READ EVERY MOLECULE DONT CONCLUDE ANYTHING BEFORE READING FULLY AS FOR THE PROTOCOL THERE ARE MANY IN THIS FORUM YOU CAN SEE YOURSELF
CHAPTER 1: UNDERSTANDING AAS
Anabolic steroids also known as anabolic androgenic steroids (AAS), are a class of drugs that are structurally related to testosterone, the main male sex hormone, and produce effects by binding to and activating the androgen receptor (AR) . The chemical form of testosterone is (androst-4-en-17β-ol-3-one) . Anabolic refers to the skeletal muscle building properties of AAS, whereas androgenic refers to the induction and maintenance of male secondary sexual characteristics
Androgen receptor is a nuclear receptor by binding with androgen receptor it releases a series of proteins and genes
The androgen receptor (AR) which is also known as NR3C4 (nuclear receptor subfamily 3, group C, member 4), is a type of nuclear receptor that is activated by binding any of the androgenic hormones, including testosterone and dihydrotestosterone in the cytoplasm and then translocating into the nucleus.
In some cell types, testosterone interacts directly with androgen receptors, whereas, in others, testosterone is converted by 5-alpha-reductase to dihydrotestosterone (DHT), an even more potent agonist for androgen receptor activation
This pub med will tell you fully how androgen receptor works i dnrd some part of this site
CHAPTER 2: AAS AND AR RECEPTOR BINDING
There are derivates of test and DHT but as you see you need to follow the one who is guiding you . but the legends of legends Avskinov i want more knowledge , ok as your wish
Natty lifting is cope. JFL at spending a decade training optimally to end up as looking like someone that has just ended his first cycle. If you're serious about Looksmaxing, you're going to take every shortcut to achieve your goal. Why should I give a shit about roiding? A body halo is...
looksmax.org
WRITINIG THIS FROM PUBMED LEGENDS DOES WHAT LEGENDS WANT
Once in the system, AAS are transported to the tissues bound to binding proteins albumin, sex hormone-binding globulin (SHBG), corticosteroid-binding globulin (CBG) and orosomucoid. Under physiological conditions, testosterone is predominately bound to the first two, leaving only 1% to 4% of circulating testosterone unbound or free test or single test . SHBG binds testosterone with high love but has a relatively low binding capacity. Conversely albumin binds testosterone with low love and cold heart but has a virtually limitless binding capacity . SHBG is present in the bloodstream as a homodimer . Under physiological conditions about one third of the binding sites is occupied by testosterone, with further occupation by several other steroids rendering about 44% of SHBG-binding sites unbound . With physiological SHBG levels in the 10–56 nmol/L range, it is clear that supraphysiological dosages of testosterone saturate its binding capacity. Besides, supraphysiological dosages strongly decrease circulating SHBG levels. Thus, increasing dosages of testosterone result in a larger fraction of albumin-bound testosterone relative to the SHBG-bound fraction . It is noteworthy that SHBG has very low affinity for other commonly used AAS, such as nandrolone, methenolone, stanozolol, methandienone, fluoxymesterone and oxymetholone which is in slayer jhonas guide
All this to explain free test btw :feelshah: now this free test will bind to AR (Androgen receptor )
Testosterone is bioactivated into a more potent androgen in tissues expressing enzymes of the 5α-reductase family. These enzymes catalyze a reduction reaction at carbon 5, adding an α-oriented hydrogen atom. With testosterone as a substrate, this reaction yields the most potent naturally occurring androgen, namely, dihydrotestosterone (DHT). And DHT or test will regulate genes AREs (ANDROGENIC RESPONSE ELEMENTS )
Anabolic–androgenic steroids (AAS) are a class of hormones that are widely abused for their muscle-building and strength-increasing properties in high, nontherapeutic, dosages. This review provides an up-to-date and comprehensive overview on how ...
so what happens is not that AR binding with AAS generate AREs the thing that happen after binding with AAS is that the hormone-AR complex moves into the nucleus, where AR molecules often form dimers (pairs). The complex binds to specific DNA sequences called Androgen Response Elements (AREs) in the promoter/enhancer regions of target genes. These are typically palindromic or direct repeat sequences (e.g., something like AGAACA-NNN-TGTTCT) . Binding recruits co-activators, coregulators, and the basal transcription machinery. This upregulates (or sometimes downregulates) expression of androgen responsive genes which will then lead to muscle growth or muscle hypertrophy in whole body , development of male secondary sexual characteristics and other stuff like facial hair growth sebum production etc
CHAPTER 3: AAS AND ITS EFFECT ON FACE
1.CHANGES OF BONEs DURING PUBERTY BY BLASTING
. Periosteal bone apposition and remodeling increase facial robusticity.
. Promotes growth of jaw (mandible), chin, brow ridge (supraorbital), cheekbones, and nose. Males develop broader foreheads, longer/stronger lower face, and more angular features.
Craniofacial growth was investigated in boys treated with low-dose testosterone for delayed puberty (> 14 years old; testicular volume < 4 ml; n = 7) and compared with controls (12-14 years; n = 37). Cephalometric radiographs, statural height and pubertal stage were recorded at the start of the study and after 1 year. Craniofacial growth was assessed by nine linear measurements. At the beginning of the study, statural height, mandibular ramus length, upper anterior face height, and total cranial base length were significantly shorter in the delayed puberty boys than in the controls. After 1 year, the growth rate of the statural height, total mandibular length, ramus length, and upper and total anterior face height was significantly higher in the treated boys than in the untreated height-matched controls (n = 7). The craniofacial measurements were similar in the treated boys as compared with the controls. These results show that statural height and craniofacial dimensions are low in boys with delayed puberty. Low doses of testosterone accelerate statural and craniofacial growth, particularly in the delayed components, thus leading towards a normalization of facial dimensions.
TLDR ; works for the guys with late puberty too
Effect of low-dose testosterone treatment on craniofacial growth in boys with delayed puberty - PubMed
THIS PAPER IS BIG HAD TO DNR BUT INCLUDES TOO
Terminal hair growth: Beard, mustache, and facial hair via effects on dermal papilla cells. cause .Androgen receptors are highly expressed in sebocytes and hair follicles
2 .Hypertrophy include skin hypertrophy so Androgens like testosterone and DHT (via AAS or natural surges) contribute to skin roughening or coarser texture primarily through increased thickness, enhanced sebum production, enlarged pores, and changes in epidermal/dermal structure. This is more pronounced on the face due to high densities of androgen receptors (AR) and 5α-reductase enzymes that convert test to potent DHT locally
Pubertal androgen surge drives sexual dimorphism in skin ( natural level of test in puberty and its changes in skin )
Male skin becomes ~20-25% thicker than female skin, with a tougher, rougher texture (thicker stratum corneum and dermis).
Increased sebum leads to oily, shiny skin with visible/coarser pores.
Acne and follicular hyperkeratinization (clogged pores) add to give rough feel.
Most prone areas on face: T-zone (forehead, nose), chin/jawline (high sebaceous activity), cheeks. Genetics (AR sensitivity) and ethnicity influence degree.
3.Androgen Response Elements (AREs) → altered expression of genes involved in adipocyte (fat cell) function, lipolysis (fat breakdown), and adipose tissue distribution. Testosterone promotes (male-pattern) fat distribution: less subcutaneous fat in limbs/face, more visceral (abdominal) fat. It reduces fat storage in estrogen-sensitive areas and enhances lipolysis via effects on adipocytes and enzymes.
Test undergoes aromatization to estradiol (estrogen), which can cause temporary fluid retention (bloat/water retention) and contribute to facial puffiness so you will also have bloated look from test reason
Elevated E2 promotes sodium retention in the kidneys (via influences on aldosterone and renin-angiotensin systems), leading to water retention
www.swintegrativemedicine.com
IMP you will get bloat acne face fat reduction and increase facial muscle and rough skin and you will grow a beard :feelshah: and if you pin it at 14 to 16 it will be the best time grow bones and bone mass and if you are 16 like from 17 to 18 the mandibular growth will remain active in many males and some residual changes possible into early 20s but little
Approximate mean ages for lengths (mandible Ar-Me and maxilla PNS-PtA)
Onset: ~8.2–8.9 years
Peak velocity: ~13.3–16 years
Cessation or slowing down : ~19.9–20 years for facial bone growth ofc
Mandible and maxilla grow similarly in timing (earlier onset, later peak/cessation than cranial base). There is substantial individual variation some people finish earlier or later. Angles (e.g., gonial) often have later cessation than linear lengths.
After natural cessation (22+): Bone growth plates are largely fused. AAS won't reopen them for significant new length growth in adults. Any changes would be more about density mineral density , remodeling, or soft tissue/muscle hypertrophy effects
remember bone density is not equal to bone growth or length increase
The study explicitly notes that, looking at averages, both mandible and maxilla cease growth at approximately age 20 in boys.
https://anatomypubs.onlinelibrary.wiley.com/doi/10.1002/ar.22918
so this apply same for supra orbital yes there is chance to grow supra till late puberty to early twenties but not as prominent growth as in early age
CHAPTER 5: UNDERSTANDING AAS IN DEPTH FOR 16 + ( AI FOR EASE )
Facial bones (craniofacial skeleton) do not close like long bone epiphyseal growth plates. Instead, they grow mainly through sutures fibrous joints and periosteal surface apposition/remodeling. Many facial sutures remain patent (open) much longer than cranial sutures, allowing growth into late teens and even early adulthood.
Maxilla (upper jaw): Growth largely completes earlier — often by 12–15 years. Forward/downward growth slows significantly after mid-teens.
Mandible (lower jaw): Continues longer. Peak growth during pubertal spurt (~13–15 years). Significant growth from 16–18 and even 18–20 years in many males. Maturity often reached around 16–18 years, but some residual changes possible up to 20–21+ years.
Facial growth in males 16 to 20 years of age - PubMed
Supra orbital ( brow ridge ) : Prominence accelerates dramatically during puberty (~12–16/17 years) due to androgen-driven periosteal apposition. Growth/robusticity largely stabilizes or gets really slowed by late teens to early 20s (~18–22 years)
Major sexual dimorphism and robust growth during puberty (12–17/18 years).
Stabilization occurs typically by 18–22 years, depending on the specific dimension (e.g., mandibular length, anterior face height). In ~20% of people, minor changes continue beyond that.
Best window (as discussed): Mid-to-late puberty (~13–17/18 years), when sutures and growth sites are still highly responsive. Low-dose T in delayed puberty boys (>14 years) accelerates mandibular length, ramus, and face height effectively.
After ~18–20: Limited skeletal expansion possible. High androgens may support minor periosteal apposition or density, but not the dramatic growth. Most adult changes are soft tissue (fat redistribution, muscle and skin).
CHAPTER 5 : ITS NOT GOOD AS ITs SOUNDS EVEN FOR EARLY TEENS
1. research is not done on healthy children's by giving them roids ( doesn't matter tho its because of ethical purpose )
2. via aromatization the free test will convert into estrogen more and will speed up the growth plate closure at growth plate chondrocytes
Weise M, De-Levi S, Barnes KM, Gafni RI, Abad V, Baron J. Effects of estrogen on growth plate senescence and epiphyseal fusion. Proc Natl Acad Sci U S A. 2001 Jun 5;98(12):6871-6. doi: 10.1073/pnas.121180498. Epub 2001 May 29. PMID: 11381135; PMCID: PMC34445.
3. it comes with health risks lol : Heart issues, infertility, endocrine crash, liver strain, potential accelerated aging or sagging long-term.
CHAPTER 6 : HOW CAN WE MANAGE AAS SIDE EFFECT FOR MOST CHANGE WHY ITS A MEH IDEA
Estrogen (from aromatization of testosterone) is the primary driver of epiphyseal (growth plate) closure and bone maturation. Lowering estrogen via AI can delay this, potentially allowing more linear growth time. Androgens (like testosterone from AAS) promote muscle, some bone density, and periosteal apposition (surface bone modeling), which in theory could influence craniofacial dimensions during active growth phases.
Using AI to Blocks aromatase → ↓ testosterone → estrogen conversion → lower circulating estrogen. This can blunt estrogen-driven sides while allowing higher androgen effects. In medical short-stature studies, AIs (with or without GH) slow bone age advancement.
The goal is to use AAS for androgenic drive on bone while using AI to keep estrogen low enough to delay growth plate closure theoretically
Yk what we actually need moderate level of estrogen blocking this completely or nuking it has its really bad side effect in ages like 14 +
PAIR
Base: Exogenous testosterone ( enanthate/cypionate) as a AAS foundation
Anastrozole (milder, easier to titrate) or letrozole (more potent). Used to suppress excess aromatization from high androgens. In studies, doses like anastrozole 1 mg/day or letrozole 2.5 mg/day are explored under monitoring, but these are for short stature
AAS raises androgens → potential periosteal bone deposition in jaw/mandible (animal data shows mandibular growth effects yeah animal data).
AI prevents estrogen rise → delays epiphyseal fusion in long bones (height) and possibly influences facial suture activity/remodeling.
More time for androgen-driven facial changes without as much estrogen-mediated maturation
Key Challenges
If too much AI → very low E2 → joint pain, dry skin, mood issues, impaired bone health (estrogen is protective for bones)
HPTA Suppression: AAS shuts down natural production; AI can further elevate androgens/LH feedback in some cases, but the overall suppression is severe.
Excessive bone growth acromegaly
No human studies support AAS + AI specifically for safe facial bone growth in healthy teens. Animal studies show AAS can increase craniofacial dimensions, but human extrapolation is poor. Medical AI use is with GH, shows height gains in select short stature cases, but adult height benefits are inconsistent, and long-term safety (e.g., bone density, vertebral issues, lipids) needs more data.
AAS often advances bone age faster AI might partially counter but not reliably for facial only benefits.
Could lead to uneven growth or later resorption.
Many changes (e.g., endocrine axis) may not fully recover.
Lack of healthy human data
THE MECHANISM PROVE THAT IT CAN WORK WITH HIGH T LEVEL IN PUBERTY IF THE PLATE IS OPEN BUT THE RISK IS THERE IF YOU WANT TO GO FOR IT YOUR CHOICE YOU DONT KNOW HOW IT WILL WORK FOR YOU . GO ROIDS FOR PHYSIQUE MOSTLY THANKS AND PLS STOP COPING MAY WORK FOR YOU AND THIS DOESNT HAVE ANY PROPER DATA OK.WE ONLY HAVE ANCEDOTES . IT CAN WORK BUT YOU MAY REGRET IT LATER
I HAVE NCLUDED RESEARCH DONE FOR HEIGHT TOO ALTHOUGH ITS DIFFERENT
pubmed.ncbi.nlm.nih.gov
pubmed.ncbi.nlm.nih.gov
CHAPTER 1: UNDERSTANDING AAS
Anabolic steroids also known as anabolic androgenic steroids (AAS), are a class of drugs that are structurally related to testosterone, the main male sex hormone, and produce effects by binding to and activating the androgen receptor (AR) . The chemical form of testosterone is (androst-4-en-17β-ol-3-one) . Anabolic refers to the skeletal muscle building properties of AAS, whereas androgenic refers to the induction and maintenance of male secondary sexual characteristics
Anabolic steroid - Wikipedia
Androgen receptor is a nuclear receptor by binding with androgen receptor it releases a series of proteins and genes
The androgen receptor (AR) which is also known as NR3C4 (nuclear receptor subfamily 3, group C, member 4), is a type of nuclear receptor that is activated by binding any of the androgenic hormones, including testosterone and dihydrotestosterone in the cytoplasm and then translocating into the nucleus.
In some cell types, testosterone interacts directly with androgen receptors, whereas, in others, testosterone is converted by 5-alpha-reductase to dihydrotestosterone (DHT), an even more potent agonist for androgen receptor activation
This pub med will tell you fully how androgen receptor works i dnrd some part of this site
Androgen Receptor Structure, Function and Biology: From Bench to Bedside - PMC
CHAPTER 2: AAS AND AR RECEPTOR BINDING
There are derivates of test and DHT but as you see you need to follow the one who is guiding you . but the legends of legends Avskinov i want more knowledge , ok as your wish
Roidmaxxing 101™ - How to get a physique halo
Natty lifting is cope. JFL at spending a decade training optimally to end up as looking like someone that has just ended his first cycle. If you're serious about Looksmaxing, you're going to take every shortcut to achieve your goal. Why should I give a shit about roiding? A body halo is...
looksmax.org
WRITINIG THIS FROM PUBMED LEGENDS DOES WHAT LEGENDS WANT
Once in the system, AAS are transported to the tissues bound to binding proteins albumin, sex hormone-binding globulin (SHBG), corticosteroid-binding globulin (CBG) and orosomucoid. Under physiological conditions, testosterone is predominately bound to the first two, leaving only 1% to 4% of circulating testosterone unbound or free test or single test . SHBG binds testosterone with high love but has a relatively low binding capacity. Conversely albumin binds testosterone with low love and cold heart but has a virtually limitless binding capacity . SHBG is present in the bloodstream as a homodimer . Under physiological conditions about one third of the binding sites is occupied by testosterone, with further occupation by several other steroids rendering about 44% of SHBG-binding sites unbound . With physiological SHBG levels in the 10–56 nmol/L range, it is clear that supraphysiological dosages of testosterone saturate its binding capacity. Besides, supraphysiological dosages strongly decrease circulating SHBG levels. Thus, increasing dosages of testosterone result in a larger fraction of albumin-bound testosterone relative to the SHBG-bound fraction . It is noteworthy that SHBG has very low affinity for other commonly used AAS, such as nandrolone, methenolone, stanozolol, methandienone, fluoxymesterone and oxymetholone which is in slayer jhonas guide
All this to explain free test btw :feelshah: now this free test will bind to AR (Androgen receptor )
Testosterone is bioactivated into a more potent androgen in tissues expressing enzymes of the 5α-reductase family. These enzymes catalyze a reduction reaction at carbon 5, adding an α-oriented hydrogen atom. With testosterone as a substrate, this reaction yields the most potent naturally occurring androgen, namely, dihydrotestosterone (DHT). And DHT or test will regulate genes AREs (ANDROGENIC RESPONSE ELEMENTS )
Anabolic–androgenic steroids: How do they work and what are the risks? - PMC
Anabolic–androgenic steroids (AAS) are a class of hormones that are widely abused for their muscle-building and strength-increasing properties in high, nontherapeutic, dosages. This review provides an up-to-date and comprehensive overview on how ...
so what happens is not that AR binding with AAS generate AREs the thing that happen after binding with AAS is that the hormone-AR complex moves into the nucleus, where AR molecules often form dimers (pairs). The complex binds to specific DNA sequences called Androgen Response Elements (AREs) in the promoter/enhancer regions of target genes. These are typically palindromic or direct repeat sequences (e.g., something like AGAACA-NNN-TGTTCT) . Binding recruits co-activators, coregulators, and the basal transcription machinery. This upregulates (or sometimes downregulates) expression of androgen responsive genes which will then lead to muscle growth or muscle hypertrophy in whole body , development of male secondary sexual characteristics and other stuff like facial hair growth sebum production etc
CHAPTER 3: AAS AND ITS EFFECT ON FACE
1.CHANGES OF BONEs DURING PUBERTY BY BLASTING
. Periosteal bone apposition and remodeling increase facial robusticity.
. Promotes growth of jaw (mandible), chin, brow ridge (supraorbital), cheekbones, and nose. Males develop broader foreheads, longer/stronger lower face, and more angular features.
Testosterone-mediated sex differences in the face shape during adolescence: Subjective impressions and objective features
Craniofacial growth was investigated in boys treated with low-dose testosterone for delayed puberty (> 14 years old; testicular volume < 4 ml; n = 7) and compared with controls (12-14 years; n = 37). Cephalometric radiographs, statural height and pubertal stage were recorded at the start of the study and after 1 year. Craniofacial growth was assessed by nine linear measurements. At the beginning of the study, statural height, mandibular ramus length, upper anterior face height, and total cranial base length were significantly shorter in the delayed puberty boys than in the controls. After 1 year, the growth rate of the statural height, total mandibular length, ramus length, and upper and total anterior face height was significantly higher in the treated boys than in the untreated height-matched controls (n = 7). The craniofacial measurements were similar in the treated boys as compared with the controls. These results show that statural height and craniofacial dimensions are low in boys with delayed puberty. Low doses of testosterone accelerate statural and craniofacial growth, particularly in the delayed components, thus leading towards a normalization of facial dimensions.
TLDR ; works for the guys with late puberty too
Effect of low-dose testosterone treatment on craniofacial growth in boys with delayed puberty - PubMed
2.CHANGES OF SKIN AND FLUIDS OR FAT DURING PUBERTY
1 .Skin changes associated with AAS appear in the form of acne, which is caused by hypertrophy and an increase in the number of sebaceous glands, and thus increased secretion of sebum . SAAs also cause increased production of skin surface lipids. These changes are caused by increased sebum synthesis through direct binding to the androgen receptor in sebocytes and indirectly through induction of nuclear peroxisome proliferator receptors (PPARs), which are involved in sebaceous cell growth and differentiation
Adolescent acne: association to sex, puberty, testosterone and dihydrotestosterone - PMC
ARTICLE: Androgens, Androgen Receptors, and the Skin: From the Laboratory to the Clinic With Emphasis on Clinical and Therapeutic Implications - JDDonline - Journal of Drugs in Dermatology
THIS PAPER IS BIG HAD TO DNR BUT INCLUDES TOO
Terminal hair growth: Beard, mustache, and facial hair via effects on dermal papilla cells. cause .Androgen receptors are highly expressed in sebocytes and hair follicles
2 .Hypertrophy include skin hypertrophy so Androgens like testosterone and DHT (via AAS or natural surges) contribute to skin roughening or coarser texture primarily through increased thickness, enhanced sebum production, enlarged pores, and changes in epidermal/dermal structure. This is more pronounced on the face due to high densities of androgen receptors (AR) and 5α-reductase enzymes that convert test to potent DHT locally
Pubertal androgen surge drives sexual dimorphism in skin ( natural level of test in puberty and its changes in skin )
Male skin becomes ~20-25% thicker than female skin, with a tougher, rougher texture (thicker stratum corneum and dermis).
Increased sebum leads to oily, shiny skin with visible/coarser pores.
Acne and follicular hyperkeratinization (clogged pores) add to give rough feel.
Most prone areas on face: T-zone (forehead, nose), chin/jawline (high sebaceous activity), cheeks. Genetics (AR sensitivity) and ethnicity influence degree.
Longdom Publishing SL | Open Access Journals
3.Androgen Response Elements (AREs) → altered expression of genes involved in adipocyte (fat cell) function, lipolysis (fat breakdown), and adipose tissue distribution. Testosterone promotes (male-pattern) fat distribution: less subcutaneous fat in limbs/face, more visceral (abdominal) fat. It reduces fat storage in estrogen-sensitive areas and enhances lipolysis via effects on adipocytes and enzymes.
Test undergoes aromatization to estradiol (estrogen), which can cause temporary fluid retention (bloat/water retention) and contribute to facial puffiness so you will also have bloated look from test reason
Elevated E2 promotes sodium retention in the kidneys (via influences on aldosterone and renin-angiotensin systems), leading to water retention
Does Estrogen Cause Fluid Retention?
This article answer the question does estrogen cause fluid retention. If you are on hormone replacement, birth control or trt, you should read this.www.swintegrativemedicine.com
IMP you will get bloat acne face fat reduction and increase facial muscle and rough skin and you will grow a beard :feelshah: and if you pin it at 14 to 16 it will be the best time grow bones and bone mass and if you are 16 like from 17 to 18 the mandibular growth will remain active in many males and some residual changes possible into early 20s but little
Approximate mean ages for lengths (mandible Ar-Me and maxilla PNS-PtA)
Onset: ~8.2–8.9 years
Peak velocity: ~13.3–16 years
Cessation or slowing down : ~19.9–20 years for facial bone growth ofc
Mandible and maxilla grow similarly in timing (earlier onset, later peak/cessation than cranial base). There is substantial individual variation some people finish earlier or later. Angles (e.g., gonial) often have later cessation than linear lengths.
After natural cessation (22+): Bone growth plates are largely fused. AAS won't reopen them for significant new length growth in adults. Any changes would be more about density mineral density , remodeling, or soft tissue/muscle hypertrophy effects
remember bone density is not equal to bone growth or length increase
The study explicitly notes that, looking at averages, both mandible and maxilla cease growth at approximately age 20 in boys.
https://anatomypubs.onlinelibrary.wiley.com/doi/10.1002/ar.22918
so this apply same for supra orbital yes there is chance to grow supra till late puberty to early twenties but not as prominent growth as in early age
CHAPTER 5: UNDERSTANDING AAS IN DEPTH FOR 16 + ( AI FOR EASE )
Facial bones (craniofacial skeleton) do not close like long bone epiphyseal growth plates. Instead, they grow mainly through sutures fibrous joints and periosteal surface apposition/remodeling. Many facial sutures remain patent (open) much longer than cranial sutures, allowing growth into late teens and even early adulthood.
Maxilla (upper jaw): Growth largely completes earlier — often by 12–15 years. Forward/downward growth slows significantly after mid-teens.
Mandible (lower jaw): Continues longer. Peak growth during pubertal spurt (~13–15 years). Significant growth from 16–18 and even 18–20 years in many males. Maturity often reached around 16–18 years, but some residual changes possible up to 20–21+ years.
Facial growth in males 16 to 20 years of age - PubMed
pubmed.ncbi.nlm.nih.gov
Supra orbital ( brow ridge ) : Prominence accelerates dramatically during puberty (~12–16/17 years) due to androgen-driven periosteal apposition. Growth/robusticity largely stabilizes or gets really slowed by late teens to early 20s (~18–22 years)
Major sexual dimorphism and robust growth during puberty (12–17/18 years).
Stabilization occurs typically by 18–22 years, depending on the specific dimension (e.g., mandibular length, anterior face height). In ~20% of people, minor changes continue beyond that.
Relevance to Exogenous Testosterone
Best window (as discussed): Mid-to-late puberty (~13–17/18 years), when sutures and growth sites are still highly responsive. Low-dose T in delayed puberty boys (>14 years) accelerates mandibular length, ramus, and face height effectively.
After ~18–20: Limited skeletal expansion possible. High androgens may support minor periosteal apposition or density, but not the dramatic growth. Most adult changes are soft tissue (fat redistribution, muscle and skin).
CHAPTER 5 : ITS NOT GOOD AS ITs SOUNDS EVEN FOR EARLY TEENS
1. research is not done on healthy children's by giving them roids ( doesn't matter tho its because of ethical purpose )
2. via aromatization the free test will convert into estrogen more and will speed up the growth plate closure at growth plate chondrocytes
Weise M, De-Levi S, Barnes KM, Gafni RI, Abad V, Baron J. Effects of estrogen on growth plate senescence and epiphyseal fusion. Proc Natl Acad Sci U S A. 2001 Jun 5;98(12):6871-6. doi: 10.1073/pnas.121180498. Epub 2001 May 29. PMID: 11381135; PMCID: PMC34445.
3. it comes with health risks lol : Heart issues, infertility, endocrine crash, liver strain, potential accelerated aging or sagging long-term.
CHAPTER 6 : HOW CAN WE MANAGE AAS SIDE EFFECT FOR MOST CHANGE WHY ITS A MEH IDEA
Estrogen (from aromatization of testosterone) is the primary driver of epiphyseal (growth plate) closure and bone maturation. Lowering estrogen via AI can delay this, potentially allowing more linear growth time. Androgens (like testosterone from AAS) promote muscle, some bone density, and periosteal apposition (surface bone modeling), which in theory could influence craniofacial dimensions during active growth phases.
Using AI to Blocks aromatase → ↓ testosterone → estrogen conversion → lower circulating estrogen. This can blunt estrogen-driven sides while allowing higher androgen effects. In medical short-stature studies, AIs (with or without GH) slow bone age advancement.
The goal is to use AAS for androgenic drive on bone while using AI to keep estrogen low enough to delay growth plate closure theoretically
Yk what we actually need moderate level of estrogen blocking this completely or nuking it has its really bad side effect in ages like 14 +
PAIR
Base: Exogenous testosterone ( enanthate/cypionate) as a AAS foundation
Anastrozole (milder, easier to titrate) or letrozole (more potent). Used to suppress excess aromatization from high androgens. In studies, doses like anastrozole 1 mg/day or letrozole 2.5 mg/day are explored under monitoring, but these are for short stature
AAS raises androgens → potential periosteal bone deposition in jaw/mandible (animal data shows mandibular growth effects yeah animal data).
AI prevents estrogen rise → delays epiphyseal fusion in long bones (height) and possibly influences facial suture activity/remodeling.
More time for androgen-driven facial changes without as much estrogen-mediated maturation
Key Challenges
If too much AI → very low E2 → joint pain, dry skin, mood issues, impaired bone health (estrogen is protective for bones)
HPTA Suppression: AAS shuts down natural production; AI can further elevate androgens/LH feedback in some cases, but the overall suppression is severe.
Excessive bone growth acromegaly
No human studies support AAS + AI specifically for safe facial bone growth in healthy teens. Animal studies show AAS can increase craniofacial dimensions, but human extrapolation is poor. Medical AI use is with GH, shows height gains in select short stature cases, but adult height benefits are inconsistent, and long-term safety (e.g., bone density, vertebral issues, lipids) needs more data.
TAKES
AAS often advances bone age faster AI might partially counter but not reliably for facial only benefits.
Could lead to uneven growth or later resorption.
Many changes (e.g., endocrine axis) may not fully recover.
Lack of healthy human data
THE MECHANISM PROVE THAT IT CAN WORK WITH HIGH T LEVEL IN PUBERTY IF THE PLATE IS OPEN BUT THE RISK IS THERE IF YOU WANT TO GO FOR IT YOUR CHOICE YOU DONT KNOW HOW IT WILL WORK FOR YOU . GO ROIDS FOR PHYSIQUE MOSTLY THANKS AND PLS STOP COPING MAY WORK FOR YOU AND THIS DOESNT HAVE ANY PROPER DATA OK.WE ONLY HAVE ANCEDOTES . IT CAN WORK BUT YOU MAY REGRET IT LATER
I HAVE NCLUDED RESEARCH DONE FOR HEIGHT TOO ALTHOUGH ITS DIFFERENT
Novel treatment of short stature with aromatase inhibitors - PubMed
Estrogens have an essential role in the regulation of bone maturation and importantly in the closure of growth plates in both sexes. This prospective, randomized, placebo-controlled study was undertaken to evaluate whether suppression of estrogen synthesis in pubertal boys delays bone maturation...pubmed.ncbi.nlm.nih.gov
Anabolic steroids and craniofacial growth in the rat - PubMed
Anabolic steroids are misused by adolescents as well as adults to increase muscle and improve appearance and athletic performance. Since these substances strongly enhance protein synthesis, it was speculated that craniofacial changes in bone size and, perhaps, skeletodental relationships might...pubmed.ncbi.nlm.nih.gov
