From The Health Journal Club comes this book review of the book by that name by Uffe Ravnskov.
=================================================
Wednesday, January 26, 2011
Book Review: "Fat and Cholesterol are Good for You!"
Uffe Ravnskov, MD PhD
Fat and cholesterol good for your?? Why its preposterous I tell you! And if this wasn't such a serious and important topic it might be worthwhile to spend a good deal of time simply on the reaction of mainstream medicine to Dr. Ravnskov's positions. To point out how this medical doctor, nephrologist and PhD could not get an English language publisher for his first book on the topic, "The Cholesterol Myths" until Sally Fallon in the alternative medicine field published it through her own company. How, despite being literally burned on a Finnish talk show, the original book was in such demand that it was selling often selling for well over 100 dollars for a used copy until the publication of the current book. Even with the publication of "Fat and Cholesterol are Good for You!" which covers and expands upon the material in the first book, used paper back copies of The Cholesterol Myths sell for over twenty dollars and new copies around $40.
The topic of heart disease is a serious one, however, and rather then spend more time on the reaction to these writings it is necessary to try and at least scratch the surface of what Dr. Ranvskov is actually saying. This is not so easy in that the numerous chapters are wide ranging, controversial and generally include some 30 - 70 references a piece. While it has become more fashionable recently to question the cholesterol lowering campaign, to my knowledge, even to the present no one has put together such a well-referenced, well organized and cogent critique of the cholesterol lowering campaign as Dr. Ravnskov. Personally, this was the first book I read which led me to begin to question much of the conventional medical wisdom I had been taught in medical school and beyond. If cholesterol lowering for heart disease may be in error, what other precepts of modern medicine might not be equally idolatrous? I also suspected when I first heard of this book, that despite the author's credentials it would almost certainly be laughably bad, well I was in for a surprise.
While every medical student is taught the results of the vaunted Framingham study which underpins much of the cholesterol lowering campaign, a stance reinforced by unanimity among instructors and peers, as well as a nearly unavoidable multi decade media blitz, Dr. Ravnskov did something I never had, he went back and looked at the relevant medical literature with a critical eye and a fine tooth comb. So for example, one learns that the Framingham study was an exception to more numerous studies at the time which found no association between cholesterol and heart disease. Without going into the compelling detail found in the book, the Framingham study itself, upon examination is shown to have serious methodological flaws which call into question it's conclusions. Similarly, multiple studies since the Framingham study, have also not documented an association between cholesterol levels and heart disease. Once the cholesterol heart disease meme became entrenched, and while not dwelt on by the author, financially profitable, the discrepant findings were ignored or explained away, often with quite convoluted reasoning.
Mainstream medicine, though it knows better, often presents cholesterol as some unmitigated evil which by happenstance exists only to predispose one to heart disease. If it only could be eliminated, there would be no more heart disease. Cholesterol itself though, is not some aberration of physiology, it is present in all membranes and is involved in numerous crucial metabolic pathways including production of steroid hormones among others. Dr. Ravnskov also points out the anti-infective properties specifically of cholesterol in conjunction with low density lipoprotein, LDL cholesterol, and notes numerous other examples of cholesterol's protective effects in disease states. To suppose that there is not the potential for deleterious effects from lowering such a ubiquitous and important molecule as cholesterol makes about as much sense as saying there is no lower healthy boundary for glucose, sodium, aldosterone etc.
Indeed, regulation of cholesterol levels is so important that dietary changes in cholesterol are compensated for by endogenous production of cholesterol by the liver. While this fact is often obliquely acknowledged by physicians Dr. Ravnskov does an excellent job of documenting that diet has zero effect on cholesterol level.
In similar fashion, the author refutes the decades old contention, first popularized by Ancel Keyes that saturated fat plays a significant role in either heart disease or obesity. Considering the enormous efforts undertaken to provide consumers with "low-fat" alternatives to all manner of healthy traditional foods it somehow feels both liberating and subversive to realize the whole low fat edifice is based on a foundation of sand. The unspoken jab in so much of the low fat marketing is that if one doesn't buy their product one is somehow a glutton. How freeing to know that if you like a big slab of grass fed cow butter on your bread you are neither being unhealthy nor any more likely to put on excess weight. Certainly the attempt to restrict dietary fat has failed miserably as a means of decreasing obesity rates. After reviewing the literature, the author concludes that you are no more likely to get fat from eating fat then you are likely to turn green from eating green vegetables.
This review has really barely scratched the surface of this mind bending, meticulous and important work. I could go on for much greater length on this book, however, Dr. Ravnskov has also just released a new work, Ignore the Awkward: How the Cholesterol Myths Are Kept Alive, and I want to give myself time to read and hopefully review that one as well. As I mentioned, heart disease is both a serious and important topic, for those who are interested in their health, it is likely worthwhile to consider the findings of one who has done an honest and exhaustive review of the literature in this area rather than only solely and uncritically accepting the stance of a media campaign for a thirty billion dollar a year industry that says buy our pill or you'll drop dead. While I don't want to overly simplify a complex topic, I suppose if there were one dramatic medical literature based finding brought out in this book that has really stuck with me it is that, on average, elderly people with high cholesterol live longer. Whoda thunk it.
"Fat and Cholesterol are Good for You" is available at Amazon.
Wednesday, January 26, 2011
Tuesday, January 25, 2011
Cost of cardiovascular disease to triple by 2030
Exerpts of an article from Prevention's The Heart.org. I do not know too much about Prevention' position on heart disease relative to mine (which should be quite obvious if you have read much of what I post here on Credible Evidence), but I thought there was some interesting observations made by Michael O'Riordan.
Please avail yourself of the link to the full article and their site for further insite from their perspective.
=========================================================
Cost of cardiovascular disease to triple by 2030
January 25, 2011
Michael O'Riordan
Dallas, TX - In the next 20 years, more than 40% of the US population is expected to have some form of cardiovascular disease, and this will triple the total direct medical costs of caring for hypertension, coronary heart disease, heart failure, stroke, and other forms of cardiovascular disease from the current $273 billion to more than $800 billion, according to a new policy statement from the American Heart Association (AHA) [1].
In addition, the AHA estimates that the prevalence of cardiovascular disease will increase by approximately 10% over the next 20 years given no changes to prevention and treatment trends. If some risk factors, such as diabetes and obesity, continue to increase rapidly, cardiovascular disease prevalence and associated costs might increase even more, write Dr Paul Heidenreich (Veteran Affairs Palo Alto Health Care System, CA) and colleagues in the report, published online January 24, 2011 in Circulation.
At present, cardiovascular disease is the leading cause of death in the US and accounts for 17% of overall healthcare expenditures. In the past, the medical costs of cardiovascular disease increased at an average annual rate of 6%, and this growth in costs has been associated with an increase in life expectancy. That said, there are "many opportunities to further improve cardiovascular health while controlling costs," according to the AHA.
Cardiovascular disease is largely preventable (emphasis by Bill Davis)
The latest 2030 prevalence estimates for hypertension, coronary heart disease, heart failure, and stroke are derived from the 1999-2006 National Health and Nutrition Examination Survey (NHANES) and Census Bureau population estimates for the years 2010 to 2030. Projections of the medical costs associated with cardiovascular disease used the 2001-2005 Medical Expenditure Panel Survey (MEPS) and did not double count expenditures resulting from individuals with multiple conditions.
By 2030, the prevalence of cardiovascular disease is expected to increase 9.9%, with the prevalence of heart failure and stroke increasing approximately 25%. Total direct costs will increase to $818 billion by 2030, according to the AHA estimates, and the total indirect cost to the US in terms of lost productivity is close to $275 billion.
.
.
.
.
.
Offering up a glass-half-full take on the data, Heidenreich and colleagues write that it is "fortunate that cardiovascular disease is largely preventable,"(emphasis by Bill Davis) and the healthcare system needs to focus on prevention and early intervention.
.
.
.
Jan 25, 2011 15:30 EST Source
1.Heidenreich PA, Trogdon JG, Khavjou OA, et al. Forecasting the future of cardiovascular disease in the United States. Circulation 2011; DOI:10.1161/CIR.0b013e31820a55f5. Available at: http://circ.ahajournals.org.
Please avail yourself of the link to the full article and their site for further insite from their perspective.
=========================================================
Cost of cardiovascular disease to triple by 2030
January 25, 2011
Michael O'Riordan
Dallas, TX - In the next 20 years, more than 40% of the US population is expected to have some form of cardiovascular disease, and this will triple the total direct medical costs of caring for hypertension, coronary heart disease, heart failure, stroke, and other forms of cardiovascular disease from the current $273 billion to more than $800 billion, according to a new policy statement from the American Heart Association (AHA) [1].
In addition, the AHA estimates that the prevalence of cardiovascular disease will increase by approximately 10% over the next 20 years given no changes to prevention and treatment trends. If some risk factors, such as diabetes and obesity, continue to increase rapidly, cardiovascular disease prevalence and associated costs might increase even more, write Dr Paul Heidenreich (Veteran Affairs Palo Alto Health Care System, CA) and colleagues in the report, published online January 24, 2011 in Circulation.
At present, cardiovascular disease is the leading cause of death in the US and accounts for 17% of overall healthcare expenditures. In the past, the medical costs of cardiovascular disease increased at an average annual rate of 6%, and this growth in costs has been associated with an increase in life expectancy. That said, there are "many opportunities to further improve cardiovascular health while controlling costs," according to the AHA.
Cardiovascular disease is largely preventable (emphasis by Bill Davis)
The latest 2030 prevalence estimates for hypertension, coronary heart disease, heart failure, and stroke are derived from the 1999-2006 National Health and Nutrition Examination Survey (NHANES) and Census Bureau population estimates for the years 2010 to 2030. Projections of the medical costs associated with cardiovascular disease used the 2001-2005 Medical Expenditure Panel Survey (MEPS) and did not double count expenditures resulting from individuals with multiple conditions.
By 2030, the prevalence of cardiovascular disease is expected to increase 9.9%, with the prevalence of heart failure and stroke increasing approximately 25%. Total direct costs will increase to $818 billion by 2030, according to the AHA estimates, and the total indirect cost to the US in terms of lost productivity is close to $275 billion.
.
.
.
.
.
Offering up a glass-half-full take on the data, Heidenreich and colleagues write that it is "fortunate that cardiovascular disease is largely preventable,"(emphasis by Bill Davis) and the healthcare system needs to focus on prevention and early intervention.
.
.
.
Jan 25, 2011 15:30 EST Source
1.Heidenreich PA, Trogdon JG, Khavjou OA, et al. Forecasting the future of cardiovascular disease in the United States. Circulation 2011; DOI:10.1161/CIR.0b013e31820a55f5. Available at: http://circ.ahajournals.org.
Sunday, January 23, 2011
The five most powerful heart disease prevention strategies
Here is a summary of the strategy from Dr Davis's blog.
Please read his complete article here.
===================================
The five most powerful heart disease prevention strategies
from Heart Scan Blog by Dr. William Davis
You've seen such lists before: 5 steps to prevent heart disease or some such thing. These lists usually say things like "cut your saturated fat," eat a "balanced diet" (whatever the heck that means), exercise, and don't smoke.
I would offer a different list. You already know that smoking is a supremely idiotic habit, so I won't repeat that. Here are the 5 most important strategies I know of that help you prevent heart disease and heart attack:
1) Eliminate wheat from the diet
2) Achieve a desirable 25-hydroxy vitamin D level
3) Supplement omega-3 fatty acids from fish
4) Normalize thyroid function
5) Make exercise fun
Note what is not on the list: cut your fat, eat more "healthy whole grains," take a cholesterol drug, take aspirin. That's the list you'd follow if you feel your hospital needs your $100,000 contribution, otherwise known as coronary bypass surgery.
Please read his complete article here.
===================================
The five most powerful heart disease prevention strategies
from Heart Scan Blog by Dr. William Davis
You've seen such lists before: 5 steps to prevent heart disease or some such thing. These lists usually say things like "cut your saturated fat," eat a "balanced diet" (whatever the heck that means), exercise, and don't smoke.
I would offer a different list. You already know that smoking is a supremely idiotic habit, so I won't repeat that. Here are the 5 most important strategies I know of that help you prevent heart disease and heart attack:
1) Eliminate wheat from the diet
2) Achieve a desirable 25-hydroxy vitamin D level
3) Supplement omega-3 fatty acids from fish
4) Normalize thyroid function
5) Make exercise fun
Note what is not on the list: cut your fat, eat more "healthy whole grains," take a cholesterol drug, take aspirin. That's the list you'd follow if you feel your hospital needs your $100,000 contribution, otherwise known as coronary bypass surgery.
Friday, January 21, 2011
Bad News For Statins Is Good News
Bad News For Statins Is Good News
Posted by Tom Naughton in Bad Medicine
Let’s hope this is the beginning of the end for statins. The so-called wonder drugs have been a cash cow for pharmaceutical companies for decades now, mostly because doctors bought into the idea that high cholesterol causes heart disease, therefore any drug that reduces cholesterol must also reduce heart disease. I’ve lost count of the people I know who don’t have atherosclerosis, but were prescribed statins simply because their cholesterol was above the supposedly magic number of 200. Their doctors weren’t treating heart disease; they were treating a cholesterol score.
While researching Fat Head, I became aware of quite a few doctors who insist that giving statins to people who don’t already have heart disease simply to beat down their cholesterol is worse than worthless … Al Sears, Mike and Mary Dan Eades, Uffe Ravnskov, Malcolm Kendrick, etc. I found the evidence they presented quite convincing. Unfortunately, the medical establishment and the media have tended to either ignore the anti-statin doctors or write them off as a bunch of kooks.
Not anymore … at least I hope not. A new meta-analysis of the effectiveness of statins (and lack thereof) was just released by the Cochrane Collaboration, and it’s bad news for the statin-makers — partly because the analysis itself isn’t flattering, and partly because the Cochrane Collaboration is a highly-respected organization whose work is considered both thorough and unbiased. Consequently, their report has generated quite a bit of media coverage. I’ve already read articles in the UK Telegraph (two), TIME’s online version, the Los Angeles Times, Miller McCune, and Reuter’s Health, among others.
If we piece together quotes from the articles, we end up with a nice summary of the statin story. Let’s start with how and why they became the best-selling drugs of all time:
Back in 1975, Henry Gadsden, the chief executive of the drug company Merck, expressed his frustration that the market for his company’s products was limited to those with some treatable illness. Ideally, he said, he would like to “sell to everyone”.
Three decades later, his dream would seem to have come true - epitomised by the most profitable class of drugs ever discovered, the cholesterol-lowering statins that are taken by an estimated seven million people in Britain, and tens of millions worldwide.
Yup, Merck and the other pharmaceuticals wanted to sell drugs to healthy people, and by gosh, they finally figured out how to do it.
The story starts with the arrival of “cholesterol consciousness”: the thesis that those indulging in (for example) bacon and eggs for breakfast boosted the cholesterol level in the blood, causing the arteries to become narrow, and making a heart attack more likely.
Although this idea has its critics, there is no doubt that the small proportion of the population with a genetic predisposition towards high cholesterol levels are at greater risk of circulatory disorders. Encouraging them to switch to a healthy diet had failed to lower that risk - so the idea gained ground that cholesterol-lowering drugs might be the answer.
The small proportion of the population with a genetic predisposition are those with familial hyperlipidemia. Their LDL is extraordinarily high because their LDL receptors don’t work and therefore don’t remove LDL from the bloodstream. Cholesterol-lowering drugs were shown to reduce their rate of heart disease by a teeny, tiny bit. From that result, the medical community decided cholesterol is a killer and we should all stop eating bacon and eggs — even though low-fat diets didn’t do diddly for the people with hyperlipidemia. Go figure.
An even more important factor, especially in the US, was the drive to establish “clinical practice guidelines”, under which panels would set the optimal treatment for any given condition. Successive guidelines have forced the “normal” level of cholesterol ever lower, resulting in leaps in the numbers deemed eligible for treatment. In the US, the figure went from 15 million to 40 million.
That’s how you sell drugs to healthy people: redefine normal cholesterol levels as dangerous. Among the un-medicated population, average total cholesterol was around 220 a few decades ago. Doctors rarely warned patients about heart disease unless their cholesterol was 250 or higher. But if 220 was the average, how did the new “normal” end up being 200?
After it was pointed out that those responsible for the most recent guidelines had failed to declare any potential conflicts of interest, it subsequently emerged that most of them had received research grants or consultancy fees from the drug companies involved in manufacturing statins.
That’s how. By declaring 200 to be the target level for cholesterol, the researchers (ahem, ahem) who wrote the guidelines guaranteed their paymasters millions of new customers.
Not surprisingly, quite a few clinical studies eventually concluded that statins prevent heart disease. I say “not surprisingly” because nearly all the studies were funded and conducted by the pharmaceutical companies. According to the Cochrane review, the studies might’ve been (surprise!) skewed to exaggerate the benefits and minimize the side effects:
In particular, while all the studies focused on benefits, only half provided information on the side effects of the drugs, said Dr. Shah Ebrahim, whose group’s findings are published by the Cochrane Collaboration, an international organization that evaluates medical research.
“There is evidence that the reports cherry-picked the best outcomes for presentation,” he added, “which will tend to inflate apparent benefits of treatment.”
While there appeared to be no difference in side effects between trials participants taking dummy pills and statins, the researchers say those results aren’t credible.
“Any appraisal we can make of adverse events is biased by failure to report these events,” Ebrahim said in an e-mail to Reuters Health. “We believe that trial funders, investigators and journal editors have failed to provide adequate information to doctors and their patients to assess the benefits and harms of statins in primary prevention.”
The good news is that while Merck and Pfizer may not report on negative side effects, more media outlets are:
Dr. Greg Burns (not his real name) is a 72-year-old retired radiologist living in Connecticut. Until early last year, he ran with his dog at canine agility meets, skied, ice skated and played 18 holes of golf. He is now unable to walk and is taking a course of medication that will postpone, by a few months, his death.
Burns’ rapid decline began in December 2007 when he suffered a short-acting stroke from which he fully recovered. His cholesterol level was elevated and so as a preventative measure his doctor prescribed a 20mg daily dose of Crestor, a cholesterol-lowering drug in the “statin” class.
A few months after beginning Crestor, Burns developed muscle cramps. He was assured by his doctors that these were not serious side effects of taking the drug. But in December 2008 when tests showed that his creatine phosphokinase - an enzyme that is released into the blood stream when muscle cells are damaged - was elevated, Dr. Burns stopped taking Crestor. When his enzyme levels returned to normal, he began taking Pravachol, another statin drug. He quickly developed weakness in his lower legs and a right foot drop.
Mayo Clinic cardiologists acknowledge that the side effects of statin drugs can include muscle pain, extreme fatigue, liver damage, digestive problems and neurological damage including memory loss.
Of course, not everyone who takes statins will experience side effects, so it’s a question of balancing benefits and risks, just like with any other drug. So let’s look at the supposed benefits.
If you’ve seen Lipitor ads on TV (and if you haven’t, it means you don’t watch TV), you know Pfizer claims Lipitor reduces the rate of heart attacks by 36%. As I’ve explained in previous posts, that figure may sound impressive, but basically it means that during the clinical trials, three out of every 100 men who took a placebo had a heart attack, while slightly less than two out of every 100 men who took Lipitor had a heart attack. So for every 100 men treated for ten years, we’re preventing (in theory) one heart attack. That’s one heart attack, not necessarily one death.
But even those unimpressive results were found only among with men with existing heart disease or multiple risk factors for heart disease — not among women, and not among otherwise healthy people who happen to have high cholesterol.
But of course, statins didn’t become the most profitable drugs in history by being prescribed solely to men with existing heart disease. Nope, statins became a cash cow when doctors started prescribing them to pretty much everybody whose cholesterol is above 200. (In the UK, you can even buy your future muscle or memory problems over the counter — yippee!)
The theory, of course, was that statins could prevent heart disease from developing in the first place, otherwise known as “primary prevention.” The Cochrane report casts more than a little doubt on that theory, as several media articles pointed out:
An authoritative review shows there is little evidence that the cholesterol-lowering drugs protect people who are not already at a high risk of heart disease.
Experts who advocate the use of statins say they have helped prolong thousands of lives by preventing heart attacks and other cardiovascular events. But a wide-ranging review of previous studies, published today in the journal The Cochrane Library, urges “caution” among GPs who prescribe them. It concludes that there is no “strong evidence” to suggest that statins reduce coronary heart disease deaths among those who have not suffered a heart attack or other cardiovascular event in the past.
Shah Ebrahim, a professor of public health at the London School of Hygiene and Tropical Medicine, who co-wrote the report, called on doctors to stop giving patients the drugs unnecessarily.
Just one life is currently saved for every 1,000 people who take them each year, the report says.
Great … so to prevent (in theory) one fatal heart attack among every 1,000 people who take statins, we’ve created lord-only-knows-how-many cases of muscle degeneration, memory loss, kidney failure, erectile dysfunction and liver damage. Of course, that works out well for Big Pharma — they sell drugs to treat those conditions, too.
I’ve said it before, and I’ll say it again: statins are some of the worst drugs ever. I’m just happy to see more people in the news media are catching on.
Posted by Tom Naughton in Bad Medicine
Let’s hope this is the beginning of the end for statins. The so-called wonder drugs have been a cash cow for pharmaceutical companies for decades now, mostly because doctors bought into the idea that high cholesterol causes heart disease, therefore any drug that reduces cholesterol must also reduce heart disease. I’ve lost count of the people I know who don’t have atherosclerosis, but were prescribed statins simply because their cholesterol was above the supposedly magic number of 200. Their doctors weren’t treating heart disease; they were treating a cholesterol score.
While researching Fat Head, I became aware of quite a few doctors who insist that giving statins to people who don’t already have heart disease simply to beat down their cholesterol is worse than worthless … Al Sears, Mike and Mary Dan Eades, Uffe Ravnskov, Malcolm Kendrick, etc. I found the evidence they presented quite convincing. Unfortunately, the medical establishment and the media have tended to either ignore the anti-statin doctors or write them off as a bunch of kooks.
Not anymore … at least I hope not. A new meta-analysis of the effectiveness of statins (and lack thereof) was just released by the Cochrane Collaboration, and it’s bad news for the statin-makers — partly because the analysis itself isn’t flattering, and partly because the Cochrane Collaboration is a highly-respected organization whose work is considered both thorough and unbiased. Consequently, their report has generated quite a bit of media coverage. I’ve already read articles in the UK Telegraph (two), TIME’s online version, the Los Angeles Times, Miller McCune, and Reuter’s Health, among others.
If we piece together quotes from the articles, we end up with a nice summary of the statin story. Let’s start with how and why they became the best-selling drugs of all time:
Back in 1975, Henry Gadsden, the chief executive of the drug company Merck, expressed his frustration that the market for his company’s products was limited to those with some treatable illness. Ideally, he said, he would like to “sell to everyone”.
Three decades later, his dream would seem to have come true - epitomised by the most profitable class of drugs ever discovered, the cholesterol-lowering statins that are taken by an estimated seven million people in Britain, and tens of millions worldwide.
Yup, Merck and the other pharmaceuticals wanted to sell drugs to healthy people, and by gosh, they finally figured out how to do it.
The story starts with the arrival of “cholesterol consciousness”: the thesis that those indulging in (for example) bacon and eggs for breakfast boosted the cholesterol level in the blood, causing the arteries to become narrow, and making a heart attack more likely.
Although this idea has its critics, there is no doubt that the small proportion of the population with a genetic predisposition towards high cholesterol levels are at greater risk of circulatory disorders. Encouraging them to switch to a healthy diet had failed to lower that risk - so the idea gained ground that cholesterol-lowering drugs might be the answer.
The small proportion of the population with a genetic predisposition are those with familial hyperlipidemia. Their LDL is extraordinarily high because their LDL receptors don’t work and therefore don’t remove LDL from the bloodstream. Cholesterol-lowering drugs were shown to reduce their rate of heart disease by a teeny, tiny bit. From that result, the medical community decided cholesterol is a killer and we should all stop eating bacon and eggs — even though low-fat diets didn’t do diddly for the people with hyperlipidemia. Go figure.
An even more important factor, especially in the US, was the drive to establish “clinical practice guidelines”, under which panels would set the optimal treatment for any given condition. Successive guidelines have forced the “normal” level of cholesterol ever lower, resulting in leaps in the numbers deemed eligible for treatment. In the US, the figure went from 15 million to 40 million.
That’s how you sell drugs to healthy people: redefine normal cholesterol levels as dangerous. Among the un-medicated population, average total cholesterol was around 220 a few decades ago. Doctors rarely warned patients about heart disease unless their cholesterol was 250 or higher. But if 220 was the average, how did the new “normal” end up being 200?
After it was pointed out that those responsible for the most recent guidelines had failed to declare any potential conflicts of interest, it subsequently emerged that most of them had received research grants or consultancy fees from the drug companies involved in manufacturing statins.
That’s how. By declaring 200 to be the target level for cholesterol, the researchers (ahem, ahem) who wrote the guidelines guaranteed their paymasters millions of new customers.
Not surprisingly, quite a few clinical studies eventually concluded that statins prevent heart disease. I say “not surprisingly” because nearly all the studies were funded and conducted by the pharmaceutical companies. According to the Cochrane review, the studies might’ve been (surprise!) skewed to exaggerate the benefits and minimize the side effects:
In particular, while all the studies focused on benefits, only half provided information on the side effects of the drugs, said Dr. Shah Ebrahim, whose group’s findings are published by the Cochrane Collaboration, an international organization that evaluates medical research.
“There is evidence that the reports cherry-picked the best outcomes for presentation,” he added, “which will tend to inflate apparent benefits of treatment.”
While there appeared to be no difference in side effects between trials participants taking dummy pills and statins, the researchers say those results aren’t credible.
“Any appraisal we can make of adverse events is biased by failure to report these events,” Ebrahim said in an e-mail to Reuters Health. “We believe that trial funders, investigators and journal editors have failed to provide adequate information to doctors and their patients to assess the benefits and harms of statins in primary prevention.”
The good news is that while Merck and Pfizer may not report on negative side effects, more media outlets are:
Dr. Greg Burns (not his real name) is a 72-year-old retired radiologist living in Connecticut. Until early last year, he ran with his dog at canine agility meets, skied, ice skated and played 18 holes of golf. He is now unable to walk and is taking a course of medication that will postpone, by a few months, his death.
Burns’ rapid decline began in December 2007 when he suffered a short-acting stroke from which he fully recovered. His cholesterol level was elevated and so as a preventative measure his doctor prescribed a 20mg daily dose of Crestor, a cholesterol-lowering drug in the “statin” class.
A few months after beginning Crestor, Burns developed muscle cramps. He was assured by his doctors that these were not serious side effects of taking the drug. But in December 2008 when tests showed that his creatine phosphokinase - an enzyme that is released into the blood stream when muscle cells are damaged - was elevated, Dr. Burns stopped taking Crestor. When his enzyme levels returned to normal, he began taking Pravachol, another statin drug. He quickly developed weakness in his lower legs and a right foot drop.
Mayo Clinic cardiologists acknowledge that the side effects of statin drugs can include muscle pain, extreme fatigue, liver damage, digestive problems and neurological damage including memory loss.
Of course, not everyone who takes statins will experience side effects, so it’s a question of balancing benefits and risks, just like with any other drug. So let’s look at the supposed benefits.
If you’ve seen Lipitor ads on TV (and if you haven’t, it means you don’t watch TV), you know Pfizer claims Lipitor reduces the rate of heart attacks by 36%. As I’ve explained in previous posts, that figure may sound impressive, but basically it means that during the clinical trials, three out of every 100 men who took a placebo had a heart attack, while slightly less than two out of every 100 men who took Lipitor had a heart attack. So for every 100 men treated for ten years, we’re preventing (in theory) one heart attack. That’s one heart attack, not necessarily one death.
But even those unimpressive results were found only among with men with existing heart disease or multiple risk factors for heart disease — not among women, and not among otherwise healthy people who happen to have high cholesterol.
But of course, statins didn’t become the most profitable drugs in history by being prescribed solely to men with existing heart disease. Nope, statins became a cash cow when doctors started prescribing them to pretty much everybody whose cholesterol is above 200. (In the UK, you can even buy your future muscle or memory problems over the counter — yippee!)
The theory, of course, was that statins could prevent heart disease from developing in the first place, otherwise known as “primary prevention.” The Cochrane report casts more than a little doubt on that theory, as several media articles pointed out:
An authoritative review shows there is little evidence that the cholesterol-lowering drugs protect people who are not already at a high risk of heart disease.
Experts who advocate the use of statins say they have helped prolong thousands of lives by preventing heart attacks and other cardiovascular events. But a wide-ranging review of previous studies, published today in the journal The Cochrane Library, urges “caution” among GPs who prescribe them. It concludes that there is no “strong evidence” to suggest that statins reduce coronary heart disease deaths among those who have not suffered a heart attack or other cardiovascular event in the past.
Shah Ebrahim, a professor of public health at the London School of Hygiene and Tropical Medicine, who co-wrote the report, called on doctors to stop giving patients the drugs unnecessarily.
Just one life is currently saved for every 1,000 people who take them each year, the report says.
Great … so to prevent (in theory) one fatal heart attack among every 1,000 people who take statins, we’ve created lord-only-knows-how-many cases of muscle degeneration, memory loss, kidney failure, erectile dysfunction and liver damage. Of course, that works out well for Big Pharma — they sell drugs to treat those conditions, too.
I’ve said it before, and I’ll say it again: statins are some of the worst drugs ever. I’m just happy to see more people in the news media are catching on.
Researchers urge caution in prescribing statins to healthy people
Good Article By Dr Briffa on statin use
===================================================
- Dr Briffa's Blog - http://www.drbriffa.com -
Researchers urge caution in prescribing statins to healthy people
Posted By John Briffa On 20 January 2011 @ 12:51 am In Cholesterol and Statins, Food and Medical Politics
My blog on Monday focused on a piece published in the American Journal of Public Health which detailed some of the tactics drug companies use to persuade doctors to prescribe their wares. The conclusion? The more aggressively a drug is marketed to doctors, the more suspicious of it we should be, basically. I ended the blog with the following remark: “Applying the inverse benefits law should, I think, cause us to be particularly wary of cholesterol reducing drugs. Let us not be too surprised, then, that the science shows statin drugs to be not-very-effective at saving lives, while at the same time putting those who take them at risk of sometimes severe adverse effects.”
What I didn’t know when I wrote this is that a review of statin treatment was about to be published by the researchers from the Cochrane Collaboration [1]. This international collective of researchers prides itself of conducting systematic, unbiased reviews of treatments. The point of this review, the researchers claimed, was to assess the risks and benefits of statin treatment in what is known as the ‘primary prevention’ setting.
Here’s some context on this from a previous blog post:
Statin therapy broadly divides into two main approaches:
Primary prevention – where statins are given to essentially healthy people with no known cardiovascular disease (i.e. there is no evidence of arterial disease and no history of a heart attack and/or stroke)
Secondary prevention – where statins are given to people with known arterial disease and/or a history of heart attack and/or stroke
This distinction is important because individuals in the secondary prevention category are at generally high risk of further problems, and stand to benefit most from statin therapy. On the other hand, individuals in the primary prevention category are at generally low risk of cardiovascular disease issues (such as heart attack and stroke), and may therefore not benefit much from a strategy or treatment intended to prevent cardiovascular disease. This primary prevention category is particularly important when one considers that the vast majority of people taking statins are in this category, and if the pharmaceutical industry and some of its hired hands in the scientific and medical community have their way, increasing numbers of people will be taking statins in the future.
In the recent Cochrane review, 14 trials were analysed. They reported, having amassed the evidence, that overall risk of death was reduced by 17 per cent, and overall risk of fatal and non-fatal cardiovascular events such as heart attacks and strokes were reduced by 30 per cent. On face value, these results look pretty good. However, the devil turns out to be in the detail.
To begin with, the researchers allowed studies in which up to 10 per cent of participants were in the secondary prevention category. What this basically means is that their assessment of the data was not really focused on the primary prevention setting. What’s required is an analysis of purely primary prevention data. The Cochrane researchers did not manage this, but other researchers have. A meta-analysis of data from individuals in the primary prevention category published just last year [2] (reported here [1]), no reduction in overall risk of death was found with statin therapy.
The Cochrane authors do mention this study, but it’s somewhat buried in the discussion. It is not mentioned at all in the introduction of their review in which they list more than one review, like theirs, that allowed secondary prevention data to corrupt the primary prevention data.
The Cochrane authors have also largely confined themselves to assessment of ‘relative risk’. However, it is well accepted that a more useful judge of the true effectiveness of a treatment is absolute risk reduction (if risk if low, relative reductions in risk translate to very small real reductions in risk) as well as ‘number need to treat’ (e.g. how many people need to be treated for one year to prevent one heart attack – generally, NNTs in primary prevention are high).
However, there are, I think, many good things about this Cochrane review. It highlights many of the deficiencies in the evidence-based regarding statin therapy. Here are a few highlights:
•Of the 14 studies reviewed, four of them were not double-blind in design (double-blind studies, where neither the researchers not the participants know whether they are taking the active drug or placebo are considered the ‘gold standard’ for good clinical research).
•11 of the 14 studies recruited individuals who, while perhaps not having a history of cardiovascular disease, nonetheless had what would traditionally be regarded as at least one major risk factor for cardiovascular disease such as raised blood fats, high blood pressure or diabetes.
•2 major trials were stopped prematurely. This is as cause for concern as may lead to “an over-estimation of treatment effects…”
•All but one of the studies was industry-funded. According to the authors, “It is now established that published pharmaceutical industry-sponsored trials are more likely than non-industry-funded trials to report results and conclusions that favour drug over placebo due to biased reporting and/or interpretation of trial results.”
•The study participants were ostensibly white, male and middle-aged (average age 57), and the authors of the Cochrane review question the appropriateness of this data in, say, older individuals and women.
•There was no evidence of significant adverse effects, though about half of the studies did not even report adverse effects. (For more on adverse effects, see the blog post I link to above).
•There was little or no significant evidence on the cost-effectiveness of statins in primary prevention.
•There was little or no significant evidence on the effects of statins on quality of life.
The authors conclude:
“This current systematic review highlights the shortcomings in the published trials and we recommend that caution should be taken in prescribing statins for primary prevention among people at low cardiovascular risk.”
While I have my reservations about this review, I do think it is high commendable that some researchers (at least) have a mind to review the data on statins with a degree of objectivity. While statins are vigorously promoted by many doctors and researchers, it is good to see some academics urging caution. It’s good that they are presenting the other side to statins. It’s a story that is rarely heard, but one that needs to be heard if individuals are going to make truly informed choices about whether they take a statin or not.
UPDATE.
After writing this post yesterday I got to talk about some of the issues the research raises on Channel 4 News here in the UK. Here’s the video…
References:
1. Taylor F, et al. Statins for the primary prevention of cardiovascular disease. Cochrane Database of Systematic Reviews 2011, Issue 1. Art. No.: CD004816. DOI: 10.1002/14651858.CD004816.pub4.
2. Ray KK, et al. Statins and all-cause mortality in high-risk primary prevention: a meta-analysis of 11 randomized controlled trials involving 65 229 participants. Arch Intern Med. 2010;170(12):1024-1031
--------------------------------------------------------------------------------
7 Comments
7 Comments To "Researchers urge caution in prescribing statins to healthy people"
#1 Comment By Chris On 20 January 2011 @ 8:05 pm
Dr Briffa, well done, an excellent summation of the Cochrane report. Congratulations too for your contribution to the debate on CH4 news.
A PDF of the report can be found [2]
It’s an uphill struggle I know, but the report did receive reasonable media coverage. BBC radio news reported it as did the [3]. BBC Breakfast News (BBC1) covered it too and invited Dr Rosemary Leonard to pass comments. Dr Leonard largely defended the use of statins. To some in the know she would, no doubt, have looked pretty dumb.
Of the papers I noticed the http://www.drbriffa.com/
Damn those html tags!
#3 Comment By Chris On 20 January 2011 @ 8:14 pm
Of the papers I noticed the [4] were quick on the uptake
#4 Comment By Jo On 21 January 2011 @ 6:54 pm
Wow, you put your case very well Dr Briffa. C4 covered this better than the BBC reports I saw. The Beeb are clinging on to the idea that statins are still a wonder drug. Their resident doc seems to push the conventional wisdom, but I imagine that’s what a state run news broadcaster is expected to do so she has to tow the line. My doc prescribed statins to me despite my cholesterol being in the ‘green’ area (they think we’re so stupid we need a traffic light system to understand). Maybe we will be once the entire population is taking these pills. I experienced memory loss and stopped taking them.
#5 Pingback By Tweets that mention Researchers urge caution in prescribing statins to healthy people
Dr Briffa’s Blog — Topsy.com On 21 January 2011 @ 9:11 pm
[...] This post was mentioned on Twitter by Jayne, H Padarin. H Padarin said: A step in the right direction… the real story of statins is finally starting to be acknowledged. Anyone on… [5] [...]
#6 Comment By gill oliver On 21 January 2011 @ 10:53 pm
I decided two months ago to stop taking statins, as i was aching all over and just didn’t feel right, i used to take anti- inflammatory tabs, plus co- codamol for my back pain, i now no longer need these and can get by on the occasional paracetamol and i feel much better in myself.
#7 Pingback By Check the links…
Pure Spontaneity On 21 January 2011 @ 11:38 pm
[...] Bad news for statins = good news. And more. [...]
--------------------------------------------------------------------------------
Article printed from Dr Briffa's Blog:
URL to article: http://www.drbriffa.com/2011/01/20/researchers-urge-caution-in-prescribing-statins-to-healthy-people/
URLs in this post:
[1] here: http://www.drbriffa.com/2010/06/30/do-statins-save-lives-in-essentially-healthy-people-no/
[2] : http://www.drbriffa.comwww.thecochranelibrary.com/details/file/985303/CD004816.html
[3] : http://www.bbc.co.uk/news/health-12224312
[4] : http://www.telegraph.co.uk/health/healthnews/8267570/Millions-taking-statins-needlessly.html
[5] : http://fb.me/SAQBLhUX
Copyright © 2010 Dr Briffa's Blog. All rights reserved.
===================================================
- Dr Briffa's Blog - http://www.drbriffa.com -
Researchers urge caution in prescribing statins to healthy people
Posted By John Briffa On 20 January 2011 @ 12:51 am In Cholesterol and Statins, Food and Medical Politics
My blog on Monday focused on a piece published in the American Journal of Public Health which detailed some of the tactics drug companies use to persuade doctors to prescribe their wares. The conclusion? The more aggressively a drug is marketed to doctors, the more suspicious of it we should be, basically. I ended the blog with the following remark: “Applying the inverse benefits law should, I think, cause us to be particularly wary of cholesterol reducing drugs. Let us not be too surprised, then, that the science shows statin drugs to be not-very-effective at saving lives, while at the same time putting those who take them at risk of sometimes severe adverse effects.”
What I didn’t know when I wrote this is that a review of statin treatment was about to be published by the researchers from the Cochrane Collaboration [1]. This international collective of researchers prides itself of conducting systematic, unbiased reviews of treatments. The point of this review, the researchers claimed, was to assess the risks and benefits of statin treatment in what is known as the ‘primary prevention’ setting.
Here’s some context on this from a previous blog post:
Statin therapy broadly divides into two main approaches:
Primary prevention – where statins are given to essentially healthy people with no known cardiovascular disease (i.e. there is no evidence of arterial disease and no history of a heart attack and/or stroke)
Secondary prevention – where statins are given to people with known arterial disease and/or a history of heart attack and/or stroke
This distinction is important because individuals in the secondary prevention category are at generally high risk of further problems, and stand to benefit most from statin therapy. On the other hand, individuals in the primary prevention category are at generally low risk of cardiovascular disease issues (such as heart attack and stroke), and may therefore not benefit much from a strategy or treatment intended to prevent cardiovascular disease. This primary prevention category is particularly important when one considers that the vast majority of people taking statins are in this category, and if the pharmaceutical industry and some of its hired hands in the scientific and medical community have their way, increasing numbers of people will be taking statins in the future.
In the recent Cochrane review, 14 trials were analysed. They reported, having amassed the evidence, that overall risk of death was reduced by 17 per cent, and overall risk of fatal and non-fatal cardiovascular events such as heart attacks and strokes were reduced by 30 per cent. On face value, these results look pretty good. However, the devil turns out to be in the detail.
To begin with, the researchers allowed studies in which up to 10 per cent of participants were in the secondary prevention category. What this basically means is that their assessment of the data was not really focused on the primary prevention setting. What’s required is an analysis of purely primary prevention data. The Cochrane researchers did not manage this, but other researchers have. A meta-analysis of data from individuals in the primary prevention category published just last year [2] (reported here [1]), no reduction in overall risk of death was found with statin therapy.
The Cochrane authors do mention this study, but it’s somewhat buried in the discussion. It is not mentioned at all in the introduction of their review in which they list more than one review, like theirs, that allowed secondary prevention data to corrupt the primary prevention data.
The Cochrane authors have also largely confined themselves to assessment of ‘relative risk’. However, it is well accepted that a more useful judge of the true effectiveness of a treatment is absolute risk reduction (if risk if low, relative reductions in risk translate to very small real reductions in risk) as well as ‘number need to treat’ (e.g. how many people need to be treated for one year to prevent one heart attack – generally, NNTs in primary prevention are high).
However, there are, I think, many good things about this Cochrane review. It highlights many of the deficiencies in the evidence-based regarding statin therapy. Here are a few highlights:
•Of the 14 studies reviewed, four of them were not double-blind in design (double-blind studies, where neither the researchers not the participants know whether they are taking the active drug or placebo are considered the ‘gold standard’ for good clinical research).
•11 of the 14 studies recruited individuals who, while perhaps not having a history of cardiovascular disease, nonetheless had what would traditionally be regarded as at least one major risk factor for cardiovascular disease such as raised blood fats, high blood pressure or diabetes.
•2 major trials were stopped prematurely. This is as cause for concern as may lead to “an over-estimation of treatment effects…”
•All but one of the studies was industry-funded. According to the authors, “It is now established that published pharmaceutical industry-sponsored trials are more likely than non-industry-funded trials to report results and conclusions that favour drug over placebo due to biased reporting and/or interpretation of trial results.”
•The study participants were ostensibly white, male and middle-aged (average age 57), and the authors of the Cochrane review question the appropriateness of this data in, say, older individuals and women.
•There was no evidence of significant adverse effects, though about half of the studies did not even report adverse effects. (For more on adverse effects, see the blog post I link to above).
•There was little or no significant evidence on the cost-effectiveness of statins in primary prevention.
•There was little or no significant evidence on the effects of statins on quality of life.
The authors conclude:
“This current systematic review highlights the shortcomings in the published trials and we recommend that caution should be taken in prescribing statins for primary prevention among people at low cardiovascular risk.”
While I have my reservations about this review, I do think it is high commendable that some researchers (at least) have a mind to review the data on statins with a degree of objectivity. While statins are vigorously promoted by many doctors and researchers, it is good to see some academics urging caution. It’s good that they are presenting the other side to statins. It’s a story that is rarely heard, but one that needs to be heard if individuals are going to make truly informed choices about whether they take a statin or not.
UPDATE.
After writing this post yesterday I got to talk about some of the issues the research raises on Channel 4 News here in the UK. Here’s the video…
References:
1. Taylor F, et al. Statins for the primary prevention of cardiovascular disease. Cochrane Database of Systematic Reviews 2011, Issue 1. Art. No.: CD004816. DOI: 10.1002/14651858.CD004816.pub4.
2. Ray KK, et al. Statins and all-cause mortality in high-risk primary prevention: a meta-analysis of 11 randomized controlled trials involving 65 229 participants. Arch Intern Med. 2010;170(12):1024-1031
--------------------------------------------------------------------------------
7 Comments
7 Comments To "Researchers urge caution in prescribing statins to healthy people"
#1 Comment By Chris On 20 January 2011 @ 8:05 pm
Dr Briffa, well done, an excellent summation of the Cochrane report. Congratulations too for your contribution to the debate on CH4 news.
A PDF of the report can be found [2]
It’s an uphill struggle I know, but the report did receive reasonable media coverage. BBC radio news reported it as did the [3]. BBC Breakfast News (BBC1) covered it too and invited Dr Rosemary Leonard to pass comments. Dr Leonard largely defended the use of statins. To some in the know she would, no doubt, have looked pretty dumb.
Of the papers I noticed the http://www.drbriffa.com/
Damn those html tags!
#3 Comment By Chris On 20 January 2011 @ 8:14 pm
Of the papers I noticed the [4] were quick on the uptake
#4 Comment By Jo On 21 January 2011 @ 6:54 pm
Wow, you put your case very well Dr Briffa. C4 covered this better than the BBC reports I saw. The Beeb are clinging on to the idea that statins are still a wonder drug. Their resident doc seems to push the conventional wisdom, but I imagine that’s what a state run news broadcaster is expected to do so she has to tow the line. My doc prescribed statins to me despite my cholesterol being in the ‘green’ area (they think we’re so stupid we need a traffic light system to understand). Maybe we will be once the entire population is taking these pills. I experienced memory loss and stopped taking them.
#5 Pingback By Tweets that mention Researchers urge caution in prescribing statins to healthy people
Dr Briffa’s Blog — Topsy.com On 21 January 2011 @ 9:11 pm
[...] This post was mentioned on Twitter by Jayne, H Padarin. H Padarin said: A step in the right direction… the real story of statins is finally starting to be acknowledged. Anyone on… [5] [...]
#6 Comment By gill oliver On 21 January 2011 @ 10:53 pm
I decided two months ago to stop taking statins, as i was aching all over and just didn’t feel right, i used to take anti- inflammatory tabs, plus co- codamol for my back pain, i now no longer need these and can get by on the occasional paracetamol and i feel much better in myself.
#7 Pingback By Check the links…
Pure Spontaneity On 21 January 2011 @ 11:38 pm
[...] Bad news for statins = good news. And more. [...]
--------------------------------------------------------------------------------
Article printed from Dr Briffa's Blog:
URL to article: http://www.drbriffa.com/2011/01/20/researchers-urge-caution-in-prescribing-statins-to-healthy-people/
URLs in this post:
[1] here: http://www.drbriffa.com/2010/06/30/do-statins-save-lives-in-essentially-healthy-people-no/
[2] : http://www.drbriffa.comwww.thecochranelibrary.com/details/file/985303/CD004816.html
[3] : http://www.bbc.co.uk/news/health-12224312
[4] : http://www.telegraph.co.uk/health/healthnews/8267570/Millions-taking-statins-needlessly.html
[5] : http://fb.me/SAQBLhUX
Copyright © 2010 Dr Briffa's Blog. All rights reserved.
Friday, January 14, 2011
MI patients with CKD not taking meds
MI patients with CKD not taking meds
January 14, 2011
Michael O'Riordan
Stanford, CA - An analysis of elderly survivors of MI shows very low rates of adherence to medical therapy for secondary prevention, with more than one-third of patients not taking their ACE inhibitors/angiotensin receptor blockers (ARBs), beta blockers, and statins at one year, and adherence rates falling off further at three years [1]. Patients with baseline kidney dysfunction are even more problematic, report investigators, with these patients less adherent to their medication than those with better kidney function at baseline.
"The results of our analysis have important clinical implications, because elderly patients with kidney dysfunction are at high risk for cardiovascular mortality and may therefore benefit the most from dedicated interventions aimed at improving long-term medication adherence," write Dr Tara Chang (Stanford University School of Medicine, CA) and colleagues in a report published online January 13, 2011 in the Clinical Journal of the American Society of Nephrology.
Previous studies by the group have shown that outpatient use of ACE inhibitors and ARBs within 90 days of hospitalization for MI were lower among patients with chronic kidney disease (CKD). The present study of more than 2100 patients 65 years of age or older enrolled in a pharmacy benefits program extends these results further, they note.
Approximately 70% of patients were adherent to each of the three medication classes (ACE inhibitors/ARBs, beta blockers, and statins) at baseline. Using pharmacy refill data to determine the percentage of days covered, only half of patients were adherent to the medication at 36 months. Adherence was defined as a percentage of days covered >80%.
Stratifying patients by estimated glomerular filtration rate (eGFR), investigators report that long-term ACE-inhibitor/ARB and beta-blocker use adherence differed by kidney function. Among those in the lowest eGFR category, defined as <30 mL/min/1.73 m2, there was a steeper drop off in medication adherence, with similar findings observed among patients taking beta blockers. There was no difference in long-term adherence to statin therapy in patients with different levels of kidney function.
Discussing the possible reasons for the poor adherence among kidney-dysfunction patients, Chang and colleagues point out that CKD patients have higher rates of functional limitations, cognitive impairment, and depression, and these are all associated with lower rates of medication adherence. Also, patients with CKD take, on average, at least eight prescribed medications, with some patients taking as many as 24 drugs, often taking different medications multiple times per day. The group points out that the prescription drug program in the present study paid for all the medications and required only small copayments.
"If long-term medication adherence is to be improved, a multifaceted approach that addresses not only financial assistance, but also a deeper understanding of physical and psychologic barriers to proper medication-taking behavior, is paramount," they conclude.
Article published here.
==================================================
My comment: Maybe it's the side effects or evidence contrary to what the main stream medical/pharmaceutical communities claim. Those are exactly what it was in my case.
January 14, 2011
Michael O'Riordan
Stanford, CA - An analysis of elderly survivors of MI shows very low rates of adherence to medical therapy for secondary prevention, with more than one-third of patients not taking their ACE inhibitors/angiotensin receptor blockers (ARBs), beta blockers, and statins at one year, and adherence rates falling off further at three years [1]. Patients with baseline kidney dysfunction are even more problematic, report investigators, with these patients less adherent to their medication than those with better kidney function at baseline.
"The results of our analysis have important clinical implications, because elderly patients with kidney dysfunction are at high risk for cardiovascular mortality and may therefore benefit the most from dedicated interventions aimed at improving long-term medication adherence," write Dr Tara Chang (Stanford University School of Medicine, CA) and colleagues in a report published online January 13, 2011 in the Clinical Journal of the American Society of Nephrology.
Previous studies by the group have shown that outpatient use of ACE inhibitors and ARBs within 90 days of hospitalization for MI were lower among patients with chronic kidney disease (CKD). The present study of more than 2100 patients 65 years of age or older enrolled in a pharmacy benefits program extends these results further, they note.
Approximately 70% of patients were adherent to each of the three medication classes (ACE inhibitors/ARBs, beta blockers, and statins) at baseline. Using pharmacy refill data to determine the percentage of days covered, only half of patients were adherent to the medication at 36 months. Adherence was defined as a percentage of days covered >80%.
Stratifying patients by estimated glomerular filtration rate (eGFR), investigators report that long-term ACE-inhibitor/ARB and beta-blocker use adherence differed by kidney function. Among those in the lowest eGFR category, defined as <30 mL/min/1.73 m2, there was a steeper drop off in medication adherence, with similar findings observed among patients taking beta blockers. There was no difference in long-term adherence to statin therapy in patients with different levels of kidney function.
Discussing the possible reasons for the poor adherence among kidney-dysfunction patients, Chang and colleagues point out that CKD patients have higher rates of functional limitations, cognitive impairment, and depression, and these are all associated with lower rates of medication adherence. Also, patients with CKD take, on average, at least eight prescribed medications, with some patients taking as many as 24 drugs, often taking different medications multiple times per day. The group points out that the prescription drug program in the present study paid for all the medications and required only small copayments.
"If long-term medication adherence is to be improved, a multifaceted approach that addresses not only financial assistance, but also a deeper understanding of physical and psychologic barriers to proper medication-taking behavior, is paramount," they conclude.
Article published here.
==================================================
My comment: Maybe it's the side effects or evidence contrary to what the main stream medical/pharmaceutical communities claim. Those are exactly what it was in my case.
Does Dietary Saturated Fat Increase Blood Cholesterol?
Does Dietary Saturated Fat Increase Blood Cholesterol? An Informal Review of Observational Studiesfrom Whole Health Source by wholehealthsource@yahoo.com (Stephan)The diet-heart hypothesis states three things:
1. Dietary saturated fat increases blood cholesterol
2. Elevated blood cholesterol increases the risk of having a heart attack
3. Therefore, dietary saturated fat increases the risk of having a heart attack
To evaluate the second contention, investigators have examined the relationship between blood cholesterol and heart attack risk. Many studies including MRFIT have shown that the two are related (1):
The relationship becomes much more complex when you consider lipoprotein subtypes, density and oxidation level, among other factors, but at the very least there is an association between habitual blood cholesterol level and heart attack risk. This is what you would want to see if your hypothesis states that high blood cholesterol causes heart attacks.
Now let's turn to the first contention, the hypothesis that dietary saturated fat increases serum cholesterol. This idea is so deeply ingrained in the scientific literature that many authors don't even bother providing references for it anymore. When references are provided, they nearly always point to the same type of study: short-term controlled diet trials, in which volunteers are fed different fats for 2-13 weeks and their blood cholesterol measured (2)*. These are the studies on which the diet-heart hypothesis was built.
But now we have a problem. Nearly every high-quality (prospective) observational study ever conducted found that saturated fat intake is not associated with heart attack risk (3). So if saturated fat increases blood cholesterol, and higher blood cholesterol is associated with an increased risk of having a heart attack, then why don't people who eat more saturated fat have more heart attacks**?
I'll begin to answer that question with another question: why do researchers almost never cite observational studies to support the idea that dietary saturated fat increases blood cholesterol? Surely if the hypothesis is correct, then people who habitually eat a lot of saturated fat should have high cholesterol, right? One reason may be that in most instances, when researchers have looked for a relationship between saturated fat intake and blood cholesterol, they haven't found one. Those findings have essentially been ignored, but let's have a look...
The Studies
It's difficult to do a complete accounting of these studies, but I've done my best to round them up. I can't claim this post is comprehensive, but I doubt I missed very many, and I certainly didn't exclude any that I came across. If you know of any I missed, please add them to the comments.
The earliest and perhaps most interesting study I found was published in the British Medical Journal in 1963 and is titled "Diet and Plasma Cholesterol in 99 Bank Men" (4). Investigators asked volunteers to weigh all food consumed at home for 1-2 weeks, and describe in detail all food consumed away from home. Compliance was good. This dietary accounting method was much more thorough than in most observational studies today***. Animal fat intake ranged from 55 to 173 grams per day, and blood cholesterol ranged from 154 to 324 mg/dL, yet there was no relationship whatsoever between the two. I'm looking at a graph of animal fat intake vs. blood cholesterol as I write this, and it looks like someone shot it with a shotgun at 50 yards. They twisted the data every which way, but were never able to squeeze even a hint of an association out of it:
Making the most out of the data in other ways- for example, by analysis of the men very stable in their diets, or in whom weighing of food intake was maximal, or where blood was taken close to the diet [measurement]- did not increase the correlation. Because the correlation coefficient is almost as often negative as positive, moreover, what is being discussed mostly is the absence of association, not merely association that is unexpectedly small.
The next study to discuss is the 1976 Tecumseh study (5). This was a large cardiovascular observational study conducted in Tecumseh, Michigan, which is often used as the basis for comparison for other cardiovascular studies in the literature. Using the 24 hour dietary recall method, including an analysis of saturated fat, the investigators found that:
Cholesterol and triglyceride levels were unrelated to quality, quantity, or proportions of fat, carbohydrate or protein consumed in the 24-hr recall period.
They also noted that the result was consistent with what had been reported in other previously published studies, including the Evans county study (6), the massive Israel Ischemic Heart Disease Study (7) and the Framingham study. One of the longest-running, most comprehensive and most highly cited observational studies, the Framingham study was organized by Harvard investigators and continues to this day. When investigators analyzed the relationship between saturated fat intake, serum cholesterol and heart attack risk, they were so disappointed that they never formally published the results. We know from multiple sources that they found no significant relationship between saturated fat intake and blood cholesterol or heart attack risk****.
The next study is the Bogalusa Heart Study, published in 1978, which studied the diet and health of 10 year old American children (8). This study found an association by one statistical method, and none by a second method*****. They found that the dietary factors they analyzed explained no more than 4% of the variation in blood cholesterol. Overall, I think this study lends little or no support to the hypothesis.
Next is the Western Electric study, published in 1981 (9). This study found an association between saturated fat intake and blood cholesterol in middle-aged men in Chicago. However, the correlation was small, and there was no association between saturated fat intake and heart attack deaths. They cited two other studies that found an association between dietary saturated fat and blood cholesterol (and did not cite any of the numerous studies that found no association). One was a very small study conducted in young men doing research in Antarctica, which did not measure saturated fat but found an association between total fat intake and blood cholesterol (10). The other studied Japanese (Nagasaki and Hiroshima) and Japanese Americans in Japan, Hawai'i and California respectively (11).
This study requires some discussion. Published in 1973, it found a correlation between saturated fat intake and blood cholesterol in Japan, Hawai'i but not in California. The strongest association was in Japan, where going from 5 to 75 g/day of saturated fat (a 15-fold change!) was associated with an increase in blood cholesterol from about 175 to 200 mg/dL. However, I don't think this study offers much support to the hypothesis upon closer examination. Food intake in Japan was collected by 24-hour recall in 1965-1967, when the diet was mostly white rice in some areas. The lower limit of saturated fat intake in Japan was 5g/day, 1/12th what was typically eaten in Hawai'i and California, and the Japanese average was 16g, with most people falling below 10g. That is an extraordinarily low saturated fat intake. I think a significant portion of the Japanese in this study, living in the war-ravaged cities of Nagasaki and Hiroshima, were over-reliant on white rice and perhaps bordering on malnourishment.
In Japanese-Americans living in Hawai'i, over a range of saturated fat intakes between 5 and 110 g/day, cholesterol went from 210 to 220 mg/dL. That was statistically significant but it's not exactly knocking my socks off, considering it's a 22-fold change in saturated fat intake. In California, going from 15 to 110 g/day of saturated fat (7.3-fold change) was not associated with a change in blood cholesterol. Blood cholesterol was 20-30 mg/dL lower in Japan than in Hawai'i or California at any given level of saturated fat intake (e.g., Japanese eating 30g per day vs. Hawai'ians eating 30g per day). I think it's probable that saturated fat is not the relevant factor here, or at least it's being trumped by other factors. An equally plausible explanation is that people in the very low range of saturated fat intake are the rural poor who eat an impoverished diet that differs in many ways from the diets at the upper end of the range.
The most recent study was the Health Professional Follow-up study, published in 1996 (12). This was a massive, well funded study that found no hint of a relationship between saturated fat intake and blood cholesterol.
Conclusion
Of all the studies I came across, only the Western Electric study found a clear association between habitual saturated fat intake and blood cholesterol, and even that association was weak. The Bogalusa Heart study and the Japanese study provided inconsistent evidence for a weak association. The other studies I cited, including the bank workers' study, the Tecumseh study, the Evans county study, the Israel Ischemic Heart study, the Framingham study and the Health Professionals Follow-up study, found no association between the two factors.
Overall, the literature does not offer much support for the idea that long term saturated fat intake has a significant effect on the concentration of blood cholesterol. If it's a factor at all, it must be rather weak, which is consistent with what has been observed in multiple non-human species (13). I think it's likely that the diet-heart hypothesis rests in part on an over-interpretation of short-term controlled feeding studies. I'd like to see a more open discussion of this in the scientific literature. In any case, these controlled studies have typically shown that saturated fat increases both LDL and HDL, so even if saturated fat did have a small long-term effect on blood cholesterol, as hinted at by some of the observational studies, its effect on heart attack risk would still be difficult to predict.
The Diet-heart Hypothesis: Stuck at the Starting Gate
Animal Models of Atherosclerosis: LDL
* As a side note, many of these studies were of poor quality, and were designed in ways that artificially inflated the effects of saturated fat on blood lipids. For example, using a run-in period high in linoleic acid, or comparing a saturated fat-rich diet to a linoleic acid-rich diet, and attributing the differences in blood cholesterol to the saturated fat. Some of them used hydrogenated seed oils as the saturated fat. Although not always consistent, I do think that overall these studies support the idea that saturated fat does have a modest ability to increase blood cholesterol in the short term.
** Besides the fact that it's a logical fallacy. Just because A causes B, and B causes C, does not mean A causes C.
*** Although I would love to hear comments from anyone who has done controlled diet trials. I'm sure this method had flaws, as it was applied in the 1960s.
**** Reference cited in the Tecumseh paper: Kannel, W et al. The Framingham Study. An epidemiological Investigation of Cardiovascular Diseases. Section 24: The Framingham Diet Study: Diet and the Regulation of Serum Cholesterol. US Government Printing Office, 1970.
***** Table 5 shows that the Pearson correlation coefficient for saturated fat intake vs. blood cholesterol is not significant; table 6 shows that children in the two highest tertiles of blood cholesterol have a significantly higher intake of saturated fat, unsaturated fat, total fat and sodium than the lowest tertile. The relationship between saturated fat and blood cholesterol shows no evidence of dose-dependence (cholesterol tertiles= 15.6g, 18.4g, 18.5g saturated fat). The investigators made no effort to adjust for confounding variables.
==================================================
The above was copied from Whole Health Source
1. Dietary saturated fat increases blood cholesterol
2. Elevated blood cholesterol increases the risk of having a heart attack
3. Therefore, dietary saturated fat increases the risk of having a heart attack
To evaluate the second contention, investigators have examined the relationship between blood cholesterol and heart attack risk. Many studies including MRFIT have shown that the two are related (1):
The relationship becomes much more complex when you consider lipoprotein subtypes, density and oxidation level, among other factors, but at the very least there is an association between habitual blood cholesterol level and heart attack risk. This is what you would want to see if your hypothesis states that high blood cholesterol causes heart attacks.
Now let's turn to the first contention, the hypothesis that dietary saturated fat increases serum cholesterol. This idea is so deeply ingrained in the scientific literature that many authors don't even bother providing references for it anymore. When references are provided, they nearly always point to the same type of study: short-term controlled diet trials, in which volunteers are fed different fats for 2-13 weeks and their blood cholesterol measured (2)*. These are the studies on which the diet-heart hypothesis was built.
But now we have a problem. Nearly every high-quality (prospective) observational study ever conducted found that saturated fat intake is not associated with heart attack risk (3). So if saturated fat increases blood cholesterol, and higher blood cholesterol is associated with an increased risk of having a heart attack, then why don't people who eat more saturated fat have more heart attacks**?
I'll begin to answer that question with another question: why do researchers almost never cite observational studies to support the idea that dietary saturated fat increases blood cholesterol? Surely if the hypothesis is correct, then people who habitually eat a lot of saturated fat should have high cholesterol, right? One reason may be that in most instances, when researchers have looked for a relationship between saturated fat intake and blood cholesterol, they haven't found one. Those findings have essentially been ignored, but let's have a look...
The Studies
It's difficult to do a complete accounting of these studies, but I've done my best to round them up. I can't claim this post is comprehensive, but I doubt I missed very many, and I certainly didn't exclude any that I came across. If you know of any I missed, please add them to the comments.
The earliest and perhaps most interesting study I found was published in the British Medical Journal in 1963 and is titled "Diet and Plasma Cholesterol in 99 Bank Men" (4). Investigators asked volunteers to weigh all food consumed at home for 1-2 weeks, and describe in detail all food consumed away from home. Compliance was good. This dietary accounting method was much more thorough than in most observational studies today***. Animal fat intake ranged from 55 to 173 grams per day, and blood cholesterol ranged from 154 to 324 mg/dL, yet there was no relationship whatsoever between the two. I'm looking at a graph of animal fat intake vs. blood cholesterol as I write this, and it looks like someone shot it with a shotgun at 50 yards. They twisted the data every which way, but were never able to squeeze even a hint of an association out of it:
Making the most out of the data in other ways- for example, by analysis of the men very stable in their diets, or in whom weighing of food intake was maximal, or where blood was taken close to the diet [measurement]- did not increase the correlation. Because the correlation coefficient is almost as often negative as positive, moreover, what is being discussed mostly is the absence of association, not merely association that is unexpectedly small.
The next study to discuss is the 1976 Tecumseh study (5). This was a large cardiovascular observational study conducted in Tecumseh, Michigan, which is often used as the basis for comparison for other cardiovascular studies in the literature. Using the 24 hour dietary recall method, including an analysis of saturated fat, the investigators found that:
Cholesterol and triglyceride levels were unrelated to quality, quantity, or proportions of fat, carbohydrate or protein consumed in the 24-hr recall period.
They also noted that the result was consistent with what had been reported in other previously published studies, including the Evans county study (6), the massive Israel Ischemic Heart Disease Study (7) and the Framingham study. One of the longest-running, most comprehensive and most highly cited observational studies, the Framingham study was organized by Harvard investigators and continues to this day. When investigators analyzed the relationship between saturated fat intake, serum cholesterol and heart attack risk, they were so disappointed that they never formally published the results. We know from multiple sources that they found no significant relationship between saturated fat intake and blood cholesterol or heart attack risk****.
The next study is the Bogalusa Heart Study, published in 1978, which studied the diet and health of 10 year old American children (8). This study found an association by one statistical method, and none by a second method*****. They found that the dietary factors they analyzed explained no more than 4% of the variation in blood cholesterol. Overall, I think this study lends little or no support to the hypothesis.
Next is the Western Electric study, published in 1981 (9). This study found an association between saturated fat intake and blood cholesterol in middle-aged men in Chicago. However, the correlation was small, and there was no association between saturated fat intake and heart attack deaths. They cited two other studies that found an association between dietary saturated fat and blood cholesterol (and did not cite any of the numerous studies that found no association). One was a very small study conducted in young men doing research in Antarctica, which did not measure saturated fat but found an association between total fat intake and blood cholesterol (10). The other studied Japanese (Nagasaki and Hiroshima) and Japanese Americans in Japan, Hawai'i and California respectively (11).
This study requires some discussion. Published in 1973, it found a correlation between saturated fat intake and blood cholesterol in Japan, Hawai'i but not in California. The strongest association was in Japan, where going from 5 to 75 g/day of saturated fat (a 15-fold change!) was associated with an increase in blood cholesterol from about 175 to 200 mg/dL. However, I don't think this study offers much support to the hypothesis upon closer examination. Food intake in Japan was collected by 24-hour recall in 1965-1967, when the diet was mostly white rice in some areas. The lower limit of saturated fat intake in Japan was 5g/day, 1/12th what was typically eaten in Hawai'i and California, and the Japanese average was 16g, with most people falling below 10g. That is an extraordinarily low saturated fat intake. I think a significant portion of the Japanese in this study, living in the war-ravaged cities of Nagasaki and Hiroshima, were over-reliant on white rice and perhaps bordering on malnourishment.
In Japanese-Americans living in Hawai'i, over a range of saturated fat intakes between 5 and 110 g/day, cholesterol went from 210 to 220 mg/dL. That was statistically significant but it's not exactly knocking my socks off, considering it's a 22-fold change in saturated fat intake. In California, going from 15 to 110 g/day of saturated fat (7.3-fold change) was not associated with a change in blood cholesterol. Blood cholesterol was 20-30 mg/dL lower in Japan than in Hawai'i or California at any given level of saturated fat intake (e.g., Japanese eating 30g per day vs. Hawai'ians eating 30g per day). I think it's probable that saturated fat is not the relevant factor here, or at least it's being trumped by other factors. An equally plausible explanation is that people in the very low range of saturated fat intake are the rural poor who eat an impoverished diet that differs in many ways from the diets at the upper end of the range.
The most recent study was the Health Professional Follow-up study, published in 1996 (12). This was a massive, well funded study that found no hint of a relationship between saturated fat intake and blood cholesterol.
Conclusion
Of all the studies I came across, only the Western Electric study found a clear association between habitual saturated fat intake and blood cholesterol, and even that association was weak. The Bogalusa Heart study and the Japanese study provided inconsistent evidence for a weak association. The other studies I cited, including the bank workers' study, the Tecumseh study, the Evans county study, the Israel Ischemic Heart study, the Framingham study and the Health Professionals Follow-up study, found no association between the two factors.
Overall, the literature does not offer much support for the idea that long term saturated fat intake has a significant effect on the concentration of blood cholesterol. If it's a factor at all, it must be rather weak, which is consistent with what has been observed in multiple non-human species (13). I think it's likely that the diet-heart hypothesis rests in part on an over-interpretation of short-term controlled feeding studies. I'd like to see a more open discussion of this in the scientific literature. In any case, these controlled studies have typically shown that saturated fat increases both LDL and HDL, so even if saturated fat did have a small long-term effect on blood cholesterol, as hinted at by some of the observational studies, its effect on heart attack risk would still be difficult to predict.
The Diet-heart Hypothesis: Stuck at the Starting Gate
Animal Models of Atherosclerosis: LDL
* As a side note, many of these studies were of poor quality, and were designed in ways that artificially inflated the effects of saturated fat on blood lipids. For example, using a run-in period high in linoleic acid, or comparing a saturated fat-rich diet to a linoleic acid-rich diet, and attributing the differences in blood cholesterol to the saturated fat. Some of them used hydrogenated seed oils as the saturated fat. Although not always consistent, I do think that overall these studies support the idea that saturated fat does have a modest ability to increase blood cholesterol in the short term.
** Besides the fact that it's a logical fallacy. Just because A causes B, and B causes C, does not mean A causes C.
*** Although I would love to hear comments from anyone who has done controlled diet trials. I'm sure this method had flaws, as it was applied in the 1960s.
**** Reference cited in the Tecumseh paper: Kannel, W et al. The Framingham Study. An epidemiological Investigation of Cardiovascular Diseases. Section 24: The Framingham Diet Study: Diet and the Regulation of Serum Cholesterol. US Government Printing Office, 1970.
***** Table 5 shows that the Pearson correlation coefficient for saturated fat intake vs. blood cholesterol is not significant; table 6 shows that children in the two highest tertiles of blood cholesterol have a significantly higher intake of saturated fat, unsaturated fat, total fat and sodium than the lowest tertile. The relationship between saturated fat and blood cholesterol shows no evidence of dose-dependence (cholesterol tertiles= 15.6g, 18.4g, 18.5g saturated fat). The investigators made no effort to adjust for confounding variables.
==================================================
The above was copied from Whole Health Source
Thursday, January 13, 2011
Fructose is a stealth poison
From the blog of Dr. William R. Davis
======================================
Restaurant eating: A fructose landmine from Heart Scan Blog by Dr. William Davis
3 people liked thisThere is no remaining question that fructose is among the worst possible things humans can consume.
Followers of the Heart Scan Blog already know this, from conversations like The LDL-Fructose Disconnect, Where do you find fructose?, and Goodbye, fructose.
But fructose, usually as either high-fructose corn syrup (44%, 55%, occasionally higher percentage fructose) or sucrose (50% fructose), is ubiquitous. I've seen it in the most improbable places, including cole slaw, mustard, and dill pickles.
It's reasonably straightforward to avoid or minimize fructose exposure while eating at home, provided you check labels and focus on foods that don't require labels (like green peppers, salmon, and olive oil, i.e., unprocessed foods). But when you choose to eat at a restaurant, then all hell can break loose and fructose exposure can explode.
So what are some common and unsuspected fructose sources when eating at a restaurant?
Salad dressings--Dressings in all stripes and flavors are now made with high-fructose corn syrup and/or sucrose. This is especially true of low-fat, non-fat, or "lite" dressings, meaning oils have been replaced by high-fructose corn syrup. It can also be true of traditional non-low-fat dressings, too, since high-fructose corn syrup is just plain cheap.
Olive oil and vinegar are still your safest bets. I will often use salsa as a dressing, which works well.
Sauces and gravies--Not only can sauces be thickened with cornstarch, many pre-mixed sauces are also made with high-fructose corn syrup or sweetened with sucrose. Barbecue sauce is a particular landmine, since it is now a rare barbecue sauce not made with high-fructose corn syrup as the first or second ingredient. Sauces for dipping are nearly always high-fructose corn syrup-based.
Ketchup--Yup. Good old ketchup even is now made with high-fructose corn syrup. In fact, you should be suspicious of any condiment.
Highball, Bloody Mary, Margarita, Daiquiri, beer--Even the before-dinner or dinner drink can have plenty of fructose, particularly if a mix is used to make it. While Blood Marys seem the most benign of all, adorned with celery, pickle, and olive, just take a look at the ingredient label on the mix used: high-fructose corn syrup.
Fructose is a stealth poison: It doesn't immediately increase blood sugar; it doesn't trigger any perceptible effect like increased energy or sleepiness. But it is responsible for an incredible amount of the health struggles in the U.S., from obesity, to diabetes, to hyperlipidemias and heart disease, to arthritis, to cataracts.
======================================
Restaurant eating: A fructose landmine from Heart Scan Blog by Dr. William Davis
3 people liked thisThere is no remaining question that fructose is among the worst possible things humans can consume.
Followers of the Heart Scan Blog already know this, from conversations like The LDL-Fructose Disconnect, Where do you find fructose?, and Goodbye, fructose.
But fructose, usually as either high-fructose corn syrup (44%, 55%, occasionally higher percentage fructose) or sucrose (50% fructose), is ubiquitous. I've seen it in the most improbable places, including cole slaw, mustard, and dill pickles.
It's reasonably straightforward to avoid or minimize fructose exposure while eating at home, provided you check labels and focus on foods that don't require labels (like green peppers, salmon, and olive oil, i.e., unprocessed foods). But when you choose to eat at a restaurant, then all hell can break loose and fructose exposure can explode.
So what are some common and unsuspected fructose sources when eating at a restaurant?
Salad dressings--Dressings in all stripes and flavors are now made with high-fructose corn syrup and/or sucrose. This is especially true of low-fat, non-fat, or "lite" dressings, meaning oils have been replaced by high-fructose corn syrup. It can also be true of traditional non-low-fat dressings, too, since high-fructose corn syrup is just plain cheap.
Olive oil and vinegar are still your safest bets. I will often use salsa as a dressing, which works well.
Sauces and gravies--Not only can sauces be thickened with cornstarch, many pre-mixed sauces are also made with high-fructose corn syrup or sweetened with sucrose. Barbecue sauce is a particular landmine, since it is now a rare barbecue sauce not made with high-fructose corn syrup as the first or second ingredient. Sauces for dipping are nearly always high-fructose corn syrup-based.
Ketchup--Yup. Good old ketchup even is now made with high-fructose corn syrup. In fact, you should be suspicious of any condiment.
Highball, Bloody Mary, Margarita, Daiquiri, beer--Even the before-dinner or dinner drink can have plenty of fructose, particularly if a mix is used to make it. While Blood Marys seem the most benign of all, adorned with celery, pickle, and olive, just take a look at the ingredient label on the mix used: high-fructose corn syrup.
Fructose is a stealth poison: It doesn't immediately increase blood sugar; it doesn't trigger any perceptible effect like increased energy or sleepiness. But it is responsible for an incredible amount of the health struggles in the U.S., from obesity, to diabetes, to hyperlipidemias and heart disease, to arthritis, to cataracts.
Wednesday, January 12, 2011
More Research of Note
Though I am usually suspicious of the terms 'correlates with', 'associated with', and 'increases/decreases risk of' etc. because when I'm lazy in my thinking I want to read them as indicating a cause not what they really are - a possible reason for much more investigation, I refer you to the following exerpt of an article by Jenny at Diabetes Update
".
.
.
3. Higher Levels of Cholesterol of ALL Types Correlates with LESS Likelihood of Alzheimers. It has long been known--though doctors have been brainwashed into ignoring it--that statins can cause permanent dementia, especially in older patients. Could it be because cholesterol is protective to the brain? This study would make you wonder.
It followed 1,130 adults 65 or older in New York City with no history of dementia or cognitive impairment.
Higher levels of HDL-C (>55 mg/dL) were associated with a decreased risk of both probable and possible A[lzheimers] D[isease] and probable AD compared with lower HDL-C levels (hazard ratio, 0.4; 95% confidence interval, 0.2-0.9; P = .03 and hazard ratio, 0.4; 95% confidence interval, 0.2-0.9; P = .03). In addition, higher levels of total and non–HDL-C were associated with a decreased risk of AD in analyses adjusting for age, sex, education, ethnic group, and APOE e4 genotype.
,
,
,
"
".
.
.
3. Higher Levels of Cholesterol of ALL Types Correlates with LESS Likelihood of Alzheimers. It has long been known--though doctors have been brainwashed into ignoring it--that statins can cause permanent dementia, especially in older patients. Could it be because cholesterol is protective to the brain? This study would make you wonder.
It followed 1,130 adults 65 or older in New York City with no history of dementia or cognitive impairment.
Higher levels of HDL-C (>55 mg/dL) were associated with a decreased risk of both probable and possible A[lzheimers] D[isease] and probable AD compared with lower HDL-C levels (hazard ratio, 0.4; 95% confidence interval, 0.2-0.9; P = .03 and hazard ratio, 0.4; 95% confidence interval, 0.2-0.9; P = .03). In addition, higher levels of total and non–HDL-C were associated with a decreased risk of AD in analyses adjusting for age, sex, education, ethnic group, and APOE e4 genotype.
,
,
,
"
The Truth About Cholesterol
Some quotes from Dr. Graveline
"For the past four decades we have all been subjected to an intense and carefully calculated program of brainwashing to believe that cholesterol is our enemy. I am sorry to admit that I was one of thousands of doctors trained to absorb this propaganda without question. In retrospect I am angry to have been so completely enmeshed in this web of deceit."
"Like puppets we wrote millions of prescriptions for whatever cholesterol buster the drug companies were promoting at the time. I was just like all the other doctors - doing what I was told, never suspecting we had functionally become employees of the pharmaceutical industry. In truth there has never been a scientific study that has been able to demonstrate a causal link between cholesterol and heart disease. The reality is that cholesterol in its natural form cannot be harmful."
".. statins significantly promote diabetes..."
"Far from being harmful, cholesterol is perhaps the most important biochemical in our bodies."
"cholesterol is the precursor for a whole class of hormones known as the steroid hormones that are absolutely critical for life as we know it."
"The large amounts of cholesterol required for both the formation and function of these basic structures argues strongly against the rationality of excessively liberal use of drugs such as statins that inhibit cholesterol synthesis."
==========================
Read the full article here. And consider buying one or more of his books.
"For the past four decades we have all been subjected to an intense and carefully calculated program of brainwashing to believe that cholesterol is our enemy. I am sorry to admit that I was one of thousands of doctors trained to absorb this propaganda without question. In retrospect I am angry to have been so completely enmeshed in this web of deceit."
"Like puppets we wrote millions of prescriptions for whatever cholesterol buster the drug companies were promoting at the time. I was just like all the other doctors - doing what I was told, never suspecting we had functionally become employees of the pharmaceutical industry. In truth there has never been a scientific study that has been able to demonstrate a causal link between cholesterol and heart disease. The reality is that cholesterol in its natural form cannot be harmful."
".. statins significantly promote diabetes..."
"Far from being harmful, cholesterol is perhaps the most important biochemical in our bodies."
"cholesterol is the precursor for a whole class of hormones known as the steroid hormones that are absolutely critical for life as we know it."
"The large amounts of cholesterol required for both the formation and function of these basic structures argues strongly against the rationality of excessively liberal use of drugs such as statins that inhibit cholesterol synthesis."
==========================
Read the full article here. And consider buying one or more of his books.
Subscribe to:
Posts (Atom)