She was 16 the first time she noticed it. Milk. From her breasts. No pregnancy. No childbirth. No explanation. She told a provider. Labs were drawn. Her prolactin was elevated. She was told it was “not a big deal.” Over the years, multiple providers suggested she must be stimulating her nipples and advised her to stop. She insisted she was not. She felt embarrassed, dismissed, and increasingly reluctant to bring it up again. She is now 32.
For more than 15 years she has had persistent galactorrhea. Repeat prolactin levels ranged between 44 and 60 nanograms per milliliter (ng/mL). She denied nipple stimulation. She was not taking opioids, antipsychotics, or other medications known to elevate prolactin. Thyroid labs, including antibodies, were normal. She also carries diagnoses of post-traumatic stress disorder (PTSD) and bipolar II disorder. Her mood instability began in early adolescence. She has a history of suicidality. Multiple antidepressant trials either failed or activated her. Although she had undergone multiple antidepressant trials, she had never been trialed on a mood stabilizer prior to presenting for care. She has lived inside a nervous system that feels unpredictable and volatile. And for over 15 years, no one sent her for a brain magnetic resonance imaging (MRI).
The clinical prevalence of elevated prolactin
Hyperprolactinemia occurs in approximately 0.4 percent of the general population, but its prevalence rises significantly in certain clinical settings. It is reported in about 5 percent of women seen in family planning clinics, 9 percent of women with amenorrhea, 17 percent of women with polycystic ovary syndrome (PCOS), and up to 36 percent of women with recurrent miscarriage. These numbers underscore that while elevated prolactin may be uncommon in the general population, it is far from rare in women presenting with reproductive or hormonal concerns.
It is also not irrelevant. Prolactin is regulated by dopamine. When dopamine tone decreases, prolactin rises. When prolactin rises, it can reflect broader neuroendocrine dysregulation. Elevated prolactin is associated with anxiety, irritability, depressive symptoms, sexual dysfunction, and menstrual disruption. Chronic stress can further dysregulate this system, creating a feedback loop between stress hormones and mood.
When psychiatric diagnoses overshadow physiology
Not every elevated prolactin level causes depression. Not every patient with mood symptoms requires endocrine imaging. But 15 years of galactorrhea deserved more than reassurance. In medicine, we are taught to look for zebras sparingly. We are also taught to investigate persistent unexplained symptoms. If a patient had 15 years of hematuria, we would not call it insignificant. If a patient had unexplained syncope for over a decade, we would not simply normalize it. Yet when psychiatric diagnoses enter the chart, physiology can quietly recede.
This is not a story about blame. It is about drift. When a patient has trauma, mood instability, and a history of suicidality, it becomes easy to attribute physical findings to stress or behavior. Suggesting self-stimulation may have seemed like a benign explanation. But when a patient repeatedly denies it and is not believed, something else happens. Trust erodes. The body becomes suspect. The patient begins to question her own credibility. Stress can elevate prolactin. Chronic psychological strain can influence the dopamine-prolactin axis. But stress does not exclude structural causes. Prolactin-secreting pituitary adenomas are common, benign, and often small. They are diagnosable. They are treatable.
The necessity of comprehensive investigation
The cost of not looking is not only biological. It is psychological. When a young woman leaks milk from her body for 15 years and is told it is insignificant or self-induced, she internalizes something about how her symptoms are valued. We often speak about integrating mental and physical health. Integration is not a slogan. It is a discipline. It requires curiosity when something does not fit neatly into a psychiatric or medical narrative. It requires believing patients when they describe their own bodies. This patient is now being referred for pituitary imaging. Perhaps her scan will be normal. Perhaps it will reveal a microadenoma. Either way, the investigation matters.
Because the deeper question is not whether she has a tumor. The question is how many times we have called something “not a big deal” or “probably behavioral” simply because the patient already carried a psychiatric diagnosis. Medicine becomes safer when we resist that reflex. Patients feel seen, heard, and taken seriously when their symptoms are investigated rather than explained away.
Carrie Friedman is a dual board-certified psychiatric and family nurse practitioner and the founder of Brain Garden Psychiatry in California. She integrates evidence-based psychopharmacology with functional and integrative psychiatry, emphasizing root-cause approaches that connect neuro-nutrition and gut–brain science, metabolic psychiatry, immunology, endocrinology, and mind–body lifestyle medicine. Carrie’s clinical focus bridges conventional psychiatry with holistic strategies to support mental health through nutrition, physiology, and sustainable lifestyle interventions. Her professional writing explores topics such as functional medicine, autism, provider well-being, and medical ethics.
