Thyroid, Mood, and Health

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The Thyroid Gland (Butterfly Shaped), Autoimmunity, Mood, and Health

The association of mood, thyroid dysfunction, and autoimmunity is a possible contributing and treatable element in mood disturbances. Integrative Psychiatry encourages looking beyond labels, symptoms, and diagnosis. An integrative approach cautions against premature jumping to treatment with what is favored, familiar, or expedient. Integrative Psychiatry fosters awareness of complexity and the possible presence of underlying and correctable factors.

There are many research studies linking thyroid and autoimmunity to mood disorders as anxiety, depression, bipolar disorder, and postpartum depression.  The human body has several important hormones producing endocrine glands.  The endocrine system is made up of all the individual endocrine glands that regulate bodily tissues. The regulation is accomplished by secretions that go directly into our circulatory system.   The endocrine hormones regulate and coordinate the body’s internal metabolism, energy level, development, reproduction, response to injury, stress, and environmental change.

If there are problems with any of the endocrine glands and their hormone production, a significant effect can occur with human behavior, cognition (thinking and thought processing), and mood. In the study of depression, mood, and the health-related quality of life, the thyroid gland has been found to affect the body’s metabolism, growth, maturation, and nervous system activity. The shape of the thyroid gland is like a butterfly in the anterior region of the neck. The thyroid is one of the largest endocrine glands in the human body.

Abnormal thyroid function, for example, has been shown to be a risk factor for changes in the neuropsychological functioning in aging populations. Neuropsychological testing suggests an association between serum thyroid hormone concentrations and the levels of memory, learning, attention, mood state, and executive, visuospatial and motor functioning. Higher total thyroxine (T4) and free thyroxine (fT4) hormone levels were associated with improved visuospatial function. Increases in age and fT4 were associated with deficits in memory and learning (Dr. Nikolas Hedberg DC DABCI DACBN BCNP) (Srishti Shresthaa, et al., 10/2016).

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Hypothyroidism, Autoimunity, and Hashimoto’s Thyroiditis

The most common thyroid dysfunction is hypothyroidism – an under active thyroid gland that does not produce enough thyroid hormone. The most common cause of hypothyroidism is an autoimmune condition called Hashimoto’s thyroiditis (HT) – an inflammation of the thyroid gland. The normal immune system is the network of cells and tissues found in the body that normally defends against intruding agents like bacteria, viruses, parasites or fungi. Their actions protect the body against disease and infection. The immune system, for unknown reasons, can begin to misidentify and attack healthy cells and tissues of the body as if they were foreign intruders. This above mechanism leads to an “autoimmune disease” with inflammation and destruction of healthy organ and body tissues. Hashimoto thyroiditis (HT) is an autoimmune thyroid disease that causes primary hypothyroidism by destroying thyroid tissue.

Symptoms that can be seen in autoimmune disease are fatigue, general malaise (feeling ill), muscle aches, low fever, and inflammation with redness, heat, pain and swelling. A pattern of flare-ups with worsening symptoms can alternate with periods of remission and improvement.

Autoimmune disease affects up to 50 million Americans, often runs in families, and is more common in women (American Autoimmune Related Diseases Association). As many as eighty types of autoimmune diseases are known. Identifying the type of autoimmune disease may involve lab testing for the specific antibodies against specific organs or tissues of the body, as anti-thyroid antibodies in the case of Hashimoto’s thyroiditis. Treatment often focuses on relieving symptoms as curative therapies continue to elude scientists. Suspected causes include:

  • genetic vulnerabilities
  • virus and bacteria
  • drugs
  • environmental and chemical triggers.

Some interventions done to alleviate the symptoms of an autoimmune disease may include medical interventions as hormone replacement therapy, anti-inflammatory medication, pain medication, immunosuppressive medication, and physical therapy. Integrative therapies may include:

  • plant based medicines and herbs
  • supplements and nutrition
  • acupuncture, somatic therapies, and exercise programs
  • stress reduction, improving rest, and sleep
  • holistic psychotherapies

Hypothyroidism and Subclinical Hypothyroidism Effects on Brain and Mood

Thyroid hormones are important for normal adult brain functioning. Hypothyroidism (the under functioning of the thyroid gland and its hormone production) affects brain function as cognition (thinking and thought processing) and affective states (emotions, moods, feelings, and attitudes).  Hypothyroidism can be associated with psychological and neuropsychiatric symptoms and disorders. Severe hypothyroidism may present as major depression and dementia. Dementia is defined as a decline in mental ability severe enough to interfere with daily life as seen with severe memory loss.

Subclinical hypothyroidism (SHT) is a condition where there is an elevated thyroid stimulating hormone (TSH) despite normal thyroid hormone concentrations. The thyroid-stimulating hormone (TSH) blood tests is used to check for thyroid gland functioning. TSH is produced when the hypothalamus part of the brain releases a substance called thyrotropin-releasing hormone (TRH). TRH then signals the pituitary gland to release TSH when the thyroid gland is possibly under functioning regarding its hormone production. TSH causes the thyroid gland to increase production of its two main hormones: triiodothyronine (T3) and thyroxine (T4). T3 and T4 help control the body’s physical and chemical processes that are necessary for the maintenance of life.

Subclinical hypothyroidism (SHT) occurs in an estimated 4 – 20% of the adult population. The exact causes are an area of ongoing research. However, it is estimated that sixty to eighty percent of subclinical hypothyroidism cases are associated with antithyroid peroxidase antibodies – a marker of chronic lymphocytic (Hashimoto’s) thyroiditis.

In both hypothyroidism and to a lesser degree in subclinical hypothyroidism, depressive symptoms when present can lead to conventional treatment with antidepressant medications.  Symptoms may include:

  • unhappiness, unease, and dissatisfaction (dysphoria)
  • irritability, depression, and anxiety
  • restlessness, agitation, and emotional lability
  • physical weakness and loss of energy
  • lack of feeling, emotion, interest, and concern (apathy)
  • impaired concentration and inattention
  • loss of interest, motivation, or pleasure in doing or experiencing things (anhedonia)
  • isolation from friends or family members
  • suspiciousness, personality changes, and suicidal ideas.

Hypothyroidism and subclinical hypothyroidism – to a lesser degree – can affect other brain, learning, and mental functioning as: memory, perceptual, language, and executive functioning; orientation to time, place and person; loss of autonomy as with self-care, emotional regulation, depersonalization (the feeling that one is observing their self from outside of the body or is living in a dream); and reduction in the speed, effectiveness and efficiency of thought processioning. Improvement can occur with thyroid hormone replacement therapy when there is deficient hormone (hypothyroidism). In subclinical hypothyroidism, there are problems with:

  1. memory, perceptual, language, and executive functioning
  2. orientation to time, place, and person
  3. loss of autonomy as with self-care
  4. emotional dysregulation
  5.  depersonalization (the feeling that one is observing their self from outside of the body or is living in a dream)
  6. reduction in the speed, effectiveness and efficiency of thought processioning

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Improvement can occur with thyroid hormone replacement therapy when there is deficient hormone (hypothyroidism). In subclinical hypothyroidism, there is variable result with thyroid hormone replacement therapy. When thyroid antibodies are present – signifying an inflammatory autoimmune process (Hashimoto’s thyroiditis), the focus of treatment will also need to be towards the reduction or abatement of the autoimmune condition (I-Ching Lin, MD, PhD, Hsin-Hung Chen, MD, et al., 02/2016.) (Dr. Nikolas Hedberg DC DABCI DACBN BCNP) (Pruneti C, et al. 2016)

In a study to evaluate the risk of depression and the effect of l-thyroxine therapy on patients with Hashimoto thyroiditis (HT) in Taiwan – with data from 1220 patients with HT and 4880 patients (89.6% of the patients were women), compared with the non-HT cohort, the HT cohort exhibited a higher prevalence of diabetes mellitus, hyperlipidemia, and coronary artery disease. The HT cohort showed a higher overall incidence of depression compared with the non-HT cohort. The risk of depression decreased after administration of l-thyroxine treatment for more than one year.  HT is felt to be influenced by hereditary factors, as seen in insulin-dependent DM and pernicious anemia.  (Hilal Bektas Uysal, et al., 2016) (I-Ching Lin, et al., 02/2016)

Hashimoto’s thyroiditis (HT), as noted above, is the most common endocrine disorder leading to hypothyroidism. HT has elevated circulating thyroid antibodies in laboratory testing, especially anti-thyroid peroxidase (anti-TPO) and anti-thyroglobulin (anti-Tg). HT is diagnosed by clinical presentation, the presence of thyroid serum antibodies. Anti-TPO is found positive in nearly 95% of the HT patients.

Hypothyroidism, Subclinical Hypothyroidism, Autoimmune Hashimoto’s Thyroiditis, and Health-related Quality of Life

When a large group of euthyroid HT patients (normal thyroid hormone levels) fill out the health-related quality of life questionnaire, higher antibody levels correlated with lower quality of life scores. Apart from hypothyroidism, it appeared that a high antibody level is a significant contributing factor for the development of HT-associated symptoms and a lower health-related quality of life. There are other contributing factors to be considered such as selenium deficiency, thyroid hormone fluctuation, and disease concerns.

All health-related quality of life scores, were significantly higher both in the anti-Tg and anti-TPO negative groups (absence of thyroid antibodies), suggesting a better quality of life than that of the antibody positive groups. Independent of hypothyroidism, a high antibody level contributed to HT associated symptoms and a lower quality of life.  Health-related quality of life (HRQoL) tests and questionnaires are a subjective assessment of how a medical situation affects the daily physical, emotional, social functioning, and well-being of a person.

In studies to date, hypothyroidism, when present, can be the main contributor to health issues, symptom, and a decreased quality of life. Thyroid disorders affect HRQoL –  independently of the thyroid function status (normal or abnormal thyroid hormone levels). Euthyroid patients with normal thyroid hormone levels can show decreased HRQoL scores. Autoimmunity affecting the thyroid gland – as with elevated anti-TPO thyroid antibodies – has been shown in studies to be closely linked with decreased quality of life and depression. (Hilal Bektas Uysal, et al., 08/2016) (Mehmet Muhittin Yalcin, Alev Eroglu Altinova, et al., 2017). Other studies support that HRQoL Health-Related Quality of Life measures, show impairment in patients with HT – independent of levothyroxine replacement therapy.

Depression and anxiety levels of these patients were higher than euthyroid subjects without HT. The indication was that thyroid autoimmunity has an impact on the psychological well-being in HT euthyroid patients (those with normal thyroid function tests).   (Mehmet Muhittin Yalcin, Alev Eroglu Altinova, et al., “Is thyroid autoimmunity itself associated with psychological well-being in euthyroid Hashimoto’s thyroiditis?”, 2017)

Thyroid, Pregnancy, and Postpartum Depression

Thyroid function abnormalities as hypothyroidism, subclinical hypothyroidism (SHT) as Hashimoto’s thyroiditis (HT), are seen in maternal postpartum depression. Postpartum depression affects 10–30% of women within one year after delivery and can present as mild transient depression (maternity blues) to severe postpartum depression and psychosis. Though not proven, there is suspicion that there is an association between TgAb (thyroid antibodies) and TPOAb (thyroid antibodies) positivity and postpartum depression. There may be a predictive value to doing an evaluation for thyroid antibody, and neuropsychological testing during pregnancy. A positive association would potentially identify women at risk for postpartum depression who may need psychological and medical treatment.

Maternal thyroid autoimmunity is seen in Hashimoto thyroiditis (HT) with normal thyroid function along with the detection of thyroid autoantibodies against thyroperoxidase (TPOAb) and thyroglobulin (TgAb). Approximately 10% of pregnant women are TPOAb positive, and about one-third to half will develop postpartum thyroiditis (PPT) within 12 months after delivery. (Maria Le Donneet, et al., 05/2017)

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Thyroid Health and Integrative Psychiatry

Integrative Psychiatry’s mission is to restore balance, integration, health, and wellbeing with an in-depth and comprehensive approach. When mood difficulties become apparent, the checking of thyroid health by a qualified integrative health care practitioner is recommended as the thyroid is an important coordinator and regulator of the body’s functions, including mood. An appropriate clinical exam would be encouraged – including blood tests as measures of thyroid hormones and antibodies, and a careful investigation of possible underlying contributory issues.

Article by Ron Parks, edited by Shan Parks

Questions:

How is your energy, mood, and quality of life?  Do you need a thyroid check?

Comment Below

Thyroid and Mood references:

Dr. Nikolas Hedberg, D.C., D.A.B.C.I., D.A.C.B.N., “Hashimoto’s Disease.” http://drhedberg.com/autoimmune-thyroid/.

———. “What Causes Hashimoto’s Thyroiditis?” http://drhedberg.com/causes-hashimotos-thyroiditis/.

Dr. Nikolas Hedberg DC DABCI DACBN BCNP. The Thyroid Alternative. https://www.amazon.com/Thyroid-Alternative-Nikolas-Robert-Hedberg/dp/0615428231/ref=sr_1_2?s=books&ie=UTF8&qid=1496454381&sr=1-2&keywords=thyroid+hedberg.

Hilal Bektas Uysal, et al. Autoimmunity Affects Health-Related Quality of Life in Patients with Hashimoto’s Thyroiditis.” Kaohsuing Journal of Medicla Science August 2016, Volume 32, Issue 8, Pages 427–433. http://www.kjms-online.com/article/S1607-551X(16)30115-2/fulltext.

I-Ching Lin, MD, PhD, Hsin-Hung Chen, MD, et al.  “Risk of Depression, Chronic Morbidities, and L-Thyroxine Treatment in Hashimoto Thyroiditis in Taiwan A Nationwide Cohort Study.” Medicine (Baltimore). 2016 Feb; 95(6): e2842. Published Online 2016 Feb 12. Doi:  10.1097/MD.0000000000002842.

Maria Le Donne, imageCarmela Mento, Salvatore Settineri,Alessandro Antonelli and Salvatore Benvenga. “Postpartum Mood Disorders and Thyroid Autoimmunity.” Front. Endocrinol., 04 May 2017 | Https://Doi.org/10.3389/fendo.2017.00091. http://journal.frontiersin.org/article/10.3389/fendo.2017.00091/full.

Mehmet Muhittin Yalcin, Alev Eroglu Altinova, et al.  “Is Thyroid Autoimmunity Itself Associated with Psychological  Well-Being in Euthyroid Hashimoto’s Thyroiditis?” Endocrine Journal 2017,  64  (4), 425-429. https://www.jstage.jst.go.jp/article/endocrj/64/4/64_EJ16-0418/_pdf.

Pruneti C, Innocenti A ., Cosentino C., et al.  “Subclinical Hypothyroidism: Behavioral and Psychophysiological Characteristics. A Pilot  Study.” International Journal of Advanced Research (2016), Volume 4, Issue 1, 249 – 255. http://s3.amazonaws.com/academia.edu.documents/42526523/003.pdf?AWSAccessKeyId=AKIAIWOWYYGZ2Y53UL3A&Expires=1494541510&Signature=JHPYu7Pmy4q9mIxclfVaj2R0e6o%3D&response-content-disposition=inline%3B%20filename%3DSubclinical_Hypothyroidism_behavioral_an.pdf.

Srishti Shresthaa, et al. “Thyroid Function and Neuropsychological Status in Older Adults.” Physiology & Behavior, Volume 164, Part A, 1 October 2016, Pages 34–39. https://doi.org/10.1016/j.physbeh.2016.05.037.

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3 thoughts on “Thyroid, Mood, and Health

  1. K. Derby wrote:
    Dear Dr. Parks,
    Reading your article helps to provide an overview and tie everything together for me. In the last three months, I have been doing some research on my overlapping conditions and am seeking the support of a psychiatrist who takes an integrative approach in lieu of medication(s) which appear to cause damage to the thyroid, such as Lithium.

    I wrote the following paper a couple of months ago to document my take on relevant research on the subject of the relationship of treating bipolar condition with Lithium and its effects on the thyroid. I developed a kind of theory, that, if you are not too busy, I hope you can take a look at.

    My theory of Lithium and its Impact on the Thyroid

    The reason Lithium works on mood control — especially mania — is because it manipulates the hormone production controlled by the thyroid. So many of the scholarly articles I am reading state that thyroid damage is a side effect of lithium. I offer that It is not incidental. It is the incident. I’ll go even further to say that the actual therapeutic effect that comes from lithium is specifically because of the toxicity introduced into the system and what the body does to control that. Research shows that there is already a high occurrence of thyroid antibodies in the systems of many people with mood conditions with or without Lithium treatment. Scientists are not sure why autoimmune exists in most of these people, but there is agreement that there is a strong genetic component. Those antibodies may indicate either the cause or effect of irregularities (depression, mania, or rapid fluctuations) in mood. When Lithium is introduced, research has shown that serves to greatly increase the presence of these antibodies. The most common result, according to research on thyroid side effects, is enlargement of the thyroid (goiter) and antibody-induced damage including nodules and significant or sub clinical hypothyroidism – very low and below normal production of the thyroid hormone.

    Normal production of the thyroid hormone regulates hormones that affect all the systems of the body. One of its primary roles is the regulation of metabolism. When the thyroid hormone is low, we have less energy, we tend to gain weight, and are more likely to be on the low end of mood or tending toward depression. Other hormones associated with mood are regulated by the thyroid, such as estrogen, progesterone, and testosterone. Impacts on the thyroid can result in disruptions in fertility or the monthly hormone cycles that are evident to most premenopausal women. Not as much is written about effects on testosterone, but there is a also a much higher occurrence of thyroid conditions in women than men.

    When Lithium is prescribed, as revealed by extensive research on side effects harming organs such as the thyroid and kidneys, it concentrates in these organs through the metabolic process. By increasing the autoimmune antibodies in those who have them (again, many with mood conditions do) and also through direct infiltration of the thyroid without the presence of antibodies, Lithium directly impacts thyroid functioning. With long- or even short-term use, it has a direct relationship to causing thyroid enlargement, or goiter, and leads to less hormone production – or hypothyroidism. In some rare cases it can lead to hyperthyroidism, or over production of the thyroid hormone where the body’s processes speed up and one may experience nervousness, anxiety, rapid heartbeat, hand tremor, excessive sweating, weight loss, and sleep problems, among other symptoms.

    When I was still on my prescribed dose of lithium, I twice experienced symptoms like those expressed above. I had never experienced anything quite like it before, even when going through mania. It was a very physical experience and both times it spun out of control into a mixed-state type of mania with continued sleep loss resulting in psychosis. I couldn’t understand why this occurred when I was on the recommended dose of Lithium which had previously served to keep me stable. Reading more on Lithium’s side effects on the thyroid leads me to a hypothesis related to Lithium induced thyroid damage that can cause not only hypothyroidism, but also hyperthyroidism. Because Lithium and/or autoimmune antibodies cause damage in the form of growths, or nodules, holes or breakage can develop in these nodules and openings in the thyroid can cause excessive release of thyroid hormone, or hyperthyroidism. Consequently, this produces the opposite of the effect that the initial hypolithium had been causing. These holes or openings are not permanent, but the result of damage occurring in the thyroid. After the temporary release, a thyroid impacted by autoimmune antibodies and Lithium can continue on the path to at least temporary hypothyroidism.

    Near hypothyroidism is the state my thyroid is in now. Tests reveal a very high release of TSH (thyroid stimulating hormone) which indicates my pituitary gland is working overtime to get my thyroid to release enough hormone (T3/T4). The blood test reveals that even with all this extra signaling by the pituitary gland my level of thyroid hormone is on the very low end of normal. Blood tests also show that I have a very high level of autoimmune antibodies in my thyroid. In combination with the hypothyroidism indicated by the low thyroid hormone, this is called Hashimoto’s disease. My endocrinologist believes that it is the result of the autoimmune disorder and not the presence of Lithium that is the main culprit in the thyroid damage. Based on the research I have done, I don’t think you can divorce the two. Most of the research I have done indicates not only that Lithium causes goiter (enlarged thyroid) resulting in hypothyroidism, but also that if autoimmune antibodies already exist in the thyroid that Lithium will serve to increase them. That is, the antibodies increase largely in the presence of Lithium, probably because it is a toxic invader.

    As a result of learning more about the connections between mood and the central importance of the thyroid to it, I am not so willing to swear allegiance to a toxic metal over alternatives that may be more healthy to my body. I recognize I have a mood condition that is and has been life threatening. It is complicated and cannot be concentrated in the brain, separated either from the outside circumstances of my life or the other important organs of my body. The nervous system is not contained within our skulls and neither are our moods. They are emotional, mental, physical, spiritual, and social. But the physical part is something we have recently tried to control with sometimes limited success. The research is abundant on organs in the body being directly impacted by Lithium, yet they treat one of the central organs that is being damaged — the thyroid — as a side effect. Isn’t it evident this is where mood control is being exerted? This appears to be where Lithium gets its efficacy. It is exerting its influence through toxic infiltration and slowing metabolic responses, including those of mood triggering hormones, such as estrogen, progesterone, testosterone, and adrenaline. Balance, including this type of extended or slow release, can be achieved with the help of our bodies’ systems or, apparently, through resistance.

    More research should be done on the immune system and its involvement in the regulation or attempt to regulate the metabolic systems. It appears, however, that for many people there is a large amount of autoimmune activity centered in the thyroid. Your average person doesn’t think of the thyroid as a hugely important organ. It is a small, butterfly shaped gland that is easily dismissed.. I might add that a large part of this dismissal may be because more women than men appear to be impacted by thyroid conditions. But it regulates just about all of our bodily functions. Is it mysterious, then, what causes the concentration of autoimmune responses in this area? It appears to register and, as a filtering gland, it is the target of foreign and possibly toxic substances in the body. For example, research shows that both the introduction of Lithium and cigarette smoke increase autoimmune responses in the thyroid.

    The question is, are there healthful alternatives – or at least supplements – for Bipolar condition that can work with your thyroid to help it do its job more efficiently? Western medicine is largely using chemicals and minerals that may appear to achieve the desired effect of balance, but at what cost? The recommendations received from doctors appear to dismiss the worth of the thyroid in favor of Lithium stability. The wording is that, when confronted with hypothyroidism and thyroid damage, the continued use of Lithium is “not contraindicated.” This means, go ahead and use Lithium at the same dosage prescribed at the cost of your thyroid. These directives appear to send the message that since we have access to the synthetic thyroid hormone the actual organ is dispensable. Doctors are not as quick to say the same about the kidneys, which are also at risk to be negatively impacted by Lithium.

    Other research has highlighted Omega 3 fatty acids as a possible replacement to or supplement of Lithium in many cases. Though Omega 3 (EPA, DHA, ALA) appears to have more antidepressant than anti-manic properties, research has shown it to be helpful in all realms of health in many organs of the body. It has also shown positive impacts on the immune system and in filtering out toxins from the body.

    More healthful alternatives need to be pursued in the area of mood stabilizing medications. If we begin to recognize the importance of the thyroid and the kidneys in the metabolic process, we will gain more insight into how to work with, rather than against these indispensable organs.

    By K. Derby
    References provided upon request.

  2. Reply from Ron Parks, MD
    Of interest is research done using a high dose of thyroid (HDT) hormone to treat and stabilize bipolar conditions as done years ago by Wybral?? at Univ. Penn. – here is a recent research article related – you might find others:

    Medical Hypotheses, Volume 97, December 2016, Pages 16-21
    A hypothesis on the mechanism of action of high-dose thyroid in refractory mood disorders, Tammas Kelly (MD), George Washington University, GWU MFA Department of Psychiatry and Behavioral Sciences, 2120 L St NW, Suite 600, Washington DC 20037, United States; The Depression & Bipolar Clinic of Colorado, 400 East Horsetooth Road, Suite 300, Fort Collins, Colorado 80525, United States; https://doi.org/10.1016/j.mehy.2016.09.022

    “Abstract: Multiple lines of evidence suggest the hypothesis that high dose thyroid therapy corrects for cellular hypothyroidism found in bipolar disorders. Evidence indicates that bipolar disorders are associated with mitochondrial dysfunction which results in low cellular adenosine 5′-triphosphate (ATP) levels. Transport of thyroid hormones into cells is energy intensive and dependent on ATP except in the pituitary gland. Inadequate ATP levels makes it difficult to get thyroid hormone into cells leading to cellular hypothyroidism.”

  3. Follow-up note from Dr. Parks:
    Many years ago, I heard a lecture by a respected physician, researcher, and scholar of the time, Dr. Whybrow. His research in bipolar disorder stabilization with high dose thyroid hormones treatment made logical sense to me at that time. As a recent comment came in on the difficulties and adverse side effects of conventional bipolar treatment, I looked for the literature on Whybrow’s work and some more recent studies on the use of high-dose thyroid to stabilize the moods fluctuations seen in bipolar disorder. References, I found on a recent search, are listed here in the event that one of the readers of this blog post, might want to research this further or to discuss with your treating physician for possible consideration.
    References:
    Andreas Baumgartner M.D., Michael Bauer M.D., Ph.D., and Rainer Hellweg M.D., 1994. “Treatment of Intractable Non-Rapid Cycling Bipolar Affective Disorder with High-Dose Thyroxine: An Open Clinical Trial.” Neuropsychopharmacology (1994) 10, 183–189. doi:10.1038/npp.1994.20. https://www.nature.com/npp/journal/v10/n3/abs/npp199420a.html.
    Harvey C. Stancer, Ph.D., MD, FRCP(C); Emmanuel Persad, MB, BS, FRCP(C). 1982. “Treatment of Intractable Rapid-Cycling Manic-Depressive Disorder with Levothyroxine.” Arch Gen Psychiatry. 1982;39(3):311-312. doi:10.1001/archpsyc.1982.04290030045008. http://jamanetwork.com/journals/jamapsychiatry/article-abstract/492747.
    Mark S. Bauer, MD; Peter C. Whybrow, MD. 1990. “Rapid Cycling Bipolar Affective Disorder. Treatment of Refractory Rapid Cycling with High-Dose Levothyroxine: A Preliminary Study.” Arch Gen Psychiatry. 1990;47(5):435-440. doi:10.1001/archpsyc.1990.01810170035006. http://jamanetwork.com/journals/jamapsychiatry/article-abstract/495022.
    Michael Bauer MD, Ph.D., Anne Berghöfer MD, et al., 2002. “Supraphysiological Doses of L-Thyroxine in the Maintenance Treatment of Prophylaxis-Resistant Affective Disorders.” Neuropsychopharmacology (2002) 27, 620–628. doi:10.1016/S0893-133X(02)00320-2. https://www.nature.com/npp/journal/v27/n4/abs/1395910a.html.
    Tammas Kelly, Daniel Z. Lieberman, 2009. “The Use of Triiodothyronine as an Augmentation Agent in Treatment-Resistant Bipolar II and Bipolar Disorder NOS.” Journal of Affective Disorders Volume 116, Issue 3, August 2009, Pages 222-226. http://www.sciencedirect.com/science/article/pii/S0165032708004850.
    Tammas Kelly (MD). 2016. “A Hypothesis on the Mechanism of Action of High-Dose Thyroid in Refractory Mood Disorders.” Medical Hypotheses Volume 97 (December): Pages 16-21.
    Whybrow PC. 1994. “The Therapeutic Use of Triiodothyronine and High Dose Thyroxine in Psychiatric Disorder.” Acta Medica Austriaca [01 Jan 1994, 21(2):47-52]. http://europepmc.org/abstract/med/7998482.