New Study Confirms Statins Cause Diabetes
Wednesday, February 17, 2010 at 06:55PM
The results of a new study have just been published in The Lancet. The researchers found that statins increase the risk for diabetes. This increased risk seems very small - its 0.4 percent. However, this is more significant than it may first seem.
The authors of the published report have stated that the benefits of statins still far outweigh the risks. But do they?
When looking at the 'benefits' of statins, we should look at how many lives are actually saved by the drugs. The JUPITER trial, which has recently been used to justify the wider use of statins, showed that statins reduce deaths from all-causes by only 0.55 percent.
This mere 0.55 percent reduction in deaths is not even the worse case scenario. Since other trials, such as the AFCAPS trial, the ASCOT trial, and the CARDS trial, all failed to show any significant reduction in deaths from all causes.
Strictly speaking, deaths from all-causes is the most important measure we should use to judge the effectiveness of a drug. Since there is not much point if the drug reduces the risk for one disease but at the same time increases the risk for another disease within the same time period. But 'experts' often focus on the cardiovascular benefits of statins in order to make the drugs appear to be better than they actually are.
Even if we do just look at cardiovascular benefits, the results are certainly nothing to shout about. The JUPITER trial mentioned above found that statins reduce the risk for ‘hard cardiac events’ (heart attack, stroke, or death from cardiovascular causes), by just 0.9 percent.
Statins can be more effective when used by people who already have heart disease. But even here the benefits in terms of actual lives saved have been mixed. And most people who take statins are at a low risk of developing heart disease.
So, when we put the 'benefits' of statins into context we can see that this increase in diabetes is by no means trivial. Any increase in diabetes should be of concern, since diabetes drastically increases the risk for heart disease, and the full extend of these risks would not be seen during a statin clinical trial. This is because statin trials are only 2 to 6 years in duration – the full extent of the increased risks associated with diabetes develop over a much longer period of time.
And we have not included in this discussion the long list of other officially recognised adverse effects associated with statins. Or the significant questions that still remain concerning statins and cancer, and statins and heart failure.
There are no published studies to show that statins provide any benefit after 5 or 6 years, yet millions of people are being asked to take the drugs for several decades. The best case scenario is that any net benefit associated with statins hangs on a knife edge. Despite this, in the UK alone, we spend hundreds of millions of pounds on these drugs every year.
There is no need for pharmaceutical companies to worry about the increased risk for diabetes associated with statins, since they have other (equally ineffective) drugs for that as well.
Note: I have used absolute percentages for this discussion. In most cases, relative percentages are used in summary reports and throughout the media. All text books on clinical research advise against the use of relative percentages in this context since relative percentages are totally misleading and do not allow people to make accurate comparisons of risk.
Reference:
Sattar N, et al. Statins and risk of incident diabetes: a collaborative meta-analysis of randomised statin trials. Lancet 2010; DOI:10.1016/S0140-6736(09)61965-6
Sunday, November 21, 2010
Ever Wondered Why Statin Drug Trials Are Stopped Early?
Ever Wondered Why Statin Drug Trials Are Stopped Early?
from Justin Smith Blog by Justin Smith
All clinical trails involving cholesterol-lowering statin drugs have been relatively short in duration. Usually they run for about 5 years and sometimes only for 2 years. There are no published trials to show the long-term effects of statins, however, patients are being asked to take statins for several decades.
This may seem slightly trivial, but it really isn't. How long a drug is consumed can have a significant effect on the risk/benefit balance. Especially where statins are concerned – since any benefit of statins already hangs by a thread.
Some adverse effects of statins can occur quickly (like muscle aches and pains) and others (like diabetes) may take longer to develop. The full extent of the adverse effects associated with statins is not seen in just 5 years – it would take much longer to see the full effects.
So, drug companies can effectively choose the duration of the trial that will show their drugs in the best possible light. Drug companies also have a history of not publishing studies that show their drugs to be ineffective or harmfull – well lets face it, they are a business at the end of the day, with immense pressures to increase profits for shareholders.
The fact that no longer-term studies have been published on statins should make us very concerned. At the very least, our health authorities (who are supposed to protect us) should be asking for at least one long-term trial. We know that money is not an issue, because the drug companies keep doing more and more relatively short trials. Instead of this repetition we could have a longer trial that might tell us something new.
In 2008, the results of the JUPITER trial were published. This trial attracted a lot of media attention around the world and I have commented on it several times before. In summary, the statin used only managed to reduce deaths from all causes by a mere 0.55 percent (despite the nonsensical relative percentages that the drug company put out to the media to exaggerate the results).
One of the many interesting aspects of the JUPITER trial is that it was stopped early. It was stopped after just 1.9 years.
I have always suspected that this trial was stopped early because if it was allowed to continue even the miniscule 0.55 percent benefit would disappear.
A few days ago, a study was published in the Journal of the American Medical Association (JAMA), that looked at the effects of stopping trials early. This study found that trials stopped early almost always show much better results for the drug being tested than if the trial was allowed to run its full duration.
In fact, the JAMA study showed that any drug benefits may be doubled by stopping the trial early. This means that the 0.55 percent reduction in deaths found in the JUPITER trial would have almost completely disappeared if the trial was allowed to run its full course.
The statin used in the JUPITER trial caused more people to develop diabetes, and all statins cause a long list of other adverse effects (some of which result in permanent damage). Knowing this, was it wise for the FDA to approve the wider use of statins based on the results of the JUPITER trial?
References:
Bassler, D et al. randomized trials early for benefit and estimation of treatment effects: systematic review and meta-regression analysis. JAMA 2010; 303(12):1180-7
Ridker PM et al. Rosuvastatin to prevent vascular events in men and women with elevated C-reactive protein. New England Journal of Medicine 2008; 359:2195–2207
from Justin Smith Blog by Justin Smith
All clinical trails involving cholesterol-lowering statin drugs have been relatively short in duration. Usually they run for about 5 years and sometimes only for 2 years. There are no published trials to show the long-term effects of statins, however, patients are being asked to take statins for several decades.
This may seem slightly trivial, but it really isn't. How long a drug is consumed can have a significant effect on the risk/benefit balance. Especially where statins are concerned – since any benefit of statins already hangs by a thread.
Some adverse effects of statins can occur quickly (like muscle aches and pains) and others (like diabetes) may take longer to develop. The full extent of the adverse effects associated with statins is not seen in just 5 years – it would take much longer to see the full effects.
So, drug companies can effectively choose the duration of the trial that will show their drugs in the best possible light. Drug companies also have a history of not publishing studies that show their drugs to be ineffective or harmfull – well lets face it, they are a business at the end of the day, with immense pressures to increase profits for shareholders.
The fact that no longer-term studies have been published on statins should make us very concerned. At the very least, our health authorities (who are supposed to protect us) should be asking for at least one long-term trial. We know that money is not an issue, because the drug companies keep doing more and more relatively short trials. Instead of this repetition we could have a longer trial that might tell us something new.
In 2008, the results of the JUPITER trial were published. This trial attracted a lot of media attention around the world and I have commented on it several times before. In summary, the statin used only managed to reduce deaths from all causes by a mere 0.55 percent (despite the nonsensical relative percentages that the drug company put out to the media to exaggerate the results).
One of the many interesting aspects of the JUPITER trial is that it was stopped early. It was stopped after just 1.9 years.
I have always suspected that this trial was stopped early because if it was allowed to continue even the miniscule 0.55 percent benefit would disappear.
A few days ago, a study was published in the Journal of the American Medical Association (JAMA), that looked at the effects of stopping trials early. This study found that trials stopped early almost always show much better results for the drug being tested than if the trial was allowed to run its full duration.
In fact, the JAMA study showed that any drug benefits may be doubled by stopping the trial early. This means that the 0.55 percent reduction in deaths found in the JUPITER trial would have almost completely disappeared if the trial was allowed to run its full course.
The statin used in the JUPITER trial caused more people to develop diabetes, and all statins cause a long list of other adverse effects (some of which result in permanent damage). Knowing this, was it wise for the FDA to approve the wider use of statins based on the results of the JUPITER trial?
References:
Bassler, D et al. randomized trials early for benefit and estimation of treatment effects: systematic review and meta-regression analysis. JAMA 2010; 303(12):1180-7
Ridker PM et al. Rosuvastatin to prevent vascular events in men and women with elevated C-reactive protein. New England Journal of Medicine 2008; 359:2195–2207
Bad Cholesterol is now Good
Bad Cholesterol is now Good - Dec092009
Wednesday, December 9, 2009 at 04:59PM
People take cholesterol-lowering statin drugs to reduce ‘bad’ cholesterol (LDL ‘cholesterol’), however ‘bad’ cholesterol may not be as bad as we think. A study published in the American Heart Journal looked at the cholesterol levels of people who had been admitted to hospital in America with heart disease. The study included 136,905 people – all of these people had their LDL level measured within 24 hours of arrival in hospital.
The graph below is taken directly from the study. I have marked on the graph the suggested ideal LDL level of 3 mmol/l (or 120 mg/dl). We are constantly told that our risk for heart disease is reduced below this level and above this level our risk increases.
We can immediately see that the majority of these people with existing heart disease had an LDL level below the suggested ideal level – LOWER levels of so called 'bad' cholesterol were much more likely to be associated with heart disease than higher levels. This of course is the opposite of what we are expected to believe.
The average LDL level for this group of people was 2.7 mmol/l (or 104 mg/dl). However, the average LDL level for the general population around the same time was 3.2 mmol/l (124 mg/dl).
If people with heart disease have lower LDL levels than the general population, then perhaps we need to rethink the policy of spending hundreds of millions of pounds on reducing LDL levels in the general population.
References:
Carroll MD et al (2005) Trends in serum lipids and lipoproteins of adults, 1960–2002. Journal of the American Medical Association 294 pp1773–1781.
Sachdeva A et al (2009) Lipid levels in patients hospitalized with coronary artery disease: an analysis of 136,905 hospitalizations in get with the guidelines. American Heart Journal 157 111–117
Wednesday, December 9, 2009 at 04:59PM
People take cholesterol-lowering statin drugs to reduce ‘bad’ cholesterol (LDL ‘cholesterol’), however ‘bad’ cholesterol may not be as bad as we think. A study published in the American Heart Journal looked at the cholesterol levels of people who had been admitted to hospital in America with heart disease. The study included 136,905 people – all of these people had their LDL level measured within 24 hours of arrival in hospital.
The graph below is taken directly from the study. I have marked on the graph the suggested ideal LDL level of 3 mmol/l (or 120 mg/dl). We are constantly told that our risk for heart disease is reduced below this level and above this level our risk increases.
We can immediately see that the majority of these people with existing heart disease had an LDL level below the suggested ideal level – LOWER levels of so called 'bad' cholesterol were much more likely to be associated with heart disease than higher levels. This of course is the opposite of what we are expected to believe.
The average LDL level for this group of people was 2.7 mmol/l (or 104 mg/dl). However, the average LDL level for the general population around the same time was 3.2 mmol/l (124 mg/dl).
If people with heart disease have lower LDL levels than the general population, then perhaps we need to rethink the policy of spending hundreds of millions of pounds on reducing LDL levels in the general population.
References:
Carroll MD et al (2005) Trends in serum lipids and lipoproteins of adults, 1960–2002. Journal of the American Medical Association 294 pp1773–1781.
Sachdeva A et al (2009) Lipid levels in patients hospitalized with coronary artery disease: an analysis of 136,905 hospitalizations in get with the guidelines. American Heart Journal 157 111–117
Wednesday, November 17, 2010
Dr. Briffa on statins and cholesterol reduction
Recent review on statins ignores body of evidence that suggests these drugs don’t work through cholesterol-reduction
http://www.drbriffa.com/blog/ November 15, 2010
Recent review on statins ignores body of evidence that suggests these drugs don’t work through cholesterol-reduction
Big cholesterol news emerged last week on the publication (much publicised) of a massive meta-analysis of statin treatment in those at relatively high risk of cardiovascular disease. The idea of this meta-analysis was to assess whether aggressive lowering of cholesterol (specifically LDL-cholesterol) brings additional benefits in terms of cardiovascular disease protection. The meta-analysis included results from a total of 26 trials (involving a total of about 170,000 individuals) [1].
What this meta-analysis found was that more intensive lowering of cholesterol was associated with a reduced risk of ‘vascular events’ such as heart attacks, fatal heart attacks and the most common form of stroke (ischaemic stroke). The authors state that for each 1.0 mmol/L (39 mg/dl) reduction in LDL-cholesterol, risk of vascular events was reduced by about a fifth. They go on to say “reduction of LDL cholesterol by 2-3 mmol/L would reduce risk by about 40-50 per cent.”
Perhaps not surprisingly, this meta-analysis is being used to ram home the conventional view that cholesterol causes cardiovascular disease, and that lower levels of LDL-cholesterol are better. However, there are a number of reasons why this study fails to tell the whole story about statins and cholesterol reduction.
Statin drugs have a number of different mechanisms which might allow them to reduce cardiovascular disease risk in a way which has nothing to do with cholesterol reduction. For example, statins have anti-inflammatory effects, which we would expect to lead to reduced risk of cardiovascular disease. Now, when we intensively lower cholesterol with these drugs, non-cholesterol-related effects (e.g. anti-inflammatory action) will generally be increased too. So, we cannot assume that any additional benefits from more intensive statin therapy have come from more intensive lowering of cholesterol.
In this meta-analysis, the results of a large number of studies was pooled. The problem is, these studies used a range of different drugs at different doses. Sometimes, the drugs were being tested against placebos, and sometimes they were being tested against other drugs. Rarely, two doses of the same drug were tested. Basically, the studies represent a huge hotchpotch of ‘methodologies’ and ‘variables’.
If you really want to take a scientific approach to assessing the role of cholesterol reduction on health, you would ‘control your variables’. This basically means changing only one thing. So, for instance, you could give two groups of people differing doses of the same statin. You could then see if the group on the higher dose had additional benefits, and also see if this appeared to be related to cholesterol reduction or something else. You’d be surprised how rarely such studies are done.
One example of such a study is the so-called TNT study [2]. Here, individuals with heart disease (very high risk of future vascular events) were given either 10 or 80 mg of atorvastatin for an average of about 5 years. The higher dose did lead to lower LDL levels and lower risk of death due to heart-related disease. The absolute reduce in risk was 0.5 per cent, by the way, so nothing to get too excited about. Plus, this study did not report on the non-cholesterol-related effects of the two different dosages, and so it’s impossible to gauge if the relative benefit of the higher dosage was down to LDL reduction and/or something else.
It should also be borne in mind, by the way, that the higher dose of statin in this study (eight times the lower dose, remember) did not lead to a reduction in overall risk of death. In other words, taking 8 times the dose of this drug for five years did not, overall, extend life by a single day, even in individuals at high risk of heart attacks and stroke.
The idea that the anti-inflammatory effects of statins (and not their cholesterol-reducing effects) may be at the heart of their benefits has been bolstered by work focusing on an inflammatory marker known as C-reactive protein (CRP). Statins are known to have the capacity to reduce CRP levels.
In one study [3] assessing the relationship between statin therapy and cholesterol and CRP levels, it was discovered that “Patients who have low CRP levels after statin therapy have better clinical outcomes than those with higher CRP levels, regardless of the resultant level of LDL cholesterol.” (emphasis mine).
In another study [4] published in the same edition of the journal, statin therapy and cardiovascular disease risk assessed using ultrasound scanning of the inside of the coronary arteries. It was found that “atherosclerosis regressed in the patients with the greatest reduction in CRP levels, but not in those with the greatest reduction in LDL cholesterol levels.”
In yet another study [5] it was found that when treating with statins, those with the highest levels of inflammatory markers at the start of the study derived the most benefit, irrespective of initial cholesterol
levels.
Evidence that statins don’t work through their cholesterol-reducing effect comes from other evidence, including the findings that:
•Statins substantially reduce the risk of stroke, despite the fact that raised cholesterol levels are a weak or non-existent risk factor for stroke [6,7].
•Statins are claimed to reduce CVD risk in individuals who have ‘normal’ or even ‘low’ cholesterol levels [8].
•More intensive cholesterol reduction does not necessarily lead to improved outcomes [9].
Despite what the authors of the recent Lancet review would have us believe, there is considerable evidence that statins primarily work through mechanism that are independent of their cholesterol-reducing effects.
Stepping aside from the science for a moment, let’s also perhaps inject some common sense. Let us not forget that cholesterol is a natural constituent of the body that is a major component in cell membranes, the brain, steroid hormones (including sex hormones) and vitamin D (which appears to have major disease-protective properties). It simply does not make sense to me that driving levels of this key substance to lower and lower levels if, in and of itself, beneficial to health. We would not make the case for driving levels of, say, sodium to lower and lower levels, would we? Or blood sugar levels?
All rationality and common sense seems to fly out of the window when certain doctors and scientists start talking about cholesterol. And when it comes to the science, it’s clear that many are ignorant of or choose to ignore the stacks of evidence that clearly contradict their stance.
References:
1. Cholesterol Treatment Trialists’ Collaboration. Efficacy and safety of more intensive lowering of LDL cholesterol: a meta-analysis of data from 170,000 participants in 26 randomised trials. Lancet 9 November 2010 [epub ahead of print]
2. La Rosa JC, et al. Intensive lipid lowering with atorvastatin in patients with stable coronary disease. N Engl J Med. 2005;352(14):1425-35
3. Ridker PM, et al. C-reactive protein levels and outcomes after statin therapy. N Engl J Med 2005;352(1):20-8
4. Nissen SE, et al. Statin therapy, LDL cholesterol, C-reactive protein and coronary artery disease. N Engl J Med. 2005;352(1):29-38
5. Ridker PM, et al. Inflammation, pravastatin, and the risk of coronary events after myocardial infarction in patients with average cholesterol levels. Cholesterol and Recurrent Events (CARE) Investigators. Circulation. 1998;98(9):839-44
6. Cholesterol, diastolic blood pressure, and stroke: 13,000 strokes in 450,000 people in 45 prospective cohorts. Prospective studies collaboration. Lancet 1995;346(8991-8992):1647-53.
7. Imamura T, et al. LDL cholesterol and the development of stroke subtypes and coronary heart disease in a general Japanese population: the Hisayama study. Stroke 2009;40(2):382-8
8. Ridker PM, et al, JUPITER Study Group. Rosuvastatin to prevent vascular events in men and women with elevated C-reactive protein. N Engl J Med 2008;359(21):2195-2207
9. Kastelein JJ, et al, ENHANCE Investigators. Simvastatin with or without ezetimibe in familial hypercholesterolemia. N Engl J Med 2008;358(14):1431-1443
http://www.drbriffa.com/blog/ November 15, 2010
Recent review on statins ignores body of evidence that suggests these drugs don’t work through cholesterol-reduction
Big cholesterol news emerged last week on the publication (much publicised) of a massive meta-analysis of statin treatment in those at relatively high risk of cardiovascular disease. The idea of this meta-analysis was to assess whether aggressive lowering of cholesterol (specifically LDL-cholesterol) brings additional benefits in terms of cardiovascular disease protection. The meta-analysis included results from a total of 26 trials (involving a total of about 170,000 individuals) [1].
What this meta-analysis found was that more intensive lowering of cholesterol was associated with a reduced risk of ‘vascular events’ such as heart attacks, fatal heart attacks and the most common form of stroke (ischaemic stroke). The authors state that for each 1.0 mmol/L (39 mg/dl) reduction in LDL-cholesterol, risk of vascular events was reduced by about a fifth. They go on to say “reduction of LDL cholesterol by 2-3 mmol/L would reduce risk by about 40-50 per cent.”
Perhaps not surprisingly, this meta-analysis is being used to ram home the conventional view that cholesterol causes cardiovascular disease, and that lower levels of LDL-cholesterol are better. However, there are a number of reasons why this study fails to tell the whole story about statins and cholesterol reduction.
Statin drugs have a number of different mechanisms which might allow them to reduce cardiovascular disease risk in a way which has nothing to do with cholesterol reduction. For example, statins have anti-inflammatory effects, which we would expect to lead to reduced risk of cardiovascular disease. Now, when we intensively lower cholesterol with these drugs, non-cholesterol-related effects (e.g. anti-inflammatory action) will generally be increased too. So, we cannot assume that any additional benefits from more intensive statin therapy have come from more intensive lowering of cholesterol.
In this meta-analysis, the results of a large number of studies was pooled. The problem is, these studies used a range of different drugs at different doses. Sometimes, the drugs were being tested against placebos, and sometimes they were being tested against other drugs. Rarely, two doses of the same drug were tested. Basically, the studies represent a huge hotchpotch of ‘methodologies’ and ‘variables’.
If you really want to take a scientific approach to assessing the role of cholesterol reduction on health, you would ‘control your variables’. This basically means changing only one thing. So, for instance, you could give two groups of people differing doses of the same statin. You could then see if the group on the higher dose had additional benefits, and also see if this appeared to be related to cholesterol reduction or something else. You’d be surprised how rarely such studies are done.
One example of such a study is the so-called TNT study [2]. Here, individuals with heart disease (very high risk of future vascular events) were given either 10 or 80 mg of atorvastatin for an average of about 5 years. The higher dose did lead to lower LDL levels and lower risk of death due to heart-related disease. The absolute reduce in risk was 0.5 per cent, by the way, so nothing to get too excited about. Plus, this study did not report on the non-cholesterol-related effects of the two different dosages, and so it’s impossible to gauge if the relative benefit of the higher dosage was down to LDL reduction and/or something else.
It should also be borne in mind, by the way, that the higher dose of statin in this study (eight times the lower dose, remember) did not lead to a reduction in overall risk of death. In other words, taking 8 times the dose of this drug for five years did not, overall, extend life by a single day, even in individuals at high risk of heart attacks and stroke.
The idea that the anti-inflammatory effects of statins (and not their cholesterol-reducing effects) may be at the heart of their benefits has been bolstered by work focusing on an inflammatory marker known as C-reactive protein (CRP). Statins are known to have the capacity to reduce CRP levels.
In one study [3] assessing the relationship between statin therapy and cholesterol and CRP levels, it was discovered that “Patients who have low CRP levels after statin therapy have better clinical outcomes than those with higher CRP levels, regardless of the resultant level of LDL cholesterol.” (emphasis mine).
In another study [4] published in the same edition of the journal, statin therapy and cardiovascular disease risk assessed using ultrasound scanning of the inside of the coronary arteries. It was found that “atherosclerosis regressed in the patients with the greatest reduction in CRP levels, but not in those with the greatest reduction in LDL cholesterol levels.”
In yet another study [5] it was found that when treating with statins, those with the highest levels of inflammatory markers at the start of the study derived the most benefit, irrespective of initial cholesterol
levels.
Evidence that statins don’t work through their cholesterol-reducing effect comes from other evidence, including the findings that:
•Statins substantially reduce the risk of stroke, despite the fact that raised cholesterol levels are a weak or non-existent risk factor for stroke [6,7].
•Statins are claimed to reduce CVD risk in individuals who have ‘normal’ or even ‘low’ cholesterol levels [8].
•More intensive cholesterol reduction does not necessarily lead to improved outcomes [9].
Despite what the authors of the recent Lancet review would have us believe, there is considerable evidence that statins primarily work through mechanism that are independent of their cholesterol-reducing effects.
Stepping aside from the science for a moment, let’s also perhaps inject some common sense. Let us not forget that cholesterol is a natural constituent of the body that is a major component in cell membranes, the brain, steroid hormones (including sex hormones) and vitamin D (which appears to have major disease-protective properties). It simply does not make sense to me that driving levels of this key substance to lower and lower levels if, in and of itself, beneficial to health. We would not make the case for driving levels of, say, sodium to lower and lower levels, would we? Or blood sugar levels?
All rationality and common sense seems to fly out of the window when certain doctors and scientists start talking about cholesterol. And when it comes to the science, it’s clear that many are ignorant of or choose to ignore the stacks of evidence that clearly contradict their stance.
References:
1. Cholesterol Treatment Trialists’ Collaboration. Efficacy and safety of more intensive lowering of LDL cholesterol: a meta-analysis of data from 170,000 participants in 26 randomised trials. Lancet 9 November 2010 [epub ahead of print]
2. La Rosa JC, et al. Intensive lipid lowering with atorvastatin in patients with stable coronary disease. N Engl J Med. 2005;352(14):1425-35
3. Ridker PM, et al. C-reactive protein levels and outcomes after statin therapy. N Engl J Med 2005;352(1):20-8
4. Nissen SE, et al. Statin therapy, LDL cholesterol, C-reactive protein and coronary artery disease. N Engl J Med. 2005;352(1):29-38
5. Ridker PM, et al. Inflammation, pravastatin, and the risk of coronary events after myocardial infarction in patients with average cholesterol levels. Cholesterol and Recurrent Events (CARE) Investigators. Circulation. 1998;98(9):839-44
6. Cholesterol, diastolic blood pressure, and stroke: 13,000 strokes in 450,000 people in 45 prospective cohorts. Prospective studies collaboration. Lancet 1995;346(8991-8992):1647-53.
7. Imamura T, et al. LDL cholesterol and the development of stroke subtypes and coronary heart disease in a general Japanese population: the Hisayama study. Stroke 2009;40(2):382-8
8. Ridker PM, et al, JUPITER Study Group. Rosuvastatin to prevent vascular events in men and women with elevated C-reactive protein. N Engl J Med 2008;359(21):2195-2207
9. Kastelein JJ, et al, ENHANCE Investigators. Simvastatin with or without ezetimibe in familial hypercholesterolemia. N Engl J Med 2008;358(14):1431-1443
Tuesday, November 9, 2010
More Misleading Information and Propaganda from the British Heart Foundation
Good new article by Justin Smith author of "$29 billion reasons to lie about cholesterol"
===================================================
More Misleading Information and Propaganda from the British Heart Foundation
Tuesday, November 9, 2010 at 11:30AM
Here is the latest headline from the British Heart Foundation (BHF):
“Research by BHF-funded scientists has shown that when it comes to cholesterol, ‘lower seems to be better’ for protecting us against heart attacks... The researchers looked at the effects of increasing the dosage of statins, a medicine that reduces cholesterol. They showed that a bigger drop in cholesterol – from more intensive treatment with statins – cut risks even more.”
This refers to a study just released in the Lancet. This study, and the media hype that the BHF have created about it, is nothing more than an attempt to confuse and mislead people.
If you read the headlines and the summary report you could certainly be forgiven for thinking that statins are wonder drugs and cholesterol really is humanity’s nemesis. This study did indeed find a reduction in heart attacks associated with more intensive use of statin drugs. However, there are at least four major reasons why the results are misleading.
The first reason is that the reduction in risk quoted in the interpretation of the study refers to a reduction in LDL cholesterol that is not normally seen in real life. This exaggerates the perceived benefits.
The interpretation refers to reductions in LDL levels of 2-3 mmol/l. The authors state that this reduction in LDL cholesterol would reduce the risk of a vascular event (such as a heart attack) by 40-50 percent.
Well, LDL cholesterol is typically around 2-3 mmol/l anyway, so the suggestion that it could be reduced by 2-3 mmol/l is nonsense – most people would have to be clinically dead to achieve this drastic reduction. So, the suggested risk reduction is completely academic and for most people could never happen.
The second reason is that, as usual, relative percentages are used instead of absolute percentages. This problem is ubiquitous in statin clinical trials and I have commented on it many times before. The risk reductions of 40-50 percent are relative percentages, which can only mislead people. In real terms, the percentages come down to single digits or less.
The third reason is that, as usual, the issue of deaths from all causes is not addressed. Statins can reduce the risk of suffering a heart attack or other cardiovascular event, but at the same time, these drugs can also increase the risk of dying from other causes, and overall, there is usually no net benefit.
There is not much point in taking an expensive medication if the risk for one disease is reduced at the cost of increasing the risk for another disease within the same time period.
I called the BHF today and asked them for the data concerning deaths from all causes. The press office said they didn't know, but they did kindly send me the full report for the study.
In this trial, the risk of dying from any cause was reduced from 2.3 percent to 2.1 percent. So, in real terms, the benefit of more intensive statin use equates to a risk reduction of just 0.2 percent.
But even this meagre 0.2 percent risk reduction may not be experienced by real people who take statins. This issue relates to the fourth problem with this study.
The forth reason why the results are misleading is that the analysis did not distinguish between people at a lower risk for a heart attack and people at a higher risk.
Around 7 million people are taking statins in England alone, and in America it is estimated that more than 20 million people may be taking them. The vast majority of these people are taking statins for primary prevention. This means that they do not have cardiovascular disease but are given the medications in the hope of preventing future disease.
To date, there is no convincing evidence that statins provide any net benefit to people when they are taken for primary prevention - they do not reduce the overall death rate. This was the conclusion of the latest analysis in the Archives of Internal Medicine.
The analysis that the BHF are supporting includes data from higher risk groups - the results do not represent the majority of people who currently take a statin.
===================================================
More Misleading Information and Propaganda from the British Heart Foundation
Tuesday, November 9, 2010 at 11:30AM
Here is the latest headline from the British Heart Foundation (BHF):
“Research by BHF-funded scientists has shown that when it comes to cholesterol, ‘lower seems to be better’ for protecting us against heart attacks... The researchers looked at the effects of increasing the dosage of statins, a medicine that reduces cholesterol. They showed that a bigger drop in cholesterol – from more intensive treatment with statins – cut risks even more.”
This refers to a study just released in the Lancet. This study, and the media hype that the BHF have created about it, is nothing more than an attempt to confuse and mislead people.
If you read the headlines and the summary report you could certainly be forgiven for thinking that statins are wonder drugs and cholesterol really is humanity’s nemesis. This study did indeed find a reduction in heart attacks associated with more intensive use of statin drugs. However, there are at least four major reasons why the results are misleading.
The first reason is that the reduction in risk quoted in the interpretation of the study refers to a reduction in LDL cholesterol that is not normally seen in real life. This exaggerates the perceived benefits.
The interpretation refers to reductions in LDL levels of 2-3 mmol/l. The authors state that this reduction in LDL cholesterol would reduce the risk of a vascular event (such as a heart attack) by 40-50 percent.
Well, LDL cholesterol is typically around 2-3 mmol/l anyway, so the suggestion that it could be reduced by 2-3 mmol/l is nonsense – most people would have to be clinically dead to achieve this drastic reduction. So, the suggested risk reduction is completely academic and for most people could never happen.
The second reason is that, as usual, relative percentages are used instead of absolute percentages. This problem is ubiquitous in statin clinical trials and I have commented on it many times before. The risk reductions of 40-50 percent are relative percentages, which can only mislead people. In real terms, the percentages come down to single digits or less.
The third reason is that, as usual, the issue of deaths from all causes is not addressed. Statins can reduce the risk of suffering a heart attack or other cardiovascular event, but at the same time, these drugs can also increase the risk of dying from other causes, and overall, there is usually no net benefit.
There is not much point in taking an expensive medication if the risk for one disease is reduced at the cost of increasing the risk for another disease within the same time period.
I called the BHF today and asked them for the data concerning deaths from all causes. The press office said they didn't know, but they did kindly send me the full report for the study.
In this trial, the risk of dying from any cause was reduced from 2.3 percent to 2.1 percent. So, in real terms, the benefit of more intensive statin use equates to a risk reduction of just 0.2 percent.
But even this meagre 0.2 percent risk reduction may not be experienced by real people who take statins. This issue relates to the fourth problem with this study.
The forth reason why the results are misleading is that the analysis did not distinguish between people at a lower risk for a heart attack and people at a higher risk.
Around 7 million people are taking statins in England alone, and in America it is estimated that more than 20 million people may be taking them. The vast majority of these people are taking statins for primary prevention. This means that they do not have cardiovascular disease but are given the medications in the hope of preventing future disease.
To date, there is no convincing evidence that statins provide any net benefit to people when they are taken for primary prevention - they do not reduce the overall death rate. This was the conclusion of the latest analysis in the Archives of Internal Medicine.
The analysis that the BHF are supporting includes data from higher risk groups - the results do not represent the majority of people who currently take a statin.
Monday, August 2, 2010
Low cholesterol levels associated with depression and other mental health issues
Dr John Briffa has a good article which states in the introductory paragraph...
"I know that some doctors and scientists would have us believe that, where cholesterol is concerned, "lower is better", but I have real difficulty mustering any entheusiasm for this stance. And one major reason for this is the fact that low levels of cholesterol are associated with enhanced risk of death, perhaps most notably from increased risk of cancer."
Please read the complete article here.
"I know that some doctors and scientists would have us believe that, where cholesterol is concerned, "lower is better", but I have real difficulty mustering any entheusiasm for this stance. And one major reason for this is the fact that low levels of cholesterol are associated with enhanced risk of death, perhaps most notably from increased risk of cancer."
Please read the complete article here.
Wednesday, July 21, 2010
The True Cause of Heart Disease – Part Two
"Dr. Dwight Lundell is on the front line fighting a health war. His mission is to find a cure for heart disease. And he believes he has done just that."
Read the full article at Total Health Breakthroughs
Read the full article at Total Health Breakthroughs
Sunday, July 18, 2010
Ten Commandments for Avoiding CHD
Not a particularly new article but one I just re-read by Sally Fallon and Mary G. Enig, PhD. It appeared in Wise Traditions in Food, Farming and the Healing Arts, the quarterly magazine of the Weston A. Price Foundation, Spring 2001.
The following excerpt appears well into the article and is a good 'cut-to-the-chase' list to summarize what to do about this scourge. I encourage all who are interested to read the full article found here.
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Again, please read and learn from the full article.
The following excerpt appears well into the article and is a good 'cut-to-the-chase' list to summarize what to do about this scourge. I encourage all who are interested to read the full article found here.
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Ten Commandments for Avoiding CHD
- Don't smoke. If you find it impossible to quit, at least try to cut back and smoke only additive-free cigarettes. Smokers should avoid polyunsaturated oils at all costs. Saturated fats and vitamins A and D are particularly protective of the lungs.
- Exercise regularly but you needn't overdo. A brisk daily walk, 10 minutes on the trampoline, swimming, and sports are all appropriate.
- Avoid overweight by eating nutrient-dense foods and keeping sweets to a minimum, but avoid crash dieting.
- Don't work too hard. Counteract stress by doing something that you love to do everyday. During periods of unavoidable hardship or loss, increase consumption of foods rich in protective nutrients.
- As much as possible, avoid exposure to fumes, chemicals, pollutants and pesticides.
- Avoid all processed foods labeled "lowfat" or that contain polyunsaturated vegetable oils, hydrogenated fats, white flour, refined sugar and additives.
- Consume high-quality animal products including a variety of seafood and milk, butter, cheese, eggs, meat, fats and organ meats from animals raised on green pasture.
- Consume a variety of fresh vegetables and fruits, preferably organically grown.
- Ensure sufficient mineral intake by using whole dairy products; bone broths; and whole grains, legumes and nuts that have been properly prepared to reduce phytic acid and other factors that block mineral absorption.41
- Supplement the diet with foods rich in protective factors including small amounts of cod liver oil (vitamins A and D); wheat germ oil (vitamin E); flax oil (omega-3 fatty acids); kelp (iodine); brewers yeast (B vitamins); desiccated liver (vitamin B12); rose hip or acerola powder (vitamin C); and coconut oil (antimicrobial fatty acids).
Again, please read and learn from the full article.
Wednesday, July 14, 2010
Dr. Dwight Lundell on omega-3s and CLA
Thursday, September 06, 2007
Dr. Dwight Lundell on omega-3s and CLA
An interview with Dr. Dwight Lundell, cardiac surgeon and author of the new book, "The Cure for Heart Disease."
Dr. Lundell comes to us with a unique pedigree. He is a cardiothoracic surgeon practicing in the Phoenix, Arizona, area. Despite having performed thousands of coronary bypass operations, including numerous "off-pump" procedures earning him a place in the Beating Heart Hall of Fame and a listing in Phoenix Magazine’s Top Doctors for 10 years, more recently Dr. Lundell has turned his attentions away from traditional surgical treatment and towards prevention of heart disease and.
In particular, Dr. Lundell is a vocal advocate for omega-3 fatty acids from fish oil and conjugated linoleic acid, or CLA.
When I heard about Dr. Lundell’s unique perspectives, I asked him if he’d like to tell us a little more about his ideas. Here follows a brief interview with Dr. Lundell.
You’re a vocal advocate of the role of omega-3 fatty acids from fish oil in heart disease prevention. Can you tell us how you use it?
In my book, I recommend 3 g of fish oil daily. This would normally yield about 1000 mg of EPA and DHA depending on the concentration of the supplement. This is approximately the dose that reduced sudden cardiac death by 50%, and all cause death, by 25% in patients with previous heart attack.
In patients with signs of chronic inflammation such as heart disease, obesity, arthritis, metabolic syndrome or depression or in those patients with elevation of CRP, I would recommend higher doses, 2000 to 3000 mg per day of EPA and DHA. The FDA has approved up to 3400 mg for treating patients with severely elevated triglycerides.
I personally take a 2000 mg EPA and DHA per day because I have calcium in my coronary arteries.
Of course, in the Track Your Plaque program we track coronary calcium scores. Do you track any measures of atherosclerosis in your patients to chart progression or regression?
Carotid ultrasound with measurement of IMT [intimal-medial thickness] has been shown to be a good surrogate marker for coronary disease, as has vascular reactivity in the arm. CT scanning with calcium scoring is a direct marker of coronary disease. CT does not differentiate between stable or unstable plaque but there is no good noninvasive way of doing this.
The dramatic value of CT scan calcium scoring is to demonstrate to people that they actually do have coronary disease and to motivate them to make the necessary lifestyle and nutritional changes to reduce it. CT scan with calcium scoring is a direct way to measure the progression or regression of coronary artery disease. If there is a choice between a direct measurement and indirect measurement, always choose the direct method.
Every patient treated with CLA in my clinic, experienced significant reductions in C-reactive protein. These patients were also on a weight-loss program, so I can't prove whether it was the CLA or the weight-loss that improved their inflammatory markers. In the animal model for arteriosclerosis, CLA has a dramatic effect of reducing and preventing plaque. This has not yet been proven in humans.
Normally, when people lose weight 20% or more of the loss is lean body mass (muscle) this lowers the metabolic rate and frustrates further weight-loss. My patient, from teenagers to retirees, lost no lean body mass and continued to have satisfactory weight-loss when CLA was used as part of the plan.
In reading your book, your use of conjugated linoleic acid (CLA) as a principal ingredient struck me. Can you elaborate on why you choose to have your patients take CLA?
My enthusiasm for CLA is based on:
1) Safety―this is of paramount importance. Animal toxicity studies have been done, as well as multiple parameters measured in human studies, both of these are well reviewed recently in the American Journal of Clinical Nutrition (2004:79(suppl)1132s). CLA, a naturally-occurring substance, is not toxic or harmful to animals or humans. The only negative report is by Riserus in Circulation (2002), where he found an elevated c- reactive protein; however, he used a preparation that is not commercially available and not found in nature as a single isomer.
2) Effectiveness―also critically important. A recent meta-analysis [a reanalysis of compiled data] in the American Journal of Clinical Nutrition (2007; 85:1203-1211) demonstrated the effectiveness of CLA in causing loss of body fat in humans. The study also reconfirmed the safety of CLA.
Since we now know that atherosclerosis is an inflammatory disorder, any strategy that reduces low-grade inflammation without significant side effects would seem to be beneficial in the treatment and prevention of atherosclerosis. CLA not only has antioxidant properties, but it modulates inflammatory cascade at multiple points. CLA reduces PGE2 (in much the same way as omega-3) CLA also has been shown to reduce IL-2, tumor necrosis factor-alpha and Cox–2. It reduces platelet deposition and macrophage accumulation in plaques. It also has some beneficial effect in the PPAR [peroxisome proliferator-activated receptors, important for lipid and inflammatory-mediator metabolism] area.
Part of the effect of CLA may be because it reduces fat mass and thus the amount of pro-inflammatory cytokines produced by fat cells.
I reiterate and fully admit that CLA has not been shown to have any effect on atherosclerosis in human beings. However, the results in the standard animal models for atherosclerosis (rabbits, hamsters,APO-E knockout mice) are very dramatic.
From all I know, it appears that the effective dose for weight loss and the animal studies in atherosclerosis would be equal to about 3 g of CLA per day. The anti-inflammatory properties of CLA seem to work better in the presence of adequate blood levels of omega-3.
I’m curious how and why a busy cardiothoracic surgeon would transform his practice so dramatically. Was there a specific event that triggered your change?
The transition from a very busy surgical practice to writing and speaking about the prevention of coronary disease has not been particularly easy, but it has been very interesting. I can't really point to any specific epiphany, it was a general feeling of frustration that we were not making any progress in curing heart disease, which is what I thought I was doing when I began my medical career.
Of course, I enjoyed the technical advances, the dramatic life-saving things that you do and I did on a daily basis. American medicine is spectacularly good at managing crises and spectacularly horrible at preventing those crises.
The lipid hypothesis is old and tired, even the most aggressive statin therapy reduces risk of heart attack by about 30% in a relatively small subset of people. It's interesting that we're now looking at statins as an anti-inflammatory agent.
Thanks, Dr. Lundell. We look forward to future conversations as your experience with CLA and heart disease prevention and reversal develops!
More about Dr. Lundell's book, The Cure for Heart Disease can be found at http://www.thecureforheartdisease.net.
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