5-HT2A possible effects on height and why it should be more looked into.

[tyrazane]

Spoiler: (dnr) Why marked under this category.

Marked as theory because I don’t know exactly how it could be applicable.

TLDR:

• 5-HT2A/2B signaling clearly affects skeletal biology, including growth-plate chondrocytes, osteoblast differentiation, and bone formation.

Sources for you incels to dig deeper-

Spoiler: Sources and what they convey

1. Hori et al. — “Regulatory mechanism of CCN2 production by serotonin (5-HT) via 5-HT2A and 5-HT2B receptors in chondrocytes” (2017)

• 5-HT2A signaling increased Akt/p38 activity and CCN2 in chondrocytes, and 5-HT2A was specifically localized to the growth plate. Mechanistically, this places 5-HT2A upstream of a cartilage-development pathway potentially relevant to longitudinal bone growth, although the study does not demonstrate increased human height. (PubMed)

1. Tanaka et al. — “Modulation of osteoblast differentiation and bone mass by 5-HT2A receptor signaling in mice” (2015)

• Pharmacologically blocking 5-HT2A reduced bone mass and impaired osteoblast differentiation, including suppression of osterix and alkaline-phosphatase activity. This suggests 5-HT2A signaling contributes to the anabolic machinery that builds bone, but bone-mass effects cannot automatically be translated into increased longitudinal growth. (PubMed)

1. Collet et al. — “The serotonin 5-HT2B receptor controls bone mass via osteoblast recruitment and proliferation” (2008)

• Removing 5-HT2B produced an osteopenic phenotype because osteoblast precursor recruitment, proliferation, differentiation, and calcium incorporation were all impaired. The key mechanistic takeaway is that 5-HT2B functions as a pro-osteogenic signal in bone-forming cells, establishing a direct serotonergic influence on skeletal tissue. (PubMed)

1. Chabbi-Alaoui et al. — “Stepwise control of osteogenic differentiation by 5-HT2B receptor signaling” (2005)

• During osteogenic differentiation, 5-HT2B signaling regulated NO, PLA2/arachidonic-acid and prostaglandin pathways; blocking its activity reduced matrix calcium incorporation by ~40%. This shows 5-HT2B is embedded directly in the signaling architecture that determines whether developing skeletal cells successfully mineralize. (PubMed)

1. Warden et al. — “Inhibition of the serotonin transporter reduces bone accrual during growth” (2005)

• Disrupting serotonin transport during skeletal growth caused reduced bone mass and impaired bone formation in mice, demonstrating that serotonergic signaling is capable of altering the developing skeleton. It is indirect evidence for 5-HT2 biology, however, because changing the serotonin transporter affects multiple serotonin receptors rather than selectively manipulating 5-HT2A/2B. (PubMed)

1. Lavoie et al. — “Serotonin regulates osteoblast proliferation and function in vitro” (2014)

• Serotonin altered osteoblast proliferation, differentiation and mineralization in a concentration-dependent manner, while osteoblasts expressed several serotonin receptors including 5-HT2A, 5-HT2B and 5-HT2C. The important point is that serotonergic effects on bone are highly context-dependent rather than simply “more serotonin = more growth,” with receptor subtype and signaling environment determining the phenotype. (PubMed)

 

[dourememberme]

tgdnr

 

[tyrazane]

tgdnr

?

 

[dourememberme]

?

to grey did NOT read
mirin effort

 

[tyrazane]

to grey did NOT read
mirin effort

Don’t throw stone from a glass house, if there is even a thing as “to gray” you are technically more gray as you have more posts and less rep.

 

[dourememberme]

Don’t throw stone from a glass house, if there is even a thing as “to gray” you are technically more gray as you have more posts and less rep.

super sensitive soy boy
my names rainbow on my screen

 

[tyrazane]

super sensitive soy boy
my names rainbow on my screen

Just not the kinda interaction i’m looking for- and good of you dude

 

[tyrazane]

Spoiler: (dnr) Why marked under this category.

Marked as theory because I don’t know exactly how it could be applicable.

TLDR:

• 5-HT2A/2B signaling clearly affects skeletal biology, including growth-plate chondrocytes, osteoblast differentiation, and bone formation.

Sources for you incels to dig deeper-

Spoiler: Sources and what they convey

1. Hori et al. — “Regulatory mechanism of CCN2 production by serotonin (5-HT) via 5-HT2A and 5-HT2B receptors in chondrocytes” (2017)

• 5-HT2A signaling increased Akt/p38 activity and CCN2 in chondrocytes, and 5-HT2A was specifically localized to the growth plate. Mechanistically, this places 5-HT2A upstream of a cartilage-development pathway potentially relevant to longitudinal bone growth, although the study does not demonstrate increased human height. (PubMed)

1. Tanaka et al. — “Modulation of osteoblast differentiation and bone mass by 5-HT2A receptor signaling in mice” (2015)

• Pharmacologically blocking 5-HT2A reduced bone mass and impaired osteoblast differentiation, including suppression of osterix and alkaline-phosphatase activity. This suggests 5-HT2A signaling contributes to the anabolic machinery that builds bone, but bone-mass effects cannot automatically be translated into increased longitudinal growth. (PubMed)

1. Collet et al. — “The serotonin 5-HT2B receptor controls bone mass via osteoblast recruitment and proliferation” (2008)

• Removing 5-HT2B produced an osteopenic phenotype because osteoblast precursor recruitment, proliferation, differentiation, and calcium incorporation were all impaired. The key mechanistic takeaway is that 5-HT2B functions as a pro-osteogenic signal in bone-forming cells, establishing a direct serotonergic influence on skeletal tissue. (PubMed)

1. Chabbi-Alaoui et al. — “Stepwise control of osteogenic differentiation by 5-HT2B receptor signaling” (2005)

• During osteogenic differentiation, 5-HT2B signaling regulated NO, PLA2/arachidonic-acid and prostaglandin pathways; blocking its activity reduced matrix calcium incorporation by ~40%. This shows 5-HT2B is embedded directly in the signaling architecture that determines whether developing skeletal cells successfully mineralize. (PubMed)

1. Warden et al. — “Inhibition of the serotonin transporter reduces bone accrual during growth” (2005)

• Disrupting serotonin transport during skeletal growth caused reduced bone mass and impaired bone formation in mice, demonstrating that serotonergic signaling is capable of altering the developing skeleton. It is indirect evidence for 5-HT2 biology, however, because changing the serotonin transporter affects multiple serotonin receptors rather than selectively manipulating 5-HT2A/2B. (PubMed)

1. Lavoie et al. — “Serotonin regulates osteoblast proliferation and function in vitro” (2014)

• Serotonin altered osteoblast proliferation, differentiation and mineralization in a concentration-dependent manner, while osteoblasts expressed several serotonin receptors including 5-HT2A, 5-HT2B and 5-HT2C. The important point is that serotonergic effects on bone are highly context-dependent rather than simply “more serotonin = more growth,” with receptor subtype and signaling environment determining the phenotype. (PubMed)

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[tyrazane]

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[India lover 52]

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