Preventing and Reversing Heart Disease - DACH

Preventing and Reversing Heart Disease, Part Three

Preventing and Reversing Heart Disease
Part Threeby Jeffrey Dach MD
This Article is Part Three.
For Part One Click Here,
and for  Part Two Click Here.

A Man with Progressive Coronary Artery Disease Unresponsive to Statins
62 year old Jim came just had his third cardiac stent.  A year ago, Jim noticed a “tight feeling” in his chest radiating to his throat, was rushed to the ER, and doctors found he was having a heart attack. A coronary angiogram showed extensive coronary artery disease with irregular plaque formation.

Progressive Coronary Artery Plaque in Spite of Low Cholesterol
For 12 years now, Jim’s cholesterol level had been driven down into the 140 area by the “top cardiologist in the area”, who prescribed a hefty dose of a statin anti-cholesterol drug.  In spite of the lowest cholesterol level on the planet,  Jim’s heart disease progressed relentlessly with worsening calcium scores, worsening angiograms, and worsening symptoms of chest pain.   His disease progression was obviously not caused by an elevated cholesterol level.  For a discussion of how elevated cholesterol is NOT the Cause of Heart Disease, see my article on patients with familial hypercholesterolemia who have very high cholesterol, yet have no heart disease, proving the hypothesis that cholesterol levels are not necessarily a risk factor for heart disease, and reducing cholesterol levels with drugs may be a fruitless endeavor.

Doctors advise Jim to Stop Testosterone
Jim had been taking topical testosterone for the past 5 years, and recently stopped it because of advice from his cardiologist who pointed a finger and said, “You should stop the testosterone….The testosterone is bad for your heart and probably caused your heart attack“.  Jim came to see me for a second opinion.

Jim’s Doctor is Right About That
Jim’s doctor is right in that a number of recent studies have shown a small increase in heart attack rate in men starting testosterone.   This is caused by increased hematocrit (red blood cell count) and increased iron stores which thicken the blood and make it more susceptible to blood clot formation, all risk factors for heart attack.  See  my article on this.  The simple solution is to monitor blood count and iron levels, and donate blood at the blood bank every 4 to 6 weeks to reduce iron and red cells.

Our Approach to Preventing Heart Disease
I must preface these remarks with our approach to prevention and reversal of heart disease which is outlined in Part One  and Part Two  of this series.  We credit and rely heavily on the  “Track Your Plaque Program ” by William Davis MD.  We also use the Linus Pauling Protocol.

Bioidentical Hormones For Prevention and Reversal of Heart Disease
In this article we will revisit the role of the testosterone and estradiol in prevention and reversal of heart disease, looking at the latest research.  Firstly, let’s try to answer the question:

” Is low testosterone a risk factor for heart diease, and is normal testosterone level protective of heart disease?” 

 

Here we assume red cell count and iron levels are kept under control with monthly trips to the blood bank, so there is no short term increase in heart attack rate from hypercoagulability, as noted in a few recent studies of men started on testosterone.

Low Testosterone is Predictive for Increased Mortality from Heart Disease
If testosterone was causative of heart disease,  one would expect men with high testosterone to have more heart disease, and men with low testosterone to have less heart disease.  This is exactly opposite of four major studies showing men with low testosterone have both increased all-cause mortality and increased heart disease mortality.(1-4)

Testosterone Levels in Men With Heart Disease
A recent study by Malkin looked at Testosterone levels in men with known underlying heart disease.  He showed that low Testosterone is common in men with underlying heart disease, and this is associated with almost double the mortality rate.(5)  Again these findings suggest that higher Testosterone is protective and prevents progression of heart disease.  The assumption that Testosterone causes progression of atherosclerosis plaque has been shown false.(6-9).
Above image: Cross section of arteries (left to right) showing development of fatty streak which enlarges into the atherosclerotic plaque.   Animal Studies on Mechanism of Protection
A number of elegant animal studies have been done to elucidate the mechanism by which testosterone is protective of heart disease.  A 1999 study by Alex Andersen in rabbits showed that testosterone reduced aortic atheroscleosis.(10)  Castrated rabbits had low testosterone levels and doubled the  aortic atherosclerosis plaque formation, suggesting that testosterone has a strong preventive effect on male atherosclerosis. In the groups receiving testosterone or DHEA they found marked inhibition of atherosclerosis compared with placebo. The mechanism was not clearly defined.  They speculated on a non-lipid mediated mechanism, possibly related to aromatase conversion of testosterone to estrogen.(10 )

Mouse Model- It’s Really the Estrogen That’s Protective
In an elegant 2001 study published in PNAS, Nathan et al used a mouse model of accelerated atherosclerosis to show that testosterone inhibits atherosclerosis by its conversion to estradiol by the aromatase enzyme.  Similar protection from atherosclerosis was obtained by administering estradiol.  In addition, blocking conversion of testosterone to estradiol with the aromatase inhibitor, anastrazole, eliminated the protective effect, and these animals had progressive atherosclerosis.(11)  Dr Nathan says:

“Testosterone attenuates early atherogenesis most likely by being converted to estrogens by the enzyme aromatase expressed in the vessel wall”.(11)

 

This information suggests that men with heart disease should NOT take arimidex (anastrazole) along with their testosterone replacement therapy.

Genetically Altered Mouse Model Provides Answers
These findings were confirmed  by Nettleship  in a 2007 study published in Circulation using the Tfm genetically modifired mouse.  This is a mouse genetically altered to have a defective androgen receptor.  In these mice,  testosterone cannot work through its normal pathway, since there is no receptor.  In spite of the lack of androgen receptor, Nettleship found that testosterone replacement in these mice attenuated atherosclerotic changes (fatty streak formation), suggesting the protective effect of testosterone was independent of the testosterone receptor.  The authors concluded that the protective benefits of testosterone were through aromatase conversion to estradiol, and then via the estrogen receptor pathways.(12)

Dr Nettleship’s findings were confirmed by Bourghardt  in a Nov 2010 study published in Endocrinology which using ”ARKO” mice, genetically modified to “knock out” the Androgen Receptor, modified to be Apo-E deficient (to accelerate atherosclerosis).  The authors showed that testosterone therapy administered to the ARKO mice inhibited atherosclerosis.  However inhibition of atherosclerosis was more profound in the wild type mice that still had intact androgen receptors.  The authors concluded the mechanism of protection of testosterone was due to both mechanisms, through the Androgen Receptor as well as through aromatase conversion to estradiol.(13 )

Conclusion:
These genetically modified mouse studies suggest that testosterone’s cardio-protective benefits are due to conversion to estrogen, and that estrogen is the cardioprotective agent.  Both estrogen and testosterone are bioidentical hormones.   Clearly the message here is Testosterone Replacement Therapy should be an important part of any heart disease prevention program,  in those patients who have low Testosterone levels.

Why Do Men Have More Heart Disease Than Women ?
Men and women are quite different when it comes to heart disease.  Men have more than twice the risk of dying from coronary disease than women. (14)  In women, coronary artery disease (CAD) develops on average 10 years later than in men.(15)  Could higher levels of estrogen (estradiol) in women explain the protection enjoyed by women?

Estrogen is Protective
Dr Xing from the University of Alabama would say, yes of course.  In a 2009 article, Dr Xing names a number of mechanisms by which estradiol protects both men and women from heart disease. He says:

“Estrogens have antiinflammatory and vasoprotective effects.  Natural endogenous estrogen 17β-estradiol (bioidentical) has been shown to cause rapid endothelium-independent dilation of coronary arteries of men and women, to augment endothelium-dependent relaxation of human coronary arteries, and improve endothelial function…Observational studies have shown substantial benefit (50% reduction in heart disease) of hormone therapy in women who choose to use menopausal hormones.”(15 )

 

Estrogen is Protective of Heart Disease
A 2010 study in European Heart by Kitamura et al  compared males to female heart attack rates. They found 61% fewer heart attacks in women of reproductive age with high estrogen levels compared to males of the same age.  The authors conclude that estrogen confers cardioprotective benefits.(16)
A review of the Nurse Health Study published in the 2000 Annals  showed 40% reduction in heart disease in hormone replacement users and that “postmenopausal hormone use decreases risk for major coronary events.” (17-18)

See my article on how estrogen protects women from heart disease: Bioidentical Hormones Prevent Heart Disease.

Comparing Three Treatment Modalities
There are three mainstream treatment modalities for coronary artery disease.
1) Surgery with coronary artery bypass.
2) Balloon angioplasty with stenting.
3) Medical Therapy with drugs such as calcium channel blockers and beta blockers.
Which one of these treatment modalities confers the most benefit? The answer is:  None of Them.
Medical Management with Drugs Provides the Same Benefit as Cardiac Angioplasty, Stenting or Bypass
Eleven randomized studies reviewed 3,000 patients with stable coronary artery disease.  Treatment with  angioplasty and stenting showed the same mortality and heart attack rate as drug treatment (also known as medical management).  They both offer the same benefit.(19)(20)
The MASS II study  published in the 2007 Circulation showed medical managment with drugs to have similar outcome to stent or bypass. (21)    A troubling fact remains that after all these studies have been completed,  there is no conclusive evidence that intervention with CABG (coronary artery bypass graft) or coronary stent  is superior to medical therapy (drugs) for treating multivessel coronary artery disease with stable angina and preserved ventricular function.(21 )  Sorano attempts to sort out the fine points of selecting between treatment modalities in her 2009 report. (22)

How Can Drugs Provide the Same Outcome as Surgery or Stenting?
The EPC, the Endothelial Progentor Cell.
Now we have an important question to ask.  How is it possible that the humble country doctor with a few drugs can provide similar outcomes when compared to the high and mighty cardiac surgeon and the interventional cardiologist?  How can drug treatment do as well or better than the cardiac stent or surgical bypass procedure?

I suggest the answer resides in the phenomenon known as “collateral vessel formation”.  The heart has the ability to grow new blood vessels which provide blood flow around the blocked artery.  Medical treatment gives the heart time to grow new collateral vessels. The key to understanding this new vessel formation is the endothelial progenitor cell, also known as the EPC. The EPC is a special type of stem cell found in the bone marrow that circulates to injured myocardium where they promote local angiogenesis, making new blood vessels. (23)

Turning On The Endothelial Progenitor Cell – How to Do It?
A previous article on telomeres and anti-aging discussed the role of estrogen as an activator of telomerase which serves as an anti-aging therapy.  Recent research shows that estrogen  activates the telomeres on endothelial progenitor cells and improves the EPC functional capacity. (24)  Another study showed reduced numbers of EPC cells in the peripheral blood of men with low testosterone levels. (25)

Estradiol Enhances Recovery After Myocardial Infarction – Collateral Vessels
An elegant mouse study was published by Isakura in 2006 Circulation .  They used a mouse model in which myocardial infarction (heart attack) was induced by ligation of the left coronary artery.  The estradiol treated mice showed increased circulating EPC’s and greater capillary density in the recovering myocardium.  This indicates enhanced recovery in the estradiol treated mice by regrowth of collateral vessels. (26)(27)(28)

A study from Bolego in Italy showed that the cardio protective benefits of estrogen could be duplicated with an estrogen receptor drug called PPT. They found that:

“myocardial ischemia-reperfusion injury was exacerbated by ovariectomy (which reduced estrogen levels).   This injury returned to baseline following treatment with estrogen-like drug PPT.”

The protective effects were linked to increased levels of endothelial progenitor cells (EPCs).(29)

Conclusion
Recent research shows the cardioprotective benefits of the bioidentical hormones, testosterone and estrogen.  Testosterone benefit appears mediated by conversion to estradiol via the aromatase enzyme.  Estradiol’s benefits appear related to activation of Endothelial Progenitor Cells which invoke new collateral circulation in areas of injury.

Another treatment modality called EECP also creates new collateral vessels.  Read my article on EECP here.
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Read the complete article here.

Healthy Men Should Not Take Statins Says JAMA - Dach

Healthy Men Should Not Take Statins Says JAMA by Jeffrey Dach MD

The title speaks for itself. This bombshell article by Rita Redberg, MD, editor of the Archives of Internal Medicine, appeared in April 2012 JAMA advising healthy men with high cholesterol to stay away from statin anti-cholesterol drugs, pointing out there is no mortality benefit.  Dr Redberg goes on with a list of adverse side effects of statin drugs,  namely, myopathy, cognitive dysfunction, etc.   This JAMA article and debate is an outgrowth of the "Less is More" series in the Archives of Internal Medicine.    For fairness, JAMA also posted the opposing view by Dr. Blaha. 

For your convenience, I have posted Dr. Rita Redberg's article here with links to the original.  Above left image: Statin Drug, Lipitor 40 mg tablets, Courtesy of The Week. Click Here for link to Dr Rita Redberg article in April 2012 JAMA.

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Healthy Men Should Not Take Statins

by Rita F. Redberg, MD; Mitchell H. Katz, MD , 

Author Affiliations: Division of Cardiology, Department of Medicine, University of California, San Francisco (Dr Redberg); and Department of Health Services, County of Los Angeles, Los Angeles, California (Dr Katz).


Left Image: Courtesy of Wall Street Journal and Dr Rita Redberg.

Dr Redberg is also Editor, Archives of Internal Medicine. Dr Katz is also Deputy Editor, Archives of Internal Medicine.

Here is the Quote from the JAMA Article:

"Should a 55-year-old man who is otherwise well, with systolic blood pressure of 110 mm Hg, total cholesterol of 250 mg/dL, and no family history of premature CHD be treated with a statin? — No "says Rita Redberg MD.

"Extensive epidemiologic data demonstrate that higher cholesterol levels are associated with a greater risk of heart disease. At the population level, higher levels of cholesterol are associated with a diet greater in fatty foods, particularly trans fat and meat, and low intake of fruits and vegetables.

The important questions for clinicians (and for patients) are as follows:

(1) does treatment of elevated cholesterol levels with statins in otherwise healthy persons decrease mortality or prevent other serious outcomes?

(2) What are the adverse effects associated with statin treatment in healthy persons?

(3) Do the potential benefits outweigh the potential risks? The answers to these questions suggest that statin therapy should not be recommended for men with elevated cholesterol who are otherwise healthy.

Benefits of Statin Therapy in Healthy Men With High Cholesterol?

Dr Ray Archives Int Med - NO Reduction in Mortality
    What is the benefit of statin therapy in healthy men with high cholesterol levels? Data from a meta-analysis of 11 trials including 65 229 persons with 244 000 person-years of follow-up in healthy but high-risk men and women showed no reduction in mortality associated with treatment with statins.(1 )

Cochrane Review - No Reduction in Mortality

A 2011 Cochrane review of treatment with statins among persons without documented coronary disease came to similar conclusions.(2) The Cochrane review also observed that all but one of the clinical trials providing evidence on this issue were sponsored by the pharmaceutical industry.

Biased Reporting in Industry Sponsored Drug Trials

It is well established that industry-sponsored trials are more likely than non–industry-sponsored trials to report favorable results for drug treatment because of biased reporting, biased interpretation, or both of trial results.(6)

Adverse Effects of Statins

What adverse effects are associated with statin treatment in healthy persons?

Myopathy, Muscle Pain, Weakness
All treatments designed to prevent disease—such as death from coronary disease—can also result in adverse effects. Data from observational studies show much higher rates for statin-associated myopathy and other adverse events in actual use than the 1% to 5% rate reported in clinical trials. This underestimation of adverse events occurs because the trials excluded up to 30% of patients with many common comorbidities, such as those with a history of muscular pains, as well as renal or hepatic insufficiency.(3)

Many randomized trials also excluded patients who had adverse effects of treatment during an open-label run-in period. For example, in the Treat to New Targets trial, after initial exclusions based on comorbidities, an additional 35% of eligible patients, or 16% of patients, were excluded during an 8-week, open-label, run-in phase because of adverse events, ischemic events, or participants' lipid levels while taking the drug not meeting entry criteria.7 Additionally, the results of randomized trials of statin treatment likely underestimate common symptoms such as myalgia, fatigue, and other minor muscle complaints because these studies often only collect data on more quantifiable adverse effects such as rhabdomyolysis.

Cognitive Impairment

    Numerous anecdotal reports as well as a small trial (8 - 9) have suggested that statin therapy causes cognitive impairment, but this adverse outcome would not have been captured in randomized trials. The true extent of cognitive impairment associated with statins remains understudied. It is disappointing that more data are not available on important adverse events associated with statin treatment, despite millions of prescriptions and many years of use. This information could be easily collected in observational studies and from registries. (8)(9)

One population-based cohort study in Great Britain of more than 2 million statin users found that statin use was associated with increased risks of moderate or serious liver dysfunction, acute renal failure, moderate or serious myopathy, and cataract.(4)

The risk of diabetes with statin use has been seen in randomized clinical trials such as JUPITER, which found a 3% risk of developing diabetes in the rosuvastatin group, significantly higher than in the placebo group.

In observational data from the Women's Health Initiative, there was an unadjusted 71% increased risk and 48% adjusted increased risk of diabetes in healthy women taking statins.(5)

Do the potential benefits outweigh the potential risks?

Based on all current evidence, a healthy man with elevated cholesterol will not live any longer if he takes statins. For every 100 patients with elevated cholesterol levels who take statins for 5 years, a myocardial infarction will be prevented in 1 or 2 patients.(7)

Preventing a heart attack is a meaningful outcome. However, by taking statins, 1 or more patients will develop diabetes and 20% or more will experience disabling symptoms, including muscle weakness, fatigue, and memory loss. (3)

NONDRUG APPROACHES TO REDUCING CORONARY RISK

There are effective methods for reducing cardiovascular risk in otherwise healthy men: dietary modification, weight loss, and increased exercise.

These strategies are effective in increasing longevity and also result in other positive benefits, including improved mood and sexual function (10) and fewer fractures. Although these strategies are challenging, prescribing a statin may undermine them. For example, some patients derive a false sense of security that because they are taking a statin they can eat whatever they want and do not have to exercise.

Belief in Benefits of Statins for Patients Without CAD

For some clinicians, evidence that statins reduce the risk of recurrent coronary events in patients with documented coronary disease leads to the belief that statins also “must” be beneficial for patients without coronary disease.

However, recent history is rife with examples of interventions that are proven to work in patients with serious disease yet are not efficacious when generalized to patients without serious disease.

CABG Not a Good Choice for Single Vessel Disease

For example, coronary artery bypass graft (CABG) surgery is lifesaving for patients with symptomatic left main disease. However, CABG surgery would not be a good choice for single-vessel coronary artery disease (CAD) because risks would outweigh benefits in less extensive CAD. Similarly, the benefits of carotid endarterectomy in preventing stroke outweigh the risks for symptomatic patients with tight carotid artery stenosis, but not for asymptomatic patients with less critical stenosis. In addition, the use of aspirin is similar to statins for prevention.

Aspirin Not Useful For Primary Prevention

The data show clear benefit for aspirin in secondary prevention of cardiovascular disease, but not for primary prevention. Practitioners should not be generalizing from other settings when good data indicate that statins are not effective in improving length or quality of life when used for primary prevention.

For the 55-year-old man in this scenario, his risk of myocardial infarction in the next 10 years based on the Framingham Risk Score varies from 10% to 20%. His risk is driven mostly by his age rather than by his cholesterol level. Increasing age has a much larger influence on risk for cardiovascular disease than do increasing levels of cholesterol.

Recent data on increased risk of diabetes, cognitive dysfunction, and muscle pain associated with statins suggest that there is risk with no evidence of benefit.

Advising healthy patients to take a drug that does not offer the possibility to feel better or live longer and has significant adverse effects with potential decrement in quality of life is not in their interest.

At the same time, there are significant opportunities for improvement in lifestyle counseling and interventions. Even small changes in diet and increases in physical activity and smoking cessation can lead to significant personal and population health benefits. Such positive lifestyle changes have the key advantage of helping patients feel better and live longer. Lifestyle counseling should remain the focus of primarily prevention efforts—at the physician and public health levels.

AUTHOR INFORMATION: Corresponding Author: Rita F. Redberg, MD, Division of Cardiology, University of California, San Francisco, 505 Parnassus Ave, M1180, San Francisco, CA 94143 (redberg@medicine.ucsf.edu).

Conflict of Interest Disclosures: Both authors have completed and submitted the ICMJE Form for Disclosure of Potential Conflicts of Interest and none were reported.


Additional Contributions: We thank Deborah Grady, MD, University of California, San Francisco, for her input in the writing of this Viewpoint. She was not compensated for her contribution." end quote


REFERENCES1) Ray KK, Seshasai SR, Erqou S,  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, PubMed

2) Taylor F, Ward K, Moore TH,  et al.  Statins for the primary prevention of cardiovascular disease.  Cochrane Database Syst Rev. 2011;(1):CD004816
PubMed

3) Fernandez G, Spatz ES, Jablecki C, Phillips PS. Statin myopathy: a common dilemma not reflected in clinical trials.  Cleve Clin J Med. 2011;78(6):393-403. PubMed

4) Hippisley-Cox J, Coupland C. Unintended effects of statins in men and women in England and Wales: population based cohort study using the QResearch database.  BMJ. 2010;340c2197. PubMed

5) Culver AL, Ockene IS, Balasubramanian R,  et al.  Statin use and risk of diabetes mellitus in postmenopausal women in the Women's Health Initiative.  Arch Intern Med. 2012;172(2):144-152. PubMed

6) Lexchin J, Bero LA, Djulbegovic B, Clark O. Pharmaceutical industry sponsorship and research outcome and quality: systematic review.  BMJ. 2003;326(7400):1167-1170 PubMed

7) LaRosa J, Grundy SM, Waters DD,  et al.  Intensive lipid lowering with atorvastatin in patients with stable coronary disease.  N Engl J Med. 2005;352(14):1425-1435 PubMed

8) Muldoon MF, Barger SD, Ryan CM,  et al.  Effects of lovastatin on cognitive function and psychological well-being.  Am J Med. 2000;108(7):538-546PubMed CrossRef

9) Muldoon MF, Ryan CM, Sereika SM, Flory JD, Manuck SB. Randomized trial of the effects of simvastatin on cognitive functioning in hypercholesterolemic adults.  Am J Med. 2004;117(11):823-829 PubMed CrossRef

10) Gupta BP, Murad MH, Clifton MM, Prokop L, Nehra A, Kopecky SL. The effect of lifestyle modification and cardiovascular risk factor reduction on erectile dysfunction: a systematic review and meta-analysis.  Arch Intern Med. 2011;171(20):1797-1803PubMed

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Links to Articles with Related Content:

You Tube Videos by Dr Dach:

Links to all four parts of this series on You Tube:

part one: http://youtube.com/watch?v=b-iUJd4IxRM

part two: http://youtube.com/watch?v=RozkhmdHPac

part three: http://www.youtube.com/watch?v=_To64-NWKao

Part four: http://youtube.com/watch?v=gd6f8_GjAsg

Links to related articles of interest:

Lipitor and The Dracula of Modern Technology by Jeffrey Dach MD
http://www.drdach.com/Lipitor_Jarvik_Dracula.html

Getting Off Statin Drug Stories
http://www.bioidenticalhormones101.com/Statin_Drug_Stories.html

How to Reverse Heart Disease with the Coronary Calcium Score by Jeffrey Dach MD
http://jeffreydach.com/2008/03/27/cat-coronary-calcium-scoring-reversing-hear...

Cholesterol Lowering Statin Drugs for Women, Just Say No
http://www.bioidenticalhormones101.com/Statin_Drugs_Women.html

Reversing Heart Disease without Drugs
http://www.drdach.com/wst_page7.html

Cholesterol Lowering Drugs for the Elderly, Bad Idea by Jeffrey Dach MD
http://jeffreydach.com/2008/08/30/cholesterol-lowering-drugs-for-the-elderly-...

A Choirboy for Cholesterol Turns Disbeliever by Jeffrey Dach MD
http://www.drdach.com/Cholesterol_Choirboy.html

More links and references

Listen to Debate Audio

http://www.ihi.org/knowledge/Pages/AudioandVideo/AIRShouldHealthyManBeTreatedWithaStatin.aspx
Audio of Debate on Statins for Healthy Men in JAMA article with  Dr Rita Redberg vs Michael Blaha (opposition)

Author in the Room: Should a Healthy 55-Year-Old Man Be Treated with a Statin?
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May 2012 Author in the Room® Teleconference

Authors and Articles:

Michael Blaha, MD, MPH, suggests that the available data do support treatment:
Statin Therapy for Healthy Men Identified as “Increased Risk”

Rita Redberg, MD, MSc, suggests that the available data do not support treatment.
Healthy Men Should Not Take Statins

Summary Points:Summary Points from Dr. Michael Blaha: High-quality literature supports statins for reduction of first heart attack and stroke, in addition to a mild decrease in all-cause mortality over 3 to 5 years.
    The key to efficient use of statins in primary prevention is risk stratification.
    We must demand high-quality evidence for benefit and for harm in a potentially beneficial medication class such as statins.
    Physicians should adhere to national guidelines to guide statin use in primary prevention.

http://www.healthnewsreview.org/2012/04/dueling-viewpoints-should-a-healthy-middle-aged-man-with-elevated-cholesterol-take-a-statin-drug/
Dueling viewpoints: Should a healthy middle-aged man with elevated cholesterol take a statin drug?  Posted by Gary Schwitzer in Journal practices

http://www.theheart.org/article/1383271.do
Should statins be used in primary prevention? JAMA gets in on the debate
April 10, 2012 Michael O'Riordan

http://www.dailymail.co.uk/debate/article-2147218/Should-everybody-fifty-Statins-reduce-health-risks.html
Should everybody over fifty take statins to reduce health risks?  By Dr Robert Lefever


http://www.vasculardoc.com/opinion-commentry/healthy-men-should-not-take-statin-drugs-for-cholesterol_133.aspx

Healthy men should not take statin drugs for cholesterol
Apr 12, 2012- In the latest issue of the Journal of the American Medical Association (JAMA – April 11, 2012) opposing viewpoints are offered by two leading cardiologists with regard to the following question:
Should a 55-year-old man who is otherwise well, with systolic blood pressure of 110 mm Hg, total cholesterol of 250 mg/dL, and no family history of premature coronary artery disease, be treated with a statin?

http://www.jonbarron.org/heart-health/statin-drugs-jama-lower-ldl-cholesterol
Statin Drugs – the JAMA Debate - The April 14th issue of the Journal of the American Medical Association inaugurated a new feature called "Viewpoint" -- an "in magazine" debating forum for arguing out key medical issues of the day. Think of it like a civilized version of Dan Aykroyd and Jane Curtain's Point/Counterpoint sketches on Saturday Night Live.1
Date: 04/23/2012 Written by: Jon Barron

http://www.natap.org/2012/HIV/041112_01.htm
Should statins be used in primary prevention?
theheart.org April 12 2012 Michael O'Riordan
Baltimore, MD and San Francisco, CA - Differing opinions on the use of statins in primary prevention make the pages of one of the leading medical journals this week, with the Journal of the American Medical Association (JAMA) the latest in a line of professional and mainstream media outlets getting in on the contentious topic [1,2]. Introduced by the JAMA editors to encourage discussion and debate [3], the inaugural "dueling viewpoints" kicks off its new series by considering the clinical question of whether or not a healthy 55-year-old male with elevated cholesterol levels should begin taking the lipid-lowering medication.


http://anthonycolpo.com/?p=3479
Why Asians Should Ignore the Cholesterol Sham, and Why Healthy People Should Not Take Statins.  Anthony Colpo | Saturday, April 28th, 2012


http://www.minnpost.com/second-opinion/2012/04/duel-over-statins-use-healthy-people-moves-new-venue
'Duel' over statins' use in healthy people moves to new venue
By Susan Perry | 04/17/12

<<<<<<<<<<<<<>>>>>>>>>>>
http://cardiobrief.org/2012/01/23/rita-redberg-and-roger-blumenthal-clash-over-statins-for-primary-prevention-in-the-wall-street-journal/
January 23, 2012     
Rita Redberg and Roger Blumenthal Clash Over Statins for Primary Prevention in the Wall Street Journal 8    by Larry Husten • Uncategorized • Tags: mortality benefit, primary prevention   

The debate over whether statins should be used for primary prevention moved to the Wall Street Journal with opposing perspectives from cardiologists Roger Blumenthal and Rita Redberg.

Blumenthal argues that “there is a mountain of high-quality scientific evidence” to support the use of statins in people without known heart disease but “demonstrated to be at high risk for heart disease.”
Redberg argues that “for most healthy people, data show that statins do not prevent heart disease, nor extend life or improve quality of life. And they come with considerable side effects. That’s why I don’t recommend giving statins to healthy people, even those with higher cholesterol.”


http://www.lifediscoverywellness.com/archives.html
Healthy Men Should Not Take Statins-Neither should Women! 04/23/2012
Most of you know what cholesterol lowering drugs are.  Below is a list of the names of the most common drugs out there.  The most unethical event is taking place to people that you know and care about.  The amount of cholesterol drugs consumed is up and the drug companies bottom line has gone up, but there is no change in the amount of heart disease.  In fact heart disease is still the number one killer by far and it continues to go up and up and up.  So what in the health are the statins for?

    Advicor  (lovastatin with niacin) – Abbott
    Altoprev (lovastatin) – Shionogi Pharma
    Caduet [atorvastatin with amlodipine (Norvasc)] – Pfizer
    Crestor (rosuvastatin) - AstraZeneca
    Lescol (fluvastatin) – Novartis
    Lipitor (atorvastatin) - Pfizer
    Mevacor (lovastatin) – Merck
    Pravachol (pravastatin) -- Bristol-Myers Squibb
    Simcor (niacin/imvastatin) – Abbott
    Vytorin (ezetimibe/simvastatin) – Merck/Schering-Plough
    Zocor (simvastatin) – Merck


http://www.ucsfhealth.org/rita.redberg

Rita Redberg, F.A.C.C., M.Sc., M.D.

Cardiologist Dr. Rita Redberg is a cardiologist specializing in heart disease in women. She earned her medical degree from the University of Pennsylvania School of Medicine, in Philadelphia. She completed her residency at Columbia-Presbyterian Medical Center in New York, where she went on to complete a fellowship in cardiology. Then she completed a fellowship in non-invasive cardiology at Mount Sinai Medical Center, also in New York. In addition, Redberg has a masters of science in health policy and administration from the London School of Economics in England. Also she is currently a Robert Wood Johnson health policy fellow.
Redberg has written, edited and contributed to many books, including "You Can Be a Woman Cardiologist," "Heart Healthy: The Step-by-Step Guide to Preventing and Healing Heart Disease," and "Coronary Disease in Women: Evidence-Based Diagnosis and Treatment."

Clinics Cardiovascular Care and Prevention Center at Mission Bay
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Statins for healthy people
Commentary by Prof John E Deanfield

Recently, prescribing statins to healthy people was discussed in the Journal of the American Medical Association. The main question is: should a healthy man aged 55 who has a blood pressure of 110 mm Hg, an LDL-cholesterol level of 6.46 mmol /L without family history take statins? Besides, the New England Journal of Medicine published a reflective publication on statins and the risk of diabetes. Links to these articles you will find below.

According to prof. John E. Deanfield (University College, London), statin therapy is a key part of multifactorial risk reduction strategies. Long term surveillance of risks and benefits are required, particularly for drugs given to very large numbers of people. The data we have so far are highly encouraging for statins.

Deanfield gives four good reasons to continue prescribing statins:

    The benefits of a healthy lifestyle should always be emphasised, but this is rarely adopted by patients.
    Statins provide an effective way of prolonging an event free survival and are generally safe, with increasing benefit over time.
    Thirdly the extremely well investigated potent statins atorvastatin and simvastatin are both generic and cheap
    It is important to consider the lifetime benefits of cardiovascular risk reduction in discussions with patients and not merely 5 and 10 year risks in those with cardiovascular disease..

References:

Healthy Men Should Not Take Statins :
JAMA. 2012;307(14):1491-1492. doi:10.1001/jama.2012.423
Rita F. Redberg, MD; Mitchell H. Katz, MD

Statin Therapy for Healthy Men Identified as “Increased Risk”
JAMA. 2012;307(14):1489-1490. doi:10.1001/jama.2012.425
Michael J. Blaha, MD, MPH; Khurram Nasir, MD, MPH; Roger S. Blumenthal, MD

Statins: Is It Really Time to Reassess Benefits and Risks?
N Engl J Med 2012; 366:1752-1755May 10, 2012
Allison B. Goldfine, M.D.

Wall Street journal - <<<<<<<<<<>>>>>>>>>>

http://online.wsj.com/article/SB10001424052970203471004577145053566185694.html

Should Healthy People Take Cholesterol Drugs to Prevent Heart Disease?


http://www.kardeanutrition.com/content/healthy-high-cholesterol-should-you-be-taking-statins

Healthy But With High Cholesterol: Should You Be Taking Statins?
Posted By Rob Leighton On 04/16/2012 - 8:05 am in the following categories :
Your healthy and feeling great, but you just found out that your LDL (bad) cholesterol is high. You do not have any of the standard risk factors, like a parent with heart disease.  Should you be taking a statin medication – perhaps for the rest of your life?

More and more doctors are coming to the conclusion that the answer is no.
In the April 2012 Journal of the American Medical Association (JAMA), two perspectives were presented.



Jeffrey Dach MD
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Myositis from Statin and PPI Drugs - Dach

A Neurosurgeon with a Painful Arm, Myositis from Statin and PPI Drugs by Jeffrey Dach MD

Sam, a 67 year old retired neurosurgeon came to see me because of pain and weakness in his right arm over the past 6 months. The pain and weakness is chronic and so severe, that he has given up Golf, his favorite pastime. His medical history is unremarkable except for his medications which includes a statin drug to lower cholesterol, simvastatin, which he has been taking for three years, and Prilosec a proton pump inhibitor (PPI) acid blocking drug for the past year for symptoms of heart burn.
Upon examination, there is diffuse tenderness of the muscles of the right shoulder and arm, as well as generalized muscle wasting.

Lab studies revealed extensive vitamin and mineral deficiencies suggesting malabsorption, B12 was low at 337 . There was a very low cholesterol level of 146.

My diagnosis was drug induced myositis from the combination of statin drug and proton pump inhibitor acid blocking drug. I advised the retired Neurosurgeon to stop these drugs and to take vitamin and mineral supplements to allow the muscles to heal.

Sam’s cardiologist and gasteroenterologist disagreed with my assessment and objected to the idea of stopping the drugs. They told Sam that these were “lifesaving drugs”. and were unlikely to be related to the muscle problems, and to continue them. In addition, Sam didn’t need any vitamins, as he was getting all his vitamins from his diet. Sam relayed this information to me on the phone. He thanked me for seeing him, but he would follow the advice of his other doctors, the cardiologist and the gasteroenterologist who he had known for years and trusted them.

Six months later, Sam’s wife called me to ask if there was anything I could do for Sam. He was still taking the statin anti-cholesterol drugs and the acid blocking drug ( PPI), and Sam’s conditionn had deteriorated to the point he was now in a wheel chair in a nursing home with early dementia.

Myopathy and Myositis are well known adverse effects of statin drugs which lower cholesterol. They also lower CoQ-10 levels and serve as mitochondrial toxins causing myopthy and dementia. The PPI drugs are also known to cause myopathy, thought to be caused by protein, mineral and vitmain malabsorption from lack of stomach acid.(1-9)



Links and References
Myopathy caused by proton pump inhibitors and statins
1) http://www.ncbi.nlm.nih.gov/pubmed/16758264
Eur J Clin Pharmacol. 2006 Jun;62(6):473-9. Epub 2006 Apr 22.
Myopathy including polymyositis: a likely class adverse effect of proton pump inhibitors? Clark DW, Strandell J.Department of Pharmacology and Toxicology, School of Medical Sciences, University of Otago, PO Box 913, Dunedin, New Zealand.
Polymyositis occurring in patients treated with omeprazole has been signalled as a possible adverse drug reaction (ADR) by the New Zealand Intensive Medicines Monitoring Programme (IMMP) and the WHO Collaborating Centre for International Drug Monitoring: the Uppsala Monitoring Centre (UMC). Polymyositis and other myopathies have also been reported in post-marketing data and in the medical literature in association with proton pump inhibitor (PPI) use. We wished to follow-up these signals and investigate the evidence of causality for the association of polymyositis and other myopathy with PPI use.
METHODS: Spontaneously reported ADRs from national monitoring centres are sent to the WHO ADR database (VigiBase). VigiBase was searched for case reports of the PPIs, omeprazole, pantoprazole, lansoprazole, esomeprazole and rabeprazole, with terms indicative of myopathy, and further information was elicited from the national centres to help establish causality. Literature sources were reviewed for the occurrence of the above terms in combination with PPIs.
RESULTS: In total, there were 292 reports of various myopathies with PPIs, excluding 868 cases of ‘myalgia’. In this analysis, 69 patients recovered when the drug was withdrawn and, in 15 patients, the reaction re-occurred when the drug was reinstated. In one-third of the 292 cases, the PPI was the single administered drug, and the PPI was the single suspected drug by the reporter in 57% of reports where concomitant medication was used. In this analysis, three index cases are documented. One involves the same patient taking three different PPIs (lansoprazole, esomeprazole and rabeprazole) at different time periods, with myalgia and muscle weakness occurring with all three drugs. In the two other index cases, myopathies with esomeprazole and omeprazole were reported with positive rechallenge, and causality was assessed as ‘possible’ and ‘certain’ by the reporting centres. In 27 cases myositis or polymyositis was reported. Other myopathies were reported, including 35 cases with rhabdomyolysis. In 9 of these cases, the PPI was withdrawn and the reaction abated. The PPI was reinstated in one patient, but the reaction did not re-occur. Time to onset was given in 17 of the rhabdomyolysis cases, rhabdomyolysis occurred with the first week in 9 cases, and in 3 cases the reaction occurred between 14 days to 3 months of treatment. In 12 of these patients, an HMG-CoA reductase inhibitor (statin) was taken concomitantly.
CONCLUSION: Case reports from the WHO ADR database, including index cases involving four out of five PPIs, along with evidence of a possible mechanism, provide compelling evidence that there is a causal association between members of the PPI drug class and myopathy including polymyositis. Evidence was also obtained to support the view that PPI use may be associated with occurrence of other myopathies, including the serious reaction rhabdomyolysis.
statin induced myopathy
2) http://www.ncbi.nlm.nih.gov/pubmed/12672737
JAMA. 2003 Apr 2;289(13):1681-90.
Statin-associated myopathy. Thompson PD, Clarkson P, Karas RH.Preventive Cardiology and Cardiovascular Research, Division of Cardiology, Hartford Hospital, Hartford, Conn 06102, USA.
Statins (3-hydroxy-3-methylglutaryl coenzyme A reductase inhibitors) are associated with skeletal muscle complaints, including clinically important myositis and rhabdomyolysis, mild serum creatine kinase (CK) elevations, myalgia with and without elevated CK levels, muscle weakness, muscle cramps, and persistent myalgia and CK elevations after statin withdrawal. We performed a literature review to provide a clinical summary of statin-associated myopathy and discuss possible mediating mechanisms. We also update the US Food and Drug Administration (FDA) reports on statin-associated rhabdomyolysis. Articles on statin myopathy were identified via a PubMed search through November 2002 and articles on statin clinical trials, case series, and review articles were identified via a PubMed search through January 2003. Adverse event reports of statin-associated rhabdomyolysis were also collected from the FDA MEDWATCH database. The literature review found that reports of muscle problems during statin clinical trials are extremely rare. The FDA MEDWATCH Reporting System lists 3339 cases of statin-associated rhabdomyolysis reported between January 1, 1990, and March 31, 2002. Cerivastatin was the most commonly implicated statin. Few data are available regarding the frequency of less-serious events such as muscle pain and weakness, which may affect 1% to 5% of patients. The risk of rhabdomyolysis and other adverse effects with statin use can be exacerbated by several factors, including compromised hepatic and renal function, hypothyroidism, diabetes, and concomitant medications. Medications such as the fibrate gemfibrozil alter statin metabolism and increase statin plasma concentration. How statins injure skeletal muscle is not clear, although recent evidence suggests that statins reduce the production of small regulatory proteins that are important for myocyte maintenance.
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3) http://www.ncbi.nlm.nih.gov/pubmed/22560377
Eur J Intern Med. 2012 Jun;23(4):317-24.
Statin induced myotoxicity. Sathasivam S. The Walton Centre NHS Foundation Trust, Lower Lane, Liverpool L9 7LJ, United Kingdom.
Statins are an effective treatment for the prevention of cardiovascular diseases and used extensively worldwide. However, myotoxicity induced by statins is a common adverse event and a major barrier to maximising cardiovascular risk reduction. The clinical spectrum of statin induced myotoxicity includes asymptomatic rise in creatine kinase concentration, myalgia, myositis and rhabdomyolysis. In certain cases, the cessation of statin therapy does not result in the resolution of muscular symptoms or the normalization of creatine kinase, raising the possibility of necrotizing autoimmune myopathy. There is increasing understanding and recognition of the pathophysiology and risk factors of statin induced myotoxicity. Careful history and physical examination in conjunction with selected investigations such as creatine kinase measurement, electromyography and muscle biopsy in appropriate clinical scenario help diagnose the condition. The management of statin induced myotoxicity involves statin cessation, the use of alternative lipid lowering agents or treatment regimes, and in the case of necrotizing autoimmune myopathy, immunosuppression.
4) http://www.ncbi.nlm.nih.gov/pubmed/22154355
Atherosclerosis. 2012 May;222(1):15-21.
Statins as a possible cause of inflammatory and necrotizing myopathies. Padala S, Thompson PD.
Department of Internal Medicine, University of Connecticut, Farmington, CT 06030, USA.
Hydroxy-methyl-glutaryl Co-A reductase (HMGCR) inhibitors or statins are a well recognized cause of a variety of skeletal myopathic effects which generally resolve on stopping the medication. Recent reports, however, suggest that statins are associated with a unique autoimmune myopathy wherein symptoms persist or even progress after statin discontinuation and require immunosuppressive therapy. We performed a systematic review to examine the association of statins with inflammatory (dermatomyositis/polymyositis) and necrotizing myopathies.
METHODS: We searched PubMed, Ovid and Scopus for English language articles addressing statin associated inflammatory and necrotizing myopathies. Given the paucity of cases, we extended the search to include articles in all languages.
RESULTS: The search yielded 14 articles reporting a possible association of statins with inflammatory myopathies describing 10 cases of polymyositis and 14 cases of dermatomyositis, and 4 articles reporting a possible association of statins with necrotizing myopathies describing 63 cases. One study identified a unique antibody directed against HMGCR in patients with necrotizing myopathy. Systemic immunosuppressive therapy was required in majority of these cases for resolution of symptoms.
CONCLUSION: Statins have recently been associated with a variety of inflammatory myopathies including polymyositis, dermatomyositis, and a necrotizing myopathy. The association of statins with necrotizing myopathy is strengthened by the discovery that the serum of some of these patients contains an anti-HMGCR antibody. This suggests that statins can cause or unmask an immune mediated myopathy.
5) http://www.if-pan.krakow.pl/pjp/pdf/2011/4_859.pdf
Pharmacol Rep. 2011;63(4):859-66.
Statin-induced myopathies. Tomaszewski M, Stępień KM, Tomaszewska J, Czuczwar SJ.
Source Department of Cardiology, Medical University of Lublin, Jaczewskiego 8, PL 20-954 Lublin, Poland.
Statins are considered to be safe, well tolerated and the most efficient drugs for the treatment of hypercholesterolemia, one of the main risk factor for atherosclerosis, and therefore they are frequently prescribed medications. The most severe adverse effect of statins is myotoxicity, in the form of myopathy, myalgia, myositis or rhabdomyolysis. Clinical trials commonly define statin toxicity as myalgia or muscle weakness with creatine kinase (CK) levels greater than 10 times the normal upper limit. Rhabdomyolysis is the most severe adverse effect of statins, which may result in acute renal failure, disseminated intravascular coagulation and death. The exact pathophysiology of statin-induced myopathy is not fully known. Multiple pathophysiological mechanisms may contribute to statin myotoxicity. This review focuses on a number of them. The prevention of statin-related myopathy involves using the lowest statin dose required to achieve therapeutic goals and avoiding polytherapy with drugs known to increase systemic exposure and myopathy risk. Currently, the only effective treatment of statin-induced myopathy is the discontinuation of statin use in patients affected by muscle aches, pains and elevated CK levels.
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6) http://www.ncbi.nlm.nih.gov/pubmed/20688875
Phys Ther. 2010 Oct;90(10):1530-42.
Effects of statins on skeletal muscle: a perspective for physical therapists.Di Stasi SL, MacLeod TD, Winters JD, Binder-Macleod SA.SourceUniversity of Delaware, Newark, Delaware, USA.
Hyperlipidemia, also known as high blood cholesterol, is a cardiovascular health risk that affects more than one third of adults in the United States. Statins are commonly prescribed and successful lipid-lowering medications that reduce the risks associated with cardiovascular disease. The side effects most commonly associated with statin use involve muscle cramping, soreness, fatigue, weakness, and, in rare cases, rapid muscle breakdown that can lead to death. Often, these side effects can become apparent during or after strenuous bouts of exercise. Although the mechanisms by which statins affect muscle performance are not entirely understood, recent research has identified some common causative factors. As musculoskeletal and exercise specialists, physical therapists have a unique opportunity to identify adverse effects related to statin use. The purposes of this perspective article are: (1) to review the metabolism and mechanisms of actions of statins, (2) to discuss the effects of statins on skeletal muscle function, (3) to detail the clinical presentation of statin-induced myopathies, (4) to outline the testing used to diagnose statin-induced myopathies, and (5) to introduce a role for the physical therapist for the screening and detection of suspected statin-induced skeletal muscle myopathy.
7) http://www.ccjm.org/content/78/6/393.long
Statin myopathy: A common dilemma not reflected in clinical trials Cleveland Clinic Journal of Medicine June 2011 vol. 78 6 393-403 GENARO FERNANDEZ, MD ERICA S. SPATZ, MD CHARLES JABLECKI, MD Department of Neurosciences, University of California San Diego, La Jolla PAUL S. PHILLIPS, MD⇓ Director, Interventional Cardiology, Department of Cardiology, Scripps Mercy Hospital, San Diego, CA
myopathy and muscle pain while on the combined treatment of atorvastatin plus ezetimibe.
8) http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2538990/
Can J Cardiol. 2006 February; 22(2): 141–144.
Ezetimibe-associated myopathy in monotherapy and in combination with a 3-hydroxy-3-methylglutaryl coenzyme A reductase inhibitor Chantale Simard, B Pharm, PhD, and Paul Poirier, MD PhD FRCPC FACC
Centre de recherche, Hôpital Laval; Faculté de Pharmacie, Université Laval, Sainte-Foy, Québec
Correspondence: Dr Chantale Simard, Centre de recherche, Hôpital Laval, 2725 chemin Sainte-Foy, Sainte-Foy, Québec
9) http://www.ncbi.nlm.nih.gov/pubmed/17768174Ann Rheum Dis. 2008 May;67(5):614-9.
Increased exposure to statins in patients developing chronic muscle diseases: a 2-year retrospective study.Sailler L, Pereira C, Bagheri A, Uro-Coste E, Roussel B, Adoue D, Fournie B, Laroche M, Zabraniecki L, Cintas P, Arlet P, Lapeyre-Mestre M, Montastruc JL.Unit of Pharmacoepidemiology, EA 3696, Clinical Pharmacology Department, Paul Sabatier University, 37 Allées Jules Guesdes, 31000 Toulouse, France.

Case reports have suggested that lipid-lowering drugs (LLDs), especially statins, could induce or reveal chronic muscle diseases. We conducted a study to evaluate the association between chronic muscle diseases and prior exposure to LLDs.METHOD:This was a retrospective study of chronic primary muscle disease cases newly diagnosed at the Toulouse University Hospitals between January 2003 and December 2004 among patients living in the Midi-Pyrénées area, France. All patients remained symptomatic for more than 1 year after drug withdrawal, or required drugs for inflammatory myopathy. Data on the patient’s exposure to LLDs and to other drugs were compared with that of matched controls (5/1) selected through the Midi-Pyrénées Health Insurance System database.RESULTS:A total of 37 patients were included in the study. Of those, 21 (56.8%) suffered from dermatomyositis (DM) or polymyositis (PM), 12 (32.4%) from genetic myopathy, and 4 (10.8%) from an unclassified disease. The prevalence of exposure to statins was 40.5% in patients and 20% in controls (odds ratio (OR) 2.73, 95% confidence interval (CI) 1.21-6.14; p<0 .01="" strong="">There was a significant positive interaction between statins and proton pump inhibitors exposure (weighted OR 3.3, 95% CI 1.37-7.54; p = 0.02).

Statin exposure rate was 47.6% among patients with DM/PM (OR 3.86, 95% CI 1.30-11.57; p<0 .01="" and="" between="" border="0" controls="" difference="" exposure="" fibrates.conclusion="" for="" img="" no="" patients="" src="http://jeffreydach.com/emoticons/tongue.png" there="" to="" was="">atients who developed chronic muscle diseases after the age of 50, including DM/PM, had a higher than expected frequency of prior exposure to statins. Further studies are needed to confirm this association and the role of proton pump inhibitors.

warmest regards,

Jeffrey Dach MD

Offices of Willow Grove

7450 Griffin Road, Suite 190

Davie, Fl 33314

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Wheat Gluten Sensitivity and Autoimmune Disease - Dach

Wheat Gluten Sensitivity and Autoimmune Disease

by Jeffrey Dach MD

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Gluten Sensitivity, Autoimmune and Neurological Disease by Jeffrey Dach MD This article is Part Three of a Series. For Previous Parts, Click Here: Part One and Part Two Two Very Mysterious and Complicated Cases caused by Gluten SensitivityWhat is wheat gluten? Gluten is a protein in grains such as wheat, rye, barley, spelt, triticale, kamut,and possibly oats. In susceptible individuals, about one per cent of the population, Wheat Gluten stimulates an immune response which may damage the inner lining of the gastrointestinal tract, or cross-react with other tissues in the body producing auto-immune, neurological and psychiatric illness. Upper left image: A variety of foods made from wheat, all containing gluten. Courtesy of the USDA and Wikimedia Commons. Celiac Disease or Gluten Sensitivity ? Shag Carpet or Flat Carpet ? The immune response to gluten may cause malabsorption, and damage to the mucosal lining of the GI tract which can be seen on endoscopic biopsy as villous atrophy (see left image). Normally, the healthy small bowel looks like a "shag carpet" under the microscope with a brush border. However, with villous atrophy, the villi or fingers are lost or shortened, and the shag carpet turns into indoor-out door carpeting with a flat surface. Left Image: Red Arrows point to Villous Atrophy. Biopsy of small bowel showing Coeliac disease manifested by blunting of villi, crypt hyperplasia, and lymphocyte infiltration of crypts, consistent with Marsh classification III. Courtesy of wikimedia commons. This advanced form is called Celiac Disease which may cause malabsorption of B12, Iron, and Calcium (leading to osteoporosis and stress fractures at a young age) . In addition, there may be malabsorption of fat with labs showing a low serum triglyceride level which may be "tip-off" for the diagnosis. (12-14) However, in many people, there may be minimal or no gastrointestinal symptoms. Rather the immune response may show up elsewhere in the body as an auto-immune disease, a neurological disease or a psychiatric manifestation. This form of the disease is called Gluten Sensitivity, a diagnosis frequently missed or ignored by mainstream medicine. Gluten Testing - Conventional Lab PanelSince Gluten sensitivity leads to villous atrophy and malabsorption of vitamins, minerals and fats, various abnormalities may show up on the conventional lab panel: Low serum triglyceride level (below 75) is a marker for gluten sensitivity.(12-14) Low Serum Iron, Ferritin and Vitamin B12 are frequently seen together as a "pattern". This pattern of malabsorption is strongly suggestive for gluten sensitivity. A clinical history of stress fracture, and osteoporosis at a young age (from calcium malabsorption) is strongly suggestive for gluten sensitivity. Enterolabs - Definitive Testing After finding the conventional blood antibody testing to be useless, we have switched to stool antibody testing with a home test kit from Enterolabs. This kit can be ordered by anyone, without a prescription, and the test performed at home. The stool sample is sent into the lab for analysis which includes immunological response to gluten, anti-gliadin antibody and genetic testing for gluten sensitivity. They offer additional panels which examine fat malabsorption (similar to the triglyreride test), and food sensitivity to dairy, egg, and soy. Dietary Trial Off-Gluten Another obvious test is a 6-week trial on a strict gluten-free diet, during which time symptoms are closely observed for improvement, indicating a gluten sensitivity. These patient should remain on a strict gluten-free diet. A 63 year old male with Recurring Cranial Nerve Palsies, Hypertransaminasemia, and Hashimotos ThyroiditisA pleasant 63 year old gentleman came to the office for a "wellness physical and some vitamins". A few years past, he had Bell's Palsy, a form of facial nerve paralysis, which had resolved. He also noticed intermittent loss of sensation involving the soles of his feet. On physical exam, he had a mild residual facial paralysis (Bell's Palsy), and a mild sensory polyneuropathy with loss of vibratory sense in the lower extremities. His lab studies showed mildly elevated liver enzymes which "had always been present over the years", and previous doctors have told him that it is "genetic", and not to worry about it. The patient also had elevated thyroid antibodies, with reduced thyroid function compatible with Hashimoto's thyroiditis. The patient was treated with thyroid hormone among other things, and did well over the next few years. However a few years later, he reported eye problems. He was unable to gaze laterally with his right eye. The opthalmologist made a diagnosis of Sixth Cranial Nerve palsy (abducens nerve to the lateral rectus eye muscle) with failure of lateral gaze. Extensive neurological workup with MRI scans was unremarkable, and his neurologist suggested a test for Lyme's Disease, which was done and found negative. Gluten and Neurological Disease The immunologic response to gluten may cross react with the nervous system, producing various neurological symptoms, such as cranial nerve palsy, and neuropathy. These may be present in the absence of any gastrointestinal symptoms. Neuropathies and psychiatric symptoms caused by consumption of wheat gluten have been reported in the medical literature.(5-7) Recurrent cranial nerve palsy has also been reported caused by ingestion of gluten. (1) Gluten Sensitivity Celiac Hashimoto's Connection Patients who have Hashimoto's thyroiditis have about 15 times greater chance of also having gluten sensitivity. One Dutch study published in 2007 showed 15% of Hashimoto's patients tested positive for gluten sensitivity or celiac disease.(2). Chronic Mild Elevation of Liver Enzymes Chronic mild elevation of liver enzymes may be a tip off of underlying gluten sensitivity.(3-4) These mild liver enzyme elevations will normalize 95% of the time by adhering to a strict gluten-free diet.(3) Treatment- Gluten Free DietThis patient ordered the Enterolabs test kit for gluten sensitivity which showed a markedly positive immunologic response to wheat gluten. After adhering to a strict gluten-free diet, the patient's symptoms of cranial nerve palsy and sensory neuropathy gradually resolved. In addition, the liver enzyme elevations normalized. A Young Patient with Systemic Lupus - Gluten Connection A 23 year old female college student with Lupus came to my office. She had been previously diagnosed with Systemic Lupus and started on Prednisone, a commonly used immune suppressive drug. She was recently hospitalized and treated with IV antibiotics for pneumonia. She was very ill, lost weight, and was amenorrheic, with menses stopping about 18 months ago. Her symptoms included joint pains, and buccal ulcerations. Physical examination showed a chronically ill, weak, cachectic young woman, with typical increased pigmentation of the palms and Lupus Butterfly Rash of the face (see left image). Above left image : Butterfly Facial Rash of Systemic Lupus Courtesy of Wikimedia Commons. This is caused by low adrenal output which stimulates increased pituitary ACTH which has Melanocyte stimulating properties. This patient needs adrenal hormones. Acetyl Co-A Deficiency in Lupus Lupus is an autoimmune disease, and blood testing shows circulating anti-nuclear antibodies as a main feature. Acetyl Co-A Deficiency in LupusMy previous article discussed the underlying defect in Lupus as an Acetyl Co-A Deficiency and how this produces adrenal insufficiency, with reduced hormone production. Adrenal insufficiency causes the pituitary to increase ACTH production which has melanocyte stimulating properties. The melanin pigment accounts for the increased skin pigmentation and facial rash of lupus (see above image). Vitamin B5, Pantothenic Acid is extremely beneficial for Lupus patients because B5 increases Acetyl-Co-A which helps the adrenals recover in their important job manufacturing adrenal hormones. My Lupus treatment program includes high dose Pantothenic Acid (300 mg three times a day of Vitamin B5), as well as direct adrenal hormones replacement with cortisol or prednisone. Over time, patients are slowly weaned off the prednisone and switched to low dose bioidentical hydro-cortisone (cortisol). Since other hormones levels are typically low in Lupus patients, we will commonly give a bioidentical hormone topical cream containing DHEA, Estradiol, Estriol (Bi-Est), Testosterone and Progesterone. Low vitamin D is frequently associated with autoimmune disease, correction is important. Her low Vitamin D levels were treated with Vitamin D3, 10,000 units per day. LDN for Autoimmune Diseases including Systemic LupusLow Dose Naltrexone is an FDA approved drug which has been used off label in a variety of auto-immune diseases such as multiple sclerosis, crohn's rheumatoid arthritis and systemic lupus, with considerable benefits for these patients. See my previous articles on LDN: LDN Part One and LDN Part Two. Lupus patients will frequently benefit from Low Dose Naltrexone Capsules 4.5 mg each evening before sleep. Gluten Free Diet Benefits Systemic Lupus PatientsMedical science considers Lupus to be an incurable disease, and relies on prednisone, a powerful immune suppressing drug to control symptoms. Prednisone is a synthetic form of hydro-cortisone, the main adrenal hormone. Systemc Lupus Cured With a Gluten Free Diet I was astounded to find a report by Jonathon Wright of 500 patients cured of Lupus with a gluten free diet. Jonathan Wright MD writes in a newsletter about how dietary exposure to wheat gluten may trigger autoimmune disease including systemic lupus. Here is an exerpt from "A Simple Solution to an Incurable Disease". (15): In 1989, my wife Holly and I visited the office of Dr. Christopher Reading in Dee Why, a suburb of Sydney, Australia. He showed us documentation of over 500 individuals who came to see him with a diagnosis of Systemic Lupus, a usually-thought-to-be incurable auto-immune disease. With hard work on their own and with Dr. Reading's treatment, these individuals eliminated all signs and symptoms of lupus as well as the patent and formerly patent medicines used to treat it. How did over 500 individuals eliminate all signs and symptoms of lupus – and all patent medicines given for it, too – over 20 years ago? Dr. Reading had them totally eliminate all gluten, all milk and dairy products, and often other foods to which they were found to be allergic.(15) Lupus is only one of a long list of auto-immune diseases triggered by Wheat Gluten Exposure. (15) Here is the complete list of auto-immune diseases triggered by gluten sensitivity: Type One Diabetes Hashimoto's thyroiditis Graves's disease Ulcerative Colitis Systemic Lupus Erythematosis (lupus) Vitiligo Addison's disease Sjogren's syndrome Pernicious anemia Scleroderma Chronic auto-immune hepatitis Dermatitis herpetiformis Polymyalgia rheumatica Celiac disease The patient was advised to adhere to a strict gluten-free diet, and eliminate dairy products as well. (8-16) She did well, and eventually tapered off the prednisone without recurrence of joint pain, and resumption of normal menses. How Many Cases of Gluten Sensitivity Are Missed by the Mainstream Medical System ? All of them. Articles with Related Interest: Wheat Gluten and Celiac Diease, Part One Gluten Sensitivity , Is Your Food Making You Sick? Part Two Minefield at the Grocery Store Fast Food in Hospitals, Selling Sickness in the Lobby