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–

MRE

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 

God help us all. 

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 

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.

A large body of evidence supports a central role for lowering levels of low-density lipoprotein cholesterol (LDL-C) in the prevention of atherosclerotic cardiovascular disease. [Uh,there is an almost nonexistent body of evidence. Certainly nothing that is conclusive.] Randomized controlled trials have established that statin-mediated reductions in LDL-C have a favorable effect on the incidence of cardiovascular events. [A couple of studies have shown a small favorable effect in people with established heart disease] As a result, LDL-C lowering has become an integral component of therapeutic strategies in the prevention of cardiovascular disease. [True, but based on very little evidence] In particular, the use of statins has become widespread. [How very true.]

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:

Funding/Support: The REVERSAL and CAMELOT studies were sponsored by Pfizer; the ASTEROID study was sponsored by AstraZeneca; and the ACTIVATE study was sponsored by Sankyo Pharma. Dr Nicholls was supported by a Ralph Reader Overseas Research Fellowship from the National Heart Foundation of Australia.

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:

Financial Disclosures: Dr Nicholls reported receiving honoraria for lectures from Pfizer, AstraZeneca, and Merck Schering-Plough; consulting fees from AstraZeneca and Anthera Pharmaceuticals; and research support from LipidSciences. Dr Tuzcu reported receiving research support from Pfizer, AstraZeneca, and Sankyo Pharma; and honoraria for lectures from Pfizer and AstraZeneca. Dr Sipahi reported receiving an educational grant from Pfizer. Dr Hazen reported receiving research support and honoraria for lectures from Pfizer, Merck, and Sankyo. Dr Grasso reported owning stock in Pfizer. Dr Schoenhagen reported giving lectures for Takeda Pharmaceuticals but noted that all honoraria were directly paid to charity. Dr Desai reported receiving honoraria for lectures from Merck and Pfizer. Dr Kapadia reported receiving honoraria for lectures from Pfizer. Dr Nissen reported receiving research support from AstraZeneca, Eli Lilly, Pfizer, Takeda, Sankyo, and Sanofi-Aventis; and consulting for a number of pharmaceutical companies without financial compensation. Dr Nissen’s honoraria, consulting fees, or other payments from any for-profit entity are paid directly to charity, so that neither income nor any tax deduction is received. No other authors reported financial disclosures.[Author's names: my bold]

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

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 

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 

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