I’m sure more than a few members here have heard the term “deca-dick.” For the guys who know the story—and the guys who don’t—let’s make some order and separate myth from actual physiology.
“Deca dick” isn’t a medical diagnosis. It’s forum slang for a cluster of symptoms some men report with nandrolone (Deca / nandrolone decanoate & nandrolone phenylpropionate): lower libido, weaker erections, reduced sensitivity, and a general “disconnect.”
The internet explanation usually defaults to one word: prolactin. Reality is more layered.
First, the prolactin myth (and what’s actually true)
Prolactin is not something a steroid “turns into”
Prolactin is a peptide hormone made by the pituitary. A steroid like nandrolone cannot be chemically converted into prolactin. So by no means does nandrolone raise prolactin serum levels. That alone kills a lot of the bro-logic.
Also, nandrolone is not “binding prolactin receptors” and forcing prolactin up the way it binds androgen receptors. If prolactin changes happen in some users, they’re indirect and not guaranteed—more about the overall endocrine + dopamine environment than about Deca being a “prolactin drug.”
So why do people blame prolactin?
Because three things happen together in real life with nandrolone:
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People experience sexual side effects (libido/erections).
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Those symptoms get associated with “prolactin issues” online.
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Nandrolone is a 19-nor steroid and can have progestin-like activity, and forums often mash “progestogenic” and “prolactinic” into one bucket.
Add the fact that most guys don’t run nandrolone in a clean, controlled setting (stacks, changing estrogen, sleep/stress, stimulants, etc.), and prolactin becomes the easiest scapegoat.
The caber reality check (important)
A lot of users report relief when adding cabergoline (caber). That can be true—and still not prove the myth.
Caber is strongly dopaminergic, and dopamine is tied to sexual drive, arousal, and erection quality. So caber can improve symptoms by:
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Improving dopamine signaling (often felt as motivation/drive returning)
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Lowering prolactin if it’s elevated
In other words: caber can relieve “deca-dick” symptoms without proving nandrolone’s primary mechanism was prolactin. It may treat a downstream pathway while the root cause remains the androgen/progestin balance and suppression picture.
The real core mechanisms behind “Deca dick”
1) Suppression: nandrolone shuts down natural testosterone
This is the boring answer, but it’s the biggest one.
Nandrolone heavily suppresses LH/FSH (as potent androgens do), so endogenous testosterone production drops. In addition, as a 19-nor steroid it has progestin-like activity at the progesterone receptor, and progestins are well known to be antigonadotropic—meaning they suppress gonadotropins and, in men, can further and significantly reduce natural testosterone output.
So with nandrolone you can get a “double hit”:
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Direct androgen negative feedback → lower LH/FSH
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Progestin-like signaling → further antigonadotropic pressure
When endogenous testosterone drops, DHT drops too, and many men will feel that as lower libido and weaker erections—regardless of any prolactin talk.
Suppression alone can create the symptom pattern. Deca just has extra quirks that make it more noticeable for some.
2) The nandrolone “quirk”: 5α-reduction can make it weaker locally
This is the Deca-specific part most people miss.
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Testosterone gets converted to DHT, which carries a 3–5× stronger androgen signal in certain androgen-sensitive tissues (discussed below).
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Nandrolone gets converted to DHN (dihydronandrolone), which is generally a weaker androgen signal than nandrolone itself.
So you can have a strong anabolic effect overall, but still end up with weaker androgen signaling in the places that matter most for sexual function.
Plain English: you can be “anabolic” in muscle yet feel under-androgenized in certain androgen-sensitive pathways relevant to sexual function—particularly on penile tissue, the prostate, and the brain—especially if your own testosterone/DHT production is suppressed.
That combination (suppression + “weaker local androgen signaling”) is one of the most coherent explanations for the classic Deca reputation.
3) Progestin-like activity: not “progesterone levels,” but “progesterone-style signaling”
This is another layer people feel but describe badly.
Nandrolone can have progestin-like effects (receptor-level behavior), which can:
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Deepen the “flat/low spark” feeling in some men
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Add to suppression/feedback effects
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Shift the overall sexual “tone” (CNS + endocrine)
This is also where the prolactin myth often gets born: guys feel progestin-like side effects and call or relate them to “prolactin,” even when prolactin isn’t the real driver.
What about estrogen — does Deca (nandrolone) aromatize?
You’ll hear two extremes:
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“Deca doesn’t aromatize, so estrogen isn’t involved.”
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“Deca is estrogenic, so estrogen is the whole cause.”
Both are oversimplified.
1) Yes — nandrolone can be converted to estrogens (E1/E2), but it doesn’t resemble testosterone in aromatization behavior
Nandrolone is 19-nortestosterone (a 19-nor steroid). There’s been debate for decades because 19-nor steroids lack the C19-methyl group that’s central to aromatase’s “classic” chemistry—yet multiple experiments still show aromatase can generate aromatized (estrogenic) products from 19-nortestosterone.
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In human placental microsomes, estrogen formation from 19-nortestosterone occurred but was lower than a typical aromatizable substrate (androstenedione): roughly 1.84 vs 8.10 pmol (E1+E2)/hr/mg protein in that setup (~23%).
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In an in-vitro study using human recombinant aromatase, 19-nortestosterone (listed as “Nan”) was rapidly converted to A-ring aromatized products, confirmed analytically (LC-MS/MS).
So the honest statement is: nandrolone is aromatizable to estrogens, but it is typically less / different in net effect than testosterone in real-world male use—especially when nandrolone is used without testosterone.
2) In actual men, estradiol often doesn’t rise on nandrolone the way it rises on testosterone — and it can even fall
A key reason is simple: most male estradiol comes from aromatizing testosterone. If nandrolone heavily suppresses your endogenous testosterone, you may reduce the main “feedstock” that keeps estradiol normal.
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In a controlled study in normal men comparing testosterone enanthate vs nandrolone decanoate, estradiol rose in the testosterone group but fell in the nandrolone group.
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Other clinical contexts can differ (for example, trials exist where estradiol is reported as not changing significantly on nandrolone).
3) Practical takeaway for the “Deca dick” discussion: estrogen is usually a modifier, not “the one hormone explanation”
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On Deca-only, a common pattern is low androgen + sometimes low/low-normal estradiol, because testosterone production is suppressed and nandrolone doesn’t replace testosterone’s full DHT/aromatization behavior.
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On Deca + high test, estrogen issues can flip the other way (more “high E2” style sides), because now you’ve added a lot of aromatizable testosterone—and when that’s paired with nandrolone’s progestin-like activity, it can be a potent recipe for more pronounced estrogenic-type side effects in susceptible users than high-dose testosterone alone.
Bottom line: estrogen matters, but the better framing is overall hormone balance + tissue androgenization. Nandrolone shifts both differently than testosterone.
Why one guy gets wrecked and another feels fine
Because sexual function is a systems output. Huge variables include:
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Baseline testosterone/estradiol/SHBG
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How hard suppression hits you
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Dopamine tone, sleep, stress, performance anxiety
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Tissue differences (enzyme expression varies)
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What else is in the stack
This is why “it’s prolactin bro” spreads easily: it’s simple. It’s just not reliable.
If you want to stop guessing and get data
Not medical advice—just the logical way to turn “forum theories” into something measurable:
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Total testosterone + free testosterone
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LH / FSH (to see suppression context)
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Estradiol
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Prolactin (measure it—don’t assume it)
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Optional: DHT, SHBG, thyroid markers if symptoms suggest
If symptoms are severe or persistent, involving a clinician is the smart move.
Bottom line (myth vs truth)
Myth: “Deca dick = prolactin.”
Truth: Nandrolone cannot be “converted to prolactin,” and it doesn’t act by binding prolactin receptors like it binds androgen receptors. If prolactin plays a role in some cases, it’s usually indirect.
Most consistent explanation:
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Suppression → low endogenous testosterone and low DHT
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Nandrolone → DHN → weaker androgen signaling in key tissues
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Progestin-like signaling → libido “tone” shift in susceptible users
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Caber can relieve symptoms via dopamine/prolactin pathways without proving prolactin was the root cause
That’s the real “science order” behind the deca-dick story.