Polycystic Ovary Syndrome (PCOS) is a common endocrine disorder characterized by hyperandrogenism (excess production of male hormones), menstrual irregularities, and often the presence of polycystic ovaries. PCOS is a spectrum of metabolic and hormonal dysfunctions that manifest differently among affected individuals. Researchers have identified distinct PCOS subtypes based on the primary source of the hormonal imbalance. Adrenal PCOS is a subtype where the excessive production of androgens originates predominantly from the adrenal glands rather than the ovaries. Focusing on adrenal function is crucial for accurate diagnosis and targeted treatment strategies.
The Role of the Adrenal Glands in Androgen Production
The adrenal glands are small, triangular organs situated atop each kidney, playing a central role in the endocrine system. They produce hormones that regulate metabolism, blood pressure, and the body’s response to stress. The outer layer, or cortex, of the adrenal gland is where androgens (male hormones) are synthesized.
A primary adrenal androgen is Dehydroepiandrosterone sulfate (DHEA-S), which serves as a precursor hormone. Unlike testosterone, which is mainly produced by the ovaries, DHEA-S is almost exclusively an adrenal product, making it a reliable marker for adrenal activity. The release of these hormones is controlled by the complex feedback system known as the Hypothalamic-Pituitary-Adrenal (HPA) axis.
The HPA axis coordinates the stress response by signaling the adrenal glands to release hormones, including cortisol and adrenal androgens. In some individuals, the adrenal cortex (specifically the zona reticularis) becomes hyper-responsive to pituitary signals. This heightened sensitivity leads to an exaggerated output of adrenal androgens like DHEA-S, even without overt HPA axis dysfunction.
Defining Adrenal Polycystic Ovary Syndrome
Adrenal Polycystic Ovary Syndrome is a specific PCOS subtype defined by the overproduction of androgens stemming from the adrenal glands. Diagnosis is strongly suggested when blood tests reveal significantly elevated levels of the adrenal androgen DHEA-S. This elevation occurs even when ovarian androgens, such as total and free testosterone, are within the normal range or only mildly elevated.
The underlying trigger for this adrenal hyperandrogenism is often linked to HPA axis dysregulation, frequently caused by chronic psychological and physiological stress. Constant activation of the stress response pathway overstimulates the adrenal glands, resulting in the chronic excess secretion of DHEA-S. This adrenal imbalance contributes to symptoms that overlap with classic PCOS.
Common manifestations include hirsutism (the growth of excess, coarse hair in a male pattern) and persistent acne, particularly along the jawline and chin. Menstrual irregularities, such as oligo- or anovulation, are also characteristic due to the disruptive effect of high androgen levels on the ovarian cycle. Unlike the more common insulin-driven PCOS, individuals with the adrenal subtype may not exhibit significant insulin resistance or the classic “string of pearls” appearance of polycystic follicles on the ovaries.
Distinguishing Adrenal PCOS from Other Subtypes
Accurately distinguishing Adrenal PCOS from other subtypes, especially the more prevalent Ovarian-driven PCOS, requires specific laboratory testing. The key diagnostic differentiator lies in measuring circulating androgen levels. A blood panel checks for both the primary adrenal androgen (DHEA-S) and the primary ovarian androgen (testosterone).
In Adrenal PCOS, the defining feature is the elevated DHEA-S level, often with total and free testosterone levels that are normal or only slightly increased. Conversely, in Ovarian-driven PCOS, testosterone levels are typically the most elevated androgen marker, while DHEA-S levels often remain within the normal range. The diagnostic process must also include testing to rule out other conditions that mimic PCOS symptoms.
A blood test for 17-hydroxyprogesterone (17-OHP) is frequently ordered to exclude Non-Classical Congenital Adrenal Hyperplasia (NCAH), a genetic condition that also causes adrenal androgen excess. Screening for cortisol-related disorders, such as Cushing’s syndrome, is necessary when specific clinical features are present, sometimes involving a dexamethasone suppression test. Focusing on the source of the androgen excess through these precise lab markers helps healthcare providers pinpoint the adrenal origin and tailor treatment accordingly.
Management Approaches for Adrenal PCOS
Because Adrenal PCOS is intrinsically linked to an overactive stress response, management strategies focus on modulating the HPA axis rather than primarily targeting insulin resistance. Lifestyle modifications are at the forefront of the treatment plan. Implementing effective stress reduction techniques is paramount, including mindfulness practices, meditation, and gentle exercises like yoga.
Improving sleep quality and maintaining consistent sleep hygiene is a foundational step, as poor sleep further dysregulates the HPA axis. Dietary support focuses on nutrient density and anti-inflammatory foods to support adrenal gland function, rather than insulin management. Specific nutritional supplements, such as B vitamins, magnesium, and adaptogenic herbs, may be recommended to support the body’s resilience to stress and promote hormonal balance.
If symptoms remain severe, pharmaceutical interventions may be introduced, though they differ from those used for other PCOS types. For significant adrenal hyperandrogenism, low-dose glucocorticoids (such as dexamethasone) may be prescribed to suppress the overproduction of DHEA-S by the adrenal glands. Anti-androgen medications or oral contraceptives may also be used to manage external symptoms like hirsutism and acne, but the root cause approach remains focused on calming the adrenal response.