Adrenopause: Causes

Pathogenesis (development of disease)

Adrenopause finds its origin in the exponential decline of DHEA production by the adrenal cortex over the entire course of adulthood, with largely normal serum ACTH levels. The temporal starting point of this progressive decline is the middle of the 4th decade of life, from about the age of 35.

Beyond the age of 50, the DHEA-S serum level (sulfated storage form of the DHEA serum level) is on average only 10-50% of the serum level measured at a young age (20-30 years). Adrenopause as an expression of a deficient DHEAS status thus only arises in connection with a decline in the performance of the adrenal cortex and a simultaneous decline in the enzymes important for adrenal function, so that adrenopause is causally caused at least in part by a partial adrenal insufficiency. This age-related adrenal insufficiency is also evident in the deficient production status of the other adrenocortical hormones, so that the production of androstenedione, testosterone, dehydrotestosterone, estradiol and pregnenolone is also more or less deficient. In this context, DHEA-S is the lead hormone of this age-related decline in adrenocortical steroids. An important exception is cortisol, which is produced by the adrenal cortex in undiminished amounts throughout life. This results in an imbalance of adrenal steroids with significant pathophysiological effects at almost all levels of the human organism.

These effects, in turn, are causally related to the increasing development of the aging process and its complaints and symptoms.

Etiology (causes)

The following diseases or circumstances may be responsible for the decrease in DHEA:

Biographical causes

  • Age – progressive decline in DHEA production from about the age of 35.

Behavioral causes

  • Stimulants
    • Alcohol
    • Tobacco
  • Physical activity
    • Lack of physical fitness
  • Overweight (BMI ≥ 25; obesity).

Disease-related causes

  • AIDS
  • Autoimmune diseases such as rheumatoid arthritis, systemic lupus erythematosus (SLE).
  • Insulin resistance – reduced effectiveness of the body’s own insulin at the target organs skeletal muscle, adipose tissue and liver.
  • Addison’s disease (primary adrenocortical insufficiency) due to various conditions such as.
    • Autoimmune adrenalitis (autoimmune adrenocortical inflammation) – most common cause; circulating antibodies to the adrenal cortex (NNR) can be detected in approximately 70% of patients with isolated Addison’s disease and nearly 100% of patients with polyglandular autoimmune syndrome.
    • Tuberculosis
    • Tumor
    • Bleeding into the adrenal cortex (NNR)
    • After adrenalectomy (removal of the adrenal gland).
  • Secondary adrenal insufficiency – due to failure of ACTH production in anterior pituitary insufficiency (failure of the anterior lobe of the pituitary gland (pituitary gland)).

Medication