Thyroid, Mood, and Health
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).
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
- 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:
- memory, perceptual, language, and executive functioning
- orientation to time, place, and person
- loss of autonomy as with self-care
- emotional dysregulation
- depersonalization (the feeling that one is observing their self from outside of the body or is living in a dream)
- 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 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)
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
How is your energy, mood, and quality of life? Do you need a thyroid check?
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.