Depression Causes Hypothyroidism [VERIFIED]
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Yes, thyroid disease can affect mood. Common thyroid disease symptoms that affect mood include anxiety or depression. In general, the more severe the thyroid disease, the more severe the mood changes.
To help your doctor figure out if your depression is because of hypothyroidism, they should test you for thyroid disorders. Blood tests can confirm them if they show low levels of a thyroid hormone called thyroxine and a high level of one called thyroid-stimulating hormone (TSH).
Studies show that if you have both hypothyroidism and depression, thyroid-replacement medications may work better than antidepressants. They boost levels of two major thyroid hormones: triiodothyronine (also called T3) and thyroxin (T4). When thyroid pills lower TSH levels, you may start feeling better.
Today, it is well recognized that disturbances in thyroid function may significantly affect mental status including emotion and cognition. Both excess and insufficient thyroid hormones can cause mood abnormalities including depression that is generally reversible with adequate thyroid treatment. On the other hand, depression can be accompanied by subtle thyroid dysfunction. Overt thyroid disease is rare in depression. One to 4% of patients with affective disorders are found to have overt hypothyroidism while subclinical hypothyroidism occurs in 4% to 40% of these patients . Furthermore, thyroid hormones are reported by many authors to be an effective adjunct treatment for depression.
On the other hand, hypothyroid patients frequently demonstrate features of depression, cognitive dysfunction, apathy, and psychomotor slowing. In severe forms of hypothyroidism, clinical symptoms may mimic that of melancholic depression and dementia . However, there is less evidence on the association of subclinical hypothyroidism with cognitive dysfunction and affective disorders particularly depression although recently, a prevalence of 63.5% of depressive symptoms was reported in an Italian population with subclinical hypothyroidism. Nevertheless, therapy with levothyroxine alone was not sufficient to induce a total remission of depressive symptoms in this population . Furthermore, Bauer et al. showed that TSH levels in hypothyroidism correlated with disease severity  and Joffe and Levitt found a disparity in depressive symptoms manifestations and severity among patients with a low-normal TSH versus those with a high-normal TSH. However, in the latter study no difference in treatment outcome was observed between the two groups . In patients treated with T4, psychological symptoms may persist even when they achieve a euthyroid state . Impaired psychological wellbeing in these subjects may be related to the occurrence of genetic polymorphisms in the D2 gene  as well as the OATPC1 encoding gene .
One mechanism explaining the increase in T4 seen in depression is the activation of hypothalamic TRH producing neurons and subsequent increase in thyroid function secondary to the rise in cortisol associated with depression [19, 24, 33]. In addition, it has been shown that elevated serum T4 levels fall after successful treatment of depression. A direct effect of antidepressants on the TRH neuron has been demonstrated resulting in an inhibition of TRH secretion . This suggests that the decrease in T4 levels with initiation of antidepressants could be secondary to a direct effect on TRH neuron and thus to a reduced stimulation of the thyroid axis.
The prolonged release of TRH in depression may be seen as a compensatory response to the decreased 5HT activity in an attempt to normalize 5HT function and maintain normal levels of thyroid hormones . An alternative explanation is that the blunted TSH response may be induced by the hypercortisolism associated with depression or the elevated thyroid hormone levels mediated by adrenergic mechanisms [60, 61].
Fewer studies assessed the efficacy of T4 in the treatment of affective disorders. Joffe and Singer found a significantly higher response to tricyclic antidepressants with T3 (53%) compared to T4 (19%) . However, use of T4 in supraphysiological doses to treatment-resistant unipolar and bipolar depression was effective in approximately 50% of patients as reported by Baumgartner in a review of eight open clinical trials (N = 78) . Surprisingly, T4 in high doses was well tolerated even in patients treated for up to 51 months. However, in healthy subjects, supraphysiological T4 doses were less well tolerated due to higher increments in thyroid hormones after supplementation . A possible explanation would be a greater inactivation of T4 to rT3 in depressed patients compared to healthy subjects .
The inconsistency in the above findings can be accounted for by the variability in the degree of hypothyroidism and the differences in the etiology and duration of the disease in the various studied populations.
The present study suggests that a clinically helpful TSH cut-off value for hypothyroidism should be based on associated symptoms, not just in population studies. Based on the assessment of depression, our study concludes that a TSH cutofff value of 2.5 MIU/L is optimal.
Abnormalities in the hypothalamus-pituitary-thyroid (HPT) axis have been reported in people with depression. In fact, several studies have confirmed the existence of classical feedback between the serotonergic and HPT systems. Thyrotropin-releasing hormone (TRH) is constantly inhibited by serotonin. On the other hand, reduced intracerebral serotonin concentration in depression could lead to increased TRH concentration in brain tissues. This mechanism is probably responsible for the blunted TSH response to TRH stimulation in depression . In animal studies, thyroid hormones influence noradrenergic and serotonergic neurotransmission, which is a target for current antidepressant therapies and plays a key role in the pathogenesis of depression .
Use of thyroid hormone for depression treatment has been controversial for a long time. For most practitioners, the normal reference range for TSH seems to be the most challenging issue in detecting thyroid problems and monitoring the effectiveness of treatment. Nevertheless, there are still unresolved disagreements about the standard upper limit of TSH . Wartofsky showed, a new TSH range was needed.
A TSH level within the laboratory reference range is not necessarily normal for every individual. Some evidences suggest that one single TSH reference range does not fit the entire population . To the best of our knowledge, no TSH cut-off value has been established for depression diagnosis. In hypothyroid patients treated with levothyroxine, psychological symptoms, especially depression, may persist even when they achieve a euthyroid state (). With this background in mind, we propose a new TSH cut-off value as a guideline to evaluate and treat depression symptoms.
Then among patients with severe depression (BDI score > 19), different TSH cut-off points were determined and compared based on severe depression. According to the ROC curve analysis, the optimal TSH cut-off point was 4 mU/L with respect to severe depression (Fig. 2 & Table 3). In addition, PPV, NPV, PLR, and NLR of different TSH cut-off points were determined and compared based on severe depression (Table 4).
The present study showed a significant correlation between the BDI score and TSH and T4 levels. Also, the findings showed that a TSH cut-off point of 2.5 mU/L is the optimal cut-off value for considering depression symptoms and treatment. To the best of our knowledge, this is the first study to focus on TSH cut-off point for depression. Many patients in spite of being euthyroid present with symptoms such as sleep disorders, fatigue, and depression in particular (). These symptoms might be related to deiodinase II  or brain thyroid hormones transporter genes such as organic anion-transporting polypeptide I (OATP-C1) polymorphisms .
The relationship between hypothyroidism and depression has been confirmed in previous literature . In fact, depression is the most common neuropsychiatric symptom in hypothyroidism . It seems that there are analogous mechanisms leading to the similarity of symptoms in hypothyroidism and depression . In addition, depression is associated with changes in the HPT axis . Since 1960, many physicians have used thyroid hormones for the treatment of depression . Zhang et al. revealed reduced serotonin levels in the dorsal raphe nucleus (DRN), resulting from inhibition by an overactive 128 lateral habenula (LHb) in depressed hypothyroid rats. It was concluded that LHb could mediate the effect of thyroid system on serotonin function in DRN .
According to the literature, 63.5% of cases with subclinical hypothyroidism have depression, and levothyroxine treatment does not lead to the full recovery of the symptoms . Although different TSH cut-off points have been introduced for the treatment of hypothyroidism in population-based studies, persistence of hypothyroidism symptoms in many patients, despite of being euthyroid, indicates the need for a symptoms-based TSH cut-off point . Obviously, the best TSH cut-off point should be based on all thyroid clinical functions and symptoms including depression, which is one of the most significant symptoms.
It seems that a TSH cut-off point of 4 mU/L (with 80.5% sensitivity and 95.6% specificity) is optimal for identifying severe depression in comparison with 3.5 and 4.5 mU/L values. In fact, this cut-off point could detect 82.9% of severely depressed cases. Also, regarding to PLR, a TSH level above 4 mU/L was 21 times less likely 153 in severely depressed individuals, compared to cases without depression. Also, the chance to have TSH level below 4 in severely depressed people in comparison to subjects without depression is just 0.2. Although studies with the aim to identify the optimal TSH cut-off point are often population-based, comparison of the findings suggests that a TSH cut-off point with respect to depression is in accordance to them. 2b1af7f3a8