'Statins' - nothing but slow poison?

[Skeptic Ginger]

....
So tell me, what are you dissing me about?

Your unsupported assertions.

 

[Sawbones79]

I can't comment about the aspects of socialized medicine, since I'm in the US. But isn't it possible that what some of your patients are saying is inaccurate?

I've seen that as a vet. A client will make a statement like that (or something similar) about another vet; yet the medical records indicate their account is far from accurate. And if I question them carefully, I'll see them retract the statement as I probe for information.

Even with friends who make such statements about their MDs and the meds prescribed-- I'll often ask questions, and find they were given information about the medication--which they may have either not understood, or didn't remember.

I don't doubt that some MDs prescribe meds as you stated. I've seen MDs that were reluctant to answer my simple, but pertinent questions, with flippant, short or nonsense answers. They are, of course, ex-MDs of mine.

Though, as SG wrote above, it's kind of off topic, it's far more troublesome for a patient to change doctors in a state-run medical system. It puts the onus of changing doctors on the patient, who will in most cases only change doctors while still being treated at the same clinic.
I'll stop derailing now, sorry. Anyway, I believe statins might often be prescribed with far too little information to the patient, since they're often part of a "parcel" of drugs prescribed to patients at risk for cardiovascular disease (the standard kit I was taught to routinely prescribe was simvastatin, salicylic acid, and an ACE-inhibitor).

 

[casebro]

Your unsupported assertions.

I've enumerated the points my conclusion is based on in post #97. Feel free to falsify my assertions.

That is the way this forum is supposed to work, isn't it? Rather than attacking me.

 

[casebro]

I want to add new assertion, in line with another poster's comment.

Regarding the way the parameter for who should take statins getting lowered. Seems they want even people with low cholesterols to take statins. Studies show that it helps. There for, I assert that the statins benefit is attained via a pathway that is exclusive of cholesterol level.

I can give you a two, and I can give you another two. If you can't have at least a 3 1/2 pop into your head, maybe the problem is in your head, not mine?

 

[Skeptic Ginger]

I've enumerated the points my conclusion is based on in post #97. Feel free to falsify my assertions.

That is the way this forum is supposed to work, isn't it? Rather than attacking me.

I don't need to discredit assertions you haven't supported. They don't have 'credit' in the first place.

 

[Skwinty]

Seems they want even people with low cholesterols to take statins. Studies show that it helps. There for, I assert that the statins benefit is attained via a pathway that is exclusive of cholesterol level.

I have type 2 diabetes and my "bad" cholestrol type is normal, however, my "good" cholestrol type is low.

Hence 1 X 20mg Simvastatin daily as per prescription along with Glucophage and Diamicron.

 

[casebro]

I don't need to discredit assertions you haven't supported. They don't have 'credit' in the first place.

Do you want to quit playing just because you can't win any more?

If I'm a poopy head, maybe somebody else will take the time to tell me why.

I believe all of my assertions are based on what is is now common knowledge. So yes, it will be hard to prove my conclusions wrong. I think.

 

[Skeptic Ginger]

So common knowledge is the source of your assertions, casebro? Not a valid source in this case. You still have nothing.

 

[casebro]

People on this thread are interested in Stain drugs.

Does anybody NOT already know as common knowledge, the assertions I enumerated in post 97?

Me thinks SG does not like the style of the emperor's new clothes.

 

[Perpetual Student]

Are there mortality studies concerning the use of statins? I am referring to mortality studies from all causes, not only from coronary disease. It seem to me that such mortality studies would help shed some light on this question.
What about the demonstrated benefit of simvastatin regarding Alzheimer's disease? For some of us that would weigh heavily as a favorable factor regardless of negative side effects.
If this has already been mentioned sorry for the redundancy.

 

[Professor Yaffle]

Are there mortality studies concerning the use of statins? I am referring to mortality studies from all causes, not only from coronary disease. It seem to me that such mortality studies would help shed some light on this question.
What about the demonstrated benefit of simvastatin regarding Alzheimer's disease? For some of us that would weigh heavily as a favorable factor regardless of negative side effects.
If this has already been mentioned sorry for the redundancy.

Here's a summary of a fairly recent metaanalysis:
http://evidencebasedmedicine.com.au/?p=1341

 

[Skwinty]

Here's a summary of a fairly recent metaanalysis:
http://evidencebasedmedicine.com.au/?p=1341

According to your link...

"
Statins were not associated with a benefit to all-cause mortality in a primary prevention setting.
Although there is some ambiguity with the data, it is very unlikely that statins are of clinical benefit in patients with low and moderate absolute cardiovascular risk.
Until more definitive evidence becomes available, statins in the primary prevention setting should be reserved for those patients who are at high risk according to the 2005 lipid management guidelines [2]"




I think I should speak to my doctor and find out why exactly I am on statins.

 

[casebro]

"All cause mortality: is de rigor in medical studies. Try googling something like <study statin mortality>. Use particular statins, lovestatin, simvistatin, etc. The typical study will show the treatment group has a 30% lower 'end point'. Ends points are death, stroke, heart attack, or surgical intervention- CABG or Angioplasty.

One place where SG and I differ is that she thinks that the 30% is prevention. I believe a better word is delay.

I'll try another post to see if I know how to post this graph I drew: http://photos.imageevent.com/bigchriscase/misc/icons/scan0001.jpg

Basically, the benefits of stain are linear. That allows us to draw a graph that extends into the future. You can see that the maximum delay in end point is the tip of the right hhand wedge,at about two years in the future. The average of the patients in that wedge is six months. So, the way I see it, 30% of the 40% of us who have heart disease (that is 12%) will live six months longer. 12% living six months longer averages out to 21 days. So, take your stains, live 21 days longer. That is not the great panacea that people expect.

Millions of people have been taking statins for 20 years. But the death rate by heart attack shows no decline in the mean time. Certainly not the 30% that those with a superficial knowledge would lead us to expect.

eta: Thanks Skwinty and Yaffle. I type slow, in the meant time you guys did some heavy lifting.

 

[Skeptic Ginger]

All cause mortality as an outcome measure is problematic. This same measure has been touted as the reason influenza vaccinations for the elderly are unnecessary. Yet studies looking for more direct measurements of the benefit of flu vaccine have demonstrated clear benefits in decreased morbidity and mortality.

When you look at all cause mortality, it is affected by external variables that vary over time. For example, you can prevent cardiovascular disease caused death but see it replaced by an increase in homicidal and suicidal deaths related to varying social issues of the time. Or you might prevent influenza and cardiac deaths but an increase in an aging population increases cancer mortality.

All cause mortality is not the end all and be all outcome measure, especially when one thinks the outcome was significant when it was actually limited in the study. Here's an earlier meta analysis with a relevant comment. I don't have access to the full article from the Professor's link to see the specific comments about the limitations of the outcome measures but without them, you should view the overall mortality measure cautiously.

We did not find a statistically significant reduction in overall mortality from statin therapy in our analysis, likely because of the relatively low risk of mortality in this patient population and insufficient length of follow-up. The overall incidence of all-cause mortality in the placebo arm of the 6 studies with available mortality data was 6.6% over 4.3 years. In contrast, in a recently published secondary prevention meta-analysis,8 the mortality rate in the placebo arm was 11.3% over approximately 5.5 years, and the reduction in overall mortality with statin therapy was statistically significant. We also did not find a statistically significant reduction in CHD death. However, the point estimate for CHD deaths seen in our study (RR reduction, 22.6%) is greater than the statistically significant 16% RR reduction reported in the Cholesterol Trialists' Collaboration19 pooled analysis of primary prevention patients. This discrepancy may be attributable to the differences in the patient population included in each analysis. The Cholesterol Trialists' Collaboration analysis included all primary prevention subjects enrolled in trials of patients with and without known vascular disease. In contrast, our analysis used aggregate data from studies in which at least 80% of subjects were classified as primary prevention.

(emphasis mine)


Here are a couple more comprehensive looks at the decision to use statins or not. The first one has an extensive discussion of the current recommendations for all adults, including the use or not of statins.
Risk assessment and lipid modification for primary and secondary prevention of cardiovascular disease: summary of NICE guidance


A systematic review and economic evaluation of statins for the prevention of coronary events.

Conclusion: There is evidence to suggest that statin therapy is associated with a statistically significant reduction in the risk of primary and secondary cardiovascular events. As the confidence intervals for each outcome in each prevention category overlap, it is not possible to differentiate, in terms of relative risk, between the effectiveness of statins in primary and secondary prevention. However, the absolute risk of CHD death/non-fatal MI is higher, and the number needed to treat to avoid such an event is consequently lower, in secondary than in primary prevention. The generalisability of these results is limited by the exclusion, in some studies, of patients who were hypersensitive to, intolerant of, or known to be unresponsive to, statins, or who were not adequately compliant with study medication during a placebo run-in phase. Consequently, the treatment effect may be reduced when statins are used in an unselected population. The results of the economic modelling show that statin therapy in secondary prevention is likely to be considered cost-effective. In primary prevention, the cost-effectiveness ratios are dependent on the level of CHD risk and age, but the results for the CVD analyses offer support for the more aggressive treatment recommendation issued by recent guidelines in UK. Evidence on clinical endpoints for rosuvastatin is awaited from on-going trials. The potential targeting of statins at low-risk populations is however associated with major uncertainties, particularly the likely uptake and long-term compliance to lifelong medication by asymptomatic younger patients. The targeting, assessment and monitoring of low-risk patients in primary care would be a major resource implication for the NHS. These areas require further research.

That doesn't say statins are not useful in low risk groups, it says the NHS hasn't determined the benefit is worth the cost. An individual should make that decision based on their own circumstances. An individual's cost-benefit analysis is very different from the group's cost-benefit factors.


The benefits of statins in people without established cardiovascular disease but with cardiovascular risk factors: meta-analysis of randomised controlled trials

Conclusion In patients without established cardiovascular disease but with cardiovascular risk factors, statin use was associated with significantly improved survival and large reductions in the risk of major cardiovascular events.

Implications of Recent Clinical Trials for the National Cholesterol Education Program Adult Treatment Panel III Guidelines

The Adult Treatment Panel III (ATP III) of the National Cholesterol Education Program issued an evidence-based set of guidelines on cholesterol management in 2001. Since the publication of ATP III, 5 major clinical trials of statin therapy with clinical end points have been published. These trials addressed issues that were not examined in previous clinical trials of cholesterol-lowering therapy. The present document reviews the results of these recent trials and assesses their implications for cholesterol management. Therapeutic lifestyle changes (TLC) remain an essential modality in clinical management. The trials confirm the benefit of cholesterol-lowering therapy in high-risk patients and support the ATP III treatment goal of low-density lipoprotein cholesterol (LDL-C) <100 mg/dL. They support the inclusion of patients with diabetes in the high-risk category and confirm the benefits of LDL-lowering therapy in these patients. They further confirm that older persons benefit from therapeutic lowering of LDL-C. The major recommendations for modifications to footnote the ATP III treatment algorithm are the following. In high-risk persons, the recommended LDL-C goal is <100 mg/dL, but when risk is very high, an LDL-C goal of <70 mg/dL is a therapeutic option, ie, a reasonable clinical strategy, on the basis of available clinical trial evidence. This therapeutic option extends also to patients at very high risk who have a baseline LDL-C <100 mg/dL. Moreover, when a high-risk patient has high triglycerides or low high-density lipoprotein cholesterol (HDL-C), consideration can be given to combining a fibrate or nicotinic acid with an LDL-lowering drug. For moderately high-risk persons (2+ risk factors and 10-year risk 10% to 20%), the recommended LDL-C goal is <130 mg/dL, but an LDL-C goal <100 mg/dL is a therapeutic option on the basis of recent trial evidence. The latter option extends also to moderately high-risk persons with a baseline LDL-C of 100 to 129 mg/dL. When LDL-lowering drug therapy is employed in high-risk or moderately high-risk persons, it is advised that intensity of therapy be sufficient to achieve at least a 30% to 40% reduction in LDL-C levels. Moreover, any person at high risk or moderately high risk who has lifestyle-related risk factors (eg, obesity, physical inactivity, elevated triglycerides, low HDL-C, or metabolic syndrome) is a candidate for TLC to modify these risk factors regardless of LDL-C level. Finally, for people in lower-risk categories, recent clinical trials do not modify the goals and cutpoints of therapy.

You should trust that your physician or nurse practitioner is following the appropriate standardized guidelines for statin use. If you don't trust that, find another provider. That doesn't mean not to ask questions or share studies you've found. I share new research with my physician all the time. I don't expect him to have read the latest research for all my medical issues, while I might have. But I give him a copy of the abstract. I want him to add that to what he already knows, I don't think I can do better on my own just reading a bit of new data.

I prefer the LDL and HDL outcome measures rather than just whether or not one is in a high or low risk category when deciding to add statins to a patient's treatment. One must consider also a myriad of other issues related to taking a drug every day and of course the side effects are an important consideration. Cost matters. I look at cost in terms of health care resource dollars, not just cost. Same with the effort to take the drugs. If you have someone who is already on a lot of meds, is adding another one better, or is it better to trade one. So you might not use the statin because an osteoporosis prevention drug is more important to that individual and both of the drugs together exceed the resources the patient has.


THE BOTTOM LINE: Don't think you can read the title of a study or a brief summary of the conclusion and consider that adequate for an informed decision. And definitely interpret the 'all mortality' measure very cautiously.

 

[fls]

Millions of people have been taking statins for 20 years. But the death rate by heart attack shows no decline in the mean time. Certainly not the 30% that those with a superficial knowledge would lead us to expect.

The death rate from cardiovascular disease has decreased by 31% over the last decade.

http://www.cdc.gov/mmwr/preview/mmwrhtml/mm6021a6.htm?s_cid=mm6021a6_x

Linda

 

[fls]

Yes but how many of those use studies been via statins? Mightn't there be an unexpected side effect to the statins, besides the claimed benefit of the lower cholesterol? Well, hell yes, per my link above some where, where in statins are shown to prevent clots, lessen inflammation, and help stabilize plaques.

A few years ago I did learn this tid bit: Cholesterol level is actually the #5 risk factor for heart disease. Risk factors are (from memory, might be in wrong order):

#1 Age, obviously
#2 Genes, relatives who had heart disease at young age
#3 Weight, probably a lot of conflation with diabetes
#4 Height, but nobody says I should cut 2" out of my femurs to prevent disease
THEN comes cholesterol level at #5

Hey, shouldn't hypertension be in there too? Lower than #5 I assume?

But, if there are four groups above cholesterol, then cholesterol can not mathematically be a risk factor bigger than 20%. And could be very minor, like only single digit?

Though it may be the risk factor with the best rate of treatment. For instance, the only way to prevent aging is death, so lowering cholesterol sure beats that.

Yet even in my morning visit to the cardiologist today, he seems to think that lowering cholesterol level will prevent any further troubles for ever. In my own lexicon, I think 'prevent' means "never happen". But the studies really only show a "lesser relative rate" actually, which is actually a 'delay'. Said delay happens in a small percent of people. Hey, 60% of people die from something else that statins have no benefit for. Cancer, pulmonary disease, brain hemorrhage, ulcers,,,

The risk factors and their Population Attributable Risk are, in order:

Lipids - 54%
Smoking - 36%
Abdominal obesity - 34%
Psychosocial - 29%
Exercise (lack) - 26%
Hypertension - 23%
Alcohol (lack) - 14%
Fruits and veggies (lack) - 13%
Diabetes - 12%

Population attributable risk is the difference in disease incidence between the current population and an unexposed population. That is a population with a favourable lipid profile would have a 54% lower incidence of cardiovascular disease.

The PAR for family history was 12%.

http://www.thelancet.com/journals/lancet/article/PIIS0140-6736(04)17018-9/abstract

(You can view the full text with free registration.)

Linda

 

[Perpetual Student]

All cause mortality as an outcome measure is problematic. This same measure has been touted as the reason influenza vaccinations for the elderly are unnecessary. Yet studies looking for more direct measurements of the benefit of flu vaccine have demonstrated clear benefits in decreased morbidity and mortality.

When you look at all cause mortality, it is affected by external variables that vary over time. For example, you can prevent cardiovascular disease caused death but see it replaced by an increase in homicidal and suicidal deaths related to varying social issues of the time. Or you might prevent influenza and cardiac deaths but an increase in an aging population increases cancer mortality.

...

If a cause of death is prevented (or delayed) by a medication or procedure, any other cause of death would logically occur later. The situations you describe above would be accounted for by using age specific mortality rates.

 

[Skeptic Ginger]

If a cause of death is prevented (or delayed) by a medication or procedure, any other cause of death would logically occur later. The situations you describe above would be accounted for by using age specific mortality rates.

Not always. Sometimes studies look at all cause mortality compared a more general variable rather than randomized matched controls. For example, there are studies re flu vaccine and mortality that don't show overall decrease in mortality correlated to an increase in vaccine use. The data makes little sense in light of the fact we have other data that the vaccine works and that influenza kills. This has come up in vaccine discussions in this forum. Some other variable is being overlooked.


Then there are limitations stated re the 'all cause' mortality outcome in some studies. If you'll notice, I bolded the limitation on that very outcome measure in the first citation I quoted from:

We did not find a statistically significant reduction in overall mortality from statin therapy in our analysis, likely because of the relatively low risk of mortality in this patient population and insufficient length of follow-up.

If one simply quoted the first line in that conclusion it is misleading.


The problem I was pointing out was the conclusion, "no change in all cause mortality" was not some magical outcome measure as is often declared in discussions such as these, and as was being touted in this discussion.

 

[Perpetual Student]

Not always. Sometimes studies look at all cause mortality compared a more general variable rather than randomized matched controls. For example, there are studies re flu vaccine and mortality that don't show overall decrease in mortality correlated to an increase in vaccine use. The data makes little sense in light of the fact we have other data that the vaccine works and that influenza kills. This has come up in vaccine discussions in this forum. Some other variable is being overlooked.

The results should always show up if the studies are properly done -- unless the medication or procedure proves to be ineffective.
Your example (comparing age specific mortality rates of those receiving flu vaccine vs. a proper control group who do not) must be flawed unless such vaccines are ineffective. We are dealing with mathematics here -- not medicine!

 

[casebro]

The risk factors and their Population Attributable Risk are, in order:

Lipids - 54%
Smoking - 36%
Abdominal obesity - 34%
Psychosocial - 29%
Exercise (lack) - 26%
Hypertension - 23%
Alcohol (lack) - 14%
Fruits and veggies (lack) - 13%
Diabetes - 12%

Population attributable risk is the difference in disease incidence between the current population and an unexposed population. That is a population with a favourable lipid profile would have a 54% lower incidence of cardiovascular disease.

The PAR for family history was 12%.

http://www.thelancet.com/journals/lancet/article/PIIS0140-6736(04)17018-9/abstract

(You can view the full text with free registration.)

Linda

But by it's very nature, isn't the PAR ignoring the biggest risk factor in the "unexposed population"?

I suspect that to be age. They left it out. I'm thinking it would be the only risk factor in the unexposed group. With such a high risk factor that all others are greatly discounted. Hey, look, the total risk factors is 255% ? Sorry, can't reduce risk factors by more than 100% EVAR. That is math.

Then also, stated as "increased risk" instead of "comparative risk" means that the 54% lipid number is exaggerated when the important point is that cutting cholesterol would cut the risk by 35%.