Updated Guidelines: Screening for Thyroid Dysfunction
USPSTF updates recommendations from 2004 guide
April 7, 2015
The U.S. Preventive Services Task Force’s updated guidelines for thyroid dysfunction screening found insufficient evidence for universal thyroid-stimulating hormone (TSH) level testing in non-pregnant, asymptomatic adults. There is currently no consensus on the correct TSH cutoff to define sub-clinical hypo- or hyperthyroidism, and so normal is defined as values that encompass approximately 95% of the population, leaving about 5% of the population with abnormal values. In addition, among the elderly, 12% of the population has a TSH above 4.5, but does not have symptoms of thyroid disease, and there is day-to-day variation in the TSH result of up to 40% to 50%. Finally, there is no evidence that screening for TSH in asymptomatic non-pregnant adults helps people by better or earlier treatment with medicines.
Citation: LeFevre ML; U.S. Preventive Services Task Force. Screening for thyroid dysfunction: U.S. Preventive Services Task Force Recommendation. Ann Intern Med. 2015. doi: 10.7326/P15-9017.
Commentary: Levothyroxine is the most commonly prescribed medication in the United States, and sub-clinical hypothyroidism, usually defined as a TSH from 5-10 mIU/L in a person who does not have symptoms, affects almost 5% of the population, with women affected more than men. About one-third of people who have sub-clinical hypothyroidism detected on exam will eventually revert back to a euthyroid state over time. The updated recommendation is that there is not enough evidence to recommend screening. This is because it is not clear that early detection—finding hypothyroidism before it clinically manifests—yields a better outcome than waiting until a patient has symptoms. If a patient has symptoms, then by all means we should do a TSH, but there is no evidence to support its use in routine screening of non-pregnant adults. –Neil Skolnik, MD
Hypothyroidism (under active thyroid) is the most common thyroid disorder and usually strikes after age 40. It is more common on women than in men, and affects 6% to 10% of women over the age of 65. The signs and symptoms of an under-active thyroid are:
slow heart rate
Hypothyroidism is diagnosed through a simple blood test. Synthetic thyroxine is a safe, effective and low-cost hormone replacement therapy. Dosing must be carefully monitored and the therapy must continue for life.
Synthetic thyroxine is one of the top three most commonly prescribed drugs in North America.
The most common cause of Hypothyroidism is an autoimmune condition called Hashimoto’s Thyroiditis in which antibodies and white blood cells attack the thyroid.
(Information based on the Thyroid Foundation of Canada Thyrobulletin, Summer 1998, Vol 19, No. 2)
You can use this checklist to bring to your doctor to help aid in getting a proper diagnosis of hypothyroidism, or as background information in your discussions regarding fine-tuning your dosage so you are at the optimal TSH level for your own level of wellness.
My risk factors for hypothyroidism include:
____ I have a family history of thyroid disease
____ I have had my thyroid “monitored” in the past to watch for changes
____ I had a previous diagnosis of goiters/nodules
____ I currently have a goiter
____ I was treated for hypothyroidism in the past
____ I had post-partum thyroiditis in the past
____ I had a temporary thyroiditis in the past
____ I have another autoimmune disease
____ I have had a baby in the past nine months
____ I have a history of miscarriage
____ I have had part/all of my thyroid removed due to cancer
____ I have had part/all of my thyroid removed due to nodules
____ I have had part/all of my thyroid removed due to Graves’ Disease/hyperthyroidism I have had radioactive iodine due to Graves’ Disease/hyperthyroidism
____ I have had anti-thyroid drugs due to Graves’ Disease/hyperthyroidism
I have the following symptoms of hypothyroidism, as detailed by the Merck Manual, the American Association of Clinical Endocrinologists, and the Thyroid Foundation of America
____ I am gaining weight inappropriately
____ I’m unable to lose weight with diet/exercise
____ I am constipated, sometimes severely
____ I have hypothermia/low body temperature (I feel cold when others feel hot, I need extra sweaters, etc.)
____ I feel fatigued, exhausted
____ Feeling run down, sluggish, lethargic
____ My hair is coarse and dry, breaking, brittle, falling out
____ My skin is coarse, dry, scaly, and thick
____ I have a hoarse or gravely voice
____ I have puffiness and swelling around the eyes and face
____ I have pains, aches in joints, hands and feet
____ I have developed carpal-tunnel syndrome, or it’s getting worse
____ I am having irregular menstrual cycles (longer, or heavier, or more frequent)
____ I am having trouble conceiving a baby
____ I feel depressed
____ I feel restless
____ My moods change easily
____ I have feelings of worthlessness
____ I have difficulty concentrating
____ I have more feelings of sadness
____ I seem to be losing interest in normal daily activities
____ I’m more forgetful lately
I also have the following additional symptoms, which have been reported more frequently in people with hypothyroidism:
____ My hair is falling out
____ I can’t seem to remember things
____ I have no sex drive
____ I am getting more frequent infections, that last longer
____ I’m snoring more lately
____ I have/may have sleep apnea
____ I feel shortness of breath and tightness in the chest
____ I feel the need to yawn to get oxygen
____ My eyes feel gritty and dry
____ My eyes feel sensitive to light
____ My eyes get jumpy/tics in eyes, which makes me dizzy/vertigo and have headaches
____ I have strange feelings in neck or throat
____ I have tinnitus (ringing in ears)
____ I get recurrent sinus infections
____ I have vertigo
____ I feel some lightheadedness
____ I have severe menstrual cramps
We use exclusively natural thyroid in our office, and a few times every day, I find myself explaining why natural thyroid is superior to Synthroid. In this article, we will explain why natural thyroid tablets are better than synthetic T4 only tablets, also called Synthroid.
Left Image: Thyroid Gland on Radionuclide Scan Courtesy of Wikimedia Commons.
What is Synthroid? What is in it?
Synthroid contains Thyroxine also called T4,which is identical hormone produced by the thyroid gland. Levothyroxine is the generic form of Synthroid. Common brand names include Thyrax, Euthyrox, Levaxin, L-thyroxine, Eltroxin and Thyrax Duotab in Europe; Thyrox in South Asia; Eutirox, Levoxyl and Synthroid in North America. Strictly speaking, Synthroid is bio-identical, even though it is synthetic.
What is in Natural Thyroid?
Natural Thyroid pills are made from desiccated porcine (pig) thyroid glands which contain Thyroxine (T4), T3, T2, T1 and Calcitonin.
Left Image: courtesy of wikimedia: Natural Thyroid tablets come from this animal, the pig.
Economics of Synthroid
As of 2005, 10 million people in the U.S. take thyroxine. When one considered that Abbott’s Synthroid is the most popular form of thyroxine, and the second-most prescribed drug in the U.S., one starts to understand the financial rivalry between Synthroid and natural thyroid competitors.
Left image: chemical structure of Tri-Iodothyronine (T3) notice three Iodine molecules. Add a fourth iodine molecule at the far left ring to make thyroxine, T4. Image courtesy of wikimedia commons.
What Does Mainstream Medicine Say ?
Here is a typical statement by Mainstream Medicine found on a popular medical informationweb site called medicine.net. Armour is a natural desiccated porcine thyroid preparation containing T1, T2, T3, T4 and calcitonin. Synthroid contains only T4.
From Medicine.Net : Answering a Viewer Question
What is your feeling regarding natural vs. synthetic replacement therapy in hypothyroid situations? Armour, for example vs. Synthroid? from L.H.
Doctor’s Answer: While it is reasonable to assume that synthetic medications are less desirable than natural counterparts, in this case- natural thyroid hormone replacement isdefinitely not an ideal solutionfor the vast majority of people.
Here’s why:Armour thyroid is derived from desiccated pig (porcine) thyroid gland. A number of years ago, these natural preparations were our only alternative. Replacement with desiccated thyroid creates dosing problems because there isno way to standardize the exact amount of the dose for each batch. As a matter of fact,these preparations do not report their dosage strength in milligrams, but rather, in grains of thyroid. This is because, they don’t really know the milligram equivalent in each dose. Dosing is also based on the assumptions that each gland has equal amounts of hormones as the next gland, and that the ratio of T4 and T3 (the more active hormone) are similar and constant in each gland from the pigs. There is no way to be certain of this, and patients on these preparations oftenhave fluctuating hormone levels, which may or may not result in symptoms.
Regardless of symptoms, the goal of replacement therapy is to keep thehormone levels as stable as possible. This is much easier to achieve with synthetic preparations such as Levoxyl and Synthroid.These preparations come in a vast number of standardized doses, allowing forminute adjustmentsin hormone dosing. There is another comment that should be made. With all the issues surrounding“mad cow disease” and other ailments, I personally am reluctant to offer animal based therapy to patients when a safe effective well studied synthetic preparation is widely available.
I hope this helps answer any questions you may have. Thank you for your question.
Medical Author: RM, M.D.
“Natural Thyroid is Not an Ideal Solution” ? !!!!
This nonsense really makes my blood boil and my eyes pop out of head.
Let’s start by doing a little research. If the above statement is true, we should expect to find that the FDAHAS NEVERrecalled Synthroid because of problems with stability or potency, and we would expect that the FDAHASrecalled natural thyroid pills because they are unstable, and vary in potency. So let’s ask the FDA about this. What do we find? In reality, the FDA says Synthroid is unstable and varies in potency, while natural thyroid from RLC labsHAS NEVERbeen recalled for instability or variation in potency.
Is Synthroid a Reliable and Stable Drug?
No, Says the FDA.
Synthroid was marketed in 1955, but not FDA approved until July 24. 2002 because of a “history of potency failures…indicates that Synthroid has not been reliably potent and stable.”– United States Food and Drug Administration Letter to Synthroid Manufacturer, Knoll Pharmaceuticals, April 26, 2001 (link)
Unstable, not of Consistent Potency from Lot to lot
Here is an FDA document August 14, 1997, Docket No. 97N-0314, which says: “The drug substance levothyroxine sodium (also called Synthroid) isunstablein the presence of light, temperature, air, and humidity. Unless the manufacturing process can be carefully and consistently controlled, orally administered levothyroxine sodium productsmay not be fully potentthrough the labeled expiration date, or be of consistent potency from lot to lot.
There is evidence from recalls, adverse drug experience reports, and inspection reports that even when a physician consistently prescribes the same brand of orally administered levothyroxine sodium, patients may receive products of variable potency at a given dose. Such variations in product potency present actual safety and effectiveness concerns.
However, no currently marketed orally administered levothyroxine sodium product has been shown to demonstrate consistent potency and stability and, thus,no currently marketed orally administered levothyroxine sodium product is generally recognized as safe and effective. ” end quotesource:http://www.gpo.gov/fdsys/pkg/FR-1997-08-14/html/97-21575.htm FDA Document [Federal Register: August 14, 1997 (Volume 62, Number 157)][Notices][Page 43535-43538]
Armour Thyroid Pill Recall 2005
To be completely fair, there was arecall of Armour thyroid in 2005, Lots manufactured in 2003 were found to have lost potency 2 years later in 2005, so Forest Labs recalled all tablets made in 2003. Since it was 2 years later, very little product from these lots was still in distribution, so it was actually a small recall.
Left Image courtesy of wikimedia commons
Change in Armour Formulation
Armour changed their thyroid tablet formulation in 2009, andwe have seen reportsfrom patients who are not happy with the new formulation. To avoid any questions, we use exclusively Naturethroid from RLC labs. After five years of clinical experience with Naturethroid from RLC labs, I can fully endorse the product as an excellent form of thyroid medication.
Naturethroid Manufacturer Speaks Out: Natural vs Synthetic
“In contrast to Naturally Desiccated Thyroid (NDT) containing T3 and T4, most synthetic medications contain T4 (or T3) only. In reality, many patients don’t start to feel normal again until they switch from synthetic to NDT (Thyroid USP). Natural Desiccated Thyroid hormone replacement has been used since the late 1800s, and it is one of the safest drugs available. It contains a full spectrum of thyroid hormones, T4 and T3 and also T2 and T1 as well.
The typical indication by the proponents of synthetic T4 is that NDT is unstable and inconsistent in its dosage. However, under the full USP monograph of both Thyroid USP as an ingredient and Thyroid USP Tablet as a finished product establishing full prescription status, this conventional argumentcould not be further from the truth. Unlike Nature-Throid™ and Westhroid™,synthetic medications have often been recalled due to batch inconsistencies. Yet most doctors are led to believe that desiccated thyroid is unstable.
To ensure that Nature-Throid™ and Westhroid™ Thyroid USP tablets are consistently potent from tablet to tablet and lot to lot, analytical tests are performed on the raw material (Thyroid USP powder) and on the actual tablets (finished product) to measure actual T4 and T3 activity.”
LeftImage courtesy of wikimedia: Conversion of T4 to T3 with IDI Deiodinase enzyme.
Conversion of T4 to T3
A common problem for many patients who don’t feel well on Synthroid is the inability toconvert T4 to T3. Synthroid contains T4 which is inactive, and must be converted to T3 by the body for it to work. This conversion is done by the De-Iodinase Enzyme (see image above). Sometimes this enzyme is deficient or not working, and many patients have an inability to convert T4 to T3. They feel much better on a natural thyroid medication which contains T3 and T4. In my experience, most patients feel much better, with more energy, and relief symptoms when switching from synthroid to a natural thyroid such as Naturethroid.
Mary Shomon on Natural Thyroid vs Synthetic
An article by Mary Shoman in the Townsend letter explains why natural thyroid treatment is better, that Synthroid and Levothyroxine are unstable, with dosage varying according to batch, and subjected to multiple recalls. Natural thyroid from RLC labs has never been recalled and is the preferred solution. Mary Shomon’s blog is an excellent resource on natural thyroid.
Left Image: Courtesy of Mary Shomon
Can I Get Mad Cow Disease from My Pig Thyroid Pill?
Millions of Americans have enjoyed ham sandwiches and pork products for decades without a single case of Mad Cow Disease ever reported. This essentially invalidates the fear of Mad Cow Disease as an argument. However, Mary Shomon advises caution with over-the-counter glandular supplements, which may contain unregulated meat products from areas of Europe known to have mad cow infected livestock.
Stop the Thyroid Madness
Another excellent resource is the Stop Your Thyroid Madness Blog and Book by Janie Bowthorpe. Janie suffered for years with low thyroid symptoms wven while on Synthroid, and had a dramatic recovery after covverting from synthroid to natural thyroid. With her blog and book, she is one of the strongest advocates for natural thyroid medication.
Left Image: Book Cover, courtesy of Janie Bowthorpe
For diagnosis of low thyroid, we use a lengthy questionnaire which reviews over 70 symptoms of low thyroid, a complete thyroid blood panel including TSH, free T3 and free T4, Thyroid antibodies and a physical examination which includes measurement of reflex time. Also included is a basal body temperature chart filled out by the patient at home. We also measure selenium and iodine levels and supplement when found low.
Once it has been determined that thyroid hormone is likely to be beneficial, a trial of low dose Nature-Throid from RLC labs is started with a Half Grain (32 mg) tablet every other morning.
A log book is kept by the patient describing benefits of increased energy, clarity of mind, etc, or adverse effects such as palpitations, feeling of warmth, anxiety or insomnia. At the end of a week, the log book is reviewed to determine if the thyroid was of benefit.
We have found that monitoring symptoms with a log book, and the Half Grain gradual increments in thyroid dosage every two to three weeks makes this program very safe. In the event of rapid heart rate or palpitations, the patient is instructed to hold the daily dosage of thyroid medication and inform the physician. This program is also excellent for switching patients from Synthroid to Natural Thyroid with patients invariably reporting dramatic improvement afterwards.
Instead of Natural Thyroid, Why Not Use Cytomel and Synthroid Together?
Cytomel is T3 and Synthroid is T4, so why not use the two together? The Cytomel provides the missing T3 to make a combination that is closer to the Natural Thyroid. Some patients arrive at my office having been given this combination from the doctor. The advantage for the prescribing doctor is that both items, Synthroid and Cytomel are available at the corner drugstore, wheras natural thyroid is available from a compounding pharmacy.
Natural Thyroid is still the preferred choice. Among other missing ingredients, the Synthroid and Cytomel lacks Calcitonin which is present in natural thyroid, and usually lacking in patients after thyroidectomy which removes the parathyroid glands. Giving back the missing calcitonin makes sense, and patients usually feel better.
Chemical and Engineering News
The Top Pharmaceuticals That Changed The World Vol. 83, Issue 25 (6/20/05)
Today, more than 10 million people in the U.S. take thyroxine. Synthroid, manufactured by Abbott Laboratories and the most popular brand of thyroxine, is the second-most prescribed drug in the U.S.
1.Treating hypothyroid patients solely with T4-only meds (synthroid)
2.Dosing solely by the TSH and the total T4, or using the outdated “Thyroid Panel”
3.Prescribing anti-depressants in lieu of evaluating and treating the free T3
4.Telling thyroid patients that desiccated natural thyroid like Armour is “unreliable”, “inconsistent”, “dangerous” or “outdated”.
5.Making lab work more important than the hypo symptoms which scream their presence
6.Failing to see the OBVIOUS symptoms of poorly treated thyroid, and instead, recommending a slew of other tests and diagnoses.
Common brand names include Thyrax, Euthyrox, Levaxin, L-thyroxine, Eltroxin and Thyrax Duotab in Europe; Thyrox in South Asia; Eutirox, Levoxyl and Synthroid in North America. There are also numerous generic versions. Synthroid is the most prescribed brand of T4 in the United States. Synthroid was marketed in 1955, but was not FDA approved at that time as it was “generally regarded safe”. In the 1990s, in response to debate as to whether Synthroid was more effective than other levothyroxine preparations, (which ended up concluding that there was little difference between Synthroid and generic brands) all levothyroxine preparations were required to undergo the formal FDA approval process. Synthroid was approved by the FDA on 24 July 2002.
Between 1991 and 1997, there were ten recalls of synthetic T4, involving over 100 million tablets.9 In nine of these recalls, the tablets had been found to be subpotent, or they were losing their potency before their expiration date; in the tenth recall, the tablets were found to be too potent. For patients, such unreliability means that the synthetic T4 they receive could be either too strong or not strong enough to treat their condition properly
Source: Federal Register 62, No. 157, 14 August 1997, pp. 43535-8.
As with all drugs, Armour’s manufacturer, Forest Laboratories, holds back samples from every lot it produces, and periodically tests those samples. When Armour Thyroid is manufactured, it has a 24-month expiration date. That means that Armour Thyroid should maintain its potency for a full two years.
What Forest found in recent sample testing was that there were several lots of Armour Thyroid that were not maintaining full potency. These lots were manufactured between March 2003 and August of 2003, and therefore they were set to expire between March 2005 and August of 2005.
The typical indication by the proponents of synthetic T4 is that NDT is unstable and inconsistent in its dosage. However, under the full USP monograph of both Thyroid USP as an ingredient and Thyroid USP Tablet as a finished product establishing full prescription status, this conventional argument could not be further from the truth. Unlike Nature-Throid™ and Westhroid™, synthetic medications have often been recalled due to batch inconsistencies. Yet most doctors are led to believe that desiccated thyroid is unstable.
Is There A Real Risk of Mad Cow Disease from Armour Thyroid?
An Update on Armour Thyroid and Glandulars by Mary Shomon
If you are willing to eat American pork products, you shouldn’t be any more concerned about Armour thyroid, as far as risk of mad cow disease. Caution is encouraged, however, with over-the-counter glandular supplements, which may contain unregulated meat products from areas of Europe known to have mad cow infected livestock.
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Copyright (c) 2013 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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1Division of Endocrinology, Georgetown University, Washington, DC, USA. Electronic address: email@example.comDepartment of Endocrinology, University of Newcastle, Newcastle, UK.
Although assigning a diagnosis of thyroid dysfunction appears quite simple, this is often not the case. Issues that make it unclear whether thyroid function is normal include transient changes in thyroid parameters, inter-individual and intra-individual differences in thyroid parameters, age-related differences, and ethnic variations. In addition, a statistically calculated distribution of thyroid analytes does not necessarily coincide with intervals or cutoffs that have predictive value for beneficial or adverse health outcomes. Based on current clincial trial data, it is unclear which individuals with mild thyroid-stimulating hormone elevations will benefit from levothyroxine treatment. For example, only a small number of patients with thyroid-stimulating hormone values of more than 10 mIU/L have been studied in a randomised manner. Even if therapy is initiated for abnormal thyroid function, not all treated individuals are maintained at the desired treatment target, and therefore might still be at risk. The consequence of this is that each patient’s thyroid function needs to be assessed on an individual basis with the entire clinical picture in mind. Monitoring also needs to be vigilant, and the targets for treatment reassessed continually.
Hashimoto’s disease is a disease, and hypothyroidism is a condition. Hypothyroidism is most commonly caused by Hashimoto’s disease, but the two terms are not interchangeable. Here is more information to help understand the difference.
Hashimoto’s vs. Hypothyroidism: What’s the Difference?
A Look at Autoimmune Thyroid Disease and Underactive Thyroid Conditions
Hashimoto’s disease, sometimes known as Hashimoto’s thyroiditis, autoimmune thyroiditis, or chronic lymphocytic thyroiditis, is an autoimmune disease. In Hashimoto’s, antibodies react against proteins in the thyroid gland, causing gradual destruction of the gland itself, and making the gland unable to produce the thyroid hormones the body needs.
Hashimoto’s disease is typically diagnosed by clinical examination that demonstrates one or more of the following findings:
Enlargement of the thyroid, known as a goiter
High levels of antibodies against thyroglobulin (TG) and thyroid peroxidase (TPO), detected via blood test
Fine needle aspiration of the thyroid (also known as a needle biopsy), which shows lymphocytes and macrophages
A radioactive uptake scan, which would show diffuse uptake in an enlarged thyroid gland
Ultrasound, which would show an enlarged thyroid gland
Symptoms of Hashimoto’s can vary. Some people have no symptoms whatsoever, and will have no demonstrable symptoms of the underlying condition. For many Hashimoto’s patients, the thyroid becomes enlarged, a condition known as a goiter. The goiter can range from slight enlargement, which may have no other symptoms, to a substantial increase in size.
Some people with Hashimoto’s, especially those with a larger goiter, may feel discomfort in the neck area. Scarves or neckties may feel uncomfortable. The neck may feel swollen or uncomfortably enlarged, even sore. Sometimes the neck and/or throat is sore or tender. Less commonly, swallowing or even breathing can become difficult if a goiter is blocking the windpipe or esophagus.
Hashimoto’s typically involves a slow but steady destruction of the gland that eventually results in the thyroid’s inability to produce sufficient thyroid hormone — the condition known as hypothyroidism. Along the way, however, there can be periods where the thyroid sputters back to life, even causing temporary hyperthyroidism, then a return to hypothyroidism. This cycling back and forth between hypothyroidism and hyperthyroidism is characteristic of Hashimoto’s disease. So, for example, periods of anxiety/insomnia/diarrhea/weight loss may be followed by periods of depression/fatigue/constipation/weight gain.
In some cases, the onset of Hashimoto’s and elevation of antibodies will be accompanied by a variety of symptoms, including anxiety, difficulty sleeping, fatigue, weight changes, depression, hair loss, muscle/joint aches and pains, and fertility problems, among others.
If a goiter causes difficulty swallowing or breathing, or is a cosmetic problem, then thyroid hormone replacement drugs (i.e., levothyroxine or natural desiccated thyroid) will usually be given to help shrink the thyroid. If drug treatment does not work, or the goiter is too invasive, then surgery to remove all or part of the thyroid may be recommended.
Except in the case of a goiter, most endocrinologists and conventional physicians will not treat Hashimoto’s disease, as diagnosed by elevated antibody levels, unless other thyroid function tests such as TSH are outside the normal range.
There are, however, some endocrinologists, as well as holistic MDs, osteopaths and other practitioners, who believe that Hashimoto’s disease — as confirmed by the presence of thyroid antibodies — along with symptoms, are enough to warrant treatment with small amounts of thyroid hormone.
The practice of treating patients who have Hashimoto’s thyroiditis but normal range thyroid function tests is supported by a study, reported on in the March 2001 issue of the journal Thyroid. In this study, German researchers reported that use of levothyroxine treatment for cases of Hashimoto’s autoimmune thyroiditis where TSH had not yet elevated beyond normal range (people who were considered “euthyroid”) could reduce the incidence and degree of autoimmune disease progression.
In the study of 21 patients with euthyroid Hashimoto’s Thyroiditis (normal range TSH, but elevated antibodies), half of the patients were treated with levothyroxine for a year, the other half were not treated. After 1 year of therapy with levothyroxine, the antibody levels and lymphocytes (evidence of inflammation) decreased significantly only in the group receiving the medication. Among the untreated group, the antibody levels rose or remained the same.
The researchers concluded that preventative treatment of normal TSH range patients with Hashimoto’s disease reduced the various markers of autoimmune thyroiditis, and speculated that that such treatment might even be able to stop the progression of Hashimoto’s disease, or perhaps even prevent development of the hypothyroidism.
You must reduce elevated TP0 antibodies down to the normal reference range to prevent hypothyroidism.
If a recent lab test has shown that you have elevated thyroid antibodies, your next question might be, “How can I bring them down to normal levels?”
When it comes to thyroid antibodies, striving for perfection may be overrated. Let’s talk about what level of antibodies you should aim for and how to reduce them.
What are Thyroid Antibodies?
Sometimes the immune system mistakenly attacks your thyroid gland with antibodies. This damages your thyroid and can lead to inflammation of the thyroid gland (thyroiditis), symptoms of hypothyroidism or hyperthyroidism, and if left unchecked, autoimmune thyroid disease.
By far, the most common cause of hypothyroidism and elevated thyroid antibodies is the autoimmune disorder Hashimoto’s thyroiditis. Elevated thyroid antibodies are also found in Graves’ Disease.
Not everyone who has thyroid antibodies is hypothyroid, but most people with elevated TPO or TG antibodies eventually become hypothyroid if the antibodies are left entirely unchecked.
What is a Healthy Level of TPO Antibodies?
There is low risk of progressing to hypothyroidism if TPO antibodies are at or below 500 IU/mL. 
I’ve commonly seen people with Hashimoto’s disease or elevated thyroid antibodies become hyper focused on reducing their antibody test results to the “normal” reference range, but is this really necessary?
It appears that the answer is no.
The normal reference range for TPO antibodies is less than 35 IU/mL, but people with elevated antibodies may have levels in the high hundreds, or even well over 1,000 IU/mL. Not all people with thyroid antibodies develop hypothyroidism, but the higher your antibodies, the higher your risk.
How Important Are Thyroid Antibodies?
Those with elevated TPO antibodies have a 9-19 chance of becoming hypothyroid after 6 years of follow up.   If we consider this, elevated thyroid antibodies are not as consequential as some would suggest.
A 2016 study published in the Journal of Hormone and Metabolic Research  found:
Those who had TPO antibodies below 500 IU/mL had a low risk of future progression to hypothyroidism.
Those who were above 500 IU/mL still only had a moderate risk.
This study suggests that you don’t have to continuously pursue lower and lower levels of antibodies with strict diets or supplements, especially if your thyroid is working well.
If you’re a patient, or a doctor working with patients, it’s important to understand that reducing TPO antibodies to under 500 IU/mL is a clinical win.
Very High Thyroid Antibodies
All that said, if your TPO antibodies are very high, reducing your antibody count is definitely a worthwhile goal. The higher the antibodies, the more likely you are to develop hypothyroidism.
The farther you reduce your antibodies, even if you can’t get them down to 500 IU/mL, the less damage to your thyroid gland. Just don’t feel discouraged by failing to get them down to the “normal” reference range.
4 Ways to Reduce Thyroid Antibodies
There are several ways you can reduce your thyroid antibodies, using diet and lifestyle.
1. Improve Your Gut Health
Preliminary evidence suggests that gut health is closely linked to thyroid health, and that improving gut health can decrease thyroid antibodies and balance your thyroid hormones. Here are several ways you can work on improving your gut health.
Anti-Inflammatory Diet: A low-quality diet is typically the single biggest source of inflammation that can impair your thyroid and immune function. But encouragingly, early evidence shows that changing your diet can lower thyroid antibodies.
A low-carbohydrate diet was shown in one study to reduce thyroid antibodies by 44% in people with Hashimoto’s thyroiditis, but not celiac disease,  while a gluten-free diet was shown to reduce thyroid antibodies in a group of women with Hashimoto’s thyroiditis.  Other studies have shown that eliminating dairy or gluten may help improve thyroid function.   A Paleo diet template is low carb, diary free, and gluten free, and may be a good place to start.
You may have heard of the Autoimmune Paleo diet, which has been shown in one small study to reduce thyroid symptoms and inflammatory markers.  Many clinicians have seen their autoimmune patients respond well to the Autoimmune Paleo diet. However, the diet has yet to be shown to reduce thyroid antibodies. This doesn’t mean it’s not useful, but it may not be necessary to follow such a restricted diet to reduce thyroid antibodies.
Gut Infections: Gut infections, such as H.pylori, SIBO (small intestinal bacterial overgrowth), and Blastocystis hominis are associated with elevated thyroid antibodies. Treating these infections may reduce thyroid antibodies.     
Probiotics: Using probiotics improves gut function and can improve your thyroid function, including antibody and thyroid hormone levels. 
Selenium: Several studies, including a meta-analysis (the highest quality science) show selenium improves thyroid antibodies for hypothyroid patients.    However, not all research agrees, and more studies need to be done.
Vitamin D: Research suggests that vitamin D deficiency is associated with higher levels of thyroid antibodies,  and that supplementation may decrease thyroid antibodies. 
CoQ10 & Magnesium: Some evidence suggests CoQ10 and Magnesium supplementation may reduce thyroid antibodies. CoQ10 has been shown to “improve thyroid vascularity,” and magnesium supports iodine uptake.  One small study demonstrated supplementation with magnesium, CoQ10, and selenium along with additional supports reduced thyroid antibodies,  while one additional study showed an association between low serum magnesium and thyroid antibodies. 
There are some encouraging data showing that low-level laser therapy can improve thyroid function and decrease TPO antibodies. The therapy also reduced the amount of levothyroxine medication the patients needed, even after 9 months of follow up.  
4. Optimize Iodine Levels
Iodine is an important nutrient for the thyroid gland, but must be used cautiously. Supplemental dietary iodine has been shown in several population-based studies to increase the incidence of autoimmune thyroid diseases.   On the other hand, too little iodine can also cause thyroid symptoms. Optimizing your iodine levels may reduce thyroid antibodies.
Suzy is a 59 year old post menopausal woman with low thyroid function. About three months ago, she started her bio-identical hormone program which included natural thyroid pills. After starting the program, she was doing well with more energy, better sleep, improved appearance of skin and hair, and resolution of her menopausal symptoms of flashes and sweats. However about 12 weeks into her program, Suzy had a visit with her primary care doctor who did a follow up thyroid panel. Her primary care doctor informed Suzy that her TSH test result was below the lab normal range, and therefore, her thyroid dose was too high, and should be reduced. (Note: TSH is Thyroid Stimulating Hormone, and is made by the pituitary gland). Above left image: Thyroid scan courtesy of wikimedia commons.
Too Many Doctors Spoil the Soup
Suzy called me at the office distraught and confused. Two doctors were telling her two different things and she didn’t know who to believe. Her primary care doctor was telling her one thing and I was telling her another. I explained to Suzy that her primary care doctor was incorrect in relying slavishly on the TSH test. Even though her TSH test was 0.15 which is below the lab reference range of 0.3, this was perfectly acceptable and indicated her thyroid medicine was suppressing the TSH to a low level which was perfectly fine. This test interpretation means she is taking thyroid pills, and the pills are working. It does not mean she is “hyperthyroid” by any stretch of the imagination.
No Clinical Evidence of Thyrotoxicosis
I also informed Suzy that her Primary Care Doctor is mistakenly relying on the TSH test to determine her thyroid dosage. The TSH test is an indirect measure of thyroid function and can be unreliable to monitor thyroid dosage. A more accurate indicator of thyroid function is the free T3, which in her case was 375, well within the normal range of 240 to 420. The Free T3 lab test together with the absence of any signs or symptoms of thyroid excess indicates she is using the correct dosage of natural thyroid medication. Symptoms of thyroid excess are rapid heartbeat or palpitations, and Suzy reported no such symptoms. In fact, Suzy said she felt fine and now that she understands it, she didn’t want to go back to feeling tired, sluggish as before she started the thyroid pills. Suzy was relieved to find out that the low TSH result was perfectly acceptable and there was nothing to worry about. This TSH scenario is a recurring event at my office.
Conventional Docs Slavishly Rely on the TSH Test
Conventional primary care doctors use an older thyroid lab panel which does not include the Free T3 test, the most informative thyroid lab test. Instead, mainstream endocrinology relies on the TSH test which is not a direct measure of thyroid function, and can, in fact, be unreliable.
Above Left image: Thyroid Gland Anatomy Diagram, courtesy of National Institute of Health, and wikimedia commons.
Most conventional doctors are unfamiliar with the use of natural thyroid which contains both T3 and T4, and instead use Synthroid which is quite different, containing only T4. Since the Primary care doctors bill the health insurance for the office visit and payment is only a few dollars, the office visit is brief, 3-5 minutes. In this short time, Primary care doctors can provide only the most basic care, which is a quick look at the TSH lab test. If the TSH is below the lab reference range the doctor gives a new prescription for Synthroid with a reduced dosage. If the TSH is above the reference range, the primary care doctor will increase the Synthroid dosage.
The Cleveland Clinic Chimes In
A few months ago, I found myself talking on the phone with an endocrinologist at the Cleveland Clinic explaining why the TSH blood test can be unreliable. He informed me I was wrong, and that he uses the TSH test as the gold standard. We agreed to disagree and parted company as friends. I have found that, in general, endocrinologists and mainstream doctors rely heavily on TSH to make a diagnosis of low thyroid.
Why Thyroid Blood Testing is Unreliable.
I recommend to you a book by Barry Durrant Peatfield, Your Thyroid and How to Keep It Healthy(1) After serving as a general practitioner in the British National Health Service, Peatfield traveled to the US to train at the Broda Barnes Institute. Peatfield later returned to England to start his own thyroid clinic. His book was written at the end of his career and contains the wisdom of 25 years of diagnosing and treating thyroid conditions. One section of the book is devoted to this question. Here it is quoted from the book: :
1) Anxiety in the medical establishment about rules and dogma has led to a slavish reliance on blood tests, such as the TSH, which are often unreliable and can actually produce a false picture.
2) Very few doctors can accept the fact that a normal, or low TSH, may still occur with low thyroid function.
3) As a result of this test (TSH), thousands are denied treatment for low thyroid condition.
Dr. Peatfield’s Reward After a LifeTime of Service
After a lifetime of work serving his community, you might imagine the honors and accolades for such a knowledgeable thyroidologist as Dr Peatfield, yet quite the opposite happened. Dr. Peatfield’s license was suspended in 2001 at the age of 68 by the General Medical Council of England.(5-6) The GMC ruling was based on “unfavorable testimony” from competing endocrinologists who “slavishly rely on the TSH test” as a measurement of thyroid function to diagnose the low thyroid condition and monitor treatment with thyroxine. Sadly, this is the sort of “Witch Hunt “which has kept medical science in the “Dark Ages” regarding the treatment of the low thyroid condition.(13)
Broda Barnes and the Low Thyroid Condition
Another useful book recommended to you is written by Broda Barnes MD on the low thyroid condition. Broda Barnes MD reported 40 years ago on the same problem of his medical colleagues relying too heavily on thyroid blood tests. The book, Hypothyroidism: The Unsuspected Illnessby Barnes, Broda is a medical classic and should be required reading for every medical student and doctor. (2) I have read the book many times. The book contains the condensed wisdom of a lifetime of research and clinical experience with the thyroid, and it rings true today as it did in 1976. Thyroid blood tests come and go, yet human physiology remains the same.
Important Point: The TSH test is unreliable for determining optimal thyroid dosage. A “below lab range” TSH is routinely encountered when patients are optimally treated with natural thyroid medication and obtain the best clinical results.
Hypothyroidism the Unsuspected Illness, by Broda Barnes MD
Broda Barnes estimated that up to 40% of the population suffers from a low thyroid condition and would benefit from thyroid medication. Of course, Barnes’ opinion differed with that of mainstream medicine of his time which relied dogmatically on thyroid blood tests to make the diagnosis of low thyroid. Barnes felt the blood tests were unreliable and instead used the basal temperature, history and physical examination. This medical debate regarding unreliability of thyroid blood testing continues today. (3,4)
Being an astute clinician, Dr. Barnes makes a number of observations about the low thyroid condition. Firstly, low thyroid is associated with a reduced immunity to infectious diseases such as TB (tuberculosis). Before the advent of modern antibiotics in the 1940’s, most low thyroid children succumbed to infectious diseases before reaching adulthood. Secondly, low thyroid is associated with a peculiar form of skin thickening called myxedema which causes a characteristic appearance of the face, puffiness around the eyes, fullness under the chin, loss of outer eyebrows, and hair thinning or hair loss.
A third observation by Dr. Barnes is that low thyroid is associated with menstrual irregularities, miscarriages and infertility. Barnes treated thousands of young women with thyroid pills which restored cycle regularity and fertility. In his day, the medical system resorted to the drastic measure of hysterectomy for uncontrolled menstrual bleeding. Although today’s use of birth control pills to regulate the cycles is admittedly a far better alternative, Barnes found that the simple administration of desiccated thyroid served quite well. Again, Barnes noted that blood testing was usually normal in these cases which respond to thyroid medication.
A lengthy chapter is devoted to heart attacks and the low thyroid condition. Based on autopsy data from Graz Austria, Barnes concluded that low thyroid patients who previously would have succumbed to infectious diseases in childhood go on years later to 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.
Important Point: A low thyroid condition is a serious risk factor for heart disease.
Dr. Barnes devotes separate chapters in the book to discussion of chronic fatigue, migraine headaches and emotional/behavioral disorders all of which respond to treatment with thyroid medication.
The final chapter describes Dr. Barnes work on obesity when he presided over a hospital ward of volunteer obese patients, and monitored everything they ate. He found that the obese patients invariably ate a high carbohydrate diet, and avoided fat. Barnes added fat back into the menu and reduced the refined carbohydrates and found that his obese patients lost 10 pounds a month with no hunger pangs.
Missing from the book are discussions of Iodine supplementation and the role of the Adrenal, both of which are covered in later updated versions of Barnes thyroid book by other authors. See Hypothyroidism Type Two by Mark Starr, and Your Thyroid by Barry Durrant Peatfield. Iodine supplementation is covered by both Derry and Brownstein. The Safe Uses of Cortisol by William McK Jefferies is the companion medical classic devoted to the adrenals and cortisol.
Broda Barnes Institute
Although Broda Barnes has since passed away, his work lives in at the Broda Barnes Institute. Patricia Puglio is the director and a great resource. She is available by phone to answer questions and offer suggestions. Here is her contact information: Patricia A. Puglio, Director, Broda O. Barnes, M.D. Research Foundation, Inc. PO Box 110098 Trumbull, CT 06611.
More on the Unreliability of the TSH Lab Test
Thanks to Jonathan Wright’s newsletter for bringing to my attention a recent article in the June 2010 International Journal of Clinical Practice by Dr. O’Reilly which summarizes the medical literature on this question of the reliability of the TSH test. (9) Essentially, Dr O’Reilly reviews the medical literature and the history thyroid medicine and provides all the medical studies and information showing that Dr Barnes and Dr Peatfield were right all along. (7-12). Here are a few quotes from Dr O’Reilly (9):
The use of the TSH measurement to assess thyroid status in patients on thyroxine (Synthroid) replacement could be considered a classic example of the misapplication of a laboratory test.”
Instead of the TSH measurement, Dr. O’Reilly recommends the T3 test for monitoring treatment with thyroid medication. He says:
“The adequacy of thyroxine (Synthroid) replacement should be assessed clinically with the serum T3 being measured, when required, to detect over-replacement”
We use the Free T3 measurement which is widely available at any lab.
In spite of the obvious need for a better approach to the low thyroid condition, there has been very little movement to rehabilitate mainstream endocrinology which dogmatically clings to the TSH test and synthetic T4 only medications (levothyroxine). Here in the state of Florida, we are fortunate that the state legislature passed a Health Freedom Law in 2001. This “Health Freedom Law” protects doctors and patients from unwarranted abuse or harassment for utilizing “outside of mainstream medical practices”, such as correct diagnosis and treatment of the low thyroid condition based on the wisdom of Drs Broda Barnes, Barry Peatfield, DS O’Reilly, Jonathan Wright, David Brownstein and many others. (14)
(3) http://ccpd.ucsf.edu/hypothyroidism.shtml Pituitary 101, UCSF California Center for Pituitary Disorders at UCSF. Web Site: “TSH is often an unreliable measure of secondary hypothyroidism and should not be used to assess the adequacy of thyroid replacement in these patients. The inappropriate use of TSH levels to determine hormone replacement is one of the more common mistakes that we see in the patients we follow, and patients should be cautious if another physician discusses changing their thyroid hormone dose. Many patients have returned for their one-year follow-up visits having had their doses lowered in response to “low TSH levels.” Most of them feel poorly, but improve after we increase or restart their medication.”
“We have long taken the view that most hypothyroid patients are content with a dose of thyroxine that restores serum concentrations of thyroid stimulating hormone to the low normal range. However, some achieve a sense of wellbeing only when serum thyroid stimulating hormone is suppressed, when we take care to ensure that serum tri-iodothyronine is unequivocally normal. Until valid evidence shows that such a policy is detrimental we will continue to treat patients holistically rather than insist on adherence to a biochemical definition of adequacy of thyroxine replacement. The issue of whether a little too much thyroxine is dangerous is likely to evaporate when appropriate preparations become available to allow treat.
Thursday, 17 May, 2001 UK Investigation into thyroid doctor. GP Dr Barry Durrant-Peatfield, 64, who has a practice in Purley, Surrey, has been stopped from working for 18 months so that the GMC can complete its investigation.
(7) http://www.ncbi.nlm.nih.gov/pubmed/8200938 J Clin Endocrinol Metab. 1994 Jun;78(6):1368-71. Comparison of second and third generation methods for measurement of serum thyrotropin in patients with overt hyperthyroidism, patients receiving thyroxine therapy, and those with nonthyroidal illness. Franklyn JA, Black EG, Betteridge J, Sheppard MC. “Undetectable TSH results, even in a third generation assay, are not diagnostic of overt hyperthyroidism, but are also found in subjects with treated thyroid disease and NTI.”
Br Med J (Clin Res Ed). 1986 September 27; 293(6550): 808–810. Are biochemical tests of thyroid function of any value in monitoring patients receiving thyroxine replacement? W D Fraser, E M Biggart, D S O’Reilly, H W Gray, J H McKillop, and J A Thomson. “These measurements are therefore of little, if any, value in monitoring patients receiving thyroxine replacement. “
Int J Clin Pract. 2010 Jun;64(7):991-4. Thyroid hormone replacement: an iatrogenic problem.O’Reilly DS.
“Thyroid hormone replacement is one of the very few medical treatments devised in the 19th century that still survive. It is safe, very effective and hailed as a major success by patients and clinicians. Currently, it is arguably the most contentious issue in clinical endocrinology. The current controversy and patient disquiet began in the early 1970s, when on theoretical grounds and without proper assessment, the serum thyrotropin (TSH) concentration was adopted as the means of assessing the adequacy of thyroxine replacement. The published literature shows that the serum TSH concentration is a poor indicator of clinical status in patients on thyroxine. The adequacy of thyroxine replacement should be assessed clinically with the serum T3 being measured, when required, to detect over-replacement.”
Ann Clin Biochem. 1987 Nov;24 ( Pt 6):614-9. Thyroid stimulating hormone measurement by an ultrasensitive assay during thyroxine replacement: comparison with other tests of thyroid function. Wheatley T, Clark PM, Clark JD, Raggatt PR, Edwards OM. “A suppressed serum TSH was found in 65% of patients with a normal serum total thyroxine. “
State of Florida Health Freedom Law: CHAPTER 2001-116 Senate Bill No. 1324 An act relating to health care; creating s. 456.41, F.S.; amending s. 381.026, F.S.; Ch. 2001-116 (S.B. 1324) Authorizes provision of and access to complementary or alternative health care treatments; requires specified disclosures by the health care practitioner and the keeping of certain records; conforms the Florida Patient’s Bill of Rights. Effective May 31, 2001.
Hypothyroidism Diagnosis and Treatment, with Ted Friedman, MD
Dr. Theodore C. Friedman, M.D., Ph.D. is Associate Professor of Medicine-UCLA, Endocrinology Division, and is also an endocrinologist in private practice. For more information about his practice, see www.goodhormonehealth.com.
In this article, he shares his thoughts about hypothyroidism diagnosis and treatment.
Hypothyroidism is a relatively common disorder. It affects more women then men, but I happen to be one of the men who does have it. Symptoms of hypothyroidism include fatigue, gradual weight gain, constipation, muscle aches, joint pain, feeling cold, menstrual irregularities, weakness, hair loss, dry, cold skin and slow reaction time. Many patients will have a goiter (enlarged thyroid). Although it has received much discussion, I believe low body temperature is not a reliable sign of hypothyroidism.
The incidence of hypothyroidism increases with increasing age. In other words, the older we get, the more likely a thyroid deficiency will show up. The most common cause of primary hypothyroidism (hypothyroidism originating in the thyroid gland itself), is Hashimoto’s Thyroiditis. Hashimoto’s is an autoimmune condition. The body’s own antibodies attack the thyroid gland and destroy it, leading to hypothyroidism. Hashimoto’s Thyroiditis may be a manifestation of multiple autoimmune syndromes and may occur in families. Hypothyroidism can also be due to a pituitary problem (central hypothyroidism).
Diagnosing all types of hypothyroidism is important, because treatment with thyroid hormone will improve symptoms in patients with hypothyroidism, but is unlikely to help those who do not have hypothyroidism. In primary hypothyroidism, the thyroid gland, located in the neck, is less able to produce the thyroid hormones, T4 and T3. The pituitary gland, located in the head, responds to this deficiency by secreting more TSH. Thus, in more mild cases of primary hypothyroidism, T4 and T3 levels are normal, but the TSH is high. In more severe cases, T4 and T3 levels drop. Although the normal range for TSH is often between 0.5 and 5 mU/mL, values at the high end of the normal range may be abnormal. T3 is the more bioactive hormone compared to T4, but T4 is more stable in the circulation.
My approach to diagnosing hypothyroidism is to start with a careful history and physical. Then an Endocrinologist should perform a hands-on thyroid examination to determine if the patient has a goiter. Blood TSH, free T4, free T3 and anti-TPO antibodies should be tested. Patients with an enlarged thyroid and/or a positive anti-TPO antibody test AND a TSH greater than 4.0 mU/mL should be considered to have primary hypothyroidism. Patients without an enlarged thyroid and without a positive anti-TPO antibody test but WITH a TSH greater than 7.5 mU/mL should also be considered to have primary hypothyroidism. Patients with a free T4 of less than 0.9 mg/dL and a TSH less than 1.0 mU/mL are likely to have central hypothyroidism. Patients with symptoms of hypothyroidism but who do not meet these criteria should be watched and retested in 6 months.
Once hypothyroidism is diagnosed, there are many treatment options, including synthetic L-thyroxine (T4) preparations (Synthroid, Levoxyl and Unithroid), synthetic L-triiodothyronine (T3) preparations (Cytomel), synthetic T4/T3 combinations (Thyrolar) and dessicated thyroid preparations (Armour, Naturethroid, Bio-Throid, and Westhroid). All of the L-thyroxine preparations contain the same active ingredient, but contain different fillers and have different quality control. Until recently, Synthroid did not have FDA approval, but now all L-thyroxine preparations have FDA approval. Thyrolar and the dessicated thyroid preparations probably have a higher T3/T4 ratio than desirable and thus, I often give a lower amounts of these preparations supplemented with T4.
Most endocrinologists use L-thyroxine preparations for the initial treatment of all forms of hypothyroidism. Although the use of L-thyroxine (T4) compared to L-triiodothyronine (T3) may be surprising as T3 is the more bioactive thyroid hormone, T4 is most frequently used. This is because tissues convert T4 to T3 to maintain physiologic levels of the T3. Thus, administration of T4 results in bioavailable T3 and T4. As T4 is more stable than T3, T4 therapy gives even blood levels, while T3 therapy leads to high levels after taking the medicine and low levels before the next dose. Armour thyroid is the least expensive preparation. Because Armour thyroid comes form pig thyroids, some Endocrinologists feel that there is high pill to pill variability, but this is unlikely to be true.
Natural desiccated thyroid has been working for over 100 years and completely changes lives. For more information on its history and details on the product itself, see the revised STTM book, Chapter 2.
Why is this page specifically on natural desiccated thyroid? Because unlike T4-only meds (Synthroid, Levoxyl, generic levothyroxine, Eltroxin, Oroxine, Levothyroid, Levaxin or Euthyrox,etc)…desiccated thyroid gives you exactly what your own thyroid would be giving you: T4, T3, T2, T1 and calcitonin. Patients around the world have found it to be a far better treatment, removes lingering symptoms, improves your immune system, gives you your life back, stops the attack of Hashimotos disease if you dose it high enough, stops adrenal fatigue (which SO many patients end up with because of the inadequacy of T4-only) and is also far better for your immune system if you’ve ever had thyroid cancer.
What are the brands of desiccated natural thyroid? The brand name “Armour” is the most well known of the Natural Desiccated Porcine Thyroid meds and oldest on the market–since early in the 20th century. Naturethroid and Westhroid came into the picture in the late 1930′s–by RLC Labs. A new generic by Acella hit the picture by late 2010. Additionally, some patients are using a natural desiccated thyroid called Thyroid-S or “Thiroyd” from Thailand with excellent results, as well as Erfa’s Thyroid from Canada. Australia uses compounded desiccated thyroid powder and there are many compounding pharmacies around the world. All desiccated thyroid comes from pig thyroid, and all most use thyroid desiccated powder which meets the stringent guidelines of the US Pharmacopeia. To see ingredients of all, go here. NOTE: you may need to chew up either Armour or Naturethroid to release the desiccated thyroid from the excess cellulose filler. To see all available options for desiccated thyroid, go here.
What are the units of measure per tablet/capsule? With the main brands, such as Naturethroid, Westhroid, Armour, Erfa, etc, each tablet/capsule is measured in milligrams (mg.). The typical tablet is 60 mg or 65 mg, which is called one grain. So, a 1/2 grain tablet is 30/32.5 mg. A 2 grain tablet is 120 mg/130. A 3 grain tablet is 180/195 mgs. A 4 grain tablet is 240/260 mg. A 5 grain tablet is 300/325 mg.
What’s in desiccated natural thyroid? Natural Desiccated Porcine Thyroid, also just called Natural Thyroid or Desiccated Thyroid, contains the same hormones that your own thyroid would produce–T4, T3, T2, T1 and calcitonin–and is why patients have found it to work so well. T4 is the storage hormone; T3 is the active, energy-giving hormone, and both are found in a 80/20 ratio in each 60 mg of desiccated thyroid. The T2, T1 and calcitonin is not measured, but it’s there, according to Forest Labs, the makers of Armour. Since porcine thyroid tends to have more T3 proportionately than human thyroids (80/20 as compared to the human 93/7), some patients add a small amount of T4, but only after they find their optimal dose of dessicated thyroid–the dose which removes all symptoms and gets the free T3 towards the upper part of the range. Many do fine on porcine thyroid alone, though.
Are there any non-prescription desiccated thyroid products? One more well-known over-the-counter (OTC) natural thyroid is called Nutri Meds which is available in either porcine or bovine desiccated thyroid. Patients find them much weaker and have to take quite a lot. You may find other fine OTC products on the shelf of your local health food store. Also check out Dr. Lowe’s ThyroGold, which seems to be stronger and workable. Neither Thyroid-S or Thiroyd from Thailand are by prescription, and patients report them working quite well.
What if I’m on T4? Many patients do their T4 one day, then stop and start on desiccated thyroid the next, with no problems whatsoever. Some doctors guide their patients to lower T4, such as by half, start on desiccated thyroid, then continue lowering the T4 as they raise the desiccated thyroid.
How do patients dose with natural desiccated thyroid? Thyroid patients and their doctors have found it wise to start on a smaller dose of desiccated thyroid than they will ultimately need, such as 1 grain (60 mg). Why? Because the body may need to adjust to getting direct T3 again, and there may be other issues which can reveal themselves, such as sluggish adrenals or low Ferritin/iron levels. Those who start on natural desiccated thyroid have discovered that it can be wise to RAISE within two weeks or less to prevent hypothyroid symptoms from returning due to the internal feedback loop in your body, which can happen if you stay on a low dose too long before raising. Most patients start to slow those raises down in the 2-3 grain area to give the T4 time to build (which can take 4-6 weeks) and show its conversion results. Many patients end up in the 3-5 grain area, but some can be on less, and some more. It’s individual.
Do I simply swallow it? Yes, you can swallow it and do great. Before Armour was reformulated and distributed in the new form in 2009, patients found it easy to do it sublingually i.e. you place the tablet under your tongue, or between your gums and inner cheek. Granted, Forest Labs did not make Armour to be sublingual, but it worked! Now, it’s more difficult since both Armour and Naturethroid have a high cellulose content. You’ll need to chew them up before swallowing. When swallowing desiccated thyroid, it will be important to avoid iron, estrogen and calcium supplements at the same time, since all bind the thyroid hormones to some degree. Canada’s “Thyroid” by Erfa can still be done sublingually, and many patients prefer it for that fact. Thailand’s Thiroyd can be done sublingually and has a slightly sweet taste, says a patient.
Do I take it once a day? To the contrary, most patients have found it beneficial to divide their dose to at least twice a day, if not more, in order to spread the energy-giving affect of T3. Desiccated thyroid contains direct T3, which is short-lived, and which peaks about 2 hours after you take it. An example is taking 2/3 or your natural desiccated thyroid in the morning, and the other 1/3 in the early afternoon. Or, for example, if you were on 3 1/2 grains, you might do 2 grains in the morning, one grain around noon, and the half grain by 2-3 pm. Some folks dose 4-5 times a day, especially in the presence of low cortisol. A few even do it once in the morning, and find that to be very effective. But the latter can stress your adrenals, or can result in fatigue later in the day. And remember: your own thyroid gives you what you need throughout the day instead of one dump; thus, multi-dosing is a way to replicate that.
How do I know when I’m on enough? Before labs were developed, doctors treated hypothyroid patients by symptoms….and successfully. Patients and many wise doctors have found this an ideal way to treat—by symptoms. One important symptom is your temperature. Temps reflect metabolism, and metabolism is controlled by your thyroid. Find a mercury or liquid oral thermometer, which is more accurate than most digitals. Generally, you want your morning temp (before rising) to be 97.8 to 98.2, and your afternoon temp to be around 98.6. You may find your temperatures correcting before you find your optimal dose. Unfortunately, doctors are trained to put a HUGE reliance on labs over symptoms. But labs only tell PART of the story. Patients have discovered that the free T3 can be the most informative. But you have to figure out where it is great for you, based on symptoms. When patients get their free T3 at the top, (or when all symptoms are eliminated), they will often have a TSH far BELOW range, i.e. below one, and that does NOT necessarily mean you are hyper. Patients have found the TSH is less important once treatment is started, and just because one’s TSH can get lower than 1 while getting the free T3 up there, does NOT mean hyper has set in. Many doctors are uninformed about this, so be prepared, and pass along to your doctor what we have learned.
Why is desiccated thyroid a better treatment? Patient experience has found desiccated thyroid to give superior results because it is natural (your body accepts ALL of it, unless you have an allergy to porcine), it contains both T4 (as the storage hormone) and T3 (the most active hormone and necessary for every cell in your body), as well as T2, T1 and calcitonin. T2 has an important role in metabolism. Calcitonin is the hormone which keeps the calcium in your bones, and certain doctors have noticed improvement in bone density with patients on natural thyroid.
Why is the T3 in desiccated thyroid so important? ”In your cells, T3 is essential to reconverting ADP (the ‘flat battery’) into ATP (the ‘charged battery’). A shortage of T3 leads to a poor ratio between ATP and ADP. That would seem to explain why a long recovery period is needed after exertion; it takes a long time, at this deficient rate, to get back to a decent level of ATP so you’re ready for more activity.” This way of explaining it comes from this website.
How do I find a doctor who understands desiccated thyroid? Patients regrettably find that many doctors are very ignorant about the efficacy and safety of natural desiccated thyroid. Be prepared. If you click on the highlighted “doctors” above, you’ll find recommendations on how to find a good doc. Consider calling the office to make sure this doc prescribes desiccated thyroid, checks the free’s, and pays attention to symptoms. If the doctor can’t do the latter, move on to another one! Another option is to visit a large pharmacy in your area and ask the pharmacist if anyone prescribes desiccated thyroid. And note that it is not uncommon to drive great distances to find a knowledgeable doctor.
How high do I raise desiccated thyroid? As your doctor helps you raise your desiccated thyroid, a certain amount may give you better energy, but may not be quite enough to stop chronic low grade depression, for example. So another raise may be warranted. By observation, it appears that many hypothyroid patients end up in the 3-5 grains, with some lower, and some higher when they find their optimal dose. It’s individual.
Are there other issues I need to correct? Often, there are other areas that need assistance when you are being treated with desiccated thyroid products. For one, many patients need to optimize their Ferritin/iron levels, which are low in many thyroid patients. Low Ferritin can cause very similar symptoms as being hypothyroid, OR can cause you to have hyper-like symptoms when you try to raise desiccated thyroid. If upon starting desiccated thyroid, you have very strange symptoms, including anxiety, insomnia, shakiness, it’s a strong sign that you may need adrenal support. Cortisol is needed to distribute thyroid hormones to your cells, and if you are not making enough cortisol from sluggish adrenals, your blood will be high in thyroid hormones, producing the above symptoms. Adrenal support is used to give back to your body what your adrenals are not, which in turn allows the thyroid hormones to get to your cells. Unless you have hypopituitary, adrenal support is not meant to be for life for most, but to allow your adrenals to rest and recover. It is strongly recommended that you do a 24 hour adrenal saliva test–there are labs you can do them with here. 24 hour saliva tests give you far better information than the one time blood test that doctors will tend to recommend. You don’t need a STIM test, by the way, unless there is strong suspicion of Addisons or a pituitary problem. Work with your doctor on all this.
Why do some patients take T3-only instead of desiccated thyroid? When your ferritin or B12 is too low, or your cortisol is too high or low, or other uncorrected issues are occurring, your body will tend to convert the T4 in desiccated thyroid to far more Reverse T3 (RT3) than you need. Excess RT3 clogs up cell receptors, preventing them from receiving optimal amounts of T3 in desiccated thyroid. You will also find yourself with excess T4 and toxic hyper-like symptoms of the excess. As a result, many patients feel the need to switch to T3-only. Cytomel is a popular brand prescribed by doctors. Chapter 12 in the STTM book is completely devoted to T3 and includes good information on RT3.
Are there any beneficial supplements that I can take with desiccated thyroid? Many patients take a Selenium tablet with their thyroid meds, which assists the T4 to T3 conversion. L-Tyrosine helps some patients, too. Zinc and Vit. C may play a role. Your need for B-vitamins will increase as you improve your energy levels. Some patients benefit from iodine supplementation. Optimizing your Vit. D levels can be important. Minerals are also important. Do research on the internet and also talk to your doctor.
Any other tips? Many patients are keen to having an emergency backup of desiccated natural thyroid just for that–emergencies! Desiccated thyroid has a long shelf life, but you can also wrap it securely to avoid damaging moisture and place it in the freezer.
Department of Endocrinology (T.D.H., V.Q.M., P.W.C., M.K.M.S.), Walter Reed National Military Medical Center, Bethesda, Maryland 20889; and Department of Preventive Medicine and Biometrics (C.H.O.), Uniformed Services University of Health Sciences, Bethesda, Maryland 20814
Address all correspondence and requests for reprints to: Mohamed K.M. Shakir, MD, Department of Endocrinology, Walter Reed National Military Medical Center, 8901 Wisconsin Avenue, Bethesda, Maryland 20889-5600. E-mail: firstname.lastname@example.org.
Context: Patients previously treated with desiccated thyroid extract (DTE), when being switched to levothyroxine (l-T4), occasionally did not feel as well despite adequate dosing based on serum TSH levels.
Objective: Our objective was to investigate the effectiveness of DTE compared with l-T4 in hypothyroid patients.
Design and Setting: We conducted a randomized, double-blind, crossover study at a tertiary care center.
Patients: Patients (n = 70, age 18–65 years) diagnosed with primary hypothyroidism on a stable dose of l-T4 for 6 months were included in the study.
Intervention: Patients were randomized to either DTE or l-T4 for 16 weeks and then crossed over for the same duration.
Outcome Measures: Biochemical and neurocognitive tests at baseline and at the end of each treatment period were evaluated.
Results: There were no differences in symptoms and neurocognitive measurements between the 2 therapies. Patients lost 3 lb on DTE treatment (172.9 ± 36.4 lb vs 175.7 ± 37.7 lb, P < .001). At the end of the study, 34 patients (48.6%) preferred DTE, 13 (18.6%) preferred l-T4, and 23 (32.9%) had no preference. In the subgroup analyses, those patients who preferred DTE lost 4 lb during the DTE treatment, and their subjective symptoms were significantly better while taking DTE as measured by the general health questionnaire-12 and thyroid symptom questionnaire (P < .001 for both). Five variables were predictors of preference for DTE.
Conclusion: DTE therapy did not result in a significant improvement in quality of life; however, DTE caused modest weight loss and nearly half (48.6%) of the study patients expressed preference for DTE over l-T4. DTE therapy may be relevant for some hypothyroid patients.
TSH Suppression Benefits and Adverse Effects by Jeffrey Dach MD
At a recent medical meeting I attended, “the danger of TSH suppression” was mentioned. The listening audience of doctors was advised not to suppress TSH with thyroid medication. We were advised to make sure the TSH always stays within the lab reference range.
Thyroid Excess and Thyrotoxicosis
Of course, we would all agree that too much thyroid medication causing thyroid excess and thyrotoxicosis is to be avoided, as this clearly is the most significant adverse effect of taking thyroid hormone pills. Taking too many pills is not a good thing, as this will cause a clinical syndrome known as thyrotoxicosis characterized by tachycardia, palpitations, insomnia, anxiety, panic attacks etc. The arrythmia, atrial fibrillation is the dreaded complication to be avoided.
Take the Time to Go Over Thyroid Excess List of Symptoms
We actually spend 5 or 10 minutes with each patient in the office talking about Thyroid excess signs and symptoms to look for, and we give each patient a print out of this list to take home and post on their bulletin board to read every day. If the patient experiences any symptoms of thyroid excess they are instructed to stop the thyroid pills. Patient selection is also a factor here, as a patient with early dementia could not be expected to have the cognitive function to recognize thyroid excess and stop their pill. The patient must be able and willing to play a role in their health care. Otherwise, they are not a candidate for natural thyroid treatment, and instead are referred to your local friendly endocrinologist for levothyroxine dosage and TSH in range.
Stop the Thyroid Pills
Thyroid excess is easily avoided by simply stopping the thyroid medication should signs of rapid resting heart rate occur. Symptoms will resolve within hours after stopping the natural thyroid pill. For T4 only levothyroxine, which has a longer half life, it takes longer for symptoms to resolve.
Is a low TSH indicative of Thyroid Excess ?
Mainstream endocrinology makes the assumption that a suppressed TSH indicates thyroid excess, and by definition, thyrotoxicosis. This is true for Graves disease and Toxic Nodular Goiter. In Graves disease with thyrotoxicosis, hypercalcemia from rapid bone turnover has beenreported. (21,22)
However, for the vast majority of hypothyroid patients taking natural dessicated thyroid (Nature-throid- RLC labs) a suppressed TSH merely indicates adequate treatment dosage with full clinical benefit, and does not correspond with the clinical signs and symptoms (or laboratory findings) of thyroid excess.
Monitoring the Other Labs and the Patient
Of course, we always monitor Free T3, Free T4, and Thyroid antibody levels, as well as monitor the patients clinical status. If the patient has a Free T3 and Free T4 in the normal range, and has no tachycardia at rest or any other symptoms of thyroid excess, then a suppressed TSH indicates adequate thyroid treatment, and by no stretch of the imagination could the patient possibly be in a state of thyroid excess or thyrotoxiciosis.
Adverse Health Effects of TSH Suppression
Another point mentioned at the medical meeting to persuade us clinicians not to suppress the TSH with thyroid mediation was the idea that there are adverse health consequences when the TSH is suppressed. The major one being loss of bone density, osteoporosis which is areal finding in long standing Graves Disease patients.
However numerous studies have examined this idea in hypothyroid patients treated with thyroid pills and found this to be a medical myth. In our patient population we see bone density improving, especially in women receiving bioidentical hormone replacement and bone supplements such as Vitamin D3, K2, magnesium and calcium..
As to the idea that there must be some adverse health effects of a suppressed TSH, this has also been examined in two groups of patients on long term TSH suppressive doses of thyroid medication, and this idea found to be false. In patients after thyroidectomy for papillary thyroid cancer who are commonly treated with TSH suppressive doses of thyroxine, there have been no adverse effects noted in many long term studies. Similarly in patients with thyroid nodules treated with TSH suppression, there have no ill effects of TSH suppression.
No Adverse Effects from Low TSH
below Reference Range in Large Scale Study
Dr Thierry Hertoghe, possibly the most recognized thyroid expert on the planet, suppresses TSH in about 30% of his patients. (personal communication)Left Image courtesy ofThierry Hertoghe.
Thyroid Receptor Mutation Requires TSH Suppressive doses of Thyroid Hormone
Another patient population are those patients with mutations in the Thyroid hormone receptor genes. The syndrome of peripheral thyroid hormone resistance was predicted and hypothesized twenty years ago, but only recently in 2013 was thegenetic defect in the receptor geneidentified. Patients with peripheral thyroid hormone resistance may require higher Free T3 levels to overcome the receptor defects.(23)
Normal Pregnant Women May Have a Suppressed TSH
During pregnancy, HCG levels rise to very high levels, and there isassociated suppression of TSH, not indicative of a hyperthyroid state. “In up to 10–20% of normal pregnant women, serum TSH concentrations are transiently low or undetectable.”(26)
Hypothalamic Dysfunction in the Chronic Fatigue Fibromyalgia – Central Hypothyroidism.(27-31)
Both Drs Kent Holtorf and Dr Jacob Teitelbaum have devoted much of their careers to the study and treatment of the chronic fatigue fibromyalgia patient. One of the keys to understanding the patho-physiology in this disorder ishypothalamic dysfunctionwhich may lead to central hypothyroidism. One of the pituitary hormones affected by hypothalamic dysfunction is the TSH (thyroid stimulating hormone) which may be paradoxically low even though the patient is in a hypothyroid state with chronic fatigue. Thus, according to both Drs Holtorf and Teitelbaum, the chronic fatigue patient may have central hypothyroidism with a suppressed TSH. (27-31) Again, it would be a clinical error to withhold thyroid hormone treatment from this patient because of a lab finding of a low or “suppressed” TSH. Left Image courtesy ofJacob Teitelbaum MD.
Chemotherapyduring cancer treatment may cause hypothalamic dysfunction in cancer-survivors. The TSH may be paradoxically low and unreliable in these cases.
It is common practice among endocrinologist to treat “euthyroid” Hashimotos patients with thyroxine (T4). “Euthyroid”, of course, meaning the TSH is in the lab reference range.Studiesshow benefit with treatment which reduces antibody levels and felt tostabilizethe autoimmune process and is recommended as soon as the diagnosis is established.
Conclusion:Long term TSH suppression in the thyroid nodule and thyroid cancer patient is a common practice of mainstream endocrinology with no adverse effects reported in many published studies. Since the TSH is a pituitary hormone, the TSH level may not always be an accurate reflection of peripheral thyroid levels, and may in fact be unreliable in chronic fatigue, fibromyalgia patients with hypothalamic dysfunction.
J Clin Endocrinol Metab. 1996 Dec;81(12):4278-89.
Effects on bone mass of long term treatment with thyroid hormones: a meta-analysis. Uzzan B1, Campos J, Cucherat M, Nony P, Boissel JP, Perret GY.
1Hôpital Avicenne, Centre Hospitale Universitaire Paris Nord, France.
Osteoporosis is the main cause of spine and hip fractures. Morbidity, mortality, and costs arising from hip fractures have been well documented. Thyroid hormones (TH) are widely prescribed, mainly in the elderly. Some studies (but not all) found a deleterious effect of suppressive TH therapy on bone mass. These conflicting data raised a controversy as to the safety of current prescribing and follow-up habits, which, in turn, raised major health-care issues. To look for a detrimental effect on bone of TH therapy, we performed a meta-analysis (by pooling standardized differences, using a fixed effect model) of all published controlled cross-sectional studies (41, including about 1250 patients) concerning the impact of TH therapy on bone mineral density (BMD). Studies with women receiving estrogen therapy were excluded a priori, as were studies with a high percentage of patients with postoperative hypoparathyroidism, when no separate data were available. We decided to stratify the data according to anatomical site, menopausal status, and suppressive or replacement TH therapy, resulting in 25 meta-analysis on 138 homogeneous subsets of data. The main sources of heterogensity between studies that we could identify were replacement or suppressive TH therapy, menopausal status, site (lumbar spine, femoral neck, Ward’s triangle, greater trochanter, midshaft and distal radius, with various percentages of cortical bone), and history of hyperthyroidism, which has recently been found to impair bone mass in a large epidemiological survey. To improve homogeneity, we excluded a posteriori 102 patients from 3 studies, who had a past history of hyperthyroidism and separate BMD data, thus allowing assessment of the TH effect in almost all 25 subset meta-analyses. However, controls were usually not matched with cases for many factors influencing bone mass, such as body weight, age at menarche and at menopause, calcium dietary intake, smoking habits, alcohol intake, exercise, etc.For lumbar spine and hip (as for all other sites), suppressive TH therapy was associated with significant bone loss in postmenopausal women (but not in premenopausal women), whereas, conversely, replacement therapy was associated with bone loss in premenopausal women (spine and hip), but not in postmenopausal women.The detrimental effect of TH appeared more marked on cortical bone than on trabecular bone. Only a large long term prospective placebo-controlled trial of TH therapy (e.g. in benign nodules) evaluating BMD (and ideally fracture rate) would provide further insight into these issues.
2)http://www.ncbi.nlm.nih.gov/pubmed/15278189 J Formos Med Assoc. 2004 Jun;103(6):442-7. Bone mineral density in women receiving thyroxine suppressive therapy for differentiated thyroid carcinoma. Chen CH1, Chen JF, Yang BY, Liu RT, Tung SC, Chien WY, Lu YC, Kuo MC, Hsieh CJ, Wang PW.
Most patients with well-differentiatedthyroid carcinomahave an excellent prognosis and are likely to live long enough to be subjected to osteoporosis. The purpose of this study was to investigate the consequences of treatment with a supraphysiological dose of levothyroxine (l-T4) on bone mineral density (BMD) in Taiwanese women with differentiated thyroid cancer.
METHODS:A total of69 (44 premenopausal, 25 postmenopausal)Taiwanese women withdifferentiated thyroid cancer were included in this retrospective study. These patients were free of disease recurrence after initial near-total thyroidectomy and I-131 radioablation, and had undergone regular l-T4 suppressive therapy for more than 3 years (mean, 7.3 +/- 3.0 years; range, 3 to 15 years). The degree of thyroid-stimulating hormone (TSH) suppression was determined based on the mean TSH score for each patient which was determined by analysis of all available follow-up TSH data, where 1 = undetectable TSH (< 0.2 mIU/mL); 2 = subnormal TSH (0.2 to 0.39 mIU/mL); 3 = normal TSH (0.4 to 4.0 mIU/mL); and 4 = elevated TSH (> 4.0 mIU/mL). The patients were divided into a full TSH suppression group with a mean TSH score in the range 1.0 to 1.99, and a partial TSH suppression group with a mean TSH score in the range 2.0 to 2.99. BMD was measured by dual-energy X-ray absorptiometry at the lumbar spine, femoral neck, Ward’s triangle and total hip. Comparisons between subgroups of patients and controls were performed by unpaired t test. Correlation between BMD and other clinical variables was assessed by Pearson’s correlation analysis.
RESULTS:Postmenopausal patients (aged 57.7 +/- 6.9 years) had significantly higher serum calcium levels and decreased BMD at all sites of the spine and hip as compared with premenopausal patients (aged 38.6 +/- 6.7 years) with similar BMI and duration of TSH suppression. Comparison of BMD between postmenopausal patients and BMI- and age-matched controls revealed that the patient group had decreased BMD at all sites of measurement, although this difference was not significant. This phenomenon was not observed in the premenopausal patients. Furthermore, when BMD was compared between patients categorized as having full and partial suppression of TSH, only patients with full suppression in the postmenopausal group showed a tendency to lower BMD.There was a strong correlation of BMD with age, BMI and serum calcium level. However, no correlation was found between BMD and degree of TSH suppression or duration of l-T4 suppression therapy.
CONCLUSION:Women with differentiated thyroid cancer who had long-term (mean, 7.3 +/- 3.0 years) l-T4 therapy and suppressed TSH levels had no evidence of lower BMD.However, patients with full suppression in the postmenopausal group showed a tendency towards lower BMD. Therefore, careful monitoring of BMD in postmenopausal women during suppression therapy is mandatory.
Endocr Regul. 2010 Apr;44(2):57-63.
Thyrotropin versus thyroid hormone in regulating bone density and turnover in premenopausal women. Baqi L1, Payer J, Killinger Z, Hruzikova P, Cierny D, Susienkova K, Langer P.
This cross-sectional study aimed to evaluate the interrelations between endogenous TSH level on one side and the status of bone mineral density (BMD) and bone metabolic turnover (BMT) on the other in pooled four groups of premenopausal women either without or with a long-term L-thyroxine treatment.
METHODS:Serum levels of free thyroxine (FT4), thyrotropin (TSH), calcium (Ca), alkaline phosphatase (ALP), osteocalcin OC) and cross linked N-telopeptide of type 1 collagen (NTx) as well as urinary calcium (U-Ca/24h), bone mineral density of lumbar spine L 1-4 (BMD-L) and femoral hip (BMD-F) were estimated in a cohort of 151 premenopausal women (median 36 years) consisting of four groups: Group 1, 40 healthy untreated women, while three other groups consisted of patients previously treated for about 5 years; Group 2, 41 patients with genuine hypothyroidism treated by L-thyroxine (50-100 microg daily); Group 3, 40 patients with genuine hyperthyroidism treated by Carbimazol (10-15 mg daily); Group 4, 30 patients treated by suppressive doses of L-thyroxine (100-150 microg daily) after thyroidectomy for thyroid cancer (n=10) or because of progressively growing benign goitre (n=20).
RESULTS:When using multiple correlation analysis (Pearson’s r) in pooled 151 women, TSH showed significant positive correlation with BMD-L (p<0.01) and BMD-F (p<0.001) and, at the same time, significant negative correlation with serum level of BMT markers such as ALP (p<0.05), OC (p<0.05) and NTx (p<0.01), while the correlation of FT4 with BMD-L, BMD-F was significantly negative (p<0.001 for both) and that with all BMT markers was significantly positive (p<0.05 to <0.001). Thus, it appeared that higher TSH level was associated with increased bone mineral density and, at the same, with decreased bone metabolic turnover. These interrelations were further supported by the findings of significantly lower BMD-F (p<0.01), BMD-L (p<0.001) and significantly higher ALP, OC and NTX (all at p<0.001) in the group of 36 women with TSH level<0.3 mU/l as compared to the group of 115 women with TSH level range of 0.35-6.3 mU/l).
CONCLUSIONS:Irrespectively of thyroid diagnosis and/or previous long term thyroxine treatment in some groups, this cross sectional study showed that, after the pooled group of 151 women has been redistributed according to the actual TSH level, the bone mineral density and the level of bone turnover markers was significantly more favorable in 115 subjects with TSH level range of 0.35-6.3 mU/l than these in 36 women with TSH<0.3 mU/l.
N Engl J Med. 1987 Jul 9;317(2):70-5.
Suppressive therapy with levothyroxine for solitary thyroid nodules. A double-blind controlled clinical study. Gharib H, James EM, Charboneau JW, Naessens JM, Offord KP, Gorman CA.
Thyroid nodules are present in up to 50 percent of adults in the fifth decade of life. Patients are often treated with thyroxine in order to reduce the size of the nodule, but the efficacy of thyrotropin-suppressive therapy with thyroxine remains uncertain. In this study,53 patientswith a colloid solitary thyroid nodule confirmed by biopsy were randomly assigned in a double-blind manner to receive placebo (n = 25) or levothyroxine (n = 28) for six months. Before treatment, pertechnetate-99m thyroid scanning showed that 22 percent of the nodules were functional, 25 percent hypofunctional, and 53 percent nonfunctional. High-resolution (10-MHz) sonography was used to measure the size of the nodules before and after treatment. Suppression of thyrotropin release was confirmed in the levothyroxine-treated group by the administration of thyrotropin-releasing hormone; thyrotropin release was normal in the placebo group. Six months of therapy did not significantly decrease the diameter or volume of the nodules in the levothyroxine group as compared with the placebo group. We conclude that the efficacy of levothyroxine therapy in reducing the size of colloid thyroid nodules is not apparent within six months, despite effective suppression of thyrotropin.
J Clin Endocrinol Metab. 2002 Nov;87(11):4928-34.
Effects of thyroid-stimulating hormone suppression with levothyroxine in reducing the volume of solitary thyroid nodules and improving extranodular nonpalpable changes: a randomized, double-blind, placebo-controlled trial by the French Thyroid Research Group. Wémeau JL1, Caron P, Schvartz C, Schlienger JL, Orgiazzi J, Cousty C, Vlaeminck-Guillem V.
The efficacy of suppressing TSH secretion with levothyroxine (L-T(4)) in reducing solitary thyroid nodule growth is still controversial. In this prospective multicenter, randomized, double-blind, placebo-controlled trial, 123 patients with a single palpable benign nodule were included and randomly allocated to an 18-month treatment with L-T(4) or placebo. Individual dose was adjusted to allow a serum TSH level below 0.3 mIU/liter. Clinical and ultrasonographic nodule characteristics were assessed before treatment and 3, 6, 12, and 18 months thereafter. The largest mean nodule size assessed on palpation and largest volume, assessed by ultrasonography, decreased in the L-T(4) group and increased slightly in the placebo group [size, -3.5 +/- 7 mm vs. +0.5 +/- 6 mm (P = 0.006); volume, -0.36 +/- 1.71 ml vs. +0.62 +/- 3.67 ml (P = 0.01), respectively]. The proportion of clinically relevant volume reduction (> or =50%) rose significantly in the L-T(4) group [26.6% vs. 16.9% (P = 0.04)]. The proportion of patients with a reduced number of infraclinical additional nodules was significantly higher in the L-T(4) group [9.4% vs. 0 (P = 0.04)]. It is concluded from this study that suppressive L-T(4) therapy is effective in reducing solitary thyroid nodule volume and improving infraclinical extranodular changes.
Ir J Med Sci. 1992 Dec;161(12):684-6.TSH as an index of L-thyroxine replacement and suppression therapy.Igoe D1, Duffy MJ, McKenna TJ.
When hypothalamic-pituitary function is normal, serum TSH levels measured by ultrasensitive assay yield bioassays of endogenous thyroid action and thus provide an ideal index of thyroid secretion and its relationship to fluctuating endogenous thyroid levels. It is theoretically possible that patients receiving exogenous L-thyroxine for primary hypothyroidismshould have suppressed TSH levels if physiological needs are constantly met. To examine this possibility free thyroxine, FT4 and TSH were measured in 90 clinically euthyroid patients receiving treatment with L-thyroxine for primary hypothyroidism.TSH levels were normal in 44, suppressed in 16 and elevated in 30 patients.FT4 levels were normal in 68, elevated in 13 and suppressed in 9 patients. Normal TSH levels were associated with normal FT4 levels in 79.5% of patients, elevated FT4 levels in 13.6% and low FT4 in 6.8%. Suppressed TSH levels were associated with elevated FT4 levels in 37.5% of patients and normal FT4 levels in 62.5%. When FT4 levels were normal, however, TSH levels were normal in only 51.5% and abnormal in 48.5%. We also examined the possibility that FT4 levels may remain within normal range when TSH is suppressed during L-thyroxine treatment for goitre or cancer. FT4 and TSH were measured in 45 patients on L-thyroxine as TSH suppression treatment.TSH was suppressed in 23 patients(51.1%), normal in 20 (44.4%) and elevated in 2 (4.5%). When TSH was suppressed, FT4 was elevated in 30.4% but normal in 69.6% of patients.(ABSTRACT TRUNCATED AT 250 WORDS)
Suppressive Therapy with Levothyroxine for Solitary Thyroid Nodules: A Double-blind Controlled Clinical Study and Cumulative Meta-analyses
Flávio Zelmanovitz 2 , Sandra Genro, and Jorge L. Gross
JCEM July 01, 2013
The data obtained in this studydo not suggest any significant decrease in BMD after 1 yr of treatment with suppressive doses of T4.However, a meta-analysis of related studies, performed by Uzzan et al., demonstrated that suppressive therapy decreased the BMD in 409 postmenopausal patients after an average of 9.6 yr (11).
Ann Intern Med. 2001 Apr 3;134(7):561-8.
Risk for fracture in women with low serum levels of thyroid-stimulating hormone.
Bauer DC1, Ettinger B, Nevitt MC, Stone KL; Study of Osteoporotic Fractures Research Group.
Biochemical evidence of hyperthyroidism may be associated with low bone mass, particularly in older postmenopausal women, but no prospective studies of thyroid function and subsequent fracture risk have been done.
OBJECTIVE:To examine the association between low levels of thyroid-stimulating hormone (TSH) and fracture in older women.
DESIGN:Prospective cohort study with case-cohort sampling.
SETTING:Four clinical centers in the United States.
PATIENTS:686 women older than 65 years of agefrom a cohort of 9704 women recruited from population-based listings between 1986 and 1988.
MEASUREMENTS:Baseline assessment of calcaneal bone mass, spine radiography, and history of thyroid disease. Spine radiography was repeated after a mean follow-up of 3.7 years; nonspine fractures were centrally adjudicated. Thyroid-stimulating hormone was measured in sera obtained at baseline from 148 women with new hip fractures, 149 women with new vertebral fractures, and a subsample of 398 women randomly selected from the cohort.
RESULTS:After adjustment for age, history of previous hyperthyroidism, self-rated health, and use of estrogen and thyroid hormone, women with a low TSH level (0.1 mU/L) had athreefold increased risk for hip fracture(relative hazard, 3.6 [95% CI, 1.0 to 12.9]) and afourfold increased risk for vertebral fracture(odds ratio, 4.5 [CI, 1.3 to 15.6]) compared with women who had normal TSH levels (0.5 to 5.5 mU/L). After adjustment for TSH level, a history of hyperthyroidism was associated with a twofold increase in hip fracture (relative hazard, 2.2 [CI, 1.0 to 4.4]), but use of thyroid hormone itself was not associated with increased risk for hip fracture (relative hazard, 0.5 [CI, 0.2 to 1.3]).
CONCLUSIONS:Women older than 65 years of age who have low serum TSH levels, indicating physiologic hyperthyroidism, are at increased risk for new hip and vertebral fractures. Use of thyroid hormone itself does not increase risk for fracture if TSH levels are normal.
Clin Endocrinol (Oxf). 1992 Dec;37(6):500-3.
Morbidity in patients on L-thyroxine: a comparison of those with a normal TSH to those with a suppressed TSH. Leese GP1, Jung RT, Guthrie C, Waugh N, Browning MC.
Patients on L-thyroxine with a ‘suppressed’ TSH (< 0.05 mU/l) were compared to those in whom TSH was detectable but not elevated (0.05-4.0 mU/l), with regard to morbidity data.
DESIGN:Biochemical data from Tayside Thyroid Register was matched to hospital admissions data obtained from Health Board Statistics.
PATIENTS:The patients were identified from those registered on the computerized Tayside Register.
MEASUREMENTS:Serum T4 and TSH assays, clinical assessment scores, and admission records with regard to ischaemic heart disease, overall fractures, fractured neck of femur and breast carcinoma.
RESULTS:Over one year, 1180 patients on thyroxine replacement had clinical and biochemical assessment; 59% had a suppressed TSH and 38% ‘normal’ TSH. Patients with a suppressed TSH exhibited higher median serum thyroxine levels (146 nmol/l, range 77-252 vs 119 nmol/l, 58-224; P < 0.001). Patients under the age of 65 years on L-thyroxine had an increased risk of ischaemic heart disease compared to the general population (female 2.7 vs 0.7%, P < 0.001; male 6.4 vs 1.7%, P < 0.01), but the risk was no different between those with suppressed and normal TSH.There was no increase in risk for overall fracture, fractured neck of femur or breast carcinoma in those on thyroxine with suppressed or normal TSH.
CONCLUSION:Patients under the age of 65 years on L-thyroxine had an increased risk of ischaemic heart disease.There was no excess of fractures in patients on L-thyroxine even if the TSH is suppressed.
J Clin Endocrinol Metab. 1997 Sep;82(9):2931-6. Low thyrotropin levels are not associated with bone loss in older women: a prospective study. Bauer DC1, Nevitt MC, Ettinger B, Stone K.
The relationship between excess thyroid hormone and bone loss is controversial. To determine whether low TSH levels, indicating excessive thyroid hormone, are associated with low bone mass or accelerated bone loss in older women, we performed a prospective cohort study of 458 women over age 65 yr participating in the multicenter Study of Osteoporotic Fractures. Three hundred and twenty-three women were randomly selected from the entire cohort of 9704; an additional 135 randomly selected thyroid hormone users were studied. Medical history, medication use, and calcaneal bone mineral density (BMD) were assessed at the baseline visit. Serum was collected and stored at -190 C. Hip and spine BMD were measured approximately 2 yr later, and follow-up calcaneal and hip BMD measurements were obtained after mean follow-up periods of 5.7 and 3.5 yr, respectively. TSH levels were determined in baseline serum samples using a third generation chemiluminescent assay. After adjustment for age, weight, previous hyperthyroidism, and use of estrogen, bone loss over 4-6 yr was similar in women with low, normal, or high TSH. For example, femoral neck bone loss was -0.3%/yr (95% confidence interval, -0.8%, 0.3%) among women with low TSH (< or = 0.1 mU/L) and -0.5%/yr (95% confidence interval, -0.7%, -0.3%) in those with normal TSH (0.1-5.5 mU/L). There were no statistically significant differences in baseline bone mass of the calcaneus, spine, or femoral neck or trochanteric hip subregions. Baseline total hip BMD was 6% lower (P = 0.01) in women with low TSH. Similar results were obtained in analyses confined to women not taking estrogens. We found no consistent evidence that low TSH, a sensitive biochemical marker of excess thyroid hormone, was associated with low BMD or accelerated bone loss in older ambulatory women.
conclusion, in this prospective study of thyroid function and skeletal health in older women,we found no consistent evidence that low TSH was associated with low bone mass or accelerated bone loss.
To determine the effect of long-term use of thyroid hormone on bone mineral density (BMD) in elderly women and the potential mitigating effects of estrogen replacement therapy.
DESIGN:Cross-sectional, community-based study.
SETTING:Rancho Bernardo, Calif.
PARTICIPANTS:A total of 991 white women aged 50 to 98 years who participated in a study of osteoporosis.
MAIN OUTCOME MEASURES:Bone mineral density at the ultradistal radius and midshaft radius using single-photon absorptiometry and at the hip and lumbar spine using dual-energy x-ray absorptiometry.
RESULTS:A total of 196 women taking thyroid hormone for a mean duration of 20.4 years were compared with 795 women who were not using thyroid hormone. Women taking daily thyroxine-equivalent doses of 200 micrograms or more had significantly lower BMD levels at the midshaft radius and hip compared with those taking less than 200 micrograms. Daily doses of 1.6 micrograms/kg and greater were associated with lower bone mass at all four sites compared with nonuse, whereas doses less than 1.6 micrograms/kg were not associated with lower BMD levels. These associations were independent of age, body mass index, smoking status, and use of thiazides, corticosteroids, and estrogen. Women taking both estrogen and a thyroid hormone dose of 1.6 micrograms/kg or greater had significantly higher BMD levels at all four sites than women taking the same thyroid hormone dose alone. Women taking both thyroid hormone and estrogen had BMD levels comparable with those observed in women taking only estrogen.
CONCLUSIONS:Long-term thyroid hormone use at thyroxine-equivalent doses of 1.6 micrograms/kg or greater was associated with significant osteopenia at the ultradistal radius, midshaft radius, hip, and lumbar spine. Estrogen use appears to negate thyroid hormone-associated loss of bone density in postmenopausal women. Women taking both thyroid hormone and estrogen had BMD levels comparable with those observed in women taking only estrogen.
J Bone Miner Res. 1997 Jan;12(1):72-7.
Skeletal integrity in men chronically treated with suppressive doses of L-thyroxine. Marcocci C1, Golia F, Vignali E, Pinchera A.
We measured bone mineral density (BMD) (lumbar spine, femoral neck, Ward’s triangle, and trochanter) in 34 men given suppressive doses of levothyroxine (L-T4) for a mean of 10.2 years. Indications for treatment were nontoxic goiter (n = 5) or thyroidectomy for differentiated thyroid cancer (n = 6) or nontoxic goiter (n = 3). Patients were followed at our institution and treated with the minimal amount of L-T4 able to suppress thyroid-stimulating hormone (TSH). At the time of evaluation, free T3 was normal in all cases, whereas free T4 was increased in 14 men (41.2%). The mean daily dose of L-T4 was 172 +/- 6 microg, and the cumulative dose of L-T4 was 673 +/- 71 mg. We found no significant difference between patients and age- and weight-matched controls in BMD (g/cm2) at any site of measurement (lumbar spine 1.144 +/- 0.12 vs. 1.168 +/- 0.15; femoral neck 0.979 +/- 0.13 vs. 1.001 +/- 0.13; Ward’s triangle 0.854 +/- 0.17 vs. 0.887 +/- 0.15; and trocanther 0.852 +/- 0.13 vs. 0.861 +/- 0.13). BMD was not correlated with the duration of therapy, cumulative or mean daily dose of L-T4, serum levels of free T4, free T3, osteocalcin, and bone alkaline phosphatase. Serum calcium and osteocalcin were slightly but significantly elevated in patients compared with controls, whereas there was no difference in intact parathyroid hormone, bone alkaline phosphatase, and sex hormone-binding globulin (marker of thyroid hormone action).Our data suggest that L-T4 suppressive therapy, if carefully carried out and monitored, using the smallest dose necessary to suppress TSH secretion, has no significant effects on bone metabolism and bone mass in men.
Carefully monitored levothyroxine suppressive therapy isnotassociated with bone loss in premenopausal women. Marcocci C, et al. J Clin Endocrinol Metab. 1994.
We measured total body and regional (lumbar spine, femoral neck, Ward’s triangle, and trochanter) bone mineral density (BMD) in 47 premenopausal women chronically treated with suppressive doses of levothyroxine (L-T4). Treatment was administered to 7 patients with nontoxic goiter or, after thyroidectomy, to 38 patients with differentiated thyroid cancer and 2 with nontoxic goiter. Patients were followed at our institution and treated with the minimal amount of L-T4 necessary to suppress TSH. At the time of evaluation, free T3 was normal in all cases, whereas free T4 was increased in 17 (36.2%). The mean daily dose of L-T4 was 154.3 +/- 5 micrograms, and the mean duration of treatment was 10.1 yr. We found no significant difference between patients and age- and weight-matched controls in BMD at any site of measurement. BMD was not correlated with duration of therapy, cumulative or mean daily dose of L-T4, serum levels of free T4, free T3, and osteocalcin. There was no difference between patients and controls in serum total calcium, intact PTH, osteocalcin, or carboxy-terminal cross-linked telopeptide of type I collagen or in the concentrations of two markers of thyroid hormone action (sex hormone-binding globulin and amino-terminal propeptide of type III procollagen).Our data suggest that L-T4 suppressive therapy, if carefully carried out and monitored, using the smallest dose necessary to suppress TSH secretion has no significant effect on bone metabolism or bone mass.
Thyroid. 1995 Apr;5(2):81-7.Possible limited bone loss with suppressive thyroxine therapy is unlikely to have clinical relevance. Müller CG1, Bayley TA, Harrison JE, Tsang R.
To determine the effect of suppressive doses of thyroxine (T4) on bone mass, we studied 50 women on suppressive doses of T4 for 3-27 years (mean of 11 years). Twenty-five had nontoxic goiter and 25 had well-differentiated thyroid carcinoma. Fifty controls were matched for age, menopausal status, and body mass index. Bone mineral density (BMD) was measured in the lumbar spine (LS), femoral neck (FN), trunk (TK), and extremities (EXT) by dual-energy X-ray absorptiometry (DXA). In addition, the trunk area was measured by neutron activation analysis and recorded as a calcium bone index (CaBI). Twenty-one patients were restudied with DXA measurements at a mean of 1.5 +/- 0.5 (1 SD) years. The total population of 50 patients showed no difference in bone mass from controls. In patients with nontoxic goiter, there was no evidence of any loss in bone mass. Cancer patients showed insignificant reductions of 2-5% in BMD of LS, FN, and TK and a significant 5% reduction in BMD of EXT, compared to controls, and a 12% reduction in CaBI compared to goiter patients. Cancer patients had a slightly higher (p < 0.001) mean daily dose of T4 than goiter patients (0.23 vs 0.15 mg/day) but had a similar degree of TSH suppression. BMD and CaBI values did not correlate with free T4 index) with the daily T4 dose, accumulative dose, or with duration of T4 therapy.There were no significant changes in bone mass in either goiter or cancer patients restudied after a mean of 1.5 years.
Thyroid. 1995 Feb;5(1):13-7.Suppressive doses of thyroxine do not accelerate age-related bone loss in late postmenopausal women.
Fujiyama K1, Kiriyama T, Ito M, Kimura H, Ashizawa K, Tsuruta M, Nagayama Y, Villadolid MC, Yokoyama N, Nagataki S.
To examine whether suppressive doses of thyroxine have any adverse effects on bone, we evaluated various bone metabolic markers (lectin-precipitated alkaline phosphatase, osteocalcin, carboxyl-terminal region of type I collagen propeptide, tartrate-resistant alkaline phosphatase, and urinary excretion of hydroxyproline and pyridinium crosslinks), incidence of vertebral deformity, total body and regional (lumbar spine and radius) bone mineral densities (BMDs), and rates of bone loss in 24 late postmenopausal (more than 5 years after menopause) women who were treated with levothyroxine (L-T4) after total thyroidectomy for differentiated carcinoma. Depending on the clinical records, including serum TSH levels measured by immunoradiometric assay, these patients were divided into two groups. One group of patients was given suppressive doses of L-T4 (TSH < 0.1 mU/L, n = 12) and the other group was given nonsuppressive doses of L-T4 (TSH > 0.1 mU/L, n = 12). There was no difference in bone metabolic markers and incidence of vertebral deformity between the groups. In patients with TSH suppression, Z-scores of BMDs calculated from age-matched healthy women (n = 179, aged 55 to 80) were nearly in the zero range of values (0.077 at total body, 0.228 at lumbar spine, and -0.117 at trabecular region of lumbar spine). The rate of bone loss in TSH-suppressed patients (-0.849 +/- 0.605%/year) was not significantly different from that of nonsuppressed patients (-0.669 +/- 0.659). These prospective and cross-sectional data suggest thatlong-term levothyroxine therapy using suppressive doses has no significant adverse effects on bone.
Clin Endocrinol (Oxf). 1993 Nov;39(5):529-33. Suppressed TSH levels secondary to thyroxine replacement therapy are not associated with osteoporosis. Grant DJ1, McMurdo ME, Mole PA, Paterson CR, Davies RR.
Recent studies have suggested that patients receiving thyroxine are at increased risk of osteoporosis. We set out to measure bone mineral densities in two groups of post-menopausal women receiving thyroxine replacement therapy (those with serum TSH levels persistently suppressed or non-suppressed) and to compare the results in both groups with those of the local control population.
PATIENTS:Seventy-eight post-menopausal women who had been treated with thyroxine for primary autoimmune or idiopathic hypothyroidism for a minimum of 5 years, 44 with TSH persistently suppressed and 34 non-suppressed. One hundred and two control subjects.
MEASUREMENTS:Forearm bone mineral density at proximal and distal sites as measured by single-photon absorptiometry.
RESULTS:Results were expressed as Z-scores, i.e. number of standard deviations from the mean of a 5-year age-band from the local control population. Mean Z-scores at proximal and distal sites for the non-suppressed patients were -0.03 and -0.07 and for the suppressed patients were -0.20 and -0.25, representing a decrease in bone mineral density of at most 5% in the suppressed patients. The differences between the three groups were not statistically significant.
CONCLUSION:In this patient population, the reduction in bone mineral density due to thyroxine is small. It is unlikely to be of clinical significance and should not on its own be an indication for reduction of thyroxine dose in patients who are clinically euthyroid.
Lack of deleterious effect on bone mineral density of long-term thyroxine suppressive therapy for differentiated thyroid carcinoma
J L Reverter, S Holgado1, N Alonso, I Salinas, M L Granada2 and A Sanmartí
Department of Endocrinology and Nutrition, Germans Trias i Pujol Hospital, Carretera de Canyet s/n. 08916, Badalona, Barcelona, Spain
1Department of Rheumatology, Germans Trias i Pujol Hospital, Badalona, Barcelona, Spain
2Hormone Laboratory, Germans Trias i Pujol Hospital, Badalona, Barcelona, Spain
The effect of subclinical hyperthyroidism on bone mineral density is controversial and could be significant in patients with differentiated thyroid carcinoma who receive suppressive doses of levothyroxine (LT4). To ascertain whether prolonged treatment with LT4 to suppress thyrotropin had a deleterious effect on bone mineral density and/or calcium metabolism in patients thyroidectomized for differentiated thyroid cancer we have performed a cross-sectional study in a group of 88 women (mean ± SD age: 51 ± 12 years) treated with LT4 after near-total thyroidectomy and in a control group of 88 healthy women (51 ± 11 years) matched for body mass index and menopausal status. We determined calcium metabolism parameters, bone turnover marker N-telopeptide and bone mass density by dual-energy X-ray absorptiometry. No differences were found between patients and controls in calcium metabolism parameters or N-telopeptide except for PTH, which was significantly increased in controls. No differences were found between groups in bone mineral density in femoral neck (0.971 ± 0.148 gr/cm2 vs 0.956 ± 0.130 gr/cm2 in patients and controls respectively, P = 0.5). In lumbar spine, bone mineral density values were lower in controls than in patients (1.058 ± 0.329 gr/cm2 vs 1.155 ± 0.224 gr/cm2 respectively, P<0.05). When premenopausal (n = 44) and postmenopausal (n = 44) patients were compared with their respective controls, bone mineral density was similar both in femoral neck and lumbar spine. The proportion of women with normal bone mass density, osteopenia and osteoporosis in patient and control groups was similar in pre- and postmenopausal women. In conclusion, long-term suppressive LT4 treatment does not appear to affect skeletal integrity in women with differentiated thyroid carcinoma.
Endocrinol Nutr. 2011 Feb;58(2):75-83. doi: 10.1016/j.endonu.2010.09.007. Epub 2011 Jan 17.
[Potential risks of the adverse effects of thyrotropin suppression in differentiated thyroid carcinoma].
[Article in Spanish]
Reverter JL1, Colomé E.
In patients with differentiated thyroid carcinoma, long-term inhibition of thyrotropin (TSH) secretion through levothyroxine administration is required when there is evidence of persistent or recurrent disease. In these cases, levothyroxine doses should be monitored to achieve the objectives of inhibiting TSH and avoiding clinical hyperthyroidism. The possibility that suppressive therapy may produce deleterious effects is still controversial, mainly in elderly patients. There are many studies on the potential harmful effects of suppressive therapy on various organs and systems with discrepant results. However, there is no scientific evidence that the clinical impact of these effects is significant.
Endocrinol Nutr. 2010 Oct;57(8):350-6. doi: 10.1016/j.endonu.2010.03.015. Epub 2010 May 24.
[Clinical endocrinologists’ perception of the deleterious effects of TSH suppressive therapy in patients with differentiated thyroid carcinoma].
[Article in Spanish]
Reverter JL1, Colomé E, Puig Domingo M, Julián T, Halperin I, Sanmartí A.
To explore the opinion of clinical endocrinologists as to the deleterious effects of thyrotropin (TSH) suppressive therapy in patients with differentiated thyroid carcinoma (DTC).
MATERIALS AND METHODS:
A self-administered survey was sent by e-mail to a group of endocrinologists with expertise in the treatment of patients with differentiated thyroid carcinoma. The questionnaire consisted of three questions related to: 1) the possible adverse effects of this therapy on different organ systems, 2) the clinical significance of these effects and 3) the usefulness of treatment guidelines for DTC.
RESULTS:A total of 91 endocrinologists responded with a wide divergence of opinions. No question had more than 80% of answers in a particular option. Of the possible side effects of suppressive therapy, a high degree of ignorance to three of them (increased left ventricular mass, reentrant tachycardia and diastolic dysfunction). Most respondents felt that the seven items, dementia and Alzheimer, decreased quality of life, decreased bone mineral density (BMD) in premenopausal women and men, thromboembolic disease, signs and symptoms of hyperthyroidism and increased risk of fractures were not affected by suppressive therapy, while most responded positively to two items (increased heart rate and decreased BMD in postmenopausal women). Eighty percent of the respondents felt that in any case these effects were not clinically significant and 33% considered that treatment guidelines should be reviewed.
CONCLUSIONS:Clinical endocrinologists seem to have a very heterogeneous opinion regarding the potential harmful effects of TSH-suppressive therapy for DTC.
We aimed to examine the safety of having a TSH which was either suppressed(≤0.03 mU/l), low (0.04–0.4 mU/l), ‘normal’ (0.4–4.0 mU/l) or raised (>4.0 mU/l)in a population-based cohort of patients all of whom were treated with thyroxine.
There were a total of16 426patients on thyroxine replacement (86% female, mean age 60 years) with a total follow-up of74 586 years. Cardiovascular disease, dysrhythmias and fractures were increased in patients with a high TSH (adjusted hazards ratio 1.95 (1.73–2.21), 1.80 (1.33–2.44) and 1.83 (1.41–2.37) respectively), and patients with a suppressed TSH (1.37 (1.17–1.6), 1.6 (1.1–2.33) and 2.02 (1.55–2.62) respectively), when compared to patients with a TSH in the laboratory reference range.Patients with a low TSH did not have an increased risk of any of these outcomes (HR: 1.1 (0.99–1.123), 1.13 (0.88–1.47) and 1.13 (0.92–1.39) respectively.
33) Nuklearmedizin. 1999;38(5):144-9.
[Effect of iodine and thyroid hormones in the induction and therapy of Hashimoto’s thyroiditis]. [Article in German] Rink T1, Schroth HJ, Holle LH, Garth H.
The effect of an iodine prophylaxis on the induction of Hashimoto’s thyroiditis as well as the influence of various therapeutic approaches on the course of antithyroglobulin (TgAb) and antiperoxidase (TPOAb) antibodies in manifest diseases are evaluated.
METHOD: A collective of 375 euthyroid subjects without relevant goiter received daily doses of 200 micrograms iodide, weekly doses of 1.53 milligrams iodide, or no medication. A second group of 377 patients suffering from Hashimoto’s thyroiditis was treated with a non-suppressive hormone medication,a suppressive hormone administration, a combination of a non-suppressive hormone therapy with low dose iodide (50-150 micrograms/day), mere iodide in doses of 200 micrograms/day, or received no therapy. The mean observation period in these two groups was 860 and 848 days, respectively.
There was no significant increase of the antibody levels in the subgroup with 200 micrograms iodide/day and in the non-treated subjects of the first collective. However, the group that received 1.53 milligrams iodide/week presented a distinct increase of the TgAb as well as the TPOAb, and the incidence of Hashimoto’s thyroiditis was 4-fold higher than in the two other subgroups. The patients of the second collective revealed a significant decrease of the TgAb in the subgroups treated with up to 200 micrograms iodide/day,while the reduction of the TPOAb depended on the thyrotropin level(TSH) and was most significant in the suppressed group(p < 0.0001).
To lower the incidence of autoimmune thyroid diseases in predisposed subjects, a daily iodine supplementation seems to be superior to high-dose weekly administrations. A hormone therapy combined with a daily, low-dose iodine medication is able to reduce the TgAb and the TPOAb levels even in patients with Hashimoto’s thyroiditis.
Hashimoto’s thyroiditis is the most frequent autoimmune thyroid disease. L-thyroxine therapy can reduce the incidence and alleviate the symptoms of this disease. The aim of this study was to evaluate the effects of prophylactic L-thyroxine treatment on clinical and laboratory findings of patients who wereeuthyroidat the time of diagnosis.
Thirty-three patients who had diagnosis of euthyroid Hashimoto’s thyroiditis were randomized to two groups, one group received prophylactic L-thyroxine treatment and the other was followed-up without treatment. Initial thyroid function tests, autoantibodies, ultrasonography, fine needle aspiration biopsy and peripheral blood lymphocyte subsets were similar in the two study groups. After 15 months of L-thyroxine treatment, there was a significant increase in free T4 and asignificant decrease in TSHand anti-thyroglobulin antibody anti-thyroid peroxidase antibody levels. CD8+ cell counts increased in both groups, CD4/CD8 levels decreased significantly because of the increase in CD8+ cell count levels. Though there was no change in cytological findings, ultrasonography showed a decrease in thyroid volume in L-thyroxine receiving patients whereas an increase was detected in patients who were followed without treatment.In conclusion, prophylactic thyroid hormone therapy can be used in patients with Hashimoto’s thyroiditis even if they are euthyroid.
Padberg, Heller K, Usadel KH, Schumm-Draeger PM
Medica Clinic l, Endocrinology, Center of Internal Medicine, Johann Wolfgang Goethe-University, Frankfurt/Main, Germany. Thyroid : Official Journal of the American Thyroid Association [2001, 11(3):249-255]
Studies in animal models of spontaneous Hashimoto’s autoimmune thyroiditis (HT) show that prophylactic treatment with levothyroxine (LT4) can reduce incidence and degree of lymphocytic infiltration in HT. The aim of the present study was to clarify whether there is a benefit of prophylactic treatment with LT4 in patients with euthyroid HT with respect to the progression of the autoimmune process. Twenty-one patients with euthyroid HT were checked for thyroid function (thyrotropin [TSH], free triiodothyronine [FT3], free thyroxine [FT4]), thyroid volume, antibodies (thyroglobulin [Tg-Ab], thyroid peroxidase [TPO-Ab]), and lymphocyte subsets. Peripheral (PBL) and thyroid-derived lymphocytes (TL) were analyzed by triple color flow cytometry. One-half of the patients with euthyroid HT were treated with LT4 for 1 year (n = 10). The other half (n = 11) were never treated with LT4. TL were obtained by fine-needle aspiration biopsy (FNAB). Thirteen healthy subjects (C) without medical history of thyroid disease served as controls concerning PBL, and patients with non-toxic nodular goiter (NG; n = 10) served as controls concerning TL. Thyroid-derived T-helper cells were found more frequently in euthyroid patients with HT compared to patients with NG (p < 0.01).After 1 year of therapy with LT4, TPO-Abs and B lymphocytes decreased significantly only in the treated group of euthyroid patients with HT (p < 0.05). In contrast, TPO-Abs levels did not change or even increased in untreated euthyroid patients with HT.Thyroid volume did not differ before and after therapy. Prophylactic treatment of euthyroid patients with HT reduced both serological and cellular markers of autoimmune thyroiditis.Therefore, prophylactic LT4 treatment might be useful to stop the progression or even manifestation of the disease.However, the long-term clinical benefit of prophylactic LT4 therapy in euthyroid patients with HT is yet to be established.
Thyroid. 2008 Jul;18(7):755-60. doi: 10.1089/thy.2008.0008.
Long-term follow-up of antithyroid peroxidase antibodies in patients with chronic autoimmune thyroiditis (Hashimoto’s thyroiditis) treated with levothyroxine.
Schmidt M1, Voell M, Rahlff I, Dietlein M, Kobe C, Faust M, Schicha H.
A number of studies show that the serum levels of antithyroid peroxidase antibodies (TPO-Ab) in patients with Hashimoto’s thyroiditis decline during levothyroxine treatment, but do not provide quantitative data or report the fraction of patients in whom test for TPO-Ab became negative (“normalization percentage”). The objective of the present study was to provide this information.
This was a retrospective study of TPO-Ab concentrations in 36 women and 2 men (mean age 51 +/- 16 years; range 19-81 years) with Hashimoto’s thyroiditis as defined by the following criteria: elevated plasma TPO-Ab and typical hypoechogenicity of the thyroid in high-resolution sonography at first presentation or during follow-up and low pertechnetate uptake in thyroid scintigraphy. When first studied 17 women and 1 man were not yet taking levothyroxine. The remaining 20 patients were receiving levothyroxine. At initial examination 18 patients had serum thyroid-stimulating hormone (TSH) concentrations above normal. Results of up to eight (mean = 5.8) measurements obtained over a mean period of 50 months while patients were receiving levothyroxine were analyzed. In addition, serum TSH, free triiodothyronine (fT3), and free thyroxine (fT4) were measured, and ultrasound of the neck was performed at each follow-up examination.
RESULTS: In terms of TPO-Ab levels,35 of 38 patients (92%) had a decrease, 2 patients had undulating levels, and 1 patient had an inverse hyperbolic increase in her TPO-Ab levels. In the 35 patients in whom there were decreasing TPO-Ab values, the mean of the first value was 4779 IU/mL with an SD of 4099 IU/mL. The mean decrease after 3 months was 8%, and after 1 year it was 45%. Five years after the first value, TPO-Ab levels were 1456 +/- 1219 IU/mL, a decrease of 70%. TPO-Ab levels became negative, < 100 IU/mL, in only six patients, a normalization percentage of 16%. There were no correlations between changes in thyroid volume and changes in TPO-Ab.
Serum TPO-Ab levels decline in most patients with Hashimoto’s thyroiditis who are taking levothyroxine, but after a mean of 50 months, TPO-Ab became negative in only a minority of patients.
It has been postulated that a decrease in thyroid size can be achieved by thyroxine treatment in patients with goitrous Hashimoto’s thyroiditis but no objective data are available. We have therefore investigated the influence of thyroxine treatment on ultrasonically determined thyroid size. We also measured serum antithyroid peroxidase antibodies.
DESIGN: Consecutive patients with goitrous Hashimoto’s thyroiditis was studied.
PATIENTS: Thirteen women participated; all had goitrous thyroiditis.
TREATMENT: To render them euthyroid thyroxine was given for 24 months.
MEASUREMENTS: Thyroid size was measured ultrasonically and antithyroid peroxidase antibodies were measured using a commercial radioimmunological method.
RESULT: Concomitant with the gradual increase in serum free thyroxine and free triiodothyronine index values and a fall in serum thyrotrophin level, a gradual decrease in thyroid volume from 50.4 +/- 6.8 ml (mean +/- SEM) to 34.1 +/- 5.7 ml (32%), P less than 0.001 was demonstrated. Antithyroid peroxidase antibodies were present in high concentrations in all subjects but the mean serum level was not significantly changed at 24 months after initiation of treatment.
CONCLUSION: A clinically significant reduction in thyroid volume related to normalization of thyroid function but unrelated to changes in antithyroid peroxidase antibody can be achieved during L-thyroxine treatment of hypothyroid goitrous Hashimoto’s thyroiditis.
Purpose To explore the relationship of regional cerebral blood flow and metabolism with cognitive function and past exposure to chemotherapy for breast cancer.
Patients and methods Subjects treated for breast cancer with adjuvant chemotherapy remotely (5–10 years previously) were studied with neuropsychologic testing and positron emission tomography (PET), and were compared with control subjects who had never received chemotherapy. [O-15] water PET scans was acquired during performance of control and memory-related tasks to evaluate cognition-related cerebral blood flow, and [F-18] fluorodeoxyglucose (FDG) PET scans were acquired to evaluate resting cerebral metabolism. PET scans were analyzed by statistical parametric mapping and region of interest methods of analysis.
Results During performance of a short-term recall task, modulation of cerebral blood flow in specific regions of frontal cortex and cerebellum was significantly altered in chemotherapy-treated subjects. Cerebral activation in chemotherapy-treated subjects differed most significantly from untreated subjects in inferior frontal gyrus, and resting metabolism in this area correlated with performance on a short-term memory task previously found to be particularly impaired in chemotherapy-treated subjects. In examining drug-class specific effects, metabolism of the basal ganglia was significantly decreased in tamoxifen + chemotherapy-treated patients compared with chemotherapy-only breast cancer subjects or with subjects who had not received chemotherapy, while chemotherapy alone was not associated with decreased basal ganglia activity relative to untreated subjects.
Conclusion Specific alterations in activity of frontal cortex, cerebellum, and basal ganglia in breast cancer survivors were documented by functional neuroimaging 5–10 years after completion of chemotherapy.
de Ruiter, Michiel B., et al. “Cerebral Hyporesponsiveness and Cognitive Impairment 10 Years After Chemotherapy for Breast Cancer.”
Chemotherapy is associated with cognitive impairment in a subgroup of breast cancer survivors, but the neural circuitry underlying this side effect is largely unknown. Moreover, long-term impairment has not been studied well. In the present study, functional magnetic resonance imaging (fMRI) and neuropsychological testing were performed in breast cancer survivors almost 10 years after high-dose adjuvant chemotherapy (chemo group, n = 19) and in breast cancer survivors for whom chemotherapy had not been indicated (control group, n = 15). BOLD activation and performance were measured during an executive function task involving planning abilities (Tower of London) and a paired associates task for assessment of episodic memory. For the chemo group versus the control group, we found hyporesponsiveness of dorsolateral prefrontal cortex in the Tower of London, and of parahippocampal gyrus in the paired associates task. Also, the chemo group showed significantly impaired planning performance and borderline significantly impaired recognition memory as compared to findings in the control group. Whole-brain analyses demonstrated hyporesponsiveness of the chemo versus the control group in very similar regions of bilateral posterior parietal cortex during both the Tower of London and the paired associates task. Neuropsychological testing showed a relatively stable pattern of cognitive impairment in the chemo group over time. These results indicate that high-dose adjuvant chemotherapy is associated with long-term cognitive impairments. These impairments are underpinned by (a) task-specific hyporesponsiveness of dorsolateral prefrontal cortex and parahippocampal gyrus, and (b) a generalized hyporesponsiveness of lateral posterior parietal cortex encompassing attentional processing.
A subgroup of patients with breast cancer suffers from mild cognitive impairment after chemotherapy. To uncover the neural substrate of these mental complaints, we examined cerebral white matter (WM) integrity after chemotherapy using magnetic resonance diffusion tensor imaging (DTI) in combination with detailed cognitive assessment. Postchemotherapy breast cancer patients (n = 17) and matched healthy controls (n = 18) were recruited for DTI and neuropsychological testing, including the self-report cognitive failure questionnaire (CFQ). Differences in DTI WM integrity parameters [fractional anisotropy (FA) and mean diffusivity (MD)] between patients and healthy controls were assessed using a voxel-based two-sample-t-test. In comparison with healthy controls, the patient group demonstrated decreased FA in frontal and temporal WM tracts and increased MD in frontal WM. These differences were also confirmed when comparing this patient group with an additional control group of nonchemotherapy-treated breast cancer patients (n = 10). To address the heterogeneity observed in cognitive function after chemotherapy, we performed a voxel-based correlation analysis between FA values and individual neuropsychological test scores. Significant correlations of FA with neuropsychological tests covering the domain of attention and processing/psychomotor speed were found in temporal and parietal WM tracts. Furthermore, CFQ scores correlated negatively in frontal and parietal WM.These studies show that chemotherapy seems to affect WM integrityand that parameters derived from DTI have the required sensitivity to quantify neural changes related to chemotherapy-induced mild cognitive impairment.
Does Thyroid Autoimmunity Cause Anxiety and Depression – The Scientific Consensus
The best evidence to date shows a significant association between
thyroid autoimmunity and depression & anxiety. But what does this
mean and what should you do about it? Let’s discuss the bottom line
regarding the best diets and natural treatment options for improving
thyroid autoimmunity and mood.
Dr. Michael Ruscio, DC: Hi, this is Dr Ruscio, and let’s
discuss the association between thyroid autoimmunity, and anxiety and
depression. Now what is thyroid autoimmunity? Thyroid autoimmunity is an
immune condition in which your immune cells attack your thyroid gland,
which they shouldn’t, and this can cause progressive damage to the gland
which can then lead to hypothyroid. It is the most common cause of
In this study, I’ll put the abstract here on the screen entitled Association of Depression and Anxiety Disorders with Autoimmune Thyroiditis, a Systematic Review and Meta Analysis.
They were looking for and tracking, and trying to answer from a high
level if there is a consistent association between thyroid autoimmunity
and depression or anxiety. To quote this study, “19 studies comparing 21
independent samples, looking at over 36,000 patients were examined.”
What they found, and I’ll quote again here, “Patients with AIT,” that’s
autoimmune thyroid, “Hashimoto’s thyroiditis, or subclinical or overt
hypothyroidism had significantly higher scores for anxiety and
DrMR: I’ll quote here their conclusion. “This meta-analysis
establishes the association between AIT, autoimmune thyroid, and
depression and anxiety disorders. Patients with AIT exhibit an increased
chance of developing symptoms of depression and anxiety, or receiving a
diagnosis of depression and anxiety disorders.” Okay, so clearly there
is an association between thyroid autoimmunity, being overtly
hypothyroid, or subclinical hypothyroid and anxiety and depression.
the question is what can you do? Well, the first thing I would do is be
very cautious with, unfortunately, with the advice that you take from
alternative natural and functional medicine. The reason for this is
because this community, which I include myself in, but I practice this,
is very quick to give people very grim diagnoses or prognoses when
they’re diagnosed with hypothyroidism, and this is incredibly damaging.
When you take someone who has a predilection toward anxiety and
depression and you paint their prognosis to be worse than it actually
is, you are in effect going to exacerbate their anxiety and depression,
and I see this all the time.
It’s very upsetting. It’s very disheartening to see people come into
the office who think that their condition is far worse than it actually
is, and they have this baseline level of anxiety and depression now
exacerbated. Because their practitioner, who’s probably operating with
virtuous intent but is trying to scare them into motivation, is actually
making the situation much, much worse. So you have to be really
careful. Unfortunately, and there’s another aspect to this, if I’m being
fully candid, which is thyroid disorders are highly marketable
Thyroid symptoms are highly marketable symptoms, and so,
unfortunately, there’s a flooding of the space on the Internet with
claims about thyroid, about how all your problems are caused by thyroid.
This further exacerbates this problem of fear, and overzealousness and
overly grim prognoses being painted for those looking to get an answer
about, “Okay, I have a thyroid condition, and I’m depressed or anxious
or have some mood disorders. What does this mean? What can I do?”
I would first offer you take a big breath in and step back and relax a
bit because much of what you are told makes a situation look far worse
than it actually is. Yes, they’re an association, but there are plenty
of things that you can do to improve your thyroid, and I would argue to
also improve your mood. You don’t need to be fear factored into thinking
that you can never eat out, have a bite of gluten, or not take handfuls
of supplements in order to feel well. Let me run through some of what
you can do, outside of being very cautious and circumspect with the
advice that you take.
Diet and Gut Health
gluten-free or gluten-reduced diet. There’s been one study to date
showing a benefit in those without celiac disease. Now the problem here
is there’s a number of studies in those with Celiac and thyroid
conditions showing improvement when going gluten-free. Yeah, that
shouldn’t be surprising. The bigger question is if you don’t have
celiac, or you have what’s known as non-celiac, gluten sensitivity, or
maybe no celiac-like diagnosis at all, but you have a thyroid condition,
and you’re gluten-free, can that improve your condition? One study has assessed that’s shown benefit(subscription required). I think it’s worthwhile to try.
I do not think you need to be strictly gluten-free if you have a
thyroid problem unless you’ve done an elimination of gluten, you feel
better, you reintroduce gluten and you clearly notice you feel worse. If
you do, then you have my full support and you should be fairly strict
with your application of a gluten-free diet. But if you don’t, this is
one of the main pain points where people I think are misled. If you’ve
eliminated and then reintroduced and you notice a little to nothing,
then eating the gluten-reduced diet is okay. Meaning you can have some
gluten from time and time, and I wouldn’t really sweat it. So, that
recommendation, gluten avoidance needs to be personalized based upon
your response to a gluten reintroduction.
could also potentially try a low FODMAP diet. Another study has looked
at essentially a paleo diet, and I’m painting a bit of an inference into
this recommendation. But essentially using a paleo diet, they showed
improvements in multiple measures in addition to the thyroid status, and
this population seemed to potentially have a FODMAP sensitivity. A few
other, well-performed analyses, have shown that those with thyroid
autoimmunity and hypothyroidism have a higher tendency to have small
intestinal bacterial overgrowth, which may benefit from a low FODMAP
diet also. So, two dietary approaches you can try in addition to the
basic advice of getting off of processed foods, trans fats, and sugars,
and sodas and things like that.
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Supplements & Medication
Now there are a few supplements that can be helpful. Vitamin D, there’s been a number of studies showing vitamin D can improve thyroid autoimmunity. Selenium,
there’s been a number of studies showing selenium can improve thyroid
autoimmunity, but not all studies have shown benefit. Some data has
shown that selenium may also improve quality of life, and we can infer
from that, that if it’s improving quality of life, people probably have a
better mood. So the whole point of the video here is the association
between thyroid disorders and mood disorders. So, there’s some evidence
that suggests that the use of selenium may help with not only thyroid
autoimmunity but with mood.
Now, the key point about selenium is you don’t need to use it
forever, three to six months if you’re not on thyroid medication. If
you’re on thyroid medication, you could make a case for using it for up
to a year, and simply track your antibodies, and you’re looking for a
significant drop in your antibody levels. Antibodies typically used,
known as TPO and you’re looking for a significant drop, but you know,
I’d say at least 300 would be what I typically would consider a
significant movement, and also your mood to improve. But remember, you
don’t have to be on selenium forever. The benefit seems to drop off
after three to six months if you’re not on thyroid medication, or about a
year if you’re on thyroid medication.
Also, CoQ10 and magnesium have also been shown to help, namely with thyroid autoimmunity.
I don’t know that there’s been a tie to mood, certainly, I have no
opposition to trying these and seeing how you feel. The other thing that
I think alludes a lot of people is improving your gut health, and
admittedly I have a gut leaning biased. However, there has now been a
number of studies documenting the gut-brain connection, and we reviewed
recently a landmark study showing that those with IBS, irritable bowel
syndromes: gas, bloating, abdominal pain, altered bowel function, have a
higher predilection or a higher prevalence of anxiety and depression.
Other data has shown that a treatment for the gut, probiotics can actually help to improve mood.
the gut can be one of these, unfortunately, overlooked pieces of the
picture that needs to be addressed. I hope people are not overlooking
their gut health, but I see this more often than I’d like to admit where
someone gets pulled into a thyroid treatment program because of, let’s
say anxiety, fatigue, and depression; all the while the gut has been
overlooked. So it’s not to say that the gut is always going to be at the
root of the problem, but it’s definitely something to consider because
there is this gut-brain connection. Inflammation in the gut, dysfunction
in the gut can cause inflammation and dysfunction in the brain,
Then lastly, I would consider, and this is something you need to take
on a case by case basis and talk with your doctor, but if you’re on a
medication, consider trying a different medication. If you’ve done any
research on thyroid, you’ve likely seen something about needing to be on
T4 plus T3. I think that recommendation is overstated, but there is
evidence to support that. Now, I wouldn’t recommend starting there. Why?
Because if you do these other things, and especially improve your gut
health, you will improve both the absorption of the medication and the
conversion of that medication from T4, the inactive form, to the active
“So, it is possible to take less medication and feel better if you
improve what absorbs and helps metabolize that medication, which is your
We’ve documented a few case studies now out of our office where
patients have felt vastly better, and at the same time, because they’re
improving their gut health, been able to decrease their dose of thyroid
medication. So, it is possible to take less medication and feel better
if you improve what absorbs and helps metabolize that medication, which
is your gut. So, switching from a T4 only formulation, like
levothyroxine or Synthroid, to a T4/T3 combination like Armor, or
Nature-Thyroid or WP Thyroid is something to consider. There’s a little
bit more nuance there for people who have chronic non-responsive
digestive issues, they may want to consider a trial on a liquid gel tab
known as Tirosint, that may also help them.
if you run through some of these steps, you have a very high
probability of improving, in my opinion, any thyroid associated anxiety
and depression. I think one of the most important things to emphasize is
that you don’t need to be scared into a corner where you have to live a
highly restrictive dietary lifestyle. A small percentage of people may
need to do that, right? Just quickly here, one Italian study
that looked at over 12,000 patients found that there was only about a
nine percent incidence of thyroid autoimmunity in those who had
non-celiac gluten sensitivity.
So they took this large group of people who had non-celiac gluten
sensitivity … or there’s large of people and they assessed who had
non-celiac gluten sensitivity. Of those who had non-celiac gluten
sensitivity, only nine percent of them had a thyroid problem. So yes,
there’s an association. Yes, it’s documentable. Yes, it’s significant.
Does it mean that every person with a thyroid problem needs to be
strict, 100 percent gluten-free? No. Why do I say that? Because the fear
and anguish that can be associated with living in this stressed out
state all the time, because you’re trying to avoid every trace of
gluten, can be problematic if you don’t need to do that.
What can you do?
to eliminate, and then reintroduce and then consume to your tolerance.
Some people need to be very strict, other people have some leeway and
it’s important to understand that. Also, to understand that a thyroid
condition is not a death sentence, it’s actually a very manageable
condition that should respond well to these therapies, plus or minus
medication if you need it. You can live a very healthy, happy,
productive life, which is important for people with thyroid problems to
hear, because you may have a tendency to be more anxious and depressed.
So we don’t want to fuel that fire.
The truth actually is that you can be very happy, very healthy and
very functional. So hopefully this is a lifeline that will pull you out
of any despair you can fall into if you’re reading the wrong information
on the Internet. So, this is Dr Ruscio with some thoughts on this
study; Looking at the connection between thyroid autoimmunity, anxiety,
I hope this information helps you get healthy and get back to your life. Thanks.
What do you think? I would like to hear your thoughts or experience with this.
The best evidence to date shows a significant association between thyroid autoimmunity and depression & anxiety. But what does this mean and what should you do about it? Let’s discuss the bottom line regarding the best diets and natural treatment options for improving thyroid autoimmunity and mood.
Leaky gut, also called “intestinal permeability” or “gut hyperpermeability”, is when the tight junctions between the cells that line your small intestine loosen.
Using a few key supplements, such as probiotics, L-glutamine, and vitamin D, helps reduce inflammation and restore the intestinal lining with leaky gut.
Probiotics perform many functions simultaneously: They repair leaky gut AND simultaneously the main causes of leaky gut, whether this is inflammation, dysbiosis, overgrowth, or infection.
L-Glutamine is an amino acid that has a significant body of research showing its restorative properties for the gut lining and gastrointestinal tract, especially during stress.
Vitamin D seems to help maintain immune system balance in the gut and prevent gut health problems.
There are a variety of other supplements that can help repair intestinal permeability including digestive enzymes, DGL, slippery elm, marshmallow root, vitamin A, zinc carnosine, fish and fish oil, immunoglobulins, gut healing foods like bone broth or collagen, and quercetin.
Though all of these supplements can be helpful for healing leaky gut, this doesn’t mean you have to use all of them to heal leaky gut.
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A quick search on Amazon for leaky gut supplements results in a long and bewildering list of recommended products. Sure, there are lots of supplements that you could use to help heal leaky gut, but you don’t need to take all of them to get well. Rather than throw the kitchen sink at leaky gut, it’s better to choose a few high quality supplements that rebalance your good and bad bacteria, restore your gut lining, and quell the GI tract inflammation that drives leaky gut.
The top three, science-based supplements I recommend to perform these functions are:
Let’s explore what leaky gut is and how these supplements can help you improve it.
What is Leaky Gut?
Leaky gut, also called “intestinal permeability” or “gut hyperpermeability”, is a loosening of the tight junctions between the cells that line your small intestine.
Your small intestine has the job of absorbing most of your nutrition from food. But poor diet,  stress,  NSAIDs (nonsteroidal anti-inflammatory drugs) such as ibuprofen or aspirin,[3, 4, 5] alcohol  or other irritants can cause inflammation of the gut lining and an increase in a protein called zonulin. Over time gaps open up in the intestinal lining and let undigested food particles and bacteria “leak” through the intestinal wall and into your bloodstream
Your body’s immune response to these unnatural particles in the bloodstream contributes to a wide variety of symptoms and some diseases, such as celiac disease and Crohn’s disease. Recognized symptoms of leaky gut include brain fog, fatigue (especially after eating), joint pain, skin conditions, and more. (For more on this, see Symptoms of Leaky Gut.)
Supplements to Heal Leaky Gut
Using a few key supplements, such as probiotics, L-glutamine, and vitamin D, helps reduce inflammation and restore the intestinal lining with leaky gut.
Here is a summary of the research that supports the use of these three supplements for healing leaky gut.
How it Helps Leaky Gut
Reduces gut inflammation Helps resolve dysbiosis or overgrowths, like SIBO Helps maintain gut lining function
The beauty of probiotics is that they perform many functions simultaneously: They repair leaky gut AND also address the main causes of leaky gut, including inflammation, dysbiosis, overgrowth, or infection.
Research shows that a healthy gut microbiome helps maintain a healthy intestinal barrier, while an overgrowth of bad gut flora or bacteria, such as SIBO (Small Intestinal Bacterial Overgrowth) can lead to increased intestinal permeability.[ 21, 22, 23, 24]
A wide variety of studies confirm that probiotics can significantly reduce the symptoms and severity of digestive disorders such as irritable bowel syndrome (IBS), Crohn’s disease, IBD, and some autoimmune diseases. [25, 26, 27, 28, 29, 30, 31]
Using one type of probiotic is good; using one from each category together is best to reset your gut health and repair leaky gut. Be sure to choose ones with colony-forming units (CFUs) in the billions. For more on how to use probiotics, check out our Probiotics Starter Guide.
Prebiotics feed the beneficial bacteria from probiotics. Prebiotics can be consumed either in the form of fiber from fruits, veggies, nuts and seeds, and whole grains, or from prebiotic supplements. However, many people with digestive issues have side effects from prebiotic foods or supplements until their guts have done some healing, so try them with caution.
Glutamine is the substance your gut naturally uses to repair intestinal cells. Supplementation with L-glutamine can help speed the repair of the intestinal lining, decrease intestinal permeability, and reduce inflammation.
L-Glutamine is an amino acid that has a significant body of research showing its restorative properties for the gut lining and gastrointestinal tract, especially during stress. [32, 33]
Though some sources claim that the benefits of L-glutamine haven’t been shown in research, a meta-analysis (the gold standard in scientific evidence) found that L-glutamine reduced markers of leaky gut and intestinal lining damage, and improved gut barrier function.
Vitamin D seems to help maintain immune system balance in the gut and prevent gut health problems.
Some studies indicate that low vitamin D is associated with greater gut lining permeability and worse outcomes for people with IBD, while increasing vitamin D reduced irritable bowel syndrome (IBS) symptoms. [35, 36, 37]
Humans naturally produce vitamin D in their skin when it’s exposed to sunlight. But as people tend to get less sun exposure in modern life and vitamin D deficiency is common. There seem to be some synergistic health benefits of vitamin D that can only be obtained by getting actual sun exposure.
Sun exposure has been shown to protect against digestive tract disease and inflammation, specifically diverticulitis and inflammatory bowel disease.  We can infer that safe sun exposure can be important for healing your leaky gut.
A general recommendation for safe sun exposure (that does not increase the risk of cancer) is 20-30 minutes of exposure while wearing a bathing suit, 1-3 days per week.
In addition to the top three supplements, there are a variety of other supplements that can help repair intestinal permeability, reduce gut inflammation, or support the healing of the gut lining. Here is a summary of others that may be useful.
Digestive Enzymes and Stomach Acid Support
Digestive enzymes help make sure that the proteins, fats, and carbohydrates you eat are fully broken down during digestion. This not only reduces wear and tear on your digestive system, but can help reduce leaky gut food sensitivity symptoms.
Along with bacterial toxins, undigested food particles may travel through the permeable gut wall and be mistaken by your body for a foreign invader and cause more systemic inflammation. 
There are many types of enzyme formulas, so be sure to find one that you tolerate well. A basic one will contain amylase, protease, and lipase to help your body digest carbohydrates, proteins, and fats.
Supporting stomach acid may also support leaky gut healing by generally supporting digestive health and helping ensure complete protein digestion. A formula that also contains betaine hydrochloride(HCL) may improve results, but isn’t necessary for everyone.
DGL, Aloe, Slippery Elm, and Marshmallow
Soothing herbs like deglycyrrhizinated licorice (DGL), aloe vera, slippery elm, and marshmallow root can help coat and soothe an irritated gut lining, and may provide therapeutic plant compounds that offer a protective benefit to the intestinal lining while healing leaky gut.  DGL and these other agents can also soothe heartburn. Be sure to choose DGL as opposed to regular licorice root, because it can lead to elevated blood pressure with continuous use. These three herbals can be combined with L-glutamine to super-charge your gut-healing protocol.
Fish and Fish Oil
Fish oil and its omega-3 fatty acids DHA & EPA have been extensively researched for their ability to help support the cardiovascular system, to promote joint, skin, gut, eye, and brain health and to help support a healthy inflammatory response. Eating wild-caught fatty fish, such as salmon and sardines, or using a DHA & EPA fish oil supplement may be beneficial for healing leaky gut.
Zinc carnosine has been shown to stabilize the gut mucosa and reduce diarrhea. [41, 42]
Vitamin A is known to affect intestinal permeability and gut lining function.  A study exploring the ways Vitamin A affects gut barrier function found that Vitamin A deficiency increases intestinal permeability, while restoring Vitamin A levels decreased intestinal permeability.  Though this study was a model-based study, it shows a likely benefit to supplementing with Vitamin A to encourage healing of leaky gut.
Immunoglobulin G (IgG) cells are a type of immune cell. They are normally present in the gut lining and bind to allergens and antigens, including bacterial toxins in the gut.
Bacterial inflammation is thought to be one of the main causes of leaky gut symptoms such as brain fog, fatigue, and joint pain. Immunoglobulin G binds these potential irritants so they can be excreted in the stool and can’t cause symptoms.
Supplemental Immunoglobulins have been shown to help IBS patients who did not respond to other treatments like diet, probiotics, antimicrobials, and soothing agents .
Gut Healing Foods
Gut healing foods like bone broth and collagen protein can support the gut lining in healing from leaky gut. Collagen is beneficial for all skin tissues.  While data are still preliminary (from animal & cell studies), we can infer that collagen is beneficial to your gut lining. [47, 48, 49]
Quercetin is a plant compound that helps restore the gut lining, and is anti-inflammatory for the gut. 
Though all of these supplements can be helpful for healing leaky gut, this doesn’t mean you have to use all of them to heal leaky gut.
Rather, I recommend focusing on the top three to start: probiotics, L-glutamine, and vitamin D from safe sun exposure. If you need additional support beyond those three, you can experiment with the other options.
And don’t forget: Eating an anti-inflammatory diet with healthy fats like coconut oil, and good daily habits, like stress reduction and getting enough sleep can be just as important as supplements. For more on other ways to help heal leaky gut, see How to Heal Leaky Gut.