Re: Statins do NOT protect against Azlheimer's
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Re: Statins do NOT protect against Azlheimer's
| Zee | 13 Feb 2005 03:41 |
Here is her CV. Not all about publish or perish. http://medicine.ucsd.edu/faculty/golomb/
No. Personal experience here means nothing. Not mine, not Michael Hope's. Why should yours be any different.
And those two studies: Prospect and HPS; are they not the studies James Wright refers to when he says he is STILL waiting for the negative results he requested from the study authors. ALL the negative results. Nada.
http://www.ti.ubc.ca/pages/letter49.htm Because large numbers of problematic patients were excluded, the HPS results cannot be used to predict the safety and tolerance of simvastatin in the general population. "
I want you to GO to that seminar. And engage "Bea" (uhuh) in discussion, or in heckle; and report back to us.
Zee
Zee
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| Sbharris[atsign]ix.netcom.com | 13 Feb 2005 03:25 |
>>Steve was not refuting ME George. Steve was refuting BEA as he so jockularly calls Dr. Beatrice Golomb, she of the 27 page cv. Hmmm. Could Steve be envious? Nahh. Our boy got big cohones: Steve's balls clank when he crosses a (news)room. What could it bea? <<
COMMENT:
I don't remember calling the lady "Bea." Did I really? Oh Bea-have.
My CV surely isn't 27 pages long. On the other hand, I don't have to publish or perish, so I don't have to generated a crappy paper every few months, in order to pad it.
I'll tell you a secret about scientific CVs. There's a big difference between somebody who's never published in a referreed journal and somebody who has. But not that much difference between somebody with a dozen papers and somebody with a hundred. Fred Sanger had a one page CV, but one paper on protein sequencing won him the Nobel prize in 1958, and another on gene sequencing won him a share of another Nobel in 1980. Quality matters. If you're not trying to be promoted (which Sanger wasn't), you can get some bench work done. That's a luxury fewer and fewer people have these days.
If Dr. Golomb is a good scientist, she won't be making numerical claims in the popular press that she hasn't published. Without seeing such a publication, I haven't a clue as to what she means by a 20% side effect rate. What is she counting as a side effect? A day of diarrhea? A stuffy nose? What? Until we know, it's impossible to evaluate this stuff, so why discuss it?
The PROSPECT study contains 8,700 patient-years of pravachol use, compared double blind with mental status testing and ability to carry out activities of daily living, with another 8,700 patient-years of placebo. That's so much more experience than any given clinician ever sees in a lifetime of prescribing any drug, that it's ridiculous. And it's all blinded, which is a luxury no clinician gets. And they saw nothing. And they published it. And if you don't like that, there are 20,000 patients in the HPS study, where this time they did have the power to see stroke reduction, and did see it. But no difference in cognitive decline, either. But no increase, either. I lay Dr. Golomb's anecdotes along side stuff like this, and what am I supposed to think?
If personal experience means anything, I've been prescribing statins for a decade and half myself, and I've taken them for years. But I know personal experience doesn't mean much. That's possibly the difference between Dr. Golomb and myself.
SBH
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| Zee | 13 Feb 2005 02:19 |
> Thank you Dr. Harris for speaking to the group with proven science and > expert analysis. No one like to see Steve post more than I do. Who cares if he is right or wrong. He's so good at it we line up to watch him do it.
I fear many lay people come here not knowing much
> about the subject and leave with a distorted view of statin therapy. You fear....????? BwahahabahaaHA. Well if they want to read a statin education in progress they can google your posts: from avid Crestor defender (my cardiologist who works at the Ontario Heart and Stroke Brothel) to sober re-think wiht a new cardiologist and a different statin.
How they fall from grace. Watch it Steve. You could end up George's yesterday's man.
> Since it would take a lifetime to refute Zee and others with their > mesianic banter about the evil associated with this class of > medications it is appreciated that you take the time to do so once in > a while. Steve was not refuting ME George. Steve was refuting BEA as he so jockularly calls Dr. Beatrice Golomb, she of the 27 page cv. Hmmm. Could Steve be envious? Nahh. Our boy got big cohones: Steve's balls clank when he crosses a (news)room. What could it bea?
> I say a lifetime because this "cause" has obviously become their main > mission in life. Well we cannot say we saved you. Because in spite of the education you have received at my and Michael Hope's expense, you still waited for your doc to change your statin to something safer.
Zee
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| George | 13 Feb 2005 01:53 |
Thank you Dr. Harris for speaking to the group with proven science and expert analysis. I fear many lay people come here not knowing much about the subject and leave with a distorted view of statin therapy.
Since it would take a lifetime to refute Zee and others with their mesianic banter about the evil associated with this class of medications it is appreciated that you take the time to do so once in a while.
I say a lifetime because this "cause" has obviously become their main mission in life.
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| Sbharris[atsign]ix.netcom.com | 12 Feb 2005 22:21 |
>>Second, the large trials enrolled people at high risk for cardiovascular disease who experience benefit from statins to nonfatal stroke, which may lead to improvements in cognition that may help to balance out harms to cognition from other mechanisms. Although there are trends toward increases in fatal stroke with statins in most of the
large statin trials, those who have died cannot complete cognitive surveys.<<
COMMENT:
Sorry, but this is a bogus argument, unless you name the studies. In the one study you DO discuss (PROSPER), there was NO possiblity that a difference between recognized nonfatal stroke or stroke influenced the cognitive outcome, because recognized stroke of any kind brought the treatment and trial to a halt for the individual patient, so no cognitive tests were done after that. All cognitive tests reported are prior to ANY stroke endpoint. They show no difference between treatment and placebo groups across more than 3 years of on-treatment testing done every 3 months, including the last set of tests before treatment end. This is NOT consistant with any negative (or positive) cognitive effect in this population. There was no difference between groups on the last on-treatment cognitive test (comparing groups) or the second-to-baseline test. Both groups decline from baseline to end, but they decline in cognitive function at the same rate.
>>Although there are trends toward increases in fatal stroke with statins in most of the large statin trials, those who have died cannot complete cognitive surveys.<<
COMMENT
NO. It's no use trying to make anything of a trend unless it's a trend in large numbers of people. The other reason this argument won't run even if testing had been done after stroke, is that when you're talking about fatal stroke, you're talking about tiny numbers. PROSPER (for example) is a study of 5800 people, and there were 14 (placebo) vs 22 (Pravachol) fatal strokes. Those extra 8 fatal strokes are not significant (p = .19) and in any case, cognitive testing NOT done on 6 dead people is certainly not going to influence any mean difference in cognitive testing in 5800 people, even if they WERE doing testing in non-fatal stroke patients (which they weren't), and the 8 dead stroke patients all came from this group. Come on. Bad inferential crap like this is why the net is called the net of a million lies. You can sometimes get away with this stuff if nobody wants to do the work to look the studies up, but sometimes you run afoul of people like me, who will. So stop it.
>>The impact on total number of strokes was unaffected in the PROSPER trial with its sole focus on the elderly population. <<
True enough. It may well be that pravachol and other statins have significant anti-stroke effect only in other well-selected groups. None was seen in this trial, though effect on TIAs barely missed significance (p = 0.051 = 94.9% chance that pravachol really did decrease TIAs in the trial).
>>In the PROSPER trial, the number of reduced transient ischemic attacks and nonfatal strokes was actually matched by a similar number of increased fatal strokes.<<
COMMENT:
Baloney-- that's quite wrong. The number of reduced transient ischemic attacks was 77 (drug) vs 102 (placebo), a difference of 25, which blows away differences in the stroke numbers (the totals for stroke plus TIA in this study I note have been mis-done in the table, for they do not add up to the stated drg/placebo 204/212, difference of 8, but are actually 212/233, difference of 21). As for total strokes they were 135 (drug) vs 131 (difference of 4 in favor of placebo), which splits up into non-fatal 116 (drug) v 119 (difference of 3 in favor of drug) and fatal 22 (drug) vs 14 (difference of 8 in favor of placebo). These number don't quite add up, either (there's one missing person), but it's clear that the differences in fatal stroke numbers are too small to decide that they simply came out of one group and went to the other. Certainly they did NOT come out of the TIA group, for the difference of 25 there is reduced merely to 21 if you add in the total stroke numbers. None of the stroke differences are significant, so nothing can be said about this, either way.
>>Finally, the HPS used what is termed an "active run-in." For six weeks, participants considered for enrollment were placed on simvastatin, and those who were not fully compliant were dropped from the study. Participants who perceived problems on the drug, including cognitive problems, may have dropped the study themselves or skipped pills intentionally. In addition, participants who developed memory problems may have had trouble remembering to take the pills even if they did not
recognize deterioration in cognitive function. This run-in process may have excluded participants who developed cognitive problems on the drug, selecting only those who did not experience problems. Over one-third of those who were interested in enrolling were excluded following this compliance run-in.<<
COMMENT: This is an interesting hypothesis, that all the people would had cognitive problems with statins were selected out in the first 6 weeks, and went out with the 1252 people given statin who didn't meet inclusion criteria or who refused to participate. But anybody who advances this argument for PROSPER had better accept the concomitant conclusion, which is that if you *don't* have problems with statins in 6 weeks, THEN you won't have any for at least 3 years. Which is what was then seen in the radomized 5804 people who went on to the next arm of the trial. You can't just hypothesize parts of explanations you like, but ignore the obligatory parts of the same hypotheses you don't.
>>Because statins reduce nonfatal stroke (and cognition is obviously not measured in people who have experienced fatal stroke), benefits by statins for cognitive function in those in whom a stroke was averted might be expected.<<
COMMENT: Nonsense, for reasons carefully explained above. The PROSPER trial measured cognition before stroke, and also the number differences between non-fatal and fatal stroke are non-significant. In any case, some hypothetical raising of mean cognitive scores by killing stroke victims is far too small to affect scoring of cognitive function in populations of patients 360 times larger than the number of excess stroke deaths.
SBH
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| Zee | 12 Feb 2005 19:02 |
> >>Another misleading subject line..... > [quoted text clipped - 23 lines] > > SBH What happens to those of us who took them for years is quite different from what happens in clincial trials. Frankie's husband for example would have been deemed a raging success 6 months out, two years out; and he is not alone. We hear from hundreds; we get corroboration from their physicians and the pattern is the same. Over and over and over. No; anecdote is not as good as fact. But it certainly raises question in any reasonable person.
statins, stroke and cognition: http://www.geriatrictimes.com/g040618.html
Second, the large trials enrolled people at high risk for cardiovascular disease who experience benefit from statins to nonfatal stroke, which may lead to improvements in cognition that may help to balance out harms to cognition from other mechanisms. Although there are trends toward increases in fatal stroke with statins in most of the large statin trials, those who have died cannot complete cognitive surveys. The impact on total number of strokes was unaffected in the PROSPER trial with its sole focus on the elderly population. In the PROSPER trial, the number of reduced transient ischemic attacks and nonfatal strokes was actually matched by a similar number of increased fatal strokes.
Finally, the HPS used what is termed an "active run-in." For six weeks, participants considered for enrollment were placed on simvastatin, and those who were not fully compliant were dropped from the study. Participants who perceived problems on the drug, including cognitive problems, may have dropped the study themselves or skipped pills intentionally. In addition, participants who developed memory problems may have had trouble remembering to take the pills even if they did not recognize deterioration in cognitive function. This run-in process may have excluded participants who developed cognitive problems on the drug, selecting only those who did not experience problems. Over one-third of those who were interested in enrolling were excluded following this compliance run-in.
Because statins reduce nonfatal stroke (and cognition is obviously not measured in people who have experienced fatal stroke), benefits by statins for cognitive function in those in whom a stroke was averted might be expected. It must be emphasized that the randomized trial evidence has, to date, uniformly failed to show cognitive benefits by statins and has supported no effect or frank and significant harm to cognitive function.
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Frisoni GB, Fratiglioni L, Fastbom J et al. (1999), Mortality in nondemented subjects with cognitive impairment: the influence of health-related factors. Am J Epidemiol 150(10):1031-1044.
Golomb BA, Kane T, Dimsdale JA (2004), Severe irritability associated with statin cholesterol-lowering drugs. QJM 97(4):229-235.
Golomb BA, Yang E, Denenberg J, Criqui M (2003), Statin-associated adverse events. P95. Presented at the 43rd Annual Conference on Cardiovascu
King DS, Jones DW, Wofford MR et al. (2001), Cognitive impairment associated with atorvastatin. Presented at the American College of Clinical Pharmacy Spring Practice and Research Forum. Salt Lake City; April 22-25.
King DS, Wilburn AJ, Wofford MR et al. (2003), Cognitive impairment associated with atorvastatin and simvastatin. Pharmacotherapy 23(12):1663-1667.
Korten AE, Jorm AF, Jiao Z et al. (1999), Health, cognitive, and psychosocial factors as predictors of mortality in an elderly community sample. J Epidemiol Community Health 53(2):83-88.
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| Sbharris[atsign]ix.netcom.com | 12 Feb 2005 18:20 |
>>Another misleading subject line..... The article makes it clear that there are conflicting studies: some show no protection against dementia, others do. Obviously, much more research is needed.
Who wouldn't hope that there *might* be some benefit from statins against this most debilitating disease, alzheimers? <<
COMMENT:
While we're visiting this subject, let us note that Alzheimer's is responsible for maybe half of dementia only. A large fraction of the other half is caused by mini-strokes and vascular disease. And of course, there's a 20 to 30% overlap of people who have both problems.
Of these, Alzheirmer's is the process I would LEAST expect statins to interfere with. They might, but they might not. However, statins have already show impressive anti-stroke capability, even in people with normal cholesterol levels. So if statins do not work in slowing or preventing progression of Alzheimer's, this in no way means we've ruled out their role in preventing "dementia."
SBH
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| listener | 11 Feb 2005 03:08 |
Another misleading subject line.....
The article makes it clear that there are conflicting studies: some show no protection against dementia, others do. Obviously, much more research is needed.
Who wouldn't hope that there *might* be some benefit from statins against this most debilitating disease, alzheimers?
L.
> Many of us who have been exposed first-hand to the devastating > cognitive adverse effects of statins have been tremendously skeptical [quoted text clipped - 72 lines] > > SOURCE: Archives of General Psychiatry, February 2005. |
| Sharon Hope | 11 Feb 2005 02:58 |
Many of us who have been exposed first-hand to the devastating cognitive adverse effects of statins have been tremendously skeptical of the "Can statins prevent Alz?????" headlines, which appeared at a time that conveniently offset articles in the popular media that exposed the memory loss caused by statins.
We doubters also questioned how the studies would differentiate between Alz and statin-induced memory loss.
As it turns out, this latest study shows that statins do NOT prevent Alzheimer's:
Statins Don't Protect Against Dementia: Study http://today.reuters.co.uk/news/newsArticle.aspx?type=healthNews&storyID=2005-02 -10T211401Z_01_B371082_RTRIDST_0_HEALTH-STATINS-DEMENTIA-DC.XML Reuters.uk, UK - 5 hours ago NEW YORK (Reuters Health) - The use of cholesterol-lowering drugs belonging to the statin family, such as Lipitor or Pravacol, does not seem to have any effect ...
Statins Don't Protect Against Dementia: Study http://www.reuters.com/newsArticle.jhtml?type=healthNews&storyID=7598600 Reuters - 5 hours ago NEW YORK (Reuters Health) - The use of cholesterol-lowering drugs belonging to the statin family, such as Lipitor or Pravacol, does not seem to have any effect ...
Statins Don't Protect Against Dementia: Study http://abcnews.go.com/Health/wireStory?id=488976 ABC News - 5 hours ago Feb 10, 2005 - NEW YORK (Reuters Health) - The use of cholesterol-lowering drugs belonging to the statin family, such as Lipitor or Pravacol, does not seem ...
Statins Don't Protect Against Dementia: Study Thu Feb 10, 2005 9:15 PM GMT
NEW YORK (Reuters Health) - The use of cholesterol-lowering drugs belonging to the statin family, such as Lipitor or Pravacol, does not seem to have any effect on the risk of dementia or Alzheimer's disease, according to findings from a new study.
This supports the results of another study, but run counter other study findings that have linked statin use with a reduced risk of dementia.
The current study involved elderly residents living in Cache County, Utah, who were evaluated for statin use and dementia between 1995 and 1997 and then again between 1998 and 2000.
Dr. John C. S. Breitner, from the VA Puget Sound Health Care System in Seattle, and colleagues report their findings in the Archives of General Psychiatry.
Of the 4,895 subjects evaluated at the initial assessment, 355 had dementia, including 200 with Alzheimer's disease. In this analysis, statin use was associated with a 56-percent reduction in risk of dementia.
During 3-year follow-up, 185 of 3308 at-risk survivors were diagnosed with dementia, including 104 with Alzheimer's disease. In this analysis, statin use at the start of the study or at follow-up had no effect on the risk of dementia or Alzheimer's disease.
One explanation for the different findings could be that after dementia sets in, patients may simply be less likely to use statins, along with other drugs.
Studies with sufficient statistical power are needed to assess the effect of statin use on dementia risk, the authors note. "Until such research is able to demonstrate more promising results, however, we suggest that costly randomized trials of statins are premature."
SOURCE: Archives of General Psychiatry, February 2005.
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