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Dear THYROID FRIENDS,
Here’s a most stunning and inspirational CHRISTMAS CARD video created by Thyroid Patient Julie! It warms your heart and gives you the most important part of the season: HOPE!!
Here’s wishing you a wonderful holiday season and may you Seize the Wisdom, Thyroid Warriors! CLICK BELOW:
P.S Join in us the Stop the Thyroid Madness STTM Facebook page:Â https://www.facebook.com/StoptheThyroidMadness
Thyroid patients are wiser!! They now know what thyroid treatment works, and what doesn’t.
And they’ve also noted common issues that they share with a large percentage of each other…one being INFLAMMATION.
Sometimes, thyroid patients don’t even know where the inflammation exists in their body, except that their high ferritin reveals it, or their C-Reactive Protein or ESR (erythrocyte sedimentation rate or sed rate) lab tests reveal it. Other times, it’s obvious by the pain they notice in their bodies.Â
Some ways to deal with inflammation, especially for Hashimotos patients, is removing gluten from the diet. Others have to ascertain if they have Lyme disease that needs treatment. Some have neither problem, but inflammation exists anyway!
Many thyroid patients take supplements to help lower that inflammation, which range from Astaxanthin to Ginger to NAC to Curcumin/Turmeric…and/or a combination of them all.Â
Here’s a great article written by Yusuf Saleeby, MD. He happens to also be a contributor to the new STOP THE THYROID MADNESS II book, which you should read, and/or give to someone you love as a Christmas present!!
The following published in May/June 2014 edition American Fitness magazine.
It has been well known and understood for years that inflammation is harmful. Inflammation essentially kills. Well, not right away or in a big flashy way, but it does hurt our chances for a healthy disease-free existence and does shorten our lifespan. Inflammation has been proven to increase your risk for heart disease, heart attacks and strokes.1-3  Inflammation is also known to increase a person’s risk for cancer.4,5  It is also linked to obesity and metabolic syndrome; even implicated in Parkinson’s and Alzheimer’s Disease.6-8,9-12
In 2011, researchers at Ohio State University found a link between inflammation and a molecule called microRNA-155 (miR-155). What they discovered was in chronic inflammatory conditions, levels of miR-155 rise and this molecule stimulates and allows for spontaneous mutations of cells contributing to tumorigenesis, the mechanism whereby normal cells become cancerous cells.13-16   While cancers are devastating diseases, all deaths due to cancer do not even come close to numbers of Americans who succumb to heart disease and stroke. So for the purpose of this article we will focus on how inflammation is a big silent killer regarding our hearts and brains; our attention will be on cardiovascular and cerebrovascular disease.
To put it simply, inflammation causes undesirable reactions on the inner lining of blood vessels. The combination of inflammation and circulating lipids is a dangerous recipe that produces something called “foam cells”. Foam cells attach to the endothelial lining of our blood vessels, such as the arteries that feed our heart and brain, and once they mature over months to years form arterial plaques. These plaques narrow the blood vessels making it an eventual challenge for oxygen carrying blood cells to pass. Distal tissues to these narrowing arteries are the ones that suffer. When cells do not get the oxygen they need the result is tissue necrosis in the form of a heart attack or a stroke. Another pathogenesis of inflammation is its impact on maturing plaques. It just happens that inflammation can cause, in a rather short time frame, the rupture of these vessel plaques. In doing so, that plaque can quickly obstruct all blood flow quite abruptly and results in significant damage downstream. One of the biomarkers we shall discuss is FDA-cleared for assessment of plaque rupture and risk of stroke.16  Specific clinically available inflammatory markers are now available for the diagnosis and management of chronic inflammatory states which can impact life and health.
With the recent availability of advanced laboratory testing with a number of inflammatory biomarkers, the clinician has the obligation of identifying inflammation and stomp it out before it puts patients at risk for some ugly disease processes. Identifying overt acute inflammation is as easy as feeling a hot knee joint for example, or identifying fever, stiffness, swelling or pain. Measuring it or quantifying it has typically been with the use of the time tested but non-specific erythrocyte sedimentation rate (ESR) and more recently the C-reactive protein (CRP) tests. However, newer, more specific and diagnostically advanced biomarkers of inflammation have arrived on the playing field to help doctors assess and gauge inflammation. They are sensitive enough to pick up harmful levels of inflammation that may go unnoticed to the casual observer (both patient and doctor). Once identified, the measured inflammation can be watched and carefully reduced by prescriptive medications (statin drugs or anti-inflammatory agents as an example), orthomolecular therapies such as glutathione (NAC), resveratrol or turmeric, and lifestyle modifications (smoke cessation, exercise and weight loss).17,18  Reassessing these inflammatory biomarkers allows clinicians to better guide their patients and assure the reduction of this disease causing entity. This article will discuss a few of these cutting edge inflammatory biomarkers that are currently being used in some clinical practices to identify people at risk for heart disease, stroke, neurodegenerative disorders and diabetes. There are other biomarkers available, many used in research and not clinically applicable or practical. At some point in the future they may find clinical application. Scientists are likely to discover even better biomarkers with more specificity and selectivity for certain conditions as research continues in this field. However, for the time being we will examine the PLAC test, the high sensitivity C-Reactive Protein, Fibrinogen, F2-Isoprostanes, Myeloperoxidase, Interleukins 6 & 17a, and Tumor Necrosis Factor-alpha. Preventive medicine physicians are measuring and monitoring these inflammatory markers to reduce the risk of end-organ damage and degenerative disease in their patients.
Lipoprotein-Associated Phospholipase A2Â (Lp-PLA2, or PLAC)
The Lp-PLA2 biomarker is an enzyme associated with plaques in the arteries. Carried mostly by LDL-Cholesterol this enzyme in high levels of circulation is found when inflammation is high and plaque rupture in eminent. When levels of this inflammatory marker remain high for long periods of time there is a very high chance for cardiovascular events and risk of ischemic stroke. Prolonged activity of this enzyme is associated with coronary calcification or ‘’hardening of the arteries”. The PLAC test was recently cleared by the FDA to assess the risk of both coronary heart disease and ischemic stroke associated with atherosclerosis.16   Nicotinic acid as well as fenofibrate therapy has effectively treated elevations in Lp-PLA2.19,20
High sensitivity C-Reactive Protein (hs-CRP)
Much like the ESR this biomarker of inflammation is non-specific; it is formed in the liver as a reaction to inflammation occurring in other parts of the body. The high sensitivity CRP is a measure of minuscule amounts of this protein that are typically associated with vascular inflammation. The chronic elevation of this acute phase reactant is used to predict risk of heart attack and undesirable events in those with angina and in those who are having a heart attack. Elevated CRP may be a better predictor of heart disease than elevations in LDL-cholesterol. 21 While Lp-PLA2 elevations can double the risk for heart attack and stroke, having both the Lp-PLA2 and hs-CRP elevated increases heart disease four-fold and stroke risk by a factor of ten. This inflammatory protein responds remarkably well to exercise. 21
Fibrinogen
Fibrinogen will convert to fibrin as blood clots form. So fibrinogen, a protein, is a good measure of acute inflammation and is associated with risks of heart disease. Elevated fibrinogen can cause platelets to clump together or aggregate, increase the viscosity of blood and embellish other clotting factors. There is a strong correlation between elevated levels of fibrinogen and acute ischemic stroke.22  Fibrinogen is therefore a good tool for evaluation of stroke risk and prediction of a future heart or brain event.  To reduce this pro-thrombotic state, a reduction of fibrinogen can be accomplished by routine aerobic exercise, smoke cessation, aspirin therapy and omega-3 fish oil supplementation and increasing endogenous glutathione with N-AcetylCystine (NAC) or bioavailable oral/IV glutathione (S-AcetylGlutathione).23
F2-Isoprostanes (F2-Isops)
While the initial implementation of exercise can often raise the F2-Isops levels, eventually sustained regular exercise lowers it to safer levels. F2-Isoprostanes are prostaglandin like compounds which are formed by the oxidation of free fatty acids by free-radicals in circulation. Poor diets, too rich in red meat, a sedentary lifestyle and cigarette smoking all contribute to the elevation of this inflammatory marker. F2-Isops is a strong predictor of coronary heart disease (CHD) as elevated levels cause oxidative stress on arterial walls and the production of atherosclerotic plaques. These isoprostanes also act as potent vasoconstrictors, which can further limit passage of blood cells through already narrowed arteries. Control of triglycerides (TG), diet and exercise combat this marker. Eicosapentaenoic acid (EPA) and docosapentaenoic acid (DHA) are two omega-3 fatty acids that are generally shown in multiple research studies to lower F2-Isoprostanes.23-26
Myeloperoxidase (MPO)
Particular white blood cells (WBC) called polymorphonuclear leukocytes and monocytes produce an enzyme called myeloperoxidase, this enzyme help your immune system fight infections only when your body uses it correctly. With chronic inflammation there is too much MPO released into circulation from WBCs and this hampers the function and bioavailability of nitric oxide. Nitric oxide (NO) is crucial to proper endothelial function in our arterial walls. MPO also causes the oxidation of HDL-C (good cholesterol) and impairs its ability to pull bad cholesterol (LDL-C) away from arteries for recycling. Additionally, the oxidizing effect of MPO on LDL-C contributes to the formation of foam cells and increases the likelihood of plaque rupture. Elevated levels of MPO in the presence of coronary artery calcium (CAC) raise the risk for a coronary event. Aspirin therapy, statin drug therapy (such as atrovastatin (Lipitor®) for example) and proper diet rich in omega-3 fatty acids (fish oil) all help lower MPO.27 Of all the biomarkers discussed here, probably the most detrimental when found elevated is the MPO. Aggressive measures should be taken to reduce this marker, especially over the long term.
Interleukin-6 (IL-6)
Interleukin-6 (IL-6) is a pro-inflammatory cytokine. Cytokines are proteins that act as cell-signaling molecules in the immune system. IL-6 can increase the aggregation of platelets causing clumping and infarction when blood vessels are narrow and blood flow is impeded. IL-6 augments the synthesis of CRP and is thus associated with increased risk of cardiovascular disease (CVD). Elevated levels of IL-6 are associated with a 2 fold increase in diabetes risk and an even higher (3-fold) risk of CVD. We know the blockade of IL-6-receptors by drugs like tocilizumab (Actemra®) in patients with rheumatoid arthritis is helpful, but whether this drug will have a similar effect on reduction of the ill effects of this circulating inflammatory cytokine on the heart or brain remains to be seen.28
Interleukin-17a (IL-17a)
Another inflammatory cytokine that has a role in vascular remodeling and function is Interleukin-17a. Elevated levels of IL-17a are responsible for vascular dysfunction and are found at increased levels in the presence of unstable angina and heart attacks. However, one study pointed out that low levels of circulating IL-17a in the presence of an acute myocardial infarction (AMI) or heart attack had poor outcomes for survival. While some studies show it as a risk factor in the asymptomatic individual, this may be untrue in the acute setting. More research is needed. Hence, blocking this interleukin too aggressively may have unwanted outcomes.29
Tumor Necrosis Factor-alpha (TNF-α)
A pro-inflammatory cytokine referred to as TNF-α is excreted from macrophages (immune system cells that fight infecting microbes). People with the autoimmune and inflammatory disease systemic lupus erythematosus (SLE) are known to be at higher risk for CVD. There is a correlation between the inflammatory TNF marker which is elevated in SLE patients and their CVD risk. Some researchers are inclined to believe that this is what causes the increased risk of heart attacks in this subset of patients. Elevated levels of this cytokine can have a negative effect on sugar metabolism by interfering with insulin receptors. Elevated TNF-α levels result in a two fold increase in CVD risk. Weight loss and statin drug therapy can lower these levels. Controlling this marker’s levels may also reduce the risk of acquiring diabetes.30
So the take home message here is that chronic inflammation is bad for your health and wellbeing. Even acute bursts of inflammation can significantly raise the risk of an acute event such as a heart attack or stroke. A very good illustration of this is found in a study in Mexico City, where air pollution levels are monitored in one of the most polluted cities in the western hemisphere. There were correlations made with rises in AMIs in a population of nursing home patients on particularly dirty air quality days in that city. The elevated air particle count attributed to an acute increase in inflammatory biomarkers and thus triggered heart attacks.31
Besides the impact on cardiovascular health, inflammation is to be avoided for many other reasons, from neurodegenerative diseases such as Parkinson’s and Alzheimer’s disease to development of cancers to destructive and degenerative diseases of our skeletal system. We are now at the cusp of clinically available, specific biomarkers of inflammation that allow doctors to identify those at risk and diligently (with periodic monitoring of serum and urine levels) evaluate therapy that reduce harmful inflammation.
ABOUT THE AUTHOR: Yusuf (JP) Saleeby, MD is a contributing editor for American Fitness magazine. He practices preventive integrative medicine and age management in Murrells Inlet & Greenville, SC. Dr. Saleeby is regional director of a direct access testing site that offers analysis of inflammatory bio-markers. He can be reached at www.saleeby.net or by e-mail at jpsaleeby@aol.com. You can also see his other website here: http://www.getmythyroidfixed.com/
SEE MORE BELOW THE REFERENCES….
 ©2013-2014
References:
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** WANT TO ORDER THE STTM BOOKS?? They are:
1) The Bible of Thyroid Treatment–all based on years of patients experiences and wisdom, called Stop the Thyroid Madness: A Patient Revolutions Against Decades of Inferior Thyroid Treatment.
2) A physician-written STTM BOOK, called Stop the Thyroid Madness II: How Thyroid Experts are Challenging Ineffective Treatments and Improving the Lives of Patients. Â Dr. Saleeby contributed Chapter 3 in this book and it’s a knockout of more information from the minds of medical professionals!
Or if you want BOTH, go here.
** HAVE YOU LIKED THE STTM FACEBOOK PAGE?? Â It’s extremely informative and speaks the TRUTH about thyroid disease, better treatments and so much more.Â
Hello to all my fellow thyroid patient friends!
I, Janie, have taken a break from the STTMÂ Â blog after the release of the fabulous Stop the Thyroid Madness II book. And it’s time to return!!
Here’s the short and sweet reason I’m writing this blog…
Listen to Kirstin Costello of Wellness Talk Radio interview me!! I think we both did a great job! Â
And once you do, spread the word by sharing the link below. Send this to your family and friends. Post it on Facebook. Let’s help reach all our fellow thyroid patients who need to learn from over a decade of thyroid patient experiences and wisdom in the treatment of hypothyroidism, adrenal fatigue/insufficiency issues, low iron and so much more.
Go here:Â https://www.youtube.com/watch?v=51-ikKxufgU
Kind regards from…
P.S. Have you read the new Stop the Thyroid Madness II book? You should.
No, this new book does not “replace” the original revised and very detailed STTM book. The latter will always have brilliant details of patient experiences and wisdom found nowhere else.
But the new STTM II book is giving you the following:
1) an excellent companion to the first book.
2) information that only certain medical practitioners can give you.
3) a strong message to all doctors since it’s written by their very colleagues.
In other words, if other practitioners continue to bash Natural Desiccated Thyroid or T3 or refer to it as “poison”, think the TSH is a great diagnostic tool to diagnose or dose by, don’t believe in low cortisol, and more…they will have to be bashing their own colleagues’ wisdom as contained on these pages.
The authors of the new STTM II book include Paige Adams FNP, Geoffrey T. Bouc MD (owner of website I want my T3!), Jeffrey Dach MD (jeffreydachmd.com), Lena D. Edwards MD, Andrew H. Heyman MD (in Virginia), Carla Heiser RDN, Paula H. Luber MD, Benjamin D. Lynch MD (aka Ben Lynch of the MTHFR website), William D. Trumbower MD, Philip L. Roberts MD, Yusuf (JP) Saleeby MD, Laura R. Stone MD, Nguyen D. Phan MD, and James C. Yang, MD.
If you haven’t yet seen or read this wonderful new book yet, go here: //www.stopthethyroidmadness.com/stop-thyroid-madness-ii
What do these people have in common: Adams, Bouc, Dach, Edwards, Heyman, Heiser, Luber, Lynch, Phan, Roberts, Saleeby, Stone, Trumbower and Yang?Â
Answer:Â Brilliance in thought, courage in action, intelligent reasoning, and a willingness to learn from their patients as medical practitioners.
And that is all exactly why each of them was chosen to contribute as an author to a new Stop the Thyroid Madness book, titled
Each of them are medical practitioners who strive to….
Why else did I choose these particular practitioners for the book?
First and foremost, it was based on patient reports. The majority of these professionals were reported by thyroid patients to be the better cream of the crop in the medical field.
Could I have chosen others?
Yes. There are others of whom patients have reported they like! But serendipity led me to each one of these masterful professionals and it has all played out like a well-tuned chorus.
How is this book different than the revised STTM book?
The revised STTM will forever stand out as a compilation of highly important and life-changing experiences and wisdom of thyroid patients worldwide.
The new STTM II book brings the minds and brilliance of medical professionals into the mix, not only giving you more details that only a trained professional can give, but the book can also be seen as a practitioner-to-practitioner book, as well. THIS is a book that will end the refrain among certain doctors “Who is Janie Bowthorpe and where is her medical degree?” (i.e. as if only someone with a medical degree can know something important medically!).
THIS is the book that you can give your doctor since it’s written by his very colleagues!
THIS is the book that will play a dynamic role in changing the worldwide medical mindset about the proper treatment of thyroid disease.
What did they write about?
CHAPTER 1 The Integrative and Functional Medicine Approach to Thyroid Diseases by James Yang, MD, MPH and Andrew Heyman, MD, MHSA
CHAPTER 2 Stress, Adrenals, Your Thyroid, and You by Laura R Stone MD, Andrew Heyman, MD MHSA and Carla Heiser MS RD LD
CHAPTER 3Â Thyroid Replacement Therapy: Natural Desiccated Thyroid (NDT)Â by Yusuf (JP)Â Saleeby, MD
CHAPTER 4 The Unreliable TSH Lab Test by Jeffrey Dach MD
CHAPTER 5 When Normal Ain’t Normal by Geoffrey T. Bouc MD
CHAPTER 6 Nutrition and Hypothyroidism by William D. Trumbower, MD
CHAPTER 7 Hashimoto’s Autoimmune Thyroid Disease by Jeffrey Dach MD
CHAPTER 8 Why Are Doctors Like That? by Nguyen D. Phan MD
CHAPTER 9 Gluten Intolerance and Thyroid Disease by Paula Luber, MD
CHAPTER 10 Thyroid Toxicity by Philip L. Roberts, MD
CHAPTER 11 Moving Forward with Reverse T3: the Causes and Health Implications by Paige Adams, FNP, B-C
CHAPTER 12Â Methylation, MTHFR and Thyroid Dysfunction by Benjamin Lynch, ND
CHAPTER 13 Hypocortisolism: An Evidence-Based Review by Lena Edwards, MD, FAARM, FICT; Andrew H. Heyman, MD MHSA; Sahar Swidan, PharmD
Who wrote the Foreword?
Dr. David Brownstein, MD.
Where can I order the book?
Currently, only at the publishing company website. It will eventually catch up to Amazon, but that can take time. You can order one or multiple copies of the new STTM II book here: http://laughinggrapepublishing.com/stop-thyroid-madness-ii-book/
Or you can order a set(s) of both the revised STTM book and the STTM II book here:Â http://laughinggrapepublishing.com/stop-thyroid-madness-books-revised-and-ii/Â ALSO NOTE that by snail mail, you can order an amount of each book. There’s an Order Form to print out on the above page.
Want to read more about each author?
Go to the following page and click on their photo: //www.stopthethyroidmadness.com/stop-thyroid-madness-ii
Have you ever had thyroid nodules? Read the real life testimony of thyroid and Hashimoto’s patient Cheryl and how she single-handedly removed her nodules with iodine and selenium…even though she has Hashimoto’s disease! ~Janie, hypothyroid patient and site creator
Remember: this is just Cheryl’s remarkable experience and information. Each person reading this has to decide for themselves or in working with their doctor.
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The new doctor I had just recently hired had decided that my thyroid looked “spongy.” I knew that an ultrasound was a step up on the ladder that would eventually lead to a diagnosis and therefore treatment.
Within three days after the ultrasound study, my doctor called me and stated she was referring me to an endocrinologist. Multiple nodules covered my thyroid and several were going to need a biopsy. It would be much later before I found out how many nodules I had and exactly what shape my thyroid was in.
Never the less, I did what so many of us do when confronted with a health issue. I hit the Internet. First, I looked up the words “Thyroid nodules.” What exactly did that mean? Was it a nice way of saying I had cancer? Thyroid nodules, according to Mayo Clinic, are “solid or fluid-filled lumps that form within your thyroid.” The article went on to state that most are benign (over 95%) and not serious. That was not enough of a definition. I wanted, needed, and felt I deserved more information.
The next site, The American Thyroid Association page (which is good with this info but lousy with other parts), said virtually the same thing, only adding that it was an abnormal growth of thyroid cells on the thyroid gland. I kept perusing the internet, reading anything and everything I could find on thyroid nodules including the size at which a nodule becomes clinically significant (1cm and over) and needs a biopsy. I also found that not all nodules are solid abnormal growths but that some are the result of tissue breakdown. Those are the fluid-filled cysts and can occur due to Hashimoto’s.
Once I was satisfied with the information I gathered on the how and why of nodules- I made it my next mission to find out about biopsies of these “abnormal growths.”
What I learned was that Fine Needle Aspiration is the preferred method to biopsy a clinically significant thyroid nodule, and the doctor usually performs it right in the office. The endocrinologist inserts a hollow needle into the “lump” and extracts a sample of cells for analysis. It is a safe and relatively painless procedure.
The biopsy went flawlessly, as they always do, and my results came back: The lumps, numbering 21, (with only two being significant), were classified as being hyperplastic (adnomatoid) nodules. Being benign, they mostly contained follicular cells, Hurthle cells, and some foamy macrophages. When I asked about treating my thyroid, the nodules, and medication, I got the usual answer. “We aren’t doing anything. We are going to watch and wait.” I left that endocrinologist’s office with a sense of defeat. I was for sure I was going to die and no one in the world was going to help me.
I was not going to “watch and wait.” “Not this girl,” I thought. It was obvious to me that my thyroid was floundering and needed help! By the time I got home from the follow up visit, about an hour and half away, I once again hit the World Wide Web to educate myself on the pathology findings. The next phase of my journey for true thyroid care began.
In the days immediately following my biopsy results, my primary care physician finally agreed to test my Free T3, Free T4, and both antibodies tests. When the results of those tests came back, they clearly proved my suspicions. My thyroid was down for the count. It was then that my doctor agreed to medication and natural desiccated thyroid was my choice (T4/T3 can work well, too). She started me off small with one 60 mg pill a day (…which is meant to be raised until we are optimal. How we raise is also in Chapter 2 of the updated revision STTM I book).
I had nodules that the field of medicine had completely disregarded. I started reading on how to treat an under medicated thyroid. I read about what nutrients and supplements the thyroid had to have for proper functioning. I started digging into benign tumors and how to treat them as well. I, then, packaged that information into a regimen of supplements made easy by online ordering.
My regimen to begin with consisted of a working NDT (From Janie: this can also be T4 and T3) and selenium. I started the selenium first because I understood that it was critical to the thyroid. So vital, in fact, that the body will take selenium from the brain for thyroid use. It was determined from the lab/biopsy results that I had Hashimoto’s and I had heard that people with Hashi’s should not take iodine. Through my research, though, I began to understand that those with Hashi’s could take iodine but do need the selenium to protect the delicate thyroid. So, I started my selenium (400 micrograms a day). I began taking it a full two weeks before my iodine. I did not want to have a Hashi’s flare from taking iodine and knew the selenium would need a while to build up completely in my system.
I had visited several sites regarding the use of iodine to cure cancers and tumors. I had joined an iodine group and absorbed Stephanie Buist’s information. I visited Breast Cancer Choices.org and found a ton of helpful information there as well. I educated myself on the many uses of iodine and the vital role it plays in the human body. I learned that as important as selenium was to the thyroid, iodine was just as important. It is the main ingredient in all thyroid hormones.
I was cautious with the iodine. I worked on building up a tolerance. I started with one drop of J.Crow’s Lugol’s 2% iodine solution a day for one week. I then “upped” the dose to 2 drops (6mg) a day for a week. And so on and so forth until I exhibited “hyper” symptoms at which time I dropped back down to the next lower dose. My body was set at 33 milligrams of iodine a day. I was going to heal my thyroid or die trying.
(From Janie: going low and slow is a good idea with iodine. It starts a detox of what we have too much of in our bodies: bromide, chloride, fluoride, etc. This is true for all but especially true if you have Hashimoto’s.)
Three months after the initial ultrasound, my doctor ordered a repeat. The results left her scratching her head and claiming divine intervention. In three months, I had lost 14 smaller clinically insignificant nodules. Fourteen nodules on my thyroid just disappeared. When I asked her, “How does that happen?” her response was “I don’t know – God.” I smirked but I knew it was the iodine and selenium I had religiously been taking.
As an experiment, and to confirm to myself what I already knew, I did come off the iodine and selenium, for a while, to see what would transpire. I told no one what I was doing, as I wanted to see it for myself, without influence or interference. For four months, I took no iodine or selenium- only the Armour. The following ultrasound showed a new nodule. That was proof enough for me. I went back on the iodine and selenium and continued to take my Armour, which, my doctor had upped to 2.5 grains a day.
I no longer have any clinically significant nodules. In fact, I only have three nodules and the ultrasound reports shows that they are shrinking as well.
However, that is not all. For the first time since my fight for thyroid care began, my thyroid itself is no longer swollen and is in “acceptable normal limits,” meaning it is a “normal” size. While I know my thyroid will need consistent life-long care, as I do have Hashimoto’s, I no longer feel like I am a slave to my supplements or that my thyroid is more of a burden than a blessing. The fight for my thyroid, as long and as arduous as it has been, has been worth it. The “the Siamese sisters of the thyroid,” what I now call selenium and iodine, have given me my thyroid, and consequently, my life back. The ultrasounds alone prove it.
Cheryl
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Read more about selenium. Here’s good information about iodine.
Keep track of any US-made desiccated thyroid products. There were three that were rightly recalled in 2020, for example.
Do you experience hyper-like symptoms when you try to raise a working desiccated thyroid or T3 in your treatment in order to get optimal? That can point to an adrenal issue. Read here.
Have you raised a working desiccated thyroid or T3 and still feel hypothyroid? Read here.
And this is your patient-to-patient book, below, with Hashimoto’s. Order here.
