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Discussion Does nicotine descend you?? (2 Viewers)

Discussion Does nicotine descend you??

Dexter

🩺 | .gg’s doctor, M.D.
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Yes go ahead
the entire process of linear growth (via chondrocyte proliferation, chondrocyte hypertrophy, matrix mineralization, osteoblastic replacement) gets interfered by smoking.

nicotine suppresses the GH-IGF1 axis.
in normal physiology, this would be the case:
hypo -> ghrh
pituitary -> pulsatile gh secretion
liver -> igf1
igf1 -> chondrocyte div in growth plates

what nicotine does:
activates alpha4beta2 nictinic acetylcholine receptor at CNS
increase dopamine and cortisol
blunts nocturnal gh pulses
reduces hepatic igf1 synthesis

Nicotine also causes chronic hypoxia at growth plate level
bcz growth plates are avascular so they rely ENTIRELY on O2 and nutrients diffusion from surrounding capillaries

what smoking introduces:
CO (carbon monoxide) -> binds Hb with 200x (iirc) affinity of O2
nicotine -> vasoconstriction (bcz of sympathetic activation)
endothelial dysfunction -> less nitric oxide available

THAT OVERALL creates functional hypoxia in the growth plates

hypoxia inhibits chondrocytic hypertrophy, accelerates premature closure of plates, activates hypoxia inducible stress pathways instead of growth pathways like in normal niggas

also cortisol is raised
cortisol inhibits collagen type II synthesis

there's a toxicity to griwth plate chondrocytes as well because tobacco smoke contains:
polycyclic aromatic hydrocarbons
cadmium
reactive oxygen species

they induce oxidative DNA damage in chondrocytes, increase apoptosis, reduce extracellular matrix production, activate inflammatory NF-kB signalling (couldn't find the symbol)

then nicotine also alters DNA methylation patterns, histone acetylation, microRNA expression related to growth and they reduce responsiveness to gh and igf1
 

tmpll

IDF soldier
Joined
Jan 16, 2026
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the entire process of linear growth (via chondrocyte proliferation, chondrocyte hypertrophy, matrix mineralization, osteoblastic replacement) gets interfered by smoking.

nicotine suppresses the GH-IGF1 axis.
in normal physiology, this would be the case:
hypo -> ghrh
pituitary -> pulsatile gh secretion
liver -> igf1
igf1 -> chondrocyte div in growth plates

what nicotine does:
activates alpha4beta2 nictinic acetylcholine receptor at CNS
increase dopamine and cortisol
blunts nocturnal gh pulses
reduces hepatic igf1 synthesis

Nicotine also causes chronic hypoxia at growth plate level
bcz growth plates are avascular so they rely ENTIRELY on O2 and nutrients diffusion from surrounding capillaries

what smoking introduces:
CO (carbon monoxide) -> binds Hb with 200x (iirc) affinity of O2
nicotine -> vasoconstriction (bcz of sympathetic activation)
endothelial dysfunction -> less nitric oxide available

THAT OVERALL creates functional hypoxia in the growth plates

hypoxia inhibits chondrocytic hypertrophy, accelerates premature closure of plates, activates hypoxia inducible stress pathways instead of growth pathways like in normal niggas

also cortisol is raised
cortisol inhibits collagen type II synthesis

there's a toxicity to griwth plate chondrocytes as well because tobacco smoke contains:
polycyclic aromatic hydrocarbons
cadmium
reactive oxygen species

they induce oxidative DNA damage in chondrocytes, increase apoptosis, reduce extracellular matrix production, activate inflammatory NF-kB signalling (couldn't find the symbol)

then nicotine also alters DNA methylation patterns, histone acetylation, microRNA expression related to growth and they reduce responsiveness to gh and igf1
high iq😍
 

Normielarper

Nosecel
Joined
Dec 27, 2025
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the entire process of linear growth (via chondrocyte proliferation, chondrocyte hypertrophy, matrix mineralization, osteoblastic replacement) gets interfered by smoking.

nicotine suppresses the GH-IGF1 axis.
in normal physiology, this would be the case:
hypo -> ghrh
pituitary -> pulsatile gh secretion
liver -> igf1
igf1 -> chondrocyte div in growth plates

what nicotine does:
activates alpha4beta2 nictinic acetylcholine receptor at CNS
increase dopamine and cortisol
blunts nocturnal gh pulses
reduces hepatic igf1 synthesis

Nicotine also causes chronic hypoxia at growth plate level
bcz growth plates are avascular so they rely ENTIRELY on O2 and nutrients diffusion from surrounding capillaries

what smoking introduces:
CO (carbon monoxide) -> binds Hb with 200x (iirc) affinity of O2
nicotine -> vasoconstriction (bcz of sympathetic activation)
endothelial dysfunction -> less nitric oxide available

THAT OVERALL creates functional hypoxia in the growth plates

hypoxia inhibits chondrocytic hypertrophy, accelerates premature closure of plates, activates hypoxia inducible stress pathways instead of growth pathways like in normal niggas

also cortisol is raised
cortisol inhibits collagen type II synthesis

there's a toxicity to griwth plate chondrocytes as well because tobacco smoke contains:
polycyclic aromatic hydrocarbons
cadmium
reactive oxygen species

they induce oxidative DNA damage in chondrocytes, increase apoptosis, reduce extracellular matrix production, activate inflammatory NF-kB signalling (couldn't find the symbol)

then nicotine also alters DNA methylation patterns, histone acetylation, microRNA expression related to growth and they reduce responsiveness to gh and igf1
what’s your iq Holy fuck
 

Mirin

Avi but hmtn
Joined
Dec 24, 2025
Posts
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the entire process of linear growth (via chondrocyte proliferation, chondrocyte hypertrophy, matrix mineralization, osteoblastic replacement) gets interfered by smoking.

nicotine suppresses the GH-IGF1 axis.
in normal physiology, this would be the case:
hypo -> ghrh
pituitary -> pulsatile gh secretion
liver -> igf1
igf1 -> chondrocyte div in growth plates

what nicotine does:
activates alpha4beta2 nictinic acetylcholine receptor at CNS
increase dopamine and cortisol
blunts nocturnal gh pulses
reduces hepatic igf1 synthesis

Nicotine also causes chronic hypoxia at growth plate level
bcz growth plates are avascular so they rely ENTIRELY on O2 and nutrients diffusion from surrounding capillaries

what smoking introduces:
CO (carbon monoxide) -> binds Hb with 200x (iirc) affinity of O2
nicotine -> vasoconstriction (bcz of sympathetic activation)
endothelial dysfunction -> less nitric oxide available

THAT OVERALL creates functional hypoxia in the growth plates

hypoxia inhibits chondrocytic hypertrophy, accelerates premature closure of plates, activates hypoxia inducible stress pathways instead of growth pathways like in normal niggas

also cortisol is raised
cortisol inhibits collagen type II synthesis

there's a toxicity to griwth plate chondrocytes as well because tobacco smoke contains:
polycyclic aromatic hydrocarbons
cadmium
reactive oxygen species

they induce oxidative DNA damage in chondrocytes, increase apoptosis, reduce extracellular matrix production, activate inflammatory NF-kB signalling (couldn't find the symbol)

then nicotine also alters DNA methylation patterns, histone acetylation, microRNA expression related to growth and they reduce responsiveness to gh and igf1
  • Stunted Height: Studies indicate that teenage boys who smoke can be, on average, 2.54 centimeters (1 inch) shorter than non-smokers.
 

carbon

Friendly guy
Joined
Jan 7, 2026
Posts
614
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the entire process of linear growth (via chondrocyte proliferation, chondrocyte hypertrophy, matrix mineralization, osteoblastic replacement) gets interfered by smoking.

nicotine suppresses the GH-IGF1 axis.
in normal physiology, this would be the case:
hypo -> ghrh
pituitary -> pulsatile gh secretion
liver -> igf1
igf1 -> chondrocyte div in growth plates

what nicotine does:
activates alpha4beta2 nictinic acetylcholine receptor at CNS
increase dopamine and cortisol
blunts nocturnal gh pulses
reduces hepatic igf1 synthesis

Nicotine also causes chronic hypoxia at growth plate level
bcz growth plates are avascular so they rely ENTIRELY on O2 and nutrients diffusion from surrounding capillaries

what smoking introduces:
CO (carbon monoxide) -> binds Hb with 200x (iirc) affinity of O2
nicotine -> vasoconstriction (bcz of sympathetic activation)
endothelial dysfunction -> less nitric oxide available

THAT OVERALL creates functional hypoxia in the growth plates

hypoxia inhibits chondrocytic hypertrophy, accelerates premature closure of plates, activates hypoxia inducible stress pathways instead of growth pathways like in normal niggas

also cortisol is raised
cortisol inhibits collagen type II synthesis

there's a toxicity to griwth plate chondrocytes as well because tobacco smoke contains:
polycyclic aromatic hydrocarbons
cadmium
reactive oxygen species

they induce oxidative DNA damage in chondrocytes, increase apoptosis, reduce extracellular matrix production, activate inflammatory NF-kB signalling (couldn't find the symbol)

then nicotine also alters DNA methylation patterns, histone acetylation, microRNA expression related to growth and they reduce responsiveness to gh and igf1
Exactly what I would’ve said
 

LifeEnjoyer

enderman
Joined
Dec 31, 2025
Posts
1,277
Reputation
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the entire process of linear growth (via chondrocyte proliferation, chondrocyte hypertrophy, matrix mineralization, osteoblastic replacement) gets interfered by smoking.

nicotine suppresses the GH-IGF1 axis.
in normal physiology, this would be the case:
hypo -> ghrh
pituitary -> pulsatile gh secretion
liver -> igf1
igf1 -> chondrocyte div in growth plates

what nicotine does:
activates alpha4beta2 nictinic acetylcholine receptor at CNS
increase dopamine and cortisol
blunts nocturnal gh pulses
reduces hepatic igf1 synthesis

Nicotine also causes chronic hypoxia at growth plate level
bcz growth plates are avascular so they rely ENTIRELY on O2 and nutrients diffusion from surrounding capillaries

what smoking introduces:
CO (carbon monoxide) -> binds Hb with 200x (iirc) affinity of O2
nicotine -> vasoconstriction (bcz of sympathetic activation)
endothelial dysfunction -> less nitric oxide available

THAT OVERALL creates functional hypoxia in the growth plates

hypoxia inhibits chondrocytic hypertrophy, accelerates premature closure of plates, activates hypoxia inducible stress pathways instead of growth pathways like in normal niggas

also cortisol is raised
cortisol inhibits collagen type II synthesis

there's a toxicity to griwth plate chondrocytes as well because tobacco smoke contains:
polycyclic aromatic hydrocarbons
cadmium
reactive oxygen species

they induce oxidative DNA damage in chondrocytes, increase apoptosis, reduce extracellular matrix production, activate inflammatory NF-kB signalling (couldn't find the symbol)

then nicotine also alters DNA methylation patterns, histone acetylation, microRNA expression related to growth and they reduce responsiveness to gh and igf1
high iq
 
Joined
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