How Stress, Cortisol, and Dopamine Contribute to High Prolactin Levels in Hypothalamic Amenorrhea (FHA)

Before we dive in, we want to give credit to the author. This was written by Cat, a graduate of our Holistic HA Practitioner (HHAP) Certification Program. Cat brings a deep understanding of the root causes of HA and is passionate about supporting women on the path to recovery through education, empowerment, and holistic strategies.

Hypothalamic Amenorrhea (HA) is a stress-related condition where the body shuts down reproductive function in response to internal or external threats. These stressors—whether psychological (emotional stress), metabolic (low energy availability), or immune/inflammatory—activate the hypothalamic-pituitary-adrenal (HPA) axis, triggering a cascade of hormonal changes (1).

One major effect of this activation is a rise in cortisol, the body’s primary stress hormone. The combination of powerful stressors in HA activate the HPA axis. This stimulates an increase in secretion of our stress hormones— namely corticotrophin releasing hormone (CRH), and cortisol-- the body’s primary stress hormone (1,2). Cortisol initially works to play a protective role, helping the body conserve energy during times of perceived danger. However, in chronic stress states, cortisol becomes dysregulated, disrupting the hypothalamic-pituitary-gonadal (HPG) axis and contributing to conditions like HA (2). Cortisol plays a myriad of roles in HA. One lesser known role is the indirect effect it has on prolactin levels.

Cortisol and Elevated Prolactin: What’s the Connection?

Prolactin is a key player in this stress-hormone interaction. It is a hormone typically associated with lactation and suppression of the reproductive system (3). It is also a hormone that is sensitive to, and responds to stress.

In HA, prolactin levels may rise even without pregnancy, or other clinical diagnoses such as a prolactinoma. The elevation of prolactin sometimes seen in HA is primarily due to changes in dopamine, a neurotransmitter that normally keeps prolactin in check (3,4).

Under chronic stress (such as with HA), cortisol can (6,7):

• Suppress dopamine production in the brain

• Desensitize D2 dopamine receptors in the pituitary gland

Since dopamine acts as the primary inhibitor of prolactin, any drop in dopamine levels or receptor function removes that inhibition 5 . The result is increased prolactin secretion, which can further disrupt ovulation, menstrual cycles, and fertility.

Think of dopamine as a security guard standing at the prolactin gate. Under normal conditions, it keeps prolactin in check, only allowing it to rise when truly necessary—like during pregnancy or breastfeeding. But when chronic stress floods the system with cortisol, that security guard gets distracted, overwhelmed, or even called off duty. Without dopamine standing watch, prolactin slips through the gate unchecked, leading to higher levels.

Temporary vs. Chronic Prolactin Spikes in FHA

Short-term stress (like exercise or anxiety) can cause brief increases in prolactin. But in functional hypothalamic amenorrhea, chronic stressors—like calorie restriction, excessive exercise, or emotional burnout—can lead to persistent hyperprolactinemia (4). In HA, this can become a vicious cycle>>>our HA tendencies cause chronic stress>>>chronic stress contributes to prolactin elevation>>>prolactin elevation AND chronic stress contribute to downregulation of the reproductive cycle and menstrual irregularities. Elevated prolactin is both a consequence and contributor to the hypothalamic suppression that defines this condition. 

Beyond Cortisol: Other Hormonal Players in FHA

While cortisol’s impact on prolactin is significant, it’s just one piece of a complex hormonal puzzle.

HA also involves:

• Changes in appetite hormones such as leptin and ghrelin (due to undernutrition)

• Suppressed kisspeptin and GnRH (which drive reproductive hormones)

• Altered beta-endorphin activity

• Low estrogen and progesterone

• Altered thyroid hormones
  

These changes further downregulate the HPG axis, disrupt the hormonal balance (including prolactin levels!) needed for regular menstrual cycles and fertility, and can contribute to elevated prolactin levels.

Key Takeaway

Chronic stress, common in HA, increases levels of cortisol. Cortisol suppresses dopamine. Why does this matter? Dopamine if the main inhibitor of prolactin. When dopamine is suppressed, prolactin levels can rise. Cortisol, along with elevated prolactin, suppresses our reproductive hormones, disrupt the HPG axis, and add fuel to the HA fire. Addressing chronic stress and restoring dopamine balance is essential for reducing prolactin and recovering your cycle!

Feeling like stress might be the missing link in your recovery?

If you're dealing with high prolactin, missing periods, or feeling stuck in HA, you're not alone—and you don’t have to figure it out by yourself. Our 1:1 coaching is designed to help you uncover the root causes, calm your nervous system, and restore your cycle with confidence. Apply HERE.

Curious to learn more about how stress affects your hormones—or want to become the kind of practitioner who can guide others through this healing process?

Explore the Holistic HA Practitioner Certification Program, where graduates like Cat learn the science-backed tools to help clients recover their cycles, restore fertility, and heal holistically.

References:

1. Podfigurna, A., & Meczekalski, B. (2017). Functional hypothalamic amenorrhea: A stress-based disease. Polish Archives of Internal Medicine, 127(6), 402–405. https://doi.org/10.20452/pamw.4049

2. Gordon, C. M., & Ackerman, K. E. (2015). Functional hypothalamic amenorrhea: Recognition and management of a challenging diagnosis. American Journal of Obstetrics and Gynecology, 213(6), 773–779. https://doi.org/10.1016/j.ajog.2015.05.001

3. Berinder, K., Nyström, T., Höybye, C., Hall, K., & Hulting, A.-L. (2007). Stress- induced hyperprolactinemia: Pathophysiology and clinical approach. European Journal of Endocrinology, 157(2), 157–163. https://doi.org/10.1530/EJE-07-0164

4. Tomatis, V., Battipaglia, C., & Genazzani, A. D. (2021). Thyroid, adrenal, PRL impairments and ovarian function. Endocrines, 2(3), 212-225. https://doi.org/10.3390/endocrines2030021​:contentReference[oaicite:0]{index=0}

5. Sonino, N., Navarrini, C., Ruini, C., Fallo, F., Boscaro, M., & Fava, G. A. (2004). Life events in the pathogenesis of hyperprolactinemia. European Journal of Endocrinology, 151(1), 61–65. https://doi.org/10.1530/eje.0.1510061

6. Bloomfield, M. A., McCutcheon, R. A., Kempton, M., Freeman, T. P., & Howes, O. (2019). The effects of psychosocial stress on dopaminergic function and the acute stress response. eLife, 8, e46797. https://doi.org/10.7554/eLife.46797

7. Blum, K. (n.d.). The impact of chronic stress on brain function and structure. Open Access Journals.