Multiple Sclerosis Drug Combined with Lipitor May Stop or Reverse Disease - Dosages Cut in Half with Fewer Negative Side Effects

March 16th 2006

Combining treatments may improve outcomes for patients with Multiple Sclerosis (MS), according to research done on mice and published online by the Journal of Clinical Investigation. Scott S. Zamvil and colleagues at the University of California, San Francisco found that mice treated with a combination of Glatiramer acetate (GA) and atorvastatin (Lipitor) demonstrated “a significant prevention and reversal of clinical MS severity” of MS symptoms.

Lipitor is a cholesterol lowering drug that has previously been shown to improve MS symptoms. Glatiramer acetate (Teva Pharmaceutical Industries Ltd.’s Copaxone) is a drug currently approved for MS treatment. The researchers found that treating MS with combinations of immune modulating drugs can greatly reduce MS disease.

According to the researchers, treating EAE (experimental autoimmune encephalomyelitis) mice with the combination therapy caused the animals to lose less myelin, prevented CNS inflammation, and MS disease incidence.

The researchers then treated isolated inflammatory cells called macrophages with these drugs and found that the combination therapy mediated its effects by promoting the secretion of the anti-inflammatory molecule IL-10 and suppressed production of the proinflammatory molecules IL-12 and TNF-alpha.

The researchers believe that the combined delivery of drugs, which act through different mechanisms, may enhance the therapeutic efficacy of MS and reduce the negative side effects. Also the drug dosages were less than the dosages used in regular single drug treatments.

Copaxone has been shown to be 30 to 35 percent effective alone. According to Bloomberg News, all MS drugs have to be injected, and have “severe side effects”. None of the MS drugs are very potent.

Lipitor on the other hand can be taken orally and is considered relatively safe. Lipitor, the best selling drug in the world, appears to block production of immune system agents, called cytokines, involved in the disease process. Currently the University of California, San Francisco is looking for 152 patients at 14 hospitals to participate in clinical trials. These trials will investigate the effect Lipitor alone has on MS. Contact the office of Scott Zamvil, associate professor of neurology at University of California, San Francisco, for more information.

There are 400,000 MS sufferers in the US. The illness causes neurological symptoms that include loss of motor control, blindness and temporary recurring paralysis. The condition occur when the body’s natural defenses are over stimulated and begin stripping the protective insulation, called myelin, from nerve fibers in the central nervous system, which includes the brain, optic nerves and spinal cord.

Dan Wilson
Best Syndication

Source

Copyright 2005 Best Syndication
Last Updated Thursday, March 16, 2006 06:07 PM

               

Clinical depression is a state of sadness or melancholia

Clinical depression is a state of sadness or melancholia that has advanced to the point of being disruptive to an individual’s social functioning and/or activities of daily living. The diagnosis may be applied when an individual meets a sufficient number of the symptomatic criteria for the depression spectrum as suggested in the DSM-IV-TR or ICD-9/10. An individual is often seen to suffer from what is termed a “clinical depression” without fully meeting the various criteria advanced for a specific diagnosis on the depression spectrum. There is an ongoing debate regarding the relative importance of genetic or environmental factors, or gross brain problems versus psychosocial functioning.

Although a mood characterized by sadness is often colloquially referred to as depression, clinical depression is something more than just a temporary state of sadness. Symptoms lasting two weeks or longer, and of a severity that begins to interfere with typical social functioning and/or activities of daily living, are considered to constitute clinical depression.

Clinical depression was originally considered to be a “chemical imbalance” in transmitters in the brain, a theory based on observations made in the 1950s of the effects of reserpine and isoniazid in altering monoamine neurotransmitter levels and affecting depressive symptoms [1]. Subsequent antidepressants have also been found to alter monoamine levels, particularly of serotonin and noradrenaline [2]. Despite a growing body of evidence suggesting otherwise, it is still a commonly held belief that depression is only a chemical imbalance. This idea is often promoted in pharmaceutical advertising, and perpetuated in everyday discussions. Despite this reliance on “common wisdom”, recent research and commentary has begun to address depression as an issue broader than this.

Clinical depression affects about 16%[3] of the population on at least one occasion in their lives. The mean age of onset, from a number of studies, is in the late 20s. About twice as many females as males report or receive treatment for clinical depression, though this imbalance is shrinking over the course of recent history; this difference seems to completely disappear after the age of 50 - 55, when most females have passed the end of menopause. Clinical depression is currently the leading cause of disability in the US as well as other countries, and is expected to become the second leading cause of disability worldwide (after heart disease) by the year 2020, according to the World Health Organization[4].

On a historical note, the modern idea of depression appears similar to the much older concept of melancholia. The name melancholia derives from ‘black bile’, one of the ‘four humours’ postulated by Galen.

The Ebers papyrus (ca 1550 BC) contains a short description of clinical depression. Though full of incantations and foul applications meant to turn away disease-causing demons and other superstition, it also evinces a long tradition of empirical practice and observation.

Source