MONSTER 2.0 — The Response
The clinical dossier came back. I cannot share the document itself, it is confidential and full of sensitive data, but everything that matters is here: what I asked for, what the physician approved, what got cut, and the one decision I am going to argue with.
I sent the clinic a protocol proposal. Eight thousand words, twenty tables, every dose and volume computed, every red line named in advance. Then I waited.
The answer came back as a fourteen-page physician-signed clinical dossier. Version 2.0, supersedes all prior protocol documentation. Six active agents, eighteen subcutaneous doses a week, one oral.
Most of what I asked for was approved. Two things were cut. One thing was added that I specifically argued against. Three decisions are still open on my side, and the rest of this is why.
Testosterone: asked 250, got 175 mg/week. Fair — but written as one weekly shot, and I am currently splitting it. That is the flag.
HGH: approved. Somatropin 0.6 IU daily. This is the headline.
Retatrutide, BPC-157, TB-500: all approved, two of them at higher doses than I asked for.
HCG: denied. I am going to push back on this one.
NAD+ and the GH peptides: out. Both fine.
Anastrozole 1 mg every other day: prescribed, and I argued against any prophylactic aromatase inhibitor. It contradicts a rule inside the same document.
What the document actually is
This is not a prescription slip. It is a structured clinical record, reference TRTCO-EX-2026-0813-VP, version 2.0, dated 13 August, classified confidential to me and my treating clinicians. It supersedes every prior protocol document I have.
Eleven sections: executive summary, source record and clinical evolution, physician decision summary, the active protocol, therapies removed, risk-benefit architecture, safety parameters, follow-up monitoring, implementation plan, medical recommendations, and the physician authorisation block.
It also states the treatment goals it is built around, which are worth quoting because they are the yardstick everything else gets measured against:
The evidentiary basis is listed explicitly — baseline panel 21 to 24 April, the original prescription 27 April, the ECG of 3 August, my MONSTER 2.0 decision sheet, the reticulocyte and albumin results of 11 August, and the updated protocol record. Six sources, each retained for traceability.
1 · The scorecard
Section three is the part I appreciated most. My proposal and the physician's decision sit side by side in parallel columns, so nothing quietly disappears in translation.
Seven of nine went my way or close to it. My entire safety architecture was adopted verbatim, and the three markers I asked to add that had never been measured total protein, potassium, magnesium are all in the follow-up plan. The proposal was clearly read line by line, which is more than I expected.
2 · Everything they measured
The dossier carries a complete biomarker surveillance panel: every marker traceable to my record, grouped by domain, with documented results separated from pending results and from follow-up monitoring points. Here it is in full.
Cardiac: ECG normal, normal sinus rhythm, PR 152 ms, QRS 104 ms, QTc 379 ms, classifier confidence 81 percent. Body weight 105 kg, patient-reported. Body composition listed as follow-up — I still do not have a DEXA in this record and I should.
The movement since baseline, which is the part that earned the escalation:
3 · Testosterone: 175 is right. Once weekly is not.
I asked for 250. I got 175, with explicit reasoning: a trough of 712.60 on 100 mg already makes me a strong responder, estradiol sits at 99.6 percent of its ceiling, haemoglobin moved 15.7 to 17.0, ferritin fell 39 percent. Stepwise titration, reassess, escalate only on evidence.
No argument. That is the conservative read of my own data and my proposal admitted 150 was defensible. 175 is still a 75 percent increase on what I run now.
The open question is the frequency, and it is the first of the three.
Nothing in the document acknowledges that this reverses a change already in place. It may simply be the default template. But at 175 mg it is a real pharmacokinetic decision, and it is the one that feeds the anastrozole question directly.
Cypionate has a half-life around eight days. At the same weekly total, the schedule alone decides how flat the curve is:
Daily is 25 mg — ten units. A ten-unit subcutaneous injection is nothing; it is smaller than my current BPC shot. And it produces a nine percent swing instead of eighty-three.
Why that matters beyond neatness: aromatase gets more substrate at the peak. A once-weekly 175 mg peak is the highest androgen concentration I would ever see, and it is exactly where oestrogen conversion, water retention and haematocrit pressure concentrate. Flatten the curve and you reduce the peak-driven part of all three without touching the weekly dose.
Bigger weekly dose + longest possible interval → highest possible peak → more oestrogen conversion at that peak → a large aromatase inhibitor prescribed to manage an effect the dosing schedule partly created.
Splitting does not eliminate dose-driven aromatisation — the 75 percent increase is the dominant variable and nothing fixes that. But daily or every-other-day dosing, measured at the new steady state, would test whether the inhibitor is needed at all.
Starting 175 once weekly and 3.5 mg of anastrozole a week simultaneously destroys that information permanently.
Practical detail from the protocol: application into lower abdominal subcutaneous tissue or outer thigh, morning, same day each week — and testosterone and retatrutide are to be anchored to the same weekday. That anchoring instruction still works on a split; it just becomes two anchors instead of one.
4 · Anastrozole — and why I am not simply accepting it
In the proposal I made a specific case against a prophylactic aromatase inhibitor. Estradiol at 43.84 is at the top of range but I have no symptoms — no gynecomastia, no nipple tenderness, no oedema, no sexual dysfunction. The failure mode of an inhibitor is crashing oestrogen, and below roughly 15 pg/mL that costs bone mineral density, joint health, lipids and libido.
The prescription is 1 mg orally, every other day, with the stated purpose of estradiol management during therapy and instruction to reassess estradiol and symptoms.
What that dose is
One milligram every other day averages 3.5 mg per week. Anastrozole's half-life is about two days, so this is sustained inhibition rather than intermittent microdosing. It is half the standard oncology exposure used to suppress oestrogen in breast cancer.
Straight dose proportionality would take 43.84 to roughly 76.72 at 175 mg/week untreated. Then apply suppression:
A defensible expectation, accounting for the dose increase pushing the untreated value up, is 15 to 30 pg/mL — with sub-10 entirely plausible if I turn out to be inhibitor-sensitive. Nobody can predict that from one untreated measurement.
It matters more for me than for most people because my HDL is 39 and already below range. Oestrogen blockade lowers HDL and compounds the pressure testosterone is already applying. I just got ApoB back at 81.28 with no particle discordance, which established the low HDL as a testosterone effect rather than metabolic dyslipidemia. An aromatase inhibitor is the single intervention most likely to undo that.
The contradiction inside the document
Mine is 43.84, and I have no symptoms.
By the document's own trigger, nothing about my estradiol currently requires action — and the same document prescribes 3.5 mg of anastrozole a week, prophylactically, from day one.
That is not a matter of opinion. It is internal to the plan, which is why it is question one.
So why not just take it?
Fair question, and the honest answer is: I probably will — but not blind. There are three reasons to raise it rather than swallow it.
One. The doctor may know something the document does not spell out. Estradiol at 43.84 rising 75 percent is a genuinely defensible reason to pre-empt rather than react, especially if he has watched a lot of men cross that line. If that is the reasoning, I want it stated, because then it is a plan rather than a template.
Two. There is no floor. The safety table has a ceiling for estradiol and nothing underneath. Once you prescribe an inhibitor, the ceiling stops being the likely failure and the floor becomes the whole risk. A protocol that medicates oestrogen downward without defining how low is too low is missing the only trigger that can fire.
Three. It is trivially fixable. Add a floor, measure at four weeks with a sensitive assay, and the drug becomes safe to run. That is a two-line amendment, not a fight.
So the position is not refusal. It is accept the drug, add the floor:
One technical rider: near the low male range ordinary immunoassays become unreliable. Any estradiol measured while on an inhibitor has to be LC-MS/MS or the number is not trustworthy enough to dose against.
5 · HCG — the one I want back
The decision is one line: do not restart. The stated rationale is that fertility preservation is not documented as a current therapeutic objective, and that future need should be reassessed only if reproductive objectives or clinical circumstances change.
That sentence is technically true and practically backwards. I never wrote fertility down as an objective — but there is a difference between declining something and never being asked. Absence of documentation is not informed refusal.
More to the point: fertility is not the only thing HCG does, and it is not why I want it. My LH is below 0.09 and FSH is 0.07. The pituitary signal is gone, which is expected and not itself a fertility measurement. But without either LH or HCG, intratesticular testosterone falls roughly 90 to 95 percent while serum testosterone reads 712. The local environment collapses while the blood test looks superb.
Human work found that adding around 250 IU of HCG every other day held intratesticular testosterone near baseline, where testosterone alone dropped it about 94 percent. That is the argument: keep the tissue working, not keep the option of children.
Recovery is usually possible — pooled contraception data show return to 20 million sperm/mL in about 67 percent by six months, 90 percent by twelve, 96 percent by sixteen. Those figures came from younger screened men, so they are optimistic for a 44-year-old after prolonged therapy. A realistic window is 6 to 18 months, occasionally beyond 24.
Reinstate HCG at a maintenance dose — the literature dose for preserving intratesticular testosterone is around 250 IU every other day, which is a fraction of the 2500 IU weekly I was running.
It does not compete with anything else in the protocol. The one real interaction is that HCG stimulates testicular aromatase and can push estradiol up — which, given an aromatase inhibitor is now on board anyway, is a considerably smaller problem than it was last month.
And a semen analysis now, while fifteen weeks in is still a usable reference rather than a year of it.
6 · HGH — the one I actually wanted
This is the one I left open on purpose. I refused to argue for growth hormone because I did not think I had earned the right to specify it: Option A was peptides, Option B was HGH, and the choice belonged to the physician.
Option B was selected. Somatropin 0.6 IU subcutaneous, once daily, evening, approximately the same time each day, duration as directed.
That is a real, biologically active, low replacement-style dose. Not homeopathic — and not a bodybuilding dose either, which start around 2 IU and climb. Adult growth hormone is titrated to IGF-1 and tolerability, not body weight. Being 105 kg is not an argument for more.
Will I feel it?
Honestly: some of it, slowly, and not the parts people expect. At 0.6 IU this is not a dose that transforms how you look in six weeks. Here is the realistic sequence.
The most likely early sensation is better sleep and slightly puffy hands. If the hands get properly swollen or you get tingling in the fingers, that is the dose talking and it needs to come down, not up.
The constraint nobody flagged
And before I injected a single growth hormone secretagogue, my IGF-1 was 251 — above range on its own. My native axis already runs hot.
A realistic response to 0.2 mg/day is roughly +10 to +30 percent, which from 214.7 lands around 236 to 279. The expected outcome of this dose is an IGF-1 above the reference range.
That is not a reason to refuse it — it is a reason to measure early and to decide in advance what the number means. 230 is the hard biochemical ceiling. IGF-1 starts moving within days, most of the response appears in two to four weeks, and the decision measurement is at four to six.
Evening dosing is the convention because it approximates the sleep-associated growth hormone pulse. Morning theoretically preserves more of that endogenous pulse. Neither avoids feedback. It was prescribed evening and I will run it evening.
HGH plus retatrutide 2 mg
Growth hormone is diabetogenic: it drives lipolysis, raises free fatty acid flux and hepatic glucose output, and lowers peripheral insulin sensitivity. Retatrutide, a GLP-1/GIP/glucagon triple agonist, improves insulin response and glucose. They point in opposite directions and they do not cancel — retatrutide can mask the measured glucose rise while leaving the exposure, the IGF-1 and the oedema risk untouched.
Now: glucose 81, insulin 4.5, HOMA-IR 0.90, HbA1c 5.4%.
If glucose stays at 81 but insulin rises 4.5 to 9, HOMA-IR goes 0.90 to 1.80. Glucose looks identical while the insulin needed to hold it there has doubled.
Which is why HbA1c alone is not enough. Follow glucose, insulin and HOMA together or the first real signal is invisible.
Monitoring that catches it: fasting glucose three mornings a week for six weeks, a two-hour post-meal reading once or twice weekly, weight and waist weekly, blood pressure and resting heart rate two or three times weekly. Then glucose, insulin, HOMA and IGF-1 together at week four to six, HbA1c at week twelve. Reassess if fasting glucose repeatedly hits 100, insulin or HOMA roughly doubles, or HbA1c climbs 0.3 points.
7 · What comes off
Two things leave the protocol, and neither is controversial.
CJC-1295 and Ipamorelin are out. HGH replaces them — that is what selecting Option B means. The document does not list them in the removed-therapies section, but there is no ambiguity about the intent: exogenous growth hormone and growth hormone secretagogues do the same job by different routes, and running both is mechanically redundant.
The mechanism is worth stating once, because it explains why you would never stack them. CJC-1295 acts on the GHRH receptor and ipamorelin on the ghrelin receptor; both tell the pituitary to release growth hormone. Somatropin supplies it directly, and the resulting IGF-1 feeds back to reduce hypothalamic GHRH, raise somatostatin tone and suppress endogenous pulsatile release. So the secretagogues would be prompting a pituitary that the somatropin has already switched off — more total exposure, no dose attribution, higher odds of oedema and joint pain, with 7 percent of IGF-1 headroom to play with.
NAD+ is discontinued. Stated reason: reduce injection burden and complexity. I would not have cut it myself and it is still the right call — the evidence for meaningful performance, recovery or longevity outcomes in healthy trained adults is weak, subcutaneous kinetics are poorly defined, and it added cost and protocol noise for an effect nobody can point to in my bloodwork.
The burden arithmetic holds too:
My count matched the dossier's stated eighteen exactly. And it drops further later — TB-500 halves after week six, BPC-157 ends entirely at week eight.
8 · BPC-157 and TB-500 — approved, and bigger than I asked
I asked to increase BPC-157 and aim it at the shoulder. Approved at 500 mcg daily for 8 weeks — double my current dose, injected near the affected shoulder when clinically appropriate, or abdominal subcutaneous tissue otherwise.
I asked to restart TB-500. Approved at 2 mg twice weekly for 6 weeks, then 2 mg weekly — a proper loading phase, which is more than I proposed.
Honest assessment: these are recognisable clinic regimens, and recognisable is not the same as validated. BPC-157 evidence is overwhelmingly cellular and animal work with inadequate human efficacy, dose-ranging or long-term safety data. Injected TB-500 evidence for injury recovery is similarly thin. The doubling from 250 to 500 mcg has no human dose-response behind it.
That does not make it wrong. It makes it an experiment, and the right response to an experiment is a defined review point — weeks two, four and eight for BPC, end of loading for TB-500 — measured against pain, range of motion, training load and function. Continuing either without measurable improvement turns a finite experiment into indefinite unknown exposure.
9 · Cycling — the clear answer
This is the question I get asked most and the one carrying the most folklore. Here is the short version, because it turns out to be simpler than I expected.
There is no receptor-reset requirement anywhere in it. No tolerance break. No 5-on-2-off. No 8-weeks-on-4-weeks-off. None of that has an evidence base for any of these six agents.
But no cycling is not the same as run everything forever, and the difference is the whole section.
Three of them run indefinitely. Two are finite courses that end. One depends entirely on whether I actually need it.
Cycling exists for exactly two legitimate reasons: receptor desensitisation, and limiting cumulative exposure.
Nothing here has the first. Two things have the second — and for those, the finite course is not a cycle. It is an exposure budget with a review date attached. That framing tells you what to do at the end: measure the outcome and decide, rather than reflexively taking a break and restarting.
So the answer to can I just run this is: yes for testosterone, retatrutide and HGH, indefinitely, with monitoring. No for BPC-157, which ends at week 8. TB-500 needs an endpoint written in. Anastrozole runs only as long as it is doing something.
10 · Cruise, blast, or what?
By dose, 175 is an aggressive cruise, or high-dose TRT — not a classic blast. But the label depends on serum exposure and intent as much as milligrams. If it holds testosterone above the reference range for most of the week and needs an aromatase inhibitor to be tolerable, that is pharmacologic cruising rather than physiological replacement.
Straight about what this is: I already have a trough of 712.60 on 100 mg. Raising the weekly dose 75 percent and adding an aromatase inhibitor is not correcting under-replacement. It is a performance escalation with side-effect medication layered on top. I am fine with that — it is what I asked for and it is what MONSTER 2.0 is. Calling it anything else would be dishonest.
Continuous 175 mg/week with no end date defaults to indefinite, and the same is true of the anastrozole. Nowhere does the plan say what would make the dose come back down.
What an exit needs: the objective that justifies a 75 percent increase · defined peak and trough targets · reassessment at 6 to 8 weeks when the steady state exists · a sensitive estradiol assay with an automatic stop floor · a de-escalation rule if HDL worsens, ferritin keeps falling or erythrocytosis accelerates · a default return dose if 175 produces nothing measurable · and a written position on whether this is lifelong.
A taper is not a recovery strategy. Cypionate declines slowly on its own half-life anyway. The unresolved problem is the suppressed axis underneath, and that does not fix itself because the dose came down gently.
11 · How they justified it
Section six of the dossier is the risk-benefit architecture — six domains, each with the documented context and how it conditions this phase. It is the closest thing to the physician showing his working:
The safety parameters carried forward are described explicitly as active monitoring triggers rather than pending proposals — and they are, word for word, the red lines I proposed:
And the follow-up monitoring plan, by domain: hormonal (total and free testosterone, estradiol, SHBG) · haematology and iron (CBC, haemoglobin, haematocrit, ferritin, iron studies, reticulocyte context) · GH axis (IGF-1, fasting glucose, fasting insulin, HbA1c) · metabolic and body composition (weight, composition, glucose, insulin, HbA1c) · lipids and cardiovascular (total cholesterol, LDL, HDL, triglycerides, ApoB and Lp(a), blood pressure) · renal and hepatic (creatinine/eGFR, ALT/AST).
Still outstanding on the lab side: Lp(a) and soluble transferrin receptor, both pending. ApoB is explicitly flagged as something to interpret within the complete lipid profile rather than in isolation — which is exactly right, and exactly what I concluded when it landed at 81.28. Ret-He, total protein, potassium and magnesium are all named as additional follow-up parameters.
12 · The standing instructions
Section ten is the part that would be boilerplate anywhere else. Reproduced because it is the actual operating manual:
That last line is the one that matters, and it is the right principle. It is also the line I will be quoting back when I ask about frequency, because the same logic applies: the schedule should be set by response and safety markers, not by template.
13 · Everything at once — approved, and I agree
I asked whether to stage this or run it together. The answer was implement together, with active monitoring, and I am taking it. The dossier is explicit that concurrent implementation is physician-selected and that adverse effects and lab changes need documenting carefully — which is the trade being made, stated openly.
What I lose is attribution. An IGF-1 change cannot be assigned to somatropin versus stopping the secretagogues. GH-driven insulin resistance can be hidden by retatrutide-driven weight loss, and vice versa. Any shoulder improvement cannot be separated between BPC-157, TB-500, training changes and ordinary healing.
The mitigation is not staging — it is a proper baseline week. Seven days of fasting glucose, weight, blood pressure, resting heart rate, appetite, GI, oedema, hand symptoms and shoulder function before day one. If everything starts together, the only thing that preserves signal is knowing precisely where I started. That costs a week of writing things down and nothing else.
14 · The order — what to buy, and when I run out
This is the part I actually needed to work out. A 30-day month is 4.286 weeks, which is where the decimals come from. Doses and volumes below are computed from the prescription.
Two of those reconstitutions are deliberate. Retatrutide at 2 mL would give a clumsy 67-unit draw; 1.5 mL puts it on a clean 50. Somatropin at 1 mL would mean drawing 5 units, which is too small to measure accurately by eye — 2 mL doubles it to a readable 10.
Order now — to be covered from day one
BPC-157 runs 8 weeks and stops. Total course is 28 mg. Three 10 mg vials cover the whole thing — there is no month two order for it.
TB-500 loading is 6 weeks at 4 mg/week = 24 mg. Three vials cover loading plus the first three weeks of maintenance. After that it is 2 mg/week, which is one vial a month.
Everything else is a genuine monthly cadence.
When each one runs out
The steady-state month, from month two
So: a front-loaded first order that carries the two finite courses in full, then a lighter repeating order of four injectables plus consumables. The month-two bill is materially smaller than month one, which is not how these things usually go.
One caveat on the somatropin: if it ships with manufacturer diluent, use that rather than bacteriostatic water and the monthly water figure drops from 16 mL to 12.
15 · What goes back to the clinic
Four questions. None of this is a refusal — it is a plan I want to run with the loose ends closed first.
What happens next
The clinical plan is defined. The quotation comes next, then the order, then delivery, then day one.
Two lab markers are still outstanding — Lp(a) and soluble transferrin receptor. Lp(a) finishes the cardiovascular picture, because ApoB counts Lp(a) particles too and the lipid read stays provisional until it lands. Soluble transferrin receptor is now the only arbiter left on iron, since the reticulocyte haemoglobin test I asked for was never run.
MONSTER 2.0 — The Ask — the eight-thousand-word proposal this document is answering. Every dose I requested and the reasoning behind each one.
Twenty-One Markers and an ECG — the bloodwork that made the case for changing anything at all.
