Outcome

Oil production plus blocked follicles, worst on back and shoulders. Tracks androgenic strength more than dose.

Hostility and short fuse. Reported consistently by users and in case series, and produced in blinded trials mainly at supraphysiological doses and mainly in a minority of people.

Restlessness, racing thoughts, a wired feeling. Multiple routes reach it: neurosteroid changes at GABA-A, glucocorticoid signalling, sleep loss and thicker blood.

Hunger drive. Some compounds raise it sharply and others kill it, and either can decide whether a diet phase works.

Plaque building in artery walls. The slow, silent, cumulative cost, driven by years of shifted lipids and pressure rather than by any single cycle.

Bile flow stalling in the liver. Itching, dark urine and jaundice, and a reason to stop rather than push through.

Blood clotting where it should not. Rises with haematocrit, and this is the reason a red cell count is worth watching rather than admiring.

Memory, focus and processing speed. It is the endpoint the nootropic peptides claim, and the one that is hardest to measure honestly outside a controlled trial.

Difficulty stopping despite harm, with low mood, lost drive and fatigue on withdrawal. Recognised as a genuine dependence syndrome in around a third of long-term users, not a character failure.

Low mood, flat drive and anhedonia. Concentrated in the withdrawal window after a cycle, when natural testosterone has not yet restarted.

Willingness to start things and to keep going. Reported separately from mood and separately from libido, and it moves separately: compounds exist that lift mood and flatten drive, and the reverse.

A narrowed range in both directions: less low, but also less warmth, less connection and less feeling for other people. Distinct from loss of pleasure, which is about reward specifically. Worth separating because the person experiencing it often rates it as an improvement while the people around them do not.

Depends on nitric oxide signalling, which needs DHT and adequate estradiol. Compounds that suppress natural testosterone without providing strong androgenic signal are the classic cause of failure here.

A lifted, expansive, everything-is-working feeling, arriving within days on some compounds. Recorded because it is real, because it is a large part of why people continue, and because it is the strongest single predictor of the dependence pattern further down. Not marked as good or bad: it is the reward that makes the rest of the list acceptable to the person having it.

Planning, switching between tasks, and holding back a response you are about to make. The last of those is the one that matters here: reported aggression on these compounds is often better described as a failure of the brake than as an increase in anger.

Total body fat. It is the endpoint the whole fat-loss class is measured on, and the one place where the incretin drugs have hard trial data rather than mechanism.

Freedom from pain, urgency and bloating. It is the outcome the gut-repair peptides are actually taken for, ahead of any measurable change to the lining.

Glandular breast tissue growth in men. Two separate routes reach it, estrogen and prolactin, and treating the wrong one does nothing.

Elevated mood, high energy, low sleep need, impaired judgement. The best-documented psychiatric effect of high-dose androgens, seen in a minority under blinded conditions.

Sperm count falling to subfertile or zero. Common on cycle, usually recovers over months to years, and occasionally does not.

Difficulty falling or staying asleep, often with night sweats. Its own problem, and an amplifier for every mood effect above it.

A lower threshold for annoyance, distinct from outright aggression and far more commonly reported.

How joints feel under load. Improved by fluid and collagen support, worsened by compounds that dry tissue out.

Muscle actually gained. The reason any of this is being taken.

Muscle lost alongside fat during rapid weight loss. Roughly a quarter to a third of the weight lost on a GLP-1 agonist without resistance training is lean tissue, which is why the newer dual agonists are engineered to spare it.

Thickened heart wall with reduced filling and relaxation. Documented in long-term users on imaging, and it does not fully reverse in everyone who stops.

Sexual desire. Needs androgen, a workable estradiol level and prolactin that is not elevated, so it fails from several directions at once.

Benign or malignant liver growths reported after prolonged high-dose oral steroid use. Rare, serious, and tied to years rather than weeks.

Things that used to be enjoyable stop landing. Distinct from low mood: a person can have normal mood and still get nothing out of food, sex, music or company. Reported most on the progestogenic and prolactin-raising compounds, and it is the effect people most often fail to name because it does not feel like sadness.

Permanent thinning at the crown and hairline in those genetically predisposed. Androgens accelerate a process that was already going to happen, and the loss does not come back.

Day-to-day mood and sense of wellbeing, as distinct from a diagnosable mood disorder. It moves in both directions on these compounds, and the direction is not predictable from how strong the compound is.

Fast shifts between states rather than a sustained one. A different claim from either raised or lowered mood, and it is the one most often reported by partners rather than by the person taking the compound.

The dose-limiting side effect of every incretin drug. It comes from the same delayed gastric emptying that produces the appetite drop, so it is not separable from the mechanism, only titratable.

Intense, unpleasant, memorable dreams, usually alongside broken sleep and night sweats. Named separately from insomnia because people report it even when total sleep time is normal, and because it is one of the few effects that reliably resolves within days of stopping.

Discrete episodes of overwhelming fear with a physical surge: pounding heart, breathlessness, a conviction that something is badly wrong. Different from sustained anxiety and worth its own entry because the plausible route is different too, running through sympathetic tone and a raised resting heart rate rather than through mood.

Suspicion of other people's motives that does not respond to evidence. Reported on the strongest compounds and named directly in the older user-facing notes on trenbolone. The evidence is case reports and self-report, and the self-report is unreliable in exactly the way the symptom predicts.

Blood-filled cavities in liver tissue. Rare, associated with long-term 17-alpha-alkylated use, and can bleed without warning.

How fast simple mental operations run. Included because it is the measure that moves with sleep debt, so it separates a genuine cognitive effect from an effect of being tired.

A larger prostate with weaker urine flow and night waking. Driven by DHT more than by testosterone itself.

Darkening of the skin, including existing moles. It is the intended effect of the melanotans and the reason dermatological review before and during use is not optional.

Breathing interruptions during sleep. Worsened by weight gain, fluid retention and neck mass, and it drives daytime blood pressure up further.

How restorative sleep is, as opposed to how much of it there is. Deep and REM sleep are where growth hormone is released and where memory is consolidated, so this is the measure that connects a sleep effect to a memory effect. A person can sleep eight hours and get almost none of this.

Mental rotation and navigation. The cognitive domain with the clearest sex difference and therefore the one most often tested in androgen studies. Effects reported are small and inconsistent.

Force produced. Rises faster than tendon and ligament can adapt, which is the risk built into the benefit.

Thoughts of ending your life, most often reported in the weeks after stopping rather than during use, when natural testosterone has not restarted and mood has not recovered. It is documented in case series and in withdrawal cohorts. It is listed here because leaving out the most serious outcome in the group would make everything above it read as the full picture.

A tendon tearing under load it should have handled. The classic pattern is a fast strength gain on a dry compound with connective tissue that has not caught up.

Shrinkage from lost LH signalling. Usually reversible, and the visible sign that the axis is switched off.

Recall of words, names and conversation. Studied in testosterone trials in older men with mixed and generally small results, which is worth stating plainly: this is one of the few cognitive measures here with any controlled human data at all, and the data does not show a large effect.

Male traits appearing in a female user: deeper voice, facial and body hair, clitoral growth. Voice change and clitoral growth are usually permanent, which makes this the one side effect that cannot be managed after the fact.

Fluid held under the skin and in tissue. Cosmetically a smoother look, clinically a blood pressure and a strain on the heart.

The cluster that arrives after stopping, while the natural axis is still shut down: flat mood, no drive, no libido, disturbed sleep, and in some cases suicidal thoughts. Separated from dependence because dependence is about the pull to continue and this is about what happens when you do not. It is the window in which almost all of the serious psychiatric events in the literature occur.

Holding and manipulating information over seconds. The cognitive measure most sensitive to lost sleep and to raised cortisol, which makes it the one most likely to move on these compounds and the one least likely to be noticed as a cognitive effect rather than as tiredness.