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Pregnancy affects the thyroid gland and its function in many ways because of the influences of hormones. Diagnosis and treatment of thyroid dysfunction during pregnancy, and in the postpartum period, is complicated. However, knowledge about the interaction between pregnancy and the thyroid gland has vastly improved overtime. Because of this interaction, laboratory tests of thyroid function must be interpreted very carefully. Thyroid function tests change as gestation continues, mostly from the influence of human chorionic gonadotropin and estrogen, which is the primary female hormone. The thyroid is functioning normally if all hormones are normal throughout pregnancy. For the first part of pregnancy the fetus is totally dependent on the mother for the production of thyroid hormone. The World Health Organization recommends iodine intake of 200 μg/day while pregnant, in order to maintain adequate thyroid hormone function. The most common forms of thyroid dysfunction in pregnancy include thyrotoxicosis, Graves’ disease, subclinical hypothyroidism, Hashimoto’s thyroiditis, silent lymphocytic thyroiditis, and thyroid cancer.

About 18% of adults in the United States have anxiety disorders, which include posttraumatic stress disorder, obsessive-compulsive disorder, and various phobias. About 7% of adults had at least one major depressive episode in the past year. Bipolar disorder affects about 2.5% of adults, and just over 1% of adults have schizophrenia. Serious mental-illness costs Americans more than $193 million in lost earnings annually. Thyroid dysfunction may be related to a variety of mental disorders. Depression is an example of a mental disorder that actually may be one of the first symptoms of thyroid dysfunction. Patients may be mislabeled as having a major mental disorder even though hypothyroidism or hyperthyroidism is causing their symptoms. When thyroid function is not normal, a variety of mental symptoms and conditions may develop. These include anxiety, bipolar disorder, depression, irritability, aggression, obsessive-compulsive disorder, panic attacks, phobia, and even schizophrenia. As many as 15% of patients treated for depression have elements of mild or overt hypothyroidism. Conditions commonly linked to mental disorders include cretinism, myxedema, and Graves’ disease with stress.

Obesity goes hand in hand with insulin resistance, which is a fundamental aspect of type 2 diabetes and is linked to hypertension, hyperlipidemia, atherosclerosis, polycystic ovarian disease, and metabolic syndrome. The human body maintains blood glucose within an extremely narrow range, utilizing the hormones insulin and glucagon, both of which are secreted by the pancreas. The production of these endocrine hormones ultimately determines if a person has disorders such as diabetes or hypoglycemia. Both hormones are secreted in response to blood glucose levels, but in opposing ways. Many mechanisms by which obesity causes systemic insulin resistance are still unknown. However, clinicians now understand the adipo-insulin axis that involves the adipocyte hormone called leptin. Its actions include the regulation of food intake and energy expenditure. Leptin also controls the insulin–glucose axis, peripheral glucose, and insulin responsiveness. This chapter focuses on the disorders of insulin regulation known as type 2 diabetes and metabolic syndrome.

The global impact of thyroid disorders, including hypothyroidism, hyperthyroidism, Graves’ disease, and thyroid cancer, is increasing by about 3.3% each year. The key determinant of thyroid disease risks is iodine nutrition. However, other factors that influence the epidemiology of thyroid disorders include aging, smoking, genetics, ethnicities, endocrine disruptors, and the use of various treatments. Hypothyroidism and hyperthyroidism, in all their forms, affect every population throughout the world. However, the prevalence and incidence of thyroid dysfunction is always changing because of differences in diagnostic thresholds, sensitivity of various tests, the populations being selected for study, and changes in the availability of dietary iodine. The burden of thyroid disorders reaches up to billions of dollars, globally, every year.

There is an increased demand for thyroid hormones during pregnancy. This is due to an increase in thyroxine-binding globulin, placental type 3 deiodinase, and placental transfer of maternal thyroxine to the fetus. Thyroxine is essential for fetal neurodevelopment. Therefore it is critical that maternal delivery of thyroxine to the fetus is ensured early in gestation. Cretinism occurs from severe iodine deficiency because the mother’s body is unable to manufacture thyroxine for transport to the fetus, especially in the first trimester. Persistently low levels of thyroxine at 12 weeks of gestation are associated with an 8–10-point deficit in mental and motor function scores in infants, compared to children of mothers with normal thyroid function. Other thyroid conditions in fetuses and newborns include congenital goiter, thyroid agenesis or dysplasia, transient hypothyroidism, and consumptive hypothyroidism.

The thyroid gland is the largest purely endocrine gland in the body. It is located in the anterior neck and has a butterfly-like shape. It curves across the anterior surface of the trachea and is slightly inferior to the larynx. This gland regulates basal body metabolism via the various hormones that it releases. The thyroid is also involved in gluconeogenesis, protein synthesis, glycogenolysis, lipogenesis, and thermogenesis. The parathyroid glands are embedded in the posterior surface of the lateral lobes of the thyroid gland and aid in calcium homeostasis.