Patient Taking Adalimumab (Humira) - Questioning Why Makers of The Drug Are Preventing Disclosure of Trial Data.

......He isn't the only one wondering what in the hell is up AbbVie's sleeve.  

I don't even take the drug, I never will, but what's the deal with withholding data like this.  Let's see it, AbbVie!  Shouldn't trial information be available to the general public in order for people to make informed decisions regarding the best treatment choice? How can people do that, when the information isn't there!?  
I visualize a bunch of robots.. The robots are the patients, they take what they are given and do as they are told.  God forbid people ask questions and want the answers and demand them.  People have the right to know this information... right?  For the people that take this stuff, they put the chemical into their body everyday and they aren't allowed to know everything there is to know about the stuff?  That just doesn't sit well with me and it shouldn't sit well with you either.  
It's sketchy.. The whole drug/medicine/medical industry can't be trusted.  They really are starting to show their faces by trying to put a curtain in front of them.  When people are told "No" to something that is usually otherwise available, it just holds a red flag to it and makes people wonder things, speculate what the reasons may be for withholding.  AbbVie is making it quite clear that they have something to hide.  Logically, what reason would they have for wanting to hold back trial data... unless the data shows something that could result in an unfavorable response.  It might make people requestion if Humira is for them or not.  Now if the data were positive, wouldn't the company want to display it for the world to see?  It would lead to more sales and continued use of the treatment.
Let's face it, your doctor isn't running down the whole list of possibly negative consequences of taking the drug before you start it.  He/she just isn't and that's that. They shine a positive outlook on the drug because they want you to take it.  In addition, THEY don't even know the ins and outs of the drug.  That's really our job and our responsibility as patients to do our homework.  Some people do their research and some  people don't, but for the ones who do, not having this information easily available or just not showing "all" of the information is just giving people a false/skewed view of what the drug really is.  
Not cool!

A patient with Crohn's disease is concerned about the attempt by the makers of adalimumab to prevent disclosure of trial data submitted during the drug's approval process, according to a personal view piece published online April 16 in BMJ.

THURSDAY, April 18 (HealthDay News) -- A patient with Crohn's disease is concerned about the attempt by the makers of adalimumab to prevent disclosure of trial data submitted during the drug's approval process, according to a personal view piece published online April 16 in BMJ.

Alex Lomas, a patient with Crohn's disease from London who has been taking adalimumab for three years with beneficial results discusses the lack of trial data available on biologicals.

Noting that part of the National Institute for Health and Care Excellence's approval for use of adalimumab for Crohn's disease was the recommendation to set up a registry to track long-term outcomes and relapse rates after treatment withdrawal, Lomas reports that registries are fragmented or are still at pilot stage. He adds that the attempt by AbbVie, the maker of adalimumab, to prevent the European Medicines Agency from disclosing recent trial data submitted during the drug's approval process is cause for concern and is preventing patients and health care providers from making informed decisions about the use of this treatment.

"As the drug industry and medical profession as a whole move towards the registration of all trials, and the publication of all trial data -- in no small way thanks to the All Trials initiative (www.alltrials.net) -- this decision by AbbVie is a backwards step and is offensive to trial participants, patients, and the wider public who ultimately pick up the tab," Lomas writes.

Health News Copyright © 2013 HealthDay. All rights reserved.

The patient Alex Lomas is taking a biological drug for Crohn’s disease, and he wants to know why the maker is trying to prevent disclosure of trial data that may well affect him

I have an obsession with data. I have instruments in my house so I know how hot each room is and to warn me if the fridge door has been open for too long. I record my weight and blood pressure using devices connected to the internet so that I can monitor long term trends. I use my smartphone to track how much walking and exercise I do.

I was diagnosed with Crohn’s disease about 20 years ago, when awareness of inflammatory bowel diseases was not as high as it is today.1 The treatment decisions made at the time of my diagnosis had unfortunate side effects for me as a teenager. High doses of prednisolone led to Cushing’s syndrome, and I was mercilessly teased about my appearance at school. With time came a reduction in the dose of steroids required, but I had to take them throughout my 20s, and control of my symptoms was still inadequate.

As a patient with Crohn’s disease, I take an active interest in my day-to-day health, but I also routinely scan news media and journal sites for new treatments and for changes to current best practice in the management of my condition. I often arrive at appointments with my consultant armed with PDFs printed from the BMJ, the Cochrane Collaboration, and the National Institute for Health and Care Excellence (NICE) to discuss the latest trials and treatment options. Yes, I’m afraid I’m one of those patients.

Three years ago my consultant suggested a new course of treatment with adalimumab (Humira), an anti-TNFα monoclonal antibody. My local primary care trust approved this new drug, which costs £352 per injection, and which I administer myself by injection each fortnight.2 Since I started taking adalimumab I have the least symptoms since diagnosis. I am no longer taking steroids; I have started to recover from 15 years of side effects; and I spend less time in clinical care and off work on sick leave.

However, anecdotes are not the foundation of evidence based medicine, and nor are they a rational basis for evaluating the cost of a treatment. On 1 April 2013 responsibility for commissioning transferred from my primary care trust to the local clinical commissioning group, bringing into sharp focus the question of whether the NHS is getting value for money in continuing my treatment.

Equally importantly, I want to be able to evaluate the benefits and risks of these costly pharmaceuticals with which I inject myself regularly. Biologicals are relatively new, and have failed spectacularly in clinical trials.3 Who knows what 20 or 30 years of data from clinical use might bring? The most recent Cochrane review of biologicals looked at nine studies, and, although it found that they were effective, it noted that none of the trials allowed for an assessment of long term adverse events nor had any trials been undertaken that compared efficacy among the available biologicals.4 My consultant recently told me that no trials had been done to determine what the minimum effective dose of adalimumab was, nor would there likely ever be; a drug company has no interest in showing you can take less of something.

Part of NICE’s approval for the use of adalimumab in treating Crohn’s disease was the recommendation that a register of patients being treated with biologicals be set up to track long term outcomes and relapse rates after withdrawal of treatment, something patient groups welcomed.5 Unfortunately it seems that such registers are fragmented, with registers of patients with rheumatoid arthritis held independently from registers of patients with inflammatory bowel disease, or are still at pilot stage.6

As a patient, I need clinicians to interpret trial data and systematic reviews of new and existing treatments so we can come to appropriate decisions about my treatment, but what if even experts don’t get to see the whole picture? How can we even know what trials are being run?

I was therefore dismayed to learn that Abbvie, the maker of adalimumab, are seeking a legal injunction to prevent the European Medicines Agency from disclosing trial data submitted during the drug’s approval process.7 With such a new drug, it is vital that all data, whether it’s good news or bad, are made available so that I, my consultant, and the care commissioning group can make informed decisions about the efficacy and cost effectiveness of treatments.

As the drug industry and medical profession as a whole move towards the registration of all trials, and the publication of all trial data—in no small way thanks to the All Trials initiative (www.alltrials.net)—this decision by Abbvie is a backwards step and is offensive to trial participants, patients, and the wider public who ultimately pick up the tab.

Notes

Cite this as: BMJ 2013;346:f2336

Footnotes

• Competing interests: I have read and understood the BMJ Group policy on declaration of interests and have no relevant interests to declare.
• Provenance and peer review: Not commissioned; not externally peer reviewed.

References

1. ↵
   Molodecky NA, Soon IS, Rabi DM, Ghali WA, Ferris M, Chernoff G, et al. Increasing incidence and prevalence of the inflammatory bowel diseases with time. Gastroenterology2012;142:46-54.

   CrossRefMedlineWeb of Science
2. ↵
   Adalimumab. British National Formulary. www.medicinescomplete.com/mc/bnf/current/PHP6632-humira.htm.
3. ↵
   Goodyear M. Learning from the TGN1412 trial. BMJ2006;0:38797.635012.47
4. ↵
   Behm BW, Bickston SJ. Tumor necrosis factor-alpha antibody for maintenance of remission in Crohn’s disease. Cochrane Database Syst Rev2008;1:CD006893.

   Medline
5. ↵
   NACC. A good decision from NICE on antiTNF treatments for Crohn’s disease. 2010. www.nacc.org.uk/downloads/media/NACC_statement_antiTNFs_4_March_2010.pdf.
6. ↵
   Alrubaiy L, Williams J, Morgan J. P422. The Biologics Register for inflammatory bowel disease in the UK: setting the clinical dataset and the IT infrastructure. ECCO, 2013. https://www.ecco-ibd.eu/publications/congress-abstract-s/item/p422-the-bi.html.
7. ↵
   Kmietowicz Z. Drug firms take legal steps to prevent European regulator releasing data. BMJ2013;346:f1636.

   FREE Full Text

I’m a patient: show me the trial data | BMJ:

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Colleen  for Following & Supporting my Blog!

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my blog want info on something, let me know

I love researching stuff and helping people.

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Researchers Report - 200 Genes Have a Connection to Crohn's Disease

Wish there was more to be said about these 200 genes they found that point to Crohn's.  Nice to know.  

Crohn's Disease, from what I read on a regular basis, is one of the most complex diseases to understand.  Scientists seem to always discover a relationship with "A" ("A" could be any of the following, I'm only listing a few:  impaired  immune response, an increased level of a serine protease, an antigen/toxin, introduced into the body,  a pathogen {a bacteria(especially MAP), virus, fungus} are associated with Crohn's, genetic factors... 200 of them apparently, drugs ( Accutane is the one I hear about the most), environmental factors such as hormonal therapy, ex. birth control.  Not enough exposure to parasites, microorganisms and infectious agents in early childhood- See: Hygiene Hypothesis.     OK that's enough.    You get the point.  

Crohn's can be associated with so many factors, but the progression to determine more components about that factor "A", may lead to other discoveries that bring understanding about how "A" and "B", but not enough to progress with more research studies. 

Then ... That's it!  Scientists reach dead ends. It seems as if the findings discovered do not provide enough concrete information to bring more understanding about the disease which halts additional  research You never hear  much more about the relationship between A & B again. This happens so much with so many of the studies that seek to understand the disease and they all seem to reach a dead end at some point during the research.  There's  a few factors that have a pretty good progression that continue to lead to more connections; & its MAP.  It is the only information that I have read  and continue to read that discover  new findings and links to Crohn's.  Scientists are able to get somewhere with their findings that allow them to be able to do more studies and they gain more  understanding about the disease. 

The other factor that stands out is the Hygiene Hypothesis.  Read about it, it makes sense. 

Of all the conditions we would have to have is one as complicated as the Crohn.    I associate the Crohn's with a nightmare person that is sorta like a stalker/rude/unpredictable/enjoys messing up my day(s) and overstays their welcome ... but they were never welocome to begin with ... The nightmare just comes right in and makes itself at home.   

Anyway... enough of my babble.  Feel free to comment on your thoughts on what research seems to stand and  make progress toward an effective treatment and maybe even a cure.  I'd love to hear what you've found .

Scientists Now See 200 Genes Linked to Crohn's Disease: MedlinePlus:

WEDNESDAY, Dec. 19 (HealthDay News) -- Using a new technique, researchers have pinpointed a large number of additional genes associated with Crohn's disease, bringing the total to 200.

The scientists at University College London, in England, created a new method to identify and map the locations of genes associated with complex inherited diseases such as Crohn's.

Crohn's disease, a type of inflammatory bowel disease, affects about 100 to 150 people out of every 100,000. Understanding more about the genes associated with the disease may lead to improved treatments, the researchers said.

The 200 genes so far linked to Crohn's are more than have been found for any other disease, according to the researchers. For example, just 66 gene regions are known for type 2 diabetes.

"The discovery of so many gene locations for Crohn's disease is an important step forward in understanding the disease, which has a very complicated genetic basis," study senior author Dr. Nikolas Maniatis said in a university news release. "We hope that the method we have used here can be used to identify the genes involved in other diseases which are similarly complex -- for example different cancers and diabetes."

The new research was published Dec. 13 in the American Journal of Human Genetics.

SOURCE: University College London, news release, Dec. 13, 2012

HealthDay

Copyright (c) 2012 HealthDay. All rights reserved.

#LDN as treatment- 4 #Fibromyalgia - Positive Results in Trial

Published in February 2013, study to determine the effectiveness of naltrexone in low doses for fibromyalgia has again displayed positive results as a good treatment option for this condition.  Low Dose Naltrexone showed significant reduction in baseline pain, improvement with general quality of life and also mood improvement.  

Abstract of study is below.

Low-dose naltrexone for the treatment of fibromyalgia: Findings of a small, randomized, double-blind, placebo-controlled, counterbalanced, crossover trial assessing daily pain levels.

Arthritis Rheum. 2013 Feb;65(2):529-38. doi: 10.1002/art.37734.

Younger J, Noor N, McCue R, Mackey S.

Source

Stanford University School of Medicine, Palo Alto, California. jarred.younger@stanford.edu.

Abstract

OBJECTIVE:

To determine whether low dosages (4.5 mg/day) of naltrexone reduce fibromyalgia severity as compared with the nonspecific effects of placebo. In this replication and extension study of a previous clinical trial, we tested the impact of low-dose naltrexone on daily self-reported pain. Secondary outcomes included general satisfaction with life, positive mood, sleep quality, and fatigue.

METHODS:

Thirty-one women with fibromyalgia participated in the randomized, double-blind, placebo-controlled, counterbalanced, crossover study. During the active drug phase, participants received 4.5 mg of oral naltrexone daily. An intensive longitudinal design was used to measure daily levels of pain.

RESULTS:

When contrasting the condition end points, we observed a significantly greater reduction of baseline pain in those taking low-dose naltrexone than in those taking placebo (28.8% reduction versus 18.0% reduction; P = 0.016). Low-dose naltrexone was also associated with improved general satisfaction with life (P = 0.045) and with improved mood (P = 0.039), but not improved fatigue or sleep. Thirty-two percent of participants met the criteria for response (defined as a significant reduction in pain plus a significant reduction in either fatigue or sleep problems) during low-dose naltrexone therapy, as contrasted with an 11% response rate during placebo therapy (P = 0.05). Low-dose naltrexone was rated equally tolerable as placebo, and no serious side effects were reported.

CONCLUSION:

The preliminary evidence continues to show that low-dose naltrexone has a specific and clinically beneficial impact on fibromyalgia pain. The medication is widely available, inexpensive, safe, and well-tolerated. Parallel-group randomized controlled trials are needed to fully determine the efficacy of the medication.

Copyright © 2013 by the American College of Rheumatology.

PMID:

 

23359310

 

[PubMed - in process]

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Low-dose naltrexone for the treatment of fib... [Arthritis Rheum. 2013] - PubMed - NCBI:

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*Videos* - Interview w/ Dr. Bihari about LDN - History of LDN

Want to know about LDN ....or  should I say.. Do you want to know MORE about LDN.?  By now, you should know the basics and then some if you have been reading my blogs that I've posted  about the treatment 

If you haven't watched anything or read anything about LDN, this is the one to watch. The doctor  answers a lot of questions and talks about how the drug works.  You'll understand it.   

Harvard-educated Bernard Bihari, MD is interviewed about his life, and his discovery of Low Dose Naltrexone (LDN) for autoimmune diseases: multiple sclerosis, lupus, rheumatoid arthritis, Crohn's disease; also HIV/AIDS and some cancers. This video was given to me by Dr. Bihari's widow, Jacqueline Young.

The video is below.  The interviewer isn't that great cause you can't hear him to well.  Despite that, the Dr. is easy to understand and follow.   This is a long video  (fyi), not all may be interested if you don't care about knowing how the drug works to treat different diseases .  I watched the whole thing because I like such action packed videos.  lol  Im such a nerd!  

I wanted to hear what the man had to say about his advancements  that he discovered through his lifetime.  He's freaking awesome.  He speaks a lot about the research he was working on before he passed away which was HIV/AIDS and cancer and how LDN really is helpful with regulating the immune system .  But he's talking about the body and how the endorphins in the body effect the immune system/response.  He touches on the following points that you may be interested in watching 

I'm glad I watched this because I have a better understanding of how the medicine works in the body and helps balance/regulate the immune system.  His theory suggests that people with cancer, aids, autoimmune diseases have a lower than normal amt of endorphins in the body.  Its all about increasing the body's endorphins!

11:40 - talks about the improvement in AIDS patients with taking ldn, also talks about cancer patients

16:10 - He speaks about LDN and the endorphins. 

18:45 - cell death (cancer cells)caused by endorphins 

**20:19 - 23:00 ** I would def watch this part.  good explaining about the importance of endorphins more about how ldn works in the body (cancer patients... speaks about low endorphins  and how LDN raises the level of endorphins in the body) 

51:10 - the different endorphin receptors and what they effect in the body. interesting 

 He says around 30K-40K people take LDN.  

& Here it is...LISTEN --->  57:09 - 100:20 Touches on Autoimmune Diseases FINALLY.  My undertsanding of how this works goes like this I think.    -   .our t-helper cells get out of wack and get impaired  some how... (probably by a bacteria,  that throws it off) that therefore effects our killer cells & macrophages which get confused with the self vs the bacteria/fungus.  They get confused and attack own tissue/cells and not the foreign bacteria.  From what he says I think the LDN enhances the functioing of the t-cells by increasing the endorphin levels, the endorphins then regulate immune response

101:13 - the amount it costs to run clinical trials for LDN for each condition.  not sure if  he said 15 or 50 million for the 1st 3 trials.  He says that finding a drug company that would want to run the trials,  work w/ FDA, ability to manufacturer , distribute and then advertise is difficult.  

1:04:40 -  talked about low toxicity rate... it doesn't exist.  That's so bomb!, the cost (super cheap)..  Those aspects are probably the main reason LDN will never get approved to treat any other condition..  There's no money to make with this medicine, what would be the incentive.... to make people better... Yeah ok!! LOL  Guess doctors will just have to continue to write it as "off label use".  

VIDEO- Low Dose Naltrexone (LDN) Pioneer Dr. Bernard Bihari Talks About His Work Through His Life

Background of Low Dose Naltrexone LDN

Naltrexone was licensed in 1984 by the FDA in a 50 mg dose as a treatment for heroin addiction. It is a pure opiate antagonist (blocking agent) and its purpose was to block the opioid receptors that heroin acts on in the brain. When it was licensed, Dr. Bihari, then involved in running programs for treating addiction, tried it in more than 50 heroin addicts who had stopped heroin use. None of the patients would stay on the drug because of side effects experienced at 50 mg such as insomnia, depression, irritability and loss of feelings of pleasure, all due to the effect of the drug at this dose in blocking endorphins. These are the hormones in the body that heroin resembles. Physicians treating heroin addicts therefore, for the most part, stopped prescribing naltrexone. In 1985, a large number of heroin addicts began to get sick with AIDS—studies showed that 50% of heroin addicts were HIV Positive.

Dr. Bihari and his colleagues decided to shift their research focus to AIDS, in particular focusing on ways of strengthening the immune system. Since endorphins are the hormones centrally involved in supporting and regulating the immune system, levels of endorphins were measured in the blood of AIDS patients. They were found to average only 25% of normal.

Naltrexone, when given to mice and people at high doses, raises endorphin levels in the body's effort to overcome the naltrexone blockade. This drug became the focus of Dr. Bihari's research group. When the group discovered that endorphins are almost all produced in the middle of the night, between 2 AM and 4 AM, the studies focused on small doses (1.5-4.5 mg at bedtime) with the hope that a brief period of endorphin blockade before 2 AM might induce an increase in the body's endorphin production. In fact, the drug did so in this dosage range. It had no effect below 1.5 mg and too much endorphin blockade at doses over 5 mg. A placebo-controlled trial in AIDS patients showed a markedly better outcome in patients on the drug as compared with those on placebo.

During the trial, a close friend of Dr. Bihari's daughter had three acute episodes of multiple sclerosis over a nine-month period with complete spontaneous recovery from each. Because of his knowledge of MS as a neurologist and of recent evidence of an autoimmune component in the disease, Dr. Bihari started his daughter's friend on naltrexone at 3 mg every night at bedtime. She took it for five years with no further attacks. At that point, when a particular month's supply ran out, she stopped it because of some denial that she had MS. Three and a half weeks later, she developed an episode of weakness, numbness, stiffness and spasms in her left arm and resumed LDN, which she has stayed on since. This episode cleared and over the 12 years since, she has had no further disease activity.

The apparent mechanism of action of LDN in this disease parallels that in AIDS and other immune-related diseases. A small dose of the drug taken nightly at bedtime doubles or triples the endorphin levels in the body all of the next day restoring levels to normal. Since endorphin levels are low in people with MS, immune function is poorly orchestrated with significant impairment of the normal immune supervisory function of CD4 cells. In the absence of normal orchestration of immune function, some of the immune system cells "forget" their genetically determined ability to distinguish between the body's 100,000 unique chemical structures (called "self") and the chemical structures of bacteria, fungi, parasites and cancer cells (called "non-self"). With this loss of immunologic memory, some cells begin to attack some of the body's unique chemical structures. In the case of people with MS, the tissue attacked by immune cells (particularly macrophages) is primarily the myelin that insulates nerve fibers. These attacks result in scars in the brain and spinal cord called plaques. LDN in such patients works by restoring endorphin levels to normal, thereby allowing the immune system to resume its normal supervision and orchestration.

There exists a common notion that the immune system in a person with an autoimmune disorder is too strong and, in its exuberance, targets a body tissue for attack. Rather, the evidence is more consistent with autoimmunity resulting from immunodeficiency.¹ Kukreja et al have demonstrated that multiple immunoregulatory T cell defects lie behind Type 1 diabetes both in humans and in non-obese diabetic mice.²

Multiple scientific papers from various other research centers have demonstrated that an underlying immunodeficiency is characteristic of any tested autoimmune disease. Examples thus far reported include multiple sclerosis, rheumatoid arthritis, Crohn's disease, and chronic fatigue syndrome.^{3, 4, 5}

Sacerdote et al measured low beta-endorphin levels in two animal examples of autoimmune disease — a mouse strain with a lupus-like syndrome and a strain of chicken with an autoimmune thyroiditis.⁶ They had significantly lower hypothalamic concentrations of the opioid than normal controls. In each case, the low levels of beta-endorphin were found well before the expression of autoimmune disease. This adds to considerable evidence of a key role for endorphins in regulating immune responses and suggests a therapeutic pathway.

Bihari et al found that a low oral dose of the opioid antagonist naltrexone, when taken at bedtime, led to a doubling or tripling of low levels of circulating beta-endorphin.⁷ Bihari has since treated some 100 people with autoimmune disorders. None of them has progressed further while the patient continued taking low dose naltrexone each night at bedtime. Since no side effects are apparently associated with its use, this medication might well be studied as a possible preventive for Type I diabetes in those youngsters with beta-cell autoantibodies.

Footnotes

1. Buckley RH. Primary Immunodeficiency Diseases Due to Defects in Lymphocytes. N Engl J Med. 2000; 343:1313-1324.
2. Kukreja A, Cost G, Marker J, et al. Multiple immuno-regulatory defects in type-1 diabetes. J Clin Invest. 2002;109(1):131-40.
3. Thewissen M, Linsen L, Somers V, Geusens P, Raus J, Stinissen P.Premature immunosenescence in rheumatoid arthritis and multiple sclerosis patients. Ann N Y Acad Sci. Jun 2005;1051: 255-62.
4. Marks DJ, Harbord MW, MacAllister R, Rahman FZ, Young J, Al-Lazikani B, Lees W, Novelli M, Bloom S, Segal AW. Defective acute inflammation in Crohn's disease: a clinical investigation. Lancet. Feb 2006;367 (9511): 668-78.
5. Vernon SD, Reeves WC. The challenge of integrating disparate high-content data: epidemiological, clinical and laboratory data collected during an in-hospital study of chronic fatigue syndrome. Pharmacogenomics. Apr 2006;7 (3): 345-54.
6. Sacerdote P, Lechner O, Sidman C, et al. Hypothalamic beta-endorphin concentrations are decreased in animals models of autoimmune disease. J Neuroimmunol. 1999;97(1-2):129-33.
7. Bihari B, Drury FM, Ragone VP, et al. Low Dose Naltrexone in the Treatment of Acquired Immune Deficiency Syndrome. Oral Presentation at the IV International AIDS Conference, Stockholm, Jun 1988.

Dr. Skip Lenz at the 08 LDN Conference at USC, 

www.skipspharmacy.com - Very good Compounding Pharmacy for LDN

Video talks about taking other drugs with LDN (pain meds)

Dr. Lenz talks about patients' symptoms prior to taking LDN, after taking LDN & side-effects

 (aw poor guy. he said he only makes 32 cents/mo from the sales of LDN (fyi-he owns skips pharmacy..

LDN CONFERENCE (the sound quality is weird)

He says about 4500 doctors write scripts for LDN in the US(these are just #'s at his pharmacy)

He mentions how many people w/ Crohns take LDN from his pharmacy, 200 I believe. and he called Crohnies amazing people.. hahaa Go to 1:33.  He mentions Crystal the chick w/ the list of all doctors that prescribes LDN across the US and many other countries.  She was very helpful to me when i was searching for a prescribing Dr. (If you'd like to know which doctors prescribe in your area, just let me know.  I will give you her contact info)  

LDN CONFERENCE CONT..

Naltrexone is an opiate antagonist drug developed in the 1970s and approved by the FDA in 1984 for opiate and drug abuse treatment. When used at much lower doses in an off-label protocol referred to as low dose naltrexone (LDN), the drug has been shown to halt disease progression in Crohn's disease and certain cancers, to reduce symptoms in multiple sclerosis and autism, and to improve numerous autoimmune and neurodegenerative conditions, including Parkinson's disease and amyotrophic lateral sclerosis (ALS).

Grounded in clinical and scientific research, this book describes the history of naltrexone, its potential therapeutic uses, its effects on the immune system, its pharmacological properties, and how the drug is administered. It also lists fillers and compounding pharmacies, doctors who prescribe LDN, and patient resources, and includes interviews with LDN patients and researchers. *Author: Moore, Elaine A./ Wilkinson, Samantha/ Agrawal, Yash Pal *Binding Type: Paperback *Number of Pages: 213 *Publication Date: 2008/12/04 *Language: English *Dimensions: 8.80 x 5.90 x 0.70 inches

Blocking Tumor-Elicited Inflammation & The Impact on Cancer Growth

Interesting short article published in Nature.  It discusses how tumor-associated inflammatory reaction can lead to cancer, but what happens when this inflammatory response is disrupted, blocked, interrupted?  Something to think about.

Blocking Tumor-Induced Inflammation Impacts Cancer Development The findings are published in the October 3, 2012 Advanced Online Edition of Nature.

Oct. 3, 2012 — Researchers at the University of California, San Diego School of Medicine report the discovery of microbial–dependent mechanisms through which some cancers mount an inflammatory response that fuels their development and growth.

The association between chronic inflammation and tumor development has long been known from the early work of German pathologist Rudolph Virchow. Harvard University pathologist Harold Dvorak later compared tumors with “wounds that never heal,” noting the similarities between normal inflammation processes that characterize wound- healing and tumorigenesis or tumor-formation.

Indeed, 15 to 20 percent of all cancers are preceded by chronic inflammation – a persistent immune response that can target both diseased and healthy tissues. Chronic hepatitis, for example, may result in hepatocellular carcinoma (liver cancer) and inflammatory bowel disease can eventually cause a form of colon cancer, known as colitis-associated cancer.

Still, most cancers are not preceded by chronic inflammation. On the other hand, they exploit ubiquitous, infiltrating immune cells to unduly provoke and hijack the host inflammatory reaction. Until now, the mechanism of so-called “tumor-elicited inflammation,” which is detected in most solid malignancies, was poorly explained.

A Mouse colorectal tumors display inflammatory infiltration by macrophages (green) and activated stromal cells (red). The question of why and how tumors recruit immune cells remains unknown. (Credit: UC San Diego School of Medicine) dd caption

“The tumor-associated inflammatory reaction is an emerging and vibrant field for biomedical studies. It may hold the keys for future preventive and therapeutic measures,” said first author Sergei Grivennikov, PhD, noting that studies of long-term users of non-steroidal anti-inflammatory drugs, such as aspirin, have revealed that general inhibition of inflammation reduces the risk of cancer death by up to 45 percent, depending on the type of cancer. “So inhibition of inflammation during cancer development may be beneficial.”

Studying early colonic tumors in humans and in animal models, the researchers, led by principal investigator Michael Karin, PhD, Distinguished Professor of Pharmacology and head of the Laboratory of Gene Regulation and Signal Transduction at UC San Diego, found that developing tumors disrupt tissue homeostasis (the normal, healthy functioning of tissues), in part because they lack a particular protective protein coating and a tight seal between their epithelial cells – a basic cell type that covers most internal surfaces and organs. Without that coating and the cellular seal, ordinarily benign, commensal bacteria present in the colon can enter the tumor to be recognized by immune cells as invaders, launching an inflammatory reaction.

In addition, said Grivennikov, who is a scientist in Karin’s lab, “cell-to-cell contacts are defective in tumors, further allowing entry of microbial products from the intestinal lumen into the tumor. These microbial products are recognized by tumor-associated macrophages and dendritic cells, which are normally isolated from commensal microflora by the intestinal barrier.”

In response, the immune cells produce signaling proteins called cytokines that further spur the inflammatory process. Chief among these is a cytokine called Interleukin-23, which regulates tumor-elicited inflammation and triggers the production of other inflammatory cytokines that promote tumor development and progression.

Grivennikov said that when researchers reduced the presence of commensal microflora through a combination of broad spectrum antibiotics, tumor-elicited inflammation and tumor growth were dampened.

“This is a very nice demonstration of how tumor-elicited inflammation in cancers that arise in the absence of underlying chronic inflammatory disease can be induced,” he said. “The next step is to look for the upregulation of Interleukin-23 and related cytokines in colon cancer patients, inhibit these cytokines and determine whether these impact cancer progression and response to therapy.”

Funding for this research came, in part, from the Crohn’s and Colitis Foundation of America, National Institutes of Health/National Institute of Diabetes and Digestive and Kidney Diseases grant K99-DK088589; UCSD DDRDC Pilot Grant DK080506; the Croucher Foundation and China Postdoctoral Science Foundation; the Strategic Young Researcher Overseas Visits Program for Accelerating Brain Circulation; SPAR Austria; National Institutes of Health grants R01CA082223, A1043477 and DK035108 and the American Association for Cancer Research.

Co-authors include Kepeng Wang, UCSD Laboratory of Gene Regulation and Signal Transduction, Department of Pharmacology and Pathology and the Biomedical Research Institute, Shenzhen-PKU-HKUST Medical Center, China; Daniel Mucida, La Jolla Institute for Allergy and Immunology and the Laboratory of Mucosal Immunology, The Rockefeller University, New York; C. Andrew Stewart, Cancer and Inflammation Program, Laboratory of Experimental Immunology, Center for Cancer Research, National Cancer Institute, National Institutes of Health; Bernd Schnabl, UCSD Department of Medicine, School of Medicine; Dominik Jauch and Guann-Yi Yu, UCSD Laboratory of Gene Regulation and Signal Transduction, Department of Pharmacology and Pathology; Koji Taniguchi, UCSD Laboratory of Gene Regulation and Signal Transduction, Department of Pharmacology and Pathology and Department of Microbiology and Immunology, Keio University School of Medicine, Tokyo; Christoph H. Österreicher, UCSD Department of Medicine, School of Medicine and Institute of Pharmacology, Center for Physiology and Pharmacology Medical University of Vienna, Austria; Kenneth E. Hung, Department of Medicine, Tufts Medical Center, Boston; Christian Datz, Department of Internal Medicine, Oberndorf Hospital, Paracelsus Medical University Salzburg, Austria; Ying Feng and Eric R. Fearon, Departments of Internal Medicine, Human Genetics and Pathology, University of Michigan Medical School; Mohamed Oukka, Seattle Children’s Research Institute, Washington; Lino Tessarollo, Mouse Cancer Genetics Program, National Cancer Institute, National Institutes of Health; Vincenzo Coppola, Department of MVIMG, Ohio State University-CCC, Wexner Medical Center; Felix Yarovinsky, Department of Immunology, University of Texas Southwestern Medical Center; Hilde Cheroutre, La Jolla Institute for Allergy and Immunology; Lars Eckmann, UCSD Department of Medicine, School of Medicine; and Giorgio Trinchieri, Cancer and Inflammation Program, Laboratory of Experimental Immunology, Center for Cancer Research, National Cancer Institute, National Institutes of Health.

Journal Reference:

1. Sergei I. Grivennikov, Kepeng Wang, Daniel Mucida, C. Andrew Stewart, Bernd Schnabl, Dominik Jauch, Koji Taniguchi, Guann-Yi Yu, Christoph H. Österreicher, Kenneth E. Hung, Christian Datz, Ying Feng, Eric R. Fearon, Mohamed Oukka, Lino Tessarollo, Vincenzo Coppola, Felix Yarovinsky, Hilde Cheroutre, Lars Eckmann, Giorgio Trinchieri, Michael Karin. Adenoma-linked barrier defects and microbial products drive IL-23/IL-17-mediated tumour growth. Nature, 2012; DOI:10.1038/nature11465

Blocking tumor-induced inflammation impacts cancer development: