한국 안산의 비즈니스 이벤트 및 컨퍼런스
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For over a century, science has recognized the connection between the thyroid axis and several commonly experienced psychiatric illnesses. Perhaps, most notably, depression.
Already in the first Greek doctors and healers, they were able to describe an association between presentations of the thyroid and thymus glands and melancholy with very little energy, sleep disturbances, weight fluctuations, lack of interest and other recurring signs and symptoms and the presence of these hormonal influences.
In the late 1800s in England, the established association between clinical thyroid disorders and psychiatric pathology, particularly affective, led to the hypothesis, presumably, that the thyroid plays an important role in mood regulation. and in the physiological pathway of its dysfunction. A great deal of research has been done in the last 35 years to identify possible thyroid function abnormalities in people with a variety of mood disorders.
There are no consistent alterations in T3 or T4 hormone levels with primary depression. However, there may be a significant change in the ratio of T4 to T3 after clinical recovery in depressed patients. This may help us better understand the biological basis of depression. TSH (thyroid-stimulating hormone) levels are very sensitive indicators of various degrees of thyroid failure, but not very sensitive indicators of mood disturbances.
There are three standardized levels of hypothyroidism (low thyroid function). Grade I or clinical hypothyroidism: has classic symptoms and abnormally low T4, T3, and elevated TSH levels; also a greater response to TRH (thyrotropin-releasing hormone).
While in so-called “subclinical” hypothyroidism, or Grade II or III hypothyroidism, it can arise from a variety of causes. The most common cause is autoimmune thyroiditis, characterized by destruction of the thyroid gland and antibodies. Approximately 5% of the general population has subclinical hypothyroidism.
The frequency can increase to 10-15% of women older than 60 years. Some studies report that this may be a risk factor for coronary artery disease due to alterations in serum lipoproteins. The incidence of heart-related mortality and morbidity is increasing in women and, in recent years, has paralleled the levels found in men.
Psychiatric sequelae of subclinical hypothyroidism may present with depression and anergy (loss of energy). These patients were substantially more likely to have a co-occurring panic disorder diagnosis. These patients are also more likely to be resistant to antidepressant therapy. This may require more than a standard first live antidepressant treatment, which may include combination or augmentation medical treatment(s) and also adjunctive thyroid replacement.
There is also a strong relationship and prevalence of grade I clinical hypothyroidism in female patients with rapid-cycling bipolar affective disease. This has led some to treat this specific form of bipolar disease with hypermetabolic doses of T4 replacement therapy.
Recent studies suggest that thyroid hormones have a direct and important effect on mature brain function. Small changes in thyroid hormone levels, within the normal range, can have significant effects on brain thyroid function. This can manifest as disturbances in mood, behavior, and cognition.
There are several hypotheses about the role of thyroid hormones in the etiology of affective illness. A prominent one is: that depression is a state of relative hyperthyroidism and that the depressive state is associated with relative increases in circulating T4 (thyroxine) levels.
Decreases in circulating T4 are also required for antidepressant response. In other words, the relative increases in T4 in depression are interpreted as a compensatory response by the thyroid to restore and maintain affective homeostasis.
Thus, thyroid hormones are mobilized during the depressive phase to allow normalization of depressed mood. It is widely believed that decreases in thyroid hormones increase vulnerability to depression, while increases in thyroid hormones promote recovery from depression.
The appearance of anxiety as a symptom of hyperthyroidism is well recognized. In one study, 29 patients were prospectively followed up and found that 23 of them were diagnosed with generalized anxiety disorder and/or panic disorder.
In 21 of the 23, they found that anxiety completely resolved with prior antithyroid therapy. This study strongly suggests that anxiety disorders are far from rare in clinical endocrinology practice and that thyroid dysfunction may be directly responsible for the appearance of anxious symptoms.
There are several reports of the occurrence of panic attacks with or without agarophobia in patients with hyperthyroidism. It would be prudent to rule out thyroid disease in patients with anxiety disorders.
Although considerations of the mechanism must remain speculative, it is clear that thyroid diseases frequently present with psychiatric symptoms. Recognition of such features is important, not only for correct diagnosis, but also for early intervention in those presentations in which changes in mood and mentality precede major changes in thyroid function.
Although no specific behavior profile has been delineated, the predictability of behavior change in thyroid disease supports the view that such states may represent the best natural model for investigation of the biology of mood, anxiety, and activity. mental.
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