Tirz/Cagri vs Tirz/Reta--

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domin8brix

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I have been on Tirz for about 16 months, currently splitting a 7.5mg dose per week. I reconstituted Reta and started 1mg of that Monday, intending to repeat on Sunday. I was hoping the stack would jump start things after being in recovery from shoulder surgery, and get me back down to fighting weight now that my working out is getting back closer to semi normal. However, I am wondering if maybe I should stack Cagri with Tirz instead of stacking Tirz and Reta. Food noise is mostly silent, though chocolate cravings can be really strong, and temptation gets to me sometimes.

Thoughts on swapping out the Reta for Cagri, or should I see how the low dose Reta boost does til that vial is done? I plan to stay on Tirz longer term bec it's helping my OCD tremendously, and the food noise silence is important to me.
 
What you posted last Friday:

domin8brix said:
Start weight 249

Current weight 117

Timeframe June 2021 to present

Protocol Bariatric surgery in June 2021, Tirzepatide in a split microdose starting Jan 2025 for food noise and OCD. Currently taking two pins a week around 3.5mg per pin. Will be stacking Reta in the coming days at a starting .5mg dose.

So what is the problem with tirz?

Of course, you could do all three (tirz + reta + cagri), but you would probably have to lower tirz somewhat.

And, of course, elora will be coming out sooner or later. So, personally, I wouldn't buy a kit of cagri. A single vial of cagri 5 mg can be less than $20 and last over two months when starting out.
 
I don't feel like I am getting the appetite suppression it was previously giving me, and I was hoping that adding the Reta might assist in that without having to increase the tirz dose that I'd adjusted down to work in the Reta. From what I've been reading, those who stacked them seemed to see more fat loss and recomp than one or the other alone. The addition of Cagri to one or both at a super tiny dose was ideally to help me further with the suppression.

Basically experimenting to find the best level of silence, fat/weight loss and suppression.
 
OH--and I don't plan to stack both or all three or some combo long term, but need to get myself back into a caloric deficit having not worked out like normal post shoulder surgery.
 
Calm Logic said:
Of course, you could do all three (tirz + reta + cagri), but you would probably have to lower tirz somewhat.

And, of course, elora will be coming out sooner or later. So, personally, I wouldn't buy a kit of cagri. A single vial of cagri 5 mg can be less than $20 and last over two months when starting out.
Stacking all three might work well--would you suggest I do Tirz/Cagri together and Reta separately? Or just rotate all three every few days?

If I try the Cagri, I will do the single vial route. I did that with Reta just to see how that worked together first.
 
Here are some projections by AI if you did all three (at current doses, adding starting dose of cagri):

Gemini said:
Estimated Weight Loss Stack (1-Year Projection) ​

Component Dose Individual 1yr Potency Contribution to Stack Primary Role in the Stack Tirzepatide 15 mg ~21.0% 18–20% The Foundation: Maximum GLP-1/GIP receptor saturation. Retatrutide 1 mg ~9.0% 1–2% The Metabolic Kick: Small Glucagon hit for thermogenesis. Cagrilintide 250 mcg ~5.0% 2–3% The Second Signal: Distinct Amylin pathway for satiety. TOTAL STACK Combined — ~23–26% Synergistic Ceiling Effect

Contribution Analysis: Why they don't simply "add up"

1. Tirzepatide (15 mg): The Heavy Lifter

In this stack, Tirzepatide is doing the vast majority of the work. Because 15 mg is the maximum dose, your GLP-1 and GIP receptors are essentially "full." Adding more GLP-1 via the Retatrutide doesn't double the weight loss; it mostly increases the potential for GI side effects.

2. Retatrutide (1 mg): The Glucagon Modifier

At this low dose, the GLP-1/GIP components are redundant. However, Retatrutide targets a third receptor: Glucagon . This helps keep the resting metabolic rate higher during a caloric deficit, acting as a "safety net" against metabolic adaptation.

3. Cagrilintide (250 mcg): The Amylin Synergy

This is actually the most effective "add-on" because it uses the Amylin pathway , which the other two do not touch. It slows gastric emptying through a different mechanism in the hindbrain, which is why even a small amount can help break a plateau when GLP-1s alone have stalled.

Note on Safety: Stacking these medications at these levels significantly increases the risk of dehydration and muscle loss. With this level of appetite suppression, focusing on high protein intake and resistance training is critical to ensure the weight lost is fat, not lean tissue.

Click to expand...

So Gemini reinforces the intution that a cleaner stack of tirz + cagri is better.

As far as splitting/spreading doses of a stack, you could do half of the whole stack twice a week. I haven't done that with stacks, but that's where I am headed, at least with a clean stack like tirz plus cagri.
 
Calm Logic said:
Here are some projections by AI if you did all three (at current doses, adding starting dose of cagri):

So Gemini reinforces the intution that a cleaner stack of tirz + cagri is better.

As far as splitting/spreading doses of a stack, you could do half of the whole stack twice a week. I haven't done that with stacks, but that's where I am headed, at least with a clean stack like tirz plus cagri.
Ok so that is awesome. THANK YOU! I will start digging into adjusting for the split.
 
I've stacked all 3 before for several months. I couldn't tell any difference when I added the Cagri. I titrated it up quite a bit. I couldn't tell any difference when I removed the Cagri.

Cagri was from PGB.
 
ktg123 said:
I've stacked all 3 before for several months. I couldn't tell any difference when I added the Cagri. I titrated it up quite a bit. I couldn't tell any difference when I removed the Cagri.

Cagri was from PGB.
Interesting...What was your dosing split with the three and prior to adding the Cagri, if you don't mind sharing?
 
ktg123 said:
I've stacked all 3 before for several months. I couldn't tell any difference when I added the Cagri. I titrated it up quite a bit. I couldn't tell any difference when I removed the Cagri.

Cagri was from PGB.

To be quoted in future promotional materials for elora, haha.
 
domin8brix said:
I don't feel like I am getting the appetite suppression it was previously giving me, and I was hoping that adding the Reta might assist in that without having to increase the tirz dose that I'd adjusted down to work in the Reta. From what I've been reading, those who stacked them seemed to see more fat loss and recomp than one or the other alone. The addition of Cagri to one or both at a super tiny dose was ideally to help me further with the suppression.

Basically experimenting to find the best level of silence, fat/weight loss and suppression.
Clenbuterol could be a solid addition. Muscle growth and fat loss through Beta 2 receptor Agonism. Shakes are dose-dependent, and its probably one of the most fear mongered drugs in this space. Can boost your metabolic rate by 21%, can lower myostatin, inhibit new fat cell growth, etc, in livestock it literally is a "partitioning agent". If anyone disagree please cite sources (not a damn case report please).
 
stoked12 said:
Clenbuterol could be a solid addition. Muscle growth and fat loss through Beta 2 receptor Agonism. Shakes are dose-dependent, and its probably one of the most fear mongered drugs in this space. Can boost your metabolic rate by 21%, can lower myostatin, inhibit new fat cell growth, etc, in livestock it literally is a "partitioning agent". If anyone disagree please cite sources (not a damn case report please).
This is the problem with bro science, and I have been guilty myself of reposting bro science, including with clen (before I knew better). I did find a doctor in an online Medscape debate/article who thought clen could be relatively safe, but I now realize he was an idiot (which is what the other doctor was basically saying).

Yes, you will lose weight with clen, but you could just be skinny for your casket. For one thing, the therapeutic window is small, and there are case reports of deaths from short-term effects (like heart attack in young adult male) and some reports from long-term effects.

Regarding your other points:

Gemini said:
Claim Status Context 21% Metabolic Boost Validated Observed in clinical settings; acts as a highly potent thermogenic. Repartitioning Agent Context-Dependent Massive effect in livestock; very weak anabolic effect in humans. Myostatin Lowering Unverified (Humans) Documented in murine/bovine models; unproven in human trials. Fat Loss Validated Primary human use; works via β2 receptor-mediated lipolysis.

Glucagon with reta is a thousand times safer than clen. For example, clen is a Schedule III controlled substance in New Mexico:

N.M. Admin. Code § 16.19.20.67 - SCHEDULE III

www.law.cornell.edu

Clen is for crazy bodybuilders trying to get ready for a competition. The biggest concern is heart enlargement (LVH) but that's not the only concern. The guys on Meso will typically favor albuterol instead (less crazy on the heart due to shorter half life).

Clen is a heart stimulant (beta 2 as you mentioned). So the exact opposite of some beta blocker blood pressure medications. But it could cause heart thickening and LVH even without much change in BP (due to the very long half-life not giving the heart a break).
 
"Skeletal muscle contains all three β -adrenoceptor subtypes ( β 1, β 2 and β 3), with about a 10-fold greater proportion of the β 2-adrenoceptor isoform than β 1 or β 3 receptors [30, 31]. The expression of subtype receptors remains to be checked under denervation condition in the future studies. Conversely, cardiac muscle contains approximately more than twofold of β 1-adrenoceptors than β 2 [1]. This forms a theoretic basis for adjusting doses of β 2 agonists to affect skeletal rather than myocardial muscles. Indeed, proper dosages of β 2 agonists, such as clenbuterol, separate the effects on different types of muscles in patients [911]. Among the known β 2 agonists, clenbuterol appears to have the safest cardiac profile. To elaborate, clenbuterol given at 1000  μ g/kg/day, caused no myocardial hypertrophy in rats, but rather skeletal muscle hypertrophy [32]. Consistently, clenbuterol (up to 720  μ g/day) promotes cardiac recovery in patients with left ventricular unloading atrophy [1214].

Physiological dose of clenbuterol in rats, 10  μ g/kg/day, attenuated denervated muscle atrophy without affecting the heart or causing myocyte death [25, 34]. That dosage was calculated based on the metabolic body weight that 10  μ g/kg/day in rats is equivalent to 1  μ g/kg/day in humans, a dose safely used in asthma treatments [25, 35]. The dose in the current study was 120  μ g/day (~2  μ g/kg/day for a 60 kg person). It was well tolerated and not associated with any obvious discomfort, except for one patient with transient nervousness. The newly occurring sinus bradycardia after the clenbuterol trial seemed not be relevant to the activation of the β 1/2 agonist, which usually leads to tachycardia. Moreover, clenbuterol at the present dose did not exacerbate preexisting minor EKG abnormalities. This is consistent with previous reports that the effects of clenbuterol on the heart are observable at a dose of up to 2100  μ g/day in combination therapy for patients using left ventricular assist device. Even at those doses, no severe adverse effects were encountered but tremors and muscle cramps [12, 13]. In our study, no adverse effects on liver, kidneys, lungs or hematopoietic system were observed after the 3-month intake of clenbuterol.

This pilot single-center study was small in scale. The efficacy would be more apparent in a larger patient population with either gradual increments of clenbuterol doses, or an on and off schedule to avoid the occurrence of receptor desensitization. Recent animal studies also show that clenbuterol is neuroprotective and promotes axon regeneration [5, 28, 29]. Thus, in combination with its antiatrophy function, clenbuterol and its kind truly represent promising and safe agents for countering nerve injuries."

This is from an actual study, Not a case report.

Clen is used for Asthma treatment in many eastern euro countries, as well as in Mexico.

Ghoul on the meso forum summarizes it really well

"

I've used clen for as long as 8 months. Off now.

I'll make the key points succinctly, if you need more details lmk.

"Tolerance" does develop quickly but it's not that simple. Metabolically 80mg of Clen, without prior use, will increase resting calorie burn by 29%, and fat lipolysis (breakdown to fatty acids) by 39%, along with increasing insulin sensitivity and other fat loss enhancing effects.

The tolerance that quickly develops primarily affects the tremors and boosted twitch speed of muscles. This accounts for only a portion of the extra resting calorie burn, and quickly diminishes as you take the same dose. Some users think that's an indication it's no longer working, which isn't accurate. I also thought increased doses to keep the tremors going and the break to reset receptors were necessary to restore the fat loss effects after you reached your max dose and the tremors stopped, but that wasn't actually necessary.

The increased fat metabolism is a direct action of Clen on fat cells, not relying on continued beta receptor sensitivity.

Air passages continue to be opened more than normal, resulting in higher resting calorie burn.

After all, when used as an asthma med it would be taken for years at the same dose. The tremors are considered a temporary side effect when treatment is initiated. No "break" or ever increasing dose is required to keep patients breathing more easily, or as we're trying to induce, additional fat oxidation.

The increased insulin sensitivity is so durable Clen has experimentally been used as a treatment for diabetes. Again, this doesn't fade with tolerance.

So do you lose some of the "free" calorie burn from a lack of tremors and muscles that have increased twitch response? Yes, how much? Not enough to warrant repeatedly going through the stress the tremor stage puts on your body in as you keep cycling over an extended period, in my opinion. The time to reset receptor sensitivity varies from person to person and protocols are all over the place, btw.

Most of the fat loss benefits will continue with sustained use, and the only way to go if you want to use this for a long period to counteract your slowed metabolism. Do something else to burn off what is perhaps 100-200 / day in extra calories from the tremor stage. The biggest benefits are the continuing enhanced lipolysis that will speed fat loss and boost energy, and better glucose control from increased insulin sensitivity. That is largely what "better metabolism" is anyway right?

So for dosing. 40ug twice a day is the asthma dose, proven to be safe for long term use. 80ug twice a day is the highest amount I've found referred to in a long term study (6 months), and those were people weakened by ALS, with no ill effects.

Because of the possible unintentional overdosing with UGL Clen I wouldn't go past 80ug a day, and would usually take that in one dose early in the morning, A split dose is better but no later than noon for the second to avoid insomnia. With pharma I'd be comfortable going up to 80ug twice a day max. Thats me, 40ug twice a day will still be effective. This is all after slow titration and dependent on how you respond. Don't go higher if you don't feel well. You've also got to monitor BP as it can drop too low if you're normal or below already. First time use 20ug for 4 days, then 40ug, 60ug, until you reach your max. Increasing every 4 days or when the tremors ease off.

Although plenty of people have gone to the hospital after taking too much, or ingesting it accidentally (an infant ate 20 tabs, and turned out ok thankfully) or it was used to cut street drugs, documented injury has only been recorded at really high doses, and thankfully very rare. No fatalities as far as I've been able to find. Definitely don't play with raws. It's essentially heart muscle damage from increased heart rate combined with insufficient oxygen supply from the low blood pressure. Again, the highest heart rate is in the tremor stage when the receptors are most sensitive, so even though the doses we're talking about shouldn't put you anywhere near the danger zone, it's another reason to not cycle back into the tremors.

Stay really well hydrated. A lot of the extra energy expenditure is going to be from expelling moisture via breathing. So not only is dehydration bad in general, it'll slow fat loss.

Your heart isn't going nuts, so the hazard of an overworking heart suffering from oxygen depravation damaging muscle cells drops precipitously. Probably back to near zero, or whatever it would normally be without clen.

There's no mysterious effect clen has that damages the heart. Your heart rate speeds up, blood pressure goes down, and if it beats too fast, for too long, the oxygen supplied by blood flow is insufficient to meet its heightened needs and some heart muscle cells die from oxygen depravation. However, this only happens at epic doses, and while the receptors are sensitive. Assuming you don't have some underlying heart issues.

"

So not trying to argue, just providing you with some information that may make you change your mind. ALSO keep in mind that many Glucagon based drugs never made it to market BECAUSE of the cardiac concerns of chronic glucagon agonism. Pretty crazy they gave people 720mcg of Clen in a medical setting, and they did not notice any significant negatives.

ClinicalTrials.gov

clinicaltrials.gov

Randomized, Double-Blind, and Placebo-Controlled Trial of Clenbuterol in Denervated Muscle Atrophy - PMC

Objectives. β 2-adrenergic agonists, such as clenbuterol, have been shown to promote the hypertrophy of healthy skeletal muscles and to ameliorate muscle wasting in a few pathological conditions in both animals and humans. We intended to investigate ...

pmc.ncbi.nlm.nih.gov

https://thinksteroids.com/community/threads/how-long-can-i-take-clen-for.134425376/page-2#posts
 
Does clen increase lifespan or quality of life in healthy human adults? The opposite would be true.

Due to FOMO, I have tried clen, albuterol, and steroids, so I know BS (bro science) when I see it. The guys at Meso rationalize all kinds of things and are addicted to feelz as much as the mirror. But like they say at Meso, albuterol would be a less risky option than clen.

My drug of choice is caffeine, and I am drinking coffee now 🙂 If I had to be on a Rx-level stimulant, I would choose modafinil, but it is a controlled substance, so non-zero legal risk for sourcing from India.

Comparing clen to some other stimulants, including glucagon with reta:

Gemini said:
Risk Rank Compound Pharmacological Class Primary Health Risks Systemic Burden & Clearance 1 (Highest) Clenbuterol Long-acting β2 Agonist Myocyte necrosis, left ventricular hypertrophy, prolonged sympathetic overdrive, localized tissue hypoxia. Severe; 36+ hour terminal half-life. 2 Amphetamines & Ephedrine Catecholamine Releasing Agents / Mixed Sympathomimetics Neurotoxicity (dopaminergic oxidative stress), hypertension, myocardial infarction risk, structural vascular damage. High; forces massive catecholamine efflux. 3 Ritalin (Methylphenidate) NDRI (Catecholamine Reuptake Inhibitor) Dose-dependent hypertension, tachycardia, vascular shear stress, anxiety, insomnia. Moderate-High; blocks DAT/NET but does not force efflux. 4 Albuterol Short-acting β2 Agonist Transient tachycardia, tremors, rapid β2 downregulation. Moderate; 4–6 hour half-life (pulsatile rather than chronic). 5 Retatrutide ("Reta") Triple Agonist Peptide (GLP-1/GIP/Glucagon) Sustained elevation in resting heart rate, cardiac arrhythmias, severe gastrointestinal distress, lean mass catabolism. High Duration / Mod. Intensity; ~6-day half-life means constant receptor activation without daily peaks and valleys. 6 Caffeine Adenosine Antagonist (Methylxanthine) Transient arrhythmias (at high doses), GI distress, sleep architecture disruption. Low-Moderate; indirect sympathetic activation. 7 (Lowest) Modafinil Atypical Eugeroic / Weak DRI Headaches, anxiety, rare dermatological reactions (e.g., Stevens-Johnson Syndrome). Low; highly stable profile without massive catecholamine surges.
 
Report of a 34-year-old woman who died from clenbuterol, just mentioned in another thread:

quoted said:
https://www.itv.com/news/2024-12-10/grieving-family-fears-illegal-weight-loss-drops-led-to-young-mums-death

Sarah’s family are adamant she would not have taken the weight loss drops if she knew the risks...

The results show the bottle contained Clenbuterol, which is a Class C controlled drug not approved for human use in the UK.

The maximum penalty for supplying the drug is 14 years in prison...

Sarah even gave a bottle of the weight loss drops to her sister, but they soon caused her heart palpitations and tremors so she stopping taking them.

After five weeks of taking the drops, Sarah too became unwell, repeatedly vomiting and unable to keep down food or liquid.

Just days later, Sarah was found dead in her bed by her 16-year-old daughter.

So probably cardiac arrest from low potassium, along with the ongoing stress on the heart. Clen can suck potassium out of the bloodstream, in addition to causing dehydration, vomiting, and GI shutdown. As with most accidental drug deaths, she probably would have lived if she got medical intervention, such as beta blockers, IV for hydration, and Zofran in the IV.
 
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