{'fraction_non_alphanumeric': 0.031206657420249653, 'fraction_numerical': 0.0062413314840499305, 'mean_word_length': 5.529411764705882, 'pattern_counts': {'":': 0, '<': 0, '<?xml version=': 0, '>': 0, 'https://': 0, 'lorem ipsum': 0, 'www.': 0, 'xml': 0}, 'pii_count': 0, 'substrings_counts': 0, 'word_list_counts': {'cursed_substrings.json': 0, 'profanity_word_list.json': 0, 'sexual_word_list.json': 0, 'zh_pornsignals.json': 0}}
[Thyroid hormones and depressive disorders--critical overview and perspectives. Part 1: Clinical aspects].

This review gives a critical synopsis of the literature on the interaction between thyroid hormones and depressive illness, a phenomenon that has been well-known for over 100 years. Possible perspectives for clinical practice and research are discussed. The most relevant conclusions and hypotheses being as follows: 1. Thyroid hormone disorders (hypo- and hyperthyroidism) may induce almost any psychiatric symptom or syndrome. However, no disease of the thyroid causes symptoms typical of a specific diagnosis. 2. Depressed patients are euthyroid, at least in terms of their laboratory values. Abnormal values are all not specific for any psychiatric diagnosis. They are probably due to intervening variables such as stress or weight loss, or simply to methodological problems. 3. Attempts to treat depressive patients with TRH or T3 have not produced any results of clinical relevance. However, some preliminary reports of a prophylactic effect of high-dose thyroxine in previously resistant "rapid-cycling" patients are most promising. 4. All antidepressant and prophylactic therapies (antidepressant drugs, sleep deprivation, ECT, lithium, and carbamazepine) affect thyroid hormone concentrations. During treatment with antidepressants, carbamezepine, and lithium, these changes are significantly correlated to clinical response.