Neuroendocrinología y conducta (I)

En este artículo se proporciona una revisión exhaustiva (en dos partes) de la investigación realizada en los 70 sobre andrógenos y conducta agresiva, tanto en animales como en humanos (1ª parte). Se propone que se adopte el modelo de la "Psicopatología de la Desinhibición" de Gorestein y Newman (1980) para el estudio de la personalidad agresiva y desinhibida caracterizada por la impulsividad y búsqueda de sensaciones novedosas entre la que es prototípica la psicopatía. Este modelo permite incluir la hipótesis aminérgica del rasgo de personalidad denominado "Búsqueda de sensaciones" que postula que los individuos desinhibidos tienen niveles bajos en la actividad MAO plaquetar, enzima que es inhibido por los estrogenos y andrógenos (2ªparte)

Neuroendocrinología y conducta (II)

En este artículo se proporciona una revisión exhaustiva (en dos partes) de la investigación realizada en los 70 sobre andrógenos y conducta agresiva, tanto en animales como en humanos (1ª parte). Se propone que se adopte el modelo de la "Psicopatología de la Desinhibición" de Gorestein y Newman (1980) para el estudio de la personalidad agresiva y desinhibida caracterizada por la impulsividad y búsqueda de sensaciones novedosas entre la que es prototípica la psicopatía. Este modelo permite incluir la hipótesis aminérgica del rasgo de personalidad denominado "Búsqueda de sensaciones" que postula que los individuos desinhibidos tienen niveles bajos en la actividad MAO plaquetar, enzima que es inhibido por los estrogenos y andrógenos (2ªparte).

Do the interactions between glucocorticoids and sex hormones regulate the development of the metabolic syndrome?

The metabolic syndrome is basically a maturity-onset disease. Typically, its manifestations begin to flourish years after the initial dietary or environmental aggression began. Since most hormonal, metabolic, or defense responses are practically immediate, the procrastinated response do not seem justified. Only in childhood, the damages of the metabolic syndrome appear with minimal delay. Sex affects the incidence of the metabolic syndrome, but this is more an effect of timing than absolute gender differences, females holding better than males up to menopause, when the differences between sexes tend to disappear. The metabolic syndrome is related to an immune response, countered by a permanent increase in glucocorticoids, which keep the immune system at bay but also induce insulin resistance, alter the lipid metabolism, favor fat deposition, mobilize protein, and decrease androgen synthesis. Androgens limit the operation of glucocorticoids, which is also partly blocked by estrogens, since they decrease inflammation (which enhances glucocorticoid release). These facts suggest that the appearance of the metabolic syndrome symptoms depends on the strength (i.e., levels) of androgens and estrogens. The predominance of glucocorticoids and the full manifestation of the syndrome in men are favored by decreased androgen activity. Low androgens can be found in infancy, maturity, advanced age, or because of their inhibition by glucocorticoids (inflammation, stress, medical treatment). Estrogens decrease inflammation and reduce the glucocorticoid response. Low estrogen (infancy, menopause) again allow the predominance of glucocorticoids and the manifestation of the metabolic syndrome. It is postulated that the equilibrium between sex hormones and glucocorticoids may be a critical element in the timing of the manifestation of metabolic syndrome-related pathologies.

Steroid hormones interrelationships in the metabolic syndrome: an introduction to the ponderostat hypothesis

Sexual dimorphism in the metabolic syndrome. The clairvoyant early implication of sex hormones in the characterization of the metabolic syndrome (MS) was detected early, and in accordance with the well-known sex-related main patterns of fat deposition in obesity: gynoid and android. The differences point to a direct implication of androgens and estrogens in the development, properties and maintenance of obesity and, by extension, to the cumulus of diseases grouped in the MS. For a long time, the key issue of the MS, i.e. the metabolic event explaining (and justifying) most of the derangements of the MS, has been considered to be insulin resistance (...)