Steroids and SARMs: Making a Bad Decision Properly

I got contacted about steroids again recently.

That “again” is the reason this page exists. It has happened several times now, from several directions, and the messages are close enough to identical that I have started recognising the shape of one before I finish reading it. Someone is about to start, or has already started, and the person asking has correctly worked out that everyone else they could ask is either selling something or moralising.

Two things, up front.

I will not help you source anything. Not a lab, not a vendor, not a name, not a “guy who is solid”. Don’t ask. I won’t answer, and if I did answer I would be wrong within six months, because the operation that was reliable last spring is now three different people using the same logo.

I will help you make the decision properly. Even when it is a bad decision. This is a bad decision. I have written that sentence in a chat window enough times now that it seemed more efficient to write it once, here, with everything that should come after it.

So this is the whole thing in one place. Every time somebody asks me from now on, they get this link.

The specific case that started this

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Someone contacted me about a guy who was about to start trenbolone. Not testosterone. Trenbolone. First cycle. No test base, no bloodwork planned, no PCT, no idea what an aromatase inhibitor was or why he might need one.

His entire reasoning was “big muscle”.

He is not an outlier. He is the median case. He is on his way to a compound that has never been approved for human use in any country, that exists to put weight on cattle before slaughter, and he thinks the worst outcome on the table is acne.

Three videos, watch them first

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Before the pharmacology, watch these. They are funny. They are supposed to be funny. Derek at More Plates More Dates has built a genre out of reading tren logs aloud, and it works because the material writes itself.

Watch them anyway, and notice the thing underneath the comedy: not one of these people thought this would happen to them. Every one of them was going to be the exception.

TREN - The Movie. Start here. It is the full arc, compressed.

16 Year Old On Tren. Sixteen. On the compound with zero human safety data, during the exact window when the axis you are shutting down has not finished forming.

Riding The Bus To Meet Fat Girls On Tren. The one that best captures what the judgement impairment actually looks like from the inside, which is to say: entirely reasonable.

The joke in all three is the same joke, and it is that the narrator cannot hear himself. That is not a personality flaw specific to those men. It is a documented, dose-dependent effect of the drug, and it is coming for your judgement too. See section 14.

1. Anabolic vs androgenic: the ratio that lies to you

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Every compound gets listed with two numbers, like “Nandrolone: 125:37”. That is the anabolic:androgenic ratio, with testosterone set at 100:100.

• Anabolic = tissue building. Muscle, bone, red blood cells, nitrogen retention.
• Androgenic = masculinising. Body hair, prostate growth, sebum, scalp hair loss, aggression, voice.

Here is the part nobody explains: both effects run through the same receptor. There is one androgen receptor. There is no muscle receptor and no separate prostate receptor.

So where does the “dissociation” come from? Almost entirely from 5α-reductase, an enzyme that is abundant in skin, scalp and prostate and nearly absent in skeletal muscle. In those tissues, testosterone becomes DHT, which binds the receptor considerably harder. A compound that gets weakened by 5α-reductase instead of amplified will look selectively anabolic. Not because it is clever. Because it does not get boosted in the tissues where boosting causes the problems.

Nandrolone is the textbook case. 5α-reduction turns it into dihydronandrolone, which binds worse than nandrolone does. Hence the flattering number.

Two things follow:

1. The ratios come from rats. Specifically, levator ani muscle weight measured against prostate and seminal vesicle weight in castrated rodents. They were never validated as predictors of human side effects, and they are not one.
2. A low androgenic rating does not mean you keep your hair. Nandrolone still causes hair loss in men who were genetically going to lose it. Ask anyone who found out the expensive way.

Treat the numbers as trivia, not as a safety rating.

2. The hormones you need to understand

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This is the part most guides skip, which is exactly why most users are flying blind. You do not need a biochemistry degree. You need five things and how they connect.

Testosterone

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The reference compound. Made in the Leydig cells of the testes, on instruction from luteinising hormone (LH).

In your blood it exists in three states:

“Free plus albumin-bound” is bioavailable testosterone, and it is what actually does anything. This matters more than people realise, because total testosterone can read perfectly fine while free testosterone is on the floor, or the reverse, depending entirely on SHBG.

What it does: muscle protein synthesis, bone density, libido, red blood cell production, mood, drive, and sperm production via its concentration inside the testes.

Estradiol (E2)

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Read this twice. Getting it wrong is the single most common self-inflicted disaster in this entire hobby.

Estradiol is made from testosterone by aromatase, mostly in fat tissue but also in brain, bone and testes. More body fat means more aromatase means more conversion.

Men need estrogen. It is not a female hormone you tolerate. It is a hormone you require.

E2 in men handles:

• Bone density. Estrogen, not testosterone, is the primary regulator of bone in men. Men with aromatase deficiency get osteoporosis on normal testosterone.
• Libido. A large fraction of male libido is E2-mediated. Crash your estrogen and your sex drive disappears even at 1,500 ng/dL of testosterone.
• Erectile function.
• HDL and lipid handling.
• Cognition and mood. Estrogen is strongly neuroprotective.
• Joints. The comfortable, lubricated kind.

Yes, too much causes gynecomastia and water retention. Too little is worse. Crashed E2 gives you joint pain, no libido at all, erectile dysfunction, depression, anhedonia, insomnia, fatigue and bone loss, and it is considerably harder to reverse quickly than high E2 is.

The most common self-destruction sequence in this space, and I have now watched it in slow motion more than once:

Guy feels bad → assumes high estrogen → takes an aromatase inhibitor → feels worse → concludes his estrogen must be even higher → takes more → crashes E2 into the floor → is now genuinely miserable and cannot work out why.

Nobody in that chain ever ordered a blood test.

DHT (dihydrotestosterone)

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Testosterone converted by 5α-reductase. Binds the androgen receptor considerably harder than testosterone and cannot be aromatised. There is no pathway from DHT to estrogen.

Responsible for: male pattern baldness in men genetically set up for it, prostate growth, body and facial hair, sebum and therefore acne, a decent share of libido and erectile function, and aggression.

The bit nobody mentions: DHT is also the precursor to 3α-androstanediol, a neurosteroid that positively modulates GABA-A receptors. It is anxiolytic. This is part of why 5α-reductase inhibitors like finasteride and dutasteride sometimes produce anxiety and depression alongside the sexual side effects. You are not only blocking hair loss. You are cutting a neurosteroid pathway.

If you are thinking about finasteride to save your hairline while running androgens, understand that you are trading one risk for a different one, not removing a risk.

Progesterone and prolactin

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The pathway everyone forgets about until there is a lump behind their nipple that an aromatase inhibitor will not touch.

19-nor compounds, meaning nandrolone and trenbolone, are significantly progestogenic. They bind the progesterone receptor directly. They also tend to push prolactin up.

Why that matters in practice:

• Progestogenic gyno is not estrogen gyno. An AI will not fix it, because estrogen is not what is causing it. So people take more and more AI, crash their E2, still have gyno, and conclude the universe is rigged.
• High prolactin causes erectile dysfunction, loss of libido, actual lactation, and gyno. This is the real mechanism behind “deca dick” and “tren dick”. Not low estrogen.
• The fix is a dopamine agonist (cabergoline, pramipexole) or dropping the compound. Not an AI.

Also worth knowing: allopregnanolone, a neurosteroid made from progesterone, is a potent GABA-A modulator, and a big part of why interfering with this axis wrecks mood and sleep so reliably.

LH, FSH, and the HPTA

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The hypothalamic-pituitary-testicular axis is the control loop you are about to break.

Hypothalamus  ──GnRH──▶  Pituitary  ──LH/FSH──▶  Testes  ──▶  Testosterone
     ▲                                                            │
     └──────────────── negative feedback ◀────────────────────────┘
                  (testosterone AND estradiol)

• LH tells the Leydig cells to make testosterone.
• FSH tells the Sertoli cells to make sperm.
• Both testosterone and estradiol feed back and shut the loop down. Estradiol is the stronger feedback signal at the hypothalamus, which is exactly why aromatase inhibitors raise LH.

When you inject exogenous testosterone, the loop reads “plenty of androgen present, stand down”. GnRH stops pulsing. LH and FSH fall to near zero. Your testes stop producing and start shrinking. And intratesticular testosterone, normally around 100 times your blood level and required for making sperm, collapses.

That is what shutdown means. It is not a figure of speech.

SHBG

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Sex hormone binding globulin, made in the liver. Binds testosterone, DHT and estradiol.

Oral 17-alpha-alkylated steroids crush SHBG. Which means:

• More free testosterone than your total-T number suggests
• Also more free estradiol, so oral-heavy cycles produce estrogenic symptoms that make no sense against the numbers
• Your total testosterone value stops being a reliable guide on its own

Get SHBG alongside total and free T, or you are interpreting a number that does not mean what you think it means.

3. The conversion map

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This one diagram explains most of what is about to happen to you.

                        ┌──────────────────┐
                        │   TESTOSTERONE   │
                        └────────┬─────────┘
                                 │
              ┌──────────────────┼──────────────────┐
              │                  │                  │
        aromatase          5α-reductase     binds AR directly
      (fat, brain,        (skin, scalp,          (muscle)
       bone, testes)        prostate)               │
              │                  │                  │
              ▼                  ▼                  ▼
      ┌───────────────┐   ┌─────────────┐   ┌───────────────┐
      │   ESTRADIOL   │   │     DHT     │   │ MUSCLE GROWTH │
      └───────┬───────┘   └──────┬──────┘   └───────────────┘
              │                  │
     bone density            hair loss
     libido                  prostate
     HDL                     acne, sebum
     mood, cognition         body hair
     joint comfort           libido, erections
     neuroprotection         aggression
              │                  │
              │                  ▼
              │          3α-androstanediol
              │         (GABA-A, anxiolytic)
              ▼
   negative feedback → shuts down LH/FSH

What falls out of it:

• Blocking aromatase does not just stop gyno. It also removes bone protection, libido, HDL support, joint comfort and neuroprotection. Use one deliberately, on evidence, or not at all.
• Blocking 5α-reductase to save your hair also removes a neurosteroid pathway and a chunk of your libido.
• Every arrow you interfere with has downstream effects you did not intend. This is a connected system, not a row of independent dials.
• Compounds that do not aromatise (tren, masteron, primo, oxandrolone, most SARMs) still shut down your natural production, but produce no estrogen of their own. Run one without a testosterone base and you get androgen high, estrogen zero. That is the joint pain, the flat mood, the dead libido, the general misery. “You need a test base” is one of the few pieces of gym-floor advice that is mechanistically correct.

4. The compounds, with half-lives

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Testosterone esters

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All of these become the same molecule. The ester only controls release rate. A milligram of testosterone is a milligram of testosterone. The difference is how fast it arrives, and how much of the weight you injected was ester rather than hormone.

19-nor compounds

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Progestogenic, prolactin-raising, heavily suppressive.

DHT derivatives

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Do not aromatise. Higher hair-loss and prostate risk.

Orals (17-alpha-alkylated)

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The alkyl group at C17 lets them survive first-pass liver metabolism. That is also precisely why they are hepatotoxic. All of them destroy HDL and raise blood pressure.

5. Trenbolone gets its own section

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Because it is the compound that prompted the whole article, and because of the three videos at the top.

What it actually is

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Trenbolone is a veterinary compound. Its legitimate use is cattle implants, to improve feed efficiency and put lean mass on animals before slaughter. It has never been approved for human use in any country. There is no human clinical dataset. There is no therapeutic dosing guidance. There is no literature on what it does to a 22-year-old over five years, because no ethics committee on earth would approve finding out.

The pharmacology, briefly

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• It binds the androgen receptor very hard. You will see “five times testosterone” repeated everywhere. The number I can actually source is from Bauer et al. 2000, who measured 17β-trenbolone’s affinity for the human androgen receptor as similar to DHT, with its main metabolites falling to under 5% of that. DHT is itself several times testosterone. So: extremely potent, yes. The specific multiplier that gets quoted on forums is softer than it sounds.
• It does not aromatise at all. No estrogen from tren, ever. It still shuts down your own production, so without a test base your estrogen goes to zero. This is why running tren alone is catastrophic rather than merely bad.
• Strongly progestogenic, and it raises prolactin. So it causes gyno that aromatase inhibitors cannot touch.
• Hard on the kidneys. Dark urine is common enough that users treat it as a normal feature, which it is not.
• Devastates HDL.

What people actually report

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The recurring pattern, and it is remarkably consistent across sources, is neuropsychiatric:

• Insomnia that does not respond to anything. Not “trouble sleeping”. Multiple consecutive nights of two or three hours.
• Drenching night sweats. Changing the sheets at three in the morning.
• Anxiety, paranoia and a very short fuse, which the user is reliably the last person to notice.
• Depersonalisation. Reports of feeling detached from themselves and from their own decisions.
• Aggression wildly out of proportion to the situation, with real consequences for relationships and jobs.
• Cardiovascular strain beyond what the dose would predict.
• Sexual dysfunction through prolactin, not estrogen.
• “Tren cough”, a violent coughing fit immediately after injecting, generally attributed to the compound reaching circulation directly.

Why it is the worst possible first compound

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1. You have no baseline. You have never run anything. You do not know how you respond to androgens at all, so you cannot attribute any effect to anything.
2. There is no dose-finding. Its potency and narrow tolerability window mean there is no gentle version to start from.
3. Two side effect channels at once, androgenic and progestogenic, which makes troubleshooting hard even for people who have done this for years.
4. The mental effects degrade your judgement, which is the exact faculty required to notice the mental effects. Watch the videos again.
5. Zero human safety data. Whatever dose you pick, you invented it.

If someone is set on using anabolics, trenbolone is not a starting point, and it is not a second cycle either. Whatever you imagine it does can be approached far more slowly with a compound your body already has machinery for.

6. SARMs, and the things sold as SARMs that aren’t

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SARMs are marketed as “steroids without the side effects”. That is false. They suppress your natural testosterone. Several are hepatotoxic. None is approved for human use anywhere. And the products sold online very often do not contain what the label says.

The label problem, with actual numbers

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Van Wagoner et al. bought 44 products marketed as SARMs online and put them through WADA-approved analysis (JAMA, 2017). The findings, stated precisely, because the precision is the point:

Read the last two rows again. In fewer than half of the products, the dose on the label was the dose in the bottle. Roughly half the time you do not know what you are taking, and a quarter of the time you are taking something nobody told you about.

That is a worse position than injecting a known steroid, which is a strange sentence to write and is true anyway.

Actual SARMs

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Sold as SARMs, but not SARMs

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This trips up nearly everyone, including people who have been buying them for years.

• Cardarine (GW-501516) is a PPARδ agonist, not a SARM. Development was abandoned after rodent studies showed cancers across multiple organ systems at high doses over long durations. The dose-relevance argument gets made in every forum thread about it. The compound was still dropped, and nobody has run the human study that would settle the argument.
• SR9009 (Stenabolic) is a REV-ERB agonist, not a SARM. Its oral bioavailability is so poor that swallowing it probably does close to nothing. You are buying an expensive placebo, which is admittedly the mildest failure mode on this page.
• MK-677 (Ibutamoren) is a ghrelin mimetic and growth hormone secretagogue, not a SARM. It does not touch androgen receptors at all. Raises GH and IGF-1. Causes serious hunger, water retention, lethargy, and insulin resistance, which is a real metabolic problem with long-term use rather than a cosmetic annoyance.

The honest summary

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They suppress you, they are unapproved, they are frequently mislabelled, some are hepatotoxic, and the human safety data ranges from thin to nonexistent. They are not a gentler on-ramp. The pharmacokinetic uncertainty plus the product quality problem makes a known testosterone ester the more predictable choice.

7. Why testosterone alone is the least-bad option

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Not safe. Least bad. The distinction is doing a lot of work in that sentence.

Testosterone cypionate, enanthate or propionate, alone, at a modest dose, is the least dangerous entry point that exists. The reasons are mechanical rather than aesthetic:

1. It is bioidentical. Your body has been running testosterone since puberty. Every enzyme, receptor and clearance pathway already exists and is calibrated for it. There is no novel molecule for your liver to puzzle over.
2. It produces its own estrogen. Because it aromatises, you avoid the androgen-high, estrogen-zero disaster that non-aromatising compounds cause. Your joints work. Your mood works. Your libido works.
3. It has an actual human safety literature, from decades of clinical TRT. We know what it does. That is not true of a single other compound on this page.
4. Predictable kinetics, so you can plan a cycle and a PCT around real numbers instead of vibes.
5. The side effects are the ones you would expect and can actually measure: hematocrit, estradiol, lipids, blood pressure.

Adding a second compound does not add a bit of risk. It multiplies your variables. When something goes wrong, and it will, you will not know which one caused it. There is no diagnostic value in a four-compound stack. There is only confusion and more organs under load.

Cypionate vs enanthate vs propionate is a scheduling question, not a safety question. Propionate needs more frequent injections and gives steadier levels. The long esters need fewer injections and take longer to clear before PCT. Pick based on how you feel about needles.

8. Bloodwork: the non-negotiable part

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Get a baseline. Before anything.

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This is the single most important test you will ever run, and you can never get it back afterwards.

Without a pre-cycle baseline you will never know whether you recovered. Post-PCT you will get a total testosterone of 480 ng/dL and have no idea whether that is your normal, or whether you used to run 750 and you have permanently lost a third of your production. That question becomes unanswerable forever the moment you inject.

One caveat that matters: testosterone is not a stable number. It varies substantially day to day and follows a diurnal rhythm, highest in the morning and declining through the day. A single reading is a snapshot with a wide error bar around it.

So: test in the morning, fasted, ideally two or three separate draws a week or two apart, and treat the resulting range as your baseline rather than any single value. Yes, that costs more. It is also the difference between having data and having a number.

The baseline panel

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Two assay notes that matter far more than they sound:

• Estradiol has to be the sensitive assay (LC-MS/MS). The standard immunoassay was designed for female-range estrogen and is unreliable at male concentrations. Ordering the wrong one and then medicating yourself based on the result is a genuinely common own goal.
• Creatinine is confounded by muscle mass. More muscle means higher creatinine with perfectly healthy kidneys. Cystatin C is not muscle-dependent, which makes it far more useful in this population specifically. If your doctor panics at your creatinine, this is the follow-up test to ask for.

Mid-cycle, around week 4 to 6

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Total and free T, sensitive E2, hematocrit, full lipids, ALT/AST/GGT, blood pressure. Add prolactin if you are on a 19-nor.

Compound-specific additions

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9. Reading your own symptoms, and why you’ll get it wrong

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Symptoms matter. They are also not a substitute for bloodwork, and this section exists mostly to show you why.

The estradiol trap

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Six of the most noticeable symptoms appear in both columns. That is the trap. You cannot tell high from low estrogen by feel, and the guess that feels most natural, “I am on steroids so it must be high”, is exactly the one that leads people to crash themselves.

The useful signs are the ones unique to one column. Joint pain out of nowhere means low. Itchy nipples mean high. Everything else is noise until you have a number.

Other patterns worth recognising

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10. Oral vs injectable vs transdermal

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Oral

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How it works: absorbed through the gut, then straight through the liver via the portal vein before reaching circulation. To survive that trip, most oral steroids carry a 17-alpha-alkyl group, which is the modification that makes them liver-toxic in the first place.

• Hepatotoxicity, from elevated enzymes through cholestasis to, rarely, liver failure. Superdrol and Anadrol are the standouts. Nothing in the class is actually benign.
• Lipid destruction. Orals suppress HDL harder than anything else here. Single-digit HDL is a routine finding on an oral cycle, and that is not a cosmetic number, it is atherosclerosis.
• SHBG suppression, which throws off the interpretation of your whole hormone panel.
• Higher blood pressure.
• Short half-lives mean daily or twice-daily dosing and unstable levels.

Alcohol multiplies all of this. Don’t.

Intramuscular injection

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How it works: oil-suspended ester deposited in muscle, slowly hydrolysed and released. Bypasses first-pass metabolism entirely.

• Much easier on the liver. This is the main reason injectables beat orals for the same compound.
• Stable blood levels with an appropriate ester and frequency.
• Injection-specific risks: infection, abscess, nerve damage, sterile inflammation, scar tissue, intravascular injection.
• Requires actual technique. See section 11.

Transdermal

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How it works: gel or cream through the skin.

• Absorption is variable and depends on skin, site and application.
• Skin is rich in 5α-reductase, so proportionally more of it converts to DHT. More hair loss and acne per unit of testosterone than injecting.
• Transfer is a real problem. Testosterone gel transfers to other people through skin contact, and there are documented cases of virilisation in partners and in children. If you share a bed or have kids, this is a practical hazard, not a footnote.
• Mostly used clinically for TRT, rarely for supraphysiological use.

Which route needs which tests

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11. Needles and injection technique

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Get this right and it is boring and uneventful, which is the entire goal. Get it wrong and you get an abscess, a nerve injury, or a hospital visit that involves explaining yourself to a stranger.

If you have read the amphetamine guide, some of the sterile-technique reasoning here will look familiar. It should. The bacteria do not care which drug you were enthusiastic about.

Watch someone do it properly

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Reading about injection technique is not the same as watching it. This is a clinic demonstrating a vastus lateralis (outer thigh) injection, which is the site I would point a first-timer at for exactly the reasons below: you can see what you are doing, you can sit down, and there is nothing important underneath.

Thigh Testosterone Injection, Victory Men’s Health. Watch the pace of the plunger, not just the stab. The slow part is the part people get wrong.

Needle sizes

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Gauge runs backwards: higher number means thinner needle.

The two-needle rule

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Draw with one needle. Bin it. Inject with a fresh one.

Not optional, and not superstition. A needle is measurably dulled after a single pass through a rubber vial stopper. A dull needle hurts more, tears tissue instead of parting it, and can core out a fragment of the stopper and carry it in with the oil. Draw-up needles are sold as such. They are not for injecting.

If you are opening glass ampoules, use a filter needle. Snapping the neck produces microscopic glass fragments that fall into the solution. A 5 μm filter needle catches them. Without one you are injecting powdered glass into your muscle, which does exactly what you would expect it to do. For ordinary rubber-stoppered vials a normal draw-up needle is fine.

Never reuse, and never share

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One puncture, then the sharps bin. Not “if it looks fine”. Not “it was only my own skin”. Not “it is the same vial”. Needles are essentially free and infections are not.

Never share anything. Not needles, not vials, not ampoules. Hepatitis B, hepatitis C and HIV all circulate in injecting populations, and steroid users are routinely left out of the harm reduction messaging that reaches other injectors, apparently on the theory that gym drugs are a different species of needle. Your gym friend’s vial is not your vial.

Sharps disposal: a proper sharps container, returned to a pharmacy or a needle exchange. Loose needles in a household bin injure waste workers, who did not sign up for your hobby.

Aseptic technique

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1. Wash your hands properly. This is the step people skip and it is the one that matters most.
2. Swab the vial stopper with alcohol and let it dry, roughly 30 seconds. Wet alcohol has not worked yet.
3. Swab the injection site, let that dry too.
4. Do not touch either afterwards. Not with a finger to check. Not with the needle tip resting against anything.
5. Do not let the needle touch any surface before it goes in.

Sites

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Vastus lateralis, the outer thigh. Easiest to self-inject and hardest to get wrong. Divide your thigh into thirds from hip to knee, use the middle third on the outer side. Large muscle, nothing important running through it, and you can see the whole thing without a mirror or a contortion.

Ventrogluteal, the side of the hip. Technically the best site: large muscle, thin fat layer, well away from the sciatic nerve. Find it by putting your palm on the bony point of your hip (greater trochanter), index finger on the front hip bone (ASIS), middle finger back along the crest, and injecting into the V between your fingers. Slightly awkward to reach on yourself. Worth learning anyway.

Dorsogluteal, upper outer buttock. The traditional site, now falling out of favour in clinical practice because of the sciatic nerve. If you use it: upper outer quadrant only, and be precise about it.

Deltoid. Small volumes only, 1 mL maximum. Easy to go too high or too deep and find bone, bursa, or the radial nerve.

Rotate. Hitting the same spot repeatedly builds scar tissue that hurts more and absorbs worse over time.

Volume: up to 2 to 3 mL in a quad or glute, 1 mL maximum in a delt. More than that in one site means pain and poor absorption.

Injecting

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Push slowly. Genuinely slowly.

Depending on gauge and oil viscosity, a full injection can take one to two minutes. That is normal. Rushing produces one of two outcomes: oil leaking back out when you withdraw, which is wasted money, or a painful lump that lasts several days, which is avoidable. Rough target: at least 10 seconds per mL, and usually a lot longer with a fine needle or thick oil.

Aspiration (pulling back on the plunger to check you are not in a vein) is genuinely contested. Modern nursing guidance for vaccines says skip it. In this context, injecting relatively large volumes of oil into big muscles, plenty of experienced users still aspirate on glute and quad, because intravascular oil is a real event and is the leading explanation for tren cough and, rarely, pulmonary oil microembolism. Both positions are defensible. If you aspirate, do it properly: pull back, wait two or three seconds, and if blood appears, withdraw and start again with a fresh needle.

Air bubbles: stop obsessing. A small bubble injected intramuscularly is harmless. Even intravenously, a fatal air embolism needs a large volume delivered fast, far more than the speck you are squinting at. Push out what comes out easily and get on with it. Anxiety about bubbles has caused more bad injections, rushed and tense and badly aimed, than bubbles ever have.

Bleeding is normal. You will nick a small vessel sometimes. It is unavoidable and usually irrelevant. Pressure, wipe, carry on. It gets rarer as your technique improves.

Do not inject a muscle you have just trained. Absorption may differ, and more usefully, you will not be able to tell post-workout soreness from an injection problem. The diagnostic clarity is worth more than the convenience.

12. Side effects and what to do about them

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Gynecomastia

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What it is: growth of actual glandular breast tissue. Not fat. Not puffiness.

Two separate mechanisms, which is precisely why people fail to treat it:

1. Estrogenic, from aromatisation. Responds to SERMs and, if genuinely warranted, to aromatase inhibitors.
2. Progestogenic and prolactin-driven, from 19-nors. Does not respond to aromatase inhibitors at all, because estrogen is not the cause.

Early signs: itching or unusual sensitivity in the nipples, then tenderness, then a firm lump directly behind the areola.

SERMs block estrogen at the breast tissue receptor while leaving circulating estrogen alone, which is exactly what you want, since you need that estrogen everywhere else.

• Tamoxifen (Nolvadex), half-life ~5–7 days. The standard choice, generally well tolerated.
• Raloxifene, with some evidence of being more effective specifically at reversing established gynecomastia.

AIs reduce estrogen production system-wide. Blunt instrument.

• Anastrozole (Arimidex), half-life ~46 h. Potent, easy to overshoot.
• Exemestane (Aromasin), irreversible inhibitor, half-life ~24 h, less rebound.
• Letrozole, very potent, and the fastest available route to a crashed E2.

Acne

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Driven by DHT and androgenic sebum production. Usually back, shoulders, chest, face.

• Shower straight after training, and do not sleep in gym clothes.
• Benzoyl peroxide wash, salicylic acid, adapalene. Over the counter in most places.
• Severe cystic acne warrants a dermatologist. Untreated cystic acne scars permanently.
• This stops being cosmetic if it gets bad. Deep cystic acne across the back is genuinely miserable and leaves marks that do not fade.

Hair loss

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If male pattern baldness runs in your family, androgens will accelerate it. Not “might”. The follicle sensitivity is genetic and the androgens are the trigger. You may compress into three years what would otherwise have taken fifteen, and once the follicle is gone it is gone.

Options, none of them clean:

• Accept it. Cheapest and most honest.
• Finasteride or dutasteride, blocking 5α-reductase. Works. Also blocks the DHT-derived neurosteroid pathway from section 2, with a documented minority experiencing sexual dysfunction and mood effects, sometimes persistent. A real trade-off, not internet paranoia.
• Topical minoxidil, no hormonal interference, but a commitment forever. Stop and you lose what you gained.
• Choose compounds with lower androgenic conversion. Helps at the margin. Does not make you immune.

Blood pressure

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Buy a cuff. €30 to €60. Upper arm, validated model, not a wrist one.

Steroids raise blood pressure through several mechanisms at once: water retention from estrogenic compounds, increased red cell mass, direct vascular effects, and simply carrying more body mass. It is the most common serious side effect, the easiest thing on this entire page to measure, and the one people most reliably ignore, because it produces no symptoms at all until something ruptures.

Take it several times a week, same time of day, seated and rested for five minutes first. Write it down.

Cholesterol and lipids

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All anabolics suppress HDL. Orals demolish it. Single-digit HDL readings are routine on oral cycles.

This is not a cosmetic number. Combined with elevated LDL and ApoB, sustained supraphysiological androgen use produces measurable atherosclerotic progression. Ask for ApoB if you can get it, because it counts atherogenic particles rather than estimating cholesterol content, and it is a better risk marker for it.

13. The cardiovascular reality

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This is the section that should change your mind, if anything on this page does.

The mortality data

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In 2025 a group at Padova published the largest study of this that exists, in the European Heart Journal. They took 20,286 male athletes who competed in 730 IFBB events between 2005 and 2020, followed them for an average of 8.1 years (190,211 athlete-years), and searched systematically for deaths through July 2023.

Available autopsies of the sudden cardiac death cases consistently showed cardiomegaly and ventricular hypertrophy.

And at the very top of the sport, restricting to bodybuilders who competed in the Mr. Olympia open category: 7 of 100 died during the study period, including five confirmed or presumed sudden cardiac deaths, at a mean age of 36.

A separate autopsy analysis, Escalante et al. 2022, looked at published autopsy reports of male bodybuilders who died before 50. Mean heart weight was 575 g against a reference of 332 g, about 74% heavier. Left ventricular wall thickness averaged 16.3 mm, roughly 125% of predicted.

That is not a heart adapted by training. That is a heart in trouble.

What is actually happening

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• Left ventricular hypertrophy. Some thickening is a normal training adaptation. Severe concentric hypertrophy is not, and the Padova authors are direct about it: it is rarely found in healthy athletes and points toward anabolic substance use, alongside increased risk of ventricular dysfunction and sudden cardiac death.
• Myocardial fibrosis. Scar tissue in the heart muscle. Fibrotic tissue conducts electricity abnormally, which is the substrate for lethal arrhythmias.
• Impaired diastolic function. The heart gets stiff and fills poorly between beats. Often the earliest detectable change.
• Accelerated atherosclerosis, from the lipid profile above.
• Polycythemia. More red cells means thicker blood means clots, and clots mean strokes and pulmonary emboli.
• Hypertension, accelerating every one of the above.

Some of this reverses when you stop. Some does not. Fibrosis does not unscar. Plaque does not unbuild.

What to actually do

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• Blood pressure cuff, weekly. The cheapest life-saving device you can own.
• Full lipids including ApoB, every cycle.
• Hematocrit monitoring. Above roughly 54%, donate blood, which has the side benefit of doing someone else some good.
• Actual cardio. Zone-2 cardiovascular training, not just lifting. Most people in this space avoid it for fear of losing size, which is a spectacularly bad trade against the numbers in that table.
• If you are in this long-term, get an echocardiogram. It is the only way to see wall thickness and ejection fraction. Ask for one and do not be dramatic about why. “I lift heavily and I want a baseline” is enough.

14. Mental health

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The most underdiscussed part of the whole topic, and the part users are least equipped to assess in themselves. Go back and watch the videos at the top if you need the illustrated version.

On cycle

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• Hypomania, irritability, aggression, short fuse. Highly dose-dependent and highly compound-dependent. 19-nors, and trenbolone in particular, are the standouts.
• Anxiety. Boldenone has a specific reputation for it. So does tren.
• Insomnia, which then amplifies everything else, because no part of your mood survives four nights of bad sleep.
• Impaired judgement about your own state. You will be the last person to notice that you have become difficult to be around. Ask someone who will tell you the truth, and then actually listen to the answer, rather than treating it as evidence that they are the problem.

Coming off

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This is the dangerous window, and almost nobody warns about it.

You have supraphysiological androgen levels for weeks, then near-zero endogenous production, then a slow and uncertain recovery. The crash is real and it is a genuine neuroendocrine event, not a character weakness.

• Depression during PCT and withdrawal is common and can be severe.
• Suicide risk in AAS withdrawal is documented. The Padova mortality data included deaths from suicide and overdose, and the authors specifically flagged the psychiatric side effects of AAS, meaning mood swings, aggression, depression and anxiety, as likely contributors.
• Losing the physique you built adds a psychological hit on top of the biochemical one.

Plan for this before you start. Tell someone you trust that you are running a cycle and that you may not be yourself for a while when you come off. Give them explicit permission to say something to you about it.

Dependence, and the thing underneath it

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AAS dependence is real and affects a substantial minority of users. The pattern is depressingly consistent: you come off, you feel terrible, you look worse, so you go back on. Then “blast and cruise”, never fully coming off, starts to sound reasonable. Then you are on for life, except now it is not a choice you made, it is a choice that was made for you by the previous eighteen months.

I have written about what that looks like from the inside, with different drugs and the same architecture.

Worth asking honestly, before the first injection: what are you actually trying to fix? Muscle dysmorphia is well documented in this population, and combined with substance use it creates conditions that amplify impulsive and self-destructive behaviour. If the honest answer is “I will finally feel okay about how I look”, the compounds will not deliver that. People who reach their goal physique and feel exactly the same afterwards are the rule, not the exception.

15. PCT: the part everyone gets wrong

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The situation you are in

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At the end of a cycle your LH and FSH are at or near zero, your testes have atrophied, and your natural production is off. Exogenous hormone is clearing from your system. Endogenous production has not restarted.

Left alone, you spend weeks to months in a hypogonadal state with no meaningful testosterone from any source. That is the depression, the fatigue, the collapsed libido, and the loss of everything you built.

PCT is the process of restarting the axis.

The mistake everyone makes: starting too early

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Do not begin PCT immediately after your last injection.

SERMs work by blocking estrogen feedback at the hypothalamus, which removes the “stand down” signal and lets GnRH pulses resume. If there is still a supraphysiological amount of testosterone circulating from your last shot, that androgen is still suppressing the axis regardless of what you do to estrogen feedback. You have spent four to six weeks of expensive SERM achieving nothing, on a body that was never going to restart during that window anyway.

Wait until the ester has substantially cleared, roughly 4 to 5 half-lives.

A common structural fix: if your cycle ends on a long ester, transition to a short ester like propionate for the last two or three weeks. That cuts the wait from three weeks of hypogonadal limbo down to a few days.

The compounds

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SERMs are the actual PCT. They block estrogen receptors at the hypothalamus, removing negative feedback, which restarts GnRH, then LH and FSH, then testosterone.

• Tamoxifen (Nolvadex), half-life ~5–7 days. Generally better tolerated than clomiphene, and directly protective against gyno at the breast tissue as a bonus.
• Clomiphene (Clomid), half-life ~5–7 days overall, but it is a mixture of two isomers: enclomiphene, the useful antagonist, and zuclomiphene, a weak agonist with a half-life around 30 days that accumulates. That accumulation is the likely reason for clomiphene’s reputation for visual disturbances and emotional side effects.
• Enclomiphene, the isolated useful isomer without the accumulating one. Cleaner, where you can get it.

hCG is useful, but it is not PCT. Human chorionic gonadotropin mimics LH and acts directly on the Leydig cells, telling them to produce testosterone regardless of what your pituitary is doing. Half-life ~24 to 36 hours.

Where hCG genuinely helps: during a cycle, or in the gap between the last injection and the start of PCT, to maintain testicular size and Leydig cell responsiveness so there is something functional left to restart. Stop it before PCT begins.

AIs during PCT: usually no. Post-cycle estradiol can rise as your body re-equilibrates and there is a temptation to control it. Generally, don’t. SERMs already block estrogen where it matters for recovery, and crashing E2 during PCT adds joint pain, depression and anhedonia to a period that is already difficult. Only with bloodwork showing genuinely high E2, and even then cautiously.

A basic structure

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Illustrative, not a prescription. Protocols vary and yours should be built around your compounds and your bloodwork.

That final blood test is the entire point. Without it you do not know whether you recovered. You only know whether you feel recovered, which is a different thing, and which is exactly what the pre-cycle baseline was for.

When recovery doesn’t happen

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It is not guaranteed. That part deserves to be said out loud.

Risk factors for permanent hypogonadism:

• Longer cycles
• Higher doses
• Starting young, before your axis had finished maturing
• 19-nors, which are notoriously slow to clear and slow to recover from
• Blast and cruise, never fully coming off
• Multiple cycles without full recovery in between

Some people never recover. They end up on testosterone replacement for the rest of their lives, which means injections forever, permanent infertility unless actively managed, and dependence on a prescription and a supply chain. Some of them started at 21, with one cycle.

If your bloods 8 weeks post-PCT show LH and FSH still flat and testosterone still low, see an endocrinologist. Not a forum. There are real medical protocols for failed recovery and they work considerably better the earlier they start.

16. Fertility

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Spermatogenesis requires intratesticular testosterone at roughly 100 times your blood concentration. That concentration only exists because LH is driving the Leydig cells locally.

Shut down LH and intratesticular testosterone collapses, even while your blood testosterone is the highest it has ever been. Sperm production stops. Many users are functionally azoospermic within months.

• Usually recovers within 6 to 12 months after stopping. Usually.
• Sometimes it does not. Duration, dose and 19-nor exposure all worsen the odds.
• hCG during a cycle helps preserve testicular function and improves the odds.
• Restoration protocols exist (hCG plus FSH or hMG, SERMs) and are run by fertility specialists.

17. What you’re actually injecting

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Everything above assumes the vial contains what the label says. Frequently it does not.

Underground lab product is made without regulatory oversight, without sterility validation, and without analytical verification. The documented problems:

• Wrong dose. Under, over, or wildly variable between vials from the same batch.
• Wrong compound entirely. Cheap testosterone sold as expensive primobolan is a running joke right up until it is your bloodwork.
• Non-sterile production, which is the direct cause of injection abscesses.
• Contamination. Heavy metals, solvent residues, particulates.
• Underdosed or fake orals. Anavar is among the most counterfeited compounds in existence.

And visual checks are close to worthless. Cloudy oil or floating particulate is a red flag, sure. But clean-looking oil tells you precisely nothing. You cannot see 200 mg/mL versus 340 mg/mL, and you cannot see the wrong molecule.

Get it tested. Properly.

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This is the part I would push hardest, because it is the one that actually converts uncertainty into information.

Janoshik Analytical is a real analytical laboratory in the Czech Republic that will test your sample. They run HPLC to quantify how many milligrams are actually in there, and mass spectrometry to confirm which molecule it is. Not a reagent colour chart. An actual lab report with a number on it.

Two things make them worth the paragraph:

1. The results are public and verifiable. Janoshik publishes results at public.janoshik.com, and each report can be checked by test ID. So when a vendor waves a Janoshik certificate at you, you do not have to take their word for it, and you do not have to trust the JPEG they posted. You look the ID up yourself. That is the whole game: a claim you can independently verify beats a claim you cannot, every time.
2. It closes the loop on your own vial. You do not have to rely on a vendor testing their own product on their own schedule. You can send yours.

A steroid quantification is on the order of a hundred dollars per sample, which is roughly one round of the bloodwork you are already committed to and considerably less than an abscess.

Your bloodwork is also an assay

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Even without sending anything anywhere, your mid-cycle bloods are a crude but genuine test of your product. If you are running 500 mg/week of testosterone and your total T comes back at 600 ng/dL, the vial is not what it claims to be. This is the strongest argument for mid-cycle bloods beyond safety: it is product verification you were going to pay for regardless.

Pharmaceutical-grade product, where you can legally obtain it, removes this entire category of risk at a stroke. That is the actual advantage of going through a doctor, and it is a bigger one than most people weigh.

18. The honest cost accounting

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The compounds are cheap. That is the trap. It makes the whole thing look accessible when it is not.

The steroids are the smallest line on that list.

The part I actually want you to take away

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If you are the person who was about to run tren as a first cycle:

1. Don’t. Not first, not second. Whatever you think it does, the cost is not what you have been told it is.
2. If you are going to use anything, testosterone alone. Bioidentical, understood, monitorable, and your body has been running it since you were fourteen.
3. Get baseline bloods before anything. You can never get them back afterwards.
4. Buy the blood pressure cuff. €40, and the highest-return purchase on this entire page.
5. Find out what is in the vial. Janoshik, or at minimum read your mid-cycle bloods as an assay.
6. Plan the PCT before the first injection, not after the last one.
7. Wait for the ester to clear before starting PCT.
8. Tell someone. Someone who will notice if you become unbearable, and who will say so out loud.
9. Understand that recovery is not guaranteed. Some people are on TRT for life because of one cycle at 21.

And honestly: the physiques that actually look good are attainable without any of this. What is genuinely rare is not access to drugs, it is ten consistent years, sleeping properly, and eating like you mean it. That is the boring answer. It is free, it does not cost you your hair, and nobody has ever needed a SERM to recover from it.

I said at the top that I would not talk you out of it, and I have not tried very hard. But I would rather you did this with a blood pressure cuff, a lab report, and a plan, than with a forum post and a vial from a guy.

Appendix: logging templates

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Copy these. The point of writing things down is not diligence for its own sake, it is that memory is extremely accommodating about what happened last month, and a table is not.

Baseline, before anything

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Cycle log

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Weekly tracking

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Injection log

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Rotating sites is much easier when you are writing them down, and so is spotting the pattern when one site keeps giving you trouble.

Sources and further reading

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• Vecchiato et al., Mortality in male bodybuilding athletes, European Heart Journal 2025, 10.1093/eurheartj/ehaf285. The mortality figures in section 13.
• Escalante et al., Dead Bodybuilders Speaking from the Heart, J Funct Morphol Kinesiol 2022, 10.3390/jfmk7040105. The autopsy analysis, with the small-n caveat noted in place.
• Van Wagoner et al., Chemical Composition and Labeling of Substances Marketed as Selective Androgen Receptor Modulators and Sold via the Internet, JAMA 2017, 10.1001/jama.2017.17069. The SARM mislabelling table in section 6.
• Bauer et al., Characterisation of the affinity of different anabolics and synthetic hormones to the human androgen receptor…, APMIS 2000, 10.1111/j.1600-0463.2000.tb00007.x. Where the trenbolone binding claim in section 5 comes from.
• Smoliga et al., Premature Death in Bodybuilders: What Do We Know?, Sports Medicine 2023.
• HAARLEM study, a prospective cohort that followed real-world AAS users through a cycle and afterwards. The closest thing to honest data this field has.
• Janoshik Analytical for compound testing, with public results at public.janoshik.com.
• More Plates More Dates for compound-specific side effect detail and bloodwork interpretation. The three videos at the top are the entertaining end of it, the technical content is the useful end.
• Your local needle exchange. They serve steroid users too, they do not report anyone, and sterile equipment is free.
• If you want to check my reasoning rather than take it: how I read a study, and the twelve-question smell test I run papers through before quoting them.

/Henrik

This is harm reduction information for people who have already made their decision. It is not medical advice, it is not encouragement, and it is not a claim that any of this is safe. Anabolic steroid use carries real risks of permanent infertility, permanent hypogonadism, irreversible cardiac remodelling, and death. If you are struggling with dependence, or with whatever is underneath the decision, help exists. In Norway, start with your fastlege, or Mental Helse on 116 123.