For more than a century, science has recognized the connection between the thyroid axis and several commonly experienced psychiatric diseases. Perhaps, most notably, depression.
As far back as the early 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 1800’s in England, the established association between clinical thyroid disorders and psychiatric, particularly affective pathology led to the hypothesis – presumptively, that thyroid plays a major role in the regulation of mood and in the path physiology of its dysfunction. The last 35 years have seen a great deal of research done in order to identify potential abnormalities of thyroid function in people with an array of mood disorders.
There are no consistent alterations of T3 levels or T4 hormone levels with primary depression. There may be however significant change in the ratio of T4 to T3 after clinical recovery in depressed patients. This can better help us to understand the biological basis of depression. TSH (thyroid stimulating hormone levels are very sensitive indicators of various degrees of thyroid failure but not very sensitive indicators of mood disturbances.
There are three standardized levels of hypothyroidism (low thyroid function). Grade I or clinical hypothyroidism – this has classic symptoms and abnormally decreased levels of T4, T3 and elevated TSH levels; also an increased response to TRH (thyrotropin releasing hormone).
Whereas in so-called “sub clinical” hypothyroidism – or Grades II or III hypothyroidism, may arise from a variety of causes. The most common cause is autoimmune thyroiditis – characterized by destruction of the thyroid gland and the antibodies. Approximately 5% of the general population has sub clinical hypothyroidism.
The frequency may increase to 10-15% of women over age 60. Some studies report that this may be a risk factor for coronary artery disease due to alterations in serum lipoproteins. The incidence of cardiac related mortality and morbidity is both on the rise in women and in these later years, parallels the levels found in men.
The psychiatric sequelae of sub clinical hypothyroidism may present with depression and anergia (loss of energy). These patients were substantially more likely to have a concurrent panic disorder diagnosis. These patients are also more likely to be resistant to antidepressant therapy. This may require more than standard, first live antidepressant treatment- which may include combination or augmentation medical treatment(s) and supplemental thyroid replacement as well.
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 hyper metabolic doses of T4 replacement therapy.
Recent studies suggest that thyroid hormones have direct and important effect on mature brain function. Small changes in thyroid hormone levels, within the normal range, may have significant effects on cerebral thyroid function. This may manifest as alterations in mood, behavior and cognition.
There are several hypotheses about the role of thyroid hormones in the etiology of affective illness. One prominently held one is: that depression is a state of relative hyperthyroidism and that the depressed state is associated with relative increases in circulating levels of T4 (Thyroxine).
Also decrements in circulating T4 are required for antidepressant response. n other words, the relative increases in T4 in depression are interpreted as being compensatory response on the part of the thyroid in order to reestablish and maintain affective homeostasis.
Thyroid hormones are therefore mobilized during the depressed phase so as to allow for normalization of the depressed mood. The widely held belief is that decreases in thyroid hormones increase vulnerability to depression whereas increases in thyroid hormone promote recovery from depression.
The occurrence of anxiety as a symptom of hyperthyroidism is well recognized. In one study, 29 patients were prospectively followed 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 antithyroid therapy above. This study strongly suggests that anxiety disorders are far from rare in clinical endocrinology practice and that the thyroid dysfunction may be directly responsible for the occurrence of the anxious symptomatology.
There are several reports of the occurrence of panic attacks with or without agarophobia in patients with hyperthyroidism. It would be prudent to rule out thyroid disease in patients presenting with anxiety disorders.
Although considerations of mechanism must remain speculative, it’s clear that thyroid diseases frequently present 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 mentation antedate gross changes in thyroid function.
Although no specific behavioral profile has been delineated, the predictability of behavioral change in thyroid disease supports the view that such states may represent the best naturally occurring model for investigation of the biology of mood, anxiety and mentation.