree.googlepages.com/
[12] Ataxia.org: http://www.ataxia.org/forum/toast.asp?action=posts&sub=search&fid=-1&author=&subject=celiac+ataxia&message=&dayprune=-1&submit.x=0&submit.y=0&submit=Submit
[13] Gluten Syndrome/Celiac Symptom Circle: http://www.glutensensitivity.net/GlutIntolCircle.pdf
[14] You Tube videos: http://healthy-family.org/caryn/360

SCLÉROSE en plaques : Soleil et vitamine D, 2 facteurs de réduction du risque

Santelog.com
10/02/2011
---

Les personnes qui vivent au soleil et ont des niveaux plus élevés de vitamine D ont moins de risque de développer une sclérose en plaques (SEP), selon cette étude canadienne publiée dans l'édition du 8 février de la revue Neurology, la revue de l'American Academy of Neurology. Mais plus intéressant encore, exposition au soleil et niveau de vitamine D sont 2 facteurs indépendants de réduction du risque de développement de la maladie.

La SEP est une maladie chronique du cerveau et moelle épinière, généralement avec des poussées récurrentes de symptômes. « Des études antérieures avaient suggéré des résultats similaires, mais cette étude est la première menée sur des patients ayant présenté les premiers symptômes de la SEP mais n’ayant pas été encore diagnostiqués», explique l’auteur de l'étude, le Pr. Robyn Lucas, de la National University de Canberra (Australie). "D'autres études ont porté sur les personnes qui avaient déjà  une SEP, il n’était pas possible de savoir si la maladie les a amenés à modifier leurs habitudes de vie, dont l’exposition au soleil ou leur alimentation."

Cette étude a été menée sur 216 personnes âgées de 18 à 59 ans ayant eu un premier événement avec des symptômes du type SAP, avec un groupe témoin de 395 participants ne présentant aucun symptôme de SEP du même âge, du même sexe et de la même région de l'Australie. Les participants ont renseigné leur exposition au soleil à chaque période de leur vie, les chercheurs ont mesuré la quantité de lésions cutanées par exposition au soleil et la quantité de mélanine dans leur peau. Les niveaux de vitamine D ont été mesurés par tests sanguins.

Le risque d'avoir un premier événement, diagnostiqué par un médecin, variait d'environ de 2 à 9 nouveaux cas pour 100.000 personnes par an, dans cette étude. L'exposition à la lumière UV des participants variait de 500 à plus de 6.000 kilojoules par mètre carré.

Les chercheurs constatent

·         que le risque d'avoir un événement de type SEP diagnostiqué est réduit de 30% pour chaque augmentation de 1000 kilojoules UV,

·         que les personnes avec lésions cutanées par exposition au soleil présentent un risque réduit de 60% de développer un premier événement par rapport aux participants sans lésions par exposition aux UV,

·         que les personnes ayant les plus hauts niveaux de vitamine D sont également moins susceptible d’avoir connu un premier épisode de symptômes de SEP que les participants ayant les niveaux moins élevés de vitamine D.



Au total, les différences d'exposition au soleil, les taux de vitamine D et le type de peau représentent une augmentation de 32 % de diagnostic d’un premier événement de SEP. Les effets liés à l'exposition au soleil et les niveaux de vitamine D sont 2 facteurs indépendants les uns des autres sur le risque de premier événement.

Néanmoins les chercheurs rappellent que l’on doit limiter son exposition au soleil en raison des risques de cancer cutané et que les risques des cabines de bronzage l’emportent de loin sur le bénéfice de protection contre la SEP.

Edgar Cayce - Lecture N° 907-1 - Etiologie de la Sclérose En Plaques

Virginia Beach, Va, 25 janvier 1939

--


1. GC: Vous allez avoir devant vous la requête du Dr Charles G. Taylor of St ..., New York, N.Y., pour une lecture de recherche concernant la maladie connue comme la Sclérose En Plaques.
Vous considérerez la déclaration suivante du Dr Taylor : "La pathologie physique de la Sclérose En Plaques est une affection des fibres nerveuses dans la moelle épiniaire et le cerveau. La gaine protectrice de ces fibres est de manière évidente attaquée par quelque agent destructeur qui cause leur 'disparition' et leur remplacement par du tissu fibreux." SVP, répondez aux questions suivantes.

2. EC: L'état de la moelle épinière et du cerveau est plutôt le résultat d'un état qui se produit dans le système de l'assimilation et de l'absence d'un équilibre dans les hormones du système sanguin.

3. Il s'agit d'un problème des nerfs, mais appauvris à partir du manque d'équilibre dans le flux sanguin ou les forces des glandes qui fournissent à partir du métabolisme les éléments nécessaires pour donner l'élasticité ou l'activité qui est nécessaire.

4. Alors, il s'agit de la source, et l'état dans la moelle épinière et le cerveau est le résultat de ce qui est appelé la Sclérose En Plaques.

5. La maladie, bien sûre, dans chaque individu, peut être considérée comme une loi en elle-même. Ceci, bien sûr, est dépendante de l'influence à partir de laquelle l'activité de la première cellule est prise dans un corps ou une entité.

6. Comme le système nerveux est le canal à travers lequel les énergies atomiques, ou les énergies électroniques passent pour produire l'activité, il y a un manque de certains éléments dans l'organisme et dans la capacité du corps de produire à travers l'activité du système d'assimilation celle de l'OR.

7. Prêt pour les questions.

8. (Q) Est-ce que cet état provient d'un régime alimentaire déséquilibré ou d'un dysfonctionnement des glandes ?
(R) Une combinaison ! Comme cela vient juste d'être indiqué, pour déterminer des facteurs dût aux glandes ou au régime alimentaire, il faut connaître l'HISTOIRE du cas considéré, et les effets qu'il y a eu, dût à aux parents quant à la quantité suffisante des forces cellulaires À PROPOS de chacune des forces atomiques qui ont permis de créer la première cellule - ou en premier le foetus lui-même.

9. (Q) Dans le cas d'un régime alimentaire inapproprié, qu'est-ce qui doit être ajouté ?
(R) Cela dépend de la progression de la maladie. Mais, comme cela a été indiqué, il s'agit de l'effet de l'or, l'effet atomique de l'or doit être ajouté au système.

10. (Q) Quelles sont les glandes impliquées ?
(R) Celles concernant le foie et les voies biliaires

11. (Q) Quelle est la nature du processus de destruction de l'enveloppe des fibres nerveuses ?
(R) La fibre nerveuse est à la fois positive et négative, ou à la fois matière blanche et matière grise comme elle passe à travers l'activité du système. Lorsqu'il y a un manque dans ce qui pourvoit à la force négative ou positive, il y a une perte qui commence à ponctionner le système. Et comme il y a un manque de ces éléments qui donnent la vitalité et l'énergie à cette portion (l'enveloppe des fibres), cela commence alors au début comme une de ces formes d'épuisement ou de fatigue et ceci GRADUELLEMENT et alors elle se retire ou se dissout, ou leurs cellules, au lieu d'être rondes, ce qui est leur état naturel, deviennent allongées et graduellement se déchirent. Ainsi, le système essaye de construire une résistance à partir des mêmes raisons qui causent la perte des énergies qui permettent de réapprovisionner le système. C'est un DÉPÉRISSEMENT.

12. (Q) Décrivez le processus original qui commence dans le foie et la région de la vésicule biliaire.
(R) La force cellulaire ici, ou l'activité glandulaire, obtenue à partir de la rate, du pancréas et des jus ou du fonctionnement excrétoire du foie, dans les activités d'assimilation avec les forces de drainage des veines lactées.
Ceci donc, dont les énergies manques, construit graduellement des conditions qui deviennent des forces sclérosantes, qui forment dans la connections entre la voie biliaire ET l'activité vers les glandes plus grandes dans leur assimilation de telle manière qu'une sclérose de cette partie commence.
Alors, ceci agit graduellement sur le système nerveux ; en premier, pour ainsi dire, la perte de la mémoire pour le moment, ensuite l'affection peut s'installer soit dans la partie basse de la moelle épinière ou ce qui concerne la fin de la brosse, ensuite ces activités augmentent graduellement jusqu'à qu'elles affectent ou se propagent le long de la moelle épinière (dans une portion de celle-ci) vers le cerveau. Et ceci commence alors dans les activités sur l'utilisation de différentes parties de l'organisme.

13. (Q) Est-ce qu'il y a un agent extérieur ou un germe impliqué dans ce processus ?
(R) Nous ne trouvons pas que ce soit le cas. Plutôt, c'est le fait de ne pas garder le bon équilibre pour chaque cellule dans leur division comme elles augmentent dans leur activité.

14. (Q) Est-ce un manque d'énergie de cette cellule particulière, ou un poison qui se forme et attaque ?
(R) Un poison naturellement. Le manque ici de suffisamment d'énergie nerveuse constitue un poison pour les autres cellules à partir de l'original, ou la force centrale pour une telle activité.

15. (Q) Qu'est-ce qui peut être fait pour prévenir cette maladie ?
(R) Garder un équilibre nominal entre les éléments dans l'organisme qui permettent de garder un équilibre normal des éléments ou des métaux dans l'organisme. La plupart de ceux-ci peuvent être testés particulièrement à partir du sperm.

16. (Q) Que veut dire cette dernière phrase ? S.V.P., expliquez.
(R) Les glandes reproductrices sont les premières informées du manque de ces éléments pour la reproduction. Donc quand ceci est découvert - un manque de ceci - il doit y avoir alors l'ajout de l'or nécessaire.

17. (Q) Est-ce qu'il est mieux de le donner vibratoirement ou de manière interne ?
(R) Vibratoirement est toujours mieux pour tout ce qui est préventif ou une force destructrice de ces influences à partir de l'intérieur d'une activité cellulaire.

18. (Q) Quelles sont les étapes générales qui doivent être suivies ?
(R) Comme cela a été indiqué, ou doit être tiré d'une analyse de ce qui vient juste d'être indiqué, il doit y avoir la bonne distribution. Ceci, bien sûr, dépend beaucoup de l'avancée de la maladie. Il est présupposé que c'est pris avec les premiers symptômes, vous voyez ? Ou au commencement de la stérilité, ou de l'inactivité de l'organisme comme cela peut être nommé. Alors l'ajout de ces forces vibratoires combinées avec les éléments du régime pour que cela fasse suffisamment d'or, d'argent et de fer dans le flux sanguin.

19. (Q) Quelles suggestions peuvent être données maintenant pour de plus amples recherches sur ce sujet à travers ce canal ? Et expliquez pour le bénéfice du Dr Taylor la source de l'information donnée ici.
(R) Ce peut être pris en commençant par examiner ce que nous venons juste d'indiquer, et comment cela se vérifie avec les états qui existent dans les diverses phases de ce qui a été appelé la Sclérose En Plaques. Donc, les questions relatives à la maladie comme elle progresse, ou les effets qui ont été et sont créés dans les différentes étapes pour chaque cas individuel. Ensuite, il peut être demandé ce qui permettrait de clarifier dans l'esprit de celui qui désire appliquer les renseignements qui ont été donnés.
Sources - la conscience universelle.

20. Nous en avons terminé pour l'instant.


Traduction 02/2011 Tdum.

Sun Exposure, Vitamin D May Lower Risk of Multiple Sclerosis

Physorg.com
Mon, 07 Feb 2011

--

People who spend more time in the sun and those with higher vitamin D levels may be less likely to develop multiple sclerosis (MS), according to a study published in the February 8, 2011, print issue of Neurology, the medical journal of the American Academy of Neurology. MS is a chronic disease of the brain and spinal cord, usually with recurrent flare-ups of symptoms. It is often preceded by a first episode (or event) of similar symptoms lasting days to weeks.

"Previous studies have found similar results, but this is the first study to look at people who have just had the first symptoms of MS and haven't even been diagnosed with the disease yet," said study author Robyn Lucas, PhD, of Australian National University in Canberra.

"Other studies have looked at people who already have MS - then it's hard to know whether having the disease led them to change their habits in the sun or in their diet."

The multi-site study involved 216 people age 18 to 59 who had a first event with symptoms of the type seen in MS. Those people were matched with 395 people with no symptoms of possible MS who were of similar ages, of the same sex and from the same regions of Australia.

The participants reported how much sun they were exposed to during different periods of their lives, and researchers also measured the amount of skin damage participants had from sun exposure and the amount of melanin in their skin. Vitamin D levels (from sun exposure, diet and supplement use) were measured by blood tests.

The risk of having a first event, diagnosed by a doctor, ranged from approximately two to nine new cases for every 100,000 people per year in this study. The reported UV light exposure of participants ranged from about 500 to over 6,000 kilojoules per meter squared. The researchers found that the risk of having a diagnosed first event decreased by 30 percent for each UV increase of 1,000 kilojoules. They also found that people with most evidence of skin damage from sun exposure were 60 percent less likely to develop a first event than the people with the least damage. People with the highest levels of vitamin D also were less likely to have a diagnosed first event than people with the lowest levels.

Studies have shown that MS is more common in latitudes further away from the equator, and this has been confirmed in Australia.

"Added together, the differences in sun exposure, vitamin D levels and skin type accounted for a 32-percent increase in a diagnosed first event from the low to the high latitude regions of Australia," Lucas said.

Lucas noted that the effects of sun exposure and vitamin D acted independently of each other on the risk of first event. "Further research should evaluate both sun exposure and vitamin D for the prevention of MS," Lucas said.

Lucas also stated that people should continue to limit their sun exposure due to skin cancer risks. She also noted that the risks of tanning beds far outweigh any possible protective effect against MS. Exposure to the sun has not been shown to benefit people who already have MS.

Source

Provided by American Academy of Neurology

Factors from Common Human Bacteria May Trigger Multiple Sclerosis

Science Daily
Tue, 24 Nov 2009

---

Current research suggests that a common oral bacterium may exacerbate autoimmune disease. Multiple sclerosis (MS), a disease where the immune system attacks the brain and spinal cord, affects nearly 1 in 700 people in the United States. Patients with multiple sclerosis have a variety of neurological symptoms, including muscle weakness, difficulty in moving, and difficulty in speech.

Porphyromas gingivalis, a common oral bacterium in humans, produces a unique type of lipid, phosphorylated dihydroceramides (DHCs), which enhance inflammatory responses. These lipids are also likely produced by bacteria found in other parts of the body including the gastrointestinal tract. To determine if these lipids accentuate immune-mediated damage in autoimmune disease, researchers led by Robert B. Clark and Frank C. Nichols of the University of Connecticut Health Center administered phosphorylated DHCs in a mouse model of MS. The severity of disease was significantly enhanced by the addition of these lipids in a manner that was dependent on activation of the immune system. These data suggest that phosphorylated DHCs from bacteria commonly found in humans may trigger or increase the severity of autoimmune diseases such as multiple sclerosis.

The authors state that "while it is clear that the immune system in most individuals has the potential to attack self-tissues, the "tipping" factors that initiate and propagate autoimmune diseases such as multiple sclerosis in only a subset of individuals remain unknown. Overall, [their] results represent the first description that phosphorylated DHCs derived from common human bacteria are capable of enhancing autoimmune disease." Thus, these lipids may function as "tipping" factors, playing a previously unrecognized role in initiating or exacerbating human autoimmune diseases. In future studies, Dr. Clark and colleagues plan to characterize the effects of phosphorylated DHCs on specific cells of the immune system and to identify how and where these lipids are deposited in tissues throughout the body. In addition to the role of these lipids in triggering and worsening MS, the authors believe that phosphorylated DHCs may have the potential to serve both as new markers of MS disease activity and as new targets for therapeutic intervention.