Research has begun to elucidate a murky pathway between thyroid imbalances and mood disorders. Clear and statistically relevant connections have been made between hypothyroidism and both major depression (and anxiety) and bipolar disorder, specifically cases that cycle rapidly. This connection has been made by the incredibly higher percentage of people with these disorders that suffer from thyroid imbalance (hypothyroidism due to auto-immune thyroid disease, such as Hashimoto’s) than the normal prevalence in the general population. Additional studies strengthened this correlation by concluding that people with bipolar disorder were less likely to get better if they suffered from low thyroid levels.
Dr. Arnold Lieber, a psychiatrist, addresses “the problem of comorbidity” by admitting that hyperthyroidism can resemble mania and hypothyroidism can resemble depression, whether or not there is a causative relationship between them (which has yet to have been discovered and/or understood). In addition, pre-existing depressive symptoms of bipolar disorder or depression and anxiety associated with major or minor depression have been proven to be more susceptible to drug resistance when thyroid levels are low. So, unless an actual blood test is carried out to sample TSH (thyroid stimulating hormone) levels, which will be elevated in response to low systemic levels of thyroid, effective treatment may be hindered. While Dr. Lieber concerns himself with the detrimental effects of the co-existence of thyroid disease with mood disorders, and how they may negatively affect the symptoms of each other, others are considering thyroid as a treatment for mood disorders, even in the preclusion of an existing thyroid auto-immune disease causing hypothyroidism.
One such study confirmed the actual thyroid levels, rather than thyroid auto-immune disease, may be the cause of symptom exacerbation, by reducing thyroid levels in euthyroid patients (whose thyroid normally fell within an acceptable range) and observing resultant increased bipolar symptoms. Successful treatments of major depression, as well as Bipolar disorders I, II, and NOS have been achieved by therapy with thyroid hormone, with one study showing improvement in 84% and full remission in 33%, all of whom were patients previously unresponsive to over a dozen traditional medications. While T4 form is usually prescribed for hypothyroidism, T3, the form to which some metabolizing tissues, including the brain, must convert T4 in order to utilize it, is generally prescribed when being used as a mood disorder treatment.
While it’s pertinent that we investigate the mechanisms through which thyroid hormone is alieving symptoms, such as to resolve some mystery associated with the pathogenesis of mood disorders, since there has been adequate observational study to permit clinical trials, and those have been successful, I see no harm in the normalization of treatment involving 1) conducting blood tests to ensure patient’s thyroid levels fall within the acceptable range if there’s any concerns about difficulty treating the patient with medications and 2) looking towards T3 therapy, leaning towards higher dosage, in the case of multiple drug resistances to treatment. The dangers implied in option 2 are not well known and hopefully long-term studies are conducted soon to survey whether there are indeed cardiac and osteoporosis risks associate with chronic hyperthyroidism, though many patients prescribed with T3 which raises their thyroid levels “above normal” don’t exhibit acute symptoms of hyperthyroidism, such as sweating, weight loss, heart palpations, and frequent bowel movements. Even in cases of little-understood mechanisms of treating mood disorders, I believe it’s very important to pursue the knowledge of their mechanisms of function in order to not only elucidate the nature of the disease, but also to improve outcomes for those suffering from multiple drug resistance, such as in patients with bipolar or schizophrenia diseases (refer to the lipodimics blog post on treating schizophrenia through ketogenesis).