Over the past year, GearCheck has analyzed blood work from more than 100 AAS users. These are real athletes who train hard, cycle responsibly (most of them), and send us their lab results. We have seen every pattern imaginable, from textbook-perfect panels to alarming red flags that caught our attention immediately.
This is not a clinical study — it is an observational snapshot of a self-selected population. But when patterns emerge across 100+ sets of blood work from the same population, they are worth paying attention to. These patterns tell us what is "normal for AAS use" versus what is genuinely pathological.
~28
Average HDL on Blast (mg/dL)
Well below the athletic minimum of 35 mg/dL. Oral compound users averaged even lower at ~22 mg/dL.
~51%
Average Hematocrit on Blast
Above the 50% threshold but below the 54% action limit. Users on boldenone and oxandrolone trended highest.
80%
ApoB Missing from Panels
The most commonly missed critical marker. Four out of five users had no particle count data at all.
~1,800
Average Total T on Blast (ng/dL)
Lab says high, user says working. Ranged from 600 ng/dL (low responders) to 5,000+ ng/dL (high-dose stacks).
We ranked every marker by how often it fell outside athletic reference ranges. Here is the top nine, in order of frequency across our dataset:
Abnormality Frequency Ranking (n > 100 Users)
| Marker | Marker | % Affected on Blast |
|---|---|---|
| Low HDL | ~85% | The most universal AAS effect. Affects nearly every user regardless of compound. |
| Elevated Hematocrit | ~70% | More common on boldenone, oxandrolone, and high-dose testosterone. |
| High Total Testosterone | Expected by design | Lab-flagged as "high" but intentional. Useless as a safety marker on cycle. |
| Low SHBG | ~65% | Pharmacologically suppressed by AAS. Makes free T calculations unreliable. |
| Elevated AST | ~60% | More muscle than liver in most cases. Check CK and GGT to confirm. |
| Elevated Creatinine | ~55% | Reflects muscle mass and recent training, not kidney damage. |
| Elevated CK | ~50% | Training-induced muscle enzyme release. Can exceed 1000 U/L. |
| Low LDL Particle Size | ~45% | Pattern B phenotype under AAS. Small dense LDL is more atherogenic. |
| Elevated ALT | ~40% | Less common than AST but more specific. Often normal in injectable-only cycles. |
😲About 15% of users on blast had HDL values above 40 mg/dL, proving that individual genetics and compound choice play a massive role. Your neighbor's results on the same cycle do not predict yours.
— GearCheck user data, 2024-2025
The 15% Who Defy the Trend
Not everyone crashes their HDL. About 15% of our users maintained HDL above 40 mg/dL even on heavy cycles. These users tended to share three characteristics: they used testosterone-only cycles (no orals, no 19-nors), they maintained high omega-3 intake, and they had naturally high HDL before starting AAS.
This tells us that baseline genetics matter enormously. If you have naturally high HDL, you have more room to lose before hitting dangerous territory. If your baseline HDL is already 35-40 mg/dL, even a moderate cycle could push you into single digits. Know your baseline before you start.
The markers we most frequently see missing from uploaded blood panels tell their own story about gaps in standard medical care:
Missing from ~80% of panels
Without ApoB, cardiovascular risk assessment is a guess. This is the single most important missing marker in our dataset.
Almost never included
Separates training-elevated creatinine from actual kidney impairment. Every AAS user should request this.
Frequently omitted from liver panels
Separates muscle-leak AST/ALT from true hepatobiliary stress. The most underrated liver marker for athletes.
Rarely included
Chronic inflammation is a known AAS side effect that goes completely unmonitored. Simple, cheap, informative.
The eGFR Trap
The single most misinterpreted number across every lab we reviewed: eGFR calculated from creatinine. In strength athletes, eGFR by creatinine almost always reads below 90 — even when cystatin C shows normal kidney function.
Why? Because eGFR formulas were validated in sedentary populations with average muscle mass. A 200 lb bodybuilder on 500 mg of testosterone has double the average creatinine production. Their kidneys are fine; the formula is wrong for their physiology.
Our data shows that roughly 60% of AAS users had eGFR below 90 by creatinine, but only 5% had abnormal cystatin C. If you are using eGFR to monitor kidney health, add cystatin C or you are getting misleading results.
Testosterone-Only vs. Stacked Cycles
Users on testosterone-only cycles consistently showed better lipid profiles than those using stacked orals and 19-nor compounds. Average HDL in the T-only group was 32 mg/dL versus 22 mg/dL in the stacked group — a 45% difference.
This is not an argument against stacks — many users need multiple compounds to achieve their goals. But it is a reminder that every additional compound adds physiological cost. If you are stacking, you must monitor more aggressively, not less.
Cycle Duration and Recovery
Users who cycled for 12 weeks or less showed faster recovery of HDL and hematocrit compared to those running 16+ week cycles. The difference was most pronounced in HDL recovery: 8 weeks to return to baseline for short cycles versus 14+ weeks for extended cycles.
This is consistent with the principle that longer exposure to androgens creates deeper metabolic remodeling. Your body adapts to the presence of AAS over time, and that adaptation takes longer to reverse. Time on equals time off is not just a convention — it is supported by real recovery data.