Unipolar depression and bipolar disorder might be characterized by a “low-thyroid function syndrome”. This thesis is sustained by the evidence that subclinical hypothyroidism appears to be the commonest abnormality found among patients with bipolar disorder and with unipolar depression.
Overt thyroid disease instead is rare among depressed patients.
However, hypothyroidism is well known to be related with anxiety or refractory depression.
AETHIOLOGY
Most patients with depression may have alterations in their thyroid function including slight elevation of the serum FT4, blunted TSH response to thyrothropin-releasing hormone (TRH) stimulation and loss of the nocturnal TSH rise and this may reflect brain hypothyroidism in the context of systemic euthyroidism.
Moreover, studies that compare depressed patients with control show that Thyroid Binding Inhibitory Immunoglobulin (TBII) levels and microsomal antibodies levels are higher in depressed patient in comparison to controls. The finding that depression often co-exists with autoimmune subclinical thyroiditis suggests that probably this condition takes part in the aethiopathogenesis of depression.
Thyroid function in clinical subtypes of major depression: an exploratory study 2004
There are several evidence about the impact of thyroid functions on the adult, mature brain, in regards to:
- NEUROTRANSMITTER SYSTEMS
Thyroid hormone receptors are widely distributed in the brain; many of the limbic system structures where these receptors are present have been implicated in the pathogenesis of mood disorders. The neurotransmitter systems originate in the brainstem and extend through the midbrain into the limbic regions and the cortex. They regulate mood by modulating the activity of these brain areas. Immunoistochemical mapping studies have shown that T3 is concentrated in the nuclei and projection sites of central noradrenergic systems, while the thyroid gland exhibits GABA transport mechanism, as well as enzyme activities for GABA synthesis and degradation. This suggest that thyroid hormones could act as neurotransmitters and neuromodulators by themselves; alternatively, their mood-regulatory properties could be mediated by interactions with the principal neurotransimitter systems.
Hypothyroidism is, thus, believed to cause depression by producing a functional decrease in:
- Noradrenergic Transmission, because of the loss of T3's property in increasing post-synaptic beta-adrenergic activity
- 5-HT Transmission, beacause of the reducing of T3's activity in reduction of the sensitivity of 5-HT 1A autoreceptors in the raphe nuclei and in increase in 5-HT 2 receptor density and sensivity in the cortex.
- BRAIN'S METABOLIC ACTIVITY
An important aspect of aethiopathogenesis is that blunted thyroid function is related with a brain's reduced metabolic activity. In a PET study of hypothyroid patients undergoing thyroid hormone replacement, reduction of the behavioural complaints during therapy was associated with a restoration of metabolic activity in brain areas that were integral to the regulation of affect and cognition.
Thyroid Functions and Bipolar Affective Disorder 2011
CONCLUSIONS
Overt thyroid dysfunction is not common in depressive patients, while, most importantly, suboptimal thyroid function is the commonest abnormality found among patients with bipolar disorder and with unipolar depression.
Depressed patients often have higher Thyroid Binding Inhibitory Immunogloblulins (TBII), wich is suggestive of the presence of an underlying autoimmune process in depression.
Thyroid function in clinical subtypes of major depression: an exploratory study 2004
