Depression affects nearly 19 million American adults. For anyone who has experienced depression, it’s not a fun place to be. The feeling of sadness and despair can hang over you even though you can’t pinpoint any specific reason for feeling so down. Although many of life circumstances can contribute to depression, it can sometimes be the result of a thyroid hormone imbalance.
Clinical depression is a mood disorder in which feelings of sadness, loss, anger, or frustration interfere with everyday life for a longer period of time. When someone develops depression, the brain usually becomes the focus of attention. But other organs can be the source of the problem. A common example is when the thyroid gland produces too little hormone — a condition known as hypothyroidism. In patients with depression, anxiety and other psychiatric problems, doctors often find abnormal blood levels of thyroid hormone. Treating the problem, they have found, can lead to improvements in mood, memory and cognition.
It is likely that some people are taking antidepressants when they should really be treating their thyroid. Nearly 10 million Americans suffer from hypothyroidism. The condition is much more common in women than in men, and becomes more prevalent with age. As many as one in five women will develop hypothyroidism by age 60.
How To Relieve Depression Symptoms?
About half of thyroid sufferers remain undiagnosed due to improper testing and because initial signs and symptoms are vague, ambiguous, and often seen in various disorders. The underlying factor contributing to infertility, hair loss, irregular menses, constipation, fatigue, weight gain, elevated cholesterol, anemia, or depression may be a malfunctioning thyroid.
Many depressed and bipolar patients have undiagnosed thyroid dysfunction as the underlying cause or major contributor to their depression that is not detected by standard thyroid tests.
The dysfunction present with these conditions includes reduced T4 to T3 conversion and reduced uptake of T4 into the cell, which blocks thyroid effect and is an indicator of reduced transport of T4 into the cell and across the blood brain barrier.
In the International Journal of Neruopsychopharmacology, Posternak M et al. published a double blind placebo control trial of 50 patients with normal thyroid function as defined by a normal TSH (1.5 +/- 0.8). The study found almost a 2-fold increase in response rate with T3 and a 4.5 times greater likelihood of experiencing a positive response at any point over a six-week period with the addition of T3.
Kelly T et al. investigated the effectiveness of T3 for the treatment of bipolar disorder in patients who had failed to adequately respond to an average of 14 medications used to treat their bipolar disorder. The medication was found to be well tolerated and 84% experienced significant improvement and 33% had a full remission.
With over 4000 patients, The Star*D Report is the largest trial comparing antidepressant effectiveness for depression. It found that 66% of patients fail to respond to antidepressants or have side-effects severe enough to discontinue use. Of those who do respond, over half will relapse within one year. The trial found that T3 was effective even when other medications — such as citalopram (Celexa), bupropion (Wellbutrin), sertraline (Zolft), venlafaxine (Effexor), or cognitive therapy – were not. It was shown to be 50% more effective, even with the less than optimal dose of 50 mcg, under direct comparison with significantly less side effects than commonly used therapeutic approaches with standard antidepressants.
With an understanding of thyroid physiology and associated dysfunction that is present in depressed patients, it is clear that timed-released T3 supplementation should be considered in all depressed and bipolar patients despite “normal” serum thyroid levels. Additionally, straight T4 should be considered inappropriate and suboptimal therapy for replacement in such patients.