'Statins' - nothing but slow poison?

Skeptic Ginger said:
You might want to consider that with prescription drugs, the people who write the prescriptions know full well how to interpret the side effects listed in the drug information by the manufacturer. In addition, if one of our patients has an unusual symptom we want to know if it might be related to the drug, we simply contact the manufacturer by phone. They maintain post market data collection and can often give additional information.

...snip...
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In the UK we have the "yellow card" system for reporting side effects: http://yellowcard.mhra.gov.uk/downloads/
 
Darat said:
I didn't know that - seems a rather OTT approach, I'd always assumed the side-effects were "calibrated" against the control group.
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He's only talking about the side effects listed in the initial studies prior to FDA approval (I would guess it was the same in the UK but I don't know) and in references that use that format.

You have to understand that how information is reported depends a lot on what the format is. So, were I doing research on a specific drug question, for example, does drug [X] cause symptom [Y], then in my conclusion I would say the data supports yes or no or is equivocal.

But when I'm filing research results with the FDA for drug approval, or writing the drug insert, then I would list all data collected and let the reader make their own determination. If you look at a drug insert you'll see the side effects listed side by side, controls vs test subjects. Also, I think for protection or for traditional reasons, the drug companies will just list all the side effects as possible. Some effects on the list are on virtually every drug insert ever. Meh, no one pays attention to those lists unless in the comparison data there is a reason to pay attention.

Anyway, the bottom line is these drug information sources, be they a manufacturer's statement or a study, have specific information in a specific format. It doesn't mean anything else.

Then for vaccines there is the VAERS reporting data. This is raw data collected on vaccine reactions which we are required by law to report. There is a list of reactions considered vaccine related, such as GBS within 12 weeks of a vaccine dose, but not 6 months after the dose. The public has access to the raw data but the CDC analyzes the data against expected baselines to pull out the relevant results.

Other adverse events following any drug dose are reportable to the FDA as are adverse events suspected to have been caused by a medical device. That data is used to monitor drug safety as well as additional data for the manufacturer.
 
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Supernaut said:
Unwilling, if you like, but I am not "expecting" anyone to "do my homework" -a rather old comeback.

Actually, I have a limited amount of time online, usually no more than a couple of hours a day (I have no connection at home, out of choice). Simple as that.

Most of the points I've made are agued for at http://www.spacedoc.net/. Knock yourself out.
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So just keep posting unsupported assertions, without evidence.

Nothing new here for a possible conspiracy theorist. "I can't think of my own ideas, I don't evaluate evidence, read someone else's web page"
 
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This thread got me to thinking about statins- again.

In particular, what do they do besides lower cholesterol? See, in previous net education, I had become aware of the fact that aspirin and statins do mostly the same thing. Aspirin cuts the 'end point' by 80% as much as statins do, but add a statin to the aspirin regimen, and only gain 20% over statin alone.

So I googled <statin anti-clotting>. Yup, that is the link. Statins actually owe much of their benefit due to anti-clotting. Here is the first hit from google:

http://heartdisease.about.com/od/cholesteroltriglyceride1/f/Why-Are-Statins-Different.htm

It does mention that other drugs may lower LDL yet have no benefit for preventing heart disease. And warns that statins are baaaad for brain hemorrhages, just like aspirin and warfarin are.

Statins also supposedly aid in plaque stabilization, and act as anti-inflammatory.

So, looks to me like it ain't the fatty diet. It ain't the cholesterol lowering of statins either. The benefits are due to anti-clotting, anti-inflammatory, and plaque stabilization. My own clogged arteries are brought about by a wheat allergy. Like the way peanuts can cause anaphylactic shock, wheat causes my angina.

eta: Addendum: So I googled <prothrombin heart disease), found this study: < http://circ.ahajournals.org/cgi/content/meeting_abstract/118/18_MeetingAbstracts/S_390-a> Conclusion was that some genetic variations in prothrombin make 1.5, 1.9. or SIX times the relative risk for ischemic heart disease.

It's not the pork, it's the clots. Take your aspirin.
 
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casebro said:
This thread got me to thinking about statins- again.

In particular, what do they do besides lower cholesterol? See, in previous net education, I had become aware of the fact that aspirin and statins do mostly the same thing. Aspirin cuts the 'end point' by 80% as much as statins do, but add a statin to the aspirin regimen, and only gain 20% over statin alone.

So I googled <statin anti-clotting>. Yup, that is the link. Statins actually owe much of their benefit due to anti-clotting. Here is the first hit from google:

http://heartdisease.about.com/od/cholesteroltriglyceride1/f/Why-Are-Statins-Different.htm

It does mention that other drugs may lower LDL yet have no benefit for preventing heart disease. And warns that statins are baaaad for brain hemorrhages, just like aspirin and warfarin are.

Statins also supposedly aid in plaque stabilization, and act as anti-inflammatory.

So, looks to me like it ain't the fatty diet. It ain't the cholesterol lowering of statins either. The benefits are due to anti-clotting, anti-inflammatory, and plaque stabilization. My own clogged arteries are brought about by a wheat allergy. Like the way peanuts can cause anaphylactic shock, wheat causes my angina.

eta: Addendum: So I googled <prothrombin heart disease), found this study: < http://circ.ahajournals.org/cgi/content/meeting_abstract/118/18_MeetingAbstracts/S_390-a> Conclusion was that some genetic variations in prothrombin make 1.5, 1.9. or SIX times the relative risk for ischemic heart disease.

It's not the pork, it's the clots. Take your aspirin.
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Your link does not support your assertion that aspirin and statins are redundant.
 
Supernaut said:
So, you're "stronger and faster" - are you saying this is thanks to statins?
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I didn't say anything about "thanks to statins."

Nevertheless, what I stated is true - I was put on statins by my GP several years ago. I am now in the best shape I've been in since my teens. You started the thread with an anecdote, I responded with personal experience.

Supernaut said:
As I asked Sputnik - do you mind my asking what age you are?
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40
 
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Supernaut said:
Basically, my conviction is that the whole saturated fat/cholesterol "causal link" with vascular and heart diesease is bunk.
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Skeptic Ginger said:
Are you familiar with the term, magical thinking?
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Although Supernaut's personal anecdote hardly qualifies as proof, there are certainly several reputable studies that support his viewpoint on saturated fat and heart disease. For example in his book "In Defense of Food" (which I have in front of me), Michael Pollan cites the following study:

"Types of Dietary Fat and Risk of Coronary Heart Disease", Frank B. Hu, et al., Journal of the American College of Nutrition, Vol. 20, 1, 5-19 (2001)

which states:
It is now increasingly recognized that the low-fat campaign has been based on little scientific evidence and may have caused unintended health consequences.
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I have not read the actual study, but Pollan says the report concludes that the amount of saturated fat has little to no impact on risk of heart disease.
 
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What are we talking about?

I am confused about the claims being made, and which aspects people take issue with. I took from the OP the following claims:

1) Connections between neurons in the brain ("synapses") are made up of cholesterol, and in general cholesterol is critical to proper brain function.

2) Statins reduce the amount of cholesterol made by the liver.

3) Statins cause people to act mentally older, i.e. lose their mind.

4) Statins cause people to act physically older, i.e. trouble walking up stairs.

Is it only 3 and 4 that are being questioned? Or are 1 and 2 questionable as well?

1 and 2 could easily be researched and sources cited, but not 3 and 4, which seem to be solely based on 2 anecdotes. But if 1 and 2 are true, it is logical to at least consider claim 3 and check for any existing studies or research which could support or refute the claim.

Claim 4 doesn't make sense to me.
 
johnnyawe said:
I am confused about the claims being made, and which aspects people take issue with. I took from the OP the following claims:

1) Connections between neurons in the brain ("synapses") are made up of cholesterol, and in general cholesterol is critical to proper brain function.
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Um cell walls are made of lipids yes, but synapses are not made of cholesterol. Synapses work through the releases and interaction of neurotransmitters.

Now if statins were shown to cause a problem with myelin that would be a real problem.
2) Statins reduce the amount of cholesterol made by the liver.

3) Statins cause people to act mentally older, i.e. lose their mind.

4) Statins cause people to act physically older, i.e. trouble walking up stairs.

Is it only 3 and 4 that are being questioned? Or are 1 and 2 questionable as well?
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1 is wrong.
1 and 2 could easily be researched and sources cited, but not 3 and 4,
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The role of statins in the early onset of dementia would be a rather easy retrospective study to design.
which seem to be solely based on 2 anecdotes.
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In defense of the OP, yes case studies can be important, but the case study should include a lot of things that an anecdote does not.
But if 1 and 2 are true, it is logical to at least consider claim 3 and check for any existing studies or research which could support or refute the claim.

Claim 4 doesn't make sense to me.
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#4 is a possible side effect of muscle aches and pains, which is a serious side effect as are some other.

But anecdotes need to become case studies with rule outs for other causes before they are useful.
 
Now has the role of serum cholesterol been overplayed, especially in the early days? Sure, I remember the 'no eggs' days.

But have there been huge data based studies that link serum cholesterol and heart disease risk, yes.

Is our understanding of the causative factors of heart disease changing, every day.

Do statins work, yes, in lowering the risk of heart disease, do we know the exact reasons, partly.

I am not a medical professional and stand to be corrected.
 
a reminder – I posted in the first place a day or two after I discovered that someone I know, who is showing a pronounced physical degeneration that seems incongruous given his age and history (55, tall and formally athletic, climber etc’) turned out to be taking Lipitor (I can't know what effect if any it may have had on his mental faculties, because it seems that he’s been taking them since before I met him).

I’m not here to crusade or push any agenda. Period. I just feel that the issue is not being discussed in the MSM as it should, notwithstanding the odd piece voicing misgivings in the press, usually to the effect that older statin users should urgently consider taking a CQ10 supplement.

I really don’t have the time or resources to devote myself to arguing and citing interminably.

For the time being I’ll leave you with this;

I cannot fathom how so many allow themselves to be convinced that "high cholesterol" is a "disease" (or even a symptom of a disease) for which the solution is to dose people in their millions pre-emptively and (presumably) for the rest of their lives with a "medicine".

Please. Just. Think. About. It
 
Dancing David said:
The role of statins in the early onset of dementia would be a rather easy retrospective study to design.
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Here is an actual study on the subject:

Statins and the risk of dementia
Interpretation
Individuals of 50 years and older who were prescribed statins had a substantially lowered risk of developing dementia, independent of the presence or absence of untreated hyperlipidaemia, or exposure to non-statin LLAs.
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(Highlighting mine.)
The Lancet, Volume 356, Issue 9242, Pages 1627 - 1631, 11 November 2000
 
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ElMondoHummus said:
Whoa, hold on.
Supernaut said:
Asserting that the constituents of the scarring (no, it is NOT “plaque”...
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Not plaque? Evidence, please?
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Supernaut (to the rest of us in this thread) said:
I really don’t have the time or resources to devote myself to arguing and citing interminably.
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Unfortunately, that seems to be a huge part of your problem: It looks like you haven't looked at this well enough or with a reasonable degree of thoroughness. You've not provided citations, references, or anything above and beyond assertion for what you've posted, the quote I questioned above being one example.

The questions are partly to see where you're coming from, and partly to see if the "place" you're coming from is valid to begin with. Frankly, without support for your arguments, it cannot be determined that it is. And given that the current medical standard of care disagrees, we're forced to conclude that it does not. That's why we ask these questions: Not to bury you in a dogpile of citations, but to discover why you're making the argument. That helps us figure out our responses.

Supernaut said:
I cannot fathom how so many allow themselves to be convinced that "high cholesterol" is a "disease" (or even a symptom of a disease) for which the solution is to dose people in their millions pre-emptively and (presumably) for the rest of their lives with a "medicine".
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Because the evidence points at not only the correlation, but a mechanism for the causation. And your post above demonstrates that you may be suffering under a misapprehension regarding the causation.

If you want to walk away from the discussion, fine. But your point gets nowhere without you providing supporting arguments. Bare assertion doesn't cut it, and yes, your post above was bare assertion.

Supernaut said:
Please. Just. Think. About. It.
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And that's the final misapprehension you suffer under: The apparent belief that we haven't already thought about it. That's not only unsupported, it's contradicted by the detail in some of the responses, and the questions we've directed back at you. We have thought about it; it's that thought and research that led us to where we are today. Using myself as an example: My late father and late maternal grandmother both had cardiovascular issues, and I'm on statins myself as a preventative against further problems. I personally am affected by this, and am by no means acting blindly. That's the same for some here, and for others, they're on the other side of the fence as care providers.

But in contrast, you are coming at this as if you only recently noticed the potential issue; your statement about only posting "in the first place a day or two after I discovered that someone I know" gives weight to that. Telling those of us who've been dealing with this for years when you yourself have only been dealing with it for a few days is a bit presumptuous. So the question in return is: Have you thought about it? Or are you merely reacting to what you saw in your friends cases?

I'm sorry, but without support for your basic presumptions - support that's missing, given that you've gone on at length from those basic presumptions but have not given support for them - it's hard to agree with you or even give your posts any credence. Again, it's your right to walk away from the discussion, but without anything other than a "Google for..." pointer, your arguments fail due to lack of support, and your point goes nowhere.

I'm sorry, but there it is. It's your choice whether to provide support for your basic presumptions or not.
 
Here's an article from SBM:

The International Network of Cholesterol Skeptics
(...)
I’ll admit there is a grain of truth in what they say. The public may falsely perceive cholesterol as some kind of “Great Satan” of heart disease, and diet has been overemphasized, and some doctors may be over-prescribing statins. But there is plenty of evidence from multiple avenues of research to show that high cholesterol is a risk factor for heart disease and that lowering it reduces risk. A Lancet article from December 2007 reviewed trials involving nearly a million people and found that “Total cholesterol was positively associated with IHD [ischemic heart disease] mortality in both middle and old age and at all blood pressure levels.”
(...)
Prevention is much more complex than just throwing statins at patients with high cholesterol. There are other ways to lower cholesterol, including weight loss. It makes a difference whether you are aiming for primary prevention (preventing disease in the first place) or secondary prevention (preventing further harm to someone who already has cardiovascular disease). A high LDL may not be as significant in a patient whose HDL (“good” cholesterol) is also high. Before prescribing, a good doctor looks at the whole patient: all the other risk factors, such as age, sex, weight, diet, exercise, family history, smoking, blood pressure, and past history. He looks at the risk/benefit ratio of statins in the patient’s particular situation. He considers the NNT (number needed to treat) to prevent one death or heart attack (which may vary from 5 to 333 depending on the situation). He looks at what other medications the patient is on, at the cost and convenience, at the patient’s personal philosophy and preferences. Ideally, the decision to use statins should be a joint decision of the patient and the doctor based on all the information available.
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http://www.sciencebasedmedicine.org/index.php/the-international-network-of-cholesterol-skeptics/
 
AdMan said:
Here is an actual study on the subject:

Statins and the risk of dementia

(Highlighting mine.)
The Lancet, Volume 356, Issue 9242, Pages 1627 - 1631, 11 November 2000
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Yeah, there are quite a few studies out there on this. A few that report an inverse correlation:
  • Use of lipid-lowering agents, indication bias, and the risk of dementia in community-dwelling elderly people, Rockwood K, Kirkland S, Hogan DB, MacKnight C, Merry H, Verreault R, Wolfson C, McDowell I, Archives of Neurology [2002, 59(2):223-7]
    While the possibility of indication bias in the original observations cannot be excluded, it was not demonstrated in LLA use in this study. Lipid-lowering agent use was associated with a lower risk of dementia, and specifically of Alzheimer disease, in those younger than 80 years. Further research is warranted.
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  • Use of statins and incidence of dementia and cognitive impairment without dementia in a cohort study, C. Cramer, PhD, M. N. Haan, DrPH, S. Galea, MD, DrPH, K. M. Langa, MD, PhD and J. D. Kalbfleisch, PhD, NeurologyJuly 29, 2008 vol. 71 no. 5 344-350
    Conclusion: Statin users were less likely to have incident dementia/cognitive impairment without dementia during a 5-year follow-up. These results add to the emerging evidence suggesting a protective effect of statin use on cognitive outcomes.
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  • The Impact of the Use of Statins on the Prevalence of Dementia and the Progression of Cognitive Impairment, Ihab Hajjara, Jeannie Schumperta, Victor Hirtha, Darryl Wielanda and G. Paul Eleazera, J Gerontol A Biol Sci Med Sci(2002) 57 (7): M414-M418.
There are more, but everyone here gets the point.

Are there any that might possibly indicate a positive correlation between statins and cognition issues? Yes, believe it or not there are:
  • Cognitive Impairment Associated with Atorvastatin and Simvastatin, Deborah S. King, Amanda J. Wilburn, Marion R. Wofford, T. Kristopher Harrell, Brent J. Lindley and Daniel W. Jones (2003). Cognitive Impairment Associated with Atorvastatin and Simvastatin. Pharmacotherapy: Volume 23, Issue 12, pp. 1663-1667.
    Emerging data associate statins with a decreased risk of Alzheimer’s disease; however, we report two women who experienced significant cognitive impairment temporally related to statin therapy. One woman took atorvastatin, and the other first took atorvastatin, then was rechallenged with simvastatin. Clinicians should be aware of cognitive impairment and dementia as potential adverse effects associated with statin therapy.
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  • Statin-Associated Memory Loss: Analysis of 60 Case Reports and Review of the Literature, Leslie R. Wagstaff, Pharm.D., Melinda W. Mitton, Pharm.D., Beth McLendon Arvik, Pharm.D., P. Murali Doraiswamy, M.D., 07/25/2003; Pharmacotherapy. 2003;23(7) © 2003 Pharmacotherapy Publications
    Conclusion: Current literature is conflicting with regard to the effects of statins on memory loss. Experimental studies support links between cholesterol intake and amyloid synthesis; observational studies indicate that patients receiving statins have a reduced risk of dementia. However, available prospective studies show no cognitive or antiamyloid benefits for any statin. In addition, case reports raise the possibility that statins, in rare cases, may be associated with cognitive impairment, though causality is not certain.
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  • Statin-associated adverse cognitive effects: survey results from 171 patients, Evans MA, Golomb BA., Pharmacotherapy. 2009 Jul;29(7):800-11.
    Patients completed a survey assessing statin-associated, cognitive-specific adverse drug reaction (ADR) characteristics, relation of the ADR to specific statin and dose (or potency), and time course of symptom onset and recovery...

    ... 128 patients (75%) experienced cognitive ADRs determined to be probably or definitely related to statin therapy. Of 143 patients (84%) who reported stopping statin therapy, 128 (90%) reported improvement in cognitive problems, sometimes within days of statin discontinuation (median time to first-noted recovery 2.5 wks). Of interest, in some patients, a diagnosis of dementia or Alzheimer's disease reportedly was reversed. Nineteen patients whose symptoms improved or resolved after they discontinued statin therapy and who underwent rechallenge with a statin exhibited cognitive problems again (multiple times in some). Within this vulnerable group, a powerful relationship was observed between potency of the statin and fraction of trials with that agent resulting in cognitive ADRs (p<0.00001). Quality of life was significantly adversely affected for each of the seven assessed domains (all p<0.00000001).

    CONCLUSION: Findings from the survey suggest that cognitive problems associated with statin therapy have variable onset and recovery courses, a clear relation to statin potency, and significant negative impact on quality-of-life. Administration of a patient-targeted questionnaire is a feasible approach that provides a useful complement to other ADR surveillance approaches.
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  • Statins and risk of polyneuropathy: A case-control study, D. Gaist, MD PhD, U. Jeppesen, MD PhD, M. Andersen, MD PhD, L. A. García Rodríguez, MD MSc, J. Hallas, MD PhD and S. H. Sindrup, MD PhD, Neurology May 14, 2002 vol. 58 no. 9 1333-1337
    Results: The authors verified a diagnosis of idiopathic polyneuropathy in 166 cases. The cases were classified as definite (35), probable (54), or possible (77). The odds ratio linking idiopathic polyneuropathy with statin use was 3.7 (95% CI 1.8 to 7.6) for all cases and 14.2 (5.3 to 38.0) for definite cases. The corresponding odds ratios in current users were 4.6 (2.1 to 10.0) for all cases and 16.1 (5.7 to 45.4) for definite cases. For patients treated with statins for 2 or more years the odds ratio of definite idiopathic polyneuropathy was 26.4 (7.8 to 45.4).

    Conclusions: Long-term exposure to statins may substantially increase the risk of polyneuropathy.
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So what's the verdict? Well, there are some indications of a type of very specific degradation in one studied population, but broader studies show negative correlation between statin use and general decline. But this isn't a vote with "X" number saying one thing and "Y" number saying another. Rather, this is representative the aggregate state of knowledge. There may be some negative effect in some specific way for some people, but for the majority of statin users, there is in fact a positive, protective neurological effect.

And that's a point that I fear that Supernaut is missing. He's working off of a pair of data points and some apparent misapprehensions of the role cholesterol plays in cardiovascular disease (someone can either correct me if I've misrepresented or mischaracterized that, but with my level of knowledge, it appears as though he's got an alternate understanding of how that disease works), while at the same time drawing conclusions about cognitive impairment in relation to statins that is not justified by the current state of knowledge. He's asking us to "think", but I'm currently not convinced that he's fully thought his way through this. Well... time will tell.
 
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