GENETICS = HEIGHT? HIGH IQ USER GTFIH

[WhoTookVendetta]

how the fuck is height genetics

dont say low iq shit like

"oh cuz higher hgh brooo"

tell me how the fuck is the genetic blueprint encoded actually effect how long the bone forms

like physically how the fuck is genetic encoded inside DNA

and in a short vs tall person

WHAT is the differences hormonally or whatever the fuck

like tell me how the genetic encoding effects the height

EXPLAIN!!!!!!!

 

[Roge]

Why dont you use search?

 

[Muttcel foid killer]

how the fuck is height genetics

dont say low iq shit like

"oh cuz higher hgh brooo"

tell me how the fuck is the genetic blueprint encoded actually effect how long the bone forms

like physically how the fuck is genetic encoded inside DNA

and in a short vs tall person

WHAT is the differences hormonally or whatever the fuck

like tell me how the genetic encoding effects the height

EXPLAIN!!!!!!!

Ancestors or some shit nigga vikings white people the weather abos evolution nigga go watch some PBS or some shit

 

[wastedspermcel]

I'm guessing more sensitive igf-1 receptors in the growth plates, less E2 receptors there too prolonging open plates

 

[Kelly Oubre Jr]

most people here are too low iq to even actually understand the question

now that i think about it OP, im also wondering the same thing, because (to my knowledge) there is not any established statistically significant correlation between height and any hormonal markers

 

[WhoTookVendetta]

I'm guessing more sensitive igf-1 receptors in the growth plates, less E2 receptors there too prolonging open plates

 

[Kelly Oubre Jr]

I'm guessing more sensitive igf-1 receptors in the growth plates, less E2 receptors there too prolonging open plates

this could be it, differences in the receptors would explain the lack of differences in the actual hormone amounts

 

[sinss]

pretty sure it has something to do with the ACAN and SHOX gene or sum shit

 

[wastedspermcel]

this could be it, differences in the receptors would explain the lack of differences in the actual hormone amounts

I mean some people have open growth plates with a lot of igf-1 (I'm talking 800ng/dl+) yet still don't grow

 

[WhoTookVendetta]

pretty sure it has something to do with the ACAN and SHOX gene or sum shit

Accountants Confidential Assistance Network (ACAN) | TXCPA

The ACAN mission is to assist Texas CPAs who have a job impairing alcohol, drug or mental health problem in order that they can return to competent practice.

www.tx.cpa

Nike Shox Shoes. Nike.com

Find Nike Shox Shoes at Nike.com. Free delivery and returns.

www.nike.com

 

[WhoTookVendetta]

I mean some people have open growth plates with a lot of igf-1 (I'm talking 800ng/dl+) yet still don't grow

maybe receptor sensetivity

thats why growth speeds up or slows down

and DNA can influence when the receptors are more sensitive to growth

 

[sinss]

Accountants Confidential Assistance Network (ACAN) | TXCPA

The ACAN mission is to assist Texas CPAs who have a job impairing alcohol, drug or mental health problem in order that they can return to competent practice.

www.tx.cpa

Nike Shox Shoes. Nike.com

Find Nike Shox Shoes at Nike.com. Free delivery and returns.

www.nike.com

literally just type "acan gene" and "shox gene"

 

[wastedspermcel]

maybe receptor sensetivity

thats why growth speeds up or slows down

and DNA can influence when the receptors are more sensitive to growth

Yeah, growth spurts are also genetic, you can't 'trigger' one necessarily

 

[WhoTookVendetta]

Yeah, growth spurts are also genetic, you can't 'trigger' one necessarily

over for retards sleeping 12hrs to HGHMAXX to grow taller

 

[xevuxia]

Height is primarily determined by a combination of genetics and environmental factors. Here’s how it works at the genetic and physiological levels:

1. Genetic Encoding: Height is influenced by many genes that affect growth plates in bones. These genes regulate proteins involved in the growth of cartilage and bone, such as collagen and growth factor proteins. Variations in these genes can lead to differences in how long bones grow.
2. Hormonal Influence: Growth hormone (GH), which is produced by the pituitary gland, plays a crucial role in growth. The way the body responds to GH can be influenced by genetic factors, determining how effectively bones elongate. Other hormones, like insulin-like growth factor 1 (IGF-1), are also involved in mediating the effects of GH on bone growth.
3. Bone Growth: Long bones grow at their growth plates (epiphyseal plates). Genetics influences how these growth plates develop and when they close. For instance, taller individuals may have a later closure of these plates, allowing for more growth over time.
4. Cellular Mechanisms: The genetic instructions encoded in DNA affect the proliferation and differentiation of chondrocytes (cartilage cells) at the growth plates. Specific genes can lead to differences in cell activity, affecting how quickly and extensively these plates grow.
5. Environmental Factors: While genetics sets the potential height range, nutrition, health, and overall environment also play significant roles. Poor nutrition or chronic illness can stunt growth, regardless of genetic predisposition.

In summary, height is a complex trait influenced by multiple genes and their interaction with hormonal pathways and environmental factors. Each component plays a specific role in how bones develop and grow.

 

[sinss]

Height is primarily determined by a combination of genetics and environmental factors. Here’s how it works at the genetic and physiological levels:

1. Genetic Encoding: Height is influenced by many genes that affect growth plates in bones. These genes regulate proteins involved in the growth of cartilage and bone, such as collagen and growth factor proteins. Variations in these genes can lead to differences in how long bones grow.
2. Hormonal Influence: Growth hormone (GH), which is produced by the pituitary gland, plays a crucial role in growth. The way the body responds to GH can be influenced by genetic factors, determining how effectively bones elongate. Other hormones, like insulin-like growth factor 1 (IGF-1), are also involved in mediating the effects of GH on bone growth.
3. Bone Growth: Long bones grow at their growth plates (epiphyseal plates). Genetics influences how these growth plates develop and when they close. For instance, taller individuals may have a later closure of these plates, allowing for more growth over time.
4. Cellular Mechanisms: The genetic instructions encoded in DNA affect the proliferation and differentiation of chondrocytes (cartilage cells) at the growth plates. Specific genes can lead to differences in cell activity, affecting how quickly and extensively these plates grow.
5. Environmental Factors: While genetics sets the potential height range, nutrition, health, and overall environment also play significant roles. Poor nutrition or chronic illness can stunt growth, regardless of genetic predisposition.

In summary, height is a complex trait influenced by multiple genes and their interaction with hormonal pathways and environmental factors. Each component plays a specific role in how bones develop and grow.

chatgpt demon + brutal post to rep ratio

 

[WhoTookVendetta]

Height is primarily determined by a combination of genetics and environmental factors. Here’s how it works at the genetic and physiological levels:

1. Genetic Encoding: Height is influenced by many genes that affect growth plates in bones. These genes regulate proteins involved in the growth of cartilage and bone, such as collagen and growth factor proteins. Variations in these genes can lead to differences in how long bones grow.
2. Hormonal Influence: Growth hormone (GH), which is produced by the pituitary gland, plays a crucial role in growth. The way the body responds to GH can be influenced by genetic factors, determining how effectively bones elongate. Other hormones, like insulin-like growth factor 1 (IGF-1), are also involved in mediating the effects of GH on bone growth.
3. Bone Growth: Long bones grow at their growth plates (epiphyseal plates). Genetics influences how these growth plates develop and when they close. For instance, taller individuals may have a later closure of these plates, allowing for more growth over time.
4. Cellular Mechanisms: The genetic instructions encoded in DNA affect the proliferation and differentiation of chondrocytes (cartilage cells) at the growth plates. Specific genes can lead to differences in cell activity, affecting how quickly and extensively these plates grow.
5. Environmental Factors: While genetics sets the potential height range, nutrition, health, and overall environment also play significant roles. Poor nutrition or chronic illness can stunt growth, regardless of genetic predisposition.

In summary, height is a complex trait influenced by multiple genes and their interaction with hormonal pathways and environmental factors. Each component plays a specific role in how bones develop and grow.

Yeah, growth spurts are also genetic, you can't 'trigger' one necessarily

literally just type "acan gene" and "shox gene"

this could be it, differences in the receptors would explain the lack of differences in the actual hormone amounts

To articulate the genetic regulation of height at a more sophisticated level, we must consider the complex interplay between polygenic inheritance and the cellular signaling pathways mediated by highly specific receptor-ligand interactions. At its core, the genetic architecture underlying height is orchestrated through a multitude of loci that influence the expression, sensitivity, and regulatory capacity of receptors embedded within growth-regulating pathways.

1. Polygenic Complexity and Receptor Pathways​

Height is governed by a polygenic framework, where additive and non-additive genetic effects converge upon signaling mechanisms that control somatic growth. The genome encodes for a diverse array of transmembrane and intracellular receptors, which are pivotal in transducing exogenous growth signals into intracellular cascades. These receptors function within highly regulated feedback loops, ensuring precise modulation of growth stimuli. For instance, IGF-1 receptor pathways are heavily involved in cellular proliferation within the epiphyseal plates, modulating the rate of chondrocyte maturation and ossification through PI3K-AKT and MAPK pathways. Variations in these receptor genes, often at non-coding regulatory regions, affect transcriptional activity, receptor density, and downstream signaling efficacy, ultimately influencing stature.

2. Receptor Sensitivity and Stoichiometric Precision​

Genetic polymorphisms affecting receptor conformational dynamics modulate ligand-binding affinities and the stoichiometry of receptor complexes, dictating the efficiency of signal transduction. For instance, subtle differences in allelic variants can lead to alterations in receptor phosphorylation states or dimerization efficiencies, which significantly impact how extracellular cues such as growth hormone (GH) and IGF-1 are interpreted by skeletal cells. Enhanced post-receptor signaling amplification, through elevated receptor sensitivity, can result in accelerated cellular proliferation in the growth plates, while diminished receptor function can constrain growth potential by attenuating the propagation of anabolic signals.

3. Epigenetic Modulation and Growth Plate Senescence​

Beyond pure genetic predisposition, epigenetic mechanisms play a crucial role in regulating receptor expression and activity. DNA methylation patterns and histone modifications at loci governing receptor genes can alter their transcriptional accessibility, thereby influencing the temporal and spatial expression of receptors throughout developmental stages. Moreover, receptor-mediated control of growth plate senescence is a key determinant of final stature. For instance, estrogen receptor-alpha (ERα) mediates the eventual closure of epiphyseal plates, and polymorphic variations in its regulatory regions can accelerate or delay this process through altered transcriptional dynamics, impacting the longevity of longitudinal bone growth.

4. Network Dynamics and Systemic Integration​

At a systemic level, height determination is not merely a function of isolated genetic signals but arises from emergent properties within a multilayered biological network. The integration of receptor-mediated pathways with endocrine signals, including thyroid hormones, androgens, estrogens, and corticosteroids, forms a complex adaptive system that calibrates growth according to genetic predispositions and environmental inputs. The cross-talk between receptor pathways, governed by feedback inhibition loops and intercellular communication, ensures the homeostatic regulation of growth processes in response to both internal and external stimuli.

5. Quantum Molecular Interactions and Receptor Efficiency​

At the quantum molecular level, electron density distributions within receptor binding pockets and ligand-receptor quantum tunneling effects may further influence receptor efficacy. Subtle shifts in molecular orbital configurations caused by genetic mutations could theoretically alter the quantum mechanical probabilities of successful ligand binding, thereby modulating growth signal reception at a fundamental level. This would provide a novel layer of control over receptor functionality that transcends classical biochemical models, suggesting that quantum biology might play an underexplored role in height determination.

Conclusion​

In sum, height is the phenotypic manifestation of an intricate genetic and epigenetic system where receptor-ligand interactions act as the pivotal mediators of growth. Through a highly regulated network of signaling pathways, governed by both genetic variants and receptor sensitivity, the human genome sculpts individual stature. The final outcome is a dynamic equilibrium between genetic potential, receptor efficiency, and environmental factors, all finely tuned within a multi-scalar biological hierarchy.

 

[sinss]

To articulate the genetic regulation of height at a more sophisticated level, we must consider the complex interplay between polygenic inheritance and the cellular signaling pathways mediated by highly specific receptor-ligand interactions. At its core, the genetic architecture underlying height is orchestrated through a multitude of loci that influence the expression, sensitivity, and regulatory capacity of receptors embedded within growth-regulating pathways.

1. Polygenic Complexity and Receptor Pathways​

Height is governed by a polygenic framework, where additive and non-additive genetic effects converge upon signaling mechanisms that control somatic growth. The genome encodes for a diverse array of transmembrane and intracellular receptors, which are pivotal in transducing exogenous growth signals into intracellular cascades. These receptors function within highly regulated feedback loops, ensuring precise modulation of growth stimuli. For instance, IGF-1 receptor pathways are heavily involved in cellular proliferation within the epiphyseal plates, modulating the rate of chondrocyte maturation and ossification through PI3K-AKT and MAPK pathways. Variations in these receptor genes, often at non-coding regulatory regions, affect transcriptional activity, receptor density, and downstream signaling efficacy, ultimately influencing stature.

2. Receptor Sensitivity and Stoichiometric Precision​

Genetic polymorphisms affecting receptor conformational dynamics modulate ligand-binding affinities and the stoichiometry of receptor complexes, dictating the efficiency of signal transduction. For instance, subtle differences in allelic variants can lead to alterations in receptor phosphorylation states or dimerization efficiencies, which significantly impact how extracellular cues such as growth hormone (GH) and IGF-1 are interpreted by skeletal cells. Enhanced post-receptor signaling amplification, through elevated receptor sensitivity, can result in accelerated cellular proliferation in the growth plates, while diminished receptor function can constrain growth potential by attenuating the propagation of anabolic signals.

3. Epigenetic Modulation and Growth Plate Senescence​

Beyond pure genetic predisposition, epigenetic mechanisms play a crucial role in regulating receptor expression and activity. DNA methylation patterns and histone modifications at loci governing receptor genes can alter their transcriptional accessibility, thereby influencing the temporal and spatial expression of receptors throughout developmental stages. Moreover, receptor-mediated control of growth plate senescence is a key determinant of final stature. For instance, estrogen receptor-alpha (ERα) mediates the eventual closure of epiphyseal plates, and polymorphic variations in its regulatory regions can accelerate or delay this process through altered transcriptional dynamics, impacting the longevity of longitudinal bone growth.

4. Network Dynamics and Systemic Integration​

At a systemic level, height determination is not merely a function of isolated genetic signals but arises from emergent properties within a multilayered biological network. The integration of receptor-mediated pathways with endocrine signals, including thyroid hormones, androgens, estrogens, and corticosteroids, forms a complex adaptive system that calibrates growth according to genetic predispositions and environmental inputs. The cross-talk between receptor pathways, governed by feedback inhibition loops and intercellular communication, ensures the homeostatic regulation of growth processes in response to both internal and external stimuli.

5. Quantum Molecular Interactions and Receptor Efficiency​

At the quantum molecular level, electron density distributions within receptor binding pockets and ligand-receptor quantum tunneling effects may further influence receptor efficacy. Subtle shifts in molecular orbital configurations caused by genetic mutations could theoretically alter the quantum mechanical probabilities of successful ligand binding, thereby modulating growth signal reception at a fundamental level. This would provide a novel layer of control over receptor functionality that transcends classical biochemical models, suggesting that quantum biology might play an underexplored role in height determination.

Conclusion​

In sum, height is the phenotypic manifestation of an intricate genetic and epigenetic system where receptor-ligand interactions act as the pivotal mediators of growth. Through a highly regulated network of signaling pathways, governed by both genetic variants and receptor sensitivity, the human genome sculpts individual stature. The final outcome is a dynamic equilibrium between genetic potential, receptor efficiency, and environmental factors, all finely tuned within a multi-scalar biological hierarchy.

tldr: just dont receive retarded genes on genetics day

 

[MA_ascender]

To articulate the genetic regulation of height at a more sophisticated level, we must consider the complex interplay between polygenic inheritance and the cellular signaling pathways mediated by highly specific receptor-ligand interactions. At its core, the genetic architecture underlying height is orchestrated through a multitude of loci that influence the expression, sensitivity, and regulatory capacity of receptors embedded within growth-regulating pathways.

1. Polygenic Complexity and Receptor Pathways​

Height is governed by a polygenic framework, where additive and non-additive genetic effects converge upon signaling mechanisms that control somatic growth. The genome encodes for a diverse array of transmembrane and intracellular receptors, which are pivotal in transducing exogenous growth signals into intracellular cascades. These receptors function within highly regulated feedback loops, ensuring precise modulation of growth stimuli. For instance, IGF-1 receptor pathways are heavily involved in cellular proliferation within the epiphyseal plates, modulating the rate of chondrocyte maturation and ossification through PI3K-AKT and MAPK pathways. Variations in these receptor genes, often at non-coding regulatory regions, affect transcriptional activity, receptor density, and downstream signaling efficacy, ultimately influencing stature.

2. Receptor Sensitivity and Stoichiometric Precision​

Genetic polymorphisms affecting receptor conformational dynamics modulate ligand-binding affinities and the stoichiometry of receptor complexes, dictating the efficiency of signal transduction. For instance, subtle differences in allelic variants can lead to alterations in receptor phosphorylation states or dimerization efficiencies, which significantly impact how extracellular cues such as growth hormone (GH) and IGF-1 are interpreted by skeletal cells. Enhanced post-receptor signaling amplification, through elevated receptor sensitivity, can result in accelerated cellular proliferation in the growth plates, while diminished receptor function can constrain growth potential by attenuating the propagation of anabolic signals.

3. Epigenetic Modulation and Growth Plate Senescence​

Beyond pure genetic predisposition, epigenetic mechanisms play a crucial role in regulating receptor expression and activity. DNA methylation patterns and histone modifications at loci governing receptor genes can alter their transcriptional accessibility, thereby influencing the temporal and spatial expression of receptors throughout developmental stages. Moreover, receptor-mediated control of growth plate senescence is a key determinant of final stature. For instance, estrogen receptor-alpha (ERα) mediates the eventual closure of epiphyseal plates, and polymorphic variations in its regulatory regions can accelerate or delay this process through altered transcriptional dynamics, impacting the longevity of longitudinal bone growth.

4. Network Dynamics and Systemic Integration​

At a systemic level, height determination is not merely a function of isolated genetic signals but arises from emergent properties within a multilayered biological network. The integration of receptor-mediated pathways with endocrine signals, including thyroid hormones, androgens, estrogens, and corticosteroids, forms a complex adaptive system that calibrates growth according to genetic predispositions and environmental inputs. The cross-talk between receptor pathways, governed by feedback inhibition loops and intercellular communication, ensures the homeostatic regulation of growth processes in response to both internal and external stimuli.

5. Quantum Molecular Interactions and Receptor Efficiency​

At the quantum molecular level, electron density distributions within receptor binding pockets and ligand-receptor quantum tunneling effects may further influence receptor efficacy. Subtle shifts in molecular orbital configurations caused by genetic mutations could theoretically alter the quantum mechanical probabilities of successful ligand binding, thereby modulating growth signal reception at a fundamental level. This would provide a novel layer of control over receptor functionality that transcends classical biochemical models, suggesting that quantum biology might play an underexplored role in height determination.

Conclusion​

In sum, height is the phenotypic manifestation of an intricate genetic and epigenetic system where receptor-ligand interactions act as the pivotal mediators of growth. Through a highly regulated network of signaling pathways, governed by both genetic variants and receptor sensitivity, the human genome sculpts individual stature. The final outcome is a dynamic equilibrium between genetic potential, receptor efficiency, and environmental factors, all finely tuned within a multi-scalar biological hierarchy.

Me when I dnrd

 

[StarvedEpi]

They are more sensitive to the hormones meaning they get more growth with the same amount, an example of high responders are west Africans, they have average amount of test but because they respond strongly they are all jacked shredded niggas