Tamoxifen is an anti-estrogenic compound. You need some estrogen levels for optimal growth however many of the beneficial effects of estrogen can be mimicked by Alfalfa. Tamoxifen induces apoptosis in growth plate chondrocytes but apoptosis is a part of endochondral ossification both as both a part of terminal differentiation and to help align the growth plate.
Too high levels of estrogen seem to have a bigger height reduction effect than too low with too high estrogen levels increasing apoptosis whereas both too high and low levels of estrogen decreased cell proliferative capacity(thus both high and low estrogen will reduce height). However, Alfalfa may be able to rescue the cell proliferating ability enabling you to safely lower estrogen without worrying about decreasing it too much.
Mice who were knockouts for GR30, which is an estrogen receptor, were found to be taller than the mice with GR30. Males and females may respond differently to estrogen.
Tamoxifen + Alfalfa may be an intriguing modality in which to increase height during development.
Tamoxifen Stimulates Cancellous Bone Formation in Long Bones of Female Mice
"Selective estrogen receptor modulators (SERMs) have been developed as a means of targeting estrogen’s protective effect on the skeleton. Although it is well established that SERMs such as tamoxifen inhibit bone resorption in a similar manner to estrogen, whether this agent shares estrogen’s stimulatory action on bone formation is currently unclear. To address this question, we compared the effect of treatment for 28 d with 17ß-estradiol (E2; 0.1, 1.0 mg/kg·d) and tamoxifen (0.1, 1.0, or 10 mg/kg·d) on cancellous bone formation at the proximal tibial metaphysis of intact female mice. E2 stimulated the formation of new cancellous bone throughout the metaphysis. A similar response was observed after administration of tamoxifen, the magnitude of which was approximately 50% of that seen after E2. As expected, E2 was found to suppress longitudinal bone growth, but in contrast, this parameter was stimulated by tamoxifen[tamoxifen also increased growth plate width]. We conclude that tamoxifen acts as an agonist with respect to estrogen’s stimulatory action on bone formation but as an antagonist in terms of estrogen’s inhibition of longitudinal growth, suggesting that the protective effect of SERMs on the skeleton is partly mediated by stimulation of osteoblast activity."
"the activity of tamoxifen requires biotransformation to 4-hydroxy-tamoxifen, which process may vary between mouse strains."<-this may explain why tamoxifen increases height in some studies but not in others.
So Tamoxifen was found to stimulate longitudinal growth in females and again male and female receptors may work differently. Here's a study that says that Tamoxifen may lower height in males:
Tamoxifen impairs both longitudinal and cortical bone growth in young male rats.
"Tamoxifen (Tam) was recently shown to inhibit the growth of cultured fetal rat metatarsal bones and thus might also affect bone growth in vivo. Four-week-old Sprague-Dawley rats were gavaged daily with vehicle alone (peanut oil), Tam (40 mg/kg/d; 1 or 4 wk), or estradiol (40 microg/kg/d; 4 wk). Five of the 10 rats in each group were killed after 4 wk and the other five after 14 wk of recovery. Bone growth was followed by repeat DXA scans, whereas other bone parameters and spine length were evaluated by pQCT and X-ray at the time of death. Four-week Tam treatment significantly decreased body weight, nose-anus distance, spinal and tibial bone lengths, trabecular BMD, cortical periosteal circumference, and bone strength and also reduced serum IGF-I levels (424 +/- 54 versus 606 +/- 53 ng/ml in control; p < 0.05). Analysis of the tibial growth plate of treated rats showed elevated chondrocyte proliferation (BrdU) and apoptosis (TUNEL), as well as decreases in the number of hypertrophic chondrocytes and in the size of terminal hypertrophic chondrocytes. Despite a complete catch-up of body weight after 14 wk of recovery, the tibia was still shorter (p < 0.001) and its cortical region was smaller. We conclude that, when administered at a clinically relevant dose, Tam causes persistent retardation of longitudinal and cortical radial bone growth in young male rats. Our findings suggest that this inhibition results from local effects on the growth plate cartilage and systemic suppression of IGF-I production. Based on these rat data, we believe that Tam, if given to growing individuals, might compromise cortical bone growth, bone strength, and adult height."
"Tam induces permanent growth arrest of cultured fetal rat metatarsal bones, an effect associated with specific elimination of chondrocytes, primarily in the resting zone of the growth plate, through apoptosis"<-regardless of apoptosis' important of apoptosis you usually want apoptosis to occur later in endochondral ossification not in the "resting zone"
"the rate of chondrocyte proliferation was increased in the Tam 1-wk (p < 0.05) and Tam 4-wk (p < 0.01) group[This is good]. In addition, 4 wk of treatment with Tam significantly enhanced the frequency of apoptosis among the same cells[Maybe Tamoxifen needs to be cycled as the increased apoptosis may be a negative feedback mechanism to Tamoxifen]"<-The study with the positive benefits of tamoxifen only did the study for 28 days(exactly four weeks) so they didn't notice the apoptosis induction.
"The findings clearly showed that the growth retardation caused by Tam is associated with both elimination of chondrocytes through apoptosis and inhibition of chondrocyte differentiation. These results are consistent with our previous observation that Tam induces apoptosis of stem-like chondrocytes in cultured fetal rat metatarsal bones"
So Tamoxifen looks like it has potential but the appropriate cycling regime needs to be be in place and it needs to be clear why there's a negative feedback to Tamoxifen. Tamoxifen has effects that cannot be rescued by Alfalfa.
And it's unknown how long off of Tamoxifen you have to be to get back the positive benefits from it. You'd have to know things like the half-life to see how long it stays in your system.
So right now Tamoxifen is too risky to add to your height increase regime but if we keep forming our collective heads together maybe we can come up with an effective cycling regime.
Estrogen reduces cellular aging in human mesenchymal stem cells and chondrocytes.
[This is contrary to other evidence that estrogen accelerates both senescence and decreases proliferation thus decreasing height]
"Chondrocyte aging is associated with cartilage degeneration and senescence impairs the regenerative potential of mesenchymal stem cells (MSCs). Physiologic premenopausal concentrations of 17β-estradiol (E(2)) significantly decelerated telomere attrition in MSCs and chondrocytes while postmenopausal E(2) concentration had no significant effects[menopause lowers estrogen levels so too high estrogen levels inhibit telomere shortening]. The estrogen agonist-antagonist tamoxifen did not affect telomere biology, but inhibited the E(2) -stimulated reduction in telomere shortening. E(2) and tamoxifen did not influence cell proliferation, cell morphology, and β-galactosidase staining in chondrogenic cells. E(2) treatment did not affect the telomere-associated proteins TRF1 and TRF2. E(2) had no regulatory effects on the expression rates of the cell cycle regulator p21 and the DNA repair proteins SIRT1 and XRCC5. In spite of reducing telomere shortening in aging MSCs and chondrocytes, estrogen is not able to prevent somatic cells from replicative exhaustion and from finally entering senescence."
So just because estrogen reduces cellular aging by telomere shortening doesn't mean that estrogen can't accelerate senescence by some other mechanism.
"The cell division-dependent telomere shortening is prohibited by the enzyme telomerase, synthesizing telomeric repeats by reverse transcription"<-Hence why Astragalus may have some role in a height increase routine.
"E2 enhances telomerase activity and the expression of the catalytic subunit hTERT via ERα."<-which tamoxifen inhibits.