Ask This Question Before Taking Statins - Penberthy

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FOR IMMEDIATE RELEASE Orthomolecular Medicine News Service, December 3, 2013 Ask This Question Before Taking Statins Commentary by W. Todd Penberthy, PhD (OMNS Dec 3, 2013) Before taking statins, ask yourself one question. Why is it, given two people with identical environmental backgrounds, that on average one of them dies early due to cardiovascular disease? Is it because that individual has taken less statin drugs? Of course not. It is likely due to something different in their genetics, which causes differences in enzymes and levels of other proteins. This leads to differing requirements for essential vitamins and minerals. Cardiovascular disease is largely caused by deficiencies of essential nutrients. Thus adjusting the diet makes sense. When your car breaks down, do you have the repair shop install a gadget not in the car's parts list? Of course not. We clean, tighten, remanufacture, or replace the correct part. Similarly, the body needs maintenance and some tender loving care. Statins are not one of our parts. Essential nutrients are what we need. The reason people die of cardiovascular disease usually begins with inflammation and progressive calcification, not cholesterol levels. The correlations between inflammation, calcification and death by cardiovascular disease (CVD) are much stronger than for correlations between cholesterol levels and death by CVD (Bolland et al, 2008). Following the guidelines of the American Heart Association (AHA) may be useful for liability and good business, but is not always useful for maintaining optimal health. To understand what's going on inside of the body, just take a look at the images of vascular calcification. In response to inflammation in arteries, plaques form. At the center of an arterial plaque sits a hard calcification that contains calcium carbonate. Around this calcified nucleus, the plaque develops with fat deposits and a fibrous cap. In many cases the plaque can be reversed with excellent nutrition. Considering the media attention given to statins, it's quite remarkable to learn that they only reduce the risk of mortality from CVD by less than 1 percent. In contrast, in clinical trials involving over 8,000 patients over 6 years, high dose niacin (3,000 mg daily) reduced mortality by 11%. And this lowered risk was tabulated 15 years after the clinical trial ended! (Canner et al., 1986) That represents a huge improvement over treatment with statins. Recent advances in molecular biology explain how this works. Niacin's amazing sustained effect is likely due to its effect on regulating sirtuin proteins that cause long lasting epigenetic changes in the structure of DNA. This type of epigenetic modulation is known to have long-lasting effects. The nutrition you get in early childhood, or even that your parents got before you were born, can affect your genes over a long period. The data from this study implies that 3,000 mg of niacin is far superior to statins for preventing CVD death. And it only costs about 35 cents per day. Anyone who has the risk factors for death from CVD would be well advised to consider taking up to three 1,000 mg daily doses (or, for less flushing, 12 doses of 250 mg) of regular "fast-release" niacin (Hoffer et al, 2012). It would also be wise to add 100 mg of the MK7 form of vitamin K2 and 1,000 mg flax seed oil with every dose of niacin. These nutrients reduce flushing and provide anti-inflammatory benefits. For a healthy heart, include 3,000-10,000 mg of vitamin C (Roberts and Hickey, 2011), 400-1200 IU natural vitamin E, and five cups of kale mixed with colorful vegetables and a bit of grass fed butter every day. Further, to remove calcifications, it may help to daily take two 200-400 mg doses of magnesium (citrate, chelate, malate, or chloride). This can help to dissolve the calcium deposits in arteries (Dean, 2007). None of these essential nutrients requires any prescription, and together they have tremendous advantages for health compared to a statin pill. (Dr. Todd Penberthy is a research consultant, medical writer and one of the world's prominent niacin researchers. A list of his recent papers is posted at http://www.cmescribe.com/resume/ ) References: Bolland, M.J., Barber, P.A., Doughty, R.N., Mason, B., Horne, A., Ames, R., Gamble, G.D., Grey, A., and Reid, I.R. Vascular events in healthy older women receiving calcium supplementation: randomised controlled trial. Bmj; 2008. 336(7638): 262-266. Canner, P.L., Berge, K.G., Wenger, N.K., Stamler, J., Friedman, L., Prineas, R.J., and Friedewald, W. Fifteen year mortality in Coronary Drug Project patients: long-term benefit with niacin. J Am Coll Cardiol; 1986. 8(6): 1245-1255. Dean, C. The Magnesium Miracle. New York, NY: Ballantine, 2007. Hoffer A, Saul AW, Foster HD. Niacin: The Real Story. Basic Health Publications, 2012. Roberts H, Hickey S. The Vitamin Cure for Heart Disease: How to Prevent and Treat Heart Disease Using Nutrition and Vitamin Supplementation. Basic Health Publications, 2011. Nutritional Medicine is Orthomolecular Medicine Orthomolecular medicine uses safe, effective nutritional therapy to fight illness. For more information: http://www.orthomolecular.org Find a Doctor To locate an orthomolecular physician near you: http://orthomolecular.org/resources/omns/v06n09.shtml The peer-reviewed Orthomolecular Medicine News Service is a non-profit and non-commercial informational resource. Editorial Review Board: Ian Brighthope, M.D. (Australia) Ralph K. Campbell, M.D. (USA) Carolyn Dean, M.D., N.D. (USA) Damien Downing, M.D. (United Kingdom) Dean Elledge, D.D.S., M.S. (USA) Michael Ellis, M.D. (Australia) Martin P. Gallagher, M.D., D.C. (USA) Michael Gonzalez, D.Sc., Ph.D. (Puerto Rico) William B. Grant, Ph.D. (USA) Steve Hickey, Ph.D. (United Kingdom) Michael Janson, M.D. (USA) Robert E. Jenkins, D.C. (USA) Bo H. Jonsson, M.D., Ph.D. (Sweden) Peter H. Lauda, M.D. (Austria) Thomas Levy, M.D., J.D. (USA) Stuart Lindsey, Pharm.D. (USA) Jorge R. Miranda-Massari, Pharm.D. (Puerto Rico) Karin Munsterhjelm-Ahumada, M.D. (Finland) Erik Paterson, M.D. (Canada) W. Todd Penberthy, Ph.D. (USA) Gert E. Schuitemaker, Ph.D. (Netherlands) Robert G. Smith, Ph.D. (USA) Jagan Nathan Vamanan, M.D. (India) Atsuo Yanagisawa, M.D., Ph.D. (Japan) Andrew W. Saul, Ph.D. (USA), Editor and contact person. Email: omns@orthomolecular.org This is a comments-only address; OMNS is unable to respond to individual reader emails. However, readers are encouraged to write in with their viewpoints. Reader comments become the property of OMNS and may or may not be used for publication. To Subscribe at no charge: http://www.orthomolecular.org/subscribe.html To Unsubscribe from this list: http://www.orthomolecular.org/unsubscribe.html

This news release was sent to bill@wmodavis.com. If you no longer wish to receive news releases, please reply to this message with "Unsubscribe" in the subject line or simply click on the following link: unsubscribe This article may be reprinted free of charge provided 1) that there is clear attribution to the Orthomolecular Medicine News Service, and 2) that both the OMNS free subscription link http://orthomolecular.org/subscribe.html and also the OMNS archive link http://orthomolecular.org/resources/omns/index.shtml are included. Orthomolecular.org | 3100 N. Hillside Ave | Wichita, KS 67219 | USA

Not Everyone is Enthusiastic - Dach

New Statin Guidelines, Not Everyone is Enthusiastic

Posted on November 14, 2013 by Jeffrey Dach

New Statin Guidelines, Not Everyone is Enthusiastic

by Jeffrey Dach MD On Tuesday, The American Heart Association and the American College of Cardiology changed the guidelines giving even more people statin drugs.  The new Guidelines increases the number of healthy people to be placed on statins by 70%..(1)
OpEd in the New York TImes

Two highly respected MDs, John Abramson and Rita Redberg have been critical of statin drugs for years. Yesterday they published an Op Ed in the New York Times skeptical of the new Guidelines .  For one thing,  the doctors on the committee had conflicts of interest.  For a second thing, the New Guidelines are not based on objective data.



Conflict of Interest  in the Committee
Once again we have a committee of doctors creating guidelines to benefit their benefactors, the drug industry:  Here is a quote from Abramson and Redberg in the New York Times: 

“The group that wrote the recommendations was not sufficiently free of conflicts of interest; several of the experts on the panel have recent or current financial ties to drug makers. In addition, both the American Heart Association and the American College of Cardiology, while nonprofit entities, are heavily supported by drug companies.”(1)

 

Another Problem – Guidelines Are Not Supported by Adequate Data Drs Abramson and Redberg go on to say the new guidelines are not supported by objective data. This is a mind boggling statement,  and that patients should be skeptical of the new guidelines.
Here is the quote:

“We believe that the new guidelines are not adequately supported by objective data, and that statins should not be recommended for this vastly expanded class of healthy Americans. Instead of converting millions of people into statin customers, we should be focusing on the real factors that undeniably reduce the risk of heart disease: healthy diets, exercise and avoiding smoking. Patients should be skeptical about the guidelines, and have a meaningful dialogue with their doctors about statins, including what the evidence does and does not show, before deciding what is best for them.”(1)

Jeffrey Dach MD 7450 Griffin Road, Suite 190 Davie, Fl 33314 954-792-4663
www.jeffreydach.com www.drdach.com
www.naturalmedicine101.com
www.bioidenticalhormones101.com
www.truemedmd.com

Articles with Related Content:
Australian Video Series on Statins and Cholesterol Mayanne DeMAsi
Getiing OFf Statin Drug Stories
Cholesterol Lowering Statin Drugs for Women Just Say No
How to Reverse Heart Disease with the Coronary Calcium Score (part one)
Reversing Heart Disease Part Three
Cholesterol Lowering Drugs for the Elderly, Bad Idea  
Healthy Men Should Not Take Statin Drugs

Jeffrey Dach MD

Links and References
(1) http://www.nytimes.com/2013/11/14/opinion/dont-give-more-patients-statins.html?_r=0 Don’t Give More Patients Statins By JOHN D. ABRAMSON and RITA F. REDBERG Published: November 13, 2013
(2) http://content.onlinejacc.org/article.aspx?articleid=1770220 2013 ACC/AHA Guideline on the Assessment of Cardiovascular Risk A Report of the American College of Cardiology/American Heart Association Task Force on Practice Guidelines ONLINE FIRST David C. Goff, MD, PhD, FACP, FAHA; Donald M. Lloyd-Jones, MD, ScM, FACC, FAHA; Glen Bennett, MPH; Christopher J. O’Donnell, MD, MPH; Sean Coady, MS; Jennifer Robinson, MD, MPH, FAHA; Ralph B. D’Agostino, PhD, FAHA; J. Sanford Schwartz, MD; Raymond Gibbons, MD, FACC, FAHA; Susan T. Shero, MS, RN; Philip Greenland, MD, FACC, FAHA; Sidney C. Smith, MD, FACC, FAHA; Daniel T. Lackland, DrPH, FAHA; Paul Sorlie, PhD; Daniel Levy, MD; Neil J. Stone, MD, FACC, FAHA; Peter W.F. Wilson, MD, FAHA [+] Author Information J Am Coll Cardiol. 2013;():.
Jeffrey Dach MD 7450 Griffin Road, Suite 190 Davie, Fl 33314 954-792-4663 www.jeffreydach.com www.drdach.com www.naturalmedicine101.com www.bioidenticalhormones101.com www.truemedmd.com Click Here for: Dr Dach’s Online Store for Pure Encapsulations Supplements
Click Here for: Dr Dach’s Online Store for Nature’s Sunshine Supplements
Web Site and Discussion Board Links: jdach1.typepad.com/blog/ disc.yourwebapps.com/Indices/244124.html disc.yourwebapps.com/Indices/244066.html disc.yourwebapps.com/Indices/244067.html disc.yourwebapps.com/Indices/244161.html disc.yourwebapps.com/Indices/244163.html Disclaimer click here: www.drdach.com/wst_page20.html
The reader is advised to discuss the comments on these pages with his/her personal physicians and to only act upon the advice of his/her personal physician. Also note that concerning an answer which appears as an electronically posted question, I am NOT creating a physician — patient relationship. Although identities will remain confidential as much as possible, as I can not control the media, I can not take responsibility for any breaches of confidentiality that may occur.
Link to this article:http://wp.me/p3gFbV-Ty Copyright (c) 2012-13 Jeffrey Dach MD All Rights Reserved. This article may be reproduced on the internet without permission, provided there is a link to this page and proper credit is given. FAIR USE NOTICE: This site contains copyrighted material the use of which has not always been specifically authorized by the copyright owner. We are making such material available in our efforts to advance understanding of issues of significance. We believe this constitutes a ‘fair use’ of any such copyrighted material as provided for in section 107 of the US Copyright Law. In accordance with Title 17 U.S.C. Section 107, the material on this site is distributed without profit to those who have expressed a prior interest in receiving the included information for research and educational purposes.
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Testosterone and the Heart Part Two - Dach

Testosterone and the Heart Part Two by Jeffrey Dach MD

Posted on November 12, 2013 by Jeffrey Dach

In Part One, we discussed a 2010 study from Boston University in which testosterone was given to immobilized, elderly, obese male smokers.  The study was halted early because of poor outcome with increased heart attacks and “cardiac events”  in the testosterone treated group.

Second Study Shows  Poor Outcome in Testosterone Group

A second study from the University of Texas was just published in JAMA .(2)  This study was done on Veterans undergoing coronary angiography with documented coronary artery disease.  Some of these Veterans had low testosterone levels (below 300) .  These veterans were given testosterone treatment and followed.  At the end of three years of follow up, the untreated men had a  20%  incidence of stroke,  heart attack or death, while the testosterone treated group had a higher 26% incidence.  This is 20% untreated, vs. 26% treated.  Clearly, the testosterone did not miraculously reverse the atherosclerosis disease in this group of veterans.(2-6)

Benefits of Testosterone Clearly Documented in Medical Literature

As discussed in part one, decades of research studies have shown that low testosterone in men is a risk factor for early mortality from cardiovascular disease, and testosterone treatment reduces mortality, especially in the diabetic males. (7-10)

Testosterone Treatment Does Not Reverse Heart Disease

However, it is clear from these two studies that testosterone by itself is insufficient as a therapy to reverse coronary artery plaque in men who have diets and lifestyles which promote heart disease, and who already have significant underlying coronary artery disease.

Left Image logo courtesy of Track Your Plaque Blog.

Track Your Plaque Program

For our office patients who are interested in reversing coronary artery plaque, we use the William Davis MD Track Your Plaque Program. This is an excellent program which is well thought out.  See my article on this: Reversing Heart Disease.


I wonder what the outcome of these two studies would have been if the testosterone treated group had been started on the Track Your Plaque Program which monitors lipo-protein profile and the Calcium Score, and uses diet and lifestyle modification and supplements to reduce Calcium Score and increase LDL particle size.

There are many unanswered questions.  I also  wonder what the Vitamin D levels were, and what the thyroid levels were on these men,   How much trans fats were they consuming?  How much were they smoking and how much alcohol did they consume?  How much overweight were they?

Conclusion

One conclusion seems clear and that is testosterone by itself does not replace the Track Your Plaque Program of Diet, Lifestyle modification and Supplements to reverse heart disease.  As these two studies show, clinical outcomes for Testosterone Treatment may actually be worse for subgroups of men with severe coronary artery disease, especially when no changes are made to the diet and lifestyles that promote heart disease.

Jeffrey Dach MD
7450 Griffin Road, Suite 180/190
Davie, Florida 33314
954-792-4663www.jeffreydach.com
www.drdach.com
www.naturalmedicine101.com
www.truemedmd.com

Articles With Related Content:

Low Testosterone Diagnosis and Treatment
HCG in Males with Low Testosterone
Testosterone Benefits, PSA and Prostate Part One
Testosterone and PSA Part Two
Clomid for Men with Low Testosterone Part One
Low Testosterone From Pain Pills
Low Testosterone Associated with Increased Mortality
Testosterone Reduces Mortality
Testosterone Blockade Increases Mortality
Testosterone Found Beneficial For Diabetes

Links and References:
(1)http://www.ncbi.nlm.nih.gov/pubmed/20592293
N Engl J Med. 2010 Jul 8;363(2):109-22. Epub 2010 Jun 30.
Adverse events associated with testosterone administration.
Basaria S, Coviello AD, Travison TG, Storer TW, Farwell WR, Jette AM, Eder R, Tennstedt S, Ulloor J, Zhang A, Choong K, Lakshman KM, Mazer NA, Miciek R, Krasnoff J, Elmi A, Knapp PE, Brooks B, Appleman E, Aggarwal S, Bhasin G, Hede-Brierley L, Bhatia A, Collins L, LeBrasseur N, Fiore LD, Bhasin S. Section of Endocrinology, Diabetes, and Nutrition, Boston University School of Medicine and Boston Medical Center, Boston, Massachusetts 02118, USA.
2) http://jama.jamanetwork.com/article.aspx?articleID=1764051  Association of Testosterone Therapy With Mortality, Myocardial Infarction, and Stroke in Men With Low Testosterone Levels  by Rebecca Vigen, MD, MSCS1; Colin I. O’Donnell, MS2,3; Anna E. Barón, PhD2,3; Gary K. Grunwald, PhD2,3; Thomas M. Maddox, MD, MSc2,3,4; Steven M. Bradley, MD, MPH2,3,4; Al Barqawi, MD3; Glenn Woning, MD3; Margaret E. Wierman, MD2,3; Mary E. Plomondon, PhD2,3,4; John S. Rumsfeld, MD, PhD2,3,4; P. Michael Ho, MD, PhD2,3,4  The University of Texas at Southwestern Medical Center, Dallas 2VA Eastern Colorado Health Care
JAMA. 2013;310(17):1829-1836.
3) http://health.clevelandclinic.org/2013/11/concerns-raised-about-testosterone-therapy/  Concerns Raised about Testosterone Therapy Study: testosterone replacement linked to heart risks By Steven Nissen, MD | 11/8/13 2:26 p.m.
4) Testosterone treatments linked with heart riskshttp://www.thetowntalk.com/viewart/20131112/LIFESTYLE/311130006/Testosterone-treatments-linked-heart-risks
5) http://online.wsj.com/news/articles/SB10001424052702303661404579180294201174958  Testosterone Therapy Tied to Heart Risks
Veterans With History of Heart Disease Had Higher Risk of Death, Heart Attack and Stroke, According
6) http://www.latimes.com/science/sciencenow/la-sci-heart-disease-testosterone-replacement-20131105,0,3592717.story  Testosterone medication may boost risk of heart attack, stroke, death
7) http://www.ncbi.nlm.nih.gov/pubmed/22496507  J Clin Endocrinol Metab. 2012 Jun;97(6):2050-8. doi: 10.1210/jc.2011-2591. Epub 2012 Apr 11.  Testosterone treatment and mortality in men with low testosterone levels. Shores MM, Smith NL, Forsberg CW, Anawalt BD, Matsumoto AM.
Source  Veterans Affairs Puget Sound Health Care System, 1660 South Columbian Way, S-116PES, Seattle, Washington 98108, USA.
8) http://www.endocrine-abstracts.org/ea/0025/ea0025p163.htm
Endocrine Abstracts (2011) 25 P163
Low testosterone predicts increased mortality and testosterone replacement therapy improves survival in men with type 2 diabetes
Vakkat Muraleedharan1,2, Hazel Marsh1 & Hugh Jones1,2
9) http://www.ncbi.nlm.nih.gov/pubmed/23999642
Eur J Endocrinol. 2013 Oct 21;169(6):725-33. doi: 10.1530/EJE-13-0321. Print 2013.
Testosterone deficiency is associated with increased risk of mortality and testosterone replacement improves survival in men with type 2 diabetes.
Muraleedharan V, Marsh H, Kapoor D, Channer KS, Jones TH.
Source  Robert Hague Centre for Diabetes and Endocrinology, Barnsley Hospital NHSFT, Gawber Road, Barnsley S75 2EP, UK.
Jeffrey Dach MD
7450 Griffin Road, Suite 180/190
Davie, Florida 33314
954-792-4663
www.jeffreydach.com
www.drdach.com
www.naturalmedicine101.com
www.truemedmd.com
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Beware: new cholesterol lowering drugs coming - Kendrick

Beware: new cholesterol lowering drugs coming

by Dr Malcolm Kendrick

‘…across the gulf of space, minds that are to our minds as ours are to those of the beasts that perish, intellects vast and cool and unsympathetic, regarded this earth with envious eyes, and slowly and surely drew their plans against us.’ War of the Worlds

An era is coming to an end. Statins, the world’s most widely prescribed and profitable drugs, have, with the exception of Crestor (rosuvastatin), all come off patent and their price has plummeted. Good news for NHS accountants: not so good for company profits.

So a supposedly new, improved, much safer and more effective generation of cholesterol lowering drugs will soon be available at a doctor’s surgery near you. At least that will be the general tone of the marketing. With 80% of the population suffering from “high” cholesterol, according to guidelines drawn up by consultants with links to drug companies, there is obviously a huge need. (For an account of how seriously we should take this “need” see Dr John Briffa’s post.)

This is obviously a great opportunity for the companies but it also faces them with a fascinating dilemma. Statins have been relentlessly promoted as the most beneficial l class of drugs ever, protecting not just against cardiovascular disease but also Alzheimer’s and Parkinson’s and being virtually side-effect free into the bargain.

An alarming press release

But if the companies are going to persuade those NHS accountants and cash-strapped GP commissioning bodies to start paying serious prices for the new drugs, they need to persuade them that statins actually had a serious problem all along but it is one that can be avoided by buying the new products.

Recently I received a press release by email that was the first sign that this process is already underway. It was a warning about something called P9 which, had I been a loyal statin believer, I would have found pretty alarming. After explaining how statins worked by targeting an enzyme known as HMG-CoA in the liver, the email went on to tell me this:

“However, statin treatments have been shown to actually stimulate the production of PCSK9, which is counterproductive, possibly damaging to the liver, and ultimately limits the treatment’s ability to lower LDL cholesterol levels.”

Why weren’t we told about this risk before?

What on earth is PCSK9, you and the medical statin believers might well ask. And if it is not only able to damage the liver but also render the whole purpose of taking a statin self-defeating, why haven’t we been told about it before?

Here was a classic marketing ploy; tell you about a problem and immediately offer a solution in the form of a drug that is able to block the production of damaging PCSK9. The full name of these new drugs is proprotein convertase subtilisin/kexin type 9 inhibitors.

And it’s not the only dauntingly high tech-new cholesterol lowering drug that could be coming your way in the not too distant future. For the sake of completeness here is a list of nearly all the new compounds waiting in the wings. Some will undoubtedly founder on the rocks of side effects that are just too dangerous, never to be seen again.

Other new drugs in the race

• Inhibitors of proprotein convertase subtilisin/kexin type 9 (PCSK9 inhibitors)
• Antisense oligonucleotides (ASOs) targeting the production of apolipoprotein B-100 (apoB-100)
• Microsomal triglyceride transfer protein inhibitors
• Squalene synthase inhibitors
• Peroxisome proliferator-activated receptor agonists
• Thyroid hormone receptor agonists

For the moment though my money for the first out of the gate are the PCSK9 inhibitors, which I will call P9 inhibitors. So what exactly are they? Well P9 is an enzyme that is found mainly in the liver. It binds to receptors that remove the “bad” LDL (low density lipoprotein) cholesterol and destroys them after they have taken just one LDL molecule out of circulation, meaning that they can’t be reused to remove more LDL.

But if you block P9, you allow LDL receptors to continue removing LDL merrily from the bloodstream, so LDL levels fall dramatically. In fact P9 inhibitors appear to lower LDL far more effectively than statins which, if you sign up to the belief that the lower your cholesterol goes the more protection you get, this can only be another major benefit.

The new statin combo

What’s clever about this is that it avoids taking on statins directly. Given how familiar doctors are with them, how most believe in them and how cheap they are, a head on attack would be doomed to failure.  The manufacturers know, damn well, that doctors are not just going to stop using statins, so their P9 inhibitors will be positioned to sit alongside statins, allowing them to work, supposedly, even more safely.  At first anyway.

But there is more to this press release and I could pick it apart for hours, marvelling at the ability to say so much – in so few words. But let’s just focus on the phrase…’possibly damaging to the liver’ in relation to statins. Now, I know that statins do damage the liver – to a greater or lesser degree. Liver enzymes in the blood (a sign of liver damage) are often raised to three times normal levels – sometimes more.

But why not focus on the side-effect that is most clearly recognised with statins?  Namely muscle damage and pain. This is the true Achilles heel of statins. Yet the press release talks about liver damage…

Danger to your liver

The most likely reason is that P9 inhibitors have been found to cause liver problems themselves in both animal studies and phase 1 studies on human volunteers. Knowing their mechanism of action, it is more than likely that PCSK9 blocking agents could damage the liver. If you over-ride negative feedback mechanisms, the body doesn’t like it very much, as you will be overloading cells with toxic waste products. Enzymes to break down LDL receptors are there for a reason.

So, we can expect P9 inhibitors are going to cause liver damage. However, by attacking statins for causing liver damage, the pharmaceutical companies will be hoping to mask the most serious adverse effect of the new drug. The words used to defuse concerns about this problem will be something along the lines of. ‘With our P9 inhibitor we have seen mild elevations of liver enzymes in clinical studies. However, they are similar to those caused by statins, are reversible and cause no long-term damage.’ Blah, blah….  ‘Move along, nothing to see here.’

This fear is not just based on a vague unease that if you block a feedback mechanism in the body you are probably heading for disaster. It is also based on the fact that, if the companies developing P9 inhibitors are already blaming statins for causing liver damage, they are doing to hide their own problems behind a smokescreen. You heard it here first.

I also predict that severe liver damage problems will take years to emerge. In most people the liver is pretty resilient – it takes a lot of alcohol and a lot of time to destroy it. I fear that clinical studies will not be long enough to demonstrate this effect –before the drugs are launched and widely prescribed. I can say all this because it is what has happened with damaging block buster drugs in the past, such as the anti-inflammatory Vioxx and and the diabetes drugs Avandia.

My predictions for P9 inhibitors:

• They will be widely promoted as the new statins
• Pfizer, or Merck, will buy out the patent to one of the new products (they may have already done this)
• They will be launched without any long-term studies to show they actually cut your chance of dying from a heart attack. They will be approved purely on the basis that they lower cholesterol/LDL cholesterol.
• They will make billions upon billions in the first two years and be hailed around the word as a new generation in cholesterol lowering. The chief executives of the companies selling these drugs will be paid massive bonuses
• Key Opinion Leaders (‘experts’) will promote them ruthlessly at major conferences and press launches
• Reports of a high level of liver damage/deaths will  start to emerge
• The companies will deny there is a problem and attack anyone who says there is one
• They will start to be withdrawn from the market two to three years after launch
• There will be lawsuits
• The companies will be fined a small fraction of the profits they made from hyping the drugs
• It will emerge that the problems with liver damage were known by the companies many years before the drugs were launched but not many people will be interested by then, as the next generation of lipid lowering agents will be arriving
• No-one will be held accountable

Yes, the great Nostrokendrickos has spoken.
In the meantime remember that ‘Something unpleasant this way comes’.
Disclosure: I do not believe that a raised LDL/cholesterol level causes heart disease.
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Getting Off Statin Drug Stories - Dach

Getting Off Statin Drug Stories by Jeffrey Dach MD

Left Image: courtesy of Uffe Ravnskov, MD Fat and Cholesterol are Good for You.Book Cover

Just Ask Judith Walsh MD in JAMA

 

 

Getting Off Statin Drug Stories
by Jeffrey Dach MD
Case Number One, Martha
Martha is 55 years old, healthy and no history of heart disease.  Nonetheless, Martha has been taking a statin drug for “high cholesterol” under the care of “the top cardiologist” in South Florida for the past five years.  Martha has also been under my care taking a bioidentical hormone program for menopausal symptoms, and doing very well.  Every six months, we run a lab panel which always shows  low cholesterol of 170, courtesy of her statin anti-cholesterol drug.


 And, every time Martha comes into the office to review her lab results, I print out a 2004 JAMA article by Judith Walsh, MD who reviewed thirteen statin drug clinical trials from 1966 to 2003.(1)  Dr. Judth Walsh concludes that cholesterol lowering drugs provide no health benefit for women.  I give her this article and, at the same time, explain to her that no woman should be on a statin drug.  Lowering cholesterol with a statin drug has no health benefit for women, that’s a fact, and public information readily available.

Playing Games With Statins

Every six months I recommend to Martha stopping the statin drug, and every six month, her cardiologist puts her back on the statin drug.  This has been going on for three years now.

Finally Success At Convincing Martha to Stop the Statin Drug

Finally this last time, Martha seems more receptive to idea that the statin drug is harming her and not helping her.  She is sitting in my office recounting multiple health problems for which she sees numerous doctors: back pain, asthma, sinus infections, skin problems, and allergies.  I suggested to Martha the possibility that many of her health problems are  caused by the low cholesterol from the statin drug.  Martha finally sees the light, goes home and tosses the bottle of pills into the garbage can.

Feeling Better

About a week later, Martha called me and reported, “I feel so much better off that statin drug, thank you so much! “.  Apparently, the statin drug was causing adverse health effects, and Martha was now feeling much better.

Believing in the Propaganda
This case illustrates the difficulty in convincing patients to stop their statin drug.  It is difficult to counter the drug company propaganda, and convince these patients they are harming their health with the statin drugs. Many continue to believe in the myth that cholesterol causes heart disease, and they go on to become statin drug medical victims.  I see them every day.  When we have a success like Martha who finally gets off her statin drug, this is a cause for celebration.


Left Image: Ignore the Awkward.: How the Cholesterol Myths Are Kept Aliveby Uffe Ravnskov MD

Case Number Two – Roger
Roger is a seventy one year old retired executive, and an avid tennis player.  He has no history of coronary artery disease and has always been healthy. Two years ago, his cardiologist said his cholesterol of 210 was “too high”, and prescribed a statin anti-cholesterol drug.  A year later, Roger’s tennis game deteriorated, he found his timing and balance was off, and he lost every game to players who could never beat him before.

Adverse Effects of the Statin Drug

I suggested to Roger that the decline in his tennis game was most likely an adverse effect of the statin drug on his muscle and nerve function.  He was losing his balance and coordination. 

I recommended stopping the statin anti-cholesterol drug.  At first, Roger resisted and said his wife wanted him to take the statin drug because she thought it was ”good medical care”, and she (mistakenly) believed that a lower cholesterol was somehow preventive of heart disease.

How to Counter the Propaganda: A Book For You
In order to counter the drug company cholesterol propaganda, I gave Roger a copy of the book, Fat and Cholesterol are Good for You, by Uffe Ravnskov MD PhD. This book reviews the medical studies which supposedly show that cholesterol is the cause of heart disease, and reveals that they do no such thing. This is a medical myth.  Neither cholesterol consumption nor cholesterol blood levels cause heart disease.  Similarly, many medical studies demonstrate that anti-cholesterol drugs work very well to reduce blood cholesterol levels, however, this treatment does not prolong life and makes most people sick with adverse side effects.

Roger was amazed and his eyes practically popped out out of his head when he “saw the light”.  The statin drugs were turning him another medical victim.  Once Roger learned the truth about the ”cholesterol causes heart disease” myth,  he took his statin drug bottle and threw it into the garbage can.  Two weeks later, off the statin drug,  Roger was back to his old self, prancing about the tennis court like a gazelle, and winning every game with ease.


Left Image : The Cholesterol Myths: Exposing the Fallacy that Saturated Fat and Cholesterol Cause Heart Disease by Uffe Ravnskov MD
 Are You Still a Believer in Anti-Cholesterol Drugs?

If you are still a believer in Statin Drugs, take a look at this primary prevention study published July 2010 in the Archives of Internal Medicine by Dr. Ray.(3)  He reviewed 11 statin drug clinical trials with 65,229 participants followed for approximately 244,000 person-years.  The astounding results showed the statin drug group all-cause mortality was THE SAME as the placebo group ! (3)  There was no benefit from the statin drugs !!!  This article was published in the mainstream medical literature !!


If cholesterol was truly the cause of heart attacks, then one would expect heart attack victims to reveal the high cholesterol causing their heart attack.   They found the opposite.  Heart attack victims have low cholesterol.  A study  analyzed 137,000 heart attack patients from 541 US hospitals and found mean cholesterol was only 174.  This is low, not high. (4)

In addition, if high cholesterol was truely the cause of heart attacks, one would expect heart attack victims with the highest cholesterol to have the worst prognosis, and lowest cholesterol to have the best prognosis.  They don’t.  A study from Henry Ford Hospital in Detroit showed that three years after a heart attack, the patients with lowest cholesterol had the highest mortality (14% vs. 7 %) (5).

Conclusion:

The cholesterol theory of heart disease is a myth maintained by drug company propaganda to support massive profits from cholesterol lowering drugs.  These drugs provide no health benefit in terms of prolonging life, and at the same time produce harm from adverse side effects.  Avoid becoming a victim of the statin drug propaganda machine.

Articles with related interest:
Heart Disease Vitamin C and Linus Pauling
Getting Off Statin Drug Stories
How to Reverse Heart Disease with the Coronary Calcium Score
Cholesterol Lowering Drugs for the Elderly, Bad Idea
Cholesterol Lowering Statin Drugs for Women Just Say No
…………………………………………………………………………………………………….

Heart Disease Part Two – Atherosclerosis: How Does it Happen?Preventing and Reversing Heart Disease Part Three by Jeffrey Dach MDHeart Disease, Ascorbate, Lysine and Linus Pauling by Jeffrey Dach MDA Choirboy for Cholesterol Turns Disbeliever by Jeffrey Dach MD
Links and References
(1) http://jama.ama-assn.org/content/291/18/2243
JAMA. 2004;291(18):2243-2252. Drug Treatment of Hyperlipidemia in Women
Judith M. E. Walsh, MD, MPH; Michael Pignone, MD, MPH
(2) Fat and Cholesterol are Good for You, Uffe Ravnskov GB Publishing (January 26, 2009)
(3) http://archinte.ama-assn.org/cgi/content/abstract/170/12/1024
Statins and All-Cause Mortality in High-Risk Primary Prevention A Meta-analysis of 11 Randomized Controlled Trials Involving 65 229 Participants. Kausik K. Ray, MD, MPhil, FACC, FESC; Sreenivasa Rao Kondapally Seshasai, MD, MPhil; Sebhat Erqou, MD, MPhil, PhD; Peter Sever, PhD, FRCP, FESC; J. Wouter Jukema, MD, PhD; Ian Ford, PhD; Naveed Sattar, FRCPath. Arch Intern Med. 2010;170(12):1024-1031.
Background  Statins have been shown to reduce the risk of all-cause mortality among individuals with clinical history of coronary heart disease. However, it remains uncertain whether statins have similar mortality benefit in a high-risk primary prevention setting. Notably, all systematic reviews to date included trials that in part incorporated participants with prior cardiovascular disease (CVD) at baseline. Our objective was to reliably determine if statin therapy reduces all-cause mortality among intermediate to high-risk individuals without a history of CVD.
Data Sources  Trials were identified through computerized literature searches of MEDLINE and Cochrane databases (January 1970-May 2009) using terms related to statins, clinical trials, and cardiovascular end points and through bibliographies of retrieved studies.
Study Selection  Prospective, randomized controlled trials of statin therapy performed in individuals free from CVD at baseline and that reported details, or could supply data, on all-cause mortality.
Data Extraction  Relevant data including the number of patients randomized, mean duration of follow-up, and the number of incident deaths were obtained from the principal publication or by correspondence with the investigators.
Data Synthesis  Data were combined from 11 studies and effect estimates were pooled using a random-effects model meta-analysis, with heterogeneity assessed with the I2 statistic. Data were available on 65 229 participants followed for approximately 244 000 person-years, during which 2793 deaths occurred.
The use of statins in this high-risk primary prevention setting was not associated with a statistically significant reduction (risk ratio, 0.91; 95% confidence interval, 0.83-1.01) in the risk of all-cause mortality. There was no statistical evidence of heterogeneity among studies (I2 = 23%; 95% confidence interval, 0%-61% [P = .23]).
Conclusion  This literature-based meta-analysis did not find evidence for the benefit of statin therapy on all-cause mortality in a high-risk primary prevention set-up.
(4) http://www.ahjonline.com/article/S0002-8703(08)00717-5/abstract
AHJ Volume 157, Issue 1, Pages 111-117.e2 (January 2009)
Lipid levels in patients hospitalized with coronary artery disease: An analysis of 136,905 hospitalizations in Get With The Guidelines. Amit Sachdeva, MDa, Christopher P. Cannon, MDb, Prakash C. Deedwania, MDc, Kenneth A. LaBresh, MDd, Sidney C. Smith Jr, MDe, David Dai, MSf, Adrian Hernandez, MDf, Gregg C. Fonarow, MDa, on behalf of the GWTG Steering Committee and Hospitals
(5) http://www.ncbi.nlm.nih.gov/pubmed/19437396
Cardiol J. 2009;16(3):227-33. Low admission LDL-cholesterol is associated with increased 3-year all-cause mortality in patients with non ST segment elevation myocardial infarction. Al-Mallah MH, Hatahet H, Cavalcante JL, Khanal S.
Abstract
BACKGROUND: The relationship between admission low-density lipoprotein (LDL) levels and long-term outcomes has not been established in patients with acute coronary syndrome. We tested the hypothesis that patients who develop non-ST segment elevation myocardial infarction (NSTEMI) despite low LDL have a worse cardiovascular outcome in the long term.
METHODS: Patients admitted with NSTEMI between 1 January 1997 and 31 December 2000 and with fasting lipid profiles measured within 24 hours of admission were selected for analysis. Baseline characteristics and 3-year all-cause mortality were compared between the patients with LDL above and below the median. Multivariate analysis was used to determine the predictors of all-cause mortality, and adjusted survival was analyzed using the Cox proportional hazard model.
RESULTS: Of the total of 517 patients, 264 had LDL dL and 253 had LDL > 105 mg/dL. There was no difference in age, gender, severity of coronary artery disease, and left ventricular ejection fraction between the 2 groups. Thirty-six percent of patients with LDL 105 mg/dL were on lipid-lowering therapy on admission.
After 3 years, patients with admission LDL dL had higher all-cause mortality rate compared to patients with LDL > 105 mg/dL (14.8% vs. 7.1%, p = 0.005). The higher all-cause mortality persisted (OR 1.8, 95% CI 1.0-3.5, p = 0.05) even after adjustment for confounding variables.

CONCLUSIONS: In our cohort, lower LDL-cholesterol at admission was associated with decreased 3-year survival in patients with NSTEMI.

Jeffrey Dach MD
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The controversial study that started the War on Cholesterol - Watson

The controversial study that started the War on Cholesterol…

      

Alan Watson | June 14, 2012   

Revisiting the Coronary Primary Prevention Trial (CPPT) – 1973 to 1984

Using "relative risk statistics" and changing the study's design, the CPPT researchers declared success and the War on Cholesterol began in earnest

 

Launched in 1973 by the National Institutes of Health, the Coronary Primary Prevention Trial (CPPT) set out to prove that lowering blood cholesterol with a drug and a low cholesterol, low saturated fat diet would reduce the risk of coronary heart disease and extend the lives of the study participants.

(As part of the study, twelve new Lipid Research Clinics were set up by the Heart Institute at large universities throughout the country including Baylor, Stanford, Johns Hopkins and the University of Washington in Seattle.)

The researchers were looking for middle-aged men with total cholesterol levels exceeding those of 95 percent of Americans. (Only men with the highest 0.8 percent total cholesterol qualified.) The CPPT researchers screened 480,000 applicants in order to select 3,806 high risk men between the ages of 35 and 59.

This meant that many of the participants had familial hypercholesterolemia, a rare genetic defect in cholesterol metabolism present in about 1 percent of the population. The trials chance of success was therefore greatly increased by focusing on this particular group of presumably vulnerable men.
In their preliminary report, CPPT researchers announced that they would study two separate outcomes:  (1) Nonfatal heart attacks and (2) fatal heart attacks or deaths from coronary heart disease. The CPPT directors emphasized that they would be satisfied with nothing less than the strongest statistical proof of their findings; they had to be “99 percent certain that the results were not due to chance.”

The researchers also announced their goal of reducing blood cholesterol in the treatment group by 25 percent and reducing the risk of heart disease in the treatment group by at least 50 percent.
Approximately half of the 3,806 men were provided low cholesterol, low saturated fat dietary advice and were treated with cholestyramine, a cholesterol-lowering bile acid resin (Questran).

(Cholestyramine lowers cholesterol by interfering with digestion. Statins such as Lipitor, Mevacor and Zocor were not available yet.)

The control group was provided the same dietary advice and an unpleasant tasting placebo – an indigestible mixture of sand, sugar and food coloring. Both trial groups suffered with moderate to severe gastrointestinal distress. There were eight gastrointestinal cancer deaths in the treatment group (out of 21 cases) and one in the placebo group (out of 11 cases).

(There were more deaths from cancer, intestinal disease, stroke, violence and suicide in the group taking the cholesterol-lowering drug, and overall mortality was essentially the same for both groups.)

Disappointing Results

In 1984, the disappointing results were tabulated. Cholesterol levels in the treatment group had decreased by no more than 7 percent. Cholestyramine and the low cholesterol, low saturated fat diet had failed to lower cholesterol enough to prove that lowering cholesterol would reduce the risk of heart disease and extend the lives in the treatment group.

The difference in nonfatal heart attacks was not statistically significant. In the treatment group, 130 participants (6.8 percent) had a heart attack versus 158 in the placebo group (8.3 percent). After 7 years, the fraction of the treatment group that had benefited was less than 2 percent.

                                       Nonfatal heart attacks               Fatal heart attacks/coronary deaths
1,900 Control Group:         158 or 8.3 percent                               38 or 2.0 percent
1,906 Treatment Group:     130 or 6.8 percent                              30 or 1.6 percent

The difference in fatal heart attacks was not significant either. In the treatment group, 30 participants (1.6 percent) suffered a fatal heart attack compared to 38 in the placebo group (2.0 percent) Again – after 7 years of taking an unpleasant drug (and following a low fat diet), the fraction of the treatment group that benefited was less than 1 percent.

However, by applying relative risk statistics (a percentage of a percentage), the CPPT researchers improved their results. They took the number of people who presumably didn’t have a heart attack because of taking the drug (28) and looked at it as a percentage of the people who did have heart attacks (158) but didn’t take the drug:

The less than 2 percent absolute difference in nonfatal heart attacks rose to a reported 19 percent reduction in risk of a heart attack!

 

In similar statistical fashion, the researchers announced a 24 percent reduction in the risk of dying from a heart attack. The 8 men or 1.6 percent out of 1,900 who presumably did not have a fatal heart attack because they took the drug became the same 24 percent who reduced their risk of mortality compared to those in the control group who did die (38) but did not take the drug.

Additional study design changes

To prop up their victory, the CPPT researchers decided to exclude  “uncertain” nonfatal heart attacks from the treatment group while including  “uncertain” fatal heart attacks in the placebo group. Also, using the original 99 percent standard, the small favorable trend in either group could only be explained by chance (as defined by the researchers themselves at the start of the trial.)
By applying the less stringent 95 percent standard and by combining the two groups into one (nonfatal and fatal heart attacks), the CPPT researchers improved their results – declared victory – while the press responded with unbridled enthusiasm.

In 1984, the press and medical journals portrayed CPPT as the long sought proof that animal fats were the cause of heart disease. It was widely reported that for the first time:

“It had been proven that lowering cholesterol would reduce the mortality from heart disease and lower the risk of having a heart attack.”

 

Much of what we hear today about diet and heart disease can be traced back to this notorious failed study. When other scientists voiced their objections to the trial’s design changes, the CPPT directors simply denied that they had ever embraced the original more stringent standards.

In January 1984, the Journal of the American Medical Association (JAMA) dutifully reported:

“The trial’s implications…could and should be extended to other age groups and women, and to others with more modest elevations of cholesterol levels. The benefits that could be expected from cholestyramine treatment are considerable.”

 

George Mann, M.D., professor in medicine and biochemistry at Vanderbilt University, severely criticized the CPPT directors and the trial’s unsupportable results:

“The managers at the National Institutes of Health have used Madison Avenue hype to sell this failed trial in the way the media people sell an underarm deodorant…”

 

 Giving cholestyramine for over seven years to 1,906 middle age men – many with a genetic predisposition to atherosclerosis – had only saved the lives of eight but the Heart Institute was now recommending that cholesterol-lowering drug treatment be extended to patient groups that had not been part of the trial.

Even without the solid evidence they sought, the medical elite in the American Heart Association and the National Institute of Health decided to push ahead with cholesterol-lowering drugs and the still unproven low cholesterol, low saturated fat diet:

 “Now we have proved that it is worthwhile to lower blood cholesterol; no more trials are necessary. Now is the time for treatment.”

 

 The long War on Cholesterol had begun
============================================================
Read the complete article here.

The controversial study that started the War on Cholesterol…

365 views

Alan Watson | June 14, 2012 | Reply

Revisiting the Coronary Primary Prevention Trial (CPPT) – 1973 to 1984

Launched in 1973 by the National Institutes of Health, the Coronary Primary Prevention Trial (CPPT) set out to prove that lowering blood cholesterol with a drug and a low cholesterol, low saturated fat diet would reduce the risk of coronary heart disease and extend the lives of the study participants.

(As part of the study, twelve new Lipid Research Clinics were set up by the Heart Institute at large universities throughout the country including Baylor, Stanford, Johns Hopkins and the University of Washington in Seattle.)

The researchers were looking for middle-aged men with total cholesterol levels exceeding those of 95 percent of Americans. (Only men with the highest 0.8 percent total cholesterol qualified.) The CPPT researchers screened 480,000 applicants in order to select 3,806 high risk men between the ages of 35 and 59.

This meant that many of the participants had familial hypercholesterolemia, a rare genetic defect in cholesterol metabolism present in about 1 percent of the population. The trials chance of success was therefore greatly increased by focusing on this particular group of presumably vulnerable men.
In their preliminary report, CPPT researchers announced that they would study two separate outcomes:  (1) Nonfatal heart attacks and (2) fatal heart attacks or deaths from coronary heart disease. The CPPT directors emphasized that they would be satisfied with nothing less than the strongest statistical proof of their findings; they had to be “99 percent certain that the results were not due to chance.”

The researchers also announced their goal of reducing blood cholesterol in the treatment group by 25 percent and reducing the risk of heart disease in the treatment group by at least 50 percent.
Approximately half of the 3,806 men were provided low cholesterol, low saturated fat dietary advice and were treated with cholestyramine, a cholesterol-lowering bile acid resin (Questran).

(Cholestyramine lowers cholesterol by interfering with digestion. Statins such as Lipitor, Mevacor and Zocor were not available yet.)

The control group was provided the same dietary advice and an unpleasant tasting placebo – an indigestible mixture of sand, sugar and food coloring. Both trial groups suffered with moderate to severe gastrointestinal distress. There were eight gastrointestinal cancer deaths in the treatment group (out of 21 cases) and one in the placebo group (out of 11 cases).

(There were more deaths from cancer, intestinal disease, stroke, violence and suicide in the group taking the cholesterol-lowering drug, and overall mortality was essentially the same for both groups.)

Disappointing Results

In 1984, the disappointing results were tabulated. Cholesterol levels in the treatment group had decreased by no more than 7 percent. Cholestyramine and the low cholesterol, low saturated fat diet had failed to lower cholesterol enough to prove that lowering cholesterol would reduce the risk of heart disease and extend the lives in the treatment group.

The difference in nonfatal heart attacks was not statistically significant. In the treatment group, 130 participants (6.8 percent) had a heart attack versus 158 in the placebo group (8.3 percent). After 7 years, the fraction of the treatment group that had benefited was less than 2 percent.

Nonfatal heart attacks                                                Fatal heart attacks/coronary deaths
1,900 Control Group:         158 or 8.3 percent                               38 or 2.0 percent
1,906 Treatment Group:   130 or 6.8 percent                              30 or 1.6 percent

The difference in fatal heart attacks was not significant either. In the treatment group, 30 participants (1.6 percent) suffered a fatal heart attack compared to 38 in the placebo group (2.0 percent) Again – after 7 years of taking an unpleasant drug (and following a low fat diet), the fraction of the treatment group that benefited was less than 1 percent.

However, by applying relative risk statistics (a percentage of a percentage), the CPPT researchers improved their results. They took the number of people who presumably didn’t have a heart attack because of taking the drug (28) and looked at it as a percentage of the people who did have heart attacks (158) but didn’t take the drug:

The less than 2 percent absolute difference in nonfatal heart attacks rose to a reported 19 percent reduction in risk of a heart attack!

 

In similar statistical fashion, the researchers announced a 24 percent reduction in the risk of dying from a heart attack. The 8 men or 1.6 percent out of 1,900 who presumably did not have a fatal heart attack because they took the drug became the same 24 percent who reduced their risk of mortality compared to those in the control group who did die (38) but did not take the drug.

Additional study design changes

To prop up their victory, the CPPT researchers decided to exclude  “uncertain” nonfatal heart attacks from the treatment group while including  “uncertain” fatal heart attacks in the placebo group. Also, using the original 99 percent standard, the small favorable trend in either group could only be explained by chance (as defined by the researchers themselves at the start of the trial.)
By applying the less stringent 95 percent standard and by combining the two groups into one (nonfatal and fatal heart attacks), the CPPT researchers improved their results – declared victory – while the press responded with unbridled enthusiasm.

In 1984, the press and medical journals portrayed CPPT as the long sought proof that animal fats were the cause of heart disease. It was widely reported that for the first time:

“It had been proven that lowering cholesterol would reduce the mortality from heart disease and lower the risk of having a heart attack.”

 

Much of what we hear today about diet and heart disease can be traced back to this notorious failed study. When other scientists voiced their objections to the trial’s design changes, the CPPT directors simply denied that they had ever embraced the original more stringent standards.

In January 1984, the Journal of the American Medical Association (JAMA) dutifully reported:

“The trial’s implications…could and should be extended to other age groups and women, and to others with more modest elevations of cholesterol levels. The benefits that could be expected from cholestyramine treatment are considerable.”

 

George Mann, M.D., professor in medicine and biochemistry at Vanderbilt University, severely criticized the CPPT directors and the trial’s unsupportable results:

“The managers at the National Institutes of Health have used Madison Avenue hype to sell this failed trial in the way the media people sell an underarm deodorant…”

 

 Giving cholestyramine for over seven years to 1,906 middle age men – many with a genetic predisposition to atherosclerosis – had only saved the lives of eight but the Heart Institute was now recommending that cholesterol-lowering drug treatment be extended to patient groups that had not been part of the trial.

Even without the solid evidence they sought, the medical elite in the American Heart Association and the National Institute of Health decided to push ahead with cholesterol-lowering drugs and the still unproven low cholesterol, low saturated fat diet:

 “Now we have proved that it is worthwhile to lower blood cholesterol; no more trials are necessary. Now is the time for treatment.”

 

 The long War on Cholesterol had begun
==================================================================
Read the complete article here.