PharmaFrontiers Corp. (OTCBB: PFTR), a company involved in the development and commercialization of cell therapies, announced today that the protocol for its Phase IIb clinical trial of Tovaxin(TM), a novel T cell therapeutic vaccine for Multiple Sclerosis (MS), has been accepted by the U.S. Food and Drug Administration's (FDA) Center for Biologics Evaluation and Research (CBER).

"PharmaFrontiers is very excited to receive a 'green light' from the FDA for our Phase IIb clinical trial. Our earlier open-label Phase I/II clinical trials not only gave us the safety and tolerability data we sought, but we also observed a trend towards a reduction in annualized relapse rate (ARR) in excess of 90%, the lowering of the myelin-peptide reactive T cells (MRTCs) in patients blood and the improvement in patients' clinical measures," said David B. McWilliams, chief executive officer of PharmaFrontiers. "The Tovaxin clinical program continues to show promising results and we believe that the completion of this Phase IIb clinical trial will allow us to launch a Phase III pivotal trial."

Tovaxin is a trivalent formulation of attenuated MRTCs, which are derived from peripheral blood and produced ex vivo as myelin basic protein (MBP), proteolipid protein (PLP) and myelin oligodendrocyte glycoprotein (MOG) reactive T cells. MRTCs are believed to play a critical role in the pathogenesis of MS. Because several myelin antigens are described as potential autoantigens for MS, depletion of MRTCs using a trivalent formulation may have enhanced therapeutic effects.

This multicenter, randomized, double blind, placebo-controlled Phase IIb clinical study is designed primarily to evaluate the efficacy, safety and tolerability of the Tovaxin T Cell therapy with clinically isolated syndrome (CIS) and early relapsing-remitting MS (RR-MS) patients. Additionally, the study of these patients will evaluate biomarkers of Tovaxin's efficacy and to evaluate the effect of Tovaxin on immune deviation and epitope spreading.

"We believe that the protocol design will allow us to study the clinical effects of Tovaxin in a group of patients requiring a safe and effective therapy," said Edward J. Fox, M.D., Ph. D., director of The MS Clinic of Central Texas (Austin) and the lead principal investigator for the upcoming clinical studies. "During this two-arm, 52-week, parallel-group study, patients will be given five subcutaneous injections at 0, 4, 8, 12 and 24 weeks. The analyses will be performed at the end of the 52-week study to assess the safety and efficacy of Tovaxin. The primary efficacy variable is the cumulative number of gadolinium-enhancing lesions on T1-weighted MRI summed over the Week 28, 36, 44, and 52 MRIs. The secondary efficacy variables are the cumulative number of new gadolinium-enhancing lesions at Weeks 28-52, the change in T2-weighted lesion volume, and the annualized relapse rate. Of the 150 patients participating in the trial, 100 will receive Tovaxin and 50 will receive the placebo."

All patients who complete the trial will be eligible to participate in an optional one-year extension study, in which they will receive Tovaxin open-label. The open-label study is being planned under a different protocol that will be submitted to the FDA.

"A patient-specific therapeutic vaccination strategy, Tovaxin T cell vaccine is formulated using the MS patient's own myelin peptide-specific activated T cell lines, which are harvested and attenuated on the day of vaccine administration," said Jim C. Williams, Ph.D., PharmaFrontiers chief operating officer. "The shelf-life of the final product is approximately three days."

PharmaFrontiers will be conducting the Phase IIb with its clinical development partner, INC Research, Raleigh, NC.

About PharmaFrontiers Corp.

PharmaFrontiers' strategy is to develop and commercialize cell therapies to treat several major disease areas such as cardiac and pancreatic conditions and Multiple Sclerosis. PharmaFrontiers owns patented and proprietary individualized cell therapies that are in FDA Phase I/II human dose ranging clinical trials to evaluate their safety and effectiveness in treating MS. The company also holds the exclusive worldwide license from the University of Chicago, through its prime contractor relationship with Argonne National Laboratory, for patents relating to the use of adult pluripotent stem cells derived from patients' own circulating blood.

Safe Harbor Statement

This press release contains "forward-looking statements," including statements about PharmaFrontiers' growth and future operating results, discovery and development of products, strategic alliances and intellectual property, as well as other matters that are not historical facts or information. These forward-looking statements are based on management's current assumptions and expectations and involve risks, uncertainties and other important factors, specifically including those relating to PharmaFrontiers' ability to obtain additional funding, develop its stem cell technologies, achieve its operational objectives, and obtain patent protection for its discoveries, that may cause PharmaFrontiers' actual results to be materially different from any future results expressed or implied by such forward-looking statements. PharmaFrontiers undertakes no obligation to update or revise any such forward-looking statements, whether as a result of new information, future events or otherwise.

Source: Business Wire

http://www.rednova.com/news/health/289627/pharmafrontiers_tovaxintm_phase_iib_multiple_sclerosis_clinical_trial_protocol_accepted/index.html?source=r_health

Category: Multiple Sclerosis News
Article Date: 30 Oct 2005

Data from the extension of a Phase II study to 12 months confirm the significant effects of FTY720, a novel oral medication, for the treatment of patients with relapsing multiple sclerosis (MS).

The data, presented at the ECTRIMS/ACTRIMS meeting in Thessalonica, Greece, showed that both patient groups taking FTY720 (1.25 mg and 5 mg) who had experienced a reduction in their annualized relapse rate of more than 50% during the first six months of the study compared to placebo maintained this low relapse rate during the subsequent six-month extension.

In patients who switched from placebo to either the 1.25 mg or 5 mg dosing of FTY720 after six months, the annualized relapse rate was reduced by at least 70% during the second six-month study phase compared to the first six months on placebo.

More than 80% of patients who received FTY720 for up to 12 months were free from lesions showing active inflammation on magnetic resonance imaging (MRI) at month twelve irrespective of their FTY720 treatment dose (1.25 mg or 5 mg).

"We are excited by these full-year study results confirming the significant effect of oral FTY720 on reducing both clinical relapses and inflammatory disease activity that we first saw during the six-month placebo-controlled phase of the study," said chief investigator Professor Ludwig Kappos, MD, Department of Neurology at the University Hospital in Basel, Switzerland, "We hope that the magnitude of benefits shown in Phase II will be confirmed in the larger scale Phase III study program expected to be launched soon." Based on the positive Phase II study results, Novartis is in discussions with regulatory authorities about the FTY720 Phase III program, which is expected to be launched by the end of 2005.

Over two million people worldwide are estimated to suffer from multiple sclerosis, which is the leading cause of neurological disability in young adults. MS is the most common chronic, disabling disease of the central nervous system affecting twice as many women than men.3 MS has a significant impact on the patient's social activities, employment and overall quality of life. Currently marketed MS therapies afford an average reduction in relapse rates of 30% in two-year studies and require frequent injections ranging from daily to weekly. , , ,

FTY720 Phase II study results

The results are from a large Phase II study conducted at 32 centers in 11 countries (Europe and Canada). In the initial, placebo-controlled part of this study, 281 patients were randomized in equal numbers to receive either placebo, 1.25 mg or 5.0 mg FTY720 orally once-daily for six months. The study evaluated the effect of FTY720 on disease activity as measured by MRI and clinical relapses as well as its tolerability and safety. After six months, patients in the placebo group were re-randomized to receive either FTY720 1.25 mg or 5 mg blinded for an additional six months, while patients already on FTY720 continued their originally-assigned treatment. A total of 98% of the 255 patients who completed the first six months volunteered to continue in the extension phase evaluating the longer-term effects of FTY720.

In the 12-month analysis, both patient groups on FTY720 (1.25 mg and 5 mg) who had experienced a reduction in their annualized relapse rate of more than 50% during the first six months compared to placebo maintained this low relapse rate during the subsequent six-month extension. In those patients who switched from placebo to either 1.25 mg or 5 mg of FTY720 after six months, the annualized relapse rate was reduced by at least 70% during the second six-month study phase compared to the first six months on placebo.

The MRI results at 12 months showed low levels of inflammatory disease activity in all FTY720 groups. In patients who switched from placebo to FTY720, the mean number of inflammatory (Gd-enhancing) lesions on MRI (at the 12th month) was reduced by more than 80% compared to the sixth month. More than 80% of patients who received FTY720 for up to 12 months were free from lesions showing active inflammation on MRI at the 12th month irrespective of their FTY720 treatment dose (1.25 mg or 5 mg).

FTY720 appeared to be well tolerated, with 91% of patients who entered the extension phase completing the 12th month on the study drug. There were no unexpected safety findings during the extension as compared to the six-month placebo-controlled phase. The most frequently reported adverse events in patients treated up to twelve months were non-serious infections (colds, influenza), headache, diarrhoea and nausea.

About FTY720

Oral FTY720 has a novel mode of action different from all available therapies. It reversibly sequesters lymphocytes away from blood and susceptible target organs such as the central nervous system (CNS), thereby reducing neuroinflammation in MS. FTY720 has been developed by Novartis Pharma and licensed from Mitsubishi Pharma Corporation.

About Multiple Sclerosis

MS is the most common inflammatory and neurodegenerative disorder of the central nervous system, including the brain, spinal cord and optic nerves. MS typically presents itself in relapsing forms. The relapsing-remitting (RRMS) course is the most common form of the disease. Patients suffer acute self-limiting attacks (relapses) of neurological dysfunction followed by complete or incomplete remission in function. Over time, transmission of electrical nerve impulses is disrupted, nerve cells are destroyed, and patients experience symptoms ranging from fatigue, tingling, numbness and blurred vision to poor muscle control with partial or complete paralysis, speech or mental impairment. About 50% of patients advance to the secondary progressive (SPMS) course within 10 years.

This release contains certain forward-looking statements relating to Novartis' business, which can be identified by the use of forward-looking terminology such as "suggest", "expected to be launched", "will be confirmed" or similar expressions, or regarding potential future revenue from FTY720. Such forward-looking statements reflect the current views of Novartis regarding future events, and involve known and unknown risks, uncertainties and other factors that may cause actual results with FTY720 to be materially different from any future results, performance or achievements expressed or implied by such statements. There can be no guarantee that FTY720 will be approved for any indications or labeling in any market. Nor can there be any guarantee of potential future sales of FTY720. Neither can there be any guarantee regarding the long-term impact of a patient's use of FTY720. In particular, management's expectations regarding commercialization of FTY720 could be affected by, among other things, unexpected clinical trial results; unexpected regulatory actions or delays or government regulation generally; Novartis' ability to obtain or maintain patent or other proprietary intellectual property protection; competition in general; government, industry and general public pricing pressures, and other risks and factors referred to in Novartis AG's current Form 20-F on file with the US Securities and Exchange Commission. Should one or more of these risks or uncertainties materialize, or should underlying assumptions prove incorrect, actual results may vary materially from those anticipated, believed, estimated or expected. Novartis is providing the information in this press release as of this date and does not undertake any obligation to update any forward-looking statements contained in this press release as a result of new information, future events or otherwise.

About Novartis

Novartis has been a leader in the neuroscience area for more than 50 years, having pioneered early breakthrough treatments for Alzheimer's disease, Parkinson's disease, attention deficit/hyperactivity disorder, epilepsy, schizophrenia and migraine. Novartis continues to be active in the research and development of new compounds, is committed to addressing unmet medical needs and to supporting patients and their families affected by these disorders.

Novartis AG (NYSE: NVS) is a world leader in pharmaceuticals and consumer health. In 2004, the Novartis group of companies' businesses achieved sales of USD 28.2 billion and pro forma net income of USD 5.8 billion. The group invested approximately USD 4.2 billion in R&D. Headquartered in Basel, Switzerland, Novartis group companies employ about 83,700 people and operate in over 140 countries around the world. For further information please consult novartis.com.

References

21st Congress of the European Committee for Treatment and Research in Multiple Sclerosis (ECTRIMS)/10th Annual Meeting of the Americas Committee for Treatment and Research in Multiple Sclerosis (ACTRIMS)

A relapse refers to the appearance of new symptoms or the aggravation of old ones, lasting for at least 24 hours.

Multiple Sclerosis International Federation
(msif.org/en/ms_the_disease/quick_facts.html)

PRISMS study group. Randomised double-blind placebo-controlled study of interferon beta-1a in relapsing-remitting multiple sclerosis. The Lancet 1998; Vol 352: 1498-1504.

LD Jacobs et al. Intramuscular Interferon beta-1a for disease progression in relapsing multiple sclerosis. Ann Neurol 1996, 39: 285-294.

IFNB Multiple Sclerosis Study Group. Interferon beta-1b is effective in relapsing-remitting multiple sclerosis. I. Clinical results of a multicenter, randomized, double-blind, placebo-controlled trial. Neurology 1993; 43: 655-661.

K.P. Johnson et al. Copolymer 1 reduces relapse rate and improves disability in relapsing-remitting multiple sclerosis: Results of a phase III multicenter, double-blind, placebo-controlled trial. Neurology 1995; 45: 1268-1276.

L. Kappos et al. Promising results with a novel oral immunomodulator - FTY720 - in relapsing MS. Clinical Abstract of data presented at the 21st Congress of the European Committee for Treatment and Research in Multiple Sclerosis (ECTRIMS)/10th Annual Meeting of the Americas Committee for Treatment and Research in Multiple Sclerosis (ACTRIMS) meeting, Thessalonica, Greece, Sept 28-Oct 1, 2005.

P. O'Connor et al. Phase II study with oral FTY720 in relapsing MS: Results of the dose-blinded active drug extension phase at 12 months. Clinical Abstract of data presented at the 21st Congress of the European Committee for Treatment and Research in Multiple Sclerosis (ECTRIMS)/10th Annual Meeting of the Americas Committee for Treatment and Research in Multiple Sclerosis (ACTRIMS) meeting, Thessalonica, Greece, Sept 28-Oct 1, 2005.

Multiple Sclerosis International Federation (msif.org/en/ms_the_disease/index.html)

Weinshenker BG. Natural history of multiple sclerosis. Ann Neurol 1994, 36: S6-S11.

Corinne Hoff
Novartis Global Media Relations
corinne.hoff@novartis.com
http://www.novartis.com

http://www.medicalnewstoday.com/medicalnews.php?newsid=32823

POSTED: 11:25 am EDT October 27, 2005

BAGHDAD, Iraq -- Marine Lt. Col. Steve Grass will be running in a Washington marathon this weekend, even though he's in Iraq.As thousands of runners circle the monuments in the nation's capital, Grass will be taking part in the Marine Corps Marathon, too. But he'll join the marathon remotely, running 26.2 miles around the Iraqi training base where he's stationed.Grass is one of 45 people who will run the marathon for Destination Cure -- The Race Against MS. The national nonprofit group is dedicated to raising money for multiple sclerosis research.Grass' mother has the disease. Last year, Grass and his fellow runners raised $300,000.

http://www.thepittsburghchannel.com/health/5188789/detail.html

Category: Multiple Sclerosis News
Article Date: 21 Oct 2005

A new study suggests that a substance made by immune cells plays a key role in the progression of a disease in animals that closely mimics multiple sclerosis (MS). The findings further suggest that blocking the molecule, known as macrophage migration inhibitory factor (MIF) might prevent the progression of the disease.

Researchers at The Ohio State University Medical Center conducted the study using mice that develop a disease that mimics MS. They compared these animals to similar mice that lacked MIF, an immune-system signaling molecule.

The results show that the animals without MIF develop the initial, acute phase of the disease, but then show no signs of further progression.

The study is published as a Cutting Edge paper in the November 1, 2005, issue of the Journal of Immunology.

"Our results suggest that MIF may be less important for initiating MS, but that it may be necessary for MS progression," says principal investigator Caroline C. Whitacre, professor of molecular virology, immunology and medical genetics.

"These findings indicate that in the future we can perhaps use MIF levels to predict the onset of a relapse. But more importantly, perhaps this study will lead to drugs that can halt the course of MS by blocking the action of MIF."

MS is an inflammatory, autoimmune disease which primarily affects the brain and spinal cord. Autoimmune diseases occur when the body's own immune cells destroy tissues in the body. In MS, immune cells destroy the myelin sheath that surrounds nerve fibers in the brain and spinal cord. Myelin is a fatty substance that insulates nerve fibers and enables them to transmit impulses.

According to the National MS Society, about 400,000 Americans are living with MS and about 10,400 new cases are diagnosed yearly. The disease usually strikes between the ages of 20 and 40, and it is more common in women. MS symptoms vary from person to person. Some individuals experience unusual fatigue, numbness and tingling; others can have loss of balance and difficulty walking; still others develop slurred speech, double vision, tremors or bladder problems.

In about 85 percent of cases, MS shows a pattern of remission and relapse, with no warning as to when a relapse will occur.

For this study, Whitacre and a group of colleagues used mice that develop the MS-like condition known as experimental autoimmune encephalomyelitis (EAE). The mice develop the disease after being inoculated with a myelin protein. The researchers compared these mice to mice that were identical except that they lacked the gene for MIF.

After inoculation, the mice with the MIF gene showed progressive EAE. In contrast, the mice lacking the MIF gene showed signs of early disease, but after about 20 days, these mice recovered and showed no further sign of progression.

The study also gave the investigators insights into the mechanism by which MIF influences the course of disease. They found that MIF blocked the steroid hormone, corticosterone (known as cortisol, in humans). Animals missing MIF had high levels of the steroid, while those with MIF showed very low levels.

The level of the steroid hormone, in turn, caused important immune-system changes in the animals that are likely to affect the disease.

For example, the mice with MIF (and low levels of the steroid hormone) showed high levels of immune-system cytokines or products that promote inflammation. Mice that lacked MIF (and had high levels of the steroid), on the other hand, showed high levels of immune-system cytokines or products that suppress inflammation .

"Our evidence overall suggests that the inhibition of this steroid hormone by MIF has an important influence on the immune system and in determining whether the disease progresses or not," Whitacre says.

Funding from the National Institute of Allergy and Infectious Diseases supported this research.

Darrell E. Ward
Darrell.Ward@osumc.edu
Ohio State University
http://researchnews.osu.edu

http://www.medicalnewstoday.com/medicalnews.php?newsid=32320

Category: Multiple Sclerosis News
Article Date: 21 Oct 2005

A new study suggests that a substance made by immune cells plays a key role in the progression of a disease in animals that closely mimics multiple sclerosis (MS). The findings further suggest that blocking the molecule, known as macrophage migration inhibitory factor (MIF) might prevent the progression of the disease.

Researchers at The Ohio State University Medical Center conducted the study using mice that develop a disease that mimics MS. They compared these animals to similar mice that lacked MIF, an immune-system signaling molecule.

The results show that the animals without MIF develop the initial, acute phase of the disease, but then show no signs of further progression.

The study is published as a Cutting Edge paper in the November 1, 2005, issue of the Journal of Immunology.

"Our results suggest that MIF may be less important for initiating MS, but that it may be necessary for MS progression," says principal investigator Caroline C. Whitacre, professor of molecular virology, immunology and medical genetics.

"These findings indicate that in the future we can perhaps use MIF levels to predict the onset of a relapse. But more importantly, perhaps this study will lead to drugs that can halt the course of MS by blocking the action of MIF."

MS is an inflammatory, autoimmune disease which primarily affects the brain and spinal cord. Autoimmune diseases occur when the body's own immune cells destroy tissues in the body. In MS, immune cells destroy the myelin sheath that surrounds nerve fibers in the brain and spinal cord. Myelin is a fatty substance that insulates nerve fibers and enables them to transmit impulses.

According to the National MS Society, about 400,000 Americans are living with MS and about 10,400 new cases are diagnosed yearly. The disease usually strikes between the ages of 20 and 40, and it is more common in women. MS symptoms vary from person to person. Some individuals experience unusual fatigue, numbness and tingling; others can have loss of balance and difficulty walking; still others develop slurred speech, double vision, tremors or bladder problems.

In about 85 percent of cases, MS shows a pattern of remission and relapse, with no warning as to when a relapse will occur.

For this study, Whitacre and a group of colleagues used mice that develop the MS-like condition known as experimental autoimmune encephalomyelitis (EAE). The mice develop the disease after being inoculated with a myelin protein. The researchers compared these mice to mice that were identical except that they lacked the gene for MIF.

After inoculation, the mice with the MIF gene showed progressive EAE. In contrast, the mice lacking the MIF gene showed signs of early disease, but after about 20 days, these mice recovered and showed no further sign of progression.

The study also gave the investigators insights into the mechanism by which MIF influences the course of disease. They found that MIF blocked the steroid hormone, corticosterone (known as cortisol, in humans). Animals missing MIF had high levels of the steroid, while those with MIF showed very low levels.

The level of the steroid hormone, in turn, caused important immune-system changes in the animals that are likely to affect the disease.

For example, the mice with MIF (and low levels of the steroid hormone) showed high levels of immune-system cytokines or products that promote inflammation. Mice that lacked MIF (and had high levels of the steroid), on the other hand, showed high levels of immune-system cytokines or products that suppress inflammation .

"Our evidence overall suggests that the inhibition of this steroid hormone by MIF has an important influence on the immune system and in determining whether the disease progresses or not," Whitacre says.

Funding from the National Institute of Allergy and Infectious Diseases supported this research.

Darrell E. Ward
Darrell.Ward@osumc.edu
Ohio State University
http://researchnews.osu.edu

http://www.medicalnewstoday.com/medicalnews.php?newsid=32320

Author(s): Zahra Pah Lavan

Abstract:

Zahra Pah Lavan gives an overview of Multiple Sclerosis and the treatments available. Zahra Pah-Lavan RN, BSc (Hons) is a freelance writer. Article accepted for publication: September 2005

Keywords:

Progressive disease Spasticity Myelin sheaths

Multiple sclerosis (MS) is an unpredictable disease of the central nervous system (CNS), with symptoms that can range from relatively benign to devastating (Compston & Coles, 2002). Current estimates are that approximately 2.5 million people worldwide have MS, with up to 62,000 cases in the UK (Compston & Coles, 2002; Toosy & Thompson, 2000).

Persons with MS may see a wide range of medical professionals depending on their symptoms (Table 1), the way MS progresses and the extent of their physical disability. A specialist or generalist nurse's role in hospital, community or long-term care is critical in providing individuals with MS and their carers with ongoing and supportive education on the disease. Nurses can work within the multidisciplinary team without losing sight of the holistic approach necessary for each individual's unique MS management (UK Multiple Sclerosis Specialist Nurse Association et al., 2001).

The name 'multiple sclerosis' signifies both a number (ie more than one) and a condition (of the scarred myelinated areas in the CNS with sclerosis being the Greek word for scarring or hardening) (www.NINDS.nih.gov). When myelin is damaged, nerve communication is disrupted and neurological transmission of messages may be slowed or blocked completely, leading to diminished or total loss of bodily functions that are controlled by areas of the CNS (Waugh & Grant, 2001).

MS affects one in 1,000 people in Western countries (USA, Europe & Australia) and is generally more common in caucasians and women (McDonald, 1998). It does not occur as frequently in every country throughout the world and seems to be related to how far a country is from the equator becoming more common the farther away a country is (Waugh & Grant, 2001; Sadovnick & Ebers, 1993). MS usually starts between the ages of 20 and 40 years but can make its first appearance in early childhood or after age 60 (McDonald, 1998). Some studies suggest that there may be a connection between where a person lived for the first 15 years of his/her life and the incidence of MS (Alvarez-Lafuente et al., 2004; Gaudet et al.,1995; Waugh & Grant, 2001).

Causes of MS
Despite a great deal of research, a specific cause of MS has not yet been determined (Alvarez-Lafuente et al., 2004). Environmental studies suggest that there is a triggering factor in the environment, such as toxins causing MS to manifest in those whose immune systems are genetically predisposed to it (Compston, 1997). It is hypothesised that, at the time of or immediately following puberty, patients acquire an infection with a long latency period. Or, conversely, people in some areas may come in contact with an unknown protective agent during the time before puberty (Waugh & Grant, 2001). Other studies suggest that the unknown element may actually be genetic predilection reflecting racial and ethnic susceptibility factors (Gold, Rieckman & Rieckman, 2000; Swanborg, Whittum-Hudson, Hudson. 2003).

Anatomy and physiology
Neuron cells: The brain, spinal cord nerves are made up of neuron cells which transmit information and control bodily functions. Each neuron has several branching structures called dendrites (responsible for receiving information from other neurons and the body), and a long arm-like nerve fibers called an axon (along which electrical signals travel passing information and instructions from the CNS to the body). Axons have a protective coating of myelin, wrapped around them like insulation to help them with their work (Waugh & Grant, 2001).

Central nervous system (CNS): This is made up of the brain and the spinal cord through which we can pick up signals from the outside world such as what we can see, smell, taste, hear and feel. The CNS also coordinates all our conscious and unconscious activities such as moving, talking, thinking, remembering and the reflex actions that happen without us thinking about them. Any

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damage to the CNS whether it is to the nerve cell or to the myelin sheath, will stop the transfer of messages carried by the nerves and produce a constellation of neurological symptoms. It is believed that in MS the nerves in the CNS are stripped of their myelin coating due to autoimmune disease (Thibodeau & Patton, 2002; Waugh & Grant, 2001).

The immune system: A complex network of specialised cells and organs - defends the body against attacks by antigens such as bacteria, viruses, fungi, and parasites. Once the immune system recognises an antigen, the first defence is an inflammatory reaction followed by the production of antibodies and migration of special cells, such as T-cells, to fight off the threat. In autoimmune disease the system fails and it begins to consider parts of itself as foreign and launches an attack on them (Thibodeau & Patton, 2002; Waugh & Grant, 2001).

Blood-Brain barrier: Although the brain is continually supplied with nutrients through the circulating blood, no blood cells cross through the walls of the blood vessels into the brain. In MS, a breach in the barrier between blood and brain brings, for the first time, the white blood cells of the immune system into direct contact with the myelin coats of nerve cells. Not having encountered myelin before, the white blood cells regard it as foreign and launch an attack stripping the nerve fibres of their protective myelin sheath. Demyelinated fibres are unable to carry out their function of carrying messages from the CNS to the rest of the body, and the symptoms of MS result (Waugh & Grant, 2001; Toosy & Thompson, 2000).

Cycle of damage and recovery: Myelin is produced by highly specialised cells (oligodendrocytes) and unfortunately, an adult brain has a limited supply of these cells which themselves only have a limited life when they are actively producing myelin. Once the inflammation within the CNS subsides, cells within the CNS can begin to repair the damaged myelin (remyelination). As the disease advances, the production of myelin cannot keep pace with its destruction resulting in an incomplete recovery of the affected function or permanent damage to the axons and complete loss of electrical signals. It is believed that permanent disability in MS could be the result of both ongoing demyelination and axonal injury (Table 2, Thibodeau & Patton, 2002; Waugh & Grant, 2001).

How is MS diagnosed?
MS diagnosis is highly dependent on the accuracy of the patient's medical history and the physician's skill in eliciting and evaluating it, however diagnosis is often delayed due to the transitory nature of the disease and the lack of specific

Table 2: Different forms of MS

1. Relapsing-remitting MS (RR-MS) Shows clearly defined relapses with some amount of recovery. It is the most common form of MS diagnosed. 2. Secondary progressive MS Initially follows a RR-MS course but over time a variable but continued loss of physical & cognitive functions starts to take over & relapses become less common. 3. Primary progressive MS Shows no relapse, & over the years there is continual loss of physical & cognitive functions. Source: Confavreux et al, 2000

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diagnostic test – specific symptoms. During a neurological consultation, Magnetic Resonance Imaging (MRI) scans, lumber puncture or evoked potentials tests may be requested (Basics of best practice in the management of Multiple Sclerosis, 1999).

MRI uses a strong magnetic field to create images of the brain and spinal cord showing defects in the white matter including patches of inflamed myelin. However, the link between the amount of disease activity shown on the MRI scan and the progress of the disease is not very clear and at present it is not possible to use the results of MRI to predict how the disease will develop (Frohman et al., 2003; Brex et al., 2002). As lesions can also occur in several other neurological disorders such as diabetes, Lyme disease, pernicious anaemia and spinocerebellar ataxias to name but a few (Waugh & Grant, 2001), they are not absolute evidence of MS. The MS diagnostic criteria (Association of British Neurologists, 2001) therefore sets out that neurological evidence of lesions or plaques in at least two distinct areas of the CNS white matter, evidence that the plaques have occurred at different points in time, and most importantly, that these plaques have no other reasonable explanation thus ruling out other illnesses that mimic MS.

Lumbar puncture involves taking a sample of the cerebrospinal fluid to check for cellular and chemical abnormalities including increased white blood cells and higher-than-average amounts of protein, especially myelin basic protein and an antibody called immunoglobulin G (Waugh & Grant, 2001; Basics of best practice in the management of Multiple Sclerosis, 1999). Evoked potentials measure responses of axons to the passage of nerve impulses from the brain to a specific part of the body that controls a particular body function, such as hearing, sight or movement. This means that when MS is present it is possible to see whether certain nervous impulses are slowed down in the demyelination of axons (Basics of best practice in the management of Multiple Sclerosis, 1999).

Finally, symptoms like numbness, tingling, or fatigue, will not be seen on any diagnostic tests and there may be cases where a person with the clinical symptoms of MS does not meet all the criteria to confirm a diagnosis of MS. A clinical diagnosis of MS may take years with a physician observing a person over a period of time before reaching a diagnosis of MS (Noseworthy et al., 2000).

MS progression
The course of the disease, and the development of disability, varies depending on the severity or location of inflammation or how quickly the myelin breaks down. After an initial event, each following episode of symptoms is called a relapse. When the inflammation is resolved, the symptoms may subside (remission). Remission may not mean a return to the way things were before the relapse and residual symptoms may be left behind (Waugh & Grant, 2001; Noseworthy et al., 2000).

It is possible to make a rough overall distinction between different types of MS according to the progress of the disease (Table 2). However, because MS varies so much between individuals, it is nearly impossible to predict how MS might affect a person or progress in the future (Confavreux et al., 2000).

Symptoms are one way to mark the progression of disease in MS. However, MS can also progress silently through axonal loss. The brain can adapt to and

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Table 1: Possible symptoms of MS
Vision disturbances and optic neuritis • One of the earliest symptoms of MS which may start with blurred vision followed by vision loss due to an inflammation of the optic nerve. • Rarely involves both eyes simultaneously. • After the initial symptoms, there is a gradual improvement, but recovery is not always complete. • Stress, fatigue or fever, may cause the blurred vision to return. This does not necessarily mean that the MS is active again. Rather, it may be the result of permanent disability that has accumulated over time. Loss of muscle strength in arms and legs • MS often affects the axons that control muscle movement. • Weakness may progress to partial or complete paralysis. Tremors, shaking or trembling of a limb or the head • May come and go and impair mobility. • Ataxia is associated with difficulty in balance and co-ordination. Spasticity Can occur either as sustained stiffness caused by increased muscle tone or as spasms that come and go, especially at night. • Occurs when opposing groups of muscles contract and relax at the same time. • Increased stiffness in the muscles means that a great deal of energy is required to perform daily activities. Impairment of the sense of touch • One of the earliest symptoms of MS. • The sensory axons in CNS provide the sense of touch in all skin, and the ability to feel cold or heat on all parts of the body. • When axons are damaged the sense of touch may be replaced by feelings of burning and crawling sensations, tingling, feelings of swelling or numbness. • Parts of the body may feel burning or cold, even though there is no heat or chill present. • If severe neurological damage to the myelin sheath takes place, then numbness may remain. Sexual Difficulties (male and female) • Includes impaired sensation, diminished orgasmic response, and decreased sexual drive loss of sexual interest. Pain • Burning pain in the arms and legs (due to damage to the sensory tracts in the spinal cord). • Trigeminal neuralgia (due to damage to the nerves of the face).	• Spasticity causes extra tension in arm and leg muscles which can be painful. • If MS has impaired the ability to walk, the extra strain in the muscles of a person’s back and legs can become painful. • Pain in the neck and shoulder muscles extending down the back, in the joints and muscles (Fibromyalgia). Bladder dysfunction • Includes increased frequency of urination, urgency, dribbling, hesitancy, inability to completely empty the bladder and incontinence. Bowel dysfunction • Includes constipation, diarrhoea and incontinence. Depression and psychotic disorders (manic-depression and paranoia) • Depression can intensify many symptoms. • May be linked directly to physical changes in the brain caused by MS. • MS-related lethargy and fatigue may be mistaken for depression or heighten its effects. • Depression may be linked to some treatments for MS that are prescribed to help to slow the progression of symptoms and/or disability. • Understandably, there may also be an emotional reaction to having the illness and coping with the symptoms and the challenges they represent. Emotional Liability and inappropriate euphoria and despair • Due to demyelination in the brainstem, that controls facial expression and emotions. • Usually seen in severe cases. Cognitive Dysfunction • Involves reasoning, verbal fluency and slower speed of thinking difficulties with concentration, attention, memory, and poor judgment. Fatigue • May be both physical and psychological and not often immediately identified as being caused by MS. • May take the form of a constant and persistent tiredness. • A person’s energy is used up every day with just a little exertion. Overdoing activities • In healthy people the body shuts down when the anaerobic threshold is reached as a lot of pain is experienced. • This warning does not occur activity is continued as no pain is experienced and the lactic acid builds up, and the body ends up recirculating carbon dioxide.
References: Soderstrom et al., 1998; Rukwied et al., 2003; Rae-Grant et al., 1999; Amato & Zipoli, 2002; Gold, Rieckmann, & Rieckmann, 2000; Johnson et al., 1996; Mahler & Benson 1990; Schurmann, Basar Eroglu & Basar, 1997; Coffey et al., 1987.

compensate for some level of damage, with symptoms being highly dependent on where the damage takes place since different parts of the brain are responsible for different activities. So a person with MS can look and feel fine, yet his or her disease may be active (Noseworthy et al., 2000).

Not all symptoms listed in Table 1 affect every MS patients and complaints may appear in various combinations depending on the area of the nervous system affected. Symptoms may be mild or severe, of long duration or short, persistent and progressive or stop from time to time (relapse & remission) and may even remit completely, leaving no residual damage, or partially leaving degrees of permanent impairment (Waugh & Grant, 2001; Compston & Coles, 2002). The erratic symptoms of MS can affect the entire family and be an emotional drain on both patient and carer (www.msfacts.org).

Can MS be treated?
Despite great strides in our understanding of MS, it still remains a lifelong disease for which there is no cure. Many patients do well with no therapy at all, especially since many medications have serious side effects (Hartung et al., 2002; Ghalie et al., 2002). Furthermore, naturally occurring or spontaneous remissions make it difficult to determine therapeutic effects of treatments, which manage symptoms and/or modify the progression of the disease. The National Institute of Clinical Excellence (NICE, 2002 & 2003) has ruled that disease modifying therapies (DMT's) such as interferon beta and glatiramer acetate should not be available on the NHS in England and Wales as they are not cost-effective. As a result the risk-sharing scheme was born, where people with MS who meet the criteria set out in guidelines from the Association of British Neurologists can be enrolled on the scheme and receive either interferon beta or glatiramer acetate treatment.

MS being a disease with a natural tendency to remit spontaneously, with no universally effective treatment and no known cause - opens the door to an array of treatments and cures from special diets, fish oils to magnetic field therapy, neural therapy and oxygen therapy. There is currently no supporting evidence for effectiveness of such therapies (MS Society, 2003). Life events have been implicated in the onset of MS including:

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Stress: During periods of stress, fatigue or fever, certain symptoms may return or be exacerbated, however, there is no evidence that daily stress or trauma causes MS or affects its course (Hartung et al., 2002).

Pregnancy: MS generally strikes during childbearing years, but there is no evidence that pregnancy and childbirth affect the overall course of the disease nor does MS hinder a woman's chance of becoming pregnant and carrying a child to full term. However, MS medications would need to be stopped as they can cause birth defects and can be passed to an infant via breast milk. Another consideration would be bringing-up a child with the additional challenges that MS can impose including the times when the MS causes people to feel less well or more tired, or if the MS becomes more progressive in the future (www.MSActiveSource.com).

Research
Currently genetic risk factors and their possible modification, environmental triggers, mechanisms of repair of the damaged blood-brain barrier and remyelination of the axons, re-educating the immune system so that it does not attack myelin, are being investigated. Furthermore, many treatments are in the experimental stages or are undergoing clinical trials.

Diagnosis of an incurable disease with potential for disability associated with loss of bodily control can cause many understandable reactions for people with MS and their carers, which at times involves young children or single parent families. But just as the symptoms and course of MS can be unpredictable, so people and carers' reactions may vary. MS is a journey into the unknown as it is impossible to predict the nature, severity or timing of progression in a given patient. With appropriate multidisciplinary management, nurses can play a key role in supporting individuals and their carers to adjust to new routines or environments in the face of disruptive symptoms (Toombs, 2004) and to grieve for the past but also to look forward and establish new roles (Jarrett, 2003).

References
Alvarez-Lafuente R., De Las Heras V., Bartolome M., Picazo J.J., Arroyo R. (2004). 'Relapsing-remitting multiple sclerosis and human herpesvirus 6 active infection'. Archives of Neurology, 61; 10: 1523-1527.
Amato M.P., Zipoli V. (2002) 'Cognitive dysfunction in multiple sclerosis: Current approaches to clinical management'. Expert Review of Neumlherapeulics, 2; 5: 731-742.
Association of British Neurologists. (2001) Guideline for tin1 Use of Beta Interferons and Gltitiramer Acetate in Multiple Sclerosis. Association of British Neurologists, London.
Basics of best practice in the management of Multiple Sclerosis 1999. The Multiple Sclerosis Society of Great Britain & Northern Ire-
land and Multiple Sclerosis Research Trust.
Brex P.A., Ciccarelli O., O'Riordan J.I., Sailer M., Thompson A.J., Miller D.H. (2002) 'A longitudinal study of abnormalities on MRI and disability from multiple sclerosis'. N Engl J Med, 346: 158-64.
British Society of Rehabilitation Medicine (BSRM). (1993) Multiple Sclerosis: A Working Party Report of the British Society of Rehabilitation Medicine. British Society of Rehabilitation Medicine & Multiple Sclerosis Society of Great Britain & Northern Ireland.
Campbell F.A., Tramer M.R., Carroll D., Reynolds D.J., Moore R.A., McQuay H.J. (2001) 'Are cannabinoids an effective and safe treatment option in the management of pain? A qualitative systematic review'. BMJ, 323: 13-6.
Coffey C.E., Weiner D., McCall W.V., Heinz E.R. (1987) 'Electroconvulsive therapy in multiple sclerosis: a magnetic resonance imaging study of the brain'. Convuls Ther, 3: 137-144.
Compston A. (1997) 'Genetic epidemiology of multiple sclerosis'. J Neuml Neurosurg Psychiatry, 62: 553-61.
Compston A., Coles A. (2002) 'Multiple sclerosis: seminar'. Lancet, 359: 1221-31.
Confavreux C., Vuskusic S., Moreau T. (2000) 'Relapses and progression of disability in multiple sclerosis'. New Eng J Med, 343: 1430-1438.
Frohman E.M., Goodin D.S., Calabresi P.A. (2003) 'The utility of MRI in suspected MS: report of the Therapeutics and Technology Assessment Subcommittee of the American Academy of Neurology'. Neurology, 61: 602-611.
Gaudet J.P.C., Hashimoto L., Sadovnick A.D., Ebers G.C. (1995) 'Is multiple sclerosis caused by late childhood infection?: a case-control study of birth order in sporadic cases of multiple sclerosis'. Acta Neurol Scand, 91: 19-21.
Ghalie R.G., Edan G., Laurent M. (2002) 'Cardiac adverse effects associated with mitoxantrone (Novantrone) therapy in patients with MS'. Neurology, 59; 6: 909-13.
Gold R., Rieckmann P., Rieckmann R. (2000) Pathogenese und Therapie der Multiplen Sklerose [Pathogenesis and therapy for multiple sclerosis]. Bremen: UNIMED Verlag, Bremen.
Hartung H.P., Gonsette R., Konig N. (2002) 'Mitoxantrone in progressive multiple sclerosis: a placebo-controlled, double blind, randomized, mulitcentre trial'. Lancet, 360: 2018-25.
Jarrett L. (2003) 'Attitudes to long term care in Multiple Sclerosis'. Nursing Standard, 17; 17: 39-44.
Johnson S.K., Deluca J., Diamond B.J., Natelson B.H. (1996) 'Selective impairment of auditory processing in chronic fatigue syndrome: A comparison with multiple sclerosis and healthy controls'. Perceptual Motor Skills, 83; 1: 51-62.
Mahler M., Benson D. (1990) 'Cognitive dysfunction in multiple sclerosis: A subcortical dementia?' In Rao S. (ed), Neurobehavioural aspects of multiple sclerosis, pp70-78. Oxford University Press, Oxford.
McDonald I. (1998) 'Diagnostic methods and investigation in multiple sclerosis'. In: Compston A. (ed), Mcalpinc's Multiple Sclerosis. Churchill, London.
MS Society. (2003) What is multiple sclerosis? MS Society: London.
NICE. (2002) Technology appraisal No 32. Guidance on the use of beta interferon and glatiramer acetate for the treatment of multiple sclerosis. National Institute for Clinical Evidence, London.
NICE. (2003) Multiple Sclerosis: Management in Primary and Secondary Care. The National Collaborating Centre for Chronic Conditions, London.
Noseworthy J.H., Lucchinetti C., Rodriguez M. (2000) 'Multiple sclerosis'. New Eng J Med, 343: 938-952.
Porter B., International Multiple Sclerosis Nursing Coalition. (2004) Topics in Multiple Sclerosis (E): An immune-logical Perspective. Multiple Sclerosis Colloquium. University of Minnesota, Minnesota, USA.
Rae-Grant A.D., Eckert N.J., Bartz S., Reed J.F. (1999) 'Sensory symptoms of multiple sclerosis: a hidden reservoir of morbidity'. Mult Scler, 5: 179-83.
Sadovnick A.D., Ebers G.C. (1993) 'Epidemiology of multiple sclerosis: a critical overview'. Can J Neurol Sd, 20:17-29.
Schurmann M., Basar C., Basar E. (1997) 'A possible role of evoked alpha in primary sensory processing: Common properties of cat intracranial recordings and human EEC and MEG'. International Journal of Psychophysiology. 20;1-3: 149-170.
Soderstrom M., Ya-Ping J., Hillert J., Link H. (1998) 'Optic neuritis: prognosis for multiple sclerosis from MRI, CSF, and HLA findings'. Neurology, 50: 708-14.
Swanborg R.H., Whittum-Hudson J.A., Hudson A.P. (2003) 'Infectious agents and multiple sclerosis: are Chlamydia pneumoniae and human herpes virus 6 involved?' J Neuroimmunol, 136: 1-8.
Thibodeau G.A., Patton K.T. (2002) The Human Body In Health and Disease. Mosby, London.
Toombs S.K. (2004) 'Living and Dying With Dignity: Reflections on Lived Experience'. Journal of Palliative Care, 20; 3: 193-200.
Toosy A., Thompson A. (2000) 'Multiple sclerosis: the disease and its treatment'. The Pharmaceutical Journal, 264: 695-700.
UK Multiple Sclerosis Specialist Nurse Association, RCN, MS Research Trust. (2001) The Key Elements for Developing MS Specialist Nurse Services in the UK. MS Research Trust, Letchworth.
Waugh A., Grant A. (2001) Ross & Wilson Anatomy and Physiology in Health and Disease. Churchill Livingstone, London.

- end of page 37 -http://www.jcn.co.uk/journal.asp?MonthNum=10&YearNum=2005&ArticleID=861

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Be Wary of Multiple Sclerosis "Cures"

Stephen Barrett, M.D.

Multiple sclerosis (MS) is a degenerative disease in which patches of inflammation and scarring interfere with the function of the brain, spinal cord, and/or the nerves to the eyes. The cause of MS is unknown, but the most attractive theory is that it is an immune reaction to the nervous system. Its symptoms include muscular weakness, loss of coordination, and difficulty with speech and vision. It occurs chiefly in young adults and, like arthritis, can have a very variable course. Some people have only a single attack. Others have only a few attacks in a lifetime, recover from these, and experience no disability except during attacks. Others have frequent attacks from which they don't recover completely, but which cause only partial disability. Still others have a slow progression of disability over a period of 10 to 25 years, which eventually leaves them helpless. When attacks occur, symptoms may come and go suddenly and may even vary from hour to hour.

MS's extreme variability makes it a perfect disease for quacks. The only way to know whether a treatment is effective is to follow many patients for years to see whether those who receive the treatment do better than those who do not. Quacks don't bother with this kind of testing, however. They simply claim credit whenever anyone who consults them improves. And since the majority of attacks are followed by complete or partial recovery, persuasive quacks can acquire patients who swear by whatever they recommend.

The Therapeutic Claims Committee of the International Federation of Multiple Sclerosis Societies has analyzed more than a hundred alleged treatments and published the results in a book called Therapeutic Claims in Multiple Sclerosis, which is revised every few years [1]. Each analysis includes a description of the method, the proponents' rationale, a scientific evaluation, estimate of risks and/or costs, and the authors' conclusion. The methods are then classified according to plausibility, extent of study, risk, and cost.

No cure is known, but a few methods are useful in shortening the duration of attacks, reducing their severity, or helping to deal with the symptoms. Methods that have a plausible rational but have not been sufficiently tested are considered "investigational." I am not listing the useful or investigational methods because I believe that advice about them should be obtained from a qualified neurologist who can thoroughly discuss them. Reliable information is also available from the National Multiple Sclerosis Society.

The committee noted that no nutritional deficiency is known to be a factor in MS, and that no special diet or the addition of vitamins or minerals has been proven to alter its course. Polyunsaturated fatty acids (PUFA) have slight immunosuppressive properties, but studies involving sunflower seed oil, evening primrose oil, safflower seed oil, and fish oils, have produced conflicting results. The committee concluded that other than a possible benefit of PUFA-containing oils, there is no evidence that any dietary change affects MS.

Methods to Avoid

The methods considered implausible or ineffective are listed below. I believe these methods should be avoided:

Adequately tested but ineffective in influencing the course of MS
Aspirin and sodium salicylate; colchicine (for immune modulation); thymectomy (removal of the thymus gland); transfer factor; myelin basic protein; hyperbaric oxygen (HBO).

Implausible and untested or inadequately tested
Various nonsteroidal antiinflammatory drugs (NSAIDs); thyrotropin-releasing hormone; cannabis (marijuana); Diltiazam; Nifedipine; Verapamil; intravenous yeasts (Proper-myl); pancreatic extract (epropanex); honey bee venom (safety is uncertain); octacosanol; superoxide dismutase (SOD); procaine hydrochloride; dimethyl sulfoxide (DMSO); Alphasal (formerly Chlororazone or Vitamin X); allergens; Rodilemid; alpha-fetoprotein; Proneut; immunobiological revitalization; proteolytic enzymes; injections of calcium orotate or calcium aminoethyl phosphate; oral calcium + magnesium +vitamin D; sodium bicarbonate or phosphate; hyperimmune colostrum ("immune milk"); Nystatin; transcutaneous nerve stimulation (TNS); ultrasound treatment applied near the spinal column; magnet therapy; dental approaches such as correction of bad bite, TMJ treatments, or removal of mercury-amalgam fillings; hysterectomy; low-fat diet; allergen-free diet; Kousmine diet; gluten-free diet; raw food diet (Evers diet); MacDougal diet; pectin- and fructose-restricted diet; sucrose- and tobacco-free diet; vitamin regimens; mineral supplements; cerebrosides; aloe vera juice; and various enzymes (Wobenzym, digestive enzymes, Vitafestal, Bilicomb, Panpur, Panzynorm).

Implausible and known to have significant risk or side effects
ACTH or other corticosteroids administered into the spinal canal; chloroquine; x-ray treatment; immunosuppression with chlorambusil (Leukoran), Lumustine, or 5-Fluorouracil; immune modulation with thymus hormones (Thymosin, Thymuline/Facteur Thymique Scrique, Thymopoetin 5, TFX-Polfa, THX, T-Activin); myelin basic protein; Interferon gamma; interferon inducers (Tilorone, Poly-ICLC, Staphage Lysate); Progabide (for spasticity); heart and pancreas extract (Pancorphen); snake venom (PROven, Venagen, Horvi MS9); cellular therapy; autogenous vaccines; chelation therapy; "metabolic therapy"; promazine hydrochloride (Sparine); Le Gac Therapy (antibiotics plus hot tubs); acupuncture; electrical stimulation of the dorsal column of the spinal cord; hyperbaric oxygen (HBO); sympathectomy; ganglionectomy; surgical spinal cord relaxation (cervicolordodesis); vertebral artery surgery; surgical implantation of pig brain tissue; Cambridge or other very-low-calorie liquid diets; high-dosage or vitamin C, and various other high-dosage vitamin or mineral regimens.

Superesonant Wavenergy (SRWE) Program

In the 1980s, Irving Dardik, M.D., a vascular surgeon, devised an exercise program which he claimed would to optimize the body's health patterns and lead to reversal of such disorders as multiple sclerosis. In 1995, New York State medical licensing authorities found him guilty of fraud, exercising undue influence, guaranteeing satisfaction or a cure, and failing to maintain adequate records. Case records indicate that he had charged four MS patients from $30,000 to $100,000 for their treatment. His New York medical license was revoked, he was fined $40,000, and his New Jersey license was subsequently revoked. One of the victimized patients, former TV investigative reporter Ellen Burstein MacFarlane, coauthored a book about her experience [2].

"Amalgam Toxicity" Scam

A few hundred phyicians and dentists have been falsely claiming that "mercury toxicity" from amalgam fillings cause multiple sclerosis and that removing them may cure it. This claim is false and fraudulent. The mercury is amalgam is tightly bound so that the amount that gets into the body over time is insigificant. Moreover, no scientific study has demonstrated that removing amalgam fillings ihelps patients with multiple sclerosis or any other ailment. I believe that pracitioners who recommend amalgam replacement as a treatment for multiple sclerosis have extremly poor judgment and should be delicensed [3].

Calcium EAP

Calcium ethylamino-phosphate (calcium EAP) has been promoted as a therapy or cure for MS and many other diseases. These claims are based on anecdotal reports rather than controlled clinical trials. The National Multiple Sclerosis Society has concluded that there is no objective evidence calcium EAP is effective against MS and "because the treatment protocol includes many different agents and may include a powerful drug that suppresses the immune system, the proposed therapy is not without serious risk." [4] The major proponent, a German physician named Hans Nieper, died in 1998, but the substance is still marketed here and abroad.

Coral Calcium

"Coral calcium" is a dietary supplement said to be derived from "remnants of living coral that have fallen from coral reefs, as a result of wave action or other natural processes." Since coral reefs are protected by law, "coral calcium" is made by grinding up limestone that no longer contains live organisms. Their principal promoter, Robert Barefoot, has claimed in widely aired infomercials that he has witnessed people with multiple sclerosis "get out of wheelchairs just by getting on the coral." He doesn't say how he determined that patients with multiple sclerosis were actually helped by coral calcium. There is neither scientific evidence nor any logical reason to believe that they were [5]. The Federal Trade Commission charged Barefoot with false advertising and obtained an injunction against furtheradvertising claims of this type.

Hydrogen Peroxide

Practitioners who advocate this type of therapy argue that diseases develop in people whose bodies lack sufficient oxygen. They claim that hydrogen peroxide is an effective treatment because it increases the cellular oxygen levels, thereby correcting the alleged deficiency. "Oxidative therapy" has also been promoted for the treatment of cancer, asthma, emphysema, AIDS, arthritis, heart disease, and Alzheimer's disease. There is no scientific evidence that lack of cellular oxygen occurs as described by "oxidative therapy" proponents, that swallowing or injecting oxygen-rich substances actually effects cellular oxygen levels, or has any effect on the diseases it is used to treat. The National Multiple Sclerosis Society [6] and the American Cancer Society [7] have both warned that hydrogen peroxide therapy has not been proven safe or effective. The National Muliple Sclerosis Society was made in response to the death of a woman who had received hydrogen peroxide therapy [8].

Prokarin

Prokarin (also called Procarin) is a skin cream that is administered using a patch that enables its ingredients to be absorbed. The treatment is based on a hypothesis that involves histamine and dates back to the 1940s. The primary promoter is Elaine DeLack, a nurse who "discovered" and patented a mixture of histamine and caffeine. Compounding pharmacists prepare the product, which is inexpensive to manufacture but is sold for about $250 for a month's supply.

In February 2002, the journal Multiple Sclerosis published the results of a 12-week study of MS patients in which 21 people took Prokarin, 5 took a placebo, and all participants were asked to limit their intake of caffeinated beverages to one cup of regular coffee per day. The authors concluded that Prokarin produced a "modest" lessening of fatigue. [9]. The National Multiple Sclerosis Society advises that the study is difficult to interpret because the number of participants was small; the numbers in the Prokarin and placebo groups were very different; the fact that Prokarin contains caffeine might mix up the results; and other reasons [10]. The Society has also warned that Prokarin lacks a scientifically plausible rationale and has not been proven to modify the course of the disease.

Prokarin proponents are promoting this study as showing that Prokarin "works." But even if it can lessen fatigue, there is no reason to believe it can influence the course of the disease, which is why most people take it. In my opinion, it is a poor investment and any marketing that arouses hope that it will influence the course of MS is both unethical and may be illegal. If you encounter a pharmacist selling Prokarin, ask the state pharmacy board to investigate what claims are being made.

Aetna's List

Aetna has issued a coverage policy bulletin that lists covered and not-covered MS treatments. The non-covered methods include linoleate supplementation to diet, low-fat diets, antilymphocyte globulin, Prokarin, oral myelin (Myloral), cladribine (Leustatin, 2-CDA), PUVA (psoralen ultraviolet light), gamma-interferon, total lymphoid irradiation, gluten-free diets, tranforming growth factor-beta (TGF), hyperbaric oxygen, tumor necrosis factor antagonists, and IL-2-toxin [11]. Aetna's list also includes other methods that are undergoing clinical trials and may have some therapeutic potential. The National Multiple Sclerosis Society maintains a list of clinical trials that are planned, in progress, or recently completed [12].

Additional Information

• Bee Venom Therapy
• MS Is Not Caused by Hepatitis B Vaccine
• MS Questionable Treatments and Claims
• Aetna Policy Coverage Bulletin
• Be Wary of Theratec Therapy
• Dubious Claims for the Molecular Magnetic Energizer
• FDA warning letter to velvet deer antler product marketer
• "MS Cures" (how people form mistaken beliefs)

References

1. Sibley W and others. Therapeutic Claims in Multiple Sclerosis, 4th edition. New York: Demos Vernande, 1996.
2. MacFarlane EB, Burstein P. Legwork: An Inspiring Journey Through a Chronic Illness. New York: MacMillin, 2000.
3. Barrett S. The mercury amalgam scam: How anti-amalgamists swindle people. Quackwatch, revised Oct 16, 2002.
4. Calcium EAP. In Multiple Sclerosis Information Sourcebook. New York: National Multiple Sclerosis Society, 2003.
5. Barrett S. Be wary of coral calcium and Robert Barefoot. Quackwatch, revised Jan 25, 2004.
6. Important medical alert: Hydrogen peroxide. National Multiple Sclerosis Society Web site, Sept 2004.
7. American Cancer Society. Questionable methods of cancer management: Hydrogen peroxide and other "hyperoxygenation" therapies. CA—A Cancer Journal for Clinicians 43:47-55, 1993.
8. Suit alleges death from IV hydrogen peroxide. Quackwatch, revised Oct 7, 2004.
9. Gillson G and others. A double-blind pilot study of the effect of Prokarin on fatigue in multiple sclerosis. Multiple Sclerosis 8:30-35, 2002.
10. NMSS Research Programs Department. Results of Prokarin to treat MS fatigue. National Multiple Sclerosis Society Research/Clinical Update, Jan 30, 2002.
11. Aetna Policy Coverage Bulletin 0264: Multiple Sclerosis Treatments, July 18, 2003
12. Clinical Trials In Multiple Sclerosis, Winter 2003 (Planned, In Progress, Recently Completed). New York: National Multiple Sclerosis Society, 2003.

This article was revised on March 12, 2005.

Last Updated Wed, 26 Oct 2005 21:59:35 EDT

CBC News

A new map of the patterns of genetic differences could help speed up the search for genes involved in diseases. "Humans are 99.9 per cent identical," said Dr. Panos Delousas, a senior investigator on the project at Britain' s Wellcome Trust Sanger Institute. Tom Hudson, director of the McGill University and Genome Quebec Innovation Centre in Montreal. "It is the tiny percentage that is different that holds the key to why some of us are more susceptible to common diseases such as diabetes or hypertension or respond differently to treatment with certain drugs." The new "HapMap" charts patterns in human genetic variation throughout the world, making it easier for scientists to identify differences in those affected by disease. More than 200 researchers from Canada, China, Japan, Nigeria, the United Kingdom and the United States worked on the HapMap, which is described in Thursday's issue of the journal Nature. The research shows the most common genetic variation, single letter differences called single nucleotide polymorphisms or SNPs, are usually found together in blocks. Investigators found the blocks, called haplotypes, by analysing DNA samples from 269 volunteers from Nigeria, Japan, China and the U.S. The haplotypes highlight areas for gene hunters to focus on. Researchers have already used the data to find a gene linked to the eye disorder macular degeneration, the leading cause of severe vision loss in the elderly. The map also guided Tom Hudson, director of the McGill University and Genome Quebec Innovation Centre in Montreal, and his team to find a gene that protects some Vietnamese and Brazilian families from leprosy. The new map will only speed up what's known about how genetics contributes to disease if the variations are common, cautioned David Goldstein and Gianpiero Cavalleri of Duke University wrote in a Nature commentary. Researchers also need to check if the four population groups studied in the HapMap project reflect variations in other human populations. A stronger case might be made for identifying differences among patients in response to difference medicines, the pair said. Canada contributed one-tenth of the funding for the $138-million US project, and Hudson's team generated 10 per cent of the data by analysing chromosomes 2 and 4p of the human genome. Headlines: Health & Science Early detection, drugs drive down breast cancer death rates: study Sharks warm up muscles to chase prey Scientists map human genetic variations Psychologist asks why campus anti-drinking campaigns fall on deaf ears Pharmacy groups disagree on internet sales of Tamiflu Tamiflu sales halted as personal stockpiles grow Use many tools to avoid waking during surgery, anesthesiologists told Occasional colonoscopy helps for family history cases: study Group angered by billboards linking breast cancer to abortion Ginseng cuts frequency of common cold: study Jobs | Contact Us | Help | RSS Terms of Use | Privacy | Copyright | Other Policies Copyright © CBC 2005 http://www.cbc.ca/story/science/national/2005/10/26/HapMap051026.html

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Wednesday October 26, 1:42 pm ET

RESEARCH TRIANGLE PARK, N.C.--(BUSINESS WIRE)--Oct. 26, 2005--Metabolon, Inc., a leader in the discovery of biomarkers using metabolomics, today announced it has been awarded a contract from the Centers for Disease Control and Prevention (CDC) to identify disease biomarkers for multiple sclerosis. MS is an autoimmune disease that affects the central nervous system by destroying myelin, the protective fatty tissue covering nerve fibers. Without myelin, nerves are unable to transmit signals to and from the brain. It is estimated that more than 2.5 million people worldwide are affected by MS, with more than 400,000 diagnosed in the United States each year.

"Multiple sclerosis is the most common neurological disease disabling young adults in the United States," said Dr. John Ryals, president and CEO of Metabolon. "Using metabolomics, we hope to find biomarkers that will determine a cause for the disease and that can be used to create a definitive diagnostic tool for MS."

There is currently no known cause of MS, but evidence indicates that it is a complex disease resulting from a combination of genetic susceptibility and environmental factors, such as heavy metals and toxic chemicals. In this study, blood samples from a group of patients diagnosed with MS and exposed to environmental factors will be compared with blood samples taken from a group of healthy subjects exposed to similar conditions. Metabolon scientists will analyze the samples to identify disease biomarkers that indicate a metabolic difference between the two subject groups. Results from this study could potentially lead to more effective diagnostics and treatments for the disease.

About Metabolon

Metabolon is an industry leader in the discovery of biomarkers through the use of metabolomics, a powerful scientific approach for the discovery and development of drugs and the early diagnosis of disease states. Metabolon's patent-pending technology is poised to dramatically impact drug discovery and development processes by accurately measuring the spectrum of biochemical changes and mapping these changes to metabolic pathways. Metabolon's technology can identify safer compounds for development, shorten the time for drugs to get to market and identify novel biomarkers for earlier disease detection. In conjunction with the NIH, Metabolon was honored as a recipient of the 2005 March of Dimes Award for Best Research in Prematurity. For additional information, visit www.metabolon.com.

---

Contact:

     Metabolon
    Stephanie Ferrell, 919-287-3359
    sferrell@metabolon.com
    or
    Maverick Marketing
    Megan Haney, 919-459-2768

http://biz.yahoo.com/bw/051026/265793.html?.v=1
    mhaney@maverickmarketing.com

By Mark Glassman Published: October 25, 2005
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IMPROVING SALES AND earnings might pacify investors when Biogen Idec (BIIB) releases its third-quarter results Wednesday after the close. But observers will be asking plenty of questions about the Cambridge, Mass., biotechnology company's long-term plans.

Biogen's biggest problem is Tysabri, the blockbuster multiple sclerosis drug it pulled from the market in February. Approved by the Food and Drug Administration last November, Tysabri was touted by analysts as a billion-dollar drug — until evidence of a serious side effect emerged. Three patients who took the drug during clinical trials developed progressive multifocal leukoencephalopathy, or PML, a debilitating brain disease. Two of the three died. On Feb. 28, the day Tysabri was pulled, Biogen's stock plunged 43% to $38.65. It has hovered around that level ever since.

Biogen hasn't thrown in the towel on Tysabri, however. Last week, along with its partner in Tysabri, Elan (ELN), Biogen announced the completion of a safety review of the drug that determined that the PML problem was limited to those three patients. The companies are now awaiting the outcome of a supplementary application to the FDA, which could make or break Tysabri and affect revenue numbers for quarters to come. Biogen and Elan have asked for a fast-track priority review, which could get Tysabri back on the shelves as early as next spring.

Despite the Tysabri troubles, Biogen is expected to post solid profits for the quarter. Analysts polled by Thomson First Call predict third-quarter earnings of 42 cents a share, up 15% year-over-year.

And Biogen is drawing plaudits for its ambitious cost-cutting efforts. On Sept. 8, the company announced it would lay off 650 employees, or about 16% of its staff. Biogen said it would incur a one-time charge of between $30 million and $40 million to pay for the downsizing. And in June, Biogen sold a manufacturing facility in Oceanside, Calif. — built last year to make Tysabri — to Genentech (DNA).

"Starting next quarter and really into 2006, they're really going to start to see substantial cost savings due to their new expectations for what the manufacturing requirements for Tysabri will be," says Bret Holly, an analyst with CIBC World Markets, a Toronto-based investment bank. "It won't have a monumental effect in the third quarter." (Holly doesn't own shares of Biogen Idec; CIBC World Markets doesn't have an investment-banking relationship with the company.)

Chris Raymond, an analyst with Robert W. Baird & Co., a Milwaukee investment bank, says cost-cutting alone won't pave the way to profit growth forever. "They have been very aggressive at keeping their costs down, which has been helpful," he says. "But the thing about biotech is that it's a growth sector. You can save your earnings numbers for only so long." (Raymond doesn't own shares of Biogen Idec; Robert W. Baird doesn't have an investment-banking relationship with the company.)

While the FDA mulls the return of Tysabri, Biogen will hope for a lift from sales of Avonex, an older multiple sclerosis drug that had been in danger of being supplanted. Considering the cannibalization — and reverse cannibalization — that has occurred between the two MS drugs this year, it's difficult to pinpoint third-quarter sales. Avonex revenues have been flat for the past three quarters.

"If it comes in flat again this quarter," Raymond says, "a reasonable question to ask is, What does this mean for the drug's prospects for next year?"

As for the pipeline, Biogen has three promising oncology drugs in Phase II clinical trials. The drug candidates target lymphoma, solid tumors and leukemia — all fairly big markets. But even under the best of circumstances, these drugs likely won't come to market for years.

One revenue stream that Biogen investors can count on now is the cancer drug Rituxan, co-marketed with Genentech. When Genentech released earnings on Oct. 10, it reported $502 million in global Rituxan sales during the third quarter. The companies haven't disclosed their revenue-sharing arrangement, but Holly estimates that Biogen should receive about 36.5% of the total third-quarter sales.

Even so, don't expect Biogen's stock to push $60 again until the company gets some good news from the FDA.

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