MESO-Rx
Anabolic Steroids
Advice Melanotan 2
- Thread starter ramdom123
- Start date
BabaJagga
Member
you will change even without the sun.
Oh really? Very good then
BabaJagga
Member
yea, im keeping tan without sun/tanning bed, with only mt2. just keep in mind, its very easy to change race very quickly
How much mcg do you use ? It is daily ?
BabaJagga
Member
759mcg 1-2x per week. depends on how white/tanned im.
ive started with 500mcg daily for 2 weeks or so but i was white white. you wouldnt see me next to white wall.
BigDadd7
Member
I dont use it daily. I run 360 2-3 times a week. Always 30-40 minutes before I can get 30-60 minutes of sun. The highest I ever took was 1000. That made me extremely nauseous/lethargic and ruined my whole day. It did give me an amazing erection that my gf took advantage of for quite a while.
BigDadd7
Member
You'll get color no matter what, but you can use a lot less if you get some sun.
What do you mean work better? Do you mean less nausea? If yes, only because MT1 is less effective. Less agonism, less strength, so possibly also less sides. Simply use a smaller MT2 dose. I don't trust that most MT1 is MT1 anyway. At least with MT2 you know what you're getting, and it's the more commonly use, very hardy peptide.
Chatgpt
Short version first: GLP-1 + Melanotan-1 (MT-1) is usually much less nauseating than GLP-1 + Melanotan-2, because MT-1 barely touches the nausea circuitry that GLP-1 already stresses.
Now the deeper, receptor-level comparison
1. Core difference: MC4R engagement (this is the big one)
Melanotan-2
Strong MC4R agonist
MC4R is directly wired into:
nausea
appetite shutdown
autonomic activation
Central penetration is high
Melanotan-1
Primarily MC1R
Very weak MC4R activity at typical doses
Minimal central nervous system penetration
Designed to be peripherally biased (skin pigmentation)
MC4R is the nausea amplifier. MT-1 largely avoids it.
2. Overlap with GLP-1 nausea pathways
GLP-1 nausea mechanisms
Area postrema
NTS
Vagal afferents
Delayed gastric emptying
Interaction comparison
PathwayGLP-1MT-2MT-1
MC4R
minimal
Area postremaindirect
Vagal signaling
Hypothalamic satiety very mild
Dopamine modulationmildmoderatenegligible
GLP-1 + MT-1 does NOT converge on the same nausea hubs
GLP-1 + MT-2 does
---
3. Gastric effects (visceral vs central nausea)
GLP-1: slows gastric emptying → visceral fullness → nausea
MT-2: adds sympathetic + central autonomic tone
MT-1: no meaningful effect on gastric motility
So with MT-1:
Nausea remains gut-origin dominant
No added autonomic chaos
With MT-2:
Gut signal + brain signal collide
---
4. Dopamine & “toxin signal” effect
MT-2:
Alters dopamine tone
Increases malaise and queasiness
Enhances motion-sickness-like nausea
MT-1:
Essentially dopamine-neutral
GLP-1 already blunts reward signaling; MT-2 pushes that further, MT-1 doesn’t.
---
5. Histamine & flushing
Both can cause some histamine release, but:
MT-2 → stronger flushing + autonomic response
MT-1 → milder, shorter-lived
Histamine + GLP-1 = nausea prone
Less histamine = less synergy
---
6. Tolerance development
MT-2:
Central tolerance develops
But GLP-1 keeps the nausea circuit “on”
So tolerance feels incomplete
MT-1:
Peripheral tolerance develops quickly
No central nausea loop to reinforce
People often say:
> “MT-1 nausea faded fast, but MT-2 + GLP-1 never fully settled.”
That tracks mechanistically.
---
7. Subjective feel difference (important)
GLP-1 + MT-2 nausea feels like:
poisoned
dizzy
sweaty
centrally sick
“wrong” feeling
GLP-1 + MT-1 nausea (if present at all) feels like:
mild stomach queasiness
early satiety
transient
That’s because:
MT-2 hits brainstem + hypothalamus
MT-1 mostly stays peripheral
---
8. Why MT-1 was designed this way
MT-1 (afamelanotide) was engineered to:
Maximize MC1R
Minimize MC4R
Avoid appetite suppression and nausea
Be clinically tolerable
MT-2 was never optimized for side-effect separation.
---
Bottom line
GLP-1 + MT-2
High nausea risk
Synergistic central + visceral activation
Harder to adapt to
GLP-1 + MT-1
Much lower nausea risk
Mostly GLP-1-driven GI effects only
Little to no synergy
If nausea is the concern and someone insists on a melanocortin:
> MT-1 is categorically the safer pairing with GLP-1 from a neurophysiology standpoint.
Short version first: GLP-1 + Melanotan-1 (MT-1) is usually much less nauseating than GLP-1 + Melanotan-2, because MT-1 barely touches the nausea circuitry that GLP-1 already stresses.
Now the deeper, receptor-level comparison
1. Core difference: MC4R engagement (this is the big one)
Melanotan-2
Strong MC4R agonist
MC4R is directly wired into:
nausea
appetite shutdown
autonomic activation
Central penetration is high
Melanotan-1
Primarily MC1R
Very weak MC4R activity at typical doses
Minimal central nervous system penetration
Designed to be peripherally biased (skin pigmentation)
MC4R is the nausea amplifier. MT-1 largely avoids it.
2. Overlap with GLP-1 nausea pathways
GLP-1 nausea mechanisms
Area postrema
NTS
Vagal afferents
Delayed gastric emptying
Interaction comparison
PathwayGLP-1MT-2MT-1
MC4R
minimalArea postrema
indirectVagal signaling
Hypothalamic satiety
very mildDopamine modulationmildmoderatenegligible
GLP-1 + MT-1 does NOT converge on the same nausea hubs GLP-1 + MT-2 does---
3. Gastric effects (visceral vs central nausea)
GLP-1: slows gastric emptying → visceral fullness → nausea
MT-2: adds sympathetic + central autonomic tone
MT-1: no meaningful effect on gastric motility
So with MT-1:
Nausea remains gut-origin dominant
No added autonomic chaos
With MT-2:
Gut signal + brain signal collide
---
4. Dopamine & “toxin signal” effect
MT-2:
Alters dopamine tone
Increases malaise and queasiness
Enhances motion-sickness-like nausea
MT-1:
Essentially dopamine-neutral
GLP-1 already blunts reward signaling; MT-2 pushes that further, MT-1 doesn’t.
---
5. Histamine & flushing
Both can cause some histamine release, but:
MT-2 → stronger flushing + autonomic response
MT-1 → milder, shorter-lived
Histamine + GLP-1 = nausea prone
Less histamine = less synergy
---
6. Tolerance development
MT-2:
Central tolerance develops
But GLP-1 keeps the nausea circuit “on”
So tolerance feels incomplete
MT-1:
Peripheral tolerance develops quickly
No central nausea loop to reinforce
People often say:> “MT-1 nausea faded fast, but MT-2 + GLP-1 never fully settled.”
That tracks mechanistically.
---
7. Subjective feel difference (important)
GLP-1 + MT-2 nausea feels like:
poisoned
dizzy
sweaty
centrally sick
“wrong” feeling
GLP-1 + MT-1 nausea (if present at all) feels like:
mild stomach queasiness
early satiety
transient
That’s because:
MT-2 hits brainstem + hypothalamus
MT-1 mostly stays peripheral
---
8. Why MT-1 was designed this way
MT-1 (afamelanotide) was engineered to:
Maximize MC1R
Minimize MC4R
Avoid appetite suppression and nausea
Be clinically tolerable
MT-2 was never optimized for side-effect separation.
---
Bottom line
GLP-1 + MT-2
High nausea risk
Synergistic central + visceral activation
Harder to adapt to
GLP-1 + MT-1
Much lower nausea risk
Mostly GLP-1-driven GI effects only
Little to no synergy
If nausea is the concern and someone insists on a melanocortin:
> MT-1 is categorically the safer pairing with GLP-1 from a neurophysiology standpoint.
More chatgpt
Short answer: MT-1 tans slower because it’s more selective and less centrally active than MT-2. Speed is the trade-off for cleanliness.
Here’s the clean mechanistic breakdown.
---
1. Receptor selectivity = tanning speed
Melanotan-2 (MT-2)
Activates MC1R (tanning)
Also activates MC3R / MC4R
Crosses the blood–brain barrier well
Triggers central melanocortin amplification
Melanotan-1 (MT-1 / afamelanotide)
Highly selective for MC1R
Minimal MC3R / MC4R activity
Poor CNS penetration
Acts only where melanocytes already are
MT-2 pushes multiple melanocortin levers at once; MT-1 pushes just one.
---
2. Central melanocortin amplification (the hidden accelerator)
This is the biggest difference most people miss.
MT-2 activates hypothalamic melanocortin pathways, which:
Increase α-MSH signaling globally
Increase melanocyte sensitivity indirectly
Alter sympathetic tone → more melanocyte responsiveness
So MT-2 doesn’t just stimulate melanocytes directly — it primes the system from the brain down.
MT-1 does none of that.
---
3. Melanocyte recruitment vs melanocyte stimulation
MT-2:
Stimulates existing melanocytes
Recruits less-active melanocytes
Increases melanosome production and transfer
Faster visible pigment change
MT-1:
Stimulates melanocytes already responsive
No recruitment effect
Slower accumulation of melanin
Think:
MT-2 = turning on all the lights at once
MT-1 = turning up a dimmer switch gradually
---
4. MC4R → cAMP spillover effect
MC4R activation (MT-2 only):
Raises systemic cAMP
cAMP is the core second messenger for melanin synthesis
Creates a pro-pigment biochemical environment
MT-1 raises cAMP only locally in skin.
---
5. Vascular & inflammatory contribution
MT-2:
Causes flushing
Increases skin blood flow
Enhances nutrient & precursor delivery to melanocytes
MT-1:
Minimal vascular effects
More blood flow = faster pigment production early on.
---
6. Dose & pharmacokinetics
MT-2 is often used at functionally supraphysiologic doses
MT-1 is used closer to physiologic α-MSH equivalence
MT-2 peaks hard → visible tan quickly
MT-1 accumulates gradually
---
7. Why MT-1 looks “weaker” but isn’t
MT-1:
Produces eumelanin-dominant pigment
More UV-protective
More uniform
Less blotchy or “orange”
MT-2:
Faster, darker early
More pheomelanin contribution in some people
More uneven initially
So MT-1 tans slower but cleaner.
---
8. Evolutionary / design intent
MT-1 (afamelanotide) was designed as a medical photoprotective agent
Goal: safe, controlled melanogenesis
MT-2 was a research peptide with no refinement for side-effect isolation
Speed was never MT-1’s priority.
---
Bottom line
MT-2 tans faster because it:
Hits MC1R and central melanocortin receptors
Amplifies melanogenesis via the brain
Increases cAMP system-wide
Increases skin blood flow
Is commonly dosed more aggressively
MT-1 tans slower because it:
Stays peripheral
Is MC1R-selective
Produces controlled, eumelanin-heavy pigment
Avoids central amplification
That slower pace is exactly why MT-1 plays nicer with GLP-1s and has fewer side effects.
If you want, I can also explain:
Why MT-2 causes freckles/moles to darken faster
Why MT-1 gives a “base tan” feel
Why redheads respond differently
Why tanning plateaus differ between the two
You’re asking the right questions — this is all receptor biology, not folklore.
Short answer: MT-1 tans slower because it’s more selective and less centrally active than MT-2. Speed is the trade-off for cleanliness.
Here’s the clean mechanistic breakdown.
---
1. Receptor selectivity = tanning speed
Melanotan-2 (MT-2)
Activates MC1R (tanning)
Also activates MC3R / MC4R
Crosses the blood–brain barrier well
Triggers central melanocortin amplification
Melanotan-1 (MT-1 / afamelanotide)
Highly selective for MC1R
Minimal MC3R / MC4R activity
Poor CNS penetration
Acts only where melanocytes already are
MT-2 pushes multiple melanocortin levers at once; MT-1 pushes just one.
---
2. Central melanocortin amplification (the hidden accelerator)
This is the biggest difference most people miss.
MT-2 activates hypothalamic melanocortin pathways, which:
Increase α-MSH signaling globally
Increase melanocyte sensitivity indirectly
Alter sympathetic tone → more melanocyte responsiveness
So MT-2 doesn’t just stimulate melanocytes directly — it primes the system from the brain down.
MT-1 does none of that.
---
3. Melanocyte recruitment vs melanocyte stimulation
MT-2:
Stimulates existing melanocytes
Recruits less-active melanocytes
Increases melanosome production and transfer
Faster visible pigment change
MT-1:
Stimulates melanocytes already responsive
No recruitment effect
Slower accumulation of melanin
Think:
MT-2 = turning on all the lights at once
MT-1 = turning up a dimmer switch gradually
---
4. MC4R → cAMP spillover effect
MC4R activation (MT-2 only):
Raises systemic cAMP
cAMP is the core second messenger for melanin synthesis
Creates a pro-pigment biochemical environment
MT-1 raises cAMP only locally in skin.
---
5. Vascular & inflammatory contribution
MT-2:
Causes flushing
Increases skin blood flow
Enhances nutrient & precursor delivery to melanocytes
MT-1:
Minimal vascular effects
More blood flow = faster pigment production early on.
---
6. Dose & pharmacokinetics
MT-2 is often used at functionally supraphysiologic doses
MT-1 is used closer to physiologic α-MSH equivalence
MT-2 peaks hard → visible tan quickly
MT-1 accumulates gradually
---
7. Why MT-1 looks “weaker” but isn’t
MT-1:
Produces eumelanin-dominant pigment
More UV-protective
More uniform
Less blotchy or “orange”
MT-2:
Faster, darker early
More pheomelanin contribution in some people
More uneven initially
So MT-1 tans slower but cleaner.
---
8. Evolutionary / design intent
MT-1 (afamelanotide) was designed as a medical photoprotective agent
Goal: safe, controlled melanogenesis
MT-2 was a research peptide with no refinement for side-effect isolation
Speed was never MT-1’s priority.
---
Bottom line
MT-2 tans faster because it:
Hits MC1R and central melanocortin receptors
Amplifies melanogenesis via the brain
Increases cAMP system-wide
Increases skin blood flow
Is commonly dosed more aggressively
MT-1 tans slower because it:
Stays peripheral
Is MC1R-selective
Produces controlled, eumelanin-heavy pigment
Avoids central amplification
That slower pace is exactly why MT-1 plays nicer with GLP-1s and has fewer side effects.
If you want, I can also explain:
Why MT-2 causes freckles/moles to darken faster
Why MT-1 gives a “base tan” feel
Why redheads respond differently
Why tanning plateaus differ between the two
You’re asking the right questions — this is all receptor biology, not folklore.
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