Tuesday, October 31, 2006

Methylthioadenosine Effective in Animal Models of Multiple Sclerosis

NEW YORK (Reuters Health) Oct 19 - Methylthioadenosine (MTA), an adenine nucleoside produced from S-adenosylmethionine, is effective in animal models of acute and chronic multiple sclerosis (MS), according to a report in the September issue of the Annals of Neurology.

"A cell compound such as methylthioadenosine is able to modulate the immune response, and it might become a useful therapy for autoimmune diseases with less toxicity than other drugs because the cell has several mechanisms to compensate its excess," Dr. Pablo Villoslada told Reuters Health.

Dr. Villoslada and colleagues from the University of Navarra, Spain studied the effects of intraperitoneal MTA in rodent experimental autoimmune encephalomyelitis (EAE, a model of MS) and in peripheral blood mononuclear cells from multiple sclerosis patients and healthy controls.

In the acute model, the authors report, MTA on the same day as induction of EAE prevented acute encephalomyelitis in 5 of 10 Lewis rats, whereas 9 of 10 placebo-treated animals developed neurological symptoms of acute EAE.

In rats with ongoing chronic-relapsing EAE, MTA also improved histological findings and decreased the rate of second relapse, the results indicate.

MTA treatment significantly attenuated the proliferative response of rat splenocytes to myelin basic protein and phytohemagglutinin, the researchers note, and had similar immunomodulatory effects on peripheral blood mononuclear cells from rats and from patients with MS.

"MTA would be an excellent candidate drug to be tested in patients with MS because it is safe and is effective in preventing brain autoimmune attack," the authors conclude.

"In addition," they write, "because MTA may have a pleiotropic mechanism of action in preventing T-cell activation, which is a critical step in autoimmune diseases, but without inducing immunosuppression, it appears an ideal candidate for combining with other immunomodulatory drugs to obtain a higher efficacy in stopping relapses and disease progression without increasing side effects."

Because the mechanism of action is immunomodulation by preventing T cell activation, "our target will be other autoimmune diseases and transplant rejection," Dr. Villoslada added. "We have preliminary data suggesting positive effects in type 1 diabetes and rheumatoid arthritis animal models."

Ann Neurol 2006;60:323-334.

Canadian Local Thought Leader Perspectives in Neurology & Neurosurgery

From Medscape Neurology & Neurosurgery

Editor's Note:
Multiple sclerosis (MS) is a chronic and often progressive inflammatory disorder of the central nervous system (CNS), and characterizing patient response to various treatments for this disease and monitoring its progression are key to patient management. Medical Editor Penelope Gray-Allan, on behalf of Medscape, discussed patient management and treatment approaches -- presented at the recent meeting of the American Academy of Neurology (AAN) -- with Mark S. Freedman, MD, Professor of Medicine (Neurology), at the University of Ottawa, in Ottawa, Ontario, Canada.

Medscape: What are the primary indicators to look for in a patient who is entering into a more progressive form of MS?

Dr. Freedman: Generally speaking, the disease is almost always progressing, but one of our primary concerns is to identify those patients before they experience rapid progression.

The primary indicators to look for include changes in physical exams, cognitive abilities, magnetic resonance images, and electrophysiology. Progression is usually indicated by relapses with a slower recovery time, a shorter time period between relapses, a reduction in the effectiveness of steroids in reducing the inflammation and leading to near complete recovery, loss of endurance, and greater difficulty doing the same tasks. A physical exam might show that there has been some accumulation of a deficit, and, if the Expanded Disability Status Scale (EDSS) is used, it will move in the absence of attacks. These indicators strongly suggest that the patient is entering into a progressive phase.

Medscape: There were a number of studies presented at the recent AAN annual meeting that looked at combination therapies, such as interferon (IFN) beta-1a and inosine,[1] IFN beta-1a and atorvastatin,[2] and IFN beta-1a and natalizumab.[3] Are these combinations showing greater promise for relapsing-remitting MS than IFN beta alone?

Dr. Freedman: Inosine and IFN beta-1a were combined in a small randomized, placebo-controlled study with 36 patients to determine the safety and tolerability of this combination as well as the effects on disease activity and progression.[1] The data suggested that this combination is safe and well tolerated with a low incidence of adverse events.

Atorvastatin is very interesting. In general, it has a different mechanism of action than IFN beta, which could complement the IFN beta activity and create synergy between the 2. However, atorvastatin requires very high doses in order to be effective, and one of its biggest side effects is hepatic problems. Side effects attributed to IFN also include liver complications, so when these therapies are combined, there may be more hepatic problems than anticipated. The other issue with high doses of statins is that they can cause muscle disease, which would be an unwanted obstacle for an individual who already has MS.

While the results of the natalizumab-IFN combination were very good,[3] 2 patients developed progressive multifocal leukoencephalopathy (PML), which is a fatal demyelinating disease of the CNS. Research is ongoing to determine the role of natalizumab but in the meantime, natalizumab has been removed from the marketplace.

There are many drugs that can potentially be added to IFN beta and to glatiramer acetate that might lead to synergy. But they're still all very much in the experimental testing phase, and no one has really been able to show definitively that combining drugs is more beneficial.

Medscape: Based on the available therapeutic agents, what do you consider to be the optimal treatment regimen for MS?

Dr. Freedman: That is a difficult question, because MS can manifest itself very differently in different people, and what may be optimal therapy for one person may not be optimal therapy for another. The clinician must tailor the treatment to the needs and the overall clinical picture of the individual patient, considering all aspects: treatment regimen, patient adherence, cost, and other complicating features, such as being realistic about the disease and the fact that the individual will need to use this medication on a regular basis.

In general, the high-dose IFNs do seem to offer more in terms of efficacy. Currently, there are ongoing studies comparing high-dose IFNs with glatiramer acetate. In 1.5-2 years, we'll know more about how they compare.

Medscape: What factors do you look for when assessing a patient for treatment failure?

Dr. Freedman: Treatment failure is so hard to define. There are very few physicians, when asked, who will define it in the same way. It seems better to define what to expect as a good response and easier to say that a patient didn't reach that optimal response. So, we prefer the term suboptimal response, which we define as a minimal amount of disease activity as determined by monitoring the relapse rate, neurologic progression, and magnetic resonance imaging (MRI) activity. Some breakthrough is normal and to be expected because the drugs are not curative.

As a member of the Canadian Multiple Sclerosis Working Group, we recently developed practical recommendations on how neurologists can assess the status of patients on disease-modifying therapies and decide when it may be necessary to modify treatment in order to optimize outcomes.[4] We fell short in that paper of actually identifying that critical number, but we provided an analog model of 3 gauges -- 1 for relapse, 1 for progression, and 1 for MRI activity. The model ranks outcomes as "low," "medium," or "high" in terms of levels of concern. If any 1 gauge reads "high," any 2 "medium," or all 3 "low," then it is likely that treatment response is suboptimal and that strategies to optimize treatment response need to be implemented. That's our hypothesis, but we need to validate it.

Medscape: At the 2005 AAN meeting, Harold Moses, MD,[5] presented results of a post hoc analysis comparing the efficacy of high-dose, high-frequency IFN beta-1a with low-dose, low-frequency IFN beta-1a among a small subgroup of patients from the EVIDENCE study. What were some of the highlights from that study?

Dr. Freedman: Physicians used to believe that patients with earlier disease might not need as much IFN. Clinicians thought that for patients with early MS, there might be a closer relationship between high-dose, high-frequency IFN beta-1a and low-dose, low-frequency IFN beta-1a, and that patients in later stages of MS might be in greater need of high-dose IFN. The study presented by Dr. Moses[5] compared IFN beta-1a 44 mcg 3 times weekly with IFN beta-1a 30 mcg once weekly, ie, 132 mcg vs 30 mcg per week, a dose that is more than 4 times greater than the low dose of IFN. There were approximately 70 early MS patients in each group. Over the entire comparative phase, 66.2% of patients who received the high dose and 53.7% of patients who received the low dose remained free from relapses. This result was not significant (P = .205). However, this favorable trend is consistent with the statistically significant results achieved during the comparative phase of the entire EVIDENCE cohort (P = .023). During the comparative phase, MRI scans showed that the mean number of T2-active lesions per patient per scan was significantly lower in the high-dose group, ie, .6 vs 1.7 in the low-dose group (P < .001).

Results from this study strongly suggest that patients in the early stages of disease do not get the full benefit of treatment if they receive low-dose IFN; there is still something to be gained by administering high-dose IFN. Remember, though, that this study was an ad hoc analysis, ie, it generates a hypothesis, but does not present proof.

Medscape: In a study you presented at the recent AAN meeting,[6] you applied treatment optimization recommendations (TOR) to the 4-year data from the PRISMS study to evaluate whether TOR disease status assessments, based on a combined evaluation of relapses and disease progression during years 1 and 2, can predict clinical outcomes during years 3-4. What were some of the highlights of that study?

Dr. Freedman: We took a database of patients who had been followed for 4 years in the PRISMS study and applied our treatment optimization recommendation tables in order to determine if we could accurately predict which of those patients would have progression or relapse. We knew that in the first 2 years they had a certain number of events, and what those events were, so we applied TOR in the first 2 years to determine how accurate we would have been at predicting which individuals would progress in years 3 and 4. We found that if we combined the progression and the relapse concerns (we didn't have the MRI data, so we left it out of the equation), we were able to predict with about 80% to 85% certainty all the individuals who either progressed or relapsed in years 3 and 4. A retrospective study like this cannot prove whether the hypothesis is true, but it does allow one to conceive of a study to test this hypothesis.

Medscape: How important are TOR for assessing MS progression?

Dr. Freedman: I think they're very useful, especially for clinicians who are not as familiar with MS and want some guidance for managing their MS patients. It's a logical approach for dealing with disease treatments that are not cures, and allows clinicians to determine just how much breakthrough is considered acceptable.

It's important to remember that patients receiving these treatments must be monitored. It's not enough to just prescribe a drug to a patient and say, "adios." Not everybody has a response to therapy that would be considered optimal. We don't have a huge armamentarium of drugs from which to choose; we have 4 drugs, 3 of which are similar, so a good rationale, such as using TOR, is necessary in order to be able to choose among them and make switches.

There are opportunities to be gained from switching from one therapy to another, and TOR can help determine when it might be appropriate to make a change. When to change the treatment is a key question. The window of opportunity for maximal benefit of treatment from the current drugs that we have is small, and recognizing that fact means that treatment is required early. Clinicians need to know how to monitor patients and to be able to determine how much breakthrough disease is too much. They also need to know how much progression will warrant moving from one therapy to another.

What drug do you switch to? What drug do you switch from? There are studies that look at just that. For example, in the ABOVE trial patients with "breakthrough" on low-dose IFN beta-1a are randomized to continue with low-dose IFN beta-1a, or switch to IFN beta-1b. The patients will be followed for 2 years. A similar study called ACHIEVE is also ongoing wherein patients with breakthrough on high-dose IFN beta-1a are randomized to either continue with their current therapy or switch to glatiramer acetate. The question is whether patients who are failing any of the disease-modifying drugs are apt to continue to fail when switched to a different one, ie, a "class" effect of failure. Alternatively, suboptimal responses to one disease-modifying drug might not necessarily mean suboptimal responses to all, and a switch to a different disease-modifying drug might lead to a successful response. MS has become a very complex disease that has become treatable; understanding the drugs and how to use them effectively and understanding how to monitor patients is a real art.

Medscape: How important is the use of MRI as a TOR tool?

Dr. Freedman: If there was a standardized MRI protocol for MS patients that was always followed, then it's possible that MRI would become much more useful as a TOR tool. All the same, that would only be true if there was enough access, and access to MRI in Canada for the most part is very limited.


Garcia DM, Marin M, Coruna A, et al. Safety and tolerability of inosine + subcutaneous interferon beta-1a (IFN beta-1a) in multiple sclerosis: could inosine protect from IFN beta -1a related adverse effects? Program and abstracts of the American Academy of Neurology 57th Annual Meeting; April 9-16, 2005; Miami Beach, Florida. Abstract P06.157.
Birnbaum G, Altafullah I. A double blind, placebo controlled combination trial of interferon beta-1a (Rebif) and atorvastatin (Lipitor) in patients with relapsing remitting multiple sclerosis. Program and abstracts of the American Academy of Neurology 57th Annual Meeting; April 9-16, 2005; Miami Beach, Florida. Abstract P06.158.
Rudick R, Stuart W, Calabresi P, et al. SENTINEL: a randomized, double-blind, placebo-controlled, multicenter trial to determine the efficacy and safety of natalizumab, when added to intramuscular interferon beta-1a, in patients with relapsing multiple sclerosis (MS). One year clinical and MRI results. Program and abstracts of the American Academy of Neurology 57th Annual Meeting; April 9-16, 2005; Miami Beach, Florida. Abstract S36.001.
Freedman MS, Patry DG, Grand'Maison F, et al. Treatment optimization in multiple sclerosis. Can J Neurol Sci. 2004;31:157-168.
Moses H. Benefits of high-dose, high frequency interferon beta-1a in early MS: comparative results from the EVIDENCE trial. Program and abstracts of the American Academy of Neurology 57th Annual Meeting; April 9-16, 2005; Miami Beach, Florida. Abstract P05.130.
Freedman MS, Forrestal FG. Treatment optimization recommendations (TOR) can predict relapse rates in patients with MS: analysis of the PRISMS study data. Program and abstracts of the American Academy of Neurology 57th Annual Meeting; April 9-16, 2005; Miami Beach, Florida. Abstract P05.128.
Funding Information
Supported by an independent educational grant from Serono Canada, Inc.

Mark S. Freedman, MD, Professor of Medicine (Neurology), University of Ottawa, Ottawa, Ontario, Canada

Disclosure: Penelope Gray-Allan has disclosed no relevant financial relationships.

Disclosure: Mark S. Freedman, MD, has disclosed that he has received grants for educational activities from Serono. Dr. Freedman has also disclosed that he has served as an advisor or consultant to Biogen Idec, Berlex, Serono, Teva, Bayer, Schering, and Pfizer.

Medscape Neurology & Neurosurgery. 2005;7(2) ©2005 Medscape

Pharmacopeia to Present at the Rodman & Renshaw 8th Annual Healthcare Conference

PRINCETON, N.J., October 31, 2006 /PRNewswire-FirstCall/ -- Pharmacopeia , an innovator in the discovery and development of novel small molecule therapeutics, today announced that Dr. Leslie J. Browne, President and Chief Executive Officer, will deliver a corporate presentation at the Rodman & Renshaw 8th Annual Healthcare Conference. The conference will be held November 6 - 8, 2006, at The New York Palace Hotel in New York City.

Dr. Browne's presentation will take place at 3:30 p.m. (local time) on Monday, November 6. The presentation will include an overview of the company's drug development pipeline, recent corporate accomplishments and expected milestones. A live webcast and 90-day archive of the presentation can be accessed at http://www.pharmacopeia.com.

Pharmacopeia's most advanced internal program is a dual-acting angiotensin and endothelin receptor antagonist (DARA) for hypertension and diabetic nephropathy that is currently in preclinical development. Pharmacopeia's internal programs in advanced optimization are: JAK3 inhibitors (immunomodulators for multiple potential indications, including transplant rejection, psoriasis and rheumatoid arthritis); CCR1 antagonists (with potential in inflammatory diseases such as rheumatoid arthritis and multiple sclerosis); adenosine A2A antagonists (with potential in neurodegenerative diseases, including Parkinson's and Alzheimer's); and avb3/avb5 inhibitors (with potential to block angiogenesis in cancer and inflammation).

Pharmacopeia currently has eleven partnered compounds in development with major pharmaceutical or biotechnology companies. Five of these compounds (representing four partnered, therapeutic programs) are currently in Phase I clinical trials for rheumatoid arthritis, an allergy/asthma indication, chronic obstructive pulmonary disease (COPD) and oncology. Six compounds are in preclinical development. Pharmacopeia will receive milestone payments for those programs that successfully advance through clinical development and royalties on the sales of any compounds that are commercialized.


Pharmacopeia is committed to creating and delivering novel therapeutics to address significant medical needs using proprietary technologies and processes. The Company is advancing multiple internal programs towards validation in clinical trials. Pharmacopeia's later stage portfolio currently comprises multiple partnered programs that have been advanced into clinical trials with further programs in preclinical development. The Company also has several internal programs - one in preclinical development and several in advanced optimization - as well as multiple partnered programs in discovery that are expected to drive the Company's clinical portfolio in the future.


Amy Sharpless


(609) 452-3643


This press release, and oral statements made with respect to information contained in this press release, constitute forward-looking statements within the meaning of the Private Securities Litigation Reform Act of 1995. Such forward-looking statements include those which express plan, anticipation, intent, goal, contingency or future development and/or otherwise are not statements of historical fact. These statements are based upon management's current expectations and are subject to risks and uncertainties, known and unknown, which could cause actual results and developments to differ materially from those expressed or implied in such statements. These forward-looking statements include, but are not limited to, statements about the successful implementation of Pharmacopeia's strategic plans, Pharmacopeia's plans to develop its DARA program and file an IND with respect to the program, Pharmacopeia's ability to successfully perform under its collaborations with Cephalon and GlaxoSmithKline, Pharmacopeia's ability to build its pipeline of novel drug candidates through its own internally funded drug discovery programs, third party collaborations and in-licensing, the continuation and funding level of such continuation of Pharmacopeia's existing drug discovery collaboration with N.V. Organon, Pharmacopeia's intentions regarding the establishment of new drug discovery collaborations with leading pharmaceutical and biotechnology organizations, Pharmacopeia's ability to raise additional capital, Pharmacopeia's expectations concerning the development priorities of its collaborators, their ability to successfully develop compounds and its receipt of milestones and royalties from the collaborations, Pharmacopeia's anticipated operating results, financial condition, liquidity and capital resources, Pharmacopeia's expectations concerning the legal protections afforded by U.S. and international patent law, Pharmacopeia's ability to pursue the development of new compounds and other business matters without infringing the patent rights of others, additional competition, and changes in economic conditions.

Further information about these and other relevant risks and uncertainties may be found in Pharmacopeia's Reports on Form 8-K, 10-Q and 10-K filed with the U.S. Securities and Exchange Commission. Pharmacopeia urges you to carefully review and consider the disclosures found in its filings which are available in the SEC EDGAR database at http://www.sec.gov and from Pharmacopeia at http://www.pharmacopeia.com. All forward-looking statements in this press release and oral statements made with respect to information contained in this press release are qualified entirely by the cautionary statements included in this press release and such filings. These risks and uncertainties could cause actual results to differ materially from results expressed or implied by such forward-looking statements. These forward-looking statements speak only as of the date of this press release. Pharmacopeia undertakes no obligation to (and expressly disclaims any such obligation to) publicly update or revise the statements made herein or the risk factors that may relate thereto whether as a result of new information, future events, or otherwise.

CONTACT: Amy Sharpless of Pharmacopeia, +1-609-452-3643 or irreq@pcop.com

Web site: http://www.pharmacopeia.com/

Ticker Symbol: (NASDAQ-NMS:PCOP)

Terms and conditions of use apply
Copyright © 2006 PR Newswire Association LLC. All rights reserved.
A United Business Media Company

Teva Announces Global In-Market Third Quarter Sales of Copaxone Increased 15% to $354 Million

JERUSALEM, Israel--(BUSINESS WIRE)--Oct 31, 2006 - Teva Pharmaceutical Industries Ltd. (Nasdaq: TEVA) announced today, in conjunction with the release of the Sanofi-Aventis group's financial results, that global in-market sales of Copaxone(R) in the third quarter of 2006 grew by 15% as compared to the third quarter of 2005 and reached a record of $354 million.

According to IMS, in the US Copaxone(R) continues to outpace the market growth strengthening its leadership position with TRx and NRx shares increasing to 34% and 35.2% respectively, as of September 2006. U.S. sales in the third quarter of 2006 increased 10% over the third quarter of 2005 to $226 million.

Outside the U.S., mainly in Europe, Copaxone(R) is the fastest growing multiple sclerosis therapy with growth of 26% over the third quarter of 2005, reaching sales of $128M.

Teva Pharmaceutical Industries Ltd., headquartered in Israel, is among the top 20 pharmaceutical companies in the world and is the leading generic pharmaceutical company. The company develops, manufactures and markets generic and innovative human pharmaceuticals and active pharmaceutical ingredients, as well as animal health pharmaceutical products. Over 80 percent of Teva's sales are in North America and Europe.

Safe Harbor Statement under the U. S. Private Securities Litigation Reform Act of 1995: This release contains forward-looking statements, which express the current beliefs and expectations of management. Such statements are based on management's current beliefs and expectations and involve a number of known and unknown risks and uncertainties that could cause Teva`s future results, performance or achievements to differ significantly from the results, performance or achievements expressed or implied by such forward-looking statements. Important factors that could cause or contribute to such differences include risks relating to Teva's ability to rapidly integrate Ivax Corporation's operations and achieve expected synergies, Teva`s ability to successfully develop and commercialize additional pharmaceutical products, the introduction of competing generic products, the impact of competition from brand-name companies that sell or license their own brand products under generic trade dress and at generic prices (so called "authorized generics") or seek to delay the introduction of generic product, the impact of consolidation of our distributors and customers, regulatory changes that may prevent Teva from exploiting exclusivity periods, potential liability for sales of generic products prior to a final resolution of outstanding litigation, including that relating to the generic versions of Allegra(R), Neurontin(R) and Zithromax(R), the effects of competition on Copaxone(R) sales, including as a result of the reintroduction of Tysabri(R) into the market, the impact of pharmaceutical industry regulation and pending legislation that could affect the pharmaceutical industry, the difficulty of predicting U.S. Food and Drug Administration, European Medicines Agency and other regulatory authority approvals, the regulatory environment and changes in the health policies and structures of various countries, Teva's ability to successfully identify, consummate and integrate acquisitions, potential exposure to product liability claims, dependence on patent and other protections for innovative products, significant operations worldwide that may be adversely affected by terrorism or major hostilities, environmental risks, fluctuations in currency, exchange and interest rates, operating results and other factors that are discussed in Teva's Annual Report on Form 20-F and its other filings with the U.S. Securities and Exchange Commission. Forward-looking statements speak only as of the date on which they are made and the Company undertakes no obligation to update publicly or revise any forward-looking statement, whether as a result of new information, future developments or otherwise.


Teva Pharmaceutical Industries Ltd.
Dan Suesskind
Chief Financial Officer
(011) 972-2-589-2840
Web Site: www.tevapharm.com
Teva North America
George Barrett
President and CEO
Teva Investor Relations
Liraz Kalif / Kevin Mannix
(011) 972-3-926-7554 / 215-591-8912

Biogen profit beats estimates

Tue Oct 31, 2006 10:47 AM ET

By Toni Clarke

BOSTON (Reuters) - Biogen Idec Inc. on Tuesday posted higher-than-expected third-quarter earnings, boosted by strong sales of its drugs for multiple sclerosis and cancer, sending its shares up nearly 6 percent.

The Cambridge, Massachusetts-based biotechnology company said net earnings jumped to $157 million, or 45 cents a share, from $27.2 million, or 8 cents a share, a year earlier, when it took big restructuring and merger charges.

Revenue rose to a higher-than-expected $703 million from $596 million a year ago.

Sales of the company's multiple sclerosis drug Avonex rose 19 percent to $445 million, helped in part by price hikes. Revenue from its joint business arrangement for the cancer drug Rituxan increased 12 percent to $204 million.

Excluding one-time items, but taking into account stock option expenses totaling 3 cents a share, the company earned 57 cents a share. Analysts' average forecast was 47 cents, according to Reuters Estimates.

"It was a fine quarter," said Eric Schmidt, an analyst at Cowen & Co. "Biogen still lacks a sexy new product, but it always helps when you can deliver more profits to the bottom line, and they certainly did that."

Biogen said sales of its recently reintroduced multiple sclerosis drug Tysabri -- which analysts had once expected to bring in billions of dollars -- were $8 million. The company said that to date, more than 2,200 patients are being treated with the drug.

Sales of Tysabri, which Biogen markets with Irish drugmaker Elan Corp. , were suspended in 2005 after the drug was linked to a rare but potentially fatal brain disease.

Biogen raised its full-year 2006 earnings forecast. It said it now expects profit, excluding one-time items, to exceed $2.20 a share. It previously forecast $1.95 to $2.10 a share.

The company said the higher forecast was driven partly by strong sales of its drugs and partly by the fact that it did not spend as much as it expected on acquisitions and other forms of business development.

Biogen said it had spent less than half the $200 million it had set aside for this purpose. Jim Mullen, the company's chief executive officer, told analysts on a conference call that competition to acquire products in late stages of development is intense.

"The most obvious deals have been done," he said. "That is driving up the pricing and valuation in certain sectors, notably oncology."

Biogen said it is considering divesting its cancer drug Zevalin, which recorded sales of just $4 million in the third quarter.

Biogen shares rose $2.59 to $46.50 in early trade on Nasdaq.

Monday, October 30, 2006

Commentary: Delaying technology is deadly

from The Washington Times

By Paul Driessen

In sub-Saharan Africa and poor areas of Asia and Latin America, diarrhea isn't just a source of mild discomfort and juvenile bathroom humor. Because of unsanitary conditions, contaminated water and food infected by bacteria in feces used for fertilizer, people in those regions endure 4 billion episodes of severe diarrhea a year. Up to 2 million die annually.

Among children in the United States, acute diarrhea accounts for more than 1.5 million outpatient visits, 200,000 hospitalizations, and 300 deaths a year. It imposes a multibillion-dollar burden on the U.S. health-care system.

But miracles of modern medical and agricultural science offer hope. For years, glucose-based rehydration solutions (similar to Pedialyte) were used to treat diarrhea. They saved countless lives, by replacing lost salts, sugars and bodily fluids. However, even with the successful health outcomes, these solutions did not reduce the incidence or severity of childhood diarrhea.

Now Ventria Bioscience has developed an advanced solution that augments standard rehydration solutions, by adding protective human proteins (lactoferrin and lysozyme) found in all human saliva and breast milk.

A recent child health study demonstrated the proteins cut the average duration of children's diarrhea by 30 percent (1-1/2 days), and patients were half as likely to get diarrhea again during the next 12 months. Equally important, Ventria produces the proteins in a special variety of rice, which makes its rehydration solution affordable, even for people in poor countries.

Ventria achieved its remarkable breakthrough by altering rice DNA and using rice plants as factories that utilize the sun, soil and water as raw materials to produce the proteins. The company extracts the proteins and adds them to rehydration solutions. Its success could convert one of the world's most essential foods into a valuable lifesaver.

In another achievement, SemBioSys Genetics created genetically engineered safflowers that produce insulin at commercial levels: An acre of safflower can produce a kilogram of insulin, enough for 2,500 patients. Fewer than 16,000 acres -- about 0.2 percent of what Iowa farmers devote to corn -- would cover projected 2010 world demand for insulin. With diabetes on the rise in India and elsewhere, this advance could be vital.

Syngenta is working on plant-based antibodies that fight infections and skin disease. Other scientists are enhancing plants to produce vaccines, hormones and enzymes that can treat HIV, cancer, heart and kidney disease, spinal cord injuries, multiple sclerosis, cystic fibrosis, hepatitis, anthrax, West Nile virus and arthritis.

It costs around $1,000 to produce 1 gram (0.035 ounce) of protein from animal cells, making many such vaccines prohibitively costly for even the wealthiest countries, and completely out of reach for destitute countries. Producing the same amount from gene-altered plants would cost less than $20 -- and that means pharmaceutical companies could give higher priority to finding cures for rare and "orphan" diseases across the globe.

But amazingly, instead of applauding these lifesaving innovations, critics attack them. Luddite radicals like the Center for Food Safety, Union of Concerned Scientists and Greenpeace assert this "Frankenstein" technology tampers with nature and could "contaminate" other crops. These groups are well funded by organic food interests and others who profit by attempting to scare the public. The European Union and organic food industries demand stringent, costly, unnecessary regulations that impose unconscionable delays and result in death for some of the world's most needy children.

Breeders have been improving plants for millennia, using various genetic technologies. Plant biotechnology is simply a refinement of the earlier, cruder techniques. Today's researchers employ genetic technologies that are far more careful and precise -- and management practices that maintain closed production systems and virtually eliminate any risks of accidental cross-pollination and gene migration.

But none of this makes any difference to "anti-humanists who put unfounded fear-mongering ahead of the world's children," says Greenpeace co-founder Patrick Moore. Healthy, well-fed, safe from diseases that kill millions in other countries, with access to abundant clean water and electricity -- they obsess about purely speculative risks from technologies that could improve and save countless lives.

In so doing, they perpetuate disease risks for countless human beings. They throw roadblocks in the path of scientific and technological progress that so far has eluded the world's poor, even as it improved our own health, nutrition, living standards and lifespans.

My personal experience with polio (luckily after receiving two Salk inoculations) made me eternally grateful that these "ethicists" weren't around 50 years ago to stymie research and field trials of that vaccine. My generation can also count its blessings for treatments, antibiotics and other vaccines that have saved many of us and our children.

It is now the responsibility of our generation to protect children, the poor and future generations from mean-spirited Luddite groups paid to undermine our humanity and technological progress. It is time for legislators, regulators, judges and people of conscience to say "enough."

The world needs these miraculous technologies -- today. And those who support radical anti-biotech organizations need to understand that, by blocking health-care innovations, they are perpetuating misery, disease and premature death in countries the world over. That is simply immoral.

Paul Driessen is senior policy adviser for the Congress of Racial Equality and Committee For A Constructive Tomorrow, and author of "Eco-Imperialism: Green power — Black death" (www.Eco-Imperialism.com).

Copyright © 2006 News World Communications, Inc. All rights reserved.

Curry spice extract may have anti-arthritis potential

By Stephen Daniells

30/10/2006- Extracts from turmeric, the yellow spice used extensively in curries, reduced the destruction of joints associated with arthritis to similar levels to pharmaceuticals, says a new animal study from the US.

The new study, published in the November issue of the journal Arthritis & Rheumatism (Vol. 54, pp. 3452-3464), is said to be the first to document the efficacy of curcumin-containing extracts for anti-arthritis activity in vivo, as well as demonstrating that the extracts studied are analogous with commercially available turmeric dietary supplements.
"Just as the willow bark provided relief for arthritis patients before the advent of aspirin, it would appear that the underground stem (rhizome) of a tropical plant [turmeric] may also hold promise [against] joint inflammation and destruction," wrote lead author Janet Funk from the University of Arizona in Tucson.

Approximately seven million people in the UK alone are reported to have long-term health problems associated with arthritis. Around 206 million working days were lost in the UK in 1999-2000, equal to £18bn (€26bn) of lost productivity.

The researchers compared the chemical composition of experimental extracts (from turmeric powder, San Francisco Herbs, Spices and Teas) with those of commercially available over the counter turmeric dietary supplements. Two experimental extracts were prepared – a crude extract with 34 per cent curcuminoids and containing essential oils, and an extract with 41 per cent curcuminoids and no essential-oils.

Funk and her co-workers report that the majority of the over-the-counter supplements were also free of essential oils and had curcuminoids contents ranging from 1.8 to 33.7 per cent.

Female rats were used to test the efficacy of the extracts in vivo. The rats were injected with either a saline solution or an arthritis-inducing solution. The animals were then injected with one of the turmeric extracts or a control solution, and joint inflammation measured.

Initial results showed that a version of turmeric extract that was free of essential oils had the most significant impact on arthritis and most closely matched the composition of commercially available supplements.

Cartilage destruction in the tibia of the rats was reduced by 66 per cent, and thigh bone mineral density (BMD) destruction was also reduced by 57 per cent, compared to the control solution.

The researchers, funded by the Office of Dietary Supplements and National Center for Complementary and Alternative Medicine of the National Institutes of Health, reported that an effective dose in rats that would be equivalent in humans to 1.5 milligrams per day of a portion of the turmeric root that makes up three per cent of dried turmeric powder.

A mechanistic study showed that the turmeric extracts appeared to work by inhibiting the protein, NF-kappaB, known to be play a key role in some inflammatory pathways.

“Given the critical role of NK-kappaB as the ‘master switch’ in innate immunity, these in vivo experiments… provide proof-of-concept for the us of this botanical in other diseases triggered by inappropriate activation of NF-kappaB–regulated inflammatory pathways, including inflammatory bowel disease, asthma, and multiple sclerosis,” said the researchers.

They noted, however, that the research did not exclude the possibility that the spice extract may also block other inflammatory processes that are parallel to the NF-kappaB process.

"Before turmeric supplements can be recommended for medicinal use, clinical trials are clearly needed to verify/determine whether… adequate doses of well-characterized turmeric extracts can indeed prevent/suppress disease flares in RA [rheumatoid arthritis] patients, as well as to explore any potential benefits of turmeric dietary supplements in the prevention or treatment of more common forms of arthritis in the general population," concluded the researchers.

Professor Robert Moots, from Liverpool University and spokesman for the British-based charity, Arthritis Research Campaign said that it was not surprising that naturally occurring compounds had similar effects to drugs.

"I do not think there is any evidence that countries that eat a lot of turmeric have a lower frequency of rheumatoid arthritis. So simply eating more spices is not likely to be effective clinically.

"What is more likely is these results will lead to the targeted development of new compounds,” he said in a statement

Copyright - Unless otherwise stated all contents of this web site are © 2000/2006 – Decision News Media SAS – All Rights Reserved. For permission to reproduce any contents of this web site, please email our Syndication department: contact our Syndication department. Full details for the use of materials on this site can be found in the Terms & Conditions.
contact the editor

Tuesday, October 24, 2006


I will be on spiritual retreat from October 25 through October 29.

Peace and good health!

US doctors still wary of Tysabri - survey

October 24, 2006 09:14

US doctors are proving more wary than many had expected about prescribing Elan's multiple sclerosis drug Tysabri, which was relaunched in July after being suspended because of safety concerns.

Over the past month or so, analysts have drawn down their 2006 sales forecasts as it becomes clear that doctors wary of the risk of the rare but potentially fatal brain disease PML are reserving the drug as a treatment of last resort.

The drug, which is made by Elan and its US Biogen Idec, had been expected by some analysts to generate sales this year of more than $100m, but those figures have dropped dramatically.

Ian Hunter, an analyst at Goodbody stockbrokers, said yesterday that he has cut his full-year Tysabri forecast to $25.7m from $78m, partly because of continuing safety concerns and the complexity of reimbursement systems in Europe.

A survey of 63 US neurologists indicates that in 2006 Tysabri will be used in less than 1% of multiple sclerosis patients - translating into revenue of under $30m.

Since July, only 47 of more than 8,500 patients treated by US physicians surveyed had used Tysabri, even though more than 700 patients had discussed using it, according to the report. And more than 75% of the patients who had used Tysabri prior to its 2005 suspension have decided not to use it since its reintroduction, the survey showed.

In taking the rare decision to allow a withdrawn drug back onto the market, the US Food and Drug Administration was partially influenced by calls from patients who said they were willing to take the risk of contracting progressive multifocal leukoencephalopathy, or PML, because of the potential benefits of the drug.

Tysabri's ultimate sales potential will depend, to an acute degree, on whether there are any more cases of PML, analysts say. Most of the respondents to the survey said they would stop using Tysabri altogether if two new PML-related deaths were associated with Tysabri.

Elan is due to report its third quarter results tomorrow.

FDA Approves Betaseron® for Use After the First Event Suggestive of Multiple Sclerosis

Early treatment with Betaseron significantly delayed the time to a second clinical event

Wayne, NJ, October 23, 2006 - Berlex, Inc., a U.S. affiliate of Schering AG, Germany (FSE: SCH; NYSE: SHR), announced today that the U.S. Food and Drug Administration (FDA) has expanded the indication of Betaseron® (interferon beta-1b) to include patients with multiple sclerosis (MS) who have experienced a first clinical episode and have MRI features consistent with MS. Betaseron is indicated for the treatment of relapsing forms of multiple sclerosis to reduce the frequency of clinical exacerbations. Betaseron is the only high-dose, high-frequency interferon beta indicated for patients at the earliest stage of MS.

The new indication is based on results from the BENEFIT (BEtaseron in Newly Emerging multiple sclerosis for Initial Treatment) Study of patients with a first clinical demyelinating event and MRI features suggestive of MS. The two-year study showed that treatment with Betaseron delayed the time to a second clinical event by one year compared to placebo. (1) BENEFIT is the only trial to demonstrate the efficacy of a high dose, high frequency interferon beta, Betaseron, as an effective treatment for patients with early MS . In addition to establishing efficacy in this group of patients, the study also showed that patients with early MS found Betaseron to be a safe and well-tolerated treatment, as evidenced by the findings that 93 percent of patients completed the study.

"We are very happy to offer people at the earliest stages of MS the benefit of an early start with high-dose, high-frequency Betaseron and its proven, long-term safety and efficacy profile," said Ludger Heeck, Ph.D., Vice President and General Manager, Specialized Therapeutics, Berlex. "Experts convened by the American Academy of Neurology (2) have suggested that higher doses of interferon beta, taken more frequently, appear to be more effective in fighting MS than lower doses taken less often. Betaseron is the only high-dose, high-frequency interferon beta approved in the U.S. for patients who have experienced a first clinical event suggestive of MS."

About the BENEFIT Study

Two-year data from the BENEFIT Study were recently published in Neurology(3). In the randomized, double-blind, placebo-controlled, multicenter trial, 468 participants were given either Betaseron 250 micrograms (mcg) subcutaneously every other day or placebo until they experienced a second clinical event or relapse, which confirms the diagnosis, or they had been followed for at least 24 months. Dose titration (increasing the dose slowly) was applied and analgesics were used prior to injection. Patients were also provided instruction on methods of self-injection.

"The BENEFIT study has taught us many things but most importantly has shown us that most patients who appear to be at high risk of developing MS do so within only two years. In the study, Betaseron cut the risk of progression to the second clinical event by nearly 50 percent compared to placebo," said Mark S. Freedman, M.D., Professor of Neurology at the University of Ottawa, Ontario, Canada, and a lead investigator of the BENEFIT Study. "We have learned from BENEFIT and other studies that early treatment is probably one of the keys to treatment success since accumulated neurological damage is often irreversible and much of this is not clinically apparent in these early phases. Betaseron is well-accepted and provides an effective first treatment option for people with relapsing MS and those with early signs of disease."

Results showed that:

- Treatment with Betaseron reduced the risk of progression to clinically definite MS by about 50 percent and to MRI-defined MS (4,5) , by 46 percent, compared to placebo.

- Treatment with Betaseron delayed the time to a second clinical event by one year compared to patients in the placebo arm.

- In the placebo group, over half of the patients reached MRI-defined MS within six months and 85 percent reached MRI-defined MS in the two-year study.

The results of the BENEFIT trial also showed that the patients were willing to initiate and continue Betaseron treatment in an effort to gain control of the disease at its earliest stages:

- More than nine out of 10 patients (93 percent) treated with Betaseron completed the study, a rate similar to placebo.

- Ninety-six percent of all eligible patients opted to participate in a three-year extension of the study. To date, no other trial involving early MS patients has demonstrated such a high level of patient acceptance.

- Only 2.7 percent of patients in the trial discontinued therapy because of adverse events.

About Betaseron

Betaseron is approved for the treatment of relapsing forms of multiple sclerosis to reduce the frequency of clinical exacerbations. Patients with multiple sclerosis in whom efficacy has been demonstrated include patients who have experienced a first clinical episode and have MRI features consistent with multiple sclerosis. Betaseron has more than 17 years of clinical experience, with a well-established safety profile resulting from more than 700,000 patient years of treatment. A long-term follow-up study demonstrated that Betaseron remains consistently safe, effective and well tolerated over the long term. Results of the study show that long-term continuous(6) use of Betaseron provided 13 years of cane-free mobility, which is, on average, six years longer than when compared to untreated patients from a natural history cohort. The study also showed that patients who continuously used Betaseron experienced a significant delay in progression to secondary progressive multiple sclerosis (SPMS) by 6.6 years compared to patients who were not on continuous Betaseron treatment.

The most commonly reported adverse reactions are lymphopenia, injection site reaction, asthenia, flu-like symptom complex, headache, and pain. Gradual dose titration and the use of analgesics during treatment initiation may help reduce flu-like symptoms. Betaseron should be used with caution in patients with depression. Injection site necrosis has been reported in five percent of patients in controlled trials. Patients should be advised of the importance of rotating injection sites. Female patients should be warned about the potential risk to pregnancy. Cases of anaphylaxis have been reported rarely. Please see full Prescribing Information available at www.betaseron.com.

(1) Based on the 25th percentile

(2) Goodin DS, Frohman EM, Garmany GP Jr, et al. Disease modifying therapies in multiple sclerosis: report of the Therapeutics and Technology Assessment Subcommitte of the American Academy of Neurology and the MS Council for Clinical Practice Guidelines. Neurology. 2002;58:169-178.

(3) Kappos L et al. Treatment with interferon beta-1b delays conversion to clinically definite and McDonald MS in patients with clinically isolated syndromes. Neurology 2006;67:1242-1249.

(4)McDonald criteria

(5) The exact relationship between MRI findings and patients' symptoms is not completely understood.

(6) Long-term continuous use is defined as > 80 percent of the study duration ( >12 years).

About Berlex

Berlex, a U.S. affiliate of Schering AG, Germany (FSE: SCH; NYSE: SHR), is committed to addressing unmet medical needs through research and development in the areas of oncology, gastroenterology, women's health, diagnostics and neurology. Berlex also markets diagnostic imaging agents, innovative treatments in the areas of female health care and oncology, as well as specialized therapeutics for life-threatening and disabling diseases of the central nervous system and cardiovascular system. Berlex has business operations in New Jersey, California and Washington. For more information, please visit www.berlex.com


Certain statements in this press release that are neither reported financial results nor other historical information are forward-looking statements, including but not limited to, statements that are predictions of or indicate future events, trends, plans or objectives. Undue reliance should not be placed on such statements because, by their nature, they are subject to known and unknown risks and uncertainties and can be affected by other factors that could cause actual results and Berlex's plans and objectives to differ materially from those expressed or implied in the forward-looking statements. Berlex, Inc. undertakes no obligation to update publicly or revise any of these forward-looking statements, whether to reflect new information or future events or circumstances or otherwise.

Monday, October 23, 2006

Multiple Sclerosis Association of America Wins Two Gold and Two Silver Awards in 2006 National Health Information Awards Program


Monday October 23, 9:00 am ET

CHERRY HILL, N.J., Oct. 23 /PRNewswire/ -- The Multiple Sclerosis Association of America (MSAA) recently received four awards in four different categories in the 13th annual National Health Information Awards competition. This program recognizes the nation's best consumer health information programs and materials.

MSAA's quarterly magazine, The Motivator, earned three awards for the following articles:

-- "Employment Strategies," featured in the Spring 2005 issue of
The Motivator, received a Gold Award for Patient Education in a
Magazine/Newspaper/Newsletter Article
-- "Planning for the Future - The Importance of Advance
Directives," featured in the Fall 2005 issue of The Motivator,
received a Gold Award for Consumer Decision Making Information in a
Magazine/Newspaper/Newsletter Article
-- "Healthcare Beyond MS," featured in the Winter 2005 issue of
The Motivator, received a Silver Award for Health Promotion/Disease and
Injury Prevention in a Magazine/Newspaper/Newsletter Article
The fourth award MSAA received was for the booklet, "All About Multiple Sclerosis," which won a Silver Award for Patient Education Information in the category of Booklet/Brochure/Pamphlet.

"We have always been very proud of our publications and this was the first year we submitted samples for judging," states MSAA President and CEO Doug Franklin. "To be awarded such honors is a tribute to our communications staff, which has always produced high-quality educational materials for the MS community."

Copies of the award-winning articles and MSAA's award-winning booklet, "All About Multiple Sclerosis," as well as all of MSAA's publications, are currently available by contacting MSAA at (800) 532-7667, or by logging onto MSAA's website (http://www.msaa.com) and clicking on the "publications" section. Copies of The Motivator and all other MSAA publications may be ordered free of charge.

The National Health Information Awards Program is coordinated by the Health Information Resource Center, a national clearinghouse for consumer health information programs and materials. The Center, which houses a large collection of such public and private sector materials, promotes the distribution of accurate and timely consumer health information materials to professionals and managers in the field. A national panel of health information experts reviewed nearly 1,000 entries from across the country for this year's program.

For more information, please contact Amanda Bednar at (800) 532-7667, extension 122 or via email at abednar@msaa.com.

The Multiple Sclerosis Association of America is a national nonprofit charitable organization dedicated to enriching the quality of life for everyone affected by multiple sclerosis. MSAA offers programs and services including a toll-free Helpline (1-800-532-7667); support groups; equipment ranging from grab bars to wheelchairs; MRI funding and insurance advocacy; educational literature including a quarterly magazine, The Motivator; Lending Library; cooling program for heat-sensitive individuals; awareness events; and more.

To make a donation to MSAA or to inquire about volunteering or fundraising, please contact MSAA at (800) 532-7667, extension 159 or visit MSAA's website at http://www.msaa.com for more information.

The most common neurological disorder diagnosed in young adults, multiple sclerosis is an autoimmune disease of the central nervous system. This disorder damages or destroys the protective covering (known as myelin) surrounding the nerves, causing reduced communication between the brain and nerve pathways. Common symptoms include visual problems, overwhelming fatigue, difficulty with balance and coordination, and various levels of impaired mobility. MS is not contagious or fatal.


Here We Go Again! Multiple Sclerosis :Multiple Sclerosis is not a terminal disease

Here we go, folks. Yet another organization insists on fighting MS by insisting that's it cannot be fatal. If these so-called MS-fighting organizations were truly serious about helping people with MS and finding a cure for the disease that the National Multiple Sclerosis Society in the United States says has "devastating effects," they would "market" their fund-raising more like the Muscular Systrophy Association, showing a public face of MS to be one where hundreds of thousands of people worldwide find themselves in wheelchairs or worse, where they can no longer work, where nerve damage can often lead to the failure of various organ systems.

Not terminal or fatal? Ask the family members and caregivers.

The following is from SpiritIndia.com:

At the MS Trust we strongly object to Multiple Sclerosis - MS being described as a terminal disease, as happened yet again yesterday in relation to the sad death of Gillian March. 'Terminal' is defined as "predicted to lead to death, especially slowly" (OED). We are all dying slowly but in fact the vast majority of people with MS will live fulfilling lives to an advanced age.

Premature death due to MS is almost invariably due either to suicide or to a failure to manage symptoms, which leads to secondary complications. With the care and treatment recommended by the NICE clinical guidelines, particularly in Mrs March's case perhaps for depression, the outcome may not have been so sad. Increased suicide rate, particularly among young, non-disabled men diagnosed with MS, is unsurprising when MS is constantly portrayed as terminal.

We have therefore today sent a letter to both the BBC and ITV asking them to consider the language they use to report news items about people with MS -- Multiple Sclerosis Trust

Saturday, October 21, 2006

Outcome not always worse for late-onset MS

Last Updated: 2006-10-06 14:51:46 -0400 (Reuters Health)
By Will Boggs, MD

NEW YORK (Reuters Health) - Individuals who develop multiple sclerosis (MS) later in life do not always have worse outcomes than those who develop the disease in early adulthood, according to a report in the journal Neurology.

It has been assumed that patients who first develop MS symptoms after around 50 years of age have a poorer prognosis than those diagnosed earlier in life, Dr. Helen Tremlett told Reuters Health. "However, our study indicates that this is not necessarily the case."

Tremlett and Dr. Virginia Devonshire from the University of British Columbia, Vancouver, Canada examined the prognosis and prognostic factors among 132 patients with MS first diagnosed at age 50 or older (late onset), and 2,603 patients with first symptoms between age 16 and 49 (adult onset).

Motor and brain symptoms were more often the first sign of MS in the late-onset group, the authors report, whereas sensory symptoms and optic neuritis were more common in the adult-onset group.

Although disease progression was significantly faster in the late-onset group (16.9 years) than in the adult-onset group (27.7 years), the results indicate, patients in the adult-onset group were significantly younger (58.4 years) than patients in the late-onset group (71.2 years) when they reached the same level of disability.

A primary progressive course was associated with more rapid progression in patients with late-onset MS and sensory symptoms were associated with a slower progression, the researchers note.

Among patients with adult-onset MS, those who had motor and brain symptoms as the first sign of illness had a more rapid disease progression. In this group, progression was slower for women and those with sensory symptoms and optic neuritis at diagnosis.

"Once the disease course was determined (i.e., relapsing or primary progressive MS) there was little difference in prognosis between late-onset or adult-onset MS," Tremlett said.

With relapsing-remitting MS, a partial or total recovery occurs after exacerbations. Most MS patients, about 85 percent, initially begin with this subtype. With primary progressive MS, symptoms begin and usually do not remit. This subtype affects about 10 percent of people with MS.

These findings have "real implications" for patients first seen for MS late in life, she continued. "Contrary to what we thought before, the prognosis...is likely to be the same as someone with adult-onset MS (once the presence of relapsing or primary progressive MS has been determined)."

Relapsing/remitting MS has a less rapid progression than does progressive MS.

"Our data do not justify recommending a different treatment approach in late-onset MS, other than on a case by case basis," the authors conclude.

SOURCE: Neurology, September 2006.
Copyright © 2006 Reuters Limited. All rights reserved. Republication or redistribution of Reuters content, including by framing or similar means, is expressly prohibited without the prior written consent of Reuters. Reuters shall not be liable for any errors or delays in the content, or for any actions taken in reliance thereon. Reuters and the Reuters sphere logo are registered trademarks and trademarks of the Reuters group of companies around the world.

Disabled set back by Medicare cuts

Policy change was aimed at curbing fraud

Associated Press
WASHINGTON - Patricia Meier, a 63-year-old quadriplegic and Medicare recipient, needs to replace the wheelchair she has used for five years.

Normally, Meier could simply use her Medicare benefits to replace the power wheelchair, which adjusts her position to prevent sores, with another one from WestMed Rehab Inc., a medical supplier near her home in Box Elder, S.D.

But WestMed, along with several other suppliers across the country, says it will no longer provide power wheelchairs to most Medicare recipients after Nov. 15, when cuts in Medicare reimbursements go into effect. WestMed planned an announcement for today.

The Medicare changes are intended to eliminate widespread fraud identified by the Health and Human Services Department, which oversees the program.

WestMed, based in Rapid City, S.D., is the only major wheelchair supplier within 300 miles of Meier's home. Concerned about the prospect of wheelchair supplies ending in their state, South Dakota's congressional delegation pressed federal health officials for more information.

If Meier were to replace her chair without using Medicare, it could cost her between $17,000 and $20,000. With Medicare, she would pay only 20 percent of that.

"When I was able-bodied, I bought cars cheaper than that," said Meier, who was injured in a car accident 20 years ago. "I don't know how I would be able to afford it."

With other suppliers saying they, too, won't be able to provide mobility equipment to many of their customers, those living with multiple sclerosis, spinal cord injuries and other conditions could be without the wheelchairs they need to get around.

Many wheelchair users "are going to have to pay out of pocket," said Tim Pederson, CEO of WestMed Rehab.

A 2004 study conducted by the HHS inspector general showed that Medicare reimbursements for certain power wheelchairs were far higher than the prices paid by consumers and suppliers. According to the Centers for Medicare and Medicaid Services, which administers both health care programs, expenditures for power wheelchairs increased by 2,705 percent between 1995 and 2003 -- from $43 million to $1.2 billion in just over just eight years.

Most suppliers have supported overhauling the system, as many companies have abused it. But they say the government has gone too far.

The changes "do eliminate the fraud and abuse, but it also eliminates the benefit," said Pederson of WestMed Rehab. "They are painting the entire industry in that broad brush, and they look at all of us as crooks."

John says 'Don't suffer MS in silence'

LIFE was going well for John Morris. He had moved to Stamford, fallen for the town’s traditional charms, and orders were rolling in for his new painting and decorating business.

But the 43-year-old’s life was turned upside down when he was diagnosed with multiple sclerosis (MS).

He says it took him a year to deal with the diagnosis.

Now he is urging other people with MS not to sufferer in silence like he did and use the help that is available.

Mr Morris knew something was seriously wrong by mid-2004 when he started to have mobility problems.

He said: “I couldn’t keep my head in the sand any more and pretend it wasn’t happening. I didn’t have a clue what MS was. It broke my heart when the doctor told me that’s what it was.”

Mr Morris’s condition means he will not be able to work again.

“To me, that is the biggest killer with this disease,” he said. “My life was so good, and I had achieved more than I had ever hoped.”

Days after his diagnosis, Mr Morris visited the MS Therapy Centre in Hartford, near Huntingdon.

He said: “There were three people in wheelchairs. I couldn’t come to terms with this and thought to myself, is this me in a couple of years’ time? I was scared. I made my excuses and left.”

Mr Morris, who now lives in Stanground, Peterborough, finally plucked up the courage to return in January this year.

And now he says the help he’s received from the centre has enabled him to get his life back together.

Not only has the centre helped his physical condition, but John says it has saved him “from going mad”.

And he believes that there are hundreds of MS sufferers in Peterborough who could benefit from the centre’s support.

Mr Morris said: “I started using an oxygen chamber that helps my condition. All the months of being alone and frightened is the opposite of how I feel right now.

“My body is still falling apart, but my mind is a lot better. To talk to people with MS, swap theories, talk about anything to do with MS and not feel intimidated is priceless.

“This place is a godsend and saved me from going mad. There are many more people that it could help if they only knew it was here.”

Mr Morris suffers from the secondary-progressive type of MS. It means his illness gets progressively worse.

The centre has 120 members who come from as far away as Saffron Walden and King’s Lynn.

Centre manager Margaret Harrison said: “The support we give to sufferers, their carers and families reminds them they are not alone.”

The centre relies on charitable donations and needs £60,000 a year to keep operating.

To contact the centre, call 01480 458688.
21 October 2006

Friday, October 20, 2006

Most Important Actors In Growth Process Of Neurons Identified

Source: Proceedings of the National Academy of Sciences
Date: October 19, 2006

Defects in the growth process of our neurons often underlie brain or nerve diseases, such as Alzheimer's disease or multiple sclerosis. Scientists from the Flanders Interuniversity Institute for Biotechnology (VIB) connected to the Katholieke Universiteit Leuven, led by Bassem Hassan, have achieved a major step in unraveling the growth process of axons, the offshoots of neurons. They have identified the JNK, Wnt and FGF signaling cascades as the most important actors and have also discovered their respective roles. Their research shows that the growth of axons and the activity of neurons are completely independent of each other. This new finding can lead to better understanding of a variety of nerve diseases.

A complex network A human being has approximately 100 billion neurons, the body's information and signal processors. The great majority of them are found in the central nervous system. The brain contains complex networks of neurons that regulate a large number of bodily functions. Because the brain and the nervous system are a delicate system, something can sometimes go seriously wrong and a brain or nerve disease appears - for example, Alzheimer's or Parkinson's disease, Amyotrophic Lateral Sclerosis (ALS), or Multiple Sclerosis (MS). In the quest for possible cures for these diseases, it is important that we understand how connections are established between neurons.

Neurons have a number of long thin offshoots - called axons - that conduct electrical impulses. These primary elements of information transfer in the nervous system can sometimes be more than a meter long. The axon's orientation as it grows is also of great importance in forming the right connection. As in-coming stimuli are converted into signals that determine the direction and speed of an axon's growth, three things can happen: the axon can grow further, pull back, or change direction. Therefore, axon growth is a process that consists of several components: growth of the axon, orientation, recognition of objectives, and finally formation of synapses in order to transmit stimuli. Unraveling precisely how this whole process works is important for understanding the development of the brain and for helping develop therapies for diseases that are the consequence of damaged or diseased neurons.

The fruit fly as model Bassem Hassan is using the fruit fly (Drosophila melanogaster) as model for his research. Many processes in this small fly are in fact comparable to processes in humans, even for something as complex as the nervous system. Axon growth is a complicated process in that it involves growth as well as orientation and recognition. So it's not surprising that many different genes are involved. To bring clarity to this complex organization, Mohammed Srahna and his colleagues, led by Bassem Hassan, have been studying the DCN (Dorsal Cluster Neurons), a group of cells in the fruit fly's brain. The DCN belong to the visual system of the adult fruit fly and stimulate the visual cortex. The axons of the DCN form a very stereotypical connection pattern. This well-ordered pattern gave the researchers the perfect starting point for studying the influence of various genes on the axon growth process.

Regulation by several genes From their study of the developing brain of an adult fruit fly, the researchers have found that axon growth is mediated by an interaction among three signal cascades: Wnt, FGF and JNK. JNK is necessary for stimulating the growth of axons. Wnt activates JNK and FGF inactivates JNK, so the right balance between Wnt and FGF provides for a precise regulation of the growth of neurons. Axonal growth turns out to be completely independent of neuronal activity. This finding brings greater clarity to the axon's growth process - knowledge that constitutes a major step forward in understanding neuronal disorders.

Wednesday, October 18, 2006

Newest drugs not always the best

By Rita Rubin, USA TODAY

If anyone has the right to say "told you so," it's Mirta Millares and her colleagues at Kaiser Permanente's Drug Information Services.

Based on advice from the staff of specially trained pharmacists, Kaiser never added Vioxx, the arthritis drug, or Tysabri, a multiple sclerosis drug, to its formulary, the list of covered prescription drugs.

In both cases, safety and cost-effectiveness concerns kept the drugs off. Doctors could prescribe them only if they believed there was no alternative.

And then, no one could get the drugs. Merck stopped selling Vioxx in September 2004, nearly five years after the Food and Drug Administration approved it. And Biogen Idec pulled Tysabri in February 2005, four months after approval.

A Merck study found patients with colon polyps who took Vioxx had twice the heart attack or stroke risk as those on a placebo. And two people in a long-term Tysabri study came down with progressive multifocal leukoencephalopathy, or PML, a rare neurological disease. One died.

Clearly, newer drugs are not always better drugs, although they're usually promoted more and pricier. Still, Arthur Levin, head of the Center for Medical Consumers in New York, cites "a cultural mindset, even among physicians, that new is an improvement on old."

A 2002 study of more than 42,000 patients found generic diuretics were not only cheaper but also more effective than newer, brand-name drugs in lowering blood pressure.

For the first year after the results came out, diuretic prescribing did rise, says lead author Curt Furberg. But since then, "it's been fairly flat." He says scientists simply can't compete with brand-name drug makers' efforts to put a positive "spin" on unfavorable findings.

When the study came out, Furberg estimated treating high blood pressure with diuretics instead of brand-name drugs could save the U.S. health care system up to $10 billion a year. Some of the brand-name drugs are now available as generics, but they're still not as effective as diuretics, and as many as half of candidates for diuretics, aren't on them, he says.

FDA's role in approval

In theory, at least, most Americans want the most effective drug, according to a USA TODAY/ABC News/Kaiser Family Foundation poll conducted Sept. 7-12. Insurers should not cover expensive new treatments unless they've been proven to be more effective than cheaper treatments, 72% of respondents said. The margin of error for that question was plus or minus 4 percentage points.

Increasingly, critics of the FDA and of the drug industry are advising doctors and patients to avoid the newest drugs when there are older, equally effective drugs.

"It is a widely held misperception that FDA approval of a new drug denotes a guarantee of safety and certainty about its risk-benefit profile," a special Institute of Medicine panel reported last month. "In fact, eliminating all uncertainties prior to approval could cause considerable delay in new products reaching patients in need."

The panel recommended Congress amend the Food, Drug, and Cosmetic Act to require new drugs carry a special symbol on their labels for their first two years on the market. The marking would alert patients and prescribers there might be uncertainties about risks and benefits.

In those first two years, panel members said they would favor a ban on direct-to-consumer advertising, although it's not clear such a move would be legal. And the FDA should review all new data about drugs after five years on the market, they said.

In last week's Archives of Internal Medicine, Furberg, Levin and three other current or former members of the FDA's Drug Safety and Risk Management Advisory Committee said the agency should be able to grant "conditional approval" for new drugs that "have clear benefits but unanswered questions regarding serious adverse events."

Conditional OK recommended

Conditional approval would press drug makers to do and report postmarket safety studies requested by the FDA, the authors wrote. For now, companies aren't doing the studies "because there is no consequence if they fail to do so," says Furberg, professor of public health sciences at Wake Forest University in Winston-Salem, N.C.

Alternatively, the FDA should re-review all drugs two to four years after initial approval, Furberg and his co-authors wrote. He says the most worrisome drugs are taken for chronic diseases over a period of years, usually far longer than pre-market clinical trials.

Spokesman Alan Goldhammer of the Pharmaceutical Research and Manufacturers of America, the main industry trade group, says stigmatizing new drugs could cause patients and doctors to shun beneficial treatments.

"Clearly, there are going to be drugs that come through the system that pose very little in terms of a risk to the patient," he says. "To single these out for special attention seems to us to be unwise."

On paper, Goldhammer says, conditional approval looks like a good way to speed promising drugs to market, but the industry is concerned insurers might not cover drugs lacking full approval.

Meanwhile, the FDA gave Biogen Idec permission to resume selling Tysabri in June. The drug's new label is topped with a black-box warning, the FDA's strongest warning, about PML.

In response to an FDA advisory committee, Biogen Idec has set up a program limiting distribution of the drug.

Whether Tysabri should now be added to the Kaiser formulary is under review.

Tuesday, October 17, 2006

Cause of nerve fiber damage in multiple sclerosis identified

New information in emerging area of MS research could aid therapy development

Irvine, Calif., October 16, 2006

Researchers have identified how the body’s own immune system contributes to the nerve fiber damage caused by multiple sclerosis, a finding that can potentially aid earlier diagnosis and improved treatment for this chronic disease.

The study reveals how immune system B-cells damage axons during MS attacks by inhibiting energy production in these nerve fiber cells, ultimately causing them to degenerate and die. Study results appear in the Oct. 15 issue of the Journal of Immunology.

B-cell-axon activity is an emerging area of MS research, one that is changing how scientists and clinicians can look at this disease. In this study, Dr. Yufen Qin and fellow researchers from UC Irvine’s School of Medicine analyzed spinal fluid and tissue samples from MS patients to identify substances that stimulate a B-cell immune response. They noted an increased level of B-cell antibodies on lesions and in spinal fluid bound to two specific enzymes – GAPDH and TPI.

These two enzymes are essential for efficient energy production. The researchers believe that the binding of these antibodies to these enzymes – GAPDH, in particular – may lower the amounts of ATP – the chemical fuel for cells – available in cells, which eventually can lead to axon cell degeneration and death. In addition to the energy-production function, GAPDH is involved with a number of genetic activities, such as RNA translocation, DNA replication and DNA repair.

Other recent studies have shown that binding of inhibitors to GAPDH and TPI causes decreased ATP production in neurons, followed by progressive neuronal degeneration and death. Moreover, patients with TPI deficiency can develop progressive neurological disorders.

“This research is exciting and potentially important for future treatments because it identifies new antibodies associated with MS that can be targeted with emerging therapies,” said Qin, an assistant professor of neurology. “Significantly, these are the first antibodies to be identified with axon activity, which is a new area researchers are exploring in the pathology of MS.”

MS is a chronic central nervous system disease that can cause blurred vision, poor coordination, slurred speech, numbness, acute fatigue and, in its most extreme form, blindness and paralysis. Some 400,000 Americans have this disease. Its causes are unknown, and symptoms are unpredictable and vary greatly in severity.

Much MS research is focused on an autoimmune process in which T-cells attack and damage myelin, the fatty insulating tissue of axons. These T-cells do not attack axons themselves; the process of demyelination interrupts electrical impulses that run through these nerve fibers, thus causing MS symptoms. Demyelination has been considered the central feature of MS.

Recently, however, Qin has been among a group of researchers who have discovered that B-cells too are involved with the autoimmune response to MS. Instead of targeting myelin, these B-cells attack axons directly. Axons are the long, slender fibers of a neuron that serve as the primary transmission lines of the nervous system, and as bundles they help make up nerves.

Research at UCI and elsewhere has shown that myelin grows back if the T-cell autoimmune response is turned off, and drugs exist or are in development to block demyelination. Axons, in turn, repair very slowly, which implies that B-cell attacks on axons may have a significant impact on the chronic central nervous system damage caused by MS.

“Since this area of research is in its early stage, it’s important to understand the process by which these B-cell responses happen,” Qin said. “Hopefully, by identifying these two crucial enzymes, it will lead to a greater understanding of MS and lead to more effective treatments for people who live with this disease.”

Johanna Kolln, Hui-Min Ren, Reng-Rong Da, Yiping Zhang, Dr. Michael Olek, Dr. Neal Hermanowicz, Lutz G. Hilgenberg, Martin A. Smith and Dr. Stanley van den Noort of UCI and Edzard Spillner of the University of Hamburg also worked on the study. The National Multiple Sclerosis Society and the National Institutes of Health provided funding support.

About the University of California, Irvine: The University of California, Irvine is a top-ranked university dedicated to research, scholarship and community service. Founded in 1965, UCI is among the fastest-growing University of California campuses, with more than 24,000 undergraduate and graduate students and about 1,400 faculty members. The second-largest employer in dynamic Orange County, UCI contributes an annual economic impact of $3.3 billion. For more UCI news, visit www.today.uci.edu.

Television: UCI has a broadcast studio available for live or taped interviews. For more information, visit www.today.uci.edu/broadcast.

News Radio: UCI maintains on campus an ISDN line for conducting interviews with its faculty and experts. The use of this line is available free-of-charge to radio news programs/stations who wish to interview UCI faculty and experts. Use of the ISDN line is subject to availability and approval by the university.

Monday, October 16, 2006

Funding kicks off new treatments for diabetes and multiple sclerosis

A $5.23 million research program that will combine stem cell therapies with a rebuilding of a key part of the immune system – the thymus – to treat diseases such as autoimmune gastritis, multiple sclerosis and diabetes is being pursued at Monash University following today's announcement that it has been funded through the National Health and Medical Research Council's Programs scheme.

The Minister for Health and Ageing, The Hon.Tony Abbott today announced funding for Monash University of more than $43 million through the NHMRC's Program, Project and Career Development schemes.

This included funding for nine Research Fellowships, two Practitioner Fellowships, two enabling grants - $2.5 million for the National Non-Human Primate Breeding and Research Facility and $1.84 million for the Australian Mouse Brain Mapping Consortium – and an $822,000 equipment grant.

Deputy Vice-Chancellor (Research) Professor Edwina Cornish said the NHMRC funding announced today was testament to the innovative medical research being pursued at Monash.

Professor Richard Boyd, principal investigator on the stem cell program, said diseases such as autoimmune gastritis, multiple sclerosis and diabetes arose because a "rogue" immune system had turned inwards to attack the body's organs. "The organ destruction follows from recognition by the immune system of specific molecules – insulin in the case of diabetes, and a protein called MOG in the case of MS - in the organs," Professor Boyd said.

"These "autoimmune" diseases are incurable and controlled mainly by long-term administration of substances that suppress the immune system, often with serious side-effects. A rational approach is to render the rogue immune system harmless by removing the immune cells that recognize these particular molecules," he said. "We plan to use stem cell therapies combined with a rejuvenated immune system to treat these diseases without the need for excessive immunosuppressive regimes that are detrimental to health and well-being."

The same technologies should be applicable to minimising or even preventing the rejection of foreign transplants, Professor Boyd said.

Other projects funded today that will be pursued at Monash include a study of Australian box jellyfish venoms, an investigation of whether coeliac disease causes a loss of coordination or cognitive impairment, the factors that affect knee structure in healthy women, and a trial of the effect of substantial weight loss on obstructive sleep apnoea.

Study: Cannabis Helps Spasticity/bladder in MS Patients

Sativex® Data Presented at ECTRIMS European Multiple Sclerosis Congress


Porton Down, UK, 3 October 2006 – GW Pharmaceuticals plc (AIM: GWP) announces today that results from two Phase III studies of Sativex ® were presented at Europe's leading multiple sclerosis (MS) conference, the 22nd Congress of the European Committee for Treatment and Research in Multiple Sclerosis ( ECTRIMS), which took place in Madrid, Spain, from 27 - 30 September. The outcome of the studies in spasticity and bladder dysfunction, both symptoms of MS, were first reported by GW earlier this year.

The MS spasticity study, which evaluated 337 patients over a 15 week period, showed a significant reduction in symptoms of spasticity in patients in the ‘per protocol' population (i.e. those patients who complied with the study protocol) with advanced MS who had severe levels of spasticity despite ongoing treatment with the best available anti-spasticity medications. In addition 36% of these patients reported at least a 30% improvement in their spasticity symptoms which was also statistically significant 1 . The ‘intention to treat' population (all patients who entered the study, some of whom may have violated the protocol) showed a trend towards Sativex but this did not reach statistical significance. Sativex-treated patients also reported improvements in secondary endpoints such as sleep assessments at clinic visits; a timed 10 metre walk, quality of life measures, spasm severity and bladder symptoms. Benefits were also reported by carers who noticed overall improvements in the Sativex group.

Professor Christine Collin, lead investigator in the study and Consultant in Neurological Rehabilitation Medicine based at The Royal Berkshire and Battle NHS Trust, Reading commented, “This study shows encouraging results in a patient population with a high level of unmet medical need. It demonstrates that Sativex can reduce spasticity in these difficult to treat patients who have failed to gain enough improvement in their spasticity from the best currently available medication. Furthermore, when these results are pooled with a previous similar trial giving a total population of over 520 MS patients with spasticity, significant benefits in favour of Sativex were seen, in the whole intention to treat population.”

A second Phase III study presented at ECTRIMS and short-listed for a prize by the scientific committee, investigated Sativex in the management of bladder problems in people with MS. Bladder problems are a very common feature in up to 75% of people with MS experiencing dysfunction including increased frequency and urgency of urination and increased incontinence2. This study in 135 patients suffering with urinary incontinence, not wholly relieved by their existing treatment, demonstrated that Sativex had a positive impact on the symptoms of over-active bladder with 84% in the Sativex treated group vs. 58% of the placebo group reporting improvements in bladder dysfunction3. Statistically significant improvements were seen in nocturia (urination during the night), number of voids per day and patients' opinion of bladder symptom severity.

Sativex contains the cannabinoids 9 -tetrahydrocannabinol (THC) and cannabidiol (CBD) and is formulated as an oromucosal spray which is administered by spraying into the mouth and allows flexible dosing which is ideally suited to the variable nature of MS. Each spray of Sativex delivers a fixed dose of 2.7mg THC and 2.5mg CBD. Sativex was generally well tolerated in both studies 1,3.

Sativex is licensed in Canada and has recently been submitted for regulatory approval in selected European countries.


GW Pharmaceuticals plc

Dr Geoffrey Guy, Executive Chairman

Tel: + 44 (0)1980 557000
Justin Gover, Managing Director

Financial Dynamics

Tel: +44 (0)20 7831 3113
David Yates, Sarah MacLeod

Notes to Editors

About GW Pharmaceuticals plc
GW was founded in 1998 and listed on the AiM, a market of the London Stock Exchange, in June 2001. Operating under licence from the UK Home Office, the Company is developing cannabis-derived pharmaceutical products for patients with multiple sclerosis, neuropathic pain, cancer pain, spinal cord injury, rheumatoid arthritis, and other severe medical conditions.

GW has assembled a team of over 100 scientists with extensive experience in developing both plant-based prescription pharmaceutical products and medicines containing controlled substances. GW is dedicated to developing treatment options that alleviate pain and other neurological symptoms in patients who suffer from serious ailments.

For further information, please visit the Company's website: www.gwpharm.com.


Collin C, Ambler Z et al. A randomised study of Sativex® in patients with symptoms of spasticity due to multiple sclerosis. Poster 412 presented at the 22nd Congress of the European Committee for Treatment and Research in Multiple Sclerosis (ECTRIMS)

de Ridder D, Constantinescu C et al. Randomised controlled study of cannabis based medicine (Sativex®) in patients suffering from multiple sclerosis associated detrusor overactivity. Poster 411 presented at the 22nd Congress of the European Committee for Treatment and Research in Multiple Sclerosis (ECTRIMS)

Sunday, October 15, 2006

Persistent Use of Emotional Acupressure Technique Eradicates Severe Symptoms of MS

Drug companies continue testing drugs to treat the symptoms associated with Multiple Sclerosis. Meanwhile, people suffering with MS are using a unique form of do-it-yourself acupressure to resolve their disabling MS symptoms. After four months of EFT treatments, one man returned to work after 24 years on disability pension and two years later, he continues to be symptom free and enjoying a full and active life.

San Francisco, CA (PRWEB) October 14, 2006 -- After being on disability for 24 years, Hank Hadley, a Multiple Sclerosis (MS) patient celebrates his second year of full time employment. After persistent application of Emotional Freedom Techniques (EFT), he is pain-free, has no symptoms of Multiple Sclerosis and works at a physically demanding job.

EFT often works where nothing else will because it addresses the emotional roots of diseases like MS. Conventional treatments for MS involve complex drug cocktails to treat the myriad of symptoms. In contrast EFT offers one simple drug-free solution to treating the physical, emotional, and cognitive components of MS. EFT can be learned without cost by downloading the free EFT Manual at http://www.emofree.com/downloadeftmanual.asp?ref=prw-MScw

After injuring his tailbone at age 10, Mr. Hadley spent the next 42 years of his life in pain. He endured 16 surgeries to his back and neck and tried to find relief with prescription addictive painkillers. He relied on crutches and a wheelchair to get around and was finally diagnosed with Multiple Sclerosis.

When he attended an EFT workshop with EFT Master, Sophia Cayer (www.solacewithsophia.com) Mr. Hadley’s pain, on a zero to 10 scale, was consistently at an 8 or 9. He had been unable to work and had been receiving disability benefits for 24 years. He was disabled and suicidal, believing that all hope of being pain free was gone.

During that EFT workshop, Mr. Hadley felt significant relief from his pain and began doing EFT work with Ms. Cayer twice weekly and doing EFT on himself 3 to 4 times a day. During their EFT sessions Mr. Hadley and Ms. Cayer addressed his emotional issues and traumatic events and as they cleared each trauma, Mr. Hadley’s pain subsided and eventually disappeared completely. Interestingly, most of his EFT treatment focused on alleviating emotional issues, not physical issues. This is a frequent finding with EFT and gives impressive weight to the mind-body connection.

After four months of EFT treatment, Mr. Hadley was off all pain medication. His MS symptoms disappeared as did arthritis symptoms and pain from scar tissue. He began working full time at a job where he was physical most of the day. Two years later he reports that with persistent daily EFT tapping, he continues to work full time and remains symptom free.

Having recently celebrated his 54th birthday, Mr. Hadley says he is, “Euphoric! I feel I am leading the best life ever, probably since I was 10 years old or younger." He is enjoying horseback riding and long walks, and theme park rides with his grandchildren; things that he had never been able to do – and never thought he would be able to do. Sophia Cayer said, “I will always remember the day Hank turned in his “Handicapped” license plate!”

Dr. Eric Robins, who uses EFT in his daily medical practice, explains how this kind of improvement is possible with EFT. “At least 85% of medical problems are physical manifestations of how stress, anxiety, and past traumas are held in and processed by the body. The best technique to address these issues and to clear them out of the body is EFT.”

This gentle, do-it-yourself form of acupressure neutralizes negative, disruptive feelings, emotions and stress and balances the energy meridians (Chi or Qi). When balance is achieved in the meridians, physical and emotional symptoms associated with diseases like MS and arthritis dissipate.

The mission of the National Multiple Sclerosis Society is to “end the devastating effects of MS”.

Gary Craig, the Stanford-trained engineer who developed EFT says, “We have spent a decade chronicling cases where people use this simple procedure to gain complete relief from the symptoms of serious diseases such as MS, diabetes, arthritis and cancer. It is time for the associations representing people with these diseases to explore ways that EFT can be used to benefit their membership.”

To ensure global accessibility to EFT, Craig makes the EFT Manual available online at no cost. The official EFT Manual has been translated by volunteer practitioners into nine languages. It can be downloaded at http://www.emofree.com/downloadeftmanual.asp?ref=prw-MScw

Although most Americans have yet to hear of it, EFT may be the world’s fastest-growing self-help technique because people are getting results where nothing else has worked. Over 350,000 have downloaded Craig’s free training manual and another 10,000 download it each month.

For further information, contact Gary Craig at 707-785-2848.