The Unified Theory of the Nervous System
and Behavior
Cognitive Philosophy /Brain Theory by Steven Michael Harris
Study: Drug May Slow Parkinson's Disease (cnn.com 12/10/2004) (link retired)
This is one of those studies that you have to be very skeptical about concerning the way it is written in this press release. It should not be trusted mostly because of what is left out.
(AP) -- A drug widely prescribed to treat symptoms of Parkinson's disease does not hasten the progression of the illness as some had feared, and it might even slow it down, a study suggests.
But the matter is far from settled. While patients in the study who used the drug showed less decline than those who didn't, brain scans suggested the drug might harm the crucial brain cells that die off in the disease.
Apart from how poorly this last paragraph is written, it is clear that this self-serving press-release (for the drug companies) is suggesting results that they admit are not “proven” even according to their own flawed rules. They tell you that the evidence is not clear at this point and it is easy to infer that the entire reason to produce such a study is to dispute the evidence that these drugs cause greater decline (while relieving some symptoms).
But doctors have debated how early in the course of the disease to prescribe it, because of laboratory evidence that it might speed up the degeneration of the brain cells whose loss brings on Parkinson's.
This laboratory evidence comes from noticing the life span of treated and untreated patients and noticing the rebound that comes from getting on and off the drugs. Apparently this study is attempting to increase the drug sales by suggesting that previous observations about the decline of these patients with this treatment is mistaken and suggesting that the drug could be used even earlier in the progression of the disease without a statistical increase in problems. But they are observing from only one point of view that must go with one very important assumption of theory: that cell loss in brain scans should be the only deciding factor regarding any impairment or decline. But they have never proven if the cell loss in the brain is the carrot or the horse (if the impairment in function causes the cell loss or if the loss of cells causes the impairment of function) and for some time it has been apparent that loss of function occurs before any loss of cells can be observed. When they say that the drug does not appear to cause degeneration, they are doing so without any mention of other methods of noticing impairment (but without using brain scans).
The new work is the first hint that levodopa might actually be protective instead, said Dr. Stanley Fahn of Columbia University Medical Center, principal researcher of the federally funded study. That isn't proven yet, he stressed, but at least "it doesn't appear to be harmful."
If you can't prove that the drug is protective with the study, you probably can't prove that it is not harmful either. When nothing is proven with a study, then it is premature to suggest that the drug is not harmful, especially with years of understanding that this drug treatment can shorten a life span over that of a patient who never takes these drugs. This statement is some evidence of where his bread is buttered as well. The paragraph takes pains to mention that this is a federally funded study, but a study can have federal funding and also have funding from the affected drug company and I am willing to bet that there is some pharmaceutical company involvement with this press release and with this study (which is purposely not mentioned). Drug history is filled with examples of medications that are claimed to be safe when they are far from safe (and currently the standard for what is safe and what is not safe is extremely suspect).
Results showed that patients who'd taken levodopa showed less worsening of their disease, suggesting levodopa had slowed progression. But the scientists also said it's possible that they didn't wait long enough for the drug's effects to wear off.
Mentioning as an afterthought that they might not have waited long enough for the drug's effects to wear off is a very important clue here. Giving time for withdrawal to occur and see what kind of decline in function and brain structure occur after waiting is crucial to such a decision about the value of this drug. Why would they not wait? Why would they release these premature results before looking again later? Will they announce the results in a press-release if the brain cells start dying at a greatly accelerated rate over normal at some point after stopping treatment? This is a very self-serving study for the makers of the levadopa drugs.
A second study in the medical journal found that the Alzheimer's disease drug rivastigmine offers modest help in dementia associated with Parkinson's. It failed to help 80 percent of the treated Parkinson's patients, but Greenamyre said the result is still important because nothing else has been proven to ease dementia in that disease.
You can't trust this last paragraph either. They don't mention placebo reports here. It failed to help 80% of the patients? What percentage of the patients report improvement with a placebo? That number could easily be more than 20%!
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