From: hound23x@gmail.com   
      
   Hope For Alzheimer's?	    
      
       
   The following is one in an ongoing series of columns entitled What Doctors   
   Don't Tell You by . View all columns in series   
   The pharmaceutical companies have spectacularly failed to move beyond the   
   'chemical imbalance' view of Alzheimer's disease. But new evidence points to   
   brain poisoning-by processed foods and heavy metals-as likely causes, and many   
   alternatives offer sound    
   possibilities of treatment without the side-effects of the current drugs on   
   offer.   
   Stand by for a battle-royal over Alzheimer's disease (AD)-to take place in the   
   British High Courts of Justice, no less. Shortly, in a unique court case, NICE   
   (National Institute for Clinical Excellence), the UK's National Health Service   
   drugs watchdog,    
   will be challenged to defend its decision not to fund Alzheimer's drugs   
   intended for use in the early stages of the disease.   
      
   Ranged on the prosecution benches will be two big guns of the pharmaceutical   
   industry, Pfizer and its marketing arm Eisai, aided and abetted by the   
   Alzheimer's Society, a vociferous patient support group that equally loudly   
   proclaims itself to have no    
   ties with any drug manufacturers.   
      
   What's all the fuss about? Are the Alzheimer's drugs any good at all, and are   
   there any alternatives? And what causes the disease in the first place?   
      
   Dementia and Alzheimer's    
   From near-obscurity only a generation ago, Alzheimer's disease is now   
   probably, after cancer, the most feared disease of old age. Alzheimer's has   
   been chillingly described as an affliction whose victims suffer the loss of   
   qualities that define human    
   existence.   
      
   Once considered a rare disorder, it is now known to be the most common type of   
   senile dementia, defined as physical damage to the brain in old age that   
   results in major changes to reasoning, memory, personality and behaviour.   
   Until recently, the only way    
   to distinguish Alzheimer's from other types of dementia was by post-mortem   
   examination of the brain. A typical AD brain is found to be partly atrophied,   
   with the brain cells clumped together in what are called 'neurofibrillary   
   tangles' or 'plaques'.   
      
   The second major type of dementia is vascular dementia, where the interruption   
   of the brain's blood supply, usually due to 'mini-strokes', causes brain cells   
   to die. These two main types of dementia can now sometimes be distinguished   
   from each other by    
   brain scans using either magnetic resonance imaging (MRI) or positron-emission   
   tomography (PET).   
      
   Senile dementia is not as inevitable as many people might imagine: between 25   
   and 50 per cent of individuals over 85 are spared it. Nevertheless, dementia   
   is on the increase, so the drug companies claim, because of the simple fact   
   that we're all living    
   longer. It is believed to be incurable.   
      
   Big Pharma's offerings   
   Any prolonged chronic illness that is only ended by death is, of course, meat   
   and drink to the pharmaceutical industry. And yet, perhaps surprisingly, there   
   are relatively few drug treat-ments available for Alzheimer's. First on the   
   market was tacrine (   
   marketed as Cognex) in 1993. Like virtually all of its successors, tacrine is   
   a so-called cholinesterase inhibitor, which acts by artificially maintaining   
   levels of acetyl-choline in the brain. This important brain chemical is known   
   to be reduced by as    
   much as 90 per cent in AD sufferers; it's also believed to be important for   
   memory, so finding a drug that can preserve the chemical in the brain makes   
   sense.   
      
   In fact, the theory is fine-the trouble is the side-effects. After just a   
   decade on the market, tacrine began to be no longer actively marketed after   
   reports of severe liver toxicity. As much as 60 per cent of patients found the   
   drug's side-effects to be    
   intolerable at high doses. The final nail in tacrine's coffin was that, after   
   all this, it really doesn't work (JAMA, 1998; 280: 1777-82).   
      
      
   Since then, three other drugs have come onto the market, all of which attempt   
   to do the same trick of increasing acetylcholine in the brain. As expected,   
   these drugs are all deadly rivals. Pfizer's Aricept (donepezil), has an   
   advertising tagline that    
   says 'when Alzheimer's hits home, Aricept can help'; Novartis' Exelon   
   (rivastigmine) claims to be 'another step forward against Alzheimer's   
   disease'; and Shire Pharmaceuticals/Janssen's Reminyl (galantamine) sells   
   itself with the somewhat vague tagline '   
   Reminyl is now'.   
      
   So far, Pfizer is the only manufacturer to have threatened a lawsuit against   
   the recent NICE ruling that none of these drugs is really worth taking in the   
   early stages of AD. Will the drugmaker win their case? Our prediction is   
   no-and, frankly, because    
   the evidence is stacked against them.   
      
   The only large-scale, truly independent clinical trial of Pfizer's Aricept was   
   carried out by a team of British researchers at the University of Birmingham.   
   In a double-blind trial that lasted for more than two years, Aricept was   
   tested head-to-head    
   against a placebo in over 500 patients who had mild-to-moderate AD.   
      
   The study's conclusions? Aricept works, but its benefits are very small-"below   
   minimally relevant thresholds" (Lancet, 2004; 363: 2105-15). As study director   
   Professor Richard Grey stated in the report: "Patients and their families   
   would probably notice    
   no difference if the drug was stopped."   
      
   What's more, even clinical trials funded by the drug companies them-selves   
   failed to show much benefit with any of their products. For example, Oxford   
   University researchers recently scrutinized data from 24 separate   
   Pfizer-sponsored Aricept trials,    
   involving more than 5000 patients at different stages of AD, and concluded   
   that "the treatment effects are small and are not always apparent in   
   practice". Add to that the strong likelihood of "many adverse events" such as   
   nausea, vomiting, diarrhoea,    
   muscle cramps, dizziness, fatigue and anorexia, and it's little wonder that   
   there's what the researchers politely refer to as a "debate" over whether   
   Aricept is worth a candle (Cochrane Database Syst Rev, 2006; 1: CD001190).   
      
      
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