Prolactin: the hormone under a dopamine brake

Prolactin is a protein hormone from the lactotrophs of the anterior pituitary. Its famous job is milk. Its quieter jobs are on the gonad, on libido, and on a breast that is already being told to grow. The control is unusual. Most pituitary hormones are switched on by a releasing hormone. Prolactin is switched off by dopamine, arriving from the hypothalamus down the portal blood and landing on D2 receptors on the lactotroph. Take the dopamine away, or block the D2 receptor, and prolactin rises. That is why some antipsychotic drugs raise it, and why a D2 agonist such as cabergoline lowers it. The brake is the physiology. Everything else is a story about the brake.

In short. Prolactin comes from the pituitary and is held down by dopamine. Block that brake and the level rises. Cabergoline pushes the brake harder, which is why it lowers prolactin.

A modest rise does not equal a discharge from the nipple, and a discharge does not equal ordinary gym gynaecomastia. Very high prolactin, the sort a prolactinoma produces, suppresses GnRH, lowers LH and testosterone, blunts libido, and can cause galactorrhoea. That is a pituitary tumour until someone has proved it is not. The levels in that disease are not the levels people screenshot after a heavy week. Stress, a poor night, a recent meal, chest-wall stimulation and even the needle itself move prolactin. A single alarmed draw, taken standing up after a row, is a bad instrument. Repeat it rested, in the morning, before you invent a tumour or a drug.

In short. Very high prolactin is a medical problem, often a pituitary adenoma, and it switches testosterone down. A single blood test after training is a poor way to catch it. Repeat it calm, in the morning.

Nandrolone and trenbolone bind the progesterone receptor, and progestogens can loosen the dopamine brake enough that prolactin drifts up in some people. They also grow breast gland through the progesterone receptor directly, which does not require prolactin to be high at all. The forum collapsed those two facts into one sentence: deca and tren raise prolactin, and prolactin is the gyno. The first half is sometimes true and often small. The second half is usually the wrong door. A man with a disc, a normal prolactin, and trenbolone in the picture has a progesterone-receptor problem. A man with prolactin five times the top of the range has a different problem, and it deserves a proper assay and a look at the pituitary, not a reflex dopamine agonist.

In short. Deca and tren can nudge prolactin up, and they can grow breast tissue through the progesterone receptor even when prolactin is normal. Most 'prolactin gyno' is the second one.

The peptide side of the same rumour is more concrete. Ghrelin receptors on the pituitary do more than release growth hormone. GHRP-6 and hexarelin push prolactin and ACTH as well as GH. That is in the original tables, which is why ipamorelin was interesting: Raun's pentapeptide was the one that spared the prolactin and cortisol lines. MK-677 occupies the same ghrelin receptor for most of a day, and prolactin can drift with it. Stack a 19-nor, which already touches the progesterone receptor, on top of a ghrelin drug that also leans on prolactin, and you have two mechanisms and one nipple. Blaming only the hormone you can buy a dopamine agonist for is how the oestrogen and progesterone receptors get ignored.

In short. GHRP-6, hexarelin and sometimes MK-677 raise prolactin because of the ghrelin receptor. Ipamorelin was picked because it mostly doesn't. A 19-nor plus one of the others is two mechanisms, not one.

Cabergoline is an ergot-derived D2 agonist. In a prolactinoma it is the drug that shrinks the tumour and brings the hormone down, and people take it for years in hospital endocrine practice. The serious stain on the class is fibrosis, including heart-valve fibrosis, shown at the much higher doses used in Parkinson's disease. Schade and colleagues, New England Journal of Medicine, 2007, is that paper. Endocrine doses are smaller, and the risk is not the Parkinson's risk copied onto a weekend, but the receptor story is the same family. Cabergoline occupies D2, the lactotroph releases less prolactin, and a breast gland that was built by oestradiol at the oestrogen receptor, or by a 19-nor at the progesterone receptor, is still there when the prolactin number was never high.

In short. Cabergoline lowers prolactin and is a real drug for pituitary tumours. At high doses it has damaged heart valves. It does not undo breast tissue that oestrogen or tren built while prolactin was normal.

Dopamine is the main brake. It is not the only input. Thyrotropin-releasing hormone nudges lactotrophs, which is why a failing thyroid can come with a higher prolactin. Oestradiol itself promotes prolactin secretion and makes the cells more numerous, so a high-aromatising cycle can raise prolactin a little without any 19-nor at all. Serotonin-reuptake antidepressants, and the antipsychotics that block D2, are common reasons for a raised number in a man who has never touched trenbolone. A drug list belongs next to the result. Stress belongs there too. Prolactin is a stress hormone as well as a milk hormone. Venepuncture, a poor night, an orgasm, a meal, and nipple stimulation all move it. The right sample is morning, rested, not straight off a session, and repeated if the first one is surprising. A single value twice the top of the range, drawn properly, is a reason to look. A single value drawn badly is a reason to draw it again.

In short. Thyroid trouble, oestradiol, some antidepressants and some antipsychotics raise prolactin without any steroid. So do stress, a meal, sex and a bad night. Repeat a surprising result in the morning before you name a cause.

The number has traps of its own. Macroprolactin is prolactin stuck to an antibody. It is biologically quiet and it inflates the immunoassay, so a man can be told he has a high prolactin and have none of the symptoms. Laboratories can precipitate it out and report the real monomer. At the other end, a very high true prolactin can swamp some assays and print a falsely normal result, the hook effect. A man with headaches, a visual-field cut, milk, and a 'normal' prolactin needs the sample diluted. These are not gym subtleties. They are why a screenshot of one number is not a diagnosis, and why a dopamine agonist started off that screenshot is a drug in search of a fact.

In short. Some high results are a harmless antibody complex, macroprolactin. Some huge real results print as normal unless the lab dilutes the sample. Either way, one number on a phone is not the whole story.

Prolactin suppresses GnRH. High enough, LH falls, testosterone falls, and desire goes with them. There is also a more local effect on erectile function that does not wait for testosterone to collapse. The levels that do this are the levels of a prolactinoma, or of a drug that has blocked dopamine hard. A 19-nor, in the studies that bothered to measure, sometimes lifts prolactin modestly and often does not lift it out of the reference range. Modest is not 'five times the limit'. Galactorrhoea, a milky discharge, is the symptom that says the lactotroph is actually overworking. An itchy nipple is not galactorrhoea. An itchy nipple is much more often the early oestrogen or progesterone signal in the duct, the same signal the gynaecomastia page is about. Treating itch with cabergoline, without a rested prolactin and without an oestradiol, is treating the wrong brake.

In short. Only a clearly high prolactin pulls testosterone down and kills desire. Deca and tren usually do not get the number that high. Milk from the nipple is prolactin. An itch is usually the breast gland, and cabergoline does not treat that.