juanson
Iron
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My theory: Anabolic signaling doesn’t just increase bone formation it also slows down bone resorption. By reducing how quickly old bone is broken down, the new matrix stays intact longer and has more time to mature and mineralize. This creates a kind of regenerative window, where the bone surface becomes temporarily more favorable for osteoblast activity. During this phase, growth factors that act downstream like GH or IGF-1 in theory could have an amplified effect because the bone is in a state that supports more efficient deposition and remodeling.
But which AAS demonstrates the greatest efficacy by concurrently enhancing osteoblastic bone formation and suppressing osteoclastic bone resorption?
Nandrolone Decanoate appears to most effectively shift the bone remodeling balance toward formation, primarily by suppressing osteoclastic resorption while simultaneously stimulating osteoblastic activity, more so than other anabolic-androgenic steroids.
Two studies—Gennari *et al.* (1989) and Dave *et al.* (2024) show something interesting about nandrolone decanoate’s (Deca) behavior in postmenopausal bone biology
Obviously this is all a theory not a lot of research so don't go run a deca only cycle to go get bonemass all that will probally happen is your dick will stop working and youll grow boobs.
But which AAS demonstrates the greatest efficacy by concurrently enhancing osteoblastic bone formation and suppressing osteoclastic bone resorption?
Nandrolone Decanoate appears to most effectively shift the bone remodeling balance toward formation, primarily by suppressing osteoclastic resorption while simultaneously stimulating osteoblastic activity, more so than other anabolic-androgenic steroids.
Two studies—Gennari *et al.* (1989) and Dave *et al.* (2024) show something interesting about nandrolone decanoate’s (Deca) behavior in postmenopausal bone biology
The 1989 double-blind trial: 50 mg of nandrolone decanoate intramuscularly every 3 or 4 weeks. low-dose DECA every three weeks led to higher lumbar spine bone mineral content (BMC), increased trabecular bone volume, and a rise in osteoid surface area. These are signs of heightened osteoblast output. Interestingly, plasma ALP (a bone formation marker) trended upward while urinary hydroxyproline (a resorption marker) trended downward. That combination implies that ND not only promotes osteoblastic differentiation but also indirectly suppresses osteoclastic activity, perhaps through local paracrine signals or androgen receptor–IGF-1 cross-talk in the bone microenvironment.
The second study Dave *et al.* (2024) was done to research osteosarcopenia, pairing Deca with alendronate. The results: simultaneous gains in bone density and lean body mass, without recorded adverse events. Mechanistically, the synergy makes sense alendronate locks down resorption at the osteoclast level, while deca enhances osteoblast productivity and calcium handling. 50 mg of nandrolone decanoate intramuscularly every 3 weeks for the first 12 weeks, followed by every 4 weeks for the remaining 9 months
Anavar – a DHT-derived anabolic steroid that’s non-aromatizable and has demonstrated *increases in bone formation markers* in burn and trauma recovery models. It enhances collagen synthesis and mineral apposition rate with fewer estrogenic interactions.
Winstrol – another non-aromatizing agent shown to *increase osteocalcin* and calcium retention, though with less impact on trabecular thickness than ND.
SARMs (e.g., ostarine, LGD-4033) – selective androgen receptor modulators designed to retain anabolic effects in bone and muscle while sparing reproductive and hepatic tissues. Early studies show they upregulate osteoblast differentiation genes (Runx2, Osterix) without significant aromatase stimulation.
Non-androgenic anabolic pathways – IGF-1 analogs, GH secretagogues, and BMP-2 agonists can potentiate osteoblastogenesis directly without invoking estrogenic feedback loops.
Winstrol – another non-aromatizing agent shown to *increase osteocalcin* and calcium retention, though with less impact on trabecular thickness than ND.
SARMs (e.g., ostarine, LGD-4033) – selective androgen receptor modulators designed to retain anabolic effects in bone and muscle while sparing reproductive and hepatic tissues. Early studies show they upregulate osteoblast differentiation genes (Runx2, Osterix) without significant aromatase stimulation.
Non-androgenic anabolic pathways – IGF-1 analogs, GH secretagogues, and BMP-2 agonists can potentiate osteoblastogenesis directly without invoking estrogenic feedback loops.
Obviously this is all a theory not a lot of research so don't go run a deca only cycle to go get bonemass all that will probally happen is your dick will stop working and youll grow boobs.
