I was catching up on my medical reading this morning when I came across an article in The Lancet from late last month that is a real jaw dropper. The article, Are lipid-lowering guidelines evidence-based?, is in the commentary section and is a pretty devastating indictment of the whole scale prescribing of statins without any evidence that such prescribing does much good.
The article gets right to the point:
The last major revision of the US guidelines, in 2001 [the guidelines I wrote about in my recent post],increased the number of Americans for whom statins are recommended from 13 million to 36 million, most of whom do not yet have but are estimated to be at moderately elevated risk of developing coronary heart disease. In support of statin therapy for the primary prevention of this disease in women and people aged over 65 years, the guidelines cite seven and nine randomised trials, respectively. Yet not one of the studies provides such evidence.
The next paragraph I don’t agree with completely:
For adults aged between 30 and 80 years old who already have occlusive vascular disease, statins confer a total and cardiovascular mortality benefit and are not controversial. The controversy involves this question: which people without evident occlusive vascular disease (true primary prevention) should be offered statins? With about three-quarters of those taking statins in this category, the answer has huge economic and health implications. In formulating recommendations for primary prevention, why do authors of guidelines not rely on the data that already exist from the primary prevention trials?
Based on my reading of the papers underlying the recommendations for adults with CHD, I don’t feel the evidence is strong enough to make the blanket statement that for these people
statins confer a total and cardiovascular mortality benefit and are not controversial.
My reading tells me that there may be a slight (a very slight) decrease in risk for another heart attack in these people if they take statins, but the lack of reduction (in some cases even an increase) in all-cause mortality, in my mind at least, negates these minimally positive effects. And when the side effects of statin therapy are taken into consideration, the positive effects are minimized even more.
The next couple of paragraphs are unbelievable. Unbelievable in the sense that I can’t believe they are published in a mainstream journal. It almost restores my faith in the unbiased nature of the medical literature.
We have pooled the data from all eight randomised trials that compared statins with placebo in primary prevention populations at increased risk. Unfortunately, our analysis is imperfect because these trials are not solely primary prevention: 8·5% of patients had occlusive vascular disease at baseline. We used two outcomes to estimate overall benefit (benefit minus harm): total mortality and total serious adverse events (SAEs). Total mortality was not reduced by statins (relative risk 0·95, 95% CI 0·89–1·01). In the two trials that reported total SAEs, such events were not reduced by statins (1·01, 0·97–1·05) (data on SAEs from the other trials were not reported). The frequency of cardiovascular events, a less encompassing outcome, was reduced by statins (relative risk 0·82, 0·77–0·87). However, the absolute risk reduction of 1·5% is small and means that 67 people have to be treated for 5 years to prevent one such event. Further analysis revealed that the benefit might be limited to high-risk men aged 30–69 years. Statins did not reduce total coronary heart disease events in 10 990 women in these primary prevention trials (relative risk 0·98, 0·85–1·12). Similarly, in 3239 men and women older than 69 years, statins did not reduce total cardiovascular events (relative risk 0·94, 0·77–1·15).
Our analysis suggests that lipid-lowering statins should not be prescribed for true primary prevention in women of any age or for men older than 69 years. High-risk men aged 30–69 years should be advised that about 50 patients need to be treated for 5 years to prevent one event. In our experience, many men presented with this evidence do not choose to take a statin, especially when informed of the potential benefits of lifestyle modification on cardiovascular risk and overall health. This approach, based on the best available evidence in the appropriate population, would lead to statins being used by a much smaller proportion of the overall population than recommended by any of the guidelines.
That pretty much says it all. I still can’t believe my eyes. Who in mainstream medicine could risk the career damage from publishing an article like this? Who are these guys?
The first author, J Abramson, is from Harvard; the second, JM Wright, is from the University of British Columbia.
Let’s look at their conflict of interest disclosures:
JMW declares no conflict of interest. JA is an expert consultant to plaintiffs’ attorneys on litigation involving the drug industry, including Pfizer for its marketing of atorvastatin.
Now I see why these guys have the guts to publish this anti-statin paper. They don’t get funding from drug companies and one of them uses his expertise to help lawyers go after drug companies.
JMW has a history of publications critical of the overprescription of statins. Here is one. Skip down to page 7 to read his Update on statin therapy.
Now if anyone says, yeah, well where are the papers? I’m not going to believe some idiot doctor who writes a blog. I want to see it in a real medical journal, you’ll be prepared.
It’s great to see someone actually putting out good information in the media. I am, however, quite surprised that it made it into a mainstream media publication. Perhaps as Bob Dylan said, “the times, they are a’changin’.” Probably not though…the pharmaceutical companies will soon bury the bodies of these two journalists in the desert and have the slate wiped clean that this article ever existed, 1984-style.
Hi Scott–
These two are not journalists; they are research scientists at major universities. That’s what makes their ‘coming out’ so newsworthy. Problem is, will the journalists pick up on it? They haven’t yet.
Cheers–
MRE
Hi Dr. Eades, I absolutely love your blog-don’t ever give it up. My wife has familial hypercholesterolemia. Is there a role for statins with that condition? Her cholesterol runs 400-500 off meds. thanks
Hi Pete–
Thanks for the kind words about the blog.
There are several different types of familial hypercholesterolemia, a number of which have no increased risk for the development of heart disease. Without knowing your wife’s history, labs, etc., I couldn’t begin to answer your question. If I did have all that info, I still couldn’t make specific recommendations to individual patients over the internet.
Best–
MRE
Dear Dr. Eades,
The author J Abramson is probably (from the book’s website in quotes) “Dr. John Abramson, M.D. is an award-winning family doctor, on the clinical faculty at Harvard Medical School, and author of the book “Overdosed America.” The URL for the website is: http://www.overdosedamerica.com/. You may have read the book. If not, I highly recommend you and everyone else to read it. I got it from my public library. If folks can’t read the whole book, read chapters 9 and 13. That’s where the real take home message is. It is a scathing indictment of today’s medical practice and Big Pharma. The editorial echoes the conclusions in the book. Keep up the great work on the blog! Many thanks to you and your wife.
Doug
Hi Doug–
Thanks for the heads up on the book. You’re the second or third person who has recommended it to me. I just ordered it through Amazon.
Best–
MRE
Have you seen the February 2007 issue of National Geographic? The cover story is called “Healing the Heart” and it purportedly focuses on new discoveries about the genetic basis of heart disease. However, the author makes repeated references to the importance of preventing heart disease by taking statins. In fact, the article reads like an ad for statins. And it is. Preceding the article is a 3-page ad for Lipitor, including an invitation for readers to learn more about heart health by visiting a webiste “brought to you by Pfizer”: http://www.nationalgeographic.com/human-heart
I am thoroughly disgusted by this irresponsible journalism from a magazine that I’ve loved since I was a little kid. I am seriously considering canceling my subscription and telling them why — not that it would help.
Beth
Hi Beth–
I did indeed see the Feb issue of NG. And I saw the article on the heart, which I skimmed while standing at the bookstore magazine rack. I noticed all the mention of statins, but I missed the three pages of Lipitor ads. Thank God I did or I might have had apoplexy. Disgusting.
Best–
MRE
consider the following:
Cholesterol Decline May Be Associated With Early Stages of Dementia
By Will Boggs, MD
NEW YORK (Reuters Health) Jan 19 – A decline in total cholesterol
levels precedes the diagnosis of dementia by at least 15 years,
according to an epidemiologic study reported in the January issue of
the Archives of Neurology.
“Studies like this are extremely valuable because they can provide a
‘window’ on to processes going on early in dementia, allowing
researchers to look back in time at people’s health and other
characteristics and compare these between people who develop dementia
and those who do not,” Dr. Robert Stewart from King’s College London,
UK told Reuters Health.
Dr. Stewart and colleagues used data from the Honolulu-Asia Aging
Study to compare the natural history of cholesterol level change over
a 26-year period between 56 men who were found to have dementia at
examination 3 years after the last cholesterol measurement and 971 men
who did not have dementia.
Total cholesterol levels at the beginning of the study did not differ
by later dementia status, the authors report, but the decline in
subsequent cholesterol levels was significantly steeper among men who
went on to develop dementia.
Adjustment for potential confounding factors strengthened the
association between cholesterol level decline and the development of
dementia, the results indicate.
The cholesterol level decline was most marked in men with dementia and
the APOE epsilon-4 allele and in those with dementia and worse self-
reported general health at the final cholesterol measurement, the
researchers note.
“The observed associations may not represent direct causal pathways,”
the investigators say. “Hypocholesterolemia is recognized to be
associated with frailty and poor general health. It also has been
found to be specifically associated with inflammatory markers and poor
nutritional status.”
Rather, they suggest, “It is possible that the decline in cholesterol
levels is a marker for early processes that reflect neurodegenerative
changes and also lead to a decline in general health status.”
The drop in cholesterol was not a result of medication. “Very few of
the participants in this study were receiving cholesterol lowering
treatment at the time the decline in cholesterol levels was observed
(there were few cholesterol lowering medications around at that time
in the 1970s), so medication was not responsible for this,” Dr.
Stewart explained.
“The drop in cholesterol was instead probably caused by some other
event and was a ‘marker’ of risk rather than actually increasing the
risk itself,” he concluded.
Arch Neurol 2007;64:103-107.
and the following:
Higher occurrence of Parkinson’s linked to low LDL cholesterol
Public release date: 19-Dec-2006
University of North Carolina School of Medicine
http://www.eurekalert.org/pub_releas…hoo121906.php#
CHAPEL HILL — People with low levels of LDL cholesterol are more
likely to have Parkinson’s disease than people with high LDL levels,
according to University of North Carolina at Chapel Hill researchers.
LDL stands for low-density lipoprotein cholesterol; low levels of LDL
cholesterol are considered an indicator of good cardiovascular health.
Earlier studies have found intriguing correlations between Parkinson’s
disease, heart attacks, stroke and smoking.
“People with Parkinson’s disease have a lower occurrence of heart
attack and stroke than people who do not have the disease,” said Dr.
Xuemei Huang, medical director of the Movement Disorder Clinic at UNC
Hospitals and an assistant professor of neurology in the UNC School of
Medicine. “Parkinson’s patients are also more likely to carry the gene
APOE-2, which is linked with lower LDL cholesterol.” And for more than
a decade, researchers have known that smoking, which increases a
person’s risk for cardiovascular disease, is also associated with a
decreased risk of Parkinson’s disease.
These findings led Huang to examine whether higher LDL cholesterol
might be associated with a decreased occurrence for Parkinson’s
disease, and vice versa. “If my hypothesis was correct,” she said,
“lower LDL-C, something that is linked to healthy hearts, would be
associated with a higher occurrence of Parkinson’s.” The results of
Huang’s study, published online Dec. 18 by the journal Movement
Disorders, confirmed her hypothesis. “We found that lower LDL
concentrations were indeed associated with a higher occurrence of
Parkinson’s disease,” Huang said. Participants with lower LDL levels
(less than 114 milligrams per deciliter) had a 3.5-fold higher
occurrence of Parkinson’s than the participants with higher LDL levels
(more than 138 milligrams per deciliter).
Huang cautioned that people should not change their eating habits, nor
their use of statins and other cholesterol-lowering drugs, because of
the results. The study was based on relatively small numbers of cases
and controls, and the results are too preliminary, she said. Further
large prospective studies are needed, Huang added.
“Parkinson’s is a disease full of paradoxes,” Huang said. “We’ve known
for years that smoking reduces the risk of developing Parkinson’s. More
than 40 studies have documented that fact. But we don’t advise people
to smoke because of the other more serious health risks,” she said.
Huang and her colleagues recruited 124 Parkinson’s patients who were
treated at the UNC Movement Disorder Clinic between July 2002 and
November 2004 to take part in the study. Another 112 people, all
spouses of patients treated in the clinic, were recruited as the
control group. Fasting cholesterol profiles were obtained from each
participant. The researchers also recorded information on each
participant’s gender, age, smoking habits and use of
cholesterol-lowering drugs.
Huang notes that the study also found participants with Parkinson’s
were much less likely to take cholesterol-lowering drugs than
participants in the control group. This, combined with the findings
about LDL cholesterol, suggests two questions for additional study,
Huang said.
“One is whether lower cholesterol predates the onset of Parkinson’s.
Number two, what is the role of statins in that? In other words, does
taking cholesterol-lowering drugs somehow protect against Parkinson’s?
We need to address these questions,” she said.
###
Hi mmeyers–
The first study you listed is one of many showing the same thing; the second is the one I posted on a couple of days ago.
Cheers–
MRE
Oy vey. My husband subscribes to National Geographic so we have the “heart” issue, too. Not very enlightening. I had my cynical cap on so as soon as I finished reading the article, I scanned the magazine for drug ads and bingo! There they were. I wasn’t surprised to read that all the cardiologists interviewed take statins themselves as a prophylactic measure.
I think I even read/heard at one point (not in the NG article) that there was a proposal to sell stains OTC in the UK! Will the madness never end?
On another unrelated note: any opinions on Jerusalem artichokes (aka sunchokes) as a good/not so good vegetable in a low carb diet? They were recommended to me but what I have found so far says that they have no starch but have fructose and inulin.
Cheers, Anna
Hi Anna–
There has been (at least tongue-in-cheek, sort of) a suggestion from the UK that statins should be put in the drinking water. The whole thing is insane. Unless, of course, you consider the French suggestion to Cherchez l’argent.
Unfortunately, I have no experience with Jerusalem artichokes. Sorry. If they contain only fructose and inulin, I wonder how much fructose. If it’s not much, I would say they’re okay.
Cheers–
MRE
Here’s an article from the “other side”. I can’t get at the original article, but the news release blurb notes the usual: “changes in all lipid parameters . . . were significant,” which of course isn’t really meaningful unless there’s a causal link between blood lipids and cardiovascular “events”.
Somewhat more interesting is the following: “Substantial atheroma regression (5 percent or more reduction in atheroma volume) was observed in patients with levels of LDL-C less than the mean (87.5 milligrams per deciliter) during treatment and percentage increases of HDL-C greater than the mean (7.5 percent).” It’s interesting that there was a measurable effect decreasing the size of plaques; on the other hand, 5% isn’t very much, and considering that a large fraction of heart attack victims have rather little in the way of atheroma formation, maybe not so exciting. That’s reinforced by the final bit of info in the press blurb: “No significant differences were found with regard to clinical events.” The trial had 1455 participants, which to me says “Doh!”
They go on to trumpet “These findings may have important implications for the management of a patient with symptomatic atherosclerotic cardiovascular disease.” That seems a rather unscientific conclusion, given that they observed zero effect on the most important measurable quantity (clinical events), and a small effect on atheroma volume, even in the face of significant modification of lipid parameters resulting from statin therapy.
Another good example of pseudo-science. The methodology is fine (I guess – hard to tell from a press release), but the conclusions are bogus because the investigators start with a 100% confidence in the lipid hypothesis. Thus, any supporting evidence is “significant”, while (both psychologically and mathematically) no amount of contradictory evidence will change their degree of belief in the hypothesis. It’s no wonder the lipid dorks like Katan have such an emotional reaction whenever the lipid hypothesis is challenged. They’re arguing from a logically untenable position, and I think that deep down, they know that, and compensate by making a lot of noise (“Ignore the man behind the curtain! I an the great and powerful Oz!”).
Dave
Hi Dave–
Sorry it took me a while to get to your comment, but I wanted to pull the paper and read it first, which took me a bit since I’m traveling.
I love the way the article starts out. The authors certainly don’t hide their bias. Here’s the first paragraph. I’ve added my commentary in brackets.
I have a couple of problems with the article. First, the patients had small occlusions. It takes at least a 90% occlusion to cause symptoms (from occlusive arterial disease); these patients had occlusions of no greater than 50%, so I don’t know what conclusions can be drawn. Second, reading the study carefully one finds that what the authors call the PAV (percent atheroma volume) actually increases with statin therapy (This is a measurement of the amount of the vascular wall that is composed of atheroma). Third, the study was actually a hodge podge of four different studies. These study combinations are often used to achieve some sort of statistical significance by accumulating data from studies in which the findings were not statistically significant. And, forth, the fingerprints of the drug industry are all over this publication.
If you look at the sponsors of the four studies, you find that they were all paid for by the pharmaceutical industry:
If you look up the National Heart Foundation of Australia, I suspect you’ll find that a portion of its funding comes from the makers of statins.
Looking at the financial disclosures of the study authors, we find the following:
The authors of the study taking funds from the makers of statins represents about three quarters of the authors of the paper. If you add to this info that all the authors are from the Cleveland Clinic, which is a hotbed of statin worshipers and funded extensively by the makers of statins, you can draw your own conclusions about bias.
Nuff said.
Cheers–
MRE
Maybe if all those statin-happy quacks keep taking their own medicine we can hope to see this nonsense die out in a couple of generations or so.
A race to see who goes first. Be sure to tell your kids and grandkids how to eat properly.
Marilyn
Hi Marilyn–
We can only hope. They are indeed statin happy, but I hate to call them quacks because they are following the precepts of mainstream medicine. They would consider me and others like me who loathe statins as the real quacks.
Cheers–
MRE
OTC Simvastatin actually began in 2004 in the UK. I don’t know if it sells particularly well though.
God help us all.
Do you know if the British Heart Foundation publish details of who funds them?
I would like to know which drug companies are making donations.
Hi Adrian–
Here is a link to their website page showing their corporate donors. It just shows their logos; it doesn’t tell how much each contributes. I went through the BHF financial reports and couldn’t find any breakdown their either.
Best–
MRE
I am 44. Until July 2006 I always had high cholesterol on blood tests, but then began an aggressive “no-animal products, no oil, no sugar, no pasta or white flour products, no salt, high fiber, whole food only, lots of salads and steamed vegetables and raw seeds and nuts” diet regime that resulted, in three months, in a rapid decrease in my overall cholesterol (240 to 160).
However, in October 2006, an ultrasound revealed soft plaque buildup of 5-10% in my carotid artery. My GP suggested, but in light of the diet, didn’t press for, Lipitor. Despite having stuck very fast to the diet and maintained the lower cholesterol level, a new ultrasound in Nov 2007 now reveals increased plaque buildup of 10-15% in my carotid arteries in several locations and my GP is now pressing me to start taking 10mg of Lipitor or other cholesterol buster plus baby aspirin, although all other heart signs are very healthy.
Would that be prevention or treatment? Am I in one of the groups who has been shown to benefit from statins? Don’t I have an elevated risk for the kind of stroke or attack that fells people who otherwise are apparently in good health but have these plaque buildups that detach and block arteries or brain vessels?
Should I give up on my diet, which causes all kinds of social stress and is a nuisance in restaurants, since cutting cholesterol through diet doesn’t seem to prevent my body from producing artery clogging lipids anyway? Should I take the statins? Help!
Hi John–
I’m sorry, but I can’t take care of your problems over the internet. These are all issues you need to address with your own physician. If he or she isn’t responsive to your questions or your needs, maybe it’s time for a switch.
The low-fat diet you have been following so assiduously despite bringing about major reductions in your cholesterol clearly hasn’t stemmed the development of carotid plaque, which is just another piece of data showing that cholesterol in the blood has little relation to the development of disease.
Best–
MRE
All my tests show no oxygen deprivation of my heart. I want to live to, BUT NOT WITHOUT MY MIND. AND MY MEMORY IS ALREADY FAILING SO MUCH THAT IT COST ME MY JOB. That’s without statin medication.
John B, perhaps you should instead of consuming no oil rather take omega-3 and omega-6(double carbon bond location) fatty-acid oils of various carbon chain lengths ie arachadonic acid, aracha doic acid, docosahexanoic acid, alpha levro-tocopherol acid (vitamin E, notice it must be levro ie left handed symetry.) Also there is some slight evidence that longercarbon chanine (thus more waxy ie high melting temperature fatty acids) of the omega-6 and omega-3 double bond structure hgelps increaase HDL which has a documented significant effect in lowerin cardiac events (I think?)