The Role of Your Thyroid in Psychiatric Illness
For more than a century, science has recognized the connection between the thyroid axis and several commonly experienced psychiatric illnesses. Perhaps, most notably, depression.
As early as the earliest Greek physicians and healers, they were able to describe an association between thyroid and thymus gland presentations and melancholia with very low energy, sleep disturbances, weight fluctuations, lack of interest, and other recurrent signs and symptoms and the presence of these hormonal influences.
In the latter part of the 1800s in England, the established association between clinical thyroid disorders and psychiatric pathology, particularly affective, led to the hypothesis, presumably, that the thyroid plays an important role in the regulation of mood. and in the physiological pathway of its dysfunction. A great deal of research has been done over the past 35 years to identify possible abnormalities of thyroid function in people with a variety of mood disorders.
There are no consistent alterations in T3 or T4 hormone levels with primary depression. However, there may be a significant change in the ratio of T4 to T3 after clinical recovery in depressed patients. This may help us better understand the biological basis of depression. TSH (thyroid-stimulating hormone) levels are very sensitive indicators of varying degrees of thyroid insufficiency, but not very sensitive indicators of mood disturbances.
There are three standardized levels of hypothyroidism (low thyroid function). Grade I or clinical hypothyroidism: has classic symptoms and abnormally low levels of T4, T3, and elevated TSH levels; also a greater response to TRH (thyrotropin releasing hormone).
Whereas in so-called “subclinical” hypothyroidism, or Grade II or III hypothyroidism, it can arise from a variety of causes. The most common cause is autoimmune thyroiditis, characterized by destruction of the thyroid gland and antibodies. Approximately 5% of the general population has subclinical hypothyroidism.
The frequency may increase to 10-15% of women over 60 years of age. Some studies report that this may be a risk factor for coronary artery disease due to alterations in serum lipoproteins. The incidence of mortality and morbidity related to the heart is increasing in women and, in recent years, is parallel to the levels found in men.
The psychiatric sequelae of subclinical hypothyroidism can present with depression and anergy (loss of energy). These patients were substantially more likely to have a diagnosis of co-occurring panic disorder. These patients are also more likely to be resistant to antidepressant therapy. This may require more than first standard in vivo antidepressant treatment, which may include augmentation or combination medical treatment(s) and also supplemental thyroid replacement.
There is also a strong relationship and prevalence of grade I clinical hypothyroidism in female patients with rapid cycling bipolar affective illness. This has led some to treat this specific form of bipolar illness with hypermetabolic doses of T4 replacement therapy.
Recent studies suggest that thyroid hormones have a direct and important effect on mature brain function. Small changes in thyroid hormone levels, within the normal range, can have significant effects on brain thyroid function. This can manifest as disturbances in mood, behavior, and cognition.
There are several hypotheses about the role of thyroid hormones in the etiology of affective illness. An outstanding one is: that depression is a state of relative hyperthyroidism and that the depressive state is associated with relative increases in circulating levels of T4 (thyroxine).
Decreases in circulating T4 are also required for antidepressant response. In other words, the relative increases in T4 in depression are interpreted as a compensatory response by the thyroid to restore and maintain affective homeostasis.
Therefore, thyroid hormones are mobilized during the depressive phase to allow normalization of depressed mood. It is widely believed that decreases in thyroid hormones increase vulnerability to depression, while increases in thyroid hormones promote recovery from depression.
The appearance of anxiety as a symptom of hyperthyroidism is well known. In one study, 29 patients were prospectively followed up and found that 23 of them were diagnosed with generalized anxiety disorder and/or panic disorder.
In 21 of the 23, they found that the anxiety resolved completely with prior antithyroid therapy. This study strongly suggests that anxiety disorders are far from rare in clinical endocrinology practice and that thyroid dysfunction may be directly responsible for the onset of anxious symptomatology.
There are several reports of the occurrence of panic attacks with or without agoraphobia in patients with hyperthyroidism. It would be prudent to rule out thyroid disease in patients with anxiety disorders.
Although mechanistic considerations remain speculative, it is clear that thyroid disease frequently presents with psychiatric symptomatology. Recognition of such features is important, not only for correct diagnosis, but also for early intervention in those presentations in which changes in mood and mindset precede major changes in thyroid function.
Although a specific behavioral profile has not been delineated, the predictability of behavioral change in thyroid disease supports the view that such states may represent the best natural model for investigation of the biology of mood, anxiety, and activity. mental.
