Hormones Mood and Cognition

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Most hormones play a significant role in affect and cognition. An example is cortisol, which is secreted by the adrenal cortex under the influence of the anterior pituitary peptide adrenocorticotropin hormone (ACTH). Cortisol hypersecretion, such as in Cushing's disease, produces psychological changes ranging from hyperphagia, insomnia, and euphoria to anxiety, panic, and mania. On the other hand, a significant number of individuals diagnosed with major depression present signs of adrenal hypertrophy and increased circulating levels of cortisol. The mechanisms hypothesized to mediate increased cortisol levels in clinically depressed patients have implicated increased activity at the level of the hypothalamus, and dysregulation of brain serotonergic and noradrenergic systems. A reduction of circulating cortisol levels, observed in patients with Addison's disease (adrenal atrophy and insufficiency), is itself correlated with irritability, apprehension, mild anxiety, and inability to concentrate. Thus, low or high circulating cortisol levels produce psychiatric symptoms.

The mechanisms whereby low cortisol levels affect mood and other cognitive functions are poorly understood. Normalization of cortisol levels usually improves the psychological profiles of these patients, and a variety of anti-depressant treatments also lead to cortisol normalization in depressed patients. Learning is also influenced by circulating cortisol levels and evidence of poor memory with either too much or too little cortisol has been documented.

Similar observations are reported with thyroid hormones (T3 and T4), which are crucial for normal brain development and function. Hypothyroidism during fetal life (a condition known as cretinism) produces short stature, sexual immaturity, and severe mental defects in afflicted individuals. In adulthood, hypothyroidism is often associated with depression, bipolar disorder, low energy, appetite and sleep changes, poor concentration, memory impairments, and apathy. The similarity of these symptoms with clinical depression routinely prompts clinicians to test thyroid functions to distinguish between the two conditions. The reverse interaction between affective illnesses, particularly major depression, and thyroid hypofunction has also been documented recently. As with cortisol, hyperthyroidism (as in Grave's disease) presents with several psychiatric symptoms including insomnia, irritability, agitation, major depression, Attention-Deficit/Hyperactivity Disorder, paranoia, and most often, Generalized Anxiety Disorder. Exactly how thyroid hormone dysregulation produces affective disorders, particularly major depression and rapid-cycling bipolar disorder, is mostly unknown. Lower thyroid hormone levels have been suggested to reduce p-adrenergic receptor activity and central serotonin activity, states often associated with a variety of affective disorders.

Growth hormone (GH—also known as somatotropin) dysregulation similarly has a variety of interactions with affect and cognition. Perhaps the most famous phenomenon associated with GH hyposecretion in children is psychosocial dwarfism, a state of short stature sustained by parental abuse. GH deficiency in adults is associated with higher incidence of affective disorders, lack of energy, and impaired self-control. GH hypersecretion can also result in affective disorders, increased appetite, and loss of drive and libido, without observable changes in intelligence or memory functions. Treatments that normalize GH levels ameliorate the psychologic symptoms produced by GH dysreg-ulation. A similar picture emerges with sex hormones, which are believed to be responsible for disturbances in memory retrieval, anger, moodiness, and anxiety associated with premenstrual syndrome (PMS) in 30% of cycling women, and perhaps some cases of major depression associated with childbirth and menopause. Elimination of ovarian cycling in PMS, or estrogen replacement at menopause, can be effective treatments for these conditions. On the other hand, several affective illnesses, as well as physical and psychological stress, are well known to interfere with sexual functions in general and with their associated hormones and cycles.

There are thus clear psychological outcomes associated with endocrine imbalances, most of which are ameliorated with hormonal normalization. Likewise, psychiatric conditions encompassing several mood disorders have a significant impact on most endocrine functions. These observations suggest a close connection between the brain substrates underlying affect and the control of endocrine systems, a connection that essentially remains to be uncovered.


Akil, H., Campeau, S., Cullinan, W. E., Lechan, R. M., Toni, R., Watson, S. J., & Moore, R. Y. (1999). Neuroendocrine systems I: Overview—Thyroid and adrenal axes. In M. J. Zigmond, F. E. Bloom, S. C. Landis, J. L. Roberts, & L. R. Squire (Eds)., Fundamental neuroscience (pp. 1127-1150). San Diego, CA: Academic Press.

Campeau, S. (2002). Psychoneuroendocrinology. In V. S. Ra-machandran (Ed.), Encyclopedia of the human brain (vol. 4, pp. 83-101). San Diego, CA: Academic Press. Frohman, L., Cameron, J., & Wise, P. (1999). Neuroendocrine system II: Growth, reproduction, and lactation. In M. J. Zigmond, F. E. Bloom, S. C. Landis, J. L. Roberts, & L. R. Squire (Eds.), Fundamental neuroscience (pp. 1151-1187). San Diego, CA: Academic Press.

McEwen, B. S. (1994). Endocrine effects on the brain and their relationship to behavior. In G. J. Siegel, B. W. Agranoff, R. W. Albers, & P. B. Molinoff (Eds.), Basic neurochemistry (pp. 10031023). New York: Raven Press. Nemeroff, C. B. (1992). Neuroendocrinology. Boca Raton, FL: CRC Press.

Nemeroff, C. B. (1999). The psychiatric clinics of North America—

Psychoneuroendocrinology (Vol. 21, no. 2). Philadelphia: W. B. Saunders.

Schulkin, J. (1999). The neuroendocrine regulation of behavior. Cambridge, UK: Cambridge University Press.

Serge Campeau

University of Colorado at Boulder See also: Anxiety; Depression; Pituitary

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