Key Benefits
'- Check for adrenal underactivity (Addison’s) by pairing cortisol with sodium and potassium.
- Spot early adrenal shortfalls; low morning cortisol strongly suggests Addison’s.
- Flag salt imbalance risks: low sodium and high potassium signal low aldosterone.
- Clarify unexplained fatigue, dizziness, weight loss, or darkened skin as adrenal-driven.
- Guide treatment planning: sodium and potassium patterns help tailor fludrocortisone dosing and salt intake.
- Protect fertility and cycles: correcting adrenal hormones stabilizes ovulation and menstrual regularity.
- Support healthy pregnancy; treat early to reduce crisis and fetal complications.
- Best interpreted with 8 a.m. cortisol timing, ACTH, renin level, and symptoms.
What are Addison’s Disease
Biomarker testing for Addison’s disease shows whether the body’s stress and fluid-balance systems are intact by tracking the hormones that link brain signals to adrenal output. Cortisol (glucocorticoid) reflects the adrenal gland’s capacity to sustain energy, blood pressure, and immune restraint, while ACTH (adrenocorticotropic hormone) reflects the pituitary “go” signal to make it. Aldosterone (mineralocorticoid) and renin map the kidney-adrenal loop that controls sodium, potassium, and blood volume (renin-angiotensin-aldosterone system). DHEA‑S (dehydroepiandrosterone sulfate) captures the adrenal androgen reserve. Autoimmune markers such as 21‑hydroxylase antibodies identify the most common cause—immune attack on the adrenal cortex—and help stage ongoing injury. Viewed together, these biomarkers locate where the chain is breaking (signal versus gland), reveal how many adrenal zones are involved (glucocorticoid, mineralocorticoid, androgen), and provide a physiological baseline for treatment and monitoring. In short, they translate symptoms like fatigue, dizziness, and salt craving into a clear map of adrenal function and guide safe hormone replacement that fits the body’s biology.
Why are Addison’s Disease biomarkers important?
Addison’s Disease biomarkers reveal how well the adrenal cortex is sustaining the body’s stress response, salt–water balance, and energy supply. Cortisol, and the aldosterone effects reflected by sodium and potassium, together forecast blood pressure stability, glucose steadiness, heart rhythm, and cognitive stamina across systems.
In healthy patterns, morning cortisol peaks—often around 10–20—and tapers through the day; feeling well usually aligns with a mid‑to‑high morning value. Sodium tends to sit near 135–145 with best function in the middle, while potassium is near 3.5–5.0 with an optimal middle range. Very high cortisol more often signals stress or steroids than Addison’s; very low sodium or very high potassium point toward mineralocorticoid loss.
When cortisol and sodium are low—and potassium is high—it reflects adrenal hormone deficiency. Too little cortisol lowers vascular tone and glucose availability, driving fatigue, weight loss, nausea, abdominal pain, and lightheadedness; ACTH rises and can deepen skin pigmentation. Aldosterone loss wastes salt and water and retains potassium, causing salt craving, muscle weakness, and heart‑rhythm risk. Women may notice low libido or menstrual changes from reduced adrenal androgens. Children can show poor growth and more hypoglycemia; pregnancy heightens risks of hyponatremia and dizziness.
Big picture, these markers sit at the crossroads of the HPA axis and the renin–angiotensin–aldosterone system, linking brain stress circuits with kidney and cardiac function. Interpreted with ACTH and renin, they map the physiology behind symptoms and the long‑term risks of adrenal crisis, arrhythmias, and chronic low‑volume states.
What Insights Will I Get?
Addison’s disease reflects failure of the adrenal cortex to sustain the body’s stress, energy, and salt–water balance systems. When these hormones are low, the whole network that maintains blood pressure, glucose stability, cognition, temperature regulation, and immune tone is strained. At Superpower, we test these specific biomarkers: Cortisol, Sodium, Potassium.
Cortisol is the primary glucocorticoid that follows a daily rhythm, peaking in the morning to mobilize energy and support vascular tone. Persistently low cortisol, especially at the expected peak, points toward adrenal insufficiency. Sodium reflects extracellular fluid balance; in Addison’s, deficient aldosterone leads to renal sodium loss and dilutional hyponatremia. Potassium tracks renal potassium excretion; with low aldosterone, potassium often rises because the kidneys cannot excrete it efficiently.
Together, these markers show system stability. Adequate cortisol supports blood pressure, glucose availability, mental clarity, and appropriate immune restraint; low values undermine these functions and increase vulnerability to stress. Sodium indicates the capacity to retain salt and water; low sodium signals impaired mineralocorticoid action and excess antidiuretic drive, risking low blood pressure and cognitive symptoms. Potassium reflects cardiac and neuromuscular safety; elevated levels increase arrhythmia risk and muscle weakness, while normal levels suggest preserved or compensated mineralocorticoid effect.
Notes: Cortisol depends on time of day, acute stress, pregnancy, and oral estrogens (via cortisol-binding globulin). Glucocorticoid therapy suppresses cortisol. Sodium and potassium are influenced by dehydration, kidney function, and drugs like diuretics, ACE inhibitors, ARBs, or potassium-sparing agents. Hemolysis can falsely elevate potassium. Assay methods and age affect reference ranges.