Though I am usually suspicious of the terms 'correlates with', 'associated with', and 'increases/decreases risk of' etc. because when I'm lazy in my thinking I want to read them as indicating a cause not what they really are - a possible reason for much more investigation, I refer you to the following exerpt of an article by Jenny at Diabetes Update
".
.
.
3. Higher Levels of Cholesterol of ALL Types Correlates with LESS Likelihood of Alzheimers. It has long been known--though doctors have been brainwashed into ignoring it--that statins can cause permanent dementia, especially in older patients. Could it be because cholesterol is protective to the brain? This study would make you wonder.
It followed 1,130 adults 65 or older in New York City with no history of dementia or cognitive impairment.
Higher levels of HDL-C (>55 mg/dL) were associated with a decreased risk of both probable and possible A[lzheimers] D[isease] and probable AD compared with lower HDL-C levels (hazard ratio, 0.4; 95% confidence interval, 0.2-0.9; P = .03 and hazard ratio, 0.4; 95% confidence interval, 0.2-0.9; P = .03). In addition, higher levels of total and non–HDL-C were associated with a decreased risk of AD in analyses adjusting for age, sex, education, ethnic group, and APOE e4 genotype.
,
,
,
"
Wednesday, January 12, 2011
The Truth About Cholesterol
Some quotes from Dr. Graveline
"For the past four decades we have all been subjected to an intense and carefully calculated program of brainwashing to believe that cholesterol is our enemy. I am sorry to admit that I was one of thousands of doctors trained to absorb this propaganda without question. In retrospect I am angry to have been so completely enmeshed in this web of deceit."
"Like puppets we wrote millions of prescriptions for whatever cholesterol buster the drug companies were promoting at the time. I was just like all the other doctors - doing what I was told, never suspecting we had functionally become employees of the pharmaceutical industry. In truth there has never been a scientific study that has been able to demonstrate a causal link between cholesterol and heart disease. The reality is that cholesterol in its natural form cannot be harmful."
".. statins significantly promote diabetes..."
"Far from being harmful, cholesterol is perhaps the most important biochemical in our bodies."
"cholesterol is the precursor for a whole class of hormones known as the steroid hormones that are absolutely critical for life as we know it."
"The large amounts of cholesterol required for both the formation and function of these basic structures argues strongly against the rationality of excessively liberal use of drugs such as statins that inhibit cholesterol synthesis."
==========================
Read the full article here. And consider buying one or more of his books.
"For the past four decades we have all been subjected to an intense and carefully calculated program of brainwashing to believe that cholesterol is our enemy. I am sorry to admit that I was one of thousands of doctors trained to absorb this propaganda without question. In retrospect I am angry to have been so completely enmeshed in this web of deceit."
"Like puppets we wrote millions of prescriptions for whatever cholesterol buster the drug companies were promoting at the time. I was just like all the other doctors - doing what I was told, never suspecting we had functionally become employees of the pharmaceutical industry. In truth there has never been a scientific study that has been able to demonstrate a causal link between cholesterol and heart disease. The reality is that cholesterol in its natural form cannot be harmful."
".. statins significantly promote diabetes..."
"Far from being harmful, cholesterol is perhaps the most important biochemical in our bodies."
"cholesterol is the precursor for a whole class of hormones known as the steroid hormones that are absolutely critical for life as we know it."
"The large amounts of cholesterol required for both the formation and function of these basic structures argues strongly against the rationality of excessively liberal use of drugs such as statins that inhibit cholesterol synthesis."
==========================
Read the full article here. And consider buying one or more of his books.
Friday, December 31, 2010
Correlation between cholesterol and heart disease
See this short YouTube video showing data of cholesterol vs heart disease presented by Dr. Malcolm Kendrick M.D. for most European countries.
Dr. Malcolm Kendrick M.D. looks at Cholesterol
Here are the last few paragraphs of Dr. Malcolm Kendrick M.D. looks at Cholesterol. Click the link and read what he has to say
============================================
Now that I know that cholesterol has nothing to do with heart disease, and that lowering it with statins is a complete waste of time, I find myself in the position of the little boy who points out that the Emperor has no Clothes. With one rather important difference.
Even though the ‘experts' have been made aware of it many times, they care not that this particular emperor has no clothes. Or, to be more accurate, they cannot and will not allow themselves to accept that it might be true. For to accept this would be far too humiliating for the great and the good. Which, I suppose, is why people become so enraged when anyone dares to point out the truth.
It is a slight comfort to know that in fifty years (hopefully many fewer than this), people will look back at cholesterol lowering and say ‘You did WHAT?' Were you MAD? Don't you know that cholesterol is absolutely vital for human health? Didn't you realise that blocking cholesterol synthesis would directly lead to nerve cell damage, muscle destruction, liver obliteration and cancer?
‘My God, you presided over the greatest iatrogenic medical disaster ever.' I, of course, will probably be dead by then. But at least I will not have poisoned my metabolism with statins.
Dr. Malcolm Kendrick (MbChB MRCGP) M.D.
Dr. Kendrick has worked in family practice for almost twenty years.
He has specialized in heart disease and set up the on-line educational website for the European Society of Cardiology.
He is a peer-reviewer for the British Medical Journal. He is a member of the International Network of Cholesterol Skeptics (THINCS) as he does not believe that a high cholesterol level causes heart disease.
============================================
Now that I know that cholesterol has nothing to do with heart disease, and that lowering it with statins is a complete waste of time, I find myself in the position of the little boy who points out that the Emperor has no Clothes. With one rather important difference.
Even though the ‘experts' have been made aware of it many times, they care not that this particular emperor has no clothes. Or, to be more accurate, they cannot and will not allow themselves to accept that it might be true. For to accept this would be far too humiliating for the great and the good. Which, I suppose, is why people become so enraged when anyone dares to point out the truth.
It is a slight comfort to know that in fifty years (hopefully many fewer than this), people will look back at cholesterol lowering and say ‘You did WHAT?' Were you MAD? Don't you know that cholesterol is absolutely vital for human health? Didn't you realise that blocking cholesterol synthesis would directly lead to nerve cell damage, muscle destruction, liver obliteration and cancer?
‘My God, you presided over the greatest iatrogenic medical disaster ever.' I, of course, will probably be dead by then. But at least I will not have poisoned my metabolism with statins.
Dr. Malcolm Kendrick (MbChB MRCGP) M.D.
Dr. Kendrick has worked in family practice for almost twenty years.
He has specialized in heart disease and set up the on-line educational website for the European Society of Cardiology.
He is a peer-reviewer for the British Medical Journal. He is a member of the International Network of Cholesterol Skeptics (THINCS) as he does not believe that a high cholesterol level causes heart disease.
Preventing and Reversing Heart Disease, Part Three
A Man with Progressive Coronary Artery Disease Unresponsive to Statins by Jeffrey Dach MD
62 year old Jim came to see me after his third cardiac stent in 10 years. About a year ago, Jim noticed a "tight feeling" in his chest radiating to his throat, was rushed to the ER, and doctors found he was having a heart attack. A coronary angiogram showed extensive coronary artery disease with irregular plaque formation virtually everywhere in his arteries. For the past 10 years, Jim had been under the care of top cardiologists who prescribed a statin cholesterol drug, and Jim's cholesterol was kept below 140 all this time. Jim's heart disease progressed relentlessly in spite of the low total cholesterol numbers clearly showing another cause at work here. It's obviously not the total cholesterol.
,,,
Our Approach
I must preface these remarks with our approach to prevention and reversal of heart disease which is outlined in Part One and Part Two of this series. We credit and rely heavily on the "Track Your Plaque Program " by William Davis MD.
,,,
=======================================
Read the full article here.
I was so interested in this article because it had many similarities to my own situation. Please read all articles in Dr. Dach's series. Part 1, Part 2, Part 3.
62 year old Jim came to see me after his third cardiac stent in 10 years. About a year ago, Jim noticed a "tight feeling" in his chest radiating to his throat, was rushed to the ER, and doctors found he was having a heart attack. A coronary angiogram showed extensive coronary artery disease with irregular plaque formation virtually everywhere in his arteries. For the past 10 years, Jim had been under the care of top cardiologists who prescribed a statin cholesterol drug, and Jim's cholesterol was kept below 140 all this time. Jim's heart disease progressed relentlessly in spite of the low total cholesterol numbers clearly showing another cause at work here. It's obviously not the total cholesterol.
,,,
Our Approach
I must preface these remarks with our approach to prevention and reversal of heart disease which is outlined in Part One and Part Two of this series. We credit and rely heavily on the "Track Your Plaque Program " by William Davis MD.
,,,
=======================================
Read the full article here.
I was so interested in this article because it had many similarities to my own situation. Please read all articles in Dr. Dach's series. Part 1, Part 2, Part 3.
Saturday, December 18, 2010
Vitamin D: Deficiency vs optimum level
Vitamin D: Deficiency vs optimum level Saturday, December 18, 2010
Dr. James Dowd of the Vitamin D Cure posted his insightful comments regarding the Institute of Medicine's inane evaluation of vitamin D.
Dr. Dowd hits a bullseye with this remark:
The IOM is focusing on deficiency when it should be focusing on optimal health values for vitamin D. The scientific community continues to argue about the lower limit of normal when we now have definitive pathologic data showing that an optimal vitamin D level is at or above 30 ng/mL. Moreover, if no credible toxicity has been reported for vitamin D levels below 200 ng/mL, why are we obsessing over whether our vitamin D level should be 20 ng/mL or 30 ng/mL?
Yes, indeed. Have no doubts: Vitamin D deficiency is among the greatest public health problems of our age; correction of vitamin D (using the human form of vitamin D, i.e., D3 or cholecalciferol, not the invertebrate or plant form, D2 or ergocalciferol) is among the most powerful health solutions.
I have seen everything from relief from winter "blues," to reversal of arthritis, to stopping the progression of aortic valve disease, to partial reversal of dementia by achieving 25-hydroxy vitamin D levels of 50 ng/ml or greater. (I aim for 60-70 ng/ml.)
The IOM's definition of vitamin D adequacy rests on what level of 25-hydroxy vitamin D reverses hyperparathyroidism (high PTH levels) and rickets. Surely there is more to health than that.
Dr. Dowd and vocal vitamin D advocate, Dr. John Cannell, continue to champion the vitamin D cause that, like many health issues, conradicts the "wisdom" of official organizations like the IOM.
Dr. James Dowd of the Vitamin D Cure posted his insightful comments regarding the Institute of Medicine's inane evaluation of vitamin D.
Dr. Dowd hits a bullseye with this remark:
The IOM is focusing on deficiency when it should be focusing on optimal health values for vitamin D. The scientific community continues to argue about the lower limit of normal when we now have definitive pathologic data showing that an optimal vitamin D level is at or above 30 ng/mL. Moreover, if no credible toxicity has been reported for vitamin D levels below 200 ng/mL, why are we obsessing over whether our vitamin D level should be 20 ng/mL or 30 ng/mL?
Yes, indeed. Have no doubts: Vitamin D deficiency is among the greatest public health problems of our age; correction of vitamin D (using the human form of vitamin D, i.e., D3 or cholecalciferol, not the invertebrate or plant form, D2 or ergocalciferol) is among the most powerful health solutions.
I have seen everything from relief from winter "blues," to reversal of arthritis, to stopping the progression of aortic valve disease, to partial reversal of dementia by achieving 25-hydroxy vitamin D levels of 50 ng/ml or greater. (I aim for 60-70 ng/ml.)
The IOM's definition of vitamin D adequacy rests on what level of 25-hydroxy vitamin D reverses hyperparathyroidism (high PTH levels) and rickets. Surely there is more to health than that.
Dr. Dowd and vocal vitamin D advocate, Dr. John Cannell, continue to champion the vitamin D cause that, like many health issues, conradicts the "wisdom" of official organizations like the IOM.
Thursday, December 2, 2010
Depression, Statins and Cardiologists
Cardiologists know that treating depression likely will benefit patients complaining of cardiovascular problems, but likely are completely unaware statin drugs may be a major contributing factor.
According to a report from a National Heart, Lung and Blood Institute (NHLBI) Working Group, and published simultaneously in Annals of Behavioral Medicine and Psychosomatic Medicine, up to 20 percent of patients with heart disease meet the American Psychiatric Association's criteria for major depression, and identifying better treatments for depression in this population could lead to improved medical, financial and psychosocial outcomes.
At almost the same time Goldstein and others of the Department of Physiology, The Hebrew University-Hadassah Medical School, Jerusalem, Israel, report in Biol Psychiatry 60(5): 491-9 on the involvement of endogenous digitalis-like compounds in depressive disorders. Cholesterol is the major precursor of these endogenous digitalis-like compounds synthesized in our adrenals.
We might have predicted the effect of this new substance in something like heart failure because of the word digitalis but who would have predicted its impact on bipolar disorder and other forms of depressive reactions?
These pleotrophic effects are due to the fact that the cellular effect of this class of drugs is on the sodium, potassium and ATPase cell wall channels in such a way as to induce calcium retention within the cells leading to altered response.
In a brain cell, mania can result from increased membrane excitability and depression from decreased transmitter release and these are only a few of the effects of these endogenous digitalis-like compounds synthesized from cholesterol.
What of the statin drugs with their ability to reduce natural cholesterol levels to values far below normal for the individual? Is there any real doubt that we now have another reason for the association of statin use with depression?
The drug industry proudly hails the ability of Lipitor®, Crestor® and Vytorin® and others to lower blood cholesterol some 40-50%. We already know what this does to the cognitive ability of many people and the erectile function of many others. And now we find another major body system completely dependent upon adequate cholesterol levels.
In addition to this mechanism for altered emotional status we also have others and all are tied to cholesterol availability. The first of these is dolichol associated glycoprotein process for neurohormone synthesis. Every emotion and mood we have are governed by the makeup of sugars and protein fragments, linked like popcorn on a string, to make up our neurohormones.
The second involves our glial cell mediated production of "on-demand" cholesterol synthesis for memory synapses, critical to the development of psychological manifestations. The third has to do with G-protein coupled receptors responsible for neurotransmitter coupling and felt to be the most important mechanism for perception of environmental factor cells.
All three of these are cholesterol dependent and therefore sensitive to statin use. The effects can be so subtle as to be hardly noticeable or so severe as to support the diagnosis of psychotic illness.
How could the designers of lucrative statin drugs two decades ago know of these effects? They obviously could not and now after 20 years of use have some very real economic reasons for not wanting to hear this. One might say that the research community is now documenting adverse reactions to statin drug use that should have been defined and warned of long before marketing.
Duane Graveline MD MPH
Former USAF Flight Surgeon
Former NASA Astronaut
Retired Family Doctor
Updated December 2010
According to a report from a National Heart, Lung and Blood Institute (NHLBI) Working Group, and published simultaneously in Annals of Behavioral Medicine and Psychosomatic Medicine, up to 20 percent of patients with heart disease meet the American Psychiatric Association's criteria for major depression, and identifying better treatments for depression in this population could lead to improved medical, financial and psychosocial outcomes.
At almost the same time Goldstein and others of the Department of Physiology, The Hebrew University-Hadassah Medical School, Jerusalem, Israel, report in Biol Psychiatry 60(5): 491-9 on the involvement of endogenous digitalis-like compounds in depressive disorders. Cholesterol is the major precursor of these endogenous digitalis-like compounds synthesized in our adrenals.
We might have predicted the effect of this new substance in something like heart failure because of the word digitalis but who would have predicted its impact on bipolar disorder and other forms of depressive reactions?
These pleotrophic effects are due to the fact that the cellular effect of this class of drugs is on the sodium, potassium and ATPase cell wall channels in such a way as to induce calcium retention within the cells leading to altered response.
In a brain cell, mania can result from increased membrane excitability and depression from decreased transmitter release and these are only a few of the effects of these endogenous digitalis-like compounds synthesized from cholesterol.
What of the statin drugs with their ability to reduce natural cholesterol levels to values far below normal for the individual? Is there any real doubt that we now have another reason for the association of statin use with depression?
The drug industry proudly hails the ability of Lipitor®, Crestor® and Vytorin® and others to lower blood cholesterol some 40-50%. We already know what this does to the cognitive ability of many people and the erectile function of many others. And now we find another major body system completely dependent upon adequate cholesterol levels.
In addition to this mechanism for altered emotional status we also have others and all are tied to cholesterol availability. The first of these is dolichol associated glycoprotein process for neurohormone synthesis. Every emotion and mood we have are governed by the makeup of sugars and protein fragments, linked like popcorn on a string, to make up our neurohormones.
The second involves our glial cell mediated production of "on-demand" cholesterol synthesis for memory synapses, critical to the development of psychological manifestations. The third has to do with G-protein coupled receptors responsible for neurotransmitter coupling and felt to be the most important mechanism for perception of environmental factor cells.
All three of these are cholesterol dependent and therefore sensitive to statin use. The effects can be so subtle as to be hardly noticeable or so severe as to support the diagnosis of psychotic illness.
How could the designers of lucrative statin drugs two decades ago know of these effects? They obviously could not and now after 20 years of use have some very real economic reasons for not wanting to hear this. One might say that the research community is now documenting adverse reactions to statin drug use that should have been defined and warned of long before marketing.
Duane Graveline MD MPH
Former USAF Flight Surgeon
Former NASA Astronaut
Retired Family Doctor
Updated December 2010
Sunday, November 21, 2010
New Study Confirms Statins Cause Diabetes
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
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
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
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