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
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.
===
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.
===
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.
The True Cause of Heart Disease
via Total Health Breakthroughs by Ian Robinson on 7/14/10
Conventional wisdom tells us that high cholesterol is the cause of heart disease. But Dr. Dwight Lundell is fighting to expose this dangerous mainstream myth.
Dr. Lundell is a pioneer and leading expert in this field. He has enjoyed a long and a distinguished career, leading his peers to new breakthroughs.. He spent 25 years as a cardiovascular surgeon and performed over 5,000 heart surgeries.
His experience in cardiovascular and thoracic surgery includes certification by the American Board of Surgery, the American Board of Thoracic Surgery, and the Society of Thoracic Surgeons. He was a pioneer in “Off-Pump” heart surgery, reducing surgical complications and recovery times. He’s in the “Beating Heart Hall of Fame” and has been listed in Phoenix Magazine’s “Top Doctors” for 10 years.
He has been recognized by his peers as a leader and has served as Chief resident at the University of Arizona and Yale University Hospitals. He later served as Chief of Staff and Chief of Surgery.
He was also one of the founding partners of the Lutheran Heart Hospital which became the second largest heart hospital in the U.S.
Dr. Lundell recently agreed to grant us an in-depth and revealing interview about the pioneering work he is currently conducting. It’s our privilege and pleasure to share part one of that exclusive interview with you today.
THB: You are the author of a controversial heart-health book called The Great Cholesterol Lie. The book challenges conventional wisdom and accepted medical theories. What’s been the response to this book?
Dr. Lundell: The response to the book has been overwhelming. I regularly correspond with people from around the world who are enjoying better health from the new understandings they gained from learning about inflammation and heart disease.
THB: That’s good to hear. It’s a seminal book that charts your professional journey as a cardiac surgeon. And, more importantly, reveals your gradual discovery of the true cause of heart disease.
If you could go back in time to when you were a young cardiac surgeon… what would you tell yourself and would you take a different path?
Dr. Lundell: I was dedicated to treating heart disease and passionate about saving lives. It was my responsibility to provide patients with a second chance.
As a young cardiac surgeon in the 1980s coronary bypass operation was the only effective treatment for people afflicted with severe coronary artery disease. So, as you can imagine, this was a very exciting time. Our ability to help people increased and the risks of surgery decreased as techniques and technology improved.
The scientific consensus at that time was elevated cholesterol levels in the blood cause a gradual deposition of cholesterol in the lumen of the blood vessel so two treatment forces were obvious: lower the levels of cholesterol in the blood or do an operation to detour the blood around the accumulated plaque thus restoring flow and heart function.
Rather than looking at more effective ways to lower blood cholesterol, there was relatively little research going on as to what was causing plaque. Everyone settled on the idea that it was as simple as controlling fat and cholesterol.
Then new research was in part driven by industry and not basic science. As balloon angioplasty emerged as an alternative to open heart surgery, the companies that produce the balloons became concerned by high rates of re-stenosis. They began funding studies to understand exactly what was happening biologically to cause the re-stenosis. (Re-stenosis means a re-narrowing of the artery after angioplasty or a stent has been inserted.)
This stimulated a lot of research and culminated in the seminal article published in 1999 in the New England Journal of Medicine announcing that “atherosclerosis [is] an inflammatory disease.”
THB: How did you discover that the true cause of heart disease was inflammation?
Dr. Lundell: I was excited to understand this new research because in the operating room I had observed the classic signs of inflammation around the coronary artery and was very disappointed that surgery, although effective at relieving symptoms and extending life, was not a cure for heart disease.
Many brilliant scientists and university centers continued to do more research that confirmed the basis for coronary disease was chronic inflammation. Sadly the attention was all directed at finding a therapy rather than looking at the cause of chronic inflammation.
Research is hugely expensive and was largely funded by drug companies who were making billions of dollars from the prescriptions for statin drugs.
One of the many side effects of statin drugs is that they seem to have a mild anti- inflammatory effect. Because of the size of the industry and how entrenched the cholesterol theory had become, the focus continues to be on treating everyone with statin drugs rather than understanding the cause and the ability to control chronic inflammation.
The makers of statin drugs have been so skillful at influencing science and controlling public policy that prescribing statins is the standard of care. Anyone questioning or disagreeing with these policies is labeled as a heretic and disregarded.
THB: Why were you so convinced inflammation was the culprit? You were so convinced that you made a major life – and career – change based on that conviction.
Dr. Lundell: I knew that I did not have enough influence to change any of the policies or practices from inside mainstream medicine. Taking a lesson from the drug makers with their direct to consumer advertising I decided to write the book and hopefully people would learn and make the changes needed to truly prevent and cure heart disease.
THB: You describe inflammation very powerfully in your book as a battleground. Can you give our readers an overview of what inflammation is?
Dr. Lundell: Inflammation truly is a battleground. For most of human history we died because of infection and trauma. Our immune system and our inflammatory systems are designed to aggressively respond to these two challenges.
If we get invaded by bacteria or injured in some way, our immune system recognizes the challenge and marshals all of the body’s resources to respond to defeat the invader and heal the wound.
We all have experienced the classic signs of inflammation: warmth, swelling, redness, and pain. Acute inflammation is the response to acute injuries. Chronic inflammation is the response to chronic smaller injuries and so we do not always get the four classic signs.
THB: You’ve taken the bold step to speak out against statin medications. But playing devil’s advocate for a moment… surely there are some situations when statin medications are effective?
Dr. Lundell: Statin medications have proven to be somewhat beneficial to a small group of people; that is a middle aged man with a previous heart attack. They have never been documented to benefit any woman of any age with any condition. They have not been documented to help people who have not had a previous heart attack of any age or gender.
There may be some people who would take great offense at the previous paragraph – especially the makers of Crestor and cardiologists who support treating almost everyone with statin drugs.
They might quote the Jupiter study which was touted as proving Crestor would reduce heart attack rates by almost 50% in otherwise healthy people. Happily, this month in The Archives of Internal Medicine, four peer reviewed articles gave a scathing rebuke to the Jupiter study – the methodology, the conflict of interest by most of the authors, the early termination of the study which almost always provides false results, and the conclusion that statin drugs were beneficial in this population of patients. At last I am getting reinforcements!
THB: That’s a good point to make - and you make it well. So, if statin meds aren’t effective, why are they so dangerous?
Dr. Lundell: Statin drugs are dangerous not necessarily because of the side effects which can be disabling or fatal, but because they divert our attention from understanding and preventing heart disease and merely treat it with statins, allowing us to think that this is beneficial.
Even some of the foremost cardiologists in the country who have written extensively about inflammation as the true cause of heart disease offer no solutions except taking statin drugs. $30,000,000,000 in worldwide sales of statin drugs has a lot to do with it.
In part two of our revealing interview, Dr. Lundell tells us why inflammation is the true cause of heart disease and offers critical solutions to prevent it. We also discover the four most common lifestyle factors that injure heart health and get expert guidance on how to improve it. All this and more in next Wednesday’s edition of Undercover.
About Dr. Lundell: Dr. Dwight Lundell is the past Chief of Staff and Chief of Surgery at Banner Heart Hospital, Mesa, AZ. He is the founder of Healthy Humans Foundation and Chief Medical Advisor for Asantae. In 2003, Dr. Lundell made the most difficult decision of his 25 year surgical career. As traditional medicine continued to chase the cholesterol theory of heart disease, Dr. Lundell closed his surgical practice. He then devoted the rest of his life to speaking the truth that inflammation causes heart disease. By lowering inflammation, heart disease has a cure.
Dr. Lundell is the author of the world-wide bestselling book, The Great Cholesterol Lie. This book is a revealing look at heart disease and the faulty theories of low-fat diets and cholesterol. He also reveals his clinically-tested recommendations for lowering inflammation that can prevent and reverse heart disease.
To your health,
Ian Robinson,
Managing Editor, Total Health Breakthroughs
Wednesday, June 30, 2010
News regarding statins.
Clare McHarris posted the following on the Stopped Out Statins Yahoo group which I pasted in its entirety here. Thank You Clare!
===========================
News regarding statins. The latest studies in the Archives of Internal Medicine are not supportive of statins. This was released today. Please read the two abstracts below.
Statins and All-Cause Mortality in High-Risk Primary Prevention
A Meta-analysis of 11 Randomized Controlled Trials Involving 65 229 Participants (click here)
Kausik K. Ray, MD, MPhil, FACC, FESC; Sreenivasa Rao Kondapally Seshasai, MD, MPhil; Sebhat Erqou, MD, MPhil, PhD; Peter Sever, PhD, FRCP, FESC; J. Wouter Jukema, MD, PhD; Ian Ford, PhD; Naveed Sattar, FRCPath
Arch Intern Med. 2010;170(12):1024-1031.
Background Statins have been shown to reduce the risk of all-cause mortality among individuals with clinical history of coronary heart disease. However, it remains uncertain whether statins have similar mortality benefit in a high-risk primary prevention setting. Notably, all systematic reviews to date included trials that in part incorporated participants with prior cardiovascular disease (CVD) at baseline. Our objective was to reliably determine if statin therapy reduces all-cause mortality among intermediate to high-risk individuals without a history of CVD.
Data Sources Trials were identified through computerized literature searches of MEDLINE and Cochrane databases (January 1970-May 2009) using terms related to statins, clinical trials, and cardiovascular end points and through bibliographies of retrieved studies.
Study Selection Prospective, randomized controlled trials of statin therapy performed in individuals free from CVD at baseline and that reported details, or could supply data, on all-cause mortality.
Data Extraction Relevant data including the number of patients randomized, mean duration of follow-up, and the number of incident deaths were obtained from the principal publication or by correspondence with the investigators.
Data Synthesis Data were combined from 11 studies and effect estimates were pooled using a random-effects model meta-analysis, with heterogeneity assessed with the I2 statistic. Data were available on 65 229 participants followed for approximately 244 000 person-years, during which 2793 deaths occurred. The use of statins in this high-risk primary prevention setting was not associated with a statistically significant reduction (risk ratio, 0.91; 95% confidence interval, 0.83-1.01) in the risk of all-cause mortality. There was no statistical evidence of heterogeneity among studies (I2 = 23%; 95% confidence interval, 0%-61% [P = .23]).
________________
Cholesterol Lowering, Cardiovascular Diseases, and the Rosuvastatin-JUPITER Controversy
A Critical Reappraisal (click here)
Michel de Lorgeril, MD; Patricia Salen, BSc; John Abramson, MD; Sylvie Dodin, MD; Tomohito Hamazaki, PhD; Willy Kostucki, MD; Harumi Okuyama, PhD; Bruno Pavy, MD; Mikael Rabaeus, MD
Arch Intern Med. 2010;170(12):1032-1036.
Background Among the recently reported cholesterol-lowering drug trials, the JUPITER (Justification for the Use of Statins in Primary Prevention) trial is unique: it reports a substantial decrease in the risk of cardiovascular diseases among patients without coronary heart disease and with normal or low cholesterol levels.
Methods Careful review of both results and methods used in the trial and comparison with expected data.
Results The trial was flawed. It was discontinued (according to prespecified rules) after fewer than 2 years of follow-up, with no differences between the 2 groups on the most objective criteria. Clinical data showed a major discrepancy between significant reduction of nonfatal stroke and myocardial infarction but no effect on mortality from stroke and myocardial infarction. Cardiovascular mortality was surprisingly low compared with total mortality—between 5% and 18%—whereas the expected rate would have been close to 40%. Finally, there was a very low case-fatality rate of myocardial infarction, far from the expected number of close to 50%. The possibility that bias entered the trial is particularly concerning because of the strong commercial interest in the study.
Conclusion The results of the trial do not support the use of statin treatment for primary prevention of cardiovascular diseases and raise troubling questions concerning the role of commercial sponsors.
===========================
News regarding statins. The latest studies in the Archives of Internal Medicine are not supportive of statins. This was released today. Please read the two abstracts below.
Statins and All-Cause Mortality in High-Risk Primary Prevention
A Meta-analysis of 11 Randomized Controlled Trials Involving 65 229 Participants (click here)
Kausik K. Ray, MD, MPhil, FACC, FESC; Sreenivasa Rao Kondapally Seshasai, MD, MPhil; Sebhat Erqou, MD, MPhil, PhD; Peter Sever, PhD, FRCP, FESC; J. Wouter Jukema, MD, PhD; Ian Ford, PhD; Naveed Sattar, FRCPath
Arch Intern Med. 2010;170(12):1024-1031.
Background Statins have been shown to reduce the risk of all-cause mortality among individuals with clinical history of coronary heart disease. However, it remains uncertain whether statins have similar mortality benefit in a high-risk primary prevention setting. Notably, all systematic reviews to date included trials that in part incorporated participants with prior cardiovascular disease (CVD) at baseline. Our objective was to reliably determine if statin therapy reduces all-cause mortality among intermediate to high-risk individuals without a history of CVD.
Data Sources Trials were identified through computerized literature searches of MEDLINE and Cochrane databases (January 1970-May 2009) using terms related to statins, clinical trials, and cardiovascular end points and through bibliographies of retrieved studies.
Study Selection Prospective, randomized controlled trials of statin therapy performed in individuals free from CVD at baseline and that reported details, or could supply data, on all-cause mortality.
Data Extraction Relevant data including the number of patients randomized, mean duration of follow-up, and the number of incident deaths were obtained from the principal publication or by correspondence with the investigators.
Data Synthesis Data were combined from 11 studies and effect estimates were pooled using a random-effects model meta-analysis, with heterogeneity assessed with the I2 statistic. Data were available on 65 229 participants followed for approximately 244 000 person-years, during which 2793 deaths occurred. The use of statins in this high-risk primary prevention setting was not associated with a statistically significant reduction (risk ratio, 0.91; 95% confidence interval, 0.83-1.01) in the risk of all-cause mortality. There was no statistical evidence of heterogeneity among studies (I2 = 23%; 95% confidence interval, 0%-61% [P = .23]).
________________
Cholesterol Lowering, Cardiovascular Diseases, and the Rosuvastatin-JUPITER Controversy
A Critical Reappraisal (click here)
Michel de Lorgeril, MD; Patricia Salen, BSc; John Abramson, MD; Sylvie Dodin, MD; Tomohito Hamazaki, PhD; Willy Kostucki, MD; Harumi Okuyama, PhD; Bruno Pavy, MD; Mikael Rabaeus, MD
Arch Intern Med. 2010;170(12):1032-1036.
Background Among the recently reported cholesterol-lowering drug trials, the JUPITER (Justification for the Use of Statins in Primary Prevention) trial is unique: it reports a substantial decrease in the risk of cardiovascular diseases among patients without coronary heart disease and with normal or low cholesterol levels.
Methods Careful review of both results and methods used in the trial and comparison with expected data.
Results The trial was flawed. It was discontinued (according to prespecified rules) after fewer than 2 years of follow-up, with no differences between the 2 groups on the most objective criteria. Clinical data showed a major discrepancy between significant reduction of nonfatal stroke and myocardial infarction but no effect on mortality from stroke and myocardial infarction. Cardiovascular mortality was surprisingly low compared with total mortality—between 5% and 18%—whereas the expected rate would have been close to 40%. Finally, there was a very low case-fatality rate of myocardial infarction, far from the expected number of close to 50%. The possibility that bias entered the trial is particularly concerning because of the strong commercial interest in the study.
Conclusion The results of the trial do not support the use of statin treatment for primary prevention of cardiovascular diseases and raise troubling questions concerning the role of commercial sponsors.
Monday, June 28, 2010
Statins, Pregnancy, Sepsis, Cancer, Heart Failure: a Critical Analysis:
Over the last few decades, the American pharmaceutical industry (henceforth, "Big Pharma") has applied a very successful formula to market fear and convert it into a multi-billion dollar industry. The algorithm goes like this:
But are they right? I think the evidence shows that very few people currently taking statin drugs are actually benefiting from them. Furthermore, many of them are actually worse off than they would have been had they never been on statins. Below, I will argue that any benefits incurred in combating heart disease are more than offset by increased susceptibility to fetal damage, toxic infection, and cancer.
...
Essentially, by taking a statin, you are shifting the odds on what you die of. Pay the money, suffer the side effects, and as a result you may end up dying of cancer or a runaway infection before you would have died of heart disease if you had never taken the drug in the first place.
...
Read the full article by Dr.Stephanie Seneff, a Principal Research Scientist at the Massachusetts Institute of Technology here.
- find a substance whose concentration can be measured cheaply
- find a prevalent disease whose presence correlates with a high concentration of that substance
- find a drug that reduces the concentration of that substance
- advertise aggressively to the general public and medical professionals, claiming a miracle cure.
But are they right? I think the evidence shows that very few people currently taking statin drugs are actually benefiting from them. Furthermore, many of them are actually worse off than they would have been had they never been on statins. Below, I will argue that any benefits incurred in combating heart disease are more than offset by increased susceptibility to fetal damage, toxic infection, and cancer.
...
Essentially, by taking a statin, you are shifting the odds on what you die of. Pay the money, suffer the side effects, and as a result you may end up dying of cancer or a runaway infection before you would have died of heart disease if you had never taken the drug in the first place.
...
Read the full article by Dr.Stephanie Seneff, a Principal Research Scientist at the Massachusetts Institute of Technology here.
Monday, March 22, 2010
Dangers of Statin Drugs - Time Magazine article
Note added July 18, 2010 - Time Magazine seems to have removed the article titled "Dangers of Statin Drugs" mentioned in this blog post from their web site. Just goes to show that MSM is not really about to give any credence to other than the mainstream view of CVD and statin drug use.
Please read this very good article on the dangers of Atorvastatin, Lovastatin, Rosuvastatin, Simvastatin etc. Also known by more common names Lipitor, Mevacor, Crestor, Zocor, Vytorin. Note this is not a complete list of statin drugs. Cerivistatin or Baycol was pulled because too many people died from taking it (the ultimate side effect).
NOTE: I removed the link to the Time article because they removed the original article which I referred to and substituted another.
Here is a link to a blog that has a copy of the article you can read.
Please read this very good article on the dangers of Atorvastatin, Lovastatin, Rosuvastatin, Simvastatin etc. Also known by more common names Lipitor, Mevacor, Crestor, Zocor, Vytorin. Note this is not a complete list of statin drugs. Cerivistatin or Baycol was pulled because too many people died from taking it (the ultimate side effect).
NOTE: I removed the link to the Time article because they removed the original article which I referred to and substituted another.
Here is a link to a blog that has a copy of the article you can read.
Tuesday, February 9, 2010
Deaths Due to Coronary Heart Disease in the Elderly
In a study published in the American Journal of Epidemiology, seven scientists concluded from the data that ...
" even a small increase in DTR is associated with a substantial increase in the deaths due to CHD."
In english that means that global warming has helped to significantly reduce the coronary heart disease death rate of the worlds elderly.
Read the complete study here.
" even a small increase in DTR is associated with a substantial increase in the deaths due to CHD."
In english that means that global warming has helped to significantly reduce the coronary heart disease death rate of the worlds elderly.
Read the complete study here.
Thursday, January 14, 2010
"...studies evaluating the association of saturated fat with cardiovascular disease"
From The American Journal of Clinical Nutrition comes a study ending this way:
"... there is no significant evidence for concluding that dietary saturated fat is associated with an increased risk of CHD or CVD." (emphasis mine)
This was the conclusion of Dr. Ronald Krauss one of the most prominent lipid researchers in the world according to Steven Guyenet whose Whole Health Source blog alerted me to the study.
P.S. I recommend Steven's Whole Health Source blog as an excellent source of credible evidence.
"... there is no significant evidence for concluding that dietary saturated fat is associated with an increased risk of CHD or CVD." (emphasis mine)
This was the conclusion of Dr. Ronald Krauss one of the most prominent lipid researchers in the world according to Steven Guyenet whose Whole Health Source blog alerted me to the study.
P.S. I recommend Steven's Whole Health Source blog as an excellent source of credible evidence.
Tuesday, January 5, 2010
The Dirty Little Secret of the Diet-Heart Hypothesis
I constantly keep my eye out for 'Credible Evidence' related especially to my own health issues which you should be able to tell if you have read this or any of the posts on this blog, is coronary artery disease.
I have just discovered Stephan Guyenet's blog Whole Health Source. In particular a recent post titled "The Dirty Little Secret of the Diet-Heart Hypothesis" was especially interesting to me and is well presented. I recommend you read it.
I will certainly be digesting more of what Stephan posts on his blog.
I have just discovered Stephan Guyenet's blog Whole Health Source. In particular a recent post titled "The Dirty Little Secret of the Diet-Heart Hypothesis" was especially interesting to me and is well presented. I recommend you read it.
I will certainly be digesting more of what Stephan posts on his blog.
Monday, January 4, 2010
The Cholesterol Theory of Heart Disease is Nonsense
Anthony Colpo who I have learned much from especially back in the days he was regularly putting out good analysis of many health items on The Omnivore.com. Here is a new newsletter I just saw published on the_omnivore@yahoogroups.com. I've provided it in full here. It is a bit long but thorough as I have found him to be. Thank You Anthony!
================================================
The Cholesterol Theory of Heart Disease is Nonsense
Posted by: "theomnivorenewsletter" ac.theomnivore@gmail.com theomnivorenewsletter
Sun Jan 3, 2010 4:30 pm (PST)
The Cholesterol Theory of Heart Disease is Nonsense
I've been telling people for years that the anti-cholesterol,
anti-saturated fat paradigm is not only nonsense but potentially
dangerous. The latest confirmation of my stance comes from two recent
studies that - in stark contrast to vigorously hyped anti-cholesterol
research – have been ignored by the mainstream health media.
The most recent of these studies was published in the November 15, 2009
issue of the New England Journal of Medicine. The ARBITER 6–HALTS
trial compared the effects of two combination therapies - either
ezetimibe+statins or niacin+statins - on carotid intima-media thickness
over a 14-month period. Measurement of carotid artery intima-media
thickness is used to indicate the extent of atherosclerosis and for
assessing cardiovascular risk.
All of the 363 subjects enrolled in the trial were already taking
cholesterol-lowering statin drugs. Statin drugs have become the darlings
of the medical establishment due to their ability to lower both total
and LDL cholesterol, while ezetimibe has become a popular adjunct to
statin treatment thanks to its LDL-lowering actions. The subjects were
randomly assigned to receive either extended-release niacin at a target
dose of 2000 mg per day or ezetimibe at a dose of 10 mg per day. The
niacin was increased from an initial dose of 500 mg at bedtime, by 500
mg every other week, to the maximum tolerated dose (up to 2000 mg at
bedtime).
The subjects were men and women (mean age 65) with atherosclerotic
cardiovascular disease or a coronary heart disease (CHD) risk
equivalent, including diabetes, a 10-year Framingham risk score of 20%
or more, or a coronary calcium score above 200 for women or 400 for men.
A total of 208 patients had completed 14 months of treatment when the
study was called to a halt. Initial LDL levels were similar in both
groups, but etezimibe produced greater reductions in LDL than niacin
(-17.6 mg/dl vs -10.0 mg/dl). If you believe the relentless barrage of
anti-LDL propaganda emanating from our ever-so-wise, impartial,
objective and totally incorruptible health authorities, then this should
have produced greater improvements in the etezimibe group.
But it didn't.
When the data was analyzed, it was observed that niacin produced a
significant reduction in carotid intima-media thickness at both 8 and 14
months. No significant overall change in carotid intima-media thickness
was seen with ezetimibe.
The researchers did however find a significant inverse relationship
between changes in LDL cholesterol and carotid intima-media thickness in
the ezetimibe group, such that a "paradoxical" increase in the
carotid intima-media thickness was seen in patients with greater
reductions in LDL cholesterol (rather than simply acknowledge the
cholesterol theory is bollocks, researchers invariably label any and
every uncomfortable contradiction to this theory a "paradox").
Major adverse cardiovascular events also occurred at a significantly
greater rate in the ezetimibe group (9 of 165 patients [5%]) than in the
niacin group (2 of 160 patients [1%]).
A peek at the dropout data also reveals some interesting findings. Among
363 patients enrolled in the trial, 44 had left the study by the time it
was terminated on June 4, 2009: 16 of 176 (9%) in the ezetimibe group
(of whom 9 had been withdrawn and 7 had died) and 28 of 187 (15%) in the
niacin group (of whom 27 had been withdrawn and 1 had died). Adverse
drug effects were cited as the reason for withdrawal in 3 of 9 patients
receiving ezetimibe and 17 of 27 patients receiving niacin. The
well-known side effect of flushing was reported in 36% of patients in
the niacin group[1].
Bottom line: Ezetimibe produced greater reductions in LDL cholesterol
(the so-called "bad" cholesterol) but resulted in no overall
improvement in carotid intima-media thickness, while individual results
showed greater thickening with greater LDL reductions. The use of
etezimibe was also accompanied by a higher number of heart attacks and
deaths.
Yep, the "paradoxes" flowed thick and fast in this study. Of
course, those of you who have read The Great Cholesterol Con will know
that there was absolutely nothing paradoxical about these findings –
the cholesterol theory is, and always has been, utter nonsense.
So Popular But So Useless
This is hardly the first time ezetimibe has shown itself to be a dud.
The SANDS trial, examining type 2 diabetic American Indians, found that ,
ezetimibe plus statins produced no greater improvement in carotid
intima-media thickness than statins alone[2].
In the Simvastatin and Ezetimibe in Aortic Stenosis (SEAS) trial, 1873
patients with mild-to-moderate, asymptomatic aortic stenosis (abnormal
narrowing of the heart's aortic valve) received either 40 mg of
simvastatin plus 10 mg of ezetimibe or placebo daily. During a follow-up
of 52.2 months, simvastatin and ezetimibe, as compared with placebo, did
not reduce the composite outcome of combined aortic valve events and
ischemic events in patients with aortic stenosis.
The simvastatin–ezetimibe group did however experience something
that the placebo group did not: an increased cancer risk. A
statistically significant excess of incident cancers was observed in the
simvastatin– ezetimibe group, with 105 in that group as compared
with 70 in the placebo group. In addition, deaths from cancer were more
frequent in the simvastatin– ezetimibe group (39 deaths vs. 23 in
the placebo group). There was also a significant increase in the number
of patients with elevated liver enzyme levels in the
simvastatin–ezetimibe group[3].
Increased cancer risk from cholesterol-lowering drugs has been observed
previously. In the PROSPER study featuring elderly subjects - the
demographic in whom you would most likely expect an increased cancer
risk to manifest itself during the relatively short duration of a
clinical trial - an increased mortality from malignant causes among
those taking pravastatin negated the reduction in cardiovascular
deaths[4]. Etezimibe, meanwhile, inhibits the absorption of phytosterols
and other phytonutrients linked to protection against cancer[5].
The ENHANCE trial was a double-blind, randomized, 24-month endeavour
comparing the effects of 80 mg of simvastatin combined with either with
placebo or with 10 mg of ezetimibe daily in 720 patients with familial
hypercholesterolemia. Mean levels of LDL cholesterol decreased from
317.8 mg/dl per to 192.7 mg/dl in the simvastatin-only group and from
319.0 mg/dl to 141.3 mg/dl in the combined-therapy group. Despite their
significantly greater decrease in LDL levels, the simvastatin+ ezetimibe
group experienced no statistically significant greater decrease in
carotid intima-media thickness.
Nor was there any advantage in incidence of regression in mean
carotid-artery intima–media thickness or new plaque formation. No
significant change was observed in mean maximum carotid-artery
intima–media thickness, mean measures of the intima–media
thickness of the common carotid artery, the carotid bulb, the internal
carotid artery, the femoral artery, nor in the average of the mean
values for intima–media thickness in the carotid and femoral
arteries. Investigator-reported cardiovascular events were noted in
seven patients in the simvastatin group (including 1 death from a
cardiovascular cause, 2 nonfatal myocardial infarctions, 1 nonfatal
stroke, and 5 coronary revascularization procedures) and in 10 patients
in the combined-therapy group (including 2 deaths from cardiovascular
causes, 3 nonfatal myocardial infarctions, 1 nonfatal stroke, and 6
coronary revascularizations)[6].
Since its introduction in 2002, ezetimibe has become the primary adjunct
to statins for reducing "elevated" LDL. This is despite the fact
that it has so far shown itself to be totally incapable of actually
producing any meaningful health benefit for the people who take it. In
today's bizarro drug company-owned health arena, where cholesterol
reduction has become a sacred end in itself, a woeful inability to
reduce heart attack or death is swept aside as a minor inconvenience.
There's money to be made in them thar lipid-lowering drugs, to hell
with any profit-destroying notion that they are largely a waste of time
and money…
WHO Says the Saturated Fat Theory is Garbage?
A recent special issue of Annals of Nutrition and Metabolism was devoted
to "Fats and Fatty Acids in Human Nutrition". This issue was the
result of a joint FAO/WHO Expert Consultation held in Geneva, November
2008 and contains "the background papers which have been prepared by
a panel of carefully selected experts and have served as the basis for
the updated dietary recommendations of FAO and WHO"[7]
One of the papers presented in this special report was a sweeping review
of both prospective epidemiological studies and clinical trials
examining the relationship between dietary fat and CHD[8]. This review
was conducted by researchers from the Department of Human Nutrition at
the University of Otago, Dunedin , New Zealand.
I must confess that when I initially pulled up the PDF of this study
(which you can freely access from the link below), I was fully expecting
more of the same old fat- and cholesterol-phobic hoopla that has
regrettably characterized public health recommendations for almost half
a century. Instead, I was pleasantly surprised. In fact, pleasantly
shocked is a more fitting description. Despite being published under the
auspices of one of the world's largest health organizations, the
report actually tells…the truth!
After examining 28 prospective epidemiological studies, the researchers
reported that:
"Intake of total fat was not significantly associated with CHD
mortality..." (p. 175)
"Intake of total fat was also unrelated to CHD events..." (p. 175)
"Intake of TFA [trans fatty acids] was strongly associated with CHD
mortality..." (p. 181)
"Intake of SFA [saturated fatty acids] was not significantly associated
with CHD mortality...
Similarly SFA intake was not significantly associated CHD events..." (p.
181)
Their pooled analysis of data from randomized controlled clinical trials
showed:
"...fatal CHD was not reduced by either the low-fat diets... or the high
P/S diets [diets high in polyunsaturated fats and low in saturated fats]
...". (p. 188)
On page 193, they conclude:
"There is probably no direct relation between total fat intake and risk
of CHD."
If you were expecting this rare gem of health authority-sanctioned
honesty and factual reporting to be reflected in said health
authority's dietary recommendations to the public, then you clearly
know little about the mechanics of these anachronistic juggernauts.
Maintaining the status quo is a self-serving activity of utmost
importance to reigning orthodoxies. Changes to currently accepted diet
and health recommendations occur almost imperceptibly over time, as
small modifications that "advance" the current body of knowledge
but never upset the underlying foundational dogma itself. Such
modifications typically include the inclusion of politically acceptable
discoveries (such as the cardiovascular benefits of omega-3 fatty acids
from fish and fish oils). However, the wholesale embrace of politically
incorrect findings is unthinkable. As such, the world's health
authorities continue to preach the kind of nonsense that rational minds
would associate with the ignorant, superstitious thinking of the Dark
Ages. Such nonsense includes the belief that cholesterol, an essential
life-sustaining substance that Mother Nature saw fit to include in the
membranes of all our cells, to protect our nervous systems, and to use
as the basis for production of our most important hormones, is in fact
toxic and must be lowered at all costs.
And so it is in this case: despite the conclusions of the aforementioned
review, WHO are still currently preaching the same old
anti-cholesterol/anti-saturate hogwash in their CHD prevention
guidelines[9].
Where's Your Head at?
Some of you reading this will do further investigation and will conclude
of your own volition that what I have reported above is factual. Some of
you will be confused and will not know what to make of what I have just
reported; it sounds compelling but at the same time you have great
difficulty accepting that so many "prestigious" health
authorities, government bodies, medical associations, doctors,
journalists, authors, and numerous other assorted talking heads could be
so wrong. Such a mindset reveals a rather naïve understanding of
human nature. No matter how prestigious and well-funded the organization
or profession, it is still comprised of fallible human individuals with
a deep-rooted evolutionary-programmed tendency to follow the herd and
subscribe to groupthink.
A minority of readers will even become angry at what I have just
written, offended by my temerity to report facts which so blatantly
contradict what they have come to believe. My response to those who fall
into this category is…too bad. After years of coming under attack
from the disgruntled worshippers of various scientifically untenable
nutrition paradigms, I'm totally over trying to reason with the
unreasonable. My aim is simply to relay research findings to those who
may find the information useful, not to pander to the fragile
sensibilities of those who attain emotional solace in certain diet and
health beliefs.
Life, if you allow it to be so, is a fascinating voyage of continual
discovery. If you wish to make any meaningful progress during this
voyage, you will frequently need to re-examine beliefs that you have
become comfortable with, and you must be prepared to discard these
beliefs if the evidence dictates.
For those prepared to do this, and who would like to further examine the
contrarian side of the cholesterol story, may I recommend the following
resources:
1. The Great Cholesterol Con by yours truly. Yes, it's my
own book and after years of extensive research and effort I would
of course be expected to gush on about what a wonderfully
ground-breaking, enlightening and beneficial tome it constitutes.
So don't listen to me; check out the non-partisan reviews by
Amazon customers and folks like Chris Masterjohn, who considers the book
"the most well-written and well-researched book on the
"skeptic" side of the debate":
http://www.cholesterol-and-health.com/Anthony-Colpo-Great-Cholesterol-Co\
n.html
A review of TGCC by Joel Kauffman can be viewed here:
http://www.jpands.org/vol11no4/bookreviews.pdf
The Amazon page for The Great Cholesterol Con can be found here:
http://www.amazon.com/Great-Cholesterol-Con-Anthony-Colpo/dp/1430309334
Those of you looking to save some money and wanting instant access to
the book can get an ebook version here:
http://www.thegreatcholesterolcon.com/
NOTE: To those of you who purchase my book (or already have it), please
read Chapter 22 – over and over. Judging by the reviews and comments
I have read about my book, that chapter appears to be overlooked by many
readers. Yet if you are truly serious about preventing coronary heart
disease, it contains the most valuable information you may ever come
across.
1. My freely available article on LDL cholesterol, which appeared in
the Journal of American Physicians and Surgeons:
http://www.jpands.org/vol10no3/colpo.pdf
Also a letter of criticism and my reply:
http://www.jpands.org/vol11no1/correspondence.pdf
1. Fat and Cholesterol are Good for You by Uffe Ravnskov. Don't
be fooled by the Atkins-like title; Uffe is a serious and
meticulous researcher with dozens of peer-reviewed research papers
to his name. I consider his writings essential reading for anyone
interested in the cholesterol debate. His book can be obtained
here:
http://www.amazon.com/Fat-Cholesterol-are-Good-You/dp/919755538X/ref=pd_\
sim_b_2
Uffe also heads a group called THINCS, whose website contains various
articles and links to resources articulating skeptical views of the
cholesterol theory:
http://www.thincs.org/
The website contains some great information; the page devoted to
unpublished correspondence (critical letters that were knocked back by
the journals they were submitted to) makes for especially
interesting reading. Please note this does not constitute a blanket
endorsement by myself of THINCS – while I find myself agreeing
with almost everything Uffe writes, I don't agree with some of
the assertions made by certain other THINCS members/contributors. I
would urge readers to be especially wary of authors who make
untenable claims about the superiority of isocaloric low-carb diets
for weight loss (claims that have been repeatedly disproved in
tightly controlled ward studies), and those who claim to have
discovered a single unifying cause of CHD whilst ignoring the critical
role of such factors as bodily iron stores, nutrition (especially
refined carbohydrate intake), vitamin and mineral status (most
notably magnesium), infectious disease, omega-3:omega-6 status,
physical activity, obesity, and/or stress.
2. Statin Drugs Side Effects and the Misguided War on Cholesterol by
Duane `Spacedoc' Graveline. This former astronaut and
physician was a key figure in alerting the public to the
little-known statin side effect of transient memory loss, which has
since been the subject of peer-reviewed articles and case reports.
Those who are being cajoled by their doctors to begin statin drug
use would be well advised to read this book:
http://www.amazon.com/Statin-Drugs-Effects-Misguided-Cholesterol/dp/0970\
081790
All the best,
Anthony Colpo.
References
1. Taylor AJ, et al. Extended-release niacin or ezetimibe and
carotid intima-media thickness. New England Journal of Medicine,
Nov 26, 2009; 361 (22): 2113-2122.
2. Fleg JL, et al. Effect of Statins Alone Versus Statins Plus
Ezetimibe on Carotid Atherosclerosis in Type 2 Diabetes. The SANDS
(Stop Atherosclerosis in Native Diabetics Study) Trial. Journal of
the American College of Cardiology, 2008; 52: 2198-2205.
http://content.onlinejacc.org/cgi/reprint/j.jacc.2008.10.031v1.pdf
3. Rossebø AB, et al. Intensive lipid lowering with
simvastatin and ezetimibe in aortic stenosis. New England Joural of
Medicine, 2008; 359: 1343-1356.
http://content.nejm.org/cgi/reprint/359/13/1343.pdf
4. Shepherd J, et al. PROspective Study of Pravastatin in the
Elderly at Risk. Pravastatin in elderly individuals at risk of
vascular disease (PROSPER): a randomised controlled trial. Lancet,
2002; 360: 1623-1630.
5. Bradford PG, Awad AB. Phytosterols as anticancer compounds.
Molecular Nutrition & Food Research, 2007; 51: 161-170.
6. Kastelein JJ, et al. Simvastatin with or without ezetimibe in
familial hypercholesterolemia. New England Joural of Medicine, Apr.
3, 2008; 358 (14): 1431-1443.
http://content.nejm.org/cgi/reprint/358/14/1431.pdf
7. Fats and Fatty Acids in Human Nutrition. Annals of Nutrition and
Metabolism, 2009; 55 (1-3). Available online:
http://content.karger.com/ProdukteDB/produkte.asp?Aktion=showproducts&se\
archWhat=books&ProduktNr=251867
8. Skeaff MC, Miller J. Dietary Fat and Coronary Heart Disease:
Summary of Evidence from Prospective Cohort and Randomised
Controlled Trials. Annals of Nutrition and Metabolism, 2009; 55:
173–201.
http://content.karger.com/ProdukteDB/produkte.asp?Aktion=ShowPDF&Artikel\
Nr=229002&Ausgabe=250361&ProduktNr=223977&filename=229002.pdf
9. http://www.fao.org/DOCREP/005/AC911E/ac911e07.htm#bm07.4.3
**CORRESPONDENCE POLICY - PLEASE READ BEFORE EMAILING**
Comments and questions from readers are always welcome, but due to time
constraints a response cannot be guaranteed. If you find lack of
response to your correspondence offensive, please don't write. Emails
with offensive, argumentative, hostile or imbecilic content will be
ignored.
**DISCLAIMER**
The information in this email is for information purposes only and is
not to be construed as medical advice. The author accepts no liability
for any harm , real or imagined, associated with the use of this
information.
================================================
The Cholesterol Theory of Heart Disease is Nonsense
Posted by: "theomnivorenewsletter" ac.theomnivore@gmail.com theomnivorenewsletter
Sun Jan 3, 2010 4:30 pm (PST)
The Cholesterol Theory of Heart Disease is Nonsense
I've been telling people for years that the anti-cholesterol,
anti-saturated fat paradigm is not only nonsense but potentially
dangerous. The latest confirmation of my stance comes from two recent
studies that - in stark contrast to vigorously hyped anti-cholesterol
research – have been ignored by the mainstream health media.
The most recent of these studies was published in the November 15, 2009
issue of the New England Journal of Medicine. The ARBITER 6–HALTS
trial compared the effects of two combination therapies - either
ezetimibe+statins or niacin+statins - on carotid intima-media thickness
over a 14-month period. Measurement of carotid artery intima-media
thickness is used to indicate the extent of atherosclerosis and for
assessing cardiovascular risk.
All of the 363 subjects enrolled in the trial were already taking
cholesterol-lowering statin drugs. Statin drugs have become the darlings
of the medical establishment due to their ability to lower both total
and LDL cholesterol, while ezetimibe has become a popular adjunct to
statin treatment thanks to its LDL-lowering actions. The subjects were
randomly assigned to receive either extended-release niacin at a target
dose of 2000 mg per day or ezetimibe at a dose of 10 mg per day. The
niacin was increased from an initial dose of 500 mg at bedtime, by 500
mg every other week, to the maximum tolerated dose (up to 2000 mg at
bedtime).
The subjects were men and women (mean age 65) with atherosclerotic
cardiovascular disease or a coronary heart disease (CHD) risk
equivalent, including diabetes, a 10-year Framingham risk score of 20%
or more, or a coronary calcium score above 200 for women or 400 for men.
A total of 208 patients had completed 14 months of treatment when the
study was called to a halt. Initial LDL levels were similar in both
groups, but etezimibe produced greater reductions in LDL than niacin
(-17.6 mg/dl vs -10.0 mg/dl). If you believe the relentless barrage of
anti-LDL propaganda emanating from our ever-so-wise, impartial,
objective and totally incorruptible health authorities, then this should
have produced greater improvements in the etezimibe group.
But it didn't.
When the data was analyzed, it was observed that niacin produced a
significant reduction in carotid intima-media thickness at both 8 and 14
months. No significant overall change in carotid intima-media thickness
was seen with ezetimibe.
The researchers did however find a significant inverse relationship
between changes in LDL cholesterol and carotid intima-media thickness in
the ezetimibe group, such that a "paradoxical" increase in the
carotid intima-media thickness was seen in patients with greater
reductions in LDL cholesterol (rather than simply acknowledge the
cholesterol theory is bollocks, researchers invariably label any and
every uncomfortable contradiction to this theory a "paradox").
Major adverse cardiovascular events also occurred at a significantly
greater rate in the ezetimibe group (9 of 165 patients [5%]) than in the
niacin group (2 of 160 patients [1%]).
A peek at the dropout data also reveals some interesting findings. Among
363 patients enrolled in the trial, 44 had left the study by the time it
was terminated on June 4, 2009: 16 of 176 (9%) in the ezetimibe group
(of whom 9 had been withdrawn and 7 had died) and 28 of 187 (15%) in the
niacin group (of whom 27 had been withdrawn and 1 had died). Adverse
drug effects were cited as the reason for withdrawal in 3 of 9 patients
receiving ezetimibe and 17 of 27 patients receiving niacin. The
well-known side effect of flushing was reported in 36% of patients in
the niacin group[1].
Bottom line: Ezetimibe produced greater reductions in LDL cholesterol
(the so-called "bad" cholesterol) but resulted in no overall
improvement in carotid intima-media thickness, while individual results
showed greater thickening with greater LDL reductions. The use of
etezimibe was also accompanied by a higher number of heart attacks and
deaths.
Yep, the "paradoxes" flowed thick and fast in this study. Of
course, those of you who have read The Great Cholesterol Con will know
that there was absolutely nothing paradoxical about these findings –
the cholesterol theory is, and always has been, utter nonsense.
So Popular But So Useless
This is hardly the first time ezetimibe has shown itself to be a dud.
The SANDS trial, examining type 2 diabetic American Indians, found that ,
ezetimibe plus statins produced no greater improvement in carotid
intima-media thickness than statins alone[2].
In the Simvastatin and Ezetimibe in Aortic Stenosis (SEAS) trial, 1873
patients with mild-to-moderate, asymptomatic aortic stenosis (abnormal
narrowing of the heart's aortic valve) received either 40 mg of
simvastatin plus 10 mg of ezetimibe or placebo daily. During a follow-up
of 52.2 months, simvastatin and ezetimibe, as compared with placebo, did
not reduce the composite outcome of combined aortic valve events and
ischemic events in patients with aortic stenosis.
The simvastatin–ezetimibe group did however experience something
that the placebo group did not: an increased cancer risk. A
statistically significant excess of incident cancers was observed in the
simvastatin– ezetimibe group, with 105 in that group as compared
with 70 in the placebo group. In addition, deaths from cancer were more
frequent in the simvastatin– ezetimibe group (39 deaths vs. 23 in
the placebo group). There was also a significant increase in the number
of patients with elevated liver enzyme levels in the
simvastatin–ezetimibe group[3].
Increased cancer risk from cholesterol-lowering drugs has been observed
previously. In the PROSPER study featuring elderly subjects - the
demographic in whom you would most likely expect an increased cancer
risk to manifest itself during the relatively short duration of a
clinical trial - an increased mortality from malignant causes among
those taking pravastatin negated the reduction in cardiovascular
deaths[4]. Etezimibe, meanwhile, inhibits the absorption of phytosterols
and other phytonutrients linked to protection against cancer[5].
The ENHANCE trial was a double-blind, randomized, 24-month endeavour
comparing the effects of 80 mg of simvastatin combined with either with
placebo or with 10 mg of ezetimibe daily in 720 patients with familial
hypercholesterolemia. Mean levels of LDL cholesterol decreased from
317.8 mg/dl per to 192.7 mg/dl in the simvastatin-only group and from
319.0 mg/dl to 141.3 mg/dl in the combined-therapy group. Despite their
significantly greater decrease in LDL levels, the simvastatin+ ezetimibe
group experienced no statistically significant greater decrease in
carotid intima-media thickness.
Nor was there any advantage in incidence of regression in mean
carotid-artery intima–media thickness or new plaque formation. No
significant change was observed in mean maximum carotid-artery
intima–media thickness, mean measures of the intima–media
thickness of the common carotid artery, the carotid bulb, the internal
carotid artery, the femoral artery, nor in the average of the mean
values for intima–media thickness in the carotid and femoral
arteries. Investigator-reported cardiovascular events were noted in
seven patients in the simvastatin group (including 1 death from a
cardiovascular cause, 2 nonfatal myocardial infarctions, 1 nonfatal
stroke, and 5 coronary revascularization procedures) and in 10 patients
in the combined-therapy group (including 2 deaths from cardiovascular
causes, 3 nonfatal myocardial infarctions, 1 nonfatal stroke, and 6
coronary revascularizations)[6].
Since its introduction in 2002, ezetimibe has become the primary adjunct
to statins for reducing "elevated" LDL. This is despite the fact
that it has so far shown itself to be totally incapable of actually
producing any meaningful health benefit for the people who take it. In
today's bizarro drug company-owned health arena, where cholesterol
reduction has become a sacred end in itself, a woeful inability to
reduce heart attack or death is swept aside as a minor inconvenience.
There's money to be made in them thar lipid-lowering drugs, to hell
with any profit-destroying notion that they are largely a waste of time
and money…
WHO Says the Saturated Fat Theory is Garbage?
A recent special issue of Annals of Nutrition and Metabolism was devoted
to "Fats and Fatty Acids in Human Nutrition". This issue was the
result of a joint FAO/WHO Expert Consultation held in Geneva, November
2008 and contains "the background papers which have been prepared by
a panel of carefully selected experts and have served as the basis for
the updated dietary recommendations of FAO and WHO"[7]
One of the papers presented in this special report was a sweeping review
of both prospective epidemiological studies and clinical trials
examining the relationship between dietary fat and CHD[8]. This review
was conducted by researchers from the Department of Human Nutrition at
the University of Otago, Dunedin , New Zealand.
I must confess that when I initially pulled up the PDF of this study
(which you can freely access from the link below), I was fully expecting
more of the same old fat- and cholesterol-phobic hoopla that has
regrettably characterized public health recommendations for almost half
a century. Instead, I was pleasantly surprised. In fact, pleasantly
shocked is a more fitting description. Despite being published under the
auspices of one of the world's largest health organizations, the
report actually tells…the truth!
After examining 28 prospective epidemiological studies, the researchers
reported that:
"Intake of total fat was not significantly associated with CHD
mortality..." (p. 175)
"Intake of total fat was also unrelated to CHD events..." (p. 175)
"Intake of TFA [trans fatty acids] was strongly associated with CHD
mortality..." (p. 181)
"Intake of SFA [saturated fatty acids] was not significantly associated
with CHD mortality...
Similarly SFA intake was not significantly associated CHD events..." (p.
181)
Their pooled analysis of data from randomized controlled clinical trials
showed:
"...fatal CHD was not reduced by either the low-fat diets... or the high
P/S diets [diets high in polyunsaturated fats and low in saturated fats]
...". (p. 188)
On page 193, they conclude:
"There is probably no direct relation between total fat intake and risk
of CHD."
If you were expecting this rare gem of health authority-sanctioned
honesty and factual reporting to be reflected in said health
authority's dietary recommendations to the public, then you clearly
know little about the mechanics of these anachronistic juggernauts.
Maintaining the status quo is a self-serving activity of utmost
importance to reigning orthodoxies. Changes to currently accepted diet
and health recommendations occur almost imperceptibly over time, as
small modifications that "advance" the current body of knowledge
but never upset the underlying foundational dogma itself. Such
modifications typically include the inclusion of politically acceptable
discoveries (such as the cardiovascular benefits of omega-3 fatty acids
from fish and fish oils). However, the wholesale embrace of politically
incorrect findings is unthinkable. As such, the world's health
authorities continue to preach the kind of nonsense that rational minds
would associate with the ignorant, superstitious thinking of the Dark
Ages. Such nonsense includes the belief that cholesterol, an essential
life-sustaining substance that Mother Nature saw fit to include in the
membranes of all our cells, to protect our nervous systems, and to use
as the basis for production of our most important hormones, is in fact
toxic and must be lowered at all costs.
And so it is in this case: despite the conclusions of the aforementioned
review, WHO are still currently preaching the same old
anti-cholesterol/anti-saturate hogwash in their CHD prevention
guidelines[9].
Where's Your Head at?
Some of you reading this will do further investigation and will conclude
of your own volition that what I have reported above is factual. Some of
you will be confused and will not know what to make of what I have just
reported; it sounds compelling but at the same time you have great
difficulty accepting that so many "prestigious" health
authorities, government bodies, medical associations, doctors,
journalists, authors, and numerous other assorted talking heads could be
so wrong. Such a mindset reveals a rather naïve understanding of
human nature. No matter how prestigious and well-funded the organization
or profession, it is still comprised of fallible human individuals with
a deep-rooted evolutionary-programmed tendency to follow the herd and
subscribe to groupthink.
A minority of readers will even become angry at what I have just
written, offended by my temerity to report facts which so blatantly
contradict what they have come to believe. My response to those who fall
into this category is…too bad. After years of coming under attack
from the disgruntled worshippers of various scientifically untenable
nutrition paradigms, I'm totally over trying to reason with the
unreasonable. My aim is simply to relay research findings to those who
may find the information useful, not to pander to the fragile
sensibilities of those who attain emotional solace in certain diet and
health beliefs.
Life, if you allow it to be so, is a fascinating voyage of continual
discovery. If you wish to make any meaningful progress during this
voyage, you will frequently need to re-examine beliefs that you have
become comfortable with, and you must be prepared to discard these
beliefs if the evidence dictates.
For those prepared to do this, and who would like to further examine the
contrarian side of the cholesterol story, may I recommend the following
resources:
1. The Great Cholesterol Con by yours truly. Yes, it's my
own book and after years of extensive research and effort I would
of course be expected to gush on about what a wonderfully
ground-breaking, enlightening and beneficial tome it constitutes.
So don't listen to me; check out the non-partisan reviews by
Amazon customers and folks like Chris Masterjohn, who considers the book
"the most well-written and well-researched book on the
"skeptic" side of the debate":
http://www.cholesterol-and-health.com/Anthony-Colpo-Great-Cholesterol-Co\
n.html
A review of TGCC by Joel Kauffman can be viewed here:
http://www.jpands.org/vol11no4/bookreviews.pdf
The Amazon page for The Great Cholesterol Con can be found here:
http://www.amazon.com/Great-Cholesterol-Con-Anthony-Colpo/dp/1430309334
Those of you looking to save some money and wanting instant access to
the book can get an ebook version here:
http://www.thegreatcholesterolcon.com/
NOTE: To those of you who purchase my book (or already have it), please
read Chapter 22 – over and over. Judging by the reviews and comments
I have read about my book, that chapter appears to be overlooked by many
readers. Yet if you are truly serious about preventing coronary heart
disease, it contains the most valuable information you may ever come
across.
1. My freely available article on LDL cholesterol, which appeared in
the Journal of American Physicians and Surgeons:
http://www.jpands.org/vol10no3/colpo.pdf
Also a letter of criticism and my reply:
http://www.jpands.org/vol11no1/correspondence.pdf
1. Fat and Cholesterol are Good for You by Uffe Ravnskov. Don't
be fooled by the Atkins-like title; Uffe is a serious and
meticulous researcher with dozens of peer-reviewed research papers
to his name. I consider his writings essential reading for anyone
interested in the cholesterol debate. His book can be obtained
here:
http://www.amazon.com/Fat-Cholesterol-are-Good-You/dp/919755538X/ref=pd_\
sim_b_2
Uffe also heads a group called THINCS, whose website contains various
articles and links to resources articulating skeptical views of the
cholesterol theory:
http://www.thincs.org/
The website contains some great information; the page devoted to
unpublished correspondence (critical letters that were knocked back by
the journals they were submitted to) makes for especially
interesting reading. Please note this does not constitute a blanket
endorsement by myself of THINCS – while I find myself agreeing
with almost everything Uffe writes, I don't agree with some of
the assertions made by certain other THINCS members/contributors. I
would urge readers to be especially wary of authors who make
untenable claims about the superiority of isocaloric low-carb diets
for weight loss (claims that have been repeatedly disproved in
tightly controlled ward studies), and those who claim to have
discovered a single unifying cause of CHD whilst ignoring the critical
role of such factors as bodily iron stores, nutrition (especially
refined carbohydrate intake), vitamin and mineral status (most
notably magnesium), infectious disease, omega-3:omega-6 status,
physical activity, obesity, and/or stress.
2. Statin Drugs Side Effects and the Misguided War on Cholesterol by
Duane `Spacedoc' Graveline. This former astronaut and
physician was a key figure in alerting the public to the
little-known statin side effect of transient memory loss, which has
since been the subject of peer-reviewed articles and case reports.
Those who are being cajoled by their doctors to begin statin drug
use would be well advised to read this book:
http://www.amazon.com/Statin-Drugs-Effects-Misguided-Cholesterol/dp/0970\
081790
All the best,
Anthony Colpo.
References
1. Taylor AJ, et al. Extended-release niacin or ezetimibe and
carotid intima-media thickness. New England Journal of Medicine,
Nov 26, 2009; 361 (22): 2113-2122.
2. Fleg JL, et al. Effect of Statins Alone Versus Statins Plus
Ezetimibe on Carotid Atherosclerosis in Type 2 Diabetes. The SANDS
(Stop Atherosclerosis in Native Diabetics Study) Trial. Journal of
the American College of Cardiology, 2008; 52: 2198-2205.
http://content.onlinejacc.org/cgi/reprint/j.jacc.2008.10.031v1.pdf
3. Rossebø AB, et al. Intensive lipid lowering with
simvastatin and ezetimibe in aortic stenosis. New England Joural of
Medicine, 2008; 359: 1343-1356.
http://content.nejm.org/cgi/reprint/359/13/1343.pdf
4. Shepherd J, et al. PROspective Study of Pravastatin in the
Elderly at Risk. Pravastatin in elderly individuals at risk of
vascular disease (PROSPER): a randomised controlled trial. Lancet,
2002; 360: 1623-1630.
5. Bradford PG, Awad AB. Phytosterols as anticancer compounds.
Molecular Nutrition & Food Research, 2007; 51: 161-170.
6. Kastelein JJ, et al. Simvastatin with or without ezetimibe in
familial hypercholesterolemia. New England Joural of Medicine, Apr.
3, 2008; 358 (14): 1431-1443.
http://content.nejm.org/cgi/reprint/358/14/1431.pdf
7. Fats and Fatty Acids in Human Nutrition. Annals of Nutrition and
Metabolism, 2009; 55 (1-3). Available online:
http://content.karger.com/ProdukteDB/produkte.asp?Aktion=showproducts&se\
archWhat=books&ProduktNr=251867
8. Skeaff MC, Miller J. Dietary Fat and Coronary Heart Disease:
Summary of Evidence from Prospective Cohort and Randomised
Controlled Trials. Annals of Nutrition and Metabolism, 2009; 55:
173–201.
http://content.karger.com/ProdukteDB/produkte.asp?Aktion=ShowPDF&Artikel\
Nr=229002&Ausgabe=250361&ProduktNr=223977&filename=229002.pdf
9. http://www.fao.org/DOCREP/005/AC911E/ac911e07.htm#bm07.4.3
**CORRESPONDENCE POLICY - PLEASE READ BEFORE EMAILING**
Comments and questions from readers are always welcome, but due to time
constraints a response cannot be guaranteed. If you find lack of
response to your correspondence offensive, please don't write. Emails
with offensive, argumentative, hostile or imbecilic content will be
ignored.
**DISCLAIMER**
The information in this email is for information purposes only and is
not to be construed as medical advice. The author accepts no liability
for any harm , real or imagined, associated with the use of this
information.
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