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Osie
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TLDR: We can learn from these studies that epiphysial fusion works differently in our vertebrae (like known previously) and that estradiol doesn’t age and inhibit the growth in our vertebrae as strongly as seen in other long bones like the tibia and femur. This idea is also demonstrated through the fact that naturally, our spines are the last growth plates to close at 18, exemplifying that estrogen needs to peak in our body for even longer times for it to close. This is also the reason why our clavicles take so long to experience complete epiphyseal fusion. This means that growth can still continue at 17,18, and possibly 19 if the spinal growth plates are open and you take high doses of AI’s and HGH.
The spinal growth dilemma
On this forum, there has been confusion and a lack of knowledge on how spinal growth works and if spinal growth plates are affected by estrogen the same way that other long bones are. We only know that spinal growth plates are the last growth plates open that affect height growth as they usually close at 18 years old. However, most people don’t see much growth after the age of 16-17 usually, despite spinal growth plates most likely being very open. So this has led me on a short journey to finding studies that demonstrate the effect of estrogen on spinal growth and fusion to possibly see if we can prevent its closure. And I was able to find two studies that discussed and described the effects of estrogen on spinal growth plates, one in female mice, and one in tall girls.The effects of estrogen in spinal growth plates of mice:
The first study we will analyze is the mice study. It is called, “Estrogen Receptor-β Inhibits Skeletal Growth and Has the Capacity to Mediate Growth Plate Fusion in Female Mice.” In this study, they used three different types of knockout mice: mice with no functioning estrogen receptor alpha (ERα), mice with no functioning estrogen receptor beta (ERβ), and mice that lacked both estrogen receptors and compared each mouse model’s vertebrae and long bone growth to each other’s. Moreover, the ERα-less mice were also exposed to supraphysiological levels of estradiol during the study and when the growth plate morphology of the mice was analyzed again 18 months later, all of the mice that had no functioning ERα and had supraphysiological levels of estradiol experienced complete epiphysial in their femur and tibia. In contrast to the other mice models, which still all had open growth plates in their tibia and femur. However, all mice models, even the ones exposed to high levels of estradiol, had open vertebra growth plates and all had the same height of the spine.This demonstrates that the cause of growth plate fusion in the vertebrae works in a different manner than other long bones. However, this difference in effects may be because the growth plates in the spine are less sensitive to estrogen as seen in the next study.
The Effects of Estrogen on Spinal Growth in Tall Girls
In this study, they analyze the effects of estradiol treatment on the bodily proportions of tall girls who want to reduce their final adult height. So before the estradiol treatment, these girls were expected to gain 5.4 cm in their sitting height (vertebra) and 4.4 cm in their leg length ( long bones like the tibia and femur) before their estimated growth plate closure. So they were expected to grow 9.8cm before growth plate fusion. However, after estradiol treatment, the girls only gained 2.9 cm in their sitting height, and 0.8 cm in their leg length by the time of growth plate fusion.
We can conclude from this study that estrogen has a less powerful effect in inhibiting growth and causing rapid growth plate aging in our vertebrae than compared to our other long bones like the tibia and femur.
