Wednesday, January 30, 2013

MAP- Where Are All the #MAP Organisms Living in Patients w/ #Crohns Disease?

Niiiiice find of information... props to PLOS for their open access (free) library of research!  There are so many good points that make sense about the link between MAP & Crohn's disease.  As you read this, you will understand what I mean - Check out what  is said about fistulas, also the location where MAP organisms may be found in large numbers within our body.  There are so many other significant postulations that are made that focus on the real cause of Crohn's that point in the direction to MAP.  

       Have Hope!!

Read this and be encouraged! Researchers and scientists are getting closer to identifying the cause of Crohn's.  Some people, a lot of people in the medical field do want to find a cure for this horrible disease, despite the downers working through our government who tend to go against the grin.  Try to be optimistic and your despair and helplessness will begin to change into enthusiasm.  

So many people have given up on their body and they no longer care what happens to it.  They are not involved with their treatment planning because they just don't care anymore, they don't make necessary (but difficult) adjustments to their lives that will lead to a better quality of life in the longterm because their hope is gone and they pretty much are just wasting away.  You have to remember YOU have Crohn's, Crohn's doesn't have you.... unless you give it permission to rule your body.  

My goal now, is to figure out how to get tested for this bacteria and where I have to go to have it done. I don't care where I have to go to have it done, who supports me & who thinks I'm wasting my time.  It doesn't matter to me what people think anymore.  This is a battle I fight daily and i'll do what it takes to get well.  

1st, do you know what MAP is ? (It stands for Mycobacterium avium subspecies paratuberculosis  - MAP)  READ THE HIGHLIGHTS FOR GENERAL INFO THAT YOU SHOULD KNOW.

I'm so fueled, not just from this article, but the list of over 15 other articles on PLOS that I haven't read yet on with the focus on MAP.  


  •  "MAP has been identified in the mucosal layer and deeper bowel wall in patients with Crohn's disease by methods other than light microscopy, and by direct visualization in small numbers by light microscopy"
  • "MAP is present in pasteurized milk [27], infant formula made from pasteurized milk[28], breast milk from women with Crohn's disease [29], surface water [30][32], soil [30], cow manure “lagoons” that can leach into surface water [33], cow manure in both solid and liquid forms that is applied as fertilizer to agricultural land [33], and municipal tap water [25],[34], providing multiple routes of transmission to humans."
  • "MAP is still not accepted as the cause of Crohn's disease. The identification of MAP by methods other than direct visualization by light microscopy, and the identification of MAP in small numbers by light microscopy, has not constituted convincing evidence of causation to the medical community at large."
  • "...MAP organisms might therefore be present in large numbers in the following locations in patients with Crohn's disease: 1)The blood vessels, lymph vessels (lymphatics), and lymph nodes in the mesentery of affected bowel wall segments. 2) The mesentery itself, i.e., the adipocytes that fill the mesentery. 3)The walls of fistulas."
  • "While other organisms have also been identified in the intestines of patients with Crohn's disease [23], no other putative pathogenic organism causes a chronic granulomatous inflammation of the intestines..."
  • "humans with Crohn's disease have antibodies to MAP antigens in their blood. ELISA studies, which detect antibodies to MAP antigens in the blood, demonstrate that anywhere from 23% to almost 90% of Crohn's patients have such antibodies [11][15][17]."

Where Are All the (MAP) Mycobacterium avium Subspecies paratuberculosis in Patients with Crohn's Disease?

  • Ellen S. Pierce mai

Tuesday, January 29, 2013

Nutrition & Crohn's Disease: Vitamins & Supplement Information From WebMD

If you have Crohn's disease, good nutrition is crucial so you can stay as healthy as possible. Unfortunately, the disease -- as well as treatments for it -- can make it much harder to get enough of the vitamins and minerals you need.
Doctors often recommend vitamins for Crohn's disease to work around this problem. Whether you need Crohn's disease vitamins -- and which ones -- depends on your case and the your medical treatments.  
Here's a rundown of the minerals and vitamins for Crohn's disease that your body might not be getting -- and advice on how to get more of them.

Crohn's Disease Nutrition

Poor nutrition has real risks if you have Crohn's disease. You may feel run-down and sick. Medications may not work as well. In children and teens, poor nutrition related to Crohn's disease can stunt growth.
Why does Crohn's disease affect nutrition? There are several reasons.
  • Inflammation and damage to the small intestine fromCrohn's diseasecan make it hard for the body to absorb substances from food, such as carbs, fats, water, and many vitamins and minerals. Surgery for Crohn’s may also make it more difficult to absorb nutrients.
  • Reduced appetite -- from pain, diarrhea, anxiety, and changes in taste -- makes it hard to eat enough.  
  • Some medications for Crohn's disease make it harder to absorb nutrients.
  • Internal bleeding in the digestive tract can lead to anemia, which can cause low levels of iron.

Crohn's Disease Nutrition: What's Missing?

What vitamins and minerals are missing in your diet? People with Crohn's disease are likely to have lower levels of:
  • Vitamin B12. After surgery in the ileum -- the lower section of the small intestine -- it may not be possible to absorb enough vitamin B12. Dietary changes and oral vitamins can help. Some people with Crohn's disease need injections of vitamin B12 or a B12 nasal spray.
  • Folic acid. Some drugs for Crohn's disease, such as sulfasalazine or methotrexate, can lower levels of folic acid. A daily 1 mg dose of a folate supplement could help. 
  • Vitamin D. Studies have shown the people with Crohn's disease often have low levels of vitamin D, which helps your body absorb calcium for strong bones.  Many people with Crohn's disease take an 800 IU supplement of vitamin D daily.
  • Vitamin A, vitamin E, and vitamin K can be low in people who have trouble absorbing fats because of surgery for Crohn's disease.
  • Calcium. Steroids for Crohn's disease can weaken bones and affect your body’s ability to absorb calcium. On top of that, some people with Crohn's disease avoid milk because they're also lactose intolerant, further reducing calcium. Up to 50% of people with Crohn's have osteopenia, or thinning of the bones. Taking additional supplements -- often 1,500 mg of calcium a day -- can help keep bones strong and prevent other problems.
  • Iron. People with active Crohn's disease may develop anemia from blood loss in the intestines. The best treatment for anemia is with iron. Most people take iron tablets or liquid, but some get infusions instead.
  • Potassium, magnesium, and zinc may be lower in people with Crohn's disease. Taking a daily supplement can help.

Friday, January 25, 2013

Donor Feces Cure Recurrent Diarrheal Infection, Study Shows - Bloomberg

Ummmm lol I still don't know about this.  There's just something that seems wrong about receiving an infusion..... of feces!

Donor Feces Cure Recurrent Diarrheal Infection, Study Shows - Bloomberg:

An infusion of feces through the nose beat the standard antibiotic as a treatment for a recurrent diarrhea-causing infection that kills about 14,000 Americans a year, a study showed.

In a trial among 43 people with recurrent diarrhea caused by a persistent bug called Clostridium difficile, 81 percent of those who received an infusion of feces from a healthy donor after treatment with vancomycin were cured, compared with only 31 percent of those treated with the drug alone, researchers from the University of Amsterdam wrote in an article published yesterday by the New England Journal of Medicine. The study was stopped early because the treatment was clearly working.
The results validate an approach called fecal microbiota transplantation, or FMT, pioneered in 1958 by doctors in Denver, and provides an alternative for the approximately one-in-four patients whose infection isn’t cleared by initial antibiotic treatment. C. difficile is the most common cause of hospital- acquired infectious diarrhea in the U.S. and costs about $1 billion a year to treat, according to the Centers for Disease Control and Prevention.
“Only patients with the most recalcitrant cases of C. difficile infection are likely to undergo FMT, usually out of desperation after multiple treatment approaches have failed,” Ciaran Kelly, a professor of medicine at Harvard Medical School, wrote in an editorial accompanying the study. The use of feces may be eliminated by the use of cultured bacteria that make the recipient resistant to C. difficile, Kelly said.

Restoring Bacteria

The procedure probably works by restoring normal gut bacteria, the researchers, led by Els van Nood, wrote in the study, which was funded by the Netherlands Organization for Health Research and Development and the Netherlands Organization for Scientific Research.
Vancomycin is sold as Vancocin by ViroPharma Inc. (VPHM) Vancocin accounted for $289 million in sales in 2011, more than half of Exton, Pennsylvania-based ViroPharma’s revenue.
A federal judge last week dismissed the company’s lawsuit against the U.S. Food and Drug Administration over generic forms of the antibiotic developed by Akorn Inc. (AKRX) and Watson Pharmaceuticals Inc. (WPI)
Optimer Pharmaceuticals Inc. (OPTR)’s Dificid, approved for sale in the U.S. in May 2011, was the first drug cleared for the infection in 25 years.
By Simeon Bennett - Jan 17, 2013 6:28 AM ET

Wednesday, January 23, 2013

Probiotics Made w/ Genetically Modified Fillers... Are they organic??

This article was on and to tell you the truth, I don't know what to believe.  Almost sounds like the writer is pushing the Sun Biotics brand.. I however, don't put much past the companies that manufacturer & produce the stuff we put in our body.  I try to have good faith in whatever it is I buy that the company is not corrupt.  Hard to tell though.  I guess it's a good idea to find a certified organic probiotic from now on. I 

(NaturalNews) A Natural News investigation into the probiotics industry has turned up alarming information about how probiotics are formulated and labeled. We've found that nearly all probiotics available in the U.S. market today are secretly formulated with genetically modified ingredients that are intentionally not listed on the label. The most common such ingredient is maltodextrin, a corn-derived flow agent.

Look for yourself at the probiotics available today, and you'll find something curious: Virtually none of them are certified USDA organic. Why is that? If you read the ingredients on the label, you might scratch your head and wonder why they can't make those ingredients organic. But the real story is found in the "dirty little secret" that probiotics supplement manufacturers are not listing on the labels: Maltodextrin and other fillers and flow agents that are derived from GM corn.

You are being lied to about probiotics ingredients

Here's the rock-bottom truth about probiotics: You are being LIED to about what they're made from because the FDA does not require manufacturers to list fillers and flow agents as ingredients.

Yep, you read that right: A probiotics manufacturer can add genetically modified corn maltodextrin to their formula and they are not required to disclose this on the label. While the maltodextrin will disqualify them from receiving organic certification, it doesn't stop them from using the word "natural" on their bottles.

Our Natural News investigation found that some probiotics contain as much as 30% maltodextrin in their formulas. Virtually all maltodextrin available today comes from genetically modified corn.

This means that consumers who think they're buying a healthy product to support digestion are actually buying products made from corn plants that are engineered to grow insecticide toxins right inside each and every kernel. Processing this into refined maltodextrin does not necessarily remove this toxin, meaning maltodextrin itself may be contaminated with the bt toxin that functions as an insecticide.

Friday, January 18, 2013

Fecal transplants cure diarrhea!! Wow what will they think of next

Interesting!!! Nuff said about this one.

Fecal transplants cure diarrhea, modulate testosterone levels

Nutella was not used as a placebo control.

From some perspectives, we humans aren't really so much individuals as we are walking ecosystems—our bodies carry more bacterial cells—with their own genomes and agendas—than the total count of human cells we're composed of. Bacteria cover our skin, get to our food before we have the chance to absorb it, and in many cases stay helpfully out of the way of the immune system.
Given all that, it shouldn't be a surprise that we're finding that bacteria can have significant effects on the human body in ways that go well beyond causing an infection. Two articles that appeared this week drive that home. In one, doctors cured a recurring, diarrhea-causing infection simply by transplanting gut bacteria from a healthy individual. And in the second, the bacterial transplants altered the progression of type 1 (autoimmune) diabetes in mice—by altering the animal's testosterone levels.

Fighting bacteria with bacteria

Clostridium difficile, or C. diff, is a bacteria that tends to cause extended bouts of diarrhea. In about 20 percent of the cases that end up under a doctor's care, it will get into the digestive system and refuse to come back out, creating recurring bouts of illness that don't respond to most antibiotics. At that point, the standard of care is an intensive course of vancomycin, which only works in about 60 percent of patients. With each further recurrence, the rate of success goes down even further.
Anecdotal evidence and case reports had suggested that the problem wasn't so much the presence of C. diff as the fact that it had grown out of balance with the rest of the gut's bacterial ecosystem. To get the gut back into balance, fecal transplants had been tried and, anecdotally at least, they worked. So some doctors in the Netherlands decided to do a clinical trial, comparing a fecal transplant to standard care with vancomycin. The trial was what the researchers called "open label," meaning that people were aware they were having a feeding tube stuffed down their nose to deliver someone else's poop into their body. (A Twitter pundit suggested a Nutella infusion might make for a good placebo control.)
A few dozen healthy volunteers were screened for a huge panel of infectious diseases, and those who came through clean were asked to rush their bodies' first deliveries of the day to the hospital, where it was mixed with saline and had the particulates removed. The results then went into the gastro-nasal tube, given to patients after their original gut flora had been cleared out by a "bowel lavage."
The authors had originally planned to get 40 patients for each group, but the fecal transplants were so successful, they stopped the trial after only 16 patients had received a transplant. Of these, 13 (80 percent) were cured after a single transplant. Two of the remaining three were cured after their second, bringing the success rate up to over 90 percent. In contrast, the success rate of vancomycin treatments was down around 30 percent.
The biggest problem? Enrolling patients. Most people who agreed to participate in the trial only did so after conventional treatments failed several times, "reflecting the reluctance of patients and physicians to choose donor-feces infusion at an early stage."

Bacteria, sex, and immunity

It's easy to view this as a demonstration of the hygiene hypothesis, which posits that all sorts of health issues are linked to exposure to a variety of infectious agents, which the immune system then learns to live in harmony with. But a second paper appeared this week that cautioned against viewing things as being quite that simple.
The paper focused on the progression of type 1 diabetes, which is the product of an autoimmune attack on the insulin-producing cells. There's a special strain of mice, called NOD (for non-obese diabetic) that are prone to developing this disorder. The mice show properties that are very much like the human version of the disease: it's genetically complex, the progression is influenced by environmental factors, and it strikes females more severely than males.
And, unexpectedly, it's influenced by gut bacteria. There was some hint of this, given that other researchers had shown that a systematic exposure to bacterial proteins was able to suppress the development of the disease. But the authors found an unexpected effect when they tested how the disorder progressed in mice raised in germ-free conditions. Rather than accelerating the development of symptoms in all mice, the germ-free conditions accelerated the progression in males, making them (at least in this assay) indistinguishable from females.
So the researchers tried an experiment: they took germ-free NOD mice and did a fecal transplant from adult male animals (mice are naturally coprophagic, so the mice took a lot less convincing than did the humans). When female NOD mice received gut bacteria from males, it actually slowed the disease progression down. The apparent sex difference in autoimmune function was mediated in part by gut bacteria.
Your first thought might be that testosterone in males could create a different environment in the gut, causing it to host a different diversity of species. It's a reasonable guess, but it's wrong. Instead, the researchers found that the transplant of gut bacteria caused a surge in testosterone production by females that lasted for up to 14 weeks. This had no effect on the female's fertility, but it did clearly alter immune function. If the authors injected these mice with a testosterone inhibitor, the diabetes protection went away.
All of which indicates that the other intuitive idea—that gut bacteria influence immune function by interacting directly with immune cells—also can't be right, or at least can't be everything. Clearly, the production of testosterone, by whatever cells may be producing it, plays a key role.
Although the papers argue against some of the simpler views of human health—bacteria are all bad, or not having exposure to pathogens means an overactive immune system—they both argue that viewing our bodies as a complex ecosystem can help provide insight into human health.
New England Journal of medicine, 2013. DOI: 10.1056/NEJMoa1205037 and Science, 2013. DOI:10.1126/science.1233521  (About DOIs).
Fecal transplants cure diarrhea, modulate testosterone levels | Ars Technica:

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Uceris Approved for Active Ulcerative Colitis #UC #IBD

Uceris sounds just like a drug that has been around for a while, Entercort (spelling?).  It works the same exact way Uceris works; it's a form of a steroid and releases in the colon.  Wonder what the difference is?/

Uceris Approved for Active Ulcerative Colitis

Santarus announced that the FDA has approved Uceris (budesonide) extended-release tablets for the induction of remission in patients with active, mild to moderate ulcerative colitis.
Uceris contains budesonide in a novel oral tablet formulation that utilizes proprietary MMX multi-matrix system technology, which is designed to result in the controlled release and distribution of budesonide throughout the length of the colon. Budesonide is a corticosteroid known to have localized anti-inflammatory effect.
Uceris will be available in 9mg extended-release tablets in 30-count bottles. Uceris is expected be available in March 2013.
For more information call (858) 314-5700 or visit

Uceris Approved for Active Ulcerative Colitis - MPR:

FDA Approves Uceris

Santarus Receives FDA Approval of Uceris (budesonide) for the Induction of Remission in Patients with Active, Mild to Moderate Ulcerative Colitis
SAN DIEGO--(BUSINESS WIRE)--Jan 15, 2013 - Santarus, Inc. announced today that the U.S. Food and Drug Administration (FDA) has approved Uceris (budesonide) extended release tablets for the induction of remission in patients with active, mild to moderate ulcerative colitis. The company expects to commence the commercial launch of Uceris in March 2013.
“The FDA approval of Uceris provides an important new therapeutic option to patients and physicians for the treatment of active, mild to moderate ulcerative colitis,” said William J. Sandborn, M.D., chief, division of Gastroenterology, director, University of California San Diego (UCSD) IBD Center and professor of clinical medicine, UCSD Health System. “Specifically, Uceris is indicated for use in the induction of remission of active disease, an acute phase of the disease often characterized by cramping, bloating, diarrhea, bleeding, fatigue, weight loss and frequent bowel movements.”Uceris contains budesonide, a corticosteroid, in a novel oral tablet formulation that utilizes proprietary MMX® multi-matrix system colonic delivery technology. The approved dosing regimen for adult patients is one 9 mg tablet taken orally once daily in the morning for up to 8 weeks. Uceris was developed in collaboration with Cosmo Technologies Limited, a subsidiary of Cosmo Pharmaceuticals S.p.A.
Gerald T. Proehl, president and CEO of Santarus, said, “We are pleased to provide a new option for patients to treat the active phase of mild to moderate ulcerative colitis. With the incremental revenue from Uceris and continued growth in our marketed products, we anticipate another robust year of solid financial results for Santarus in 2013. We expect total revenues of $320 million to $325 million, representing significant double-digit growth over our 2012 revenue guidance."

Important Safety Information About Uceris

Uceris is a prescription corticosteroid medicine used to help get mild to moderate ulcerative colitis under control. Uceris is taken once daily in the morning with or without food for up to 8 weeks.
  • Do not take Uceris if you are allergic to budesonide or any of the ingredients in Uceris.
  • Before you take Uceris, tell your doctor if you have liver problems, are planning to have surgery, have chickenpox or measles or have recently been near someone with chickenpox or measles, have or had a family history of diabetes, cataracts or glaucoma, have high blood pressure (hypertension), decreased bone mineral density (osteoporosis), stomach ulcers, any other medical condition, are pregnant or plan to become pregnant, or breastfeed or plan to breastfeed.
  • Tell your doctor about all the medications you take, including prescription and over-the-counter vitamins and herbal supplements. Uceris and other medicines may affect each other, causing side effects.
  • Do not eat grapefruit or drink grapefruit juice while taking Uceris because these can increase the level of Uceris in your blood.
  • Long-time use of Uceris can cause you to have too much glucocorticosteroid medicine in your blood (hypercorticism). Tell your doctor if you have any of the following signs and symptoms of hypercorticism: acne, bruise easily, rounding of your face (moon face), ankle swelling, thicker or more hair on your body and face, a fatty pad or hump between your shoulders (buffalo hump), or pink or purple stretch marks on the skin of your abdomen, thighs, breasts, and arms.
  • When Uceris is taken for a long period of time, the adrenal glands do not make enough steroid hormones. Tell your doctor if you are under stress or have any symptoms of adrenal suppression during treatment with Uceris, including tiredness, weakness, nausea and vomiting, and low blood pressure.
  • Uceris weakens your immune system. Taking medicines that weaken your immune system makes you more likely to get infections. Avoid contact with people who have contagious diseases such as chickenpox or measles while taking Uceris. Tell your doctor about any signs or symptoms of infection, including fever, pain, aches, chills, feeling tired, or nausea and vomiting.
  • If you take certain other corticosteroid medicines to treat allergies (e.g., eczema, rhinitis), switching to Uceris may cause your allergies to come back. Tell your doctor if any of your allergies become worse while taking Uceris.
  • The most common side effects with Uceris are headache, nausea, decreased blood cortisol levels, stomach-area pain, tiredness, stomach or intestinal gas, bloating, acne, urinary tract infection, joint pain, and constipation.
Uceris is available by prescription only. For additional information, talk to your healthcare provider and see the Full Prescribing Information including Patient Labeling.

Wednesday, January 09, 2013

LDN to treat Autoimmune Diseases - Clinical Trials

LDN Clinical Trials:
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Clinical Trials

Am J Gastroenterol. 2007 Apr;102(4):820-8. Epub 2007 Jan 11.
Low-dose naltrexone therapy improves active Crohn's disease.
Smith JP, Stock H, Bingaman S, Mauger D, Rogosnitzky M, Zagon IS.
Department of Medicine, Pennsylvania State University College of Medicine, Hershey, Pennsylvania 17033, USA.
OBJECTIVES: Endogenous opioids and opioid antagonists have been shown to play a role in healing and repair of tissues. In an open-labeled pilot prospective trial, the safety and efficacy of low-dose naltrexone (LDN), an opioid antagonist, were tested in patients with active Crohn's disease.
METHODS: Eligible subjects with histologically and endoscopically confirmed active Crohn's disease activity index (CDAI) score of 220-450 were enrolled in a study using 4.5mg naltrexone/day. Infliximab was not allowed for a minimum of 8 wk prior to study initiation. Other therapy for Crohn's disease that was at a stable dose for 4 wk prior to enrollment was continued at the same doses. Patients completed the inflammatory bowel disease questionnaire (IBDQ) and the short-form (SF-36) quality of life surveys and CDAI scores were assessed pretreatment, every 4 wk on therapy and 4 wk after completion of the study drug. Drug was administered by mouth each evening for a 12-wk period.
RESULTS: Seventeen patients with a mean CDAI score of 356 +/- 27 were enrolled. CDAI scores decreased significantly (P=0.01) with LDN, and remained lower than baseline 4 wk after completing therapy. Eighty-nine percent of patients exhibited a response to therapy and 67% achieved a remission (P < 0.001). Improvement was recorded in both quality of life surveys with LDN compared with baseline. No laboratory abnormalities were noted. The most common side effect was sleep disturbances, occurring in seven patients.
CONCLUSIONS: LDN therapy appears effective and safe in subjects with active Crohn's disease. Further studies are needed to explore the use of this compound.
PMID: 17222320

Integr Cancer Ther. 2007 Sep;6(3):293-6.
Reversal of signs and symptoms of a B-cell lymphoma in a patient using only low-dose naltrexone.
Berkson BM, Rubin DM, Berkson AJ.
Integrative Medical Center of New Mexico, Las Cruces, USA.
PMID: 17761642

Mult Scler. 2008 Sep;14(8):1076-83.
A pilot trial of low-dose naltrexone in primary progressive multiple sclerosis.
Gironi M, Martinelli-Boneschi F, Sacerdote P, Solaro C, Zaffaroni M, Cavarretta R, Moiola L, Bucello S, Radaelli M, Pilato V, Rodegher M, Cursi M, Franchi S, Martinelli V, Nemni R, Comi G, Martino G.
Institute of Experimental Neurology (INSPE) and Department of Neurology, San Raffaele Scientific Institute, Via Olgettina 58, Milan, Italy.
A sixth month phase II multicenter-pilot trial with a low dose of the opiate antagonist Naltrexone (LDN) has been carried out in 40 patients with primary progressive multiple sclerosis (PPMS). The primary end points were safety and tolerability. Secondary outcomes were efficacy on spasticity, pain, fatigue, depression, and quality of life. Clinical and biochemical evaluations were serially performed. Protein concentration of beta-endorphins (BE) and mRNA levels and allelic variants of the mu-opiod receptor gene (OPRM1) were analyzed. Five dropouts and two major adverse events occurred. The remaining adverse events did not interfere with daily living. Neurological disability progressed in only one patient. A significant reduction of spasticity was measured at the end of the trial. BE concentration increased during the trial, but no association was found between OPRM1 variants and improvement of spasticity. Our data clearly indicate that LDN is safe and well tolerated in patients with PPMS.
PMID: 18728058

Pain Med. 2009 May-Jun;10(4):663-72. Epub 2009 Apr 22.
Fibromyalgia symptoms are reduced by low-dose naltrexone: a pilot study.
Younger J, Mackey S.
School of Medicine, Department of Anesthesia, Division of Pain Management, Stanford University, 780 Welch Road, Suite 208, Palo Alto, CA 94304-1573, USA.
OBJECTIVE: Fibromyalgia is a chronic pain disorder that is characterized by diffuse musculoskeletal pain and sensitivity to mechanical stimulation. In this pilot clinical trial, we tested the effectiveness of low-dose naltrexone in treating the symptoms of fibromyalgia.
DESIGN: Participants completed a single-blind, crossover trial with the following time line: baseline (2 weeks), placebo (2 weeks), drug (8 weeks), and washout (2 weeks).
PATIENTS: Ten women meeting criteria for fibromyalgia and not taking an opioid medication.
INTERVENTIONS: Naltrexone, in addition to antagonizing opioid receptors on neurons, also inhibits microglia activity in the central nervous system. At low doses (4.5 mg), naltrexone may inhibit the activity of microglia and reverse central and peripheral inflammation.
OUTCOME MEASURES: Participants completed reports of symptom severity everyday, using a handheld computer. In addition, participants visited the lab every 2 weeks for tests of mechanical, heat, and cold pain sensitivity.
RESULTS: Low-dose naltrexone reduced fibromyalgia symptoms in the entire cohort, with a greater than 30% reduction of symptoms over placebo. In addition, laboratory visits showed that mechanical and heat pain thresholds were improved by the drug. Side effects (including insomnia and vivid dreams) were rare, and described as minor and transient. Baseline erythrocyte sedimentation rate predicted over 80% of the variance in drug response. Individuals with higher sedimentation rates (indicating general inflammatory processes) had the greatest reduction of symptoms in response to low-dose naltrexone.
CONCLUSIONS: We conclude that low-dose naltrexone may be an effective, highly tolerable, and inexpensive treatment for fibromyalgia.
PMID: 19453963

Inflamm Bowel Dis.. [Epub ahead of print]
Low-dose naltrexone for treatment of duodenal Crohn's disease in a pediatric patient.
Shannon A, Alkhouri N, Mayacy S, Kaplan B, Mahajan L.
Department of Pediatric Gastroenterology, Cleveland Clinic Pediatric Institute, Cleveland, Ohio.
PMID: 20014017

Annals of Neurology, Volume 9999, Issue 999A, Feb 2010
Pilot trial of low dose naltrexone and quality of life in MS
Bruce A.C. Cree, Elena Kornyeyeva, Douglas S. Goodin
Multiple Sclerosis Center at Univ. of Calif. in San Francisco 350 Parnassus Ave., Suite 908, San Francisco, CA 94117  USA
Objective: To evaluate the efficacy of 4.5 mg nightly naltrexone on the quality of life of multiple sclerosis patients.
Methods: This single center, double-masked, placebo-controlled, crossover studied evaluated the efficacy of eight weeks of treatment with 4.5 mg nightly naltrexone (Low dose naltrexone or LDN) on self reported quality of life of MS patients.
Results: 80 subjects with clinically definite multiple sclerosis were enrolled and 60 subjects completed the trial. 10 withdrew before completing the first trial period: 8 for personal reasons, 1 for a non-MS related adverse event and 1 for perceived benefit. Database management errors occurred in 4 other subjects and quality of life surveys were incomplete in 6 subjects for unknown reasons. The high rate of subject dropout and data management errors substantially reduced the trial's statistical power. LDN was well tolerated and serious adverse events did not occur. LDN was associated with significant improvement on the following mental health quality of life measures: a 3.3 point improvement on the Mental Component Summary score of the SF-36 (P=.04), a 6 point improvement on the Mental Health Inventory (P<.01), a 1.6 point improvement on the Pain Effects Scale (P=.04) and a 2.4 point improvement on the Perceived Deficits Questionnaire (P=.05).
Interpretation: LDN significantly improved mental health quality of life indices. Further studies with LDN in MS are warranted.
Who is LDNscience?  This is what they say......
LDNscience™ is a public information project of theMedInsight® Research Institute.
The MedInsight® Research Institute is a U.S.-based 501(c)(3) nonprofit working to bridge the ever-widening gap between medical research and actual medical practice. We are dedicated to bringing relief to those who suffer from cancer or chronic medical conditions by raising awareness of:
  • • Commercially unsponsored medications.
  • • Off-label or secondary uses for approved medications.
  • • Specialized tests that enable treatments to be tailored to the individual.
MedInsight's co-founder, Moshe Rogosnitzky, is an expert in the clinical application of Low Dose Naltrexone (LDN)Opioid Growth Factor (OGF) and related therapies, which have made incredible inroads with Crohn’s disease, cancer and other serious diseases. He collaborates in research with the discoverers of LDN and OGFDr. Ian S. Zagon and Dr. Patricia J. McLaughlin of Hershey Medical Center, Penn State University, as well as with Dr. Jill P. Smith of Hershey Medical Center, who conducts clinical research into LDN and OGF.
This site is intended to provide you with general information on the background, use of and evidence forLDNOGF and related therapies, and to answer any questions on these therapies and our work.  If you cannot find the answer to your particular question, please submit your question and we will respond to you as soon as possible.
To become a much-valued supporter of this site or of our life-changing research into LDNOGF and related therapies, please visit:  Join Our Supporters.
medinsight_logo_1Thank you,
The LDNscience™ Team

Tuesday, January 08, 2013

Research Article-IL-13 Promotes Collagen Accumulation in Crohn’s Disease Fibrosis by Down-Regulation of Fibroblast MMP Synthesis

Plos One Research Article.  Fibrosis is a serious consequence of Crohn’s disease (CD), often necessitating surgical resection. Research study examined the hypothesis that IL-13 may promote collagen accumulation within the CD muscle microenvironment. (Not written in layman terms.  Written using medical terminology which may be confusing for some to understand)

PLOS ONE: IL-13 Promotes Collagen Accumulation in Crohn’s Disease Fibrosis by Down-Regulation of Fibroblast MMP Synthesis: A Role for Innate Lymphoid Cells?



Fibrosis is a serious consequence of Crohn’s disease (CD), often necessitating surgical resection. We examined the hypothesis that IL-13 may promote collagen accumulation within the CD muscle microenvironment.


Factors potentially modulating collagen deposition were examined in intestinal tissue samples from fibrotic (f) CD and compared with cancer control (C), ulcerative colitis (UC) and uninvolved (u) CD. Mechanisms attributable to IL-13 were analysed using cell lines derived from uninvolved muscle tissue and tissue explants.


In fCD muscle extracts, collagen synthesis was significantly increased compared to other groups, but MMP-2 was not co-ordinately increased. IL-13 transcripts were highest in fCD muscle compared to muscle from other groups. IL-13 receptor (R) α1 was expressed by intestinal muscle smooth muscle, nerve and KIR+ cells. Fibroblasts from intestinal muscle expressed Rα1, phosphorylated STAT6 in response to IL-13, and subsequently down-regulated MMP-2 and TNF-α-induced MMP-1 and MMP-9 synthesis. Cells with the phenotype KIR+CD45+CD56+/−CD3 were significantly increased in fCD muscle compared to all other groups, expressed Rα1 and membrane IL-13, and transcribed high levels of IL-13. In explanted CD muscle, these cells did not phosphorylate STAT6 in response to exogenous IL-13.


The data indicate that in fibrotic intestinal muscle of Crohn’s patients, the IL-13 pathway is stimulated, involving a novel population of infiltrating IL-13Rα1+, KIR+ innate lymphoid cells, producing IL-13 which inhibits fibroblast MMP synthesis. Consequently, matrix degradation is down-regulated and this leads to excessive collagen deposition.