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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. Maybe, especially, depression.

As far back as the early Greek doctors and healers, they were able to describe an association between thyroid and thymus gland presentations and melancholia with very low energy, sleep disorders, weight fluctuations, lack of interest and other recurring 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, especially affective pathology led to the hypothesis – presumably, that the thyroid gland plays a major role in the regulation of mood and in the path physiology of his dysfunction. The last 35 years have seen a lot of research done to identify potential abnormalities of thyroid function in people with a variety of mood disorders.

There are no consistent changes of T3 levels or T4 hormone levels with primary depression. However, there may be 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 various degrees of thyroid failure, but not very sensitive indicators of mood disorders.

There are three standardized levels of hypothyroidism (low thyroid function). Grade I or clinical hypothyroidism – this has classic symptoms and abnormally reduced levels of T4, T3 and increased TSH levels; also an increased response to TRH (thyrotropin-releasing hormone).

While in so-called “subclinical” hypothyroidism – or grade II or III hypothyroidism, can 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 subclinical 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 changes in serum lipoproteins. The incidence of heart-related mortality and morbidity is both on the rise in women and in these later years, similar to the levels found in men.

The psychiatric consequences of subclinical hypothyroidism can present with depression and anergia (loss of energy). These patients were substantially more likely to have a concurrent diagnosis of panic disorder. 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) as well as additional thyroid replacement.

There is also a strong relationship and prevalence of class I clinical hypothyroidism in female patients with rapid 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 significant influence on adult brain function. Small changes in thyroid hormone levels, within the normal range, can have significant effects on cerebral thyroid function. This can manifest as changes 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 depressive state is associated with relative increase in circulating levels of T4 (Thyroxine).

Also decrements in circulating T4 are necessary for antidepressant response. in other words, the relative increase of T4 in depression are interpreted as compensatory response of the thyroid gland to restore and maintain affective homeostasis.

Thyroid hormones are therefore mobilized during the depressive phase to normalize the depressed mood. The widely held belief is that decreases in thyroid hormones increase vulnerability to depression, while increases in thyroid hormones promote recovery from depression.

The occurrence of anxiety as a symptom of hyperthyroidism is well recognized. In one study, 29 patients were followed prospectively 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 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 is clear that thyroid diseases often present with psychiatric symptomatology. Recognition of such characteristics 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 mapped, the predictability of behavioral change in thyroid disease supports the view that such states may represent the best naturally occurring model for research into the biology of mood, anxiety, and mentation.

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