Thyroid Pills & Heart Disease - Dach

Thyroid Pills Prevent Heart Attacks by Jeffrey Dach MD

Thyroid Pills Prevent Heart Attacks by Jeffrey Dach MD

The Low Thyroid Condition and Heart Disease

In 1976 Broda Barnes was the first to connect low thyroid function with heart attacks and heart disease.  His book is called, Hypothyroidism The Unsuspected Illness by Broda Barnes, Click Here to read my Book Review..

Above Left Image: Photo of WP Thyroid Pills Bottle courtesy of RLC labs Natural thyroid pills

Discovering the Connection
How did Broda Barnes discover the connection between low thyroid and heart disease?  Barnes took summer vacations in Graz Austria every year to study the autopsy files.  Graz had a high prevalence of thyroid disorders, and anyone in Graz who died over the past 100 years required an autopsy to determine cause of death, as mandated by the authorities.  This rather large amount of autopsy data showed that low thyroid patients survived the usual childhood infectious diseases thanks to the invention of antibiotics, and years later develop heart disease.  Barnes also found that thyroid treatment was protective in preventing heart attacks, based on his own clinical experience.  Likewise for diabetes, Dr. Barnes found that adding thyroid medication was beneficial at preventing the onset of vascular disease in diabetics.  Again, blood tests are usually normal.
New research like the Hunt Study confirms that Broda Barnes was right all along, creating a paradigm shift in thyroid treatment, and constituting a frontal assault on the Institution of Medicine’s thyroid dogma.

The Hunt Study - Thyroid Function and  Heart Disease
 
TSH is short for thyroid stimulating hormone, made by the pituitary gland.  TSH actually stimulates the thyroid gland to make more thyroid hormone, and can therefore be used as a barometer of thyroid function.  If thyroid function is low, the pituitary sends out more TSH to stimulate the thyroid to make more thyroid hormone.  
Mainstream Medicine regards the TSH as the single most important test for determining thyroid function. High TSH means low thyroid function, and a Low TSH means normal or high thyroid function.


What Did The Hunt Study Find?
The Hunt Study from the April 2008 Archives of Internal Medicine examined mortality from coronary heart disease (CHD) and TSH level.  The authors conclude,
“The results indicate that relatively low but clinically normal thyroid function may increase the risk of fatal CHD.”
Above Image: Thyroid Gland makes thyroid hormone.

The Hunt Study measured thyroid function with the TSH test in 17,000 women and 8,000 men with no known thyroid disease or heart disease. All patients had “normal TSH” levels meaning the TSH values were in the lab reference range of 0.5 to 3.5.   The women were stratified into three groups, lower TSH, intermediate and upper TSH levels, and mortality from heart disease was recorded over an 8 year observation period.

 (see chart below).
70% Increase in Heart Disease Mortality for TSH in Upper Normal Range
The Hunt study found that group with the higher TSH had a 70% increased mortality from heart disease compared to the lower TSH group.  Remember all these TSH vales were in the normal lab range. See chart below for results of the Hunt Study:

Left Image: Heart with Occluded Coronary Artery and Infarction at the apex, courtesy of wikimedia commons.

Results of the Hunt Study:

	TSH	Death from Heart Disease
Group 1	0.50-1.4	baseline risk
Group 2	1.5-2.4	40% higher than baseline
Group 3	2.5-3.5	70% higher than baseline

This Finding is Earthshaking !!

This means that merely by taking natural thyroid pills to reduce TSH to the low end of “normal” (0.5), one can reduce death from cardiovascular disease by 70 percent.  This mortality benefit is mind boggling and far exceeds any drug intervention available.

Thyroid Hormone Also Improves LDL Lipo-Proteins
Another report from the Hunt Study published in 2007 showed that LDL cholesterol was linearly associated with TSH level. (see chart below).
Below Chart showing LDL cholesterol (non-HDL) goes up as TSH goes up.  Note that TSH always remains within in the lab “normal range” (0.5-3.5).
Above chart shows linear increase in LDL cholesterol as TSH increases. Image Courtesy of Hunt Study European Journal of Endocrinology, Vol 156, Issue 2, 181-186, 2007
The Conclusion is Clear:
The best way to normalize lipoprotein profile and reduce mortality from heart disease is to reduce TSH to the lower end of the normal range with thyroid medication.  A TSH in the upper end of the normal range is associated with increased cardiovascular mortality and elevations in LDL lipo-protein measurements.  A TSH at the lower end of the normal range is associated with protection from heart disease.

Statin Drugs or Thyroid to Prevent Heart Disease in Women?

My previous article discussed the issue of statin drugs for women.  Decades of published statin drug studies show that statin drugs simply don’t work for women, and don’t reduce mortality from heart disease in women.  But on the other hand, the HUNT study shows that TSH levels in the lower normal range provide a 70% reduction in heart disease mortality for women.  This can be accomplished safely with inexpensive thyroid medication under a physician’s supervision.  So for women concerned about preventing heart disease, this is good news, pointing out a natural alternative to statin drugs that works much better.

Natural Thyroid is Better
Rather than Synthroid, we prefer to use natural thyroid which is a dessicated porcine thyroid gland from RLC Labs.  The reason for this is that we have seen better clinical results with the natural thyroid preparations compared to synthroid.
Above image: thyroid hormone Courtesy Wikimedia .
Natural Thyroid is Safer, but can Cause Adverse Effects of Palpitations
Although natural thyroid is safe, there is always the possibility of adverse effects from thyroid excess, defined as too much thyroid medication.  The first sign of thyroid excess is usually a rapid heart rate at rest or perhaps palpitations (at rest).  We spend about five minutes at the office going over this adverse effect before starting patients on thyroid medication.  Usually patients will notice the heart rate going up or the heart beat sounding louder than usual as the first sign that can be easily recognized.  Once recognized, the patient is instructed to stop the thyroid medication, and symptoms usually resolve within 6 hours (for natural thyroid).  It is perfectly safe to stop the thyroid medication at any time, as there will be no acute changes, merely a gradual reversion to the original state that existed before starting the thyroid pills.

Some patients are very sensitive to thyroid medication and will have thyroid excess symptoms such as rapid heart rate and palpitations from small amounts of thyroid medication.  These are usually the elderly with underlying heart disease and/or magnesium deficiency, and we usually avoid giving thyroid medication to these patients.  We also liberally supplement everyone with magnesium if their RBC magnesium levels are low.

About 5 per cent of our patients initially started on thyroid will notice symptoms of thyroid excess with a rapid heart rate, and they will stop the medication for a day or two and restart at a lower dosage with no problem.  This is more common in Hashimoto’s patients whose own production of thyroid hormones may fluctuate from month to month.  Patients with magnesium deficiency or adrenal fatigue with low cortisol output on salivary testing will also tend to be more sensitive to small amounts of thyroid medication, so caution is advised in these groups as well.

Thyroid Excess Can Rarely Cause Atrial Fibrillation
Upper Image: EKG strip with Red Arrow shows atrial fibrillation, no recognizable P-wave.  Lower Image: EKG strip with normal rhythm with recognizable P wave (blue arrow). Courtesy of Wikimedia Commons.
So far, we have not had a patient go into atrial fibrillation from thyroid medication, probably because we spend so much time with each patient discussing the symptoms of thyroid excess, and the importance of stopping the thyroid medication if these symptoms are noted.

Mainstream Docs Don’t Have Time To Discuss Adverse Effects
One of the reasons the mainstream conventional docs will give only a minuscule amount of synthroid to the low thyroid patient is that they simply don’t have the time to discuss thyroid excess and can’t afford an adverse event which is more likely if the patient doesn’t have a clue about what to watch out for.  In addition, mainstream medical docs don’t recognize the syndrome of adrenal fatigue or magnesium deficiency , so they can run into problems with thyroid excess without understanding why, and this also makes them very cautious, tending to under treat.
Left Image: Doctor thinking about thyroid dosage.
In patients with underlying heart disease who are prone to cardiac arrhythmias, thyroid excess can cause atrial fibrillation with characteristic EKG appearance.  Atrial fibrillation can be a problem, because if it becomes chronic and doesn’t go away on its own, the cardiologist will try a maneuver called cardioversion, the application of an electrical shock to restart a normal cardiac rhythm.  Or, if that doesn’t work, prescribe blood thinners, all of which is not without risk.  So it is better to avoid atrial fibrillation altogether by simply stopping the thyroid pills whenever symptoms of rapid heart rate or palpitations are noted while at rest.  Exercise induced rapid heart rate, of course, doesn’t count since that is normal cardiovascular response to exercise.

How To Design A Better Hunt Study
How would I design an even better Hunt Study? That’s easy. Include another group of patients with TSH levels above and below the study group, namely, below 0.5, and above 3.5.  I would also include data on annual CAT coronary calcium scores.  I would predict that the lower TSH group (below 0.5) would have even less heart disease than the higher TSH group, and that coronary calcium score, indicating plaque burden, would go up as TSH went up.

Read More About the Hunt Study from William Davis MD and Jacob Teitelbaum MD:
Is normal TSH too high?   by William Davis MD
Low Thyroid (Even if Tests are Normal) is a Major Cause of Heart Attacks by Jacob Teitelbaum, MD.

Credit and Thanks is given to William Davis MD and Jacob Teitelbaum MD for bringing the Hunt Study to my attention.

For more information on thyroid and heart disease, read my previous articles:
Saving Time Russert and George Carlin
Healthy Men Should Not Take Statin Drugs
Heart Disease Vitamin C and Linus Pauling
Getting Off Statin Drug Stories
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
Cholesterol Lowering Statin Drugs for Women Just Say No

Jeffrey Dach MD
7450 Griffin Road Suite 190
Davie Florida 33314
954-792-4663
www.jeffreydach.com
www.drdach.com
www.naturalmedicine101.com
www.truemedmd.com
(c) 20013 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.
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Links and References:
http://archinte.ama-assn.org/cgi/content/abstract/168/8/855
Arch Intern Med. 2008;168(8):855-860. Thyrotropin Levels and Risk of Fatal Coronary Heart Disease,
The HUNT Study
Arch Intern Med. 2008;168(8):855-860. Background  Recent studies suggest that relatively low thyroid function within the clinical reference range is positively associated with risk factors for coronary heart disease (CHD), but the association with CHD mortality is not resolved.
Methods  In a Norwegian population-based cohort study, we prospectively studied the association between thyrotropin levels and fatal CHD in 17 311 women and 8002 men without known thyroid or cardiovascular disease or diabetes mellitus at baseline.
Results  During median follow-up of 8.3 years, 228 women and 182 men died of CHD. Of these, 192 women and 164 men had thyrotropin levels within the clinical reference range of 0.50 to 3.5 mIU/L. Overall, thyrotropin levels within the reference range were positively associated with CHD mortality (P for trend = .01); the trend was statistically significant in women (P for trend = .005) but not in men. Compared with women in the lower part of the reference range (thyrotropin level, 0.50-1.4 mIU/L), the hazard ratios for coronary death were 1.41 (95% confidence interval [CI], 1.02-1.96) and 1.69 (95% CI, 1.14-2.52) for women in the intermediate (thyrotropin level, 1.5-2.4 mIU/L) and higher (thyrotropin level, 2.5-3.5 mIU/L) categories, respectively.
Conclusions  Thyrotropin levels within the reference range were positively and linearly associated with CHD mortality in women. The results indicate that relatively low but clinically normal thyroid function may increase the risk of fatal CHD.
Author Affiliations: Department of Public Health, Faculty of Medicine (Drs Åsvold and Vatten), and Human Movement Science Programme (Dr Nilsen), Norwegian University of Science and Technology, Trondheim, Norway; St Olavs Hospital, Trondheim University Hospital, Trondheim (Dr Åsvold); Department of Medical Biochemistry, Rikshospitalet-Radiumhospitalet Medical Center, Oslo, Norway (Dr Bjøro); and Department of Social Medicine, University of Bristol, Bristol, England (Dr Gunnell).
http://www.eje-online.org/cgi/content/full/156/2/181
European Journal of Endocrinology, Vol 156, Issue 2, 181-186, 2007  CLINICAL STUDY  The association between TSH within the reference range and serum lipid concentrations in a population-based study. The HUNT Study
Bjørn O Åsvold1,2, Lars J Vatten1, Tom I L Nilsen1 and Trine Bjøro3  1 Department of Public Health, Faculty of Medicine, Norwegian University of Science and Technology, N-7489 Trondheim, Norway, 2 St Olavs Hospital, Trondheim University Hospital, Trondheim, Norway and 3 Department of Medical Biochemistry, Rikshospitalet-Radiumhospitalet Medical Center, Oslo, Norway (Correspondence should be addressed to L J Vatten
Jacob Teitelbaum MD
http://www.endfatigue.com/health_articles_f-n/Heart-low_thyroid_major_cause_heart_attacks.html
Jacob Teitelbaum, MD. Low Thyroid (Even if Tests are Normal) is a Major Cause of Heart Attacks,
William Davis MD
http://heartscanblog.blogspot.com/2008/06/is-normal-tsh-too-high.html
William Davis MD, begin quote:”Is normal TSH too high? There’s no doubt that low thyroid function results in fatigue, weight gain, hair loss, along with rises in LDL cholesterol and other fractions of lipids. It can also result in increasing Lp(a), diabetes, and accelerated heart disease, even heart failure.  But how do we distinguish “normal” thryoid function from “low” thyroid function? This has proven a surprisingly knotty question that has generated a great deal of controversy.  Thyroid stimulating hormone, or TSH, is now the most commonly used index of the adequacy of thyroid gland function, having replaced a number of older measures. TSH is a pituitary gland hormone that goes up when the pituitary senses insufficient thyroid hormone, and a compensatory increase of thyroid hormone is triggered; if the pituitary senses adequate or excessive thyroid hormone, it is triggered to decrease release of TSH. Thus, TSH participates in a so-called “negative feedback loop:” If the thyroid is active, pituitary TSH is suppressed; if thyroid activity is low, pituitary TSH increases.  An active source of debate over the past 10 years has been what a normal TSH level is. In clinical practice, a TSH in the range of 0.4-5.0 mIU/L is considered normal. (Lower TSH is hyperthyroidism, or overactive thyroid; high TSH is hypothyroidism, or underactive thyroid.)  The data from a very fascinating and substantial observation called the HUNT Study, however, is likely to change these commonly-held thyroid “rules.” endquote WIlliam Davis MD
International Hormone Societyhttp://www.intlhormonesociety.org/ref_cons/
Ref_cons_9_thryoid_treatment_of_clinically_hypothyroid_biochemically_hypothyroid_patients.pdf
International Hormone Society, references, clinically hypothyroid , lab euthyrroid
Other Blogs:
http://thyroid.blogspot.com/
Thyroid Blog by Dr. Richard B. Guttler M.D., F.A.C.E.
Location: Santa Monica, California, United States
http://www.stopthethyroidmadness.com/
Stop the Thyroid Madness Blog – a patient tries in vain to convince soctors to switch from Synthroid to Armour
http://thyroid.about.com/
MAry Shomon thyroid blog
Disclaimer click here: http://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.  Finally, the material produced by myself may be reproduced for personal use, provided that appropriate credit is given
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(c) 2007-2013 Jeffrey Dach MD All Rights reserved. This article may be copied or reproduced on the internet provided a link and credit is given.

 

What Causes Elevated LDL Particle Number? - Kresser

What Causes Elevated LDL Particle Number?

By Chris Kresser on May 3, 2013

 

In the last article in this series, I explained that LDL particle number (LDL-P) is a much more accurate predictor of cardiovascular disease risk than either LDL or total cholesterol. In this article, I’m going to briefly outline the five primary causes of elevated LDL-P.

Conventional medicine is primarily focused on suppressing symptoms. If your blood pressure is high, you take a medication to lower it. If your blood sugar is high, you take a medication to lower it. If your cholesterol is high, you take a medication to lower it. In most cases there is rarely any investigation into why these markers are high in the first place, with the possible exception of some basic (but often incorrect) counseling on diet and exercise.

On the other hand, functional medicine—which is what I practice—focuses on treating the underlying cause of health problems instead of just suppressing symptoms. If your blood sugar, blood pressure or cholesterol are high, the first question a functional medicine practitioner will ask is “why?” If we can identify the root cause of the problem, and address it at that level, medication is often unnecessary.

To use a simple analogy, if you have weeds in your garden, what happens if you just cut the weeds from the top? They grow right back—and sometimes faster than before! If you really want to get rid of them once and for all, you have to pull them up by their roots.

With this in mind, let’s look at some of the potential causes of elevated LDL particle number. If your LDL-P is high, it makes sense to test for and treat any of the conditions below (with the exception of the last, which is genetic and thus can’t be treated) before—or at least along with—taking pharmaceutical drugs.

Insulin resistance and metabolic syndrome

LDL particles don’t just carry cholesterol; they also carry triglycerides, fat-soluble vitamins and antioxidants. You can think of LDL as a taxi service that delivers important nutrients to the cells and tissues of the body.

As you might expect, there’s a limit to how much “stuff” that each LDL particle can carry. Each LDL particle has a certain number of cholesterol molecules and a certain number of triglycerides. As the number of triglycerides increases, the amount of cholesterol it can carry decreases, and the liver will have to make more LDL particles to carry a given amount of cholesterol around the body. This person will end up with a higher number of LDL particles.

Consider two hypothetical people. Both have an LDL cholesterol level of 130 mg/dL, but one has high triglycerides and the other has low triglycerides. The one with the high triglyceride level will need more LDL particles to transport that same amount of cholesterol around the body than the one with a low triglyceride level.

Numerous studies have found an association between increased LDL particle number, and metabolic syndrome. One study measured ApoB, a marker for LDL particle number, in a group of 1,400 young Finns with no established disease. The participants with the highest LDL particle number were 2.8 times more likely to have metabolic syndrome than those with the lowest levels of LDL-P. (1) A much larger study of over 300,000 men also found a strong association between LDL-P and metabolic syndrome and its components (i.e. insulin resistance, abdominal obesity, high blood pressure, etc.). (2)

Poor thyroid function

Poor thyroid function is another potential cause of elevated particle number. Thyroid hormone has multiple effects on the regulation of lipid production, absorption, and metabolism. It stimulates the expression of HMG-CoA reductase, which is an enzyme in the liver involved in the production of cholesterol. (As a side note, one way that statins work is by inhibiting the HMG-CoA reductase enzyme.) Thyroid hormone also increases the expression of LDL receptors on the surface of cells in the liver and in other tissues. In hypothyroidism, the number of receptors for LDL on cells will be decreased. This leads to reduced clearance of LDL from the blood and thus higher LDL levels. Hypothyroidism may also lead to higher cholesterol by acting on Niemann-Pick C1-like 1 protein, which plays a critical role in the intestinal absorption of cholesterol. (3, 4)

Studies show that LDL particle number is higher even in subclinical hypothyroidism (high TSH with normal T4 and T3), and that LDL particle number will decrease after treatment with thyroid hormone. (5)

Infections

Another cause of high cholesterol profile is infection. Multiple studies have shown associations between bacterial infections like Chlamydia pneumoniae and H. pylori, which is the bacterium causes duodenal ulcers, and viral infections like herpes and cytomegalovirus and elevated lipids. (6) For example, H. pylori leads to elevated levels of total cholesterol, LDL cholesterol, lipoprotein (a), ApoB or LDL particle number, and triglyceride concentrations as well as decreased levels of HDL. (7)

Several mechanisms have been proposed to explain the association between infections and elevated blood lipids. Some evidence suggests that viral and bacterial infections directly alter the lipid metabolism of infected cells, and other evidence suggests that lipids increase as a result of the body’s attempt to fight off infection. Other evidence suggests that LDL has antimicrobial properties and is directly involved in inactivating microbial pathogens. This has been confirmed by studies showing that mice with defective LDL receptors—and thus very high levels of LDL—are protected against infection by gram-negative bacteria like H. pylori. (8)

Leaky gut

One of the primary functions of the intestinal barrier is to make sure that stuff that belongs in the gut stays in the gut. When this barrier fails, endotoxins such as lipopolysaccharide (LPS) produced by certain species of gut bacteria can enter the bloodstream and provoke an immune response. Part of that immune response involves LDL particles, which as I mentioned above, have an anti-microbial effect. A protein called LPS-binding protein, which circulates with LDL particles, has been shown to reduce the toxic properties of LPS by directly binding to it and removing it from the circulation. (9) Studies have also shown significant increases in LPS-binding protein (and thus LDL particles) in cases of endotoxemia—a condition caused by large amounts of circulating endotoxins. (10)

Though more research is needed in this area, the studies above suggest that a leaky gut could increase the level of LPS and other endotoxins in the blood, and thus increase LDL particle number as a result. I have seen this in my practice. I recently had a patient with high LDL-P and no other risk factors. I tested his gut and discovered H. pylori and small intestine bacterial overgrowth (SIBO). After treating his gut, his LDL-P came down to normal levels.

Genetics

The final cause of elevated LDL-P is genetics. Familial hypercholesterolemia, or FH, involves a mutation of a gene that codes for the LDL receptor or the gene that codes for apolipoprotein B (ApoB). The LDL receptor sits on the outside of cells; the LDL particle has to attach to the LDL receptor in order to deliver the nutrients it’s carrying and be removed from the circulation. ApoB is the part of the LDL particle that binds to the receptor. If we use a door lock as an analogy, apolipoprotein B would be the key, and the LDL receptor is the lock. They both need to be working properly for LDL to deliver its cargo and to be removed from the bloodstream.

Homozygous carriers of FH have two copies of the mutated gene. This condition is very rare. It affects approximately 1 in a million people. And people that are homozygous for this mutation have extremely high total cholesterol levels, often as high as 1000 mg/dL. And unfortunately they usually die from severe atherosclerosis and heart disease before the age of 25.

Heterozygous carriers, however, only have a single copy of the mutated gene, and the other copy is functioning normally. This is much more common. The prevalence is between 1 in 300 to 1 in 500 people, depending on which study you look at. These heterozygous carriers of FH have total cholesterol levels that often range between 350 and 550 mg/dL, along with very high LDL particle number. They have about three times higher risk of death from heart disease than people without FH if it goes untreated.

It’s important to note that people with FH have primarily large, buoyant LDL particles, and yet are still at much higher risk for cardiovascular disease. While it’s true that small, dense, oxidized LDL particles are more likely to cause atherosclerosis, large, buoyant particles can also be harmful when their concentration is high enough. This is one reason why LDL particle number is a superior marker to LDL particle size.

In the next article in this series, I will debunk the myth that statins extend lifespan in healthy people with no pre-existing heart disease.
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Read the complete article here.

Why Doesn’t My Doctor Know All of This?

The following is not specifically about heart disease or cholesterol as is most of this blog content. But it does apply. Thyroid dysfunction can be tied in with heart disease if in no other way than making certain lipid abnormalities difficult or nearly impossible to normalize in the quest to reduce plaque growth. In short, I believe this is a valuable discussion of an important issue applicable to CAD.

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Why Doesn’t My Endocrinologist Know All of This?

A question often raised by patients is: “Why doesn’t my physician know about the inaccuracies and limitations of standard thyroid tests?” The reason is that the overwhelming majority of physicians (endocrinologists, internists, family practitioners, rheumatologists, etc.) do not read medical journals. When asked, most doctors will claim that they routinely read medical journals, but this has been shown not to be the case. Many reasons exist, but it comes down to the fact that doctors do not have the time — they are too busy running their practices. The overwhelming majority of physicians rely on what they have learned in medical school and on consensus statements by medical societies, such as the Endocrine Society, the American Association of Clinical Endocrinologists or the American Thyroid Association, to direct treatment decisions.

Historically, relying on a consensus statement to treat or not to treat a particular patient has been shown to result in poor care and, as such, society consensus statements and practice guidelines are considered to be worst level of evidence in support of a particular therapy or treatment. A number of organizations, including the World Health Organization and others, have ranked the strength and accuracy of various types of evidence used in the medical decision process. In all scoring systems, the highest strength of evidence is randomized control trials and meta-analyses, with lower scores for other types of evidence. All grading systems place consensus statements and expert opinion by respected authorities (societies) as the poorest level of evidence, because historically they have failed to adopt new concepts and treatments based on new knowledge or new-found understanding demonstrated in the medical literature (1-6).

For instance, a recent study published in the 2009 Journal of American Medical Association studied the evidence supporting the practice guidelines and consensus statements published by the American College of Cardiology and the American Heart Association. It was found that only 11% of the recommendations, practice guidelines and consensus statements were based on quality evidence and over half were based on poor quality evidence that was little more than the panel’s opinion. The review also found that even the strongest (Class 1) recommendations, which are considered medical dogma, cited as a legal standards and often go unquestioned as medical fact, were only supported by high quality evidence 19% of the time and not revised based on new evidence (6).

Similarly, the Endocrine Society, the American Association of Clinical Endocrinologists and the American Thyroid Association also have a long history of guidelines and recommendations that are not supported by the medical literature and fail to adjust or abandon recommendations when new understanding and knowledge contradicts their recommendations. A case in point is the recommendation by these societies that a normal TSH adequately rules out thyroid dysfunction, despite massive amounts of literature that demonstrate this not to be the case (see Diagnosis of Hypothyroidism) or that T4 only replacement is adequate for most patients. A doctor who simply follows outdated society treatment guidelines that relies on a simple laboratory test and ignores the clinical aspects of a patient is not practicing evidence-based medicine. (1-7). Such doctors may be adequate as lab technicians, but as doctors and clinicians they fall short (1-7). This method of practice is consistently rebuked as improper and poor medicine, but has become the standard used by a large percentage of endocrinologists and physicians who feel medicine can be related to simply reading “normal” or “abnormal” in a laboratory column.

Discussing the lack of scientific basis of most medical society’s consensus statements and treatment guidelines in Internal Medicine News, Dr. Diana Petritti, states, “Expert opinion and consensus statements can be quite misleading when used as the basis for a practice. Expert opinions imply that there is something that the experts know that clinician doesn’t know. I don’t think it’s always appreciated that it’s only opinion. There is a tendency to make guidelines and recommendations seem authoritative. I believe that physicians think that there is a great deal more behind authoritative recommendations than there might be when you lift the lid of the box and see what’s underneath(8).”

There has been significant concern by health care organizations and medical experts that physicians are placing too much reliance on consensus statements and failing to learn of new information presented in medical journals. Thus, they lack the ability to translate this new information into treatments for their patients. The concern is that doctors fail to practice evidence-based medicine, erroneously relying on what they have previously been taught and on “expert” societies instead of changing treatment philosophies based on new information as it becomes available. This is especially true for endocrinological conditions, where physicians are very resistant to changing old concepts of diagnosis and treatment — despite overwhelming evidence to the contrary — because it is not what they were taught in medical school and endocrinology residency.

This concern is particularly clear in an article published in the New England Journal of Medicine entitled “Clinical Research to Clinical Practice: Lost in Translation” (9). The article was written by Claude Lenfant, M.D., Director of National Heart, Lung and Blood Institute, and it is well supported. He states that there is great concern that doctors continue to rely on what they learned 20 years before and are uninformed about scientific findings. According to Dr. Lenfant, medical researchers, along with public officials and political leaders, are increasingly concerned about physicians’ inability to translate research findings in their medical practice to benefit their patients. He says that very few physicians learn about new discoveries from reading medical journals or by attending scientific conferences; thus, they lack the ability to translate new knowledge in the field into enhanced treatments for their patients. He states that a review of past medical discoveries reveals how excruciatingly slow the medical establishment is to adopt novel concepts, noting that even simple methods to improve medical quality are often met with fierce resistance. “Given the ever-growing sophistication of our scientific knowledge and the additional new discoveries that are likely in the future, many of us harbor an uneasy, but quite realistic suspicion that this gap between what we know about disease and what we do to prevent and treat them will become even wider. And it is not just recent research results that are not finding their way into clinical practice; there is plenty of evidence that ‘old’ research outcome have been lost in translation as well (1).”

Dr. Lenfant discusses the fact that the proper practice of medicine involves the combination of medical knowledge, intuition and judgment and that physicians’ knowledge is lacking because they don’t keep up with the medical literature. He states that there is often a difference of opinion among physicians and reviewing entities, but that judgment and knowledge of the research pertaining to the patient’s condition is central to the responsible practice of medicine. “Enormous amounts of new knowledge are barreling down the information highway, but they are not arriving at the doorsteps of our patients. (9).”

These thoughts are echoed by physicians who have researched this issue as well, such as William Shankle, M.D., Professor, University of California, Irvine. He states, “Most doctors are practicing 10 to 20 years behind the available medical literature and continue to practice what they learned in medical school….There is a breakdown in the transfer of information from the research to the overwhelming majority of practicing physicians. Doctors do not seek to implement new treatments that are supported in the literature or change treatments that are not (10).”

This view is echoed by the Dean of Stanford University School of Medicine who states that in the absence of translational medicine the delivery of medical care would remain stagnant and uninformed by the tremendous progress taking place in science and medicine (11).

This concern has also received significant publicity in the mainstream media. An example is an article by Sidney Smith, M.D., former president of the American Heart Association, published in 2003 in the Wall Street Journal entitled Too Many Patients Never Reap the Benefits of Great Research. Dr. Smith is very critical of physicians for not seeking out available information and applying that information to their patients, arguing that doctors feel the best medicine is what they’ve been doing and thinking for years. They discount new research, Dr. Smith says, because it is not what they have been taught or practiced, and they refuse to admit that what they have been doing or thinking for many years is not the best medicine. He states, “A large part of the problem is the real resistance of physicians…; many of these independent-minded souls don’t like being told that science knows best, and the way they’ve always done things is second-rate (12).” The National Center for Policy Analysis also expresses concern for the lack of ability of physicians to translate medical therapies into practice (13).

A review published in The Annals of Internal Medicine found that there is clearly a problem of physicians not seeking to advance their knowledge by reviewing the current literature, believing proper care is what they learned in medical school or residency and not basing their treatments on the most current research. The review found that the longer a physician is in practice, the more inappropriate and substandard the care (14). Thus, it is not a surprise that the scientific evidence as expressed in the literature is often opposite to what is continually repeated as dogma by most physicians and those considered to be “experts.”

Another example is a study published in the Journal of the American Medical Informatics Association (15). In reviewing the study, the National Institute of Medicine reports that there is an unacceptable lag between the discovery of new treatment modalities and their acceptance into routine care: “The lag between the discovery of more effective forms of treatment and their incorporation into routine patient care averages 17 years.” (16) In response to this unacceptable lag, the Business and Professions Code passed an amendment relating to the healing arts. This amendment — CA Assembly Bill 592; An Act to Amend Section 2234.1 of the Business and Professions Code — states: Since the National Institute of Medicine has reported that it can take up to 17 years for a new best practice to reach the average physician and surgeon, it is prudent to give attention to new developments not only in general medical care but in the actual treatment of specific diseases, particularly those that are not yet broadly recognized [such as the concept of tissue hypothyroidism, chronic fatigue syndrome and fibromyalgia] (17).

The Principals of Medical Ethics adopted by the American Medical Association in 1980 states that a physician shall continue to study, apply, and advance scientific knowledge, make relevant information available to patients, colleagues, and the public (18). This has, unfortunately, been replaced with a goal of providing merely “adequate” care. The current insurance reimbursement system in the United States fosters this thinking, as the worst physicians are financially rewarded by insurance companies. While it is true that the best physicians are continually fighting to provide cutting edge treatments and superior care that the insurance companies deem not medically necessary, even these physicians eventually get worn down and are forced to capitulate to the current system that promotes substandard care.

This was clearly demonstrated in a study published in the March 2006 edition of The New England Journal of Medicine entitled “Who is at Greater Risk for Receiving Poor-Quality Health Care.” The study found that the majority of individuals received substandard, poor-quality care, and that there was no significant difference among different income levels or whether or not the individual was covered by insurance. It used to be the case that only those in low socioeconomic classes without insurance received poor-quality care. But insurance company restrictions on treatments and diagnostic procedures have made the same poor care afforded to those of low socioeconomic status the new standard-of-care for society at large (19). An example of this is a physician’s failing to spend the time to adequately assess a potential hypothyroid patient and instead simply does a TSH test.

Most physicians will satisfy their required amount of continuing medical education (CME) by going to a conference a year, usually at a highly desirable location that has skiing, golf, boating, etc. Physicians are rarely monitored as to whether or not they actually showed up for the lectures or went skiing instead. One must also understand that the majority of conferences organized by medical societies are in fact sponsored by pharmaceutical companies. These payments by pharmaceutical companies are called unrestricted grants, so that the society has free reign to do what they want with the money and thus can claim there is no influence of lecture content by the companies. The problem, however, is that if the society wants to continue getting these “unrestricted” grants, they must think twice about providing content that the sponsoring pharmaceutical company might disapprove of. Consequently, ground breaking research that goes against the status quo and does not support the drug industry receives little attention.

Evidence-based medicine involves the synthesis of all available data when comparing therapeutic options for patients. Evidence-based medicine does not mean that data should be ignored until a randomized control trial of a particular size and duration is completed. A physician who tries to avoid the need of being a physician and is fine with just being a technician or health care provider will adamantly defend the “one-size fits all” method of diagnosis and treatment. But the best doctors who truly practice evidence-based medicine and not merely the perception of such will not rely on consensus statements to best provide their patients. Instead of relying on old dogma, the best physicians will seek out and translate both basic science results and clinical outcomes to decide on the safest, most efficacious treatment for their patients. Further, the best physicians will continually assess the current available data to decide which therapies are likely to carry the greatest benefits for patients and involve the lowest risks.

http://nahypothyroidism.org/why-doesn%E2%80%99t-my-doctor-know-all-of-this/