Friday, January 28, 2011

New study adds to the growing evidence that cholesterol reduction has dubious benefits for health

Dr. Briffa's 'A Good Look at Good Health', which I subscribe to and follow, has a good article about the growing evidence against low cholesterol and use of statin drugs.

New study adds to the growing evidence that cholesterol reduction has dubious benefits for health

Posted By John Briffa On 28 January 2011 @ 2:40 pm In Cholesterol and Statins

Statins reduce cholesterol-levels and have the ability to reduce heart disease risk. However, some researchers have asked if the primary mode of action of statins is cholesterol reduction. After all, statins have several effects in the body which might reduce the risk of heart disease in ways that have essentially nothing to do with cholesterol. For example, statins enhance nitric oxide production (this helps dilate blood vessels), have anti-inflammatory effects (see below), and also have the ability to reduce clotting in the blood (e.g. reduced fibrinogen levels and inhibition of platelet adhesion and aggregation).
Today saw the publication of a study which reinforced this idea. It involved the treatment of individuals deemed to be at high risk of cardiovascular disease with a statin (simvastatin) or placebo [1]. This research was designed to assess whether the effect of statin therapy was in any way influenced by levels of a substance known as C-reactive protein (CRP) in the body. CRP is a marker of inflammation, and inflammation is a key underlying process in heart disease. Statins are anti-inflammatory. Could it be, therefore, that statins work between in individuals with raised CRP levels. In short, this study found that risk reduction was essentially the same across different levels of CRP. In other words, in the study, CRP levels did not appear to help identify individuals who might benefit most from statin therapy.
But an interesting finding from this study, I think, is the fact that statin therapy appeared to reduce cardiovascular events (such as heart attack and stroke) in individuals with low LDL-cholesterol (supposedly ‘unhealthy’) levels. Now, low levels of cholesterol are not a risk factor for cardiovascular disease. So, if statins broadly help individuals with low LDL levels, that does suggest their main mode or modes of action here do not relate to cholesterol reduction.
This is not, however, the first time research has found statins reduce cardiovascular disease risk in individuals with ‘normal’ or even ‘low’ cholesterol levels [2]. It is also interesting to note that statins substantially reduce the risk of stroke, despite the fact that raised cholesterol levels are a weak or non-existent risk factor for stroke [3,4]. Also, more intensive cholesterol reduction does not necessarily lead to improved outcomes [5].
All of this also calls into question the wisdom of cholesterol reduction generally. If cholesterol reduction does indeed have broad benefits for health, we would expect to see positive effects from cholesterol-reducing strategies in terms of risk of total mortality. However, in a meta-analysis (pooling together of several similar studies) of a variety of cholesterol-reducing strategies including drug treatments [6], neither fibrates nor resins (two forms of cholesterol-reducing drugs) were found to reduce overall mortality. In fact, in this meta-analysis, other than statins, no cholesterol-reducing strategy analysed was found to reduce overall mortality.

Some argue that other cholesterol-reducing strategies fail to reduce cholesterol enough compared to statins. However, in this meta-analysis statin therapy was found to reduce cholesterol by 20 per cent on average, and this was associated with reduced mortality. This level of cholesterol reduction was matched by resin therapy in those with a prior history of cardiovascular disease, yet there was no reduction in overall mortality here.

In 2002, a new type of cholesterol-reducing drug – ezetimibe – was licensed for use. The basis for this decision was ezetimibe’s proven cholesterol-reducing effect. However, to date, no studies have been published which show that this agent has the capacity to reduce CVD risk or mortality.

Moreover, one trial found that treatment with ezetimibe actually increased thickening in the wall of the arteries (carotid artery intima thickness). Most importantly, ezetimibe use was associated with five times the risk of cardiovascular events (e.g. heart attacks, stroke) compared to another treatment (niacin – a form of vitamin B3) [7]. Such findings clearly call into question the view that cholesterol reduction, through whatever means, is beneficial to cardiovascular and general health.

The reason that this is important is because that we are generally encouraged to drive our cholesterol levels to ever-lower levels, and there is good evidence which questions the fundamental assumptions on which this approach is based. Research suggests that cholesterol reduction, per se, does not have broad benefits for health. Though I do admit the drugs companies and the researchers in their pay have done a generally very good job of persuading us otherwise.

1. Heart Protection Study Collaborative Group. C-reactive protein concentration and the vascular benefits of statin therapy: an analysis of 20 536 patients in the Heart Protection Study. The Lancet, Early Online Publication, 28 January 2011

2. Ridker PM, et al, JUPITER Study Group. Rosuvastatin to prevent vascular events in men and women with elevated C-reactive protein. N Engl J Med 2008;359(21):2195-2207

3. Cholesterol, diastolic blood pressure, and stroke: 13,000 strokes in 450,000 people in 45 prospective cohorts. Prospective studies collaboration. Lancet 1995;346(8991-8992):1647-53.

4. Imamura T, et al. LDL cholesterol and the development of stroke subtypes and coronary heart disease in a general Japanese population: the Hisayama study. Stroke 2009;40(2):382-8
5. Kastelein JJ, et al, ENHANCE Investigators. Simvastatin with or without ezetimibe in familial hypercholesterolemia. N Engl J Med 2008;358(14):1431-1443
6. Studer M, et al. Effect of different antilipidemic agents and diets on mortality: a systematic review. Arch Intern Med 2005;165(7):725-30
7. Taylor AJ, et al. Extended-Release Niacin or Ezetimibe and Carotid Intima–Media Thickness. N Engl J Med 2009; 361:2113-2122]


The Polypill

From Prevention                    When will all this nonsense end?


WHO trial shows acceptability of polypill in a developing county

January 28, 2011
Lisa Nainggolan

Winston-Salem, NC - A pilot trial of a polypill for primary prevention of cardiovascular disease in Sri Lanka has shown this approach to be practical in a developing country and demonstrated that the polypill is highly acceptable among both patients and doctors [1].

"This study has fulfilled its purpose; we wanted to check the feasibility of doing a large-scale clinical trial with a polypill in a developing country, and from this perspective we now know that it's feasible," lead author Dr Elsayed Z Soliman (Wake Forest University School of Medicine, Winston-Salem, NC) told heartwire. Soliman and colleagues report their findings, the only such study sponsored by the World Health Organization (WHO), online January 5, 2011 in Trials.

The polypill was as effective as standard treatment in the population studied, but Soliman points out that "standard" treatment in this trial was administered from a tertiary-care center, and so it was "very sophisticated, complicated therapy."

And he says that although feasibility has been demonstrated, there are many questions to resolve before going forward with future, large trials of polypills. First, which patient population should a polypill be aimed at: primary or secondary prevention? What components and what doses should be in the pill? He notes that there is now a question mark over aspirin, at least in the primary-prevention population. And what should it be compared with? The separate components of the pill, placebo, or "standard treatment," and if the latter, how should that be defined? "All of these questions will never be answered by a single trial," he notes.

Polypill deemed acceptable by 90% of patients and >80% of doctors

Soliman et al conducted an open-label, parallel-group, randomized clinical trial that enrolled a total of 216 patients without established cardiovascular disease with an estimated 10-year total CVD risk score >20% from three sites in Sri Lanka. Patients were randomized to a polypill containing 75 mg of aspirin, 20 mg of simvastatin, 10 mg of lisinopril, and 12.5 mg of hydrochlorothiazide (Red Heart pill 2b; Reddy's Laboratories, India) or to standard practice and followed for three months.

Prespecified primary outcomes included reduction in systolic BP, total cholesterol, and estimated 10-year CVD risk. The researchers also assessed the recruitment process and the acceptability of the polypill by physicians and patients.

Of the patients, 203 completed the three-month treatment and returned for their three-month follow-up visit; both the polypill and standard treatment resulted in marked reductions in systolic BP, cholesterol, and 10-year risk of CVD, but there was no significant difference between the groups.
Of the patients who completed the trial, 90% said they would take the polypill "for life" if it were proven to be effective in reducing CVD risk; 86% of doctors supported the use of the polypill for primary prevention and 93% for secondary prevention.
Lessons learned should guide future studies
Soliman and colleagues explain they were unable to estimate the risk-factor reductions on the polypill "because the control group received similar treatment with individual drugs." However, they note that the polypill was "simpler" and achieved comparable risk-factor reductions, "highlighting its potential usefulness in the prevention of CVD."
And they point out that the three tertiary-care hospitals involved in this study "do not reflect the level of medical care provided at primary-care centers and secondary-level hospitals in Sri Lanka. Thus, the findings from the selected trial sites cannot be generalized to other levels of care.
"Further studies assessing the polypill in developing countries should take into consideration the study design lessons and challenges that we encountered," they conclude.
Other polypill trials are ongoing, including the TIPS 2 study and a collaborative effort called Single Pill to Avert Cardiovascular Events (SPACE), which includes the Use of a Multidrug Pill in Reducing Cardiovascular Events (UMPIRE), the Kanyini Guidelines Adherence with the Polypill (Kanyini GAP) and Improving Adherence Using Combination Therapy (IMPACT) trials.
UPDATE: Sept 8, 2014 -  An FDA advisory committee looks at a new cardiovascular polypill about which FDA staff expressed serious reservations

Thursday, January 27, 2011

Statins and the Cholesterol Hypothesis – Part I

Not a newly discovered article, rather one in my 'to be read' pile that I finally got to, but here it is in full (it was too hard to select just an exerpt). From Kurt G. Harris MD at his PāNu blog. There is a lot on his site I need to read.


Statins and the Cholesterol Hypothesis – Part I

Wednesday, July 21, 2010 at 10:31AM

Reader Stephen is a young man I have corresponded with a few times on the subject of his diagnosis of FH (heterozygous Familial Hypercholesterolemia) and what he should do about it. His TC runs about 467 mg/dl and his LDL about 333 mg/dl. He has a CAC (calcium score) of 16, which is very high for a 24 year old man. This would be at about the 50th percentile for a 50 year old male on the SAD.

Stephen has of course given me permission to discuss his case here.

This is his most recent email to me:

Hi Dr. Harris,

It's been awhile since I last emailed you about any recent information regarding my heart scan. I also forgot to thank you for your last response and really appreciate the help you've given me. I recently had more lab work done and I am waiting to hear back for the results, although not much has changed since our last correspondence. However, now that I'm back in Dallas for my summer break I was able to get a proper heart scan at the Cooper Clinic. My CAC score was 16. I attended the Metabolism Society Symposium conference in Seattle a few months back and spoke with Jimmy Moore and a few others about my situation and they recommended I send Dr. Davis an email to get his advice on the matter. I recently heard back from him telling me basically that he strongly believes I go on statins while maintaining my current diet. Jimmy asked me to keep him posted about Dr. Davis' recommendations, so I emailed him, and he is now interested in posting a blog about it and asking others for suggestions since he is strongly against statin use. Anyways, I just wanted to update you, since you mentioned an interest in eventually making a post about this as well. If you're interested in having a look at the scan I can send another copy over to you as well as the results of the NMR profile I drew blood for a few days ago. If not, I completely understand as well, you have a lot on your plate as is. Let me know what you'd prefer and I'll do whatever works best for you. I look forward to hearing back from you.

Thanks again,

Stephen U.

By now you already know that I personally would avoid statins under any circumstances as they only work at all on heart attack risk via their effects on inflammation. Taking a sledgehammer to the entire cholesterol machinery has all kinds of negative knock-on effects, including promotion of cancer and interference with muscle and liver function, in addition to the accidental side benefit of reducing inflammation. It’s a crude approach, it has side effects that make all cause mortality over long periods of time likely to be worse, and the only group with any demonstrated benefit is men with established disease. The vast majority of those taking statins have no scientific basis for taking them. The rest, including those who have had an MI already, could likely accomplish far greater improvements in health with non-drug dietary measures like improved glucoregulatory control, and avoidance of the Neolithic agents of disease.

Let me summarize what we know about statins

1) A few older trials show an all-cause mortality benefit to statins in secondary prevention IN MEN (not women). The relative risk reduction is at most about 30% and the maximum absolute risk reduction is about 1% per year. (This means you still have about 70% of the relative risk of dying you had before the drug. Is it possible dietary changes could decrease your risk more substantially? I think so.) Secondary prevention means you have already had a heart attack or been proven to have coronary artery disease (CAD). If you only have high TC or LDL, this does not include you, and this does not include the majority of those now taking statins.

2) Other trials, especially more recent ones, are less likely to show a benefit, even in secondary prevention

3) For primary prevention, there is no demonstrated mortality benefit to taking statins.

4) When there are decreased deaths from cardiac events in primary prevention, there are more deaths by other causes. You may well be trading your heart attack for cancer. Because of the long lead time for cancer deaths, there are good theoretical reasons to believe that over periods of time - much longer than a few years (the length of the typical drug trial) all cause mortality could easily be higher when taking a statin for primary prevention.

5) When statins do work, they work by accident via their effects on inflammation. The side effects may be related to the lowering of LDL, but the benefits are not. Trials have failed to show the linear relationship between LDL lowering and cardiac end-points that one would expect if the effect were due to the LDL level.

I do not believe in any of the versions of the lipid hypothesis, ranging from Ancel Keys' original idea that cholesterol or dietary fat clogs the arteries, to the currently fashionable one that “small, dense” LDL particles are like microscopic rodents that are designed to burrow under the intima of your blood vessels and kill you.

Neither cholesterol nor any of the lipoproteins nor LP(a) is a "cause" of CAD (coronary artery disease). There is no evidence that “fixing” these numbers is of benefit other than by accident and there is plenty of evidence that you can kill people by trying to do so.

HDL, particle numbers, particle sizes, LP(a) are all parameters that are more or less associated with CAD. If they respond positively to changes in diet, then they are just covariant with decreased risk of CAD or MI due to the changes you made in your diet. They are not necessarily, and not usually the direct mediators of the decreased risk.

They may track the positive changes you make in your diet, but they are not causing heart attacks any more than shoe size causes height!

You cannot decrease your stature by amputating your toes. Believing any of the lipid hypotheses or the cholesterol hypothesis is the intellectual equivalent of amputating toes to decrease height because shoe size causes stature.

Correlation is not causation. Causation can cause a correlation to occur, but proof of correlation is not sufficient to prove causation. None of the lipid hypotheses are biologically plausible, and all have failed to be proven despite decades of research and billions in expenditure.

Say you observe that the neighborhoods that have the most numbers of police on patrol have more crime. A neighborhood in downtown Milwaukee has more than 8 times the per capita police presence than in Sturgeon Bay 120 miles to the north. The crime rate in downtown Milwaukee is also more than an order of magnitude higher. Say the calculated correlation coefficient is .85 – with 0 being no correlation and 1.0 perfect correlation. Is it reasonable to propose we reduce the number of police in Milwaukee in order to effect a lower crime rate? There is a very high (and statistically significant) correlation, but if we think of mechanisms, and how police presence relates to crime, we would probably think that the police are there in response to the crime and are not likely causing it. We might go a step further and say that it might be dangerous to reduce the number of police, as for all we know the city has put them there for good reason, and the crime differential between our two towns might become even greater without them.

In the same way, although high HDL indeed correlates with lower risk of MI (heart attack or myocardial infarction) and CAD (coronary artery disease), when we understand the biology of HDL production, we might be wary of approaches that attempt to increase HDL as if HDL is the agent protecting your heart. It might well matter how we alter HDL. It might be that HDL is high in response to whatever lowers heart attack risk.

It might be (In fact I think it is) that a diet high in saturated fat protects against atherosclerosis and also affects the numerical value of HDL (most of you know it does because you see it happen to you), such that the association of HDL and lower MI risk is because they are caused by the same thing (diet) instead of because one “causes” the other.

Consider the particle du jour of LP(a). Measured Lipoprotein (a) has a correlation with MI risk. It’s not really that high as a risk factor (not even remotely close to glycated hemoglobin or calcium score), but there is a positive correlation. In an individual human, Lipoprotein (a) could be high as an adaptive response to having lots of oxidized LDL and thereby may indicate you have an atherogenic diet, like the crime ridden neighborhood that has a substantial police presence. Or you could be just born with high levels of LP (a). In the same way a somewhat paranoid and wealthy community has lots of policemen on patrol even though the crime rate is low, you might have patrol cars of LP (a) cruising around even though you do not have intimal damage occurring.

Sidenote: I admit I have a bias towards this interpretation. My Lp(a) level is 85 yet my CIMT* measurement would be normal for someone 15 years younger and my CAC score is zero. Lp(a) levels can be highly heritable, and longevity and freedom from atherosclerosis runs in my family. As Peter would say, some of us may just be born with more sticking plasters, and some of us make more sticking plasters because we have more damage. It should be noted that the best way to decrease LP (a) is increasing saturated fat intake, but also that although there is positive correlation of LP(a) with disease on a population level, there is not yet a shred of evidence that any intervention to modify your LP(a) level modifies your risk.

The point is that just by observing more police patrols or more Lp(a), even in the context of a true correlation between crime and police and Lp(a) and MI, you cannot necessarily tell why the police are there or why the Lp(a) is elevated. More importantly, the idea that reducing the number of police will reduce crime or that pharmacologically altering Lp(a) will reduce risk may be not only false, but dangerously false. Some neighborhoods need their police, and some humans may need their Lp(a), just like some humans may have more heart attacks when we “help” them by pharmacologically jacking up their HDL.

This is in fact precisely the story of torcetrapib. This drug cost Pfizer over 800 million dollars to develop. Torcetrapib is an inhibitor of CETP - cholesterol ester transfer protein. CETP facilitates the transfer of cholesterol from HLD to VLDL or LDL. Now, if you believe version 3.0 of the lipid hypothesis, there are these things called “good” and “bad” cholesterol. This is cardiologist shorthand for lipoprotein-cholesterol complexes that cause or prevent heart disease. HDL is the good one and we want it to be high, so it can hoover up the cholesterol from arterial plaque (a ridiculous idea that as Malcolm Kendrick pointed out defies physical chemistry – Ornish’s “garbage trucks”) and shrink them. LDL is the bad one and we want it to be low, as it is constantly fighting to transport cholesterol to the arterial plaque.

Cardiologists and Pfizer actually believe that LDL is trying to kill you and HDL is trying to save you at the same time. They figured, why not throw our pharmacological weight into the fight? If we inhibit CETP, the level of HDL will rise, and the level of LDL will fall. They actually combined torcetrapib with an extant statin (atorvastatin or Lipitor) to really, really get the LDL down as well as the HDL up.

So how did it work? Well, it worked spectacularly. HDL levels soared and LDL levels went down. I mean, we are talking HDL to LDL ratios that epidemiologists and cardiologists would say should reduce the risk of heart attack to zero. There was a glitch, though. Although the HDL and LDL went exactly the way they wanted, the risk of death in the group that got the torcetrapib was 60% higher. The trial was halted early.

Sidenote: We could belabor the police metaphor by saying pharmacologic elevation of HDL with torcetrapib was a bit like recruiting Alex’s droogs into the police in “Clockwork Orange”. The crime rate would go up with more police recruited from among those who are themselves criminals.

So do you think it is plausible that LDL causes heart disease and HDL saves us from it? Or is it more likely that these laboratory numbers are merely epiphenomena to the real primary process?

Is it really plausible that our bodies evolved to simultaneously create two substances that are like some perverse yin and yang, with good HDL trying to save us from the LDL that is furiously trying to clog our arteries with cholesterol?

Or is this all a bunch of biologically implausible nonsense?

Taking all the evidence in its totality, I’ve see no compelling use for statins for anyone if they have truly optimized their diet, and very little even if they haven’t. The benefits of statins are unrelated to their effects on “cholesterol” or lipoprotein levels, are small and are accidental.

The risk/benefit ratio and effect size of dietary modifications are likely to be superior to any of the current statin drugs.

I do believe there are dietary ways that we can minimize the risk of atherosclerosis and other inflammatory processes, minimize the risk of acute plaque rupture and thrombosis if we do have atherosclerosis, and minimize the risk of a fatal arrhythmia if these upstream steps fail

I don’t believe once you have taken these steps, that pharmacology targeted to “cholesterol” or lipoproteins has anything to add.

I suggest:

1) Avoidance of excess PUFA in the diet that leads to oxidized LDL and possible endothelial damage
2) Avoidance of all the causes of leaky gut that may lead to the suite of inflammatory processes known as the metabolic syndrome – avoid excess PUFA (esp. linoleic acid), wheat, and fructose
3) Plenty of saturated fat intake
4) If your glucoregulation is impaired, reduce carbohydrate consumption to whatever is necessary to minimize glycation and endothelial damage. Minimize glycated hemoglobin (Hemoglobin A1c) to the degree possible
5) Replacement of essential micronutrients that may be deficient on the SAD. Magnesium, sunshine, pastured butter for Vit K2.

Those are my general recommendations for everyone.

So what if you have FH? Are the recommendations different?

More discussion in the next post.

*CIMT is carotid intima/media thickness - easily measured noninvasively with ultrasound and a more sensitive measure of early atherosclerosis than CAC (calcium score) in men under 40 and women under 50

Cholesterol: Friend Or Foe?

Natasha Campbell-McBride, MD, wrote an article with the title "Cholesterol: Friend Or Foe? " that appears here. Her last paragraph states:

"In conclusion, cholesterol is one of the most important substances in the body. We cannot live without it, let alone function well. The pernicious diet-heart hypothesis has vilified this essential substance. Unfortunately, this hypothesis has served many commercial and political interests far too well, so they ensure its long survival. However, the life of the diet-heart hypothesis is coming to an end as we become aware that cholesterol has been mistakenly blamed for the crime just because it was found at the scene."

Please avail yourself of the full article. You may find out some almost new information about cholesterol.


Wednesday, January 26, 2011

The Statin Scam

Several lines that say a lot from Dr Lundell's post on Spacedoc.net about - yes you guessed it - statins. I have added emphasis by bolding key (to me) words.


Treating or attempting to prevent heart disease with statin drugs is dangerous and fraudulent for two reasons:

1.) Serious, deadly and disabling side effects which are largely ignored by the medical profession and suppressed by the statin makers. These side effects have been brilliantly documented by Dr. Duane Graveline and other brave doctors who dare to speak out against the official religion of cholesterol and saturated fat.

2.) Continued focus on this ineffective treatment diverts attention from truly understanding and controlling heart disease, and gives patients a false sense of security that prevents them from making the lifestyle changes that would truly prevent and reverse heart disease.

Consider also the following:

1.) Statins have not been proven to help any woman of any age!

2.) Statins have not been proven to help anyone over the age of 65!

3.) The only group of patients who may, and I emphasize "may" get any benefit, are middle aged men who have had a previous heart attack.

It is amazing to see all the medical literature that is funded by the statin makers and delivered to doctors' offices by enthusiastic young drug reps that purport to prove that statins are beneficial.

Read the doctors full article here

I fall under point 3 above. 'I may have gotten some benefit...'

My cholesterol which was controlled over the course of my life by nearly every statin then available (including baycol - fortunate for my dear wife, it was for only a short period of time) was low enough to make the most skeptical cardiolodist grin like a chesire cat and pat himself on the back for 'saving' another potential CVD patient from what they really do most (CABG, stent etc).

I responded well on their primary objective. Life saving Zocor, Lipitor, Baycol, Mevacor etc - caused my cholesterol to take the sought for plunge to safety well below the current target. What a model I was. With a mother who was a pharmacist and numerous doctors in the family I was a well behaved obedient patient. Heck, I didn't want to die young (I was in my late 20's or early 30's when I got on the S wagon) of something so easily treated by not taking my pill. I knew the miracle power of the pill.

The aspect I didn't do quite as well on was the persistent muscle aches which prevented sleep and were, I was told, a small price to pay in trade for the most 'tremendous benefit' -  prevention of 'The widowmaker'. The main thing I was told about these aches was they were NOT related to the medication but other age related things that you couldn't do anything about. They hadn't yet invented the aging prevention pill.

Here and now let me admit that I have experimented with drugs. Oops now it's out. Yes I did. I'm happy to say I did! No! Not that kind. But the kind associated with this topic.

Experiment: Without full disclosure, I cold turkey stopped taking my statins. (don't tell my dr - I withheld that info from him. After all this was MY experiment and I knew what he would say 'don't stop we'll try another one. There are lots of flavors'.)
Result: After a period of time I could sleep better due to lack of aching muscles. Sure, it could have been some other non-controlled or confounding factor skewing my perception.
Repeatablity: I'm a skeptic but after I was admonished to 'think of my wife and go back on the S wagon', and complying, the aches returned. Second time, perhaps with a bit more attention to what was going on, ooooh, same 'non-related' outcome.

There were some other tests of sneaking off the wagon.

The 'experimental' phase was undertaken at least partly because after roughly 10 years on statins I was rushed into the ER and the EKG tech spotted the (don't breathe this out loud as he did causing him to receive strong admonishment from those agast at his breech in front of the patient) 'toumbstone effect' on my trace. This shouldn't happen - I'm protected!

Subsequent History: MI(cabg), MI(stent), MI, drug free, MI(stent), MI(stent in a stent), GIST, basal cell carcinoma. Note: the last two items 'may' have nothing to do with long term drug (statin) use/abuse.

Darn! All that with near ideal cholesterol. What gives here?

When will the real honest true truth become mainstream? I sincerely thank those who try like Dr Lundell and Dr Duane Graveline and others who are on the front lines trying to breech the wall.

MMR vaccines and symptoms of autism

Oh Horrors! The BMJ couldn't/wouldn't do a thing like that - would they?

Not my usual topic on this blog but my humble opinion deems it quite interesting in spite of the lack of mentioning the 'C' word or 'S' word.


Dr Wakefield demands retraction from BMJ after documents prove innocence from allegations of vaccine autism data fraud

by Mike Adams, the Health Ranger, NaturalNews Editor

(NaturalNews) In light of new evidence that has emerged clearing Dr Wakefield of the allegations that he fabricated study data involving MMR vaccines and symptoms of autism, Dr Wakefield is now publicly demanding a retraction from the British Medical Journal and author Brian Deer. Documents just made public reveal that another medical research team which included a senior pathologist independently documented evidence of a possible MMR vaccine - autism link 14 months before Dr Wakefield's paper first appears in The Lancet -- based on several of the same children appearing in Dr Wakefield's study. (http://www.naturalnews.com/031116_D...)

These documents include detailed clinical notes describing the pathology in seven children following MMR vaccination. These notes include references to "autism" and chronic gastrointestinal inflammation, among others.

This evidence, which was just made public, refutes the accusations of fraud leveled against Dr Andrew Wakefield by the British Medical Journal and reporter Brian Deer. This evidence was made available to the BMJ before the publication of their accusations, but they chose to ignore it. Dr Wakefield, in essence, has been falsely accused by the BMJ in what is now being widely recognized as a political witch hunt against the most visible researcher questioning the safety of MMR vaccines.

BMJ caught in highly politicized scientific fraud

The BMJ, in essence, has been caught pulling off what may be the largest scientific fraud ever perpetrated by any medical journal in the history of the world. It grossly misrepresented the facts in falsely accusing Dr Wakefield of fabricating the clinical trial data that led to his landmark study being published in The Lancet in 1998. The innocence of Dr Wakefield has now been established by these newly-released documents.

The British Medical Journal also failed to disclose that its own finances are largely funded by vaccine manufacturers who fill the journal with paid advertising, and that such financial ties may have influenced the journal's decision to attempt to destroy the reputation of a researcher whose findings threatened the profits of its top sponsors. If you follow the money in this story, in other words, it leads right to the editors of BMJ, whose salaries are effectively financed by vaccine manufacturers. This all-important conflict of interest is almost never discussed in the mainstream media, by the way.

In light of the evidence that has now been made public, clearing Dr Andrew Wakefield of any wrongdoing, Dr Wakefield is publicly demanding that the BMJ issue a full retraction of its Brian Deer article accusing Dr Wakefield of fabricating the data. His statement is entitled, "Uncovered Documents Prove There Was No Fraud in Lancet Case Series" and is included here in its entirety:


Uncovered Documents Prove There Was No Fraud in Lancet Case Series

British Medical Journal and Sunday Times author Brian Deer misrepresent facts in latest articles wrongly accusing Dr. Wakefield of altering clinical histories of autistic children

In a series of articles published in the UK Sunday Times and the British Medical Journal (BMJ), written by freelance journalist Brian Deer and BMJ editor Dr. Fiona Godlee (1), I am accused of altering the clinical histories and test results in autistic children in order to manufacture a novel disease – a disease described in The Lancet in 1998 that Brian Deer claims does not exist. I have documents that confirm beyond a shadow of a doubt that I did not falsify this data; that the finding of bowel disease in these children is real; and that these findings were accurately reported in The Lancet in 1998.

The first document (2) describes 7 of The Lancet children and was written by Professor John Walker-Smith in December 1996, 14 months before The Lancet paper was published. Professor Walker-Smith prepared this document in an exercise that, in his words, “was totally unrelated to Andy Wakefield” (3). The document was a report prepared for a scientific meeting, and was based upon Professor Walker-Smith’s own independent assessment of the children’s condition.

He was assisted by a senior pathologist and an expert in bowel disease, Dr. Dhillon, who reported on the microscopic findings in the children’s intestinal tissues. This independent analysis was conducted to a high level of scientific rigor, and are the precise findings reported in The Lancet.

These documents, including Professor Walker-Smith’s report; the transcript of his sworn testimony before the UK medical regulator (2), the General Medical Council (GMC), and the relevant sections of the statement of Dr. Dhillon to the GMC3; were available to Deer and the editors of the BMJ well in advance of their recent publication. (4) They knew, or should have known, that their allegations against me were false. It is clear that the BMJ acted recklessly by failing to check these facts adequately before making their false allegations.

On the basis of this evidence, the British Medical Journal must retract these articles, or face the consequences.

(1) Author of BMJ articles only
(2) http://www.vaccinesafetyfirst.com/p...
(3) http://www.vaccinesafetyfirst.com/p...
(4) Callous Disregard: Autism and Vaccines - The Truth Behind a Tragedy, published by Skyhorse Publishing in May 2010 and Wakefield’s complaint about Brian Deer to the UK’s Press Complaints Commission at www.cryshame.org
Read Callous Disregard to learn more truth

Dr Andrew Wakefield is the author of Callous Disregard, the book that documents the truth behind conventional medicine's political witch hunt to destroy anyone who questions the safety of vaccines. The book is sold everywhere, including Amazon.com: http://www.amazon.com/Callous-Disre...
Sources for this story include:

Read the article here.

Book Review: Fat and Cholesterol are Good for You!

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.

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.

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.

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.

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.
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…
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 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
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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.

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.

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.