thyroid

Thyroid Disease and Testing During Pregnancy

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One in five women of reproductive age suffers from some form of thyroid disease, mostly hypothyroidism (Gharib et al. 2005; Hollowell et al. 2002). In adult women, 95% of clinical hypothyroidism results from primary disease of the thyroid gland, generally, the autoimmune condition Hashimoto thyroiditis (Wartofsky et al., 2006). Autoimmune thyroid disease is also common among women with Type 1 diabetes mellitus, Sjogren syndrome, Addison disease, or pernicious anemia. Up to 25% of patients with Type 1 diabetes will develop postpartum thyroid disease (Alvarez-Marfany et al., 1994).

Hypothyroidism During Pregnancy

What happens when a woman with untreated thyroid disease gets pregnant? Depending upon the diagnostic criteria, hypothyroidism affects 0.3% (Casey & Leveno, 2006) to 5% (Gharib et al. 2005) of pregnancies. The symptoms are vague and are similar to other pregnancy concerns making diagnoses based on clinical symptoms alone difficult. Hypothyroid symptoms include fatigue, constipation, cold intolerance, muscle cramps, insomnia, weight gain, carpal tunnel syndrome, hair loss, voice changes, and slowed thinking.

The consequences of undiagnosed hypothyroidism during pregnancy are significant. Hypothyroidism is associated with premature birth, pre-eclampsia, abruption, low birth weight (LBW), postpartum hemorrhage, and impaired neuropsychological development in childhood (Burman, 2009). Research found that fetal loss was higher in untreated hypothyroid women (29%) vs hypothyroid women taking levothyroxine (6%), highlighting the need for early detection (Hallengren 2009).

Hyperthyroidism During Pregnancy

Hyperthyroidism, the result of an excess of thyroid hormones, complicates less than 1% of pregnancies (ACOG Practice Bulletin, 2002). Symptoms of hyperthyroidism are uncommon in normal pregnancy and thus somewhat easier to identify clinically. Maternal symptoms include weight loss or failed weight gain despite increased dietary intake, resting tachycardia, hypertension, tremor, eye stare, eyelid lag, proptosis, and thyroid enlargement or nodule.

Graves’ disease, an autoimmune disorder occurring in 0.5% of the population, accounts for more than 90% of the hyperthyroidism associated with pregnancy. Complications associated with undiagnosed or poorly managed hyperthyroidism during pregnancy include pre-term labor, pre-eclampsia and maternal thyroid storm, fetal tachycardia, low birth weight, congenital abnormalities, and stillbirth.

Should Pregnant Women Be Tested for Thyroid Disease?

Yes, but there is little consensus among the major medical associations regarding who, when, and how to test for thyroid function during pregnancy. It is argued that by the time TSH (the gold standard in thyroid diagnostics) becomes hyper-elevated and the clinical symptoms emerge, the damage to fetal neurodevelopment related to insufficient maternal T4 stores, has already been done (Calvo et al. 2002).  Emerging evidence suggests that maternal T4 levels may not track directly with elevated TSH levels especially in the first trimester when the demands for maternal T4 are greatest (Morreale de Escobar et al. 2000), making the need for more advanced testing techniques even more important.

Iodine Deficiency and Hypothyroidism: One More Factor to Consider

Complicating matters even further, in iodine-deficient populations, neither TSH, T4 nor T3 denote the underlying deficiency, which as it progresses, inevitably elicits the range of fetal developmental issues and maternal complications associated with hypothyroidism. In the US, approximately 10% of the population is iodine deficient while 50% of Europe is iodine deficient (Zimmerman 2009). In recent years, iodine deficiency has increased in the US in women of reproductive age with 14.9% percent potentially iodine deficient (Hollowell et al. 1998). Similarly, the incidence of congenital hypothyroidism in newborns has also increased in the US over the last two decades (Parks et al. 2010).

Iodine deficiency in women can lead to overt hypothyroidism and consequent anovulation, infertility, gestational hypertension, spontaneous first-trimester abortion, and stillbirth (DeLong et al., 1997). Iodine deficiency is also associated with an increased risk for thyroid carcinoma in animal models and humans (Mellemgaard et al., 1998). In the Bryansk region of Russia, an area of known radioactive I-131 exposure following the Chernobyl disaster, the risk of all types of thyroid cancer was inversely associated with urinary iodine excretion levels (WHO Health Risk Assessment).

What Constitutes Hypothyroidism in Pregnant Women?

In addition to the debate over whether to test pregnant moms routinely for thyroid disease, especially hypothyroid moms, there is much debate regarding what constitutes elevated TSH and whether to include subclinical hypothyroidism (SCH) or mild hypothyroid cases in the testing matrix (Fatourechi 2009; Surks et al. 2004). SCH or mild hypothyroidism is suggested by only slightly elevated TSH concentrations without the normally accompanying changes in T4.  Arguments against testing for SCH include the enormous increase in cases; up to 28 million more people could be diagnosed with hypothyroidism, and the conflicting data regarding treatment benefits and disease progression. Moreover, recent evidence suggests significant age and race-based differences in TSH reference ranges across the non-pregnant population complicating diagnoses even further (Surks & Boucai 2010).

Given the dire consequences of untreated thyroid dysfunction during pregnancy, there is a need for more accurate, non-invasive and less expensive thyroid function tests with reference ranges specifically identified for this population of women. Screening for thyroid function in women of reproductive age and in pregnant women could reduce maternal and fetal complications.

Our view on thyroid disorders during pregnancy can be summarized as follows:

  • Thyroid disease is common in pregnancy.
  • Hypothyroidism and hyperthyroidism are associated with adverse pregnancy outcomes, and treatment may improve these outcomes.
  • Untreated hypothyroidism during pregnancy is associated with impaired intellectual development in childhood.
  • Routine, universal screening for thyroid function in women of reproductive age and in pregnant women could reduce could reduce maternal and fetal complications
  • Normal reference ranges for thyroid function tests in pregnancy must be established

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Postscript: This article was originally published on February 21, 2012 and updated on July 11, 2014. If I were to rewrite this post now, I would attribute much of the thyroid dysfunction to nutrient deficiencies. 

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Vitamin D Plays an Integral Role in Adaptive Immunity

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Severe Adverse Reactions Include Vitamin D Deficiency and Autoimmunity

Hormones Matter researchers discovered that, inter alia, severe adverse reactions to any of the surveyed drugs trigger significant but varying autoimmune responses. Moreover, the research revealed an underlying consistency involving all reviewed drugs: vitamin D deficiency.

Vitamin D Helps Regulate the Adaptive Immune System

The adaptive immune system comprises the body’s intricate network of antibodies and special types of white blood cells (called sensitized lymphocytes ) to thwart new and previous invaders including viruses, bacteria, and drugs. When the adaptive immune system is not strong enough to endure external disruptions such as severe side effects of drugs, it can go awry by signaling antibodies and sensitized lymphocytes to attack healthy cells. This response is called autoimmunity—when the adaptive immune system’s cells do not recognize previous invaders and designate healthy cells as those invaders. In other words, the body’s immune cells attack its own healthy cells.

Scientific research over the past three decades solidifies the connection between vitamin D and autoimmunity. Vitamin D plays an integral role in the regulation of the adaptive immune system. Adequate vitamin D in our bodies can protect us from autoimmunity because adaptive immune cells contain vitamin D receptors (VDRs). These receptors are attached to the surface of the adaptive immune system’s antibodies and sensitized lymphocytes. The VDRs act as “gate keepers” by signaling what external substances, e.g., components of medications, can enter a cell. The VDRs must be replete with vitamin D to effectively regulate adaptive immunity. When the VDRs receive adequate amounts of vitamin D, they enable the adaptive immune system to function properly by attacking new and previous invaders.

When the VDRs attached to the adaptive immune system’s cells do not contain sufficient vitamin D to attack invaders, autoimmunity may kick in, causing the death of healthy immune cells. Thus, low vitamin D levels can lead to autoimmune diseases including thyroid disorders such as Hashimoto’s and demyelinating diseases including multiple sclerosis (MS).

Vitamin D and Hashimoto’s Autoimmune Thyroid Disease

The Real Women, Real Data research also uncovered another consistency among severe adverse reactions to the reviewed drugs: Hashimoto’s thyroiditis, an autoimmune disease caused by abnormal cells constantly assaulting the thyroid gland
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Vitamin D receptors are present in the thyroid as well as the pituitary, the pea-shaped gland that controls the thyroid. Not surprisingly, low levels of serum vitamin D have been linked to Hashimoto’s thyroiditis, according to recent Turkish medical research:

Published in a 2013 issue of the journal Endocrine Practice, a study conducted at a training and research hospital in Ankara demonstrated that serum vitamin D levels of female chronic Hashimoto’s patients were significantly lower than healthy subjects. Furthermore, the researchers discovered a direct correlation between serum vitamin D levels and thyroid volume as well as an inverse correlation to the antibodies involved in the thyroid.

Researchers at Medeniyet University’s Goztepe Education and Research Hospital in Istanbul learned that 92 per cent of their 161 Hashimoto’s thyroiditis cases had serum vitamin D levels lower than 30 ng/mL (12 nmol/L), a value characterized as “insufficient.” Published in a 2011 issue of the journal Thyroid, the study reports an association between vitamin D insufficiency and Hashimoto’s thyroiditis.

Vitamin D and Demyelinating Disorders

Another disturbing outcome of the Real Woman, Real Data research is the reporting of neurological and neuromuscular symptoms, many which of are consistent with demyelinating disorders such as MS, an autoimmune disease. The development of MS occurs when a poorly functioning, adaptive immune system gradually attacks the protective covering of the nerve cells (called the myelin sheath) of the brain and spinal cord. This potentially debilitating process is called demyelination.

Scientific—primarily epidemiological—research indicates an association between vitamin D levels and the risk of developing a demyelinating disorder such as MS. VDRs exist on nerve cells and the myelin sheath. When the VDRs receive adequate amounts of vitamin D, they help protect the integrity of the myelin sheath. However, when the VDRs do not contain sufficient vitamin D, autoimmunity may occur, resulting in the death of healthy nerve cells. Numerous clinical trials are underway to assess the connection between vitamin D status and the likelihood of developing demyelinating disorders.

Low Vitamin D: The Chicken or the Egg?

The connection between low vitamin D status and the development of autoimmune disease is genuine. However, medical research has not yet determined if vitamin D deficiency plays a role in the development of autoimmune disease, if low vitamin D levels are a consequence of the disease itself, or if vitamin D deficiency acts as both a cause and effect. The authors of the aforementioned 2013 Hashimoto’s study concluded,

“Finally, our results suggested that there may be a causal relation between vitamin D deficiency and development of Hashimoto’s thyroiditis. On the other hand, there might be a possible relation between severity of vitamin D deficiency and progression of thyroid damage. However, further studies are needed especially about the effects of vitamin D supplementation on prevention and/or progression of autoimmune thyroid disease.”

Proactive Protection against Severe Adverse Reactions

We could wait years (or decades) to garner the results of further scientific studies and clinical trials to define the exact relationship between vitamin status and severe adverse reactions to vaccines and medications that culminate in autoimmune disorders. Or we could be proactive by taking daily vitamin supplements and enjoying moderate sunlight exposure to increase our vitamin D levels.

It is imperative to take enough vitamin D3 so this essential nutrient will be stored in your cells to help regulate your immune system. The greater your serum vitamin D level (easily obtained from a simple blood test called 25(OH) D, the more likely you will benefit from a stronger immune system that protects your body’s cells from attacking one another.

No one wants to endure severe adverse reactions to drugs such as Gardasil and Lupron, let alone an autoimmune disease. Attaining and maintaining adequate supplementation provides a safe, easy, and inexpensive approach to improved preventive health. By empowering yourself with adequate vitamin D, you may reap the benefits of avoiding disease and enjoying better quality of life.

Copyright © 2013 by Susan Rex Ryan. All rights reserved.

This article was published previously on Hormone Matter in September 2013.

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Why Fatigue Matters in Thyroid Disease

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The notion that unremitting fatigue is a core clinical symptom is difficult for many physicians and patients to reconcile with its ubiquitous nature in illness. Here is yet another example of the importance of recognizing fatigue and the constellation of other clinical signs that manifest concurrently in thyroid disease. Here we see that fatigue represents a loss of mitochondrial function that, if left untreated, has some subtle and not so subtle effects on central nervous system functioning.

Some Background: Fatigue and the Mitochondrial Connection

Fatigue is one of the most common signs of mitochondrial dysfunction or deficit. Mitochondria, the energy factories within our cells, produce the ATP or cellular energy, that our bodies require to function. This process is called oxidative metabolism. As Dr. Lonsdale wrote about in How can Something as Simple as Thiamine Cause So Many Problems, consider each mitochondrion as a mini, combustion engine.

 Fuel + Oxygen + Catalyst = Energy

 Each of our one hundred trillion body/brain cells is kept alive and functioning because of this reaction. It all takes place in micro “fireplaces” known as mitochondria. Oxygen combines with fuel (food) to cause burning or the combustion – think fuel combustion engine. We need fuel, or gasoline, to burn and spark plugs to ignite in order for the engines to run.

In our body/brain cells it is called oxidation. The catalysts are the naturally occurring chemicals we call vitamins (vital to life). Like a spark plug, they “ignite” the food (fuel). Absence of ANY of the three components spells death.

Antioxidants like vitamin C protect us from the predictable “sparks” (as a normal effect of combustion) known as “oxidative stress”.  Vitamin B1, is the spark plug, the catalyst for these reactions.

 

When there is dysfunction within this pathway, which is also called the OXPHOS or oxidative phosphorylation, when the engine doesn’t get the fuel it needs or the spark plugs don’t work, fatigue and other symptoms arise. Fatigue is an important clinical sign that something is amiss in our cellular combustion engines.

Mitochondria and Hypothyroidism – Beyond One Test One Drug

In chronic hypothyroidism, chronic mitochondrial deficits are clinical signs that can be recognized, if one is looking for them. They present as fatigue, and when chronic, as balance and gait disorders. Recall our discussion and videos on Hashimoto’s disease associated with walking and balance difficulties: Adverse Reactions, Hashimoto’s Thyroiditis, Gait Balance and Tremors –  those examples pointed to mitochondrial dysfunction. Here is yet another example of the importance of recognizing subtle clinical signs of mitochondrial damage.

Watch and listen for the clinical signs. How many do you have?

Notice, he speaks of the importance of proper nutrition, of reducing inflammation, and of exercise and other modalities to correct the functional deficits of hypothyroidism and mitochondrial dysfunction. Notice also, the improvement in functioning after only eight weeks of treatment.

Datis Kharrazian: Developing the Clinical Eye to Discover the Causes of Fatigue from The Institute for Functional Med on Vimeo.

If you or a loved one suffers from chronic and unremitting fatigue rule out thyroid dysfunction and its sister condition mitochondrial damage. A simple TSH test, as is commonly considered, is not sufficient to find thyroid dysfunction. A full panel must given. Once a diagnosis is reached, remember thyroid medications, though they may be necessary, are not enough to correct mitochondrial damage. Diet and nutrients must considered. Put it all together and live healthier.

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Hormones Matter needs funding now. Our research funding was cut recently and because of our commitment to independent health research and journalism unbiased by commercial interests we allow minimal advertising on the site. That means all funding must come from you, our readers. Don’t let Hormones Matter die.

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This article was published originally on Hormones Matter on November 7, 2013. 

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Vitamin D3 and Thyroid Health

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The benefits of vitamin D3 garner a plethora of glowing press these days but little information has been reported about how this essential nutrient may be associated with thyroid disorders. An alarming number of Americans—over 25 million—suffer from thyroid disease. Women are four times more likely than men to develop a thyroid disorder. The thyroid, a butterfly-shaped gland located in your neck, regulates your metabolism and affects every cell in your body. When your thyroid is not working properly, your body becomes unbalanced, potentially causing symptoms including weight gain or loss and chronic fatigue as well as autoimmune disease and cancer. Let’s look at how vitamin D3 may affect thyroid health:

Thyroid Hormonal Balance

Vitamin D receptors (VDR) are present in the cells of the pituitary, the pea-sized gland located at the base of the brain that controls your thyroid. The pituitary produces a hormone called thyroid stimulating hormone (TSH) that signals your thyroid gland to make thyroid hormone (T3 and T4). Thyroid hormone constantly circulates throughout your body, regulating metabolism. Either inadequate or excessive thyroid hormone can wreak havoc to your health, culminating in hypo- or hyperthyroidism. Understanding the regulating effects of VDR in our cells, I surmise that the amount of activated vitamin D3 in the pituitary’s VDR may be connected to the balance of thyroid hormone.

Autoimmune Thyroid Diseases

Adequate levels of vitamin D3 may protect the immune system from attacking itself. Low vitamin D3 levels have been linked to autoimmune thyroid diseases including Hashimoto’s and Graves’ thyroiditis.

Discovered one hundred years ago by a Japanese physician, Hashimoto’s disease is caused by abnormal blood cells and white blood cells constantly attacking and damaging the thyroid. About 95 per cent of Hashimoto’s disease patients are women. A study published in a 2011 issue of the journal Thyroid revealed that 92 per cent of Hashimoto’s thyroiditis cases had insufficient circulating vitamin D3 levels.

Ten times more likely to develop in women than men, Graves’ disease is caused by antibodies that overstimulate thyroid hormone production, causing hyperthyroidism. Researchers, who investigated Japanese female and male patients with Graves’ disease over a one-year period, found a high prevalence of woefully low circulating vitamin D3 in the female patients compared to the male subjects.

Thyroid Cancer

Incidences of thyroid cancer have doubled over the past four decades. The likelihood of women developing thyroid cancer is three times greater than for men. Activated vitamin D3 regulates cell differentiation, cell proliferation, and cell death. If these vital functions go awry, cancer may develop. Epidemiological studies indicate a link between vitamin D3 and thyroid cancer. Vitamin D researcher W.B. Grant, Ph.D. published a paper in a 2012 issue of the journal Anticancer Research that indicated an association between solar ultraviolet B, vitamin D3, and cancers including thyroid.

A relatively rare form of thyroid cancer—medullary thyroid cancer—originates in the thyroid C cells where a hormone called calcitonin is secreted. Calcitonin’s functions include stimulation of vitamin D3 production in the kidneys. The measurement of calcitonin is a diagnostic screening tool for medullary thyroid cancer. VDR are present in the thyroid C cells. Understanding the powerful effect of activated VDR on cell regulation, I hypothesize that activated VDR in the C cells may possibly prevent the development of medullary thyroid cancer.

In conclusion, recent medical literature suggests a connection between vitamin D3 and thyroid health. However, additional research is required to determine if thyroid dysfunction may cause vitamin D3 deficiency, or low vitamin D3 status may contribute to thyroid disorders.

Copyright ©2012 by Susan Rex Ryan, all rights reserved.

This post was published previously on Hormones Matter in September 2012.

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Hormones Matter Top 100 Articles of 2015

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Happy New Year, everyone. We have another remarkable year under our belts. Hormones Matter continues to grow month after month. This year, despite the site being down for a month in September, we had over 815,000 visitors, most staying quite a while to read our articles.

Since inception, we’ve published close to 900 articles, many are read by thousands of readers every month. The hysterectomy and endometriosis articles continue to draw large crowds, demonstrating the great need for information in these areas of women’s health.

Our success is thanks to a fantastic crew of volunteer writers who spend countless hours researching complex medical topics, making connections, identifying unconventional therapeutic opportunities, and bringing to light, what are often, invisible illnesses. Without these incredibly talented and compassionate individuals, Hormones Matter would not exist.

Before we begin the new year in earnest, let us take a moment to thank all of the writers of Hormones Matter.

Thank You Hormones Matter Writers!

 

Below are the articles and authors who made the top 100 list for 2015. If you haven’t read these articles, it’s time to do so. If you like them, share them and share our site so we can continue to grow. If you were helped by any of our articles, take a moment and send the writer a thank you note.

This year, we thought we’d do something a little different and include the 25 all-time favorite articles on Hormones Matter. Be sure to scroll down to the second table and take a look. The numbers are quite impressive.

Since we are run by volunteers and unfunded, feel free contribute a few dollars to cover the costs of maintaining operations. Crowdfund Hormones Matter. Every dollar helps.

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Hormones Matter Top 100 Articles of 2015

Article Title and Author

Reads

1. Post Hysterectomy Skeletal and Anatomical Changes -WS 50,814
2. Sex in a Bottle: the Latest Drugs for Female Sexual Desire – Chandler Marrs 47,910
3. Sexual Function after Hysterectomy – WS 28,898
4. In the ER Again – Heavy Menstrual Bleeding -Lisbeth Prifogle 25,326
5. Endometrial Ablation – Hysterectomy Alternative or Trap? -WS 25,048
7.  Adhesions: Cause, Consequence and Collateral Damage – David Wiseman 22, 868
8. Is Sciatic Endometriosis Possible? – Center for Endometriosis Care 11,701
9. Endometriosis: A Husband’s Perspective – Jeremy Bridge Cook 11,626
10. A Connection between Hypothyroidism and PCOS – Sergei Avdiushko 11,024
11. Often Injured, Rarely Treated: Tailbone Misalignment – Leslie Wakefield 10,580
12. Hysterectomy: Impact on Pelvic Floor and Organ Function – WS 8,494
13. Pill Bleeds are not Periods – Lara Briden 8,440
14. Silent Death – Serotonin Syndrome – Angela Stanton 8,408
15.  An Often Overlooked Cause of Fatigue: Low Ferritin – Philippa Bridge-Cook 8,374
16. Wide Awake: A Hysterectomy Story – Robin Karr 7,733
17. How Hair Loss Changed My Life – Suki Eleuterio
18. The High Cost of Endometriosis – Philippa Bridge-Cook 7,170
19. Skin Disorders post Gardasil – Chandler Marrs 6,891
20. Essure Sterilization: The Good, the Bad and the Ugly – Margaret Aranda 6,820
21. Love Hurts – Sex with Endometriosis – Rachel Cohen 6,779
22. Dehydration and Salt Deficiency Migraines – Angela Stanton 6,638
23.  Adverse Reactions, Hashimoto’s Thyroiditis, Gait, Balance and Tremors – Chandler Marrs 6,445
24.  Stop the Metformin Madness – Chandler Marrs 6,400
25. Lupron, Estradiol and the Mitochondria: A Pathway to Adverse Reactions – Chandler Marrs 6,110
26. Endometriosis after Hysterectomy – Rosemary Finnegan 6,093
27. The Reality of Endometriosis in the ER – Rachel Cohen 5,962
28. Mittelschmerz – what should you know – Sergei Avdiushko 5,780
29.  Red Raspberry Leaf Tea to Relieve Menstrual Pain – Lisbeth Prifogle 5,586
30. Mommy Brain: Pregnancy and Postpartum Memory Deficits – Chandler Marrs 5,437
31. Parasites: A Possible Cause of Endometriosis, PCOS, and Other Chronic, Degenerative Illnesses – Dorothy Harpley-Garcia 5,414
32.  Endometriosis and Risk of Suicide – Philippa Bridge-Cook 5,413
33.  Fluoroquinolone Antibiotics and Thyroid Problems: Is there a Connection? – JMR 5, 228
34. Adenomyosis – Philippa Bridge-Cook 5,022
35.  Gardasil: The Controversy Continues – Lisbeth Prifogle 4,809
36.  Hyperemesis Gravidarum – Severe Morning Sickness: Are Mitochondria Involved? – Chandler Marrs 4,801
37.  Oral Contraceptives, Epigenetics, and Autism – Kim Elizabeth Strifert 4,452
38.  High Blood Pressure in Women: Could Progesterone be to Blame? – Chandler Marrs 4,446
39. My Battle with Endometriosis: Hysterectomy at 23 – Samantha Bowick 4,288
40. Thiamine Deficiency Testing: Understanding the Labs – Derrick Lonsdale 4,045
41. My Battle with Endometriosis and Migraines – Angela Kawakami 3,839
42. Tampons with Glyphosate: Underpinnings of Modern Period Problems? – Chandler Marrs 3,835
43. Cipro, Levaquin and Avelox are Chemo Drugs – Lisa Bloomquist 3,792
44. Hysterectomy or Not – Angela’s Endometriosis Update – Angela Kawakami 3,750
45. Warning to Floxies: Beware of New Med for Psoriatic Arthritis – Debra Anderson 3,691
46.  DES – The Drug to Prevent Miscarriage Ruins Lives of Millions – DES Daughter 3,655
47.   Sphincter of Oddi Dysfunction (SOD) – Brooke Keefer 3,540
48. Progesterone for Peripheral Neuropathy – Chandler Marrs 3,278
49. The Fluoroquinolone Time Bomb – Answers in the Mitochondria – Lisa Bloomquist 3,251
50. Why is PCOS so Common? – Lara Briden 3,211
51.  Pregnancy Toes – What Sugar does to Feet – Angela Stanton 2,971
52.  Five Half-truths of Hormonal Contraceptives – The Pill, Patch and Ring – Joe Malone 2,834
53.  Five Years After Gardasil – Ashley Adair 2,831
54. Bleeding Disorders Overlooked in Women with Heavy Periods – Philippa Bridge Cook 2,826
55.  Is Gardasil Mandated in Your State? – Lisbeth Prifogle 2,814
56.  Is Prenatal Dexamethasone Safe: The Baby Makers’ Hubris – Chandler Marrs 2,808
57. Porn Brain – A Leading Cause of Erectile Dysfunction – Chandler Marrs 2,792
58. Lupron and Endometriosis – Jordan Davidson 2,752
59.  Endometriosis, Adhesions and Physical Therapy – Philippa Bridge-Cook 2,746
60.  Glabrata – A Deadly Post Fluoroquinolone Risk You’ve Never Heard About – Debra Anderson 2,703
61. Are You Vitamin B12 Deficient? – Chandler Marrs 2,635
62. Topamax: The Drug with 9 Lives – Angela Stanton 2,635
63.  Cyclic Vomiting Syndrome – Philippa Bridge-Cook 2,622
64.  The Endo Diet: Part 1 – Kelsey Chin 2,614
65.  Endometriosis and Adhesions –  Angela Kawakami 2,544
66.  Thyroid Disease Plus Migraines – Nancy Bonk 2,530
67.  Is it Endometriosis? – Rosalie Miletich 2,414
68. Hysterectomy, Hormones, and Suicide – Robin Karr 2,412
69.  Why I am Backing the Sweetening the Pill Documentary – Laura Wershler 2,321
70.  I Wanted to Die Last Night: Endometriosis and Suicide – Rachel Cohen 2,271
71.  How Can Something As Simple As Thiamine Cause So Many Problems? – Derrick Lonsdale 2,456
72.  Thyroid Dysfunction with Medication or Vaccine Induced Demyelinating Diseases – Chandler Marrs 2,034
73. Angela’s Endometriosis Post Operative Update –  Angela Kawakami 2,017
74.  Fluoroquinolone Antibiotics Damage Mitochondria – FDA Does Little – Lisa Bloomquist 1,993
75.  Endometriosis and Pregnancy at a Glance – Center for Endometriosis Care 1,969
76.  Don’t Take Cipro, Levaquin or Avelox If…. – Lisa Bloomquist 1,960
77.  Gardasil Injured – Dollie Duckworth 1,898
78. Fear of Childbirth Prolongs Labor – Elena Perez 1,888
79. Fluoroquinolone Poisoning: A Tale from the Twilight Zone – Kristen Weber 1,883
80. Personal Story: Thyroid Cancer – Myrna Wooders 1,880
81. Recurrent Miscarriage – Philippa Bridge-Cook 1,873
82. Recovering from the Gardasil Vaccine: A Long and Complicated Process – Charlotte Nielsen 1,842
83. Pelvic Therapy for Endometriosis, Adhesions and Sexual Pain – Belinda Wurn 1,818
84. Hormones, Hysterectomy and the Hippocampus – Chandler Marrs 1,777
85. Why Fatigue Matters in Thyroid Disease – Chandler Marrs 1,718
86. How Do You Deal with the Lasting Effects of Endometriosis? – Samantha Bowick 1,697
87. Depression with Endometriosis – Samantha Bowick 1,678
88. Easing Endometriosis Pain and Inflammation with Nutrition –  Erin Luyendyk 1,648
89. Anti-NMDAR Encephalitis and Ovarian Teratomas – Chandler Marrs 1,634
90. Autoinflammatory Syndromes Induced by Adjuvants: A Case for PFAPA – Sarah Flynn 1,595
91. Endometriosis Awareness Month: A Wish Noted – Philippa Bridge-Cook 1,513
92. The Role of Androgens in Postmenopausal Women – Sergei Avdiushko 1,477
93. It Wasn’t by Choice: Dysautonomia – Margaret Aranda 1,454
94. Fluoroquinolone Antibiotics Associated with Nervous System Damage – Lisa Bloomquist 1,453
95.  Vitamin D3 and Thyroid Health – Susan Rex Ryan 1,439
96. Dealing with Doctors When You Have Undiagnosed Endometriosis -Angela Kawakami 1,439
97. Endometriosis and Being a Trans Person: Beyond Gendered Reproductive Health – Luke Fox 1,436
98. Cyclic Vomiting Syndrome and Mitochondrial Dysfunction: Research and Treatments – Philippa Bridge-Cook 1,430
99. Living with Ehlers Danlos is Hell – Debra Anderson 1,420
100. What is Fluoroquinolone Toxicity? – Lisa Bloomquist 1,415

Hormones Matter All-Time Top 25 Articles

Article Title and Author

Reads

1. Post Hysterectomy Skeletal and Anatomical Changes -WS 105,336
2. Sex in a Bottle: the Latest Drugs for Female Sexual Desire – Chandler Marrs 99,098
3. Endometrial Ablation – Hysterectomy Alternative or Trap? -WS 70,999
4. Adhesions: Cause, Consequence and Collateral Damage – David Wiseman 40,299
5. In the ER Again – Heavy Menstrual Bleeding -Lisbeth Prifogle 39,821
7.  Sexual Function after Hysterectomy – WS 35,188
8. A Connection between Hypothyroidism and PCOS – Sergei Avdiushko 31,193
9. Is Sciatic Endometriosis Possible? – Center for Endometriosis Care 24,691
10. Endometriosis: A Husband’s Perspective – Jeremy Bridge-Cook 23,251
11. Skin Disorders post Gardasil – Chandler Marrs 18,105
12.  Gardasil: The Controversy Continues – Lisbeth Prifogle 14,174
13.  Wide Awake: A Hysterectomy Story – Robin Karr 14,134
14.  Endometriosis and Risk of Suicide – Philippa Bridge-Cook 13,836
15.  Love Hurts – Sex with Endometriosis – Rachel Cohen 13,782
16. Endometriosis after Hysterectomy – Rosemary Finnegan 13,294
17. Hysterectomy: Impact on Pelvic Floor and Organ Function – WS 13,056
18.  Adverse Reactions, Hashimoto’s Thyroiditis, Gait, Balance and Tremors – Chandler Marrs 12,901
19.  How Hair Loss Changed My Life – Suki Eleuterio 12,835
20. Mittelschmerz – what should you know – Sergei Avdiushko 11,919
21.  Often Injured, Rarely Treated: Tailbone Misalignment – Leslie Wakefield 11,521
22.  An Often Overlooked Cause of Fatigue: Low Ferritin – Philippa Bridge-Cook 10,821
23.  Mommy Brain: Pregnancy and Postpartum Memory Deficits – Chandler Marrs 10,591
24. Adenomyosis – Philippa Bridge-Cook 10,249
25.  I Wanted to Die Last Night: Endometriosis and Suicide – Rachel Cohen 9,826
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Thyroid Dysfunction with Medication or Vaccine Induced Demyelinating Diseases

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It is always amazing to me when seemingly disparate research articles come across my desk and within an instant there is a shift in understanding. That is what happened over the last two weeks, community members from different disease groups shared research articles. From the Gardasil community: CNS Demyelination and Quadrivalent HPV Vaccination .  From our friends at Thyroid Change: Triiodothyronine Administration Ameliorates the Demyelination/Remyelination Ratio in a Non-Human Primate Model of Multiple Sclerosis by Correcting Tissue Hypothyroidism. And I connected some dots.

Thyroid and Neuromuscular Reactions to Gardasil and Lupron

Among the more common side-effects reported by Gardasil injured and a group we are just beginning to study, Lupron injured women, include decreased thyroid function, sometimes associated with Hashimoto’s, thyrotoxicosis or even thyroid cancer. Simultaneously, but frequently viewed as separate or unrelated disease processes, both groups of women report a constellation of neurological and neuromuscular symptoms, many consistent with demyelinating disorders such as multiple sclerosis (MS). Indeed, case reports of central nervous system (CNS) demyelination or MS and Gardasil have been reported (cited above). There may be a connection between the demyelination process and the thyroid injury that develops as an adverse immune response to a drug or vaccine. More importantly, there may be a treatment opportunity.

Thyroid Hormones Affect Myelination

Almost a decade of research conducted solely in animals, rodents and monkeys, shows a connection between decreased thyroid function and demyelination disorders. Specifically, researchers found that administration of the thyroid hormone triiodothyronine (T3) not only improves the clinical course of the MS – like symptoms but effectively switches the disease process from a primarily demyelinating progression to remyelination. That is, the T3 induces cell level responses that regrow the protective myelin sheaths around CNS axons and corrects the medication-induced, tissue level, hypothyroidism. For the young women experiencing the host of neurological and neuromuscular symptoms post HPV vaccine, Gardasil or Cervarix, and/or post Lupron, this research may point to both an etiology and a treatment opportunity – disrupted thyroid metabolism mediated by an inflammatory reaction and T3 supplementation, respectively.

Dysregulated Thyroid in Critical and Chronic Illness

Vast amounts of research show a connection between thyroid function and critical and chronic illness. Hypothyroidism is common in what are otherwise considered ‘euthryoid’ or ‘normal’ thyroid individuals, but whose physiology is so severely stressed by disease or injury, thyroid function is affected. The presentation of diminished thyroid function during severe or chronic illness of unrelated etiology is often difficult to determine and its treatment is controversial. In these cases, thyroid stimulating hormone (TSH) is within the normal range in all but about 10% of patients and thyroxine (T4) may or may not be reduced. If and when further analysis is completed, T3, however, is often shown to be significantly diminished, the T4/T3 ratio is larger, reverse T3 (rT3), the T3 deactivating hormone is increased, while the enzymes responsible for converting T4 to T3 are reduced; clear evidence of disrupted thyroid metabolism that can be missed with traditional testing.

With the mixed laboratory presentation and evidence that supplementing with levothyroxine (synthetic T4) does little to improve patient outcomes, treating illness induced thyroid dysfunction is controversial, many physicians and medical organizations argue against treatment. Indeed, even in primary hypothyroidism, treatment with anything other than levothyroxine – T4 is controversial. Perhaps it shouldn’t be. The evidence reported in these animal studies, clearly indicates, T3 dysfunction and consequent supplementation controls the demyelination and remyelination process at the cell level and may improve clinical outcomes.  In this research, T3 supplementation also improved T4 levels without a concomitant onset of hyperthyroidism, the reason often cited for not utilizing T3.

What This Means

If you or your child are suffering with the constellation of symptoms associated with an inflammatory nerve disease such as multiple sclerosis and/or if you have known hypothyroid symptoms in combination with undiagnosed neuromuscular symptoms, it’s time to connect the dots. The two may be related and may require T3 supplementation. Whether these symptoms were initiated with an adverse reaction to a medication such as Lupron, a vaccine such as Gardasil or Cervarix, or by some other process entirely, the research presented here clearly suggests a role for T3 in the array of symptoms associated hypothyroid disease and CNS demyelinating diseases.

Some of the symptoms associated with MS include:

  • Vision problems (optic neuritis)
  • Numbness or tingling of the face, arms, legs
  • Chronic, unexplained pain
  • Muscle spasms – painful muscle contractions
  • Uncontrollable, often painful jerking of the arms or legs
  • Extreme fatigue and weakness
  • Dizziness
  • Vertigo (spinning)
  • Balance or gait (walking) problems
  • Hearing problems or loss
  • Seizures
  • Uncontrollable shaking
  • Breathing problems
  • Slurred speech
  • Trouble swallowing
  • Dysfunctional bladder urinating frequently, strong urges to urinate, or inability to hold in urine
  • Bowel problems – constipation, diarrhea, or loss of bowel control
  • Memory problems
  • Concentration problems
  • Language/speaking
  • Depression
  • Rapidly switching moods
  • Uncontrollable moods
  • Inappropriate moods

These symptoms have been noted in post Gardasil or Cervarix reactions, and as we are learning, in post Lupron reactions as well.  Even though these are two entirely different medications with entirely different mechanisms of action, the core reaction illness that ensues is inflammatory and often attacks the thyroid. When the thyroid is compromised, a range of other pathophysiological processes emerge, including demyelination. Certainly, additional research is warranted, but in the absence of time, and in the face of great suffering, T3 testing and supplementation may be indicated.

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This article was published previously on Hormones Matter in August 2013.

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Thyroid Hormones and Cardiovascular Function: New Research, New Neurons

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Thyroid dysfunction affects approximately 12% of the US population and up to 30% of the world population, especially in iodine deficient regions.  According to the American Thyroid Association, women are eight times more likely to have thyroid disease than men and up to 60% of those with thyroid disease may be undiagnosed. The thyroid gland, located in base of the neck, produces two primary hormones thyroxine (T4) and triiodothyronine (T3) that travel throughout the body and bind to thyroid receptors that then control a myriad of physiological processes including temperature regulation, skeletal muscle, fat metabolism and cardiovascular function. Thyroid hormones also impact brain function and are linked to a range of neuropsychological functions including cognition, depression, anxiety and even psychosis.

Hypothalamic Pituitary Thyroid Axis

The thyroid hormones are controlled from a region in the brain about the size of an almond called the hypothalamus. The hypothalamus is the master regulator for all hormone systems and hormone related activity including feeding, sleeping, reproduction, fight, flight, energy usage – basically every aspect of human and animal survival. It sits at the interface between the central nervous system functioning and the endocrine system functioning.

To regulate thyroid function, the hypothalamus releases a hormone called thyrotropin releasing hormone (TRH), which signals the pituitary gland to release thyroid stimulating hormone (TSH). TSH then activates the thyroid gland to produce and release thyroxine or T4.  If all is well, T4 is converted to T3, which then binds to thyroid receptors located throughout the body and thyroid modulated functions are regulated appropriately. Too much or not enough circulating thyroid hormones, because of their broad reaching effects can, and often do, destabilize homeostatic balance throughout the body.

Thyroid Hormones and Cardiovascular Function

Thyroid hormones have a profound effect on cardiovascular function. Hyperthyroidism evokes heart palpitations, tachycardia, and high blood pressure. While hypothyroidism, elicits bradycardia and low blood pressure consistent with its slowing of metabolism in general. These effects were believed to be mediated solely through the thyroid hormone – thyroid receptor complex on the heart itself. New research shows that there may be an additional, more direct route for thyroid control of cardiovascular function – the brain’s autonomic system.

Researchers have identified a new set neurons in the anterior hypothalamus that suggest a site for central nervous system – autonomic control of thyroid mediated cardiovascular function. That is, these neurons directly control heart rate and blood pressure.

Anterior Hypothalamic Neurons Contain Thyroid Receptors

For over 50 years, researchers have known that lesions to this region of the hypothalamus cause heart rate and blood pressure to skyrocket. Conversely, stimulation causes heart rate and blood pressure to drop. What they didn’t know is how neurons in the anterior hypothalamus controlled cardiovascular function. It turns out, there are thyroid receptors in a set of nuclei called the parvalbuminergic neurons that directly control cardiovascular function. Mutations that specifically affect those thyroid receptors in the parvalbumiergic neurons have drastic affects on heart rate, blood pressure and thermosensation – the ability to sense temperature change and regulate the body’s response accordingly.

In the present study, mutations to the thyroid receptors located on the parvalbumiergic neurons in the anterior hypothalamus directly altered cardiovascular function, suggesting direct and specific autonomic control of cardiovascular function. The mutation to these thyroid receptors evoked high blood pressure and elevated heart rate in conjunction with thermosensation and in states of hypothyroidism. That is, temperature change evoked the cardiovascular effects. When animals with the defunct thyroid receptor in the anterior hypothalamus were exposed to cold, heart rate and blood pressure skyrocketed. In conditions where the ambient temperature was normal, only minimal tachycardia was observed. Since hypothyroid patients have difficulty maintaining core body heat, finding an association between cold exposure and impaired cardiovascular functioning, was particularly interesting.

Hypothyroidism, is not normally normally considered a risk for high blood pressure and high heart rate, at least initially. As other systems, affected by low thyroid hormones become damaged, however, high blood pressure can emerge.  The data from this study suggest a direct mechanism for high blood pressure in some hypothyroid patients. The mutation affecting the thyroid receptors in the hypothalamic neurons can elicit increased heart rate and blood pressure relative to cold exposure, irrespective of circulating thyroid hormone concentrations, adding yet another layer of complexity to thyroid disease management.

 

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A Call for Improved Thyroid Treatment Options

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Did you know that there is a controversy regarding the treatment of thyroid disease? Harvard Health estimates that more than 12 million Americans have thyroid disease, many of whom don’t even realize it. Thyroid patients insist that current treatment standards leave too many patients suffering from a lack of diagnosis or ineffective treatment. Both patient populations are left with a diminished quality of life, yet there are few doctors willing to step outside of the current guidelines. In an effort to change this situation a team of patients created ThyroidChange, a nonprofit organization dedicated to improving the treatment of thyroid disease.

What is Thyroid Dysfunction?

The thyroid is a gland in your body which is located at the base of your neck. Go ahead, touch it! Just above your collar bone and just below your “Adam’s apple.” This gland is shaped like a butterfly with two lobes which stretch around your trachea – hence its nickname the butterfly gland. This gland is key to your body’s metabolism. The hormones it secretes kick-start the energy in every cell of your body like a spark plug in your engine or flint to a match. Without appropriate amounts of thyroid hormones, whether too high or too low, the function of your body is greatly impacted. There are over 300 symptoms of insufficient thyroid hormone and they represent dysfunction in every major organ. Thyroid dysfunction is so common that you or someone you know is probably impacted or will be in the future.

Thyroid hormone is a broad term. The thyroid secretes many hormones, but the two most important for this conversation are thyroxine (T4) and triiodothyronine (T3). The pituitary gland located in your brain senses the level of hormones in that area of your brain, and sends out thyroid stimulating hormone (TSH) which excites your thyroid and causes it to release hormones. T3 is used immediately by various cells and T4 is called the storage hormone because it cannot be used by the cells. It is stored to later be converted to the useable and valuable T3. When a patient does not have sufficient levels of T3 in their blood stream, physicians expect a patient’s TSH level to increase, demonstrating the demand for more hormone by the pituitary gland. If a patient’s thyroid is producing too many hormones, the TSH lab value should decrease to tell it to “decelerate” its production.

An individual whose thyroid gland makes too much thyroid hormone is hyperthyroid. Some patients are rendered hyperthyroid due to an autoimmune disease called Graves’. One can also have cancer of the thyroid gland. Treatments for these can vary, but inevitably it leads to a lifetime of hypothyroidism.

One who has insufficient T3 available to their cells is called hypothyroid. The leading cause of insufficient thyroid hormone is the autoimmune disease, Hashimoto’s Thyroiditis. This disease causes one’s own body attacks their thyroid gland making it inefficient.

What is the Current Treatment standard? Why is it Flawed?

The flawed TSH test is used to diagnose and treat individuals. A physician will run the TSH and if the value is above a particular threshold, the physician will declare a patient hypothyroid. The physician will usually prescribe levothyroxine which is synthetic T4. The dosage will be determined by the TSH lab value. Once it hits a number determined by the physician, the patient will be determined as “euthyroid” or “good as new.”

How many disorders are you aware of that have one lab test and one prescribed treatment? Even though there is research demonstrating that the TSH lab test is flawed and that there are alternative treatments to effectively treat thyroid disease, thyroid patients have difficulty accessing these research-proven methods. We have not even begun to discuss that a majority of hypothyroidism is caused by an autoimmune disease that is seen as insignificant and is not necessarily tested for when a patient is being treated for the resulting hormone imbalance.

What is the Change Being Sought by Thyroid Patients?

One can plainly see that current treatments are solely based on T4 substitution and the ability of an individual’s body to convert the prescribed hormone to the active hormone T3. Patient experience shows that if a patient continues to complain about lingering symptoms, physicians focus on current guidelines which promote the flawed TSH lab value instead of drawing additional labs. This further testing may well demonstrate that a patient is lacking the necessary T3 to function properly, but as so few physicians are willing to perform this, many patients continue to suffer.

In a person with low Free T3, raising T4 doses will not alleviate symptoms. These patients are often prescribed drugs such as antidepressants and cholesterol-lowering drugs to mask the symptoms of insufficient T3. (If you are on one of these medications, have you had your thyroid tested? If you are on thyroid medication, have you had your Free T3 tested?). Adding medications increases side effects and does not restore balance to the patient’s hormones. Simple blood tests can demonstrate to a physician why symptoms persist after the employment of current treatment guidelines. Tests such as Free T4 and Free T3 can indicate how much Free and useable T4 and T3 are in a person’s bloodstream. These tests in combination with antibody testing can help to shed light on a patient’s persistent symptoms.

As per the current guidelines in the treatment of hypothyroidism, based on TSH testing most patients are sufficiently relieved of their symptoms by T4-only treatment. Those who are not in the majority are left to struggle for a doctor willing to listen and run extended lab tests. Complicating this further, many doctors and patients are not only unaware of additional lab work, but also of the many treatment options that one can use to treat thyroid disease.

Levothyroxine or synthetic T4 will restore health in some patients. There are also various T3-containing treatment options such as natural thyroid extract and synthetic T3 which can be used to supplement or substitute T4 treatment. Each patient is unique. We need to make sure that each patient has access to the treatment approach to best restore his or her health. ThyroidChange is about patients advocating for other patients.

Who is ThyroidChange?

ThyroidChange is a nonprofit organization advocating for the use of extended lab testing (Free T4, Free T3, TSH, Reverse T3 and thyroid antibodies) and access to various treatment options to suit the individual patient. We host a petition to appeal for such changes and this has garnered more than 16,000 signatures worldwide, demonstrating that there is indeed a genuine need for change in thyroid treatment. Our community unites patient advocacy groups in an effort to gain better care for thyroid patients and to raise awareness of this widespread problem. ThyroidChange also aims to work with medical oversight agencies in order to create a unified standard of care for thyroid patients to increase patient access to effective, modern treatment.

Please help this effort by visiting www.ThyroidChange.org to sign the petition and unite for better thyroid care, or contact ThyroidChange to discuss how you can support this initiative.

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