Answer to Question 1
Like the SAM and HPA axis, the action for the thyroxine axis begins with the hypothalamus. The paraventricular nucleus of the hypothalamus responds to the demands on our systems to increase metabolism by releasing a polypeptide messenger releasing factor into the portal system of the anterior pituitary. This biochemical messenger prompts the anterior pituitary to release a compound called thyroid stimulating hormone (TSH). TSH then travels through the blood stream to the thyroid gland, a gland shaped like a butterfly that sits just below the larynx (the Adams apple is a good outer reference point for the larynx), prompting the release of thyroxine.
Answer to Question 2
High levels of thyroxine can produce feelings of nervousness or anxiety, insomnia, increased heart rate, increased respiration leading to a sensation of shortness of breath, excessive sweating, diarrhea (due to increased gastric secretions and motility), and feelings of tiredness. The hormone can also amplify the effects of epinephrine, causing persons to experience more intense stress reactions to acute stressors than their normal reactions. Given its longevity and staying power relative to the majority of other stress-related hormones, the effects of thyroxine may explain why some individuals under chronic stress have difficulty returning to baseline levels once they leave a stressful environment. For example, some people have difficulty relaxing even during a one or two week vacation.
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The hypothalamic–pituitary–adrenal axis