• Whether you are a VET or a beginner, this is the place to be. Click the REGISTER link below to proceed. Give us an intro after joining!

Anabolic Steroids and Organ Systems

Durro NoHurtNoBigShirt

EL SuperMod
Staff member
SUPER MOD
Messages
1,075
Reaction score
1,937
Points
113

The Scientific Breakdown: Anabolics and Organ Systems​

Liver (Hepatic system):
Oral anabolic steroids are often 17α-alkylated, meaning they’re chemically modified to survive digestion. This puts the liver front and center as the filtration battleground.
Moderate/controlled use: The liver usually adapts, processing the compounds without lasting harm if cycles are short and monitored. Enzymes like ALT and AST may elevate but can return to baseline after discontinuation.
Abuse: Prolonged or high-dose use can trigger cholestasis (blocked bile flow), hepatocellular damage, and in extreme cases, liver tumors or peliosis hepatis (blood-filled cysts that can rupture). Essentially, the liver becomes a clogged, overstressed filter.

Cardiovascular system (Heart and blood vessels):
Steroids shift the lipid balance in your blood.
Controlled use: Even small doses can lower HDL (“good” cholesterol) and raise LDL (“bad” cholesterol). Blood pressure might creep upward as water and salt retention increase.
Abuse: The heart muscle itself thickens (left ventricular hypertrophy), arteries stiffen, and plaque builds faster. The risk of myocardial infarction (heart attack) and sudden cardiac death skyrockets, especially when paired with stimulants or poor diet.

Kidneys (Renal system):
The kidneys filter waste and regulate electrolytes.
Controlled use: They’re not directly targeted by most injectables, but increased blood pressure and elevated protein metabolism can still add stress.
Abuse: Long-term high doses can cause focal segmental glomerulosclerosis (scarring in the kidney’s filtration units). Combine that with hypertension, and you’ve got progressive kidney damage.

Endocrine system (Hormone regulation):
Steroids mimic testosterone, overriding the hypothalamic-pituitary-gonadal (HPG) axis.
Controlled use: The brain senses extra androgens and temporarily shuts down natural testosterone production. After a cycle, post-cycle therapy (PCT) can help restart it.
Abuse: Chronic use can lead to permanent suppression, testicular atrophy (shrinking), infertility, and gynecomastia (male breast tissue growth) from estrogen conversion.

Brain and Mood (Neuroendocrine effects):
Androgens influence neurotransmitters like dopamine and serotonin.
Controlled use: Users may feel more driven, focused, confident, and sexually energized.
Abuse: “Roid rage” isn’t just gym folklore, it’s linked to dysregulated serotonin and increased aggression. Long-term abuse is associated with anxiety, depression, and even structural brain changes in memory and emotional centers.

Other Organs/Tissues:
Skin:
Moderate androgen use can thicken skin and increase oil production (sometimes a plus for youthfulness). Abuse tends to cause severe acne and cysts.
Immune system: Short-term androgens can stimulate repair and recovery. Long-term abuse weakens immunity, leaving the body more open to infections.

Below is an AAS monitoring Panel:
Screen Shot 2025-08-26 at 08.38.42.webp



Example cycle timeline data:

Screen Shot 2025-08-26 at 08.42.18.webp


Lipids chart: HDL (protective) typically falls, LDL (atherogenic) rises on AAS—especially with 17-alpha-alkylated/oral compounds. If your HDL line dives under ~40 and LDL climbs past ~160, risk is stacking.
Screen Shot 2025-08-26 at 08.46.15.webp



Hematocrit + Blood Pressure: Androgens stimulate red-cell production. Hematocrit (Hct) often creeps up to 54% is a red flag threshold used in testosterone guidelines. Rising blood pressure adds load to the heart. If your Hct line kisses 54% or systolic BP pushes 140+, that’s where you “park the car and check the engine.
output.webp




Liver enzymes (ALT/AST): Orals and 17α-alkylated agents can cause hepatocellular stress and cholestasis. Transaminases above 3× ULN or persistent bilirubin/ALP/GGT elevation means stop and evaluate (jaundice/dark urine is also urgent).
Screen Shot 2025-08-26 at 08.46.55.webp



Hormonal axis: On-cycle, LH/FSH flatline (pituitary shuts down); total T can look sky high if you’re pinning testosterone, but that’s external, not natural production. After PCT, LH/FSH should rebound; if they don’t, you’re not recovering. Long term AAS use is linked to cardiac remodeling and premature atherosclerosis, this is where the hematocrit/lipids/BP cocktail bites

Screen Shot 2025-08-26 at 09.00.59.webp

What to test, why it matters

Use the AAS Monitoring Panel table I dropped above as your checklist. Here are the biggest tripwires and what they mean.

Hematocrit 54% hold or reduce androgens; rule out sleep apnea, your clinician may consider therapeutic phlebotomy.
HDL 40 mg/dL + LDL 160 mg/dL (or ApoB 90 mg/dL)you’re building plaque faster; discuss stopping orals, lowering dose, adding lipid therapy. AAS induced HDL collapse is a known phenomenon.
ALT/AST 3× ULN or bilirubin/ALP/GGT up suspect drug induced liver injury, especially with 17α-alkylated orals; cholestasis and even peliosis hepatis are documented.
eGFR declining or urine albumin creatinine 30 mg/gearly kidney stress; FSGS has been reported in long-term AAS using bodybuilders.
BP persistently 140/90 cardiac risk accelerates; combine with lipid/Hct elevations and the risk gets non linear. Long-term AAS use is associated with LV dysfunction and atherosclerosis.

Interpretation cheat codes
If your HDL line plunges & LDL/ApoB climb:
Pull oral AAS first, cut dose, push omega-3s/fiber/steps, and talk with your clinician about lipid lowering if the graph doesn’t bend.

If Hct rises toward 54% while BP ticks up: Blood is literally getting thicker while pipes are pressurized. Lower dose, hydrate, check sleep apnea, and coordinate care; do not tough it out.

If ALT/AST drift up mildly during hard training: Trend them, disproportionate GGT/ALP/bilirubin changes point more toward cholestasis than muscle breakdown. Orals notoriously drive that pattern.

If LH stays flat post-PCT: Your pituitary hasn’t woken up... That’s when fertility/libido/mood issues drag. Re-test in 2–4 weeks and plan with a physician.

A word on kidneys

Big muscle mass can nudge creatinine up even if kidneys are fine, that’s why pairing eGFR with cystatin-C and urine albumin-creatinine is smart. When users take AAS long term, there are published clusters of FSGS, that’s scarring of the filters, often with protein in urine first. Don’t wait for swelling; watch the urine marker.

In Conclusion

In small, controlled doses with medical oversight, anabolics can drive muscle growth, boost recovery, and give a temporary edge. However, the organs always pay a service fee, such as altered lipids, mild strain on liver and kidneys, and suppressed hormone production. When pushed into abusive territory high doses, stacked compounds, and long cycles the price escalates to organ damage, cardiovascular disease, and irreversible endocrine dysfunction.

The more you know!
 
Always check, before, during, after. That cruise phase is crucial.
 
Back
Top