Retatrutide - Possibly better than semaglutide b/c lower nausea/side effect profile, but higher heart rate

#406

Please share this contacts. What shop is it? Have you try this?

And anyone - can you give me a contacts of reliable cheap chinese shop, maybe from made-in-china.com? or any other site.

#407

If looking for Chinese grey peptides, read this Retatrutide - Possibly better than semaglutide b/c lower nausea/side effect profile, but higher heart rate - #248 by qBx123Yk

#408

Thanks. But its a bad site. No list of vendors, unnecessary accent on cryptocurrencies. All the normal sellers use bank transfer, and have representatives on major sites like alibaba, made-in-china ans so on. No need to play spygames “wwooooh, we are on a DARK NET!”
Just need a contact as in the thread for indian pharmacies for Rapamycin.

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#409

Understood. You should be able to find sites saying they sell peptides from a relatively simple internet search then.

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#410

I agree on this. But I disagree that cryptocurrencies are necessary. A lot of these vendors get blacklisted by banks and are forced to use cryptocurrency.

These type of grey market peptide vendors often come and go a lot more than the Indian pharmacies so it’s harder to keep track of what is good and what is not. This has caused people to say “just do your own research” to find the best vendor but I think we should aim to have a list of viable vendors in the same way we have Indian pharmacies here.

Not everyone has time to deep dive on researching Chinese vendors and it is very tiresome, but people who do look into it often vet many and can list ones they’ve found to be reliable at the time.

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#411

Thanks. https://glp1forum.com for example. I found it very helpful with a real (i hope, they look like) reviews on sellers and with many tests of batches.

#412

I continue to benefit from 1.0 mg. It is the best item in my stack, but not the only good one.

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#413

Actually I have found that my initial hypothesis that Telmisartan acts synergistically to reta is probably accurate…

So, I initially found it tough to go above around 4mg-5 mg without strong appetite suppression (too strong, I want to enjoy food and stop the weight loss where it is)… during this time period I was concerned about the fact that I was hovering near hypotension so I tried to quit telmisartan for a few weeks… it was during that time period where the appetite suppression was gone and I moved up in mg… Once I got my blood work that shown for me positive results taking both reta/telmisartan and hovering near hypotension (without symptoms) I made the guess that near hypotension doesn’t have to be bad and I started taking both again… during that time have had to down regulate reta again due to bothersome appetite suppression

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#414

I also dropped telmisartan due to Reta but am not planning to re-introduce it for now

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#415

1. Executive Summary

This is an opinion-framed “mind changed” video from a creator (self-identified as a neuroscience PhD, referred to as “Nick” in the Q&A) who describes shifting from GLP-1 skepticism toward viewing these drugs as broadly beneficial well beyond weight loss. He frames this explicitly as personal opinion, not medical advice, and states he has no pharma financial ties.

The video moves through six parts: societal framing (adoption trends, obesity rate shifts, food industry response), common safety concerns (muscle loss, bone health, eye health, thyroid risk), the three “generations” of GLP-1-class drugs ending with the triple agonist retatrutide, weight-independent effects (Alzheimer’s pathology, osteoarthritis/cartilage), combination therapies for simultaneous fat loss and muscle gain (myostatin/activin-A inhibitors, ATX304), and an audience Q&A covering oral GLP-1s, rebound weight gain, addiction/craving effects, and gastroparesis.

He closes by stating his current view is that benefits outweigh risks for most people, “provided someone doesn’t lose too much weight” — explicitly flagged as opinion, not a medical claim.

2. Actionable Insights

Resistance training + protein target during GLP-1 use

  • What: 3+ resistance sessions/week, ~0.7–1g protein per lb of lean mass while losing weight
  • Risk: Low — standard sports-nutrition guidance, not GLP-1-specific
  • Evidence tier: Stated by the speaker as “a reasonable rule of thumb,” not tied to a specific trial in the transcript — treat as practitioner heuristic

Slow dose titration + avoiding overeating (gastroparesis mitigation)

  • What: Start low, escalate slowly, avoid large meals especially at high doses
  • Risk: Low — sensible general guidance
  • Evidence tier: General clinical reasoning stated in transcript, not tied to a specific study

Oral GLP-1 (orforglipron — transcript garbles the name)

  • What: Non-peptide oral GLP-1; transcript states ~11.2% body weight reduction over 72 weeks
  • Risk: Low-moderate, described as similar profile to existing GLP-1s
  • Evidence tier: Human RCT — verified below in Claims Requiring Scrutiny; the exact figure needs a small correction

ATX304 (AMPK activator)

  • What: Framed as pulling fuel into muscle while increasing fat oxidation; speaker mentions personal use (lowered his fasting glucose by 6 mg/dL) and recommending it to two family members
  • Risk: Speculative-to-high — unapproved research compound, no human data for this specific compound in the transcript. The personal/family anecdotes are testimonial, not evidence, and the speaker explicitly says “not medical advice”
  • Evidence tier: Animal only. Transcript specifies a 32-day study, 21% body weight reduction, “100% from fat”; species not named in transcript — this is a gap, not filled in here. The “no lean mass loss when combined with GLP-1s” claim is also animal-only per transcript, species again unspecified.

Myostatin/activin-A inhibitors + GLP-1

  • What: Blocking muscle-growth “brakes” alongside GLP-1s for simultaneous fat loss/muscle gain
  • Risk: Speculative — early-stage, not accessible outside trials
  • Evidence tier: Animal — monkey (specified in transcript) for the 50% fat mass loss / 6% lean mass gain result. The human figure cited (3kg lean gained, 4kg fat lost over 8 weeks) needs correction — see Claims Requiring Scrutiny below.

Testosterone replacement for diagnosed hypogonadism (context within the Nicholas N case study)

  • What: 200mg/week testosterone, replacement-dose (not supraphysiologic), prescribed for medically diagnosed low testosterone, alongside retatrutide, diet, and resistance training
  • Risk: Low when medically diagnosed and monitored — standard-of-care hormone replacement, not off-label enhancement — but only applies to someone with an actual diagnosis, not a general recommendation
  • Evidence tier: Single case study (n=1), not a controlled trial

3. Safety Concerns

  • Thyroid: Warning specifically for personal/family history of medullary thyroid carcinoma or MEN2 syndrome. Concern originates from rodent studies per the transcript, not established human carcinogenicity.
  • Eyes (NAION): Transcript cites “a 2026 systematic review” finding no significant association, with an absolute risk estimate of “something like half a percent in patients with diabetes over 5 years” — unverified, see below. Caution flagged for pre-existing retinal or diabetic eye disease regardless.
  • Gastroparesis: True pathologic stomach paralysis is distinguished from the drug’s intended slowed-gastric-emptying mechanism. Severity/prevalence figures beyond “relatively uncommon” aren’t given.
  • Cardiac load (retatrutide specifically): Increased resting heart rate and cardiac load from the glucagon-receptor component flagged as an open long-term question by the speaker himself.
  • Populations needing more caution per transcript: pre-existing retinal disease, personal/family thyroid cancer history, MEN2.
  • Not mentioned in transcript but worth flagging: pregnancy, pancreatitis history, and gallbladder disease are commonly discussed GLP-1 contraindications elsewhere that this video doesn’t address — a notable omission if you’re using this as a source.

4. Signals Worth Watching

Retatrutide’s proposed PCSK9-lowering mechanism

  • What/stage: Speaker’s own n=1 self-experiment (1–2mg for 4 weeks), reporting LDL/ApoB drops he attributes partly to glucagon-receptor-mediated PCSK9 reduction
  • Vs. existing interventions: Mechanistically distinct from statins (HMG-CoA reductase inhibition) or PCSK9 monoclonal antibodies (evolocumab/alirocumab) — not stated in transcript, added for context
  • What’s needed: The transcript notes a confounding second compound taken concurrently (“azetoide”). A controlled trial isolating retatrutide’s independent lipid effect is needed.

FGF-21-mediated muscle-sparing hypothesis for retatrutide

  • What/stage: Explicitly the speaker’s own unpublished hypothesis about FGF-21 resistance in obese vs. lean populations
  • Comparison: Mechanistically novel relative to behavioral muscle-preservation strategies (resistance training/protein) — an endocrine rather than behavioral lever
  • What’s needed: Direct comparison of FGF-21 sensitivity and lean mass outcomes across BMI strata on retatrutide specifically

GLP-1 and Alzheimer’s pathology (BACE1/amyloid, GSK-3β/tau)

  • What/stage: Population correlational data plus two proposed direct mechanisms — GLP-1 inhibiting BACE1 and improving brain insulin signaling to reduce GSK-3β-driven tau hyperphosphorylation
  • Comparison: Places GLP-1s in a different category from anti-amyloid monoclonal antibodies (lecanemab, donanemab) — not mentioned in transcript, added for context
  • What’s needed: RCTs with cognitive/biomarker endpoints in non-diabetic, non-obese populations to separate direct brain effects from metabolic-improvement confounding

Cartilage thickening / osteoarthritis effects

  • What/stage: “A 2026 study” (unnamed) reporting GLP-1 association with cartilage thickening in humans
  • What’s needed: The specific study, its design, and whether thickening correlates with functional/pain outcomes — none of this is in the transcript, and I did not locate it in this pass

5. Deep Dive

  • DEXA lean-mass-vs-liver-mass claim: The underlying DEXA critique is legitimate — DEXA genuinely cannot separate contractile protein from glycogen-bound water, organ mass, or connective tissue. But no study is named, and “preferentially reduce liver mass” is doing significant work: hepatic steatosis reduction on GLP-1s is well-documented, but whether that fully accounts for the 25–40% lean-mass-loss figure cited elsewhere is left unresolved.
  • Bone: The osteoblast-stimulating/osteoclast-inhibiting framing is mechanistically plausible, and the rat insulin-resistance study is specified as animal in the transcript. But the downstream signaling from “GLP-1 receptors in bone cells” to osteoblast/osteoclast balance is stated without receptor subtype or pathway detail.
  • Generation classification and weight-loss percentages: The three-generation framing is standard for how the field discusses this progression. The figures given (10–15% / ~20% / ~24%, ~28% in women) are broadly in range of published retatrutide data, likely TRIUMPH-1, but the transcript names no trial.
  • “Wanting vs. liking” framing: A legitimate, well-established distinction in addiction neuroscience, applied correctly at a conceptual level, though the specific genetic-variant studies referenced aren’t named.
  • PCSK9 mechanism plausibility: Glucagon receptor agonism affecting PCSK9 expression is biologically plausible, but presented via a single confounded self-experiment — far short of establishing the mechanism.

6. Claims Requiring Scrutiny

“US obesity rate fallen from ~40% to ~37%… 7.6 million fewer obese adults”
Checked against Gallup’s National Health and Well-Being Index — this is accurate. Obesity peaked at 39.9% in 2022 and fell to 37.0% in 2025, ~7.6 million fewer obese adults, alongside GLP-1 use for weight loss rising from 5.8% (Feb 2024) to 12.4% (2025). Caveat Gallup itself notes: this is self-reported survey data, and the obesity decline is correlational with GLP-1 uptake, not proven causal — other factors aren’t ruled out.

Oral GLP-1 (orforglipron) — “11.2% body weight reduction over 72 weeks”
Checked against the published ATTAIN-1 Phase 3 trial (NEJM) — the actual figure is 12.4% weight reduction (27.3 lbs) at the highest (36mg) dose at 72 weeks. Close to the video’s number but not exact, and the video doesn’t specify dose. Use 12.4% at 36mg if citing this.

Myostatin/activin-A human trial (“3kg lean mass gained, 4kg fat lost over 8 weeks, single treatment”)
This appears to be a garbled recollection of the real BELIEVE trial (bimagrumab + semaglutide, published in Nature Medicine, presented at ADA 2025) — but the actual numbers don’t match. BELIEVE ran 48–72 weeks with repeated dosing, not a single 8-week treatment. In the combination arm, lean mass was reduced by 2.9% (better preserved than semaglutide alone’s 7.4% loss, but not a gain); bimagrumab monotherapy alone showed a 2.5% lean mass increase. The “3kg gained / 4kg lost” figures don’t appear in the sources I found. Treat this as likely misstated — cite the actual BELIEVE data instead if you cover it.

“2026 systematic review found no significant association” (NAION/vision)
Not verified in this pass — I could not locate a specific named 2026 systematic review on GLP-1s and NAION. This doesn’t mean one doesn’t exist, but the claim remains as unsourced as the transcript presents it.

“A 2026 study” on cartilage thickening / osteoarthritis, and “2026 research” on DEXA/liver mass
Not checked in this pass — no compound or trial name in the transcript to search against.

Overall thesis (“maybe everyone should be taking a GLP-1”)
Not a factual claim — explicitly rhetorical framing per the speaker, who hedges by the end.

ATX304 anecdote and Nicholas N case study
Not independently checkable — personal testimonial and single self-reported case, not verifiable trial data.

7. Discussion Prompts

What happens to a food and pharmaceutical economy that reorganizes itself around a drug class whose 20-year cardiovascular and cancer safety data don’t yet exist — and is the individual risk/benefit calculus (“is this good for me”) actually a different question from whether society adapting its infrastructure around these drugs this quickly is a good idea?

The FGF-21 muscle-sparing hypothesis is explicitly the speaker’s own unpublished idea, not literature consensus — if a claim like this spreads faster than its evidentiary basis, what’s the mechanism by which it usually gets corrected or reinforced within the biohacker/longevity information ecosystem, and does that mechanism work fast enough?

8. Citations

No sources named with full detail anywhere in the transcript. Referenced but unnamed: “a 2026 systematic review” (NAION), “2026 research” (DEXA/liver mass), “a 2026 study” (osteoarthritis/cartilage). Named individual: “Nicholas N” (community case study, self-reported, n=1). Named product/newsletter: metabetism.com (“Stay Curious”). Verified externally in this pass: Gallup National Health and Well-Being Index (obesity/GLP-1 usage stats), Lilly’s ATTAIN-1 Phase 3 trial (orforglipron), the BELIEVE trial (bimagrumab + semaglutide, Nature Medicine).

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#416

The path used by retatrutide to lower LDL is thought to be ANGPTL3/8 pathway. From ESC 365 - Reduction of triglyceride-rich lipoproteins with retatrutide in type 2 diabetes may be explained by concurrent reduction in ANGPTL3/8 levels

Baseline ANGPTL3/8 levels (mean 26.3 ng/mL, IQR 17.4-33.0 ng/mL) were not different among all study groups. Mean percent changes of ANGPTL3/8 from baseline at week 24 were -1.3%, -12.0%, -48.7% and -51.0% in 0.5 mg, 4 mg, 8 mg and 12 mg retatrutide groups, respectively (Figure). Percent changes of ANGPTL3/8 in 8 mg and 12 mg retatrutide groups were significantly different from placebo group (p < 0.0001). Mean
percent changes of PCSK9 levels from baseline to 24 weeks were not different from placebo for any treatment arm (+6.2%, -3.9%, -3.8% and -9.6% for retatrutide 0.5 mg, 4 mg, 8 mg and 12 mg groups, respectively, and -1.5% for dulaglutide and -6.5% for placebo).

Here’s what AI says about how retatrutide uses this pathway to help lower LDL

This is another way to lower LDL, but not panacea. I didn’t see any additional lowering of LDL in my case by adding retatrutide. In my case, blocking absorption was much, much more effective via Ezetimibe.

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#417

I’ve bought it from some obscure supplier. 1st dose was 0,5, second 1,5, now made 3mg. Was on tirza 3-6mg for several months, and sema for 1,5 years.
I do feel nothing. May it be too low dose for not-naive person? Or may it be fake reta from china? Frankly there are not much bad stories about 0% of active peptides in an already recieved parcels. Scam happens, but nobody send nothing at all usually.
So I think its too low dose for me, but a lot of people say its “very powerful” and so on. Should I wait more weeks? Should I go up, maybe to 4-5-6mg? My appetite is normal. Not completely gone as it was on sema for a first 1-3 months. Sometimes I really feel hungry. And for 3 weeks no weight loss. Not gain either.
I’m a bit confused.

#418

Your dose is most likely too low, but I wouldn’t discard the possibility that you got 0% active ingredients, especially since I’ve seen a huge spikes in those lately. Do you have a third party test for your batch?

I would increase my dose, especially since 2mg is the starting dose in all trials. Pick a dose and stay on it for 4 weeks, this is how long the medicine takes to reach a steady state. The dose schedule on most trials has been 2mg,4,6,9,12mg, each dose held over 4 weeks.

Usually on retatrutide, people report less hunger suppression. Watch for the scale to move, not for hunger suppression to kick in, hunger suppression is not weight loss. I’m able to lose weight on retatrutide without my hunger being too affected.

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#419

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