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Like cortisol, aldosterone is a steroid hormone.

1. Formation of aldosterone

Cholesterol is converted to aldosterone via pregnenolone and progesterone.

Aldosterone is formed in the outermost layer of the adrenal cortex, the zona glomerulosa.

The half-life of aldosterone is 20 minutes.

The breakdown of aldosterone to (mainly) tetrahydro-glucuronide derivatives takes place in the liver, and to a lesser extent to an 18-glucuronide in the liver and kidneys. Excretion takes place via the urine.

1.1. Aldosterone agonists

  • Stress
    • ACTH
  • Renin from the kidney1
  • Reduction in blood volume and blood pressure
    • Operations
    • Hyperaldosteronism (due to angiotensin II at AT1 receptors)
      • Angiotensin II is increased by
        • Sodium deficiency
        • Hypovolemia (blood deficiency)
        • Decrease in renal blood flow.
  • Hyperkalemia (too high potassium blood level)1
  • Hyponatremia (low sodium blood level)

1.2. Aldosterone antagonists

  • Spironolactone
  • Canrenoat
  • Eplerenone
  • Hypernatremia (high sodium blood level)

2. Effect of aldosterone

  • Is increasingly released in the event of a lack of fluids
    • Conveys a feeling of thirst
  • Regulation of blood pressure (significant)
  • Electrolyte balance
    • Aldosterone deficiency triggers salt cravings
  • Binding to mineralocorticoid receptor (MR)2
  • With the same receptor affinity, aldosterone is 1000 times more effective than cortisol.
    This is because cortisol is converted to cortisone in the aldosterone-sensitive cells by 11β-hydroxysteroid dehydrogenase type 2. Cortisol cannot activate the receptor

3. Aldosterone deficiency

3.1. Effect of an aldosterone deficiency

  • Hyponatremia (sodium deficiency)
  • Hyperkalemia (excess potassium)
  • Reduction of the plasma volume
  • Hypotension
  • Circulatory insufficiency
  • Shock

3.2. Causes of aldosterone deficiency

This can be caused by disorders of aldosterone biosynthesis. These are very rare.

  • 21-hydroxylase deficiency
    • Varying extent
    • Partial 21-hydroxylase deficiency (reduction of aldosterone production to 1-2%) can maintain sufficient mineralocorticoid function3
      Further effects need to be checked
  • Aldosterone synthetase deficiency
  • 3b-hydroxysteroid dehydrogenase deficiency
  • Cholesterol desmolase deficiency
  • Primary adrenal insufficiency
    • While central (secondary and tertiary) adrenal insufficiency usually “only” involves a significant glucocorticoid deficiency, primary adrenal insufficiency usually involves deficiency symptoms of glucocorticoids, mineralocorticoids (aldosterone) and androgens (e.g. dehydroepiandrosterone = DHEA).4

In general, aldosterone deficiency is more common in a low cortisol stress response and alpha-amylase stress response, as is typical in atopy (inflammatory health problems).5

3.3. Treatment of aldosterone deficiency

In primary adrenal insufficiency, aldosterone is usually substituted in addition to cortisol. This is done using the mineralocorticoid fludrocortisone.
A lack of cortisol due to a failure of the pituitary gland does not usually require the administration of aldosterone.

There is also so-called pseudohypoaldosteronism, where the body produces sufficient or even too much aldosterone, but this is not recognized as such by the target organs. Pseudohypoaldosteronism thus causes the same symptoms as an aldosterone deficiency in the blood.6

3.4. Hypothesis: Aldosterone deficiency as a contributory cause of ADHD-HI

We hypothesize, purely theoretically, that aldosterone deficiency could be a contributing cause of ADHD-HI (with hyperactivity / decreased cortisol stress response).

ADHD-HI can be viewed from the perspective that the insufficient cortisol stress response causes a deficient shutdown of the HPA axis, which triggers an endurance run of the stress system of the HPA axis including the resulting phenomena of inability to recover and thus causes a self-reinforcing permanent stress reaction.
Aldosterone binds to mineralocorticoid receptors (MR). If there is an aldosterone deficiency, the MRs are too weakly occupied. In an acute stress situation, cortisol must first address the unoccupied MR before it can occupy the less affine glucocorticoid receptors (GR), which cause the HPA axis to be switched off again. Above a certain level of aldosterone deficiency and low cortisol stress response, the system is no longer able to bind enough GR to shut down the HPA axis after activation by an acute stressor.

In SHR (Spontanuous hypertensive rat) rats, which are model animals for a purely genetic causative model of ADHD-HI (with hyperactivity) and hypertension, significantly decreased basal aldosterone levels (in addition to decreased corticosterone, which is the predominant glucocorticoid in rats) were found.7

A search for “aldosterone” and “ADHD” in PubMed did not yield any relevant references. This possible connection seems to have been completely ignored so far.

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