NICOTINE'S EFFECTS ON GROWTH PLATES, AND HOW TO PREVENT THEM (NICOTINECELS GTFIH!!!)

[thaum]

Hello all! This is my first thread referencing nicotine and it's effects on your system. I have noticed a LOT of misinformation regarding it's effects so I figured I should create a thread.

OVERVIEW ON NICOTINE​

Spoiler: General Knowledge

Nicotine is a commonly consumed psychoactive stimulant that acts on nicotinic acetylcholine receptors. This interaction leads to dopaminergic effects, as well as stimulating the release of norepinephrine and your sympathetic nervous system (what gives you the focus benefits). The effects of nicotine on the brain are not relevant to the post, so no further information about them will be provided in this thread.

nAChR RECEPTORS AND THEIR FUNCTION​

nicotinic acetylcholine receptors (commonly referred to as nAChRs for short) are present throughout your body and are responsible for most of nicotine's effects. This receptor serves as a fast ion channel, which is required in many parts of your body, such as the nervous system and skeletal muscle.

HOW DOES THIS RELATE TO GROWTH AND FAH?​

nAChRs exist in epiphyseal plates too, which is precisely how nicotine acts on the growth plates, and why prolonged nicotine use can be dangerous to maximising your height. When one of these receptors is activated in the growth plate, it has the following effects:

• Surpressed Differentiation: Nicotine binds to alpha-7 nAChRs on chondrocytes, actively blocking them from maturing. This slows the growth process significantly, and is the primary reason we see growth retardation in nicotine users.​
• Decreased Extracellular Matrix Synthesis: This interaction with chondrocytes inhibits their ability to create the skeletal framework, which can potentially result in the cartilage matrix being stunted.​
• IGF-1 Signal Disruption: Nicotine downregulates parts of the IGF-1 pathway within the growth plate, leading to less response to IGF-1 and therefore a shorter FAH.​
• Necrosis: Nicotine is suggested to accelerate cell death in the growth plate, leading to dead chondrocytes building up.​

(source, source)
​

So, now that the effects of nicotine on the growth plates have been made clear, lets move on to potential workarounds (if quitting isn't an option)

PHARMACOLOGICAL INTERVENTION
​

We need to find a way to stop nicotine from binding to these nAChRs specifically, without affecting the ones in the brain and CNS (or else there'd be no point in using it at all since you wouldn't get it's positive effects). To achieve this, we need to find a way to block it from interacting with the alpha-7 subtype specifically, as that would keep its positive effects while preventing its interaction with the growth plates.

This is unfortunately not possible to do safely, with the only known solution being:

Methyllycaconitine (MLA)
​

This compound was researched in this study for preventing this interaction, and was found to be successful.

"Methyllycaconitine (MLA), a specific antagonist of alpha7 nAChR, reversed the inhibition of matrix synthesis and functional calcium signal by nicotine in human growth plate chondrocytes in vitro."
​

MLA is a potent toxin directly because of its effects on the alpha-7 nAChR, leading to muscular paralysis, impairment of breathing and heart function, and death.

CONCLUSION
​

Nicotine affects growth plates through alpha-7 nAChRs, leading to a decreased growth velocity and potentially a lower FAH. Its use should therefore be suspended. MLA, the only well-documented way of preventing this interaction, is not suitable as a method of harm reduction because it interferes with the alpha-7 receptor's normal functions as well, which can be deadly. In short, this interaction can not be prevented, and it is therefore advised to taper off and quit using nicotine if you care about your height, as no other option to prevent this interaction is available.

TLDR FOR LAZY FUCKS
Nicotine's effects on the growth plate can not be prevented, because the receptors it interacts with are vital for your heart and lung function. You can only prevent these interactions with the cessation of nicotine consumption as a result.

 

[Navity]

> Yo bro how are you a 6' chad?
>"Just nicotinemaxx sir"

BRUTAL

 

[thaum]

> Yo bro how are you a 6' chad?
>"Just nicotinemaxx sir"

BRUTAL

if only it increased FAH

i have to quit now FML

 

[Shirobon]

Hello all! This is my first thread referencing nicotine and it's effects on your system. I have noticed a LOT of misinformation regarding it's effects so I figured I should create a thread.

OVERVIEW ON NICOTINE​

Spoiler: General Knowledge

Nicotine is a commonly consumed psychoactive stimulant that acts on nicotinic acetylcholine receptors. This interaction leads to dopaminergic effects, as well as stimulating the release of norepinephrine and your sympathetic nervous system (what gives you the focus benefits). The effects of nicotine on the brain are not relevant to the post, so no further information about them will be provided in this thread.

nAChR RECEPTORS AND THEIR FUNCTION​

nicotinic acetylcholine receptors (commonly referred to as nAChRs for short) are present throughout your body and are responsible for most of nicotine's effects. This receptor serves as a fast ion channel, which is required in many parts of your body, such as the nervous system and skeletal muscle.

HOW DOES THIS RELATE TO GROWTH AND FAH?​

nAChRs exist in epiphyseal plates too, which is precisely how nicotine acts on the growth plates, and why prolonged nicotine use can be dangerous to maximising your height. When one of these receptors is activated in the growth plate, it has the following effects:

• Surpressed Differentiation: Nicotine binds to alpha-7 nAChRs on chondrocytes, actively blocking them from maturing. This slows the growth process significantly, and is the primary reason we see growth retardation in nicotine users.​
• Decreased Extracellular Matrix Synthesis: This interaction with chondrocytes inhibits their ability to create the skeletal framework, which can potentially result in the cartilage matrix being stunted.​
• IGF-1 Signal Disruption: Nicotine downregulates parts of the IGF-1 pathway within the growth plate, leading to less response to IGF-1 and therefore a shorter FAH.​
• Necrosis: Nicotine is suggested to accelerate cell death in the growth plate, leading to dead chondrocytes building up.​

(source, source)
​

So, now that the effects of nicotine on the growth plates have been made clear, lets move on to potential workarounds (if quitting isn't an option)

PHARMACOLOGICAL INTERVENTION
​

We need to find a way to stop nicotine from binding to these nAChRs specifically, without affecting the ones in the brain and CNS (or else there'd be no point in using it at all since you wouldn't get it's positive effects). To achieve this, we need to find a way to block it from interacting with the alpha-7 subtype specifically, as that would keep its positive effects while preventing its interaction with the growth plates.

This is unfortunately not possible to do safely, with the only known solution being:

Methyllycaconitine (MLA)
​

This compound was researched in this study for preventing this interaction, and was found to be successful.

"Methyllycaconitine (MLA), a specific antagonist of alpha7 nAChR, reversed the inhibition of matrix synthesis and functional calcium signal by nicotine in human growth plate chondrocytes in vitro."
​

MLA is a potent toxin directly because of its effects on the alpha-7 nAChR, leading to muscular paralysis, impairment of breathing and heart function, and death.

CONCLUSION
​

Nicotine affects growth plates through alpha-7 nAChRs, leading to a decreased growth velocity and potentially a lower FAH. Its use should therefore be suspended. MLA, the only well-documented way of preventing this interaction, is not suitable as a method of harm reduction because it interferes with the alpha-7 receptor's normal functions as well, which can be deadly. In short, this interaction can not be prevented, and it is therefore advised to taper off and quit using nicotine if you care about your height, as no other option to prevent this interaction is available.

TLDR FOR LAZY FUCKS
Nicotine's effects on the growth plate can not be prevented, because the receptors it interacts with are vital for your heart and lung function. You can only prevent these interactions with the cessation of nicotine consumption as a result.

very cool brah

 

[thaum]

bump

why everyone DNR my post

 

[thaum]

Hello all! This is my first thread referencing nicotine and it's effects on your system. I have noticed a LOT of misinformation regarding it's effects so I figured I should create a thread.

OVERVIEW ON NICOTINE​

Spoiler: General Knowledge

Nicotine is a commonly consumed psychoactive stimulant that acts on nicotinic acetylcholine receptors. This interaction leads to dopaminergic effects, as well as stimulating the release of norepinephrine and your sympathetic nervous system (what gives you the focus benefits). The effects of nicotine on the brain are not relevant to the post, so no further information about them will be provided in this thread.

nAChR RECEPTORS AND THEIR FUNCTION​

nicotinic acetylcholine receptors (commonly referred to as nAChRs for short) are present throughout your body and are responsible for most of nicotine's effects. This receptor serves as a fast ion channel, which is required in many parts of your body, such as the nervous system and skeletal muscle.

HOW DOES THIS RELATE TO GROWTH AND FAH?​

nAChRs exist in epiphyseal plates too, which is precisely how nicotine acts on the growth plates, and why prolonged nicotine use can be dangerous to maximising your height. When one of these receptors is activated in the growth plate, it has the following effects:

• Surpressed Differentiation: Nicotine binds to alpha-7 nAChRs on chondrocytes, actively blocking them from maturing. This slows the growth process significantly, and is the primary reason we see growth retardation in nicotine users.​
• Decreased Extracellular Matrix Synthesis: This interaction with chondrocytes inhibits their ability to create the skeletal framework, which can potentially result in the cartilage matrix being stunted.​
• IGF-1 Signal Disruption: Nicotine downregulates parts of the IGF-1 pathway within the growth plate, leading to less response to IGF-1 and therefore a shorter FAH.​
• Necrosis: Nicotine is suggested to accelerate cell death in the growth plate, leading to dead chondrocytes building up.​

(source, source)
​

So, now that the effects of nicotine on the growth plates have been made clear, lets move on to potential workarounds (if quitting isn't an option)

PHARMACOLOGICAL INTERVENTION
​

We need to find a way to stop nicotine from binding to these nAChRs specifically, without affecting the ones in the brain and CNS (or else there'd be no point in using it at all since you wouldn't get it's positive effects). To achieve this, we need to find a way to block it from interacting with the alpha-7 subtype specifically, as that would keep its positive effects while preventing its interaction with the growth plates.

This is unfortunately not possible to do safely, with the only known solution being:

Methyllycaconitine (MLA)
​

This compound was researched in this study for preventing this interaction, and was found to be successful.

"Methyllycaconitine (MLA), a specific antagonist of alpha7 nAChR, reversed the inhibition of matrix synthesis and functional calcium signal by nicotine in human growth plate chondrocytes in vitro."
​

MLA is a potent toxin directly because of its effects on the alpha-7 nAChR, leading to muscular paralysis, impairment of breathing and heart function, and death.

CONCLUSION
​

Nicotine affects growth plates through alpha-7 nAChRs, leading to a decreased growth velocity and potentially a lower FAH. Its use should therefore be suspended. MLA, the only well-documented way of preventing this interaction, is not suitable as a method of harm reduction because it interferes with the alpha-7 receptor's normal functions as well, which can be deadly. In short, this interaction can not be prevented, and it is therefore advised to taper off and quit using nicotine if you care about your height, as no other option to prevent this interaction is available.

TLDR FOR LAZY FUCKS
Nicotine's effects on the growth plate can not be prevented, because the receptors it interacts with are vital for your heart and lung function. You can only prevent these interactions with the cessation of nicotine consumption as a result.

EDIT:

I just want to add that if you are currently using nicotine, and do not want to quit, there is a way to minimise these effects.

now it won't get rid of them for reasons i'll explain later but it will keep them to a minimum.

If you avoid nicotine 4 hours before bed, you should avoid about 90% of these effects (as it has a halflife of 1-2 hours)
However, cotinine (the metabolite of nicotine) has a much longer halflife of about 20 hours, and it too can act on nAChRs (although with 100x less binding affinity compared to nicotine), so you won't avoid the effects entirely.