Bone remodeling operates on a balanced system between two opposing but interdependent forces: osteoblasts, which synthesize and mineralize new bone matrix, and osteoclasts, which resorb old or micro damaged bone tissue. Their coordination is regulated by several converging molecular pathways, primarily the mTOR (mechanistic target of rapamycin) and LKB1–AMPK–SIRT1 axis, which function as the body’s energy and growth sensors. mTOR, activated by sufficient amino acids, insulin, and IGF-1, signals the cell that nutrient and energy status are high, stimulating protein synthesis, osteoblast differentiation, and cellular proliferation. The LKB1–AMPK–SIRT1 axis, on the other hand, becomes dominant under conditions of energy scarcity such as fasting or caloric restriction; it promotes autophagy, energy conservation, and, paradoxically, long-term cellular health. The contradiction lies in that mTOR activation drives anabolic growth but accelerates aging and resource consumption, while AMPK activation extends cellular lifespan at the cost of suppressing growth. Yet both are required, osteoblasts require mTOR for expansion, but osteoclasts rely partly on AMPK signaling for bone resorption and metabolic recycling, maintaining dynamic equilibrium.
A theoretical “trick” to gain both benefits is through intermittent activation, cycling between high mTOR and high AMPK states in short, strategic windows. For example, training or mechanical loading while fasted (AMPK high) creates a stress signal and increases sensitivity to growth factors, then breaking the fast with a nutrient-rich, protein-heavy meal spikes insulin, IGF-1, and mTOR, switching the system from catabolic to anabolic. This oscillation may allow simultaneous autophagic cleansing and growth stimulus, avoiding the chronic suppression of one pathway. Leucine, insulin, and IGF-1 serve as the primary mTOR triggers, while fasting, cold exposure, and NAD+ elevation drive the LKB1–AMPK–SIRT1 cascade.
In this context, LIPUS (Low-Intensity Pulsed Ultrasound) acts as a mechanical-biophysical signal that mimics micro-fracture stress, stimulating osteoblast differentiation via mechanotransduction pathways, including integrin FAK–MAPK and potentially mTORC1. When paired with a local increase in GH or IGF-1, the osteogenic potential could, in theory, multiply: the mechanical stimulus directs where to build, while the hormones supply the signal to build more. This dual-input model parallels how natural bone healing occurs under load and hormonal stimulation. However, the issue is that excessive GH or IGF-1, especially during adolescence, can dysregulate this feedback, triggering abnormal bone growth, insulin resistance, or disproportionate tissue hypertrophy.
here's an example of the device itself
I also have a friend who's used this device for this exact reason at a young age, will be talking with him regarding the matter.
hormones further modulate this environment. DHT (dihydrotestosterone) increases local mTOR activity and osteoblast differentiation, particularly in androgen receptor, places like the mandible and zygomatics , while estrogen plays a dual role, it limits osteoclast overactivity (preventing bone resorption) but also constrains mTOR-driven overgrowth (but we obviously can't be injecting estro). especially in the male face, seem to emerge from a precise ratio: sufficient DHT to drive anabolic remodeling and local mTOR activation, balanced by estrogen’s regulatory feedback preventing chaotic over-mineralization.
the system operates like a controlled feedback loop: mechanical loading or LIPUS provides the spatial cue for bone remodeling; mTOR and IGF-1 provide the anabolic drive; AMPK and SIRT1 maintain metabolic discipline; and sex hormones fine-tune the balance between growth and regulation. The grand theory is that controlled cycling as well as fasting to activate AMPK and autophagy, followed by refeeding to spike mTOR and osteoblast activity, allows one to use both regenerative and growth pathways simultaneously.. When paired with localized mechanical or ultrasonic stimuli, the body can theoretically be nudged to remodel specific structures, provided the biochemical environment is primed for it, this obviously needs to be at a pretty young age, but you'd reap many rewards doing this at 16>
doing more research and will update on this matter.
here are some things you can further read if your interested.
https://pubmed.ncbi.nlm.nih.gov/8865143/
https://pmc.ncbi.nlm.nih.gov/articles/PMC5651475/?utm_
https://pmc.ncbi.nlm.nih.gov/articles/PMC3971652/?utm_
https://pubmed.ncbi.nlm.nih.gov/27500435/
https://pubmed.ncbi.nlm.nih.gov/15838623/
A theoretical “trick” to gain both benefits is through intermittent activation, cycling between high mTOR and high AMPK states in short, strategic windows. For example, training or mechanical loading while fasted (AMPK high) creates a stress signal and increases sensitivity to growth factors, then breaking the fast with a nutrient-rich, protein-heavy meal spikes insulin, IGF-1, and mTOR, switching the system from catabolic to anabolic. This oscillation may allow simultaneous autophagic cleansing and growth stimulus, avoiding the chronic suppression of one pathway. Leucine, insulin, and IGF-1 serve as the primary mTOR triggers, while fasting, cold exposure, and NAD+ elevation drive the LKB1–AMPK–SIRT1 cascade.
In this context, LIPUS (Low-Intensity Pulsed Ultrasound) acts as a mechanical-biophysical signal that mimics micro-fracture stress, stimulating osteoblast differentiation via mechanotransduction pathways, including integrin FAK–MAPK and potentially mTORC1. When paired with a local increase in GH or IGF-1, the osteogenic potential could, in theory, multiply: the mechanical stimulus directs where to build, while the hormones supply the signal to build more. This dual-input model parallels how natural bone healing occurs under load and hormonal stimulation. However, the issue is that excessive GH or IGF-1, especially during adolescence, can dysregulate this feedback, triggering abnormal bone growth, insulin resistance, or disproportionate tissue hypertrophy.
here's an example of the device itself
I also have a friend who's used this device for this exact reason at a young age, will be talking with him regarding the matter.
hormones further modulate this environment. DHT (dihydrotestosterone) increases local mTOR activity and osteoblast differentiation, particularly in androgen receptor, places like the mandible and zygomatics , while estrogen plays a dual role, it limits osteoclast overactivity (preventing bone resorption) but also constrains mTOR-driven overgrowth (but we obviously can't be injecting estro). especially in the male face, seem to emerge from a precise ratio: sufficient DHT to drive anabolic remodeling and local mTOR activation, balanced by estrogen’s regulatory feedback preventing chaotic over-mineralization.
the system operates like a controlled feedback loop: mechanical loading or LIPUS provides the spatial cue for bone remodeling; mTOR and IGF-1 provide the anabolic drive; AMPK and SIRT1 maintain metabolic discipline; and sex hormones fine-tune the balance between growth and regulation. The grand theory is that controlled cycling as well as fasting to activate AMPK and autophagy, followed by refeeding to spike mTOR and osteoblast activity, allows one to use both regenerative and growth pathways simultaneously.. When paired with localized mechanical or ultrasonic stimuli, the body can theoretically be nudged to remodel specific structures, provided the biochemical environment is primed for it, this obviously needs to be at a pretty young age, but you'd reap many rewards doing this at 16>
doing more research and will update on this matter.
here are some things you can further read if your interested.
https://pubmed.ncbi.nlm.nih.gov/8865143/
https://pmc.ncbi.nlm.nih.gov/articles/PMC5651475/?utm_
https://pmc.ncbi.nlm.nih.gov/articles/PMC3971652/?utm_
https://pubmed.ncbi.nlm.nih.gov/27500435/
https://pubmed.ncbi.nlm.nih.gov/15838623/
