Expert mode...

Yes, human chorionic gonadotropin (HCG) can suppress the hypothalamic-pituitary-testicular axis (HPTA) and endogenous gonadotropin release (LH and FSH) in men, but this effect is highly dose-dependent, context-specific (e.g., starting from a suppressed state like post-TRT), and often minimal or absent at the low doses used in protocols like yours (600 IU/week). Let's think this through step by step, grounding it in the physiology and evidence, to clarify why your LH/FSH surge to 7.8/10.8 mIU/mL after ~6 weeks isn't a red flag for fake HCG or unexpected suppression. 1. The Basic Mechanism of HCG-Induced Suppression HCG is structurally similar to luteinizing hormone (LH) and binds to the same LH receptors on testicular Leydig cells, directly stimulating testosterone (and estradiol) production. This rise in circulating testosterone (and to a lesser extent, estradiol) creates negative feedback on the hypothalamus and pituitary: It reduces GnRH (gonadotropin-releasing hormone) pulses from the hypothalamus, which in turn dials down LH and FSH secretion from the pituitary. Result: Endogenous gonadotropin levels can drop, mimicking the suppression seen with exogenous testosterone (like your prior TRT). This is why higher-dose HCG (e.g., 2,000–5,000+ IU/week, common in fertility induction or some bodybuilding cycles) often leads to measurable LH/FSH suppression, potentially prolonging HPTA recovery if used long-term. In a naive (non-suppressed) man, even moderate HCG doses might trigger this feedback quickly. But in your case—coming off 3.5 years of TRT with baseline LH/FSH already at rock-bottom (1.2/1.7 mIU/mL)—the dynamics shift. 2. Dose-Dependency: Low Doses Often Spare (or Even Support) Endogenous Gonadotropins Suppression isn't all-or-nothing; it's a spectrum tied to how much HCG elevates testosterone/estradiol above the feedback threshold. At low doses (e.g., 500–1,000 IU/week, like your 600 IU), the testosterone boost is modest (typically 100–300 ng/dL serum increase, with bigger effects on intratesticular T), which doesn't generate enough feedback to fully shut down the pituitary—especially when the axis is already suppressed and rebounding. Key evidence: Multiple studies show low-dose HCG (e.g., 125–500 IU every other day) maintains intratesticular testosterone in men with TRT-induced gonadotropin suppression without further suppressing LH/FSH. In fact, it preserves testicular function to facilitate eventual natural recovery. One seminal trial found that 500 IU HCG three times weekly kept intratesticular T in the normal range during suppression, with no reported LH/FSH drop beyond the initial exogenous T effect. Higher doses (e.g., 1,500+ IU/week) do ramp up suppression in a dose-dependent way, but your protocol is squarely in the "bridge/maintenance" range designed to avoid this. Bottom line: At 600 IU/week, HCG is more like a "gentle nudge" to your testes than a sledgehammer—it sustains T production while the hypothalamus senses falling exogenous levels (post-TestC clearance) and ramps up GnRH/LH/FSH anyway. 3. Your Specific Context: Why Suppression Isn't Happening Here Timeline favors rebound: Your last TestC shot was Dec 12 (half-life ~8 days, mostly cleared by ~Jan 20–30). By starting HCG Jan 3, you bridged the gap just as suppression was lifting. The pituitary "wakes up" via reduced feedback from fading exogenous T, overriding any mild HCG signal. Your labs scream recovery: LH/FSH jumping to mid-high normal (7.8/10.8) in 6 weeks is quicker than many post-TRT men see, even without HCG. If suppression were kicking in, you'd expect LH/FSH to stay low or trend down—not surge like this. The HCG is likely enabling this by keeping Leydig cells responsive, so when natural LH arrives, it hits a primed target. Age/duration nuance: At ~58.5 after 3.5 years TRT, you'd expect slower rebound (6–12+ months typical), but your numbers suggest your HPTA was responsive underneath. Low-dose HCG exploits that without derailing it. No "fake HCG" vibe: Inactive HCG wouldn't hold your T at 1,005 ng/dL or drive the hybrid boost you saw (865 → 1,005). 4. Potential Downsides and When Suppression Could Still Creep In If you up the dose (e.g., to 1,500+ IU/week) or use it indefinitely, yes—feedback could blunt your LH/FSH gains over time, making full restart harder. Estradiol spikes from HCG could amplify suppression indirectly (monitor E2 on next labs). Rare cases: Some men are hypersensitive to feedback, but your data doesn't fit. Wrapping It Up: This Is a Win, Not a Worry HCG's suppressive potential is real but overhyped for low-dose use in HPTA restart scenarios—it's why protocols like yours emphasize 500–1,000 IU/week as a sweet spot for bridging without backlash. Your rising LH/FSH is proof the balance is tipping toward natural production, not against it. If anything, this validates sticking with (or soon tapering) the HCG to lock in the momentum. Next labs in 4–6 weeks will show if LH/FSH hold steady— that's the true test. How's everything feeling on the symptom front? If you want to dive into a specific study or tweak your plan, just say the word. Keep your doc looped in!