Thyroid Disease and Mental Disorders: Cause and Effect or Only comorbidity?

Robertas Bunevičius; Arthur J. Prange Jr


Curr Opin Psychiatry. 2010;23(4):363-368. 

In This Article


Alterations in thyroid hormone activity impair development of the fetal brain as well as function of the mature brain. During brain development, thyroid hormone deficiency causes mental retardation and cretinism. Endemic dietary iodine deficiency and congenital thyroid malformations are major causes of systemic hypothyroidism. DIO2 polymorphism and timing of thyroid hormone dysfunction are two variables that determine neurological deficits. Specific neuronal hypothyroidism due to MCT8 gene mutation and thus loss of T3 transport into the neuron also causes severe mental retardation and indicates that T3 is critically important.

In the adult brain, compared with the developing brain, thyroid–brain relationships are less apparent but still important. Most adults with thyroid dysfunction will develop mental symptoms. In overt hyperthyroidism, adrenergic hyperactivity is a causal factor for psychiatric symptoms. Thus, beta-adrenergic antagonists are effective against mental symptoms. Although most patients with severe hypothyroidism will also demonstrate some mental symptoms, causality is not so evident as in overt hyperthyroidism.

Data from epidemiological community-based samples, in contrast to clinical samples, provide conflicting results regarding associations between thyroid disorders and mental symptoms. There are several possible explanations. Chief among them is this: when mental symptoms occur in the general population, they may have any of many causes, of which thyroid dysfunction is but one.

Genetic factors may critically determine the differential effects sometimes observed between the outcomes of treatment with T4 alone versus treatment with a combination of T4 and T3.

Thyroid autoimmunity itself, even in the absence of a change in thyroid state, may contribute to mental symptoms in vulnerable patients. Thus, the brain may be more involved in autoimmune processes than previously realized.


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