After all the research we have done, something that is often asked by readers is what can they do or what supplements can they take to at least delay the fact that their growth plates will close and not reopen.

The most common reply by some of the regular readers is to use compounds that can inhibit or block the effects of estrogen. They are called the aromatase inhibitors. The two most common types that is talked about and tried out to cause growth plate closure delay are Letrozole and Anavar. Both prevent the ability of estrogen from reaching the right type of receptor. The effect that estrogen seems to have on the growth plate is that it increases the rate at which the number of chondrocytes in the resting zone of the epiphyseal plate to be used up.

From the studies “Depletion of resting zone chondrocytes during growth plate senescence.” and “Effects of estrogen on growth plate senescence and epiphyseal fusion.”

The conclusion from the 1st study is…

Our findings support the hypotheses that growth plate senescence is caused by qualitative and quantitative depletion of stem-like cells in the resting zone and that growth-inhibiting conditions, such as glucocorticoid excess, slow senescence by slowing resting zone chondrocyte proliferation and slowing the numerical depletion of these cells, thereby conserving the proliferative capacity of the growth plate. We speculate that estrogen might accelerate senescence by a proliferation-independent mechanism, or by increasing the loss of proliferative capacity per cell cycle.

The conclusion that is stated very clearly by the 2nd study was…

“Our data suggest that (i) epiphyseal fusion is triggered when the proliferative potential of growth plate chondrocytes is exhausted; and (ii) estrogen does not induce growth plate ossification directly; instead, estrogen accelerates the programmed senescence of the growth plate, thus causing earlier proliferative exhaustion and consequently earlier fusion.”

The growth plate goes through senescence or the act/ process of aging. From aging its activity and ability to proliferate decreases. The stem like cells in the resting zone gets used up. It seems seems from the 1st study that one idea is to increase the amount of glucocorticoid to both inhibit growth and slow down resting zone chondrocyte proliferation and the number of chondrocytes being depleted. Both of the studies suggest that estrogen acts in an indirect pathway to drop the number of chondrocytes available to be proliferated by increased the rate the chondrocytes get depleted.

In some studies it is suggested that the compounds like gluccocorticoids and dexamethasone can slow down growth plate senescence, but there have been other studies which show that gluccocorticoids and deamethasone also decrease chondrocyte proliferation, and actually decrease longitudinal lengthening like “Dexamethasone-induced growth inhibition of porcine growth plate chondrocytes is accompanied by changes in levels of IGF axis components.” and “Growth retardation induced by dexamethasone is associated with increased apoptosis of the growth plate chondrocytes”

This shows that dexamethasone may be able to slow down the rate of senescence but it might also contribute to it since it increases the rate of apoptosis of growth plate chondrocytes. If there was any ideas on using glucocorticoids or dexamethasone to delay puberty, I personally would not suggest it since what you are hoping for is that from the delaying and inihbition of the depletion of the chondrocytes, you will get “catch-up growth” afters to compensate for the longitudinal growth that was not achieved in the earlier stages when the chondrocytes could have been proliferating and going through senescence in a normal rate.

The other option I’ve seen to prevent the penetration through the perichondrium that is protecting the epiphyseal hyaline cartilage from the blood vessels and the vascularization and ossification of all the cartilage has been a compound that has not be looked at by other height increase researchers yet, Chondromodulin, types I and type II. Technically the Chondromodulin protein is termed a Cartilage- derived angiogenesis inhibitor.

I wrote two posts before on the possibility on using this compound to help keep the cartilage from being infiltrated and calsified too quickly with “Increase Height And Grow Taller Using Chondromodulin-1” and “Further Analysis On The Possibility Of Using Chondromodulin-I and Chondromodulin-II To Increase Height”

From my reading on the periosteum and the perichondrium it seems to suggest that the perichondrium might turn into the periosteum in a sort of differentiation pathway or process. Both of them surround a specific type of tissue. The perichondrium is wrapped around developing hyaline cartilage specifically to prevent vascularization. Cartilage themselves get the neccesary nutrients not through blood vessels but diffusion. From vascularization, the hyaline cartilage will lead to calcification. This would imply that if we can get more chondromodulin into our system, specifically to protect the hyaline cartilage from being penetrated, we might be able to extend the lifespan of the growth plates slightly longer.

This may be just a repost of the previous post but I wanted to cite 3 PubMed studies again, all showing that Chondromodulin Type I has chondroprotective properties.

PubMed study #1

“Our findings indicate that the antiangiogenic factor chondromodulin 1 stabilizes the chondrocyte phenotype by supporting chondrogenesis but inhibiting chondrocyte hypertrophy and endochondral ossification.”

PubMed study #2

“Cartilage-generated matrix components chondromodulin-I (ChM-I) synergistically stimulates growth and differentiation of chondrocytes in the presence or absence of FGF-2. In contrast, ChM-I inhibits the proliferation of vascular endothelial cells and tube formation, thereby further stimulating cartilage growth and inhibiting replacing cartilage by bone in an early stage. Another cartilage-derived chondromodulin-II (ChM-II) also stimulates cartilage growth. However, ChM-II does not inhibit vascularization but stimulates osteoclast differentiation.”

PubMed study #3

“Chondromodulin 1 stabilizes the chondrocyte phenotype and inhibits endochondral ossification of porcine cartilage repair tissue.”

CONCLUSION:

Our findings indicate that the antiangiogenic factor chondromodulin 1 stabilizes the chondrocyte phenotype by supporting chondrogenesis but inhibiting chondrocyte hypertrophy and endochondral ossification.

Interpretation:

Technically Chondromodulin Type I does disrupt the bone formation process. The researchers state that it gets in the way of endochondral ossification, which is what actually causes longitudinal growth on long bones. We would find out from the study “What makes the permanent articular cartilage permanent?” that is is Chondromoduline Type I which keeps the articular cartilage relatively permanent unlike the epiphyseal cartilage. What I have always proposed is that as long as there is some type of cartilage, preferrably hyaline cartilage with its uniform collagenous fibers we can more easily cause longitudinal growth. I am willing to propose that some of the results we find from LSJL is from the fact that the individual might have had some cartilage in their long bone to begin with, whether epiphyseal or other which meant that from just a mechanical point of view, they could have just squeezed the bone laterally and then would have made the relatively flexible elastic cartilage push out and lengthen causing longitudinal growth.

At this point, I would say that the best way to delay the end of puberty and extend the growth period is to get some injections of chondromodulin close to the growth plate regions in the body. This would cause the cartilage to not ossify as quickly. It would give more time to use certain techniques like PEMF or LSJL to gain some extra height and growth.

Tyler-Here’s another study

The effects of delayed puberty on the growth plate.

“Many athletes are beginning intense training before puberty, a time of increased bone accrual when up to 25% of total bone mineral accrual occurs. Female athletes experiencing late or delayed pubertal onset may have open epiphyseal plates open that are vulnerable to injury. This investigation’s purpose was to determine whether a delay in puberty (primary amenorrhea) affects the growth plate immediately post-puberty and at maturity.

Forty-eight female Sprague–Dawley rats (23days-of-age) were randomly assigned to four groups (n=12); short-term control (C-ST), long-term control (C-LT), short-term GnRH antagonist (G-ST) and long-term GnRH antagonist (G-LT). At 25days-of-age, daily gonadotropin-releasing hormone antagonist (GnRH-a; Cetrotide™, Serono, Inc.) injections were administered delaying pubertal onset. Left tibias were analyzed. Stained frontal slices of proximal tibia (5 μm thick) were analyzed in hypertrophic, proliferative and reserve zones for total height, zone height, and cell/ column counts. All procedures were approved by (IACUC) at Brooklyn College.

Growth plate height was 19.7% wider in delayed puberty (G-ST) group and at maturity was 27.9% greater in G-LT group compared to control (C-LT) (p<0.05){but increased growth plate height does not always result in larger final height}. No significant differences were found in short or long-term growth plate zone heights or cell/column counts between groups (p>0.05). Growth plate zone height normalized to total height resulted in 28.7 % larger reserve zone in the short term GnRH-a group (G-ST) but the proliferative zone was 8.5 % larger in the long-term group compared to the control group (p<0.05). Normalized to growth plate height a significant decrease was found in column counts in proliferative zones of the short and long-term GnRH-a groups.

Current data illustrates delayed puberty using GnRH-a injections results in significant growth plate height and decreases proliferative column counts and zone height\potentially contributing to decreases in bone mass at maturity.”

“Data from this study also showed delayed pubertal onset in the GnRH-a groups resulted in increased height but bone bridging would indicate that even though statistically growth plates are at different heights senescence was near with growth plate fusion at a time point similar to control animals.”