How to Grow Taller if your Growth Plates are still open

Here's a list of supplements by risk versus reward stated as benefit.  The most beneficial supplements have the most validated effects, tend to always be beneficial without needing an equilibrium value, and the most pro-chondrogenic:

Most Beneficial: Milk(Cycle), Choindroitin, Hyaluronic Acid
Medium: LSJL, PEMF, LIPUS, Lovastatin, Creatine
Least Beneficial: Other(See LSJL supplement page)

First, the growth plate closing does not inhibit height increase from occuring.  Their are still mesenchymal stem cells in the epiphyseal bone marrow.  It's just that there are no chondrocytes proliferating and differentiating.  If new stem cells proceeded to differentiate into chondrocytes then growth plate activity would be restored. This is what Lateral Synovial Joint Loading does, it encourages stem cells to differentiate into chondrocytes by altering intracellular calcium secretions via interstitial fluid flow and hydrostatic pressure.

The best supplements to increase height are hyaluronic acid and choindroitin.  Their are countless studies that show the pro-chondrogenic effects of hyaluronic acid and choindroitin and their ability to induce chondrogenic differentiation.  Their are even studies that show that Hyaluronic Acid supplementation does increase serum levels of HA.

LIPUS is also a potential way to grow taller for open plates as well as epiphysis with no active proliferating and differentiating chondrocytes.  Their are countless studies that show the prochondrogenic effects of LIPUS.  Unfortunately, the optimal setting has not been determined.  An experimental routine is provided here.

Yet another way to increase height is anabolic(anabolic = increase cellular proliferation and differentiation) factors like IGF-1 and Insulin.  Milk increases IGF-1 but needs to be cycled after age 5.  It would be better for somehow the milk to be lactose free as lactose enhances FGF21 signaling. I'm not sure how it should be cycled.  Insulin is controversial as there is evidence that insulin resistance increases height.  IGF-1 is pro-chondrogenic

Whether you still have active proliferating chondrocytes or not, what you want to do to achieve growth is pretty much the same.  First, the most important thing to do is to inhibit myostatin.  Myostatin is a regulator of stem cell proliferation and differentiation.  Now that doesn't mean that you can't achieve extra stem cell proliferation and differentiation in the presence of myostatin.  Compare it to muscle growth, it's easier if myostatin is inhibited but it's still possible if it's not.  Creatine is a myostatin inhibitor that has other pro-chondrogenic effects as well.

Lovastatin which is in Red Yeast Rice may help increase height as well but it hasn't been well documented.

There's also electrical methods.

You would also want to find a way to enhance the amount of C-type nautriuretic peptides that you express.  There's a product coming out that releases guanyl Cyclase B which enhances your expression of C-type nautriuretic peptides.  CNP increases height by increasing chondrocyte hypertrophy and inhibits FGFR3 and keeps Sox9 in check when it wants to inhibit the cell cycle by inhibiting CyclinD

But even if you are doing LSJL to try to re-activate your growth plates you still ideally want both of these substances.  You want your stem cells to proliferate and differentiate.  You want your chondrocytes to proliferate or differentiate when the stem cells differentiate into them.  The difference between growth plates open or not is that if your growth plates are "closed" you need to first initiate reform growth plates via mesenchymal condensation and chondrogenesis.

Another way to grow is to inhibit estrogen.  There's an equilibrium quantity of estrogen however so you have to be careful not to go below this quantity.  However, being at too high level of estrogen is more damaging to height than too low way.

The problem with this is negative feedback.  Scientists have tried injecting extraneous HGH into children and only found an increase in growth rate but not final adult height.  The reason that extraneous HGH doesn't work is negative feedback.  Most of the causes of Gigantism involve an alteration in the bodies homeostatic mechanisms(like the pituitary gland).  They have even found causes of Gigantism with low HGH levels due to an increase in tissue sensitivity to HGH.  There is evidence that the genes related to HGH is involved in height growth but there's also a lot of evidence that HGH isn't the be-all/end-all to height growth.

Here are other supplements that may help.

So, pretty much everything you want to do to grow taller is pretty much the same whether you have existing chondrocytes proliferating and differentiating in the growth plate or not.  The difference is getting new MSCs to differentiate into chondrocytes and form ectopic growth plates within bone in fused bone.

Chondrocyte injection in distraction epiphysiolysis (rabbit model).

"The purpose of this study was to determine if cultured chondrocytes could prevent premature closure of the physis after physeal distraction in a rabbit model. Epiphyseal distraction at the proximal tibial epiphysis was performed in 24 immature rabbits. Chondrocytes were harvested from the iliac apophysis. The animals were divided into three groups: A, epiphyseal distraction alone; B, injection of phosphate buffered saline (PBS) after epiphyseal distraction; and C, injection of cultured chondrocytes after epiphyseal distraction. After epiphyseal separation was noted radiographically, each animal was evaluated at routine intervals. At 2 to 4 weeks, significant tibial lengthening as compared to the contralateral tibia was noted in all three groups. At 10 weeks, lengthening was apparent only in group C; in groups A and B, the operated tibia was shorter than the unoperated one. Histologic examination at 4 weeks revealed partial bony bridge formation with cell clustering in the fibrocartilaginous matrix in groups A and B. In group C, the matrix showed a typical hyaline aspect with cells organized in columns at the injection site. The zone of hypertrophic chondrocytes was enlarged. It appears that the injected cells differentiated into hypertrophic chondrocytes and delayed premature physeal closure. At 10 weeks after distraction of the physis, the width of the physis was restored to 75% of normal, but disordered chondrocyte growth with cell clustering was present in the cell-injected group."

"Physeal distraction is a relatively simple method of limb lengthening in which the epiphysis is pulled away from the metaphysis at a slow, controlled rate. The physis separates without osteotomy and distraction can be applied through an external fixator."

"the lengthening obtained often is lost by growth retardation caused by premature physeal closure after removal of the fixator."

"Skeletally immature, 6-week-old New Zealand white rabbits were ideal for study because these animals approach physeal closure (maturity) at 4 to 6 months."

"In group C, physeal defects were primarily filled with abundant hypertrophic cartilage. A few islands of calcified cartilage were seen in the separated defect in the lower portion of the separated physis at 4 weeks
The matrix showed a typical hyaline aspect with cells organizein columns at the injection site. Most of the cells were viable and exhibited a delimited nucleus. The cellularity of the repair tissue was greater than that of the adjacent normal cartilage.  The injected cells seemed to attach to the bottom of the separated physis and incorporate as hypertrophic chondrocytes, thus delaying premature closure of the physis.At 10 weeks after initiation of distraction, the defect was filled primarily with mixed fibro-hyaline cartilage and the thickness of the physis was restored to 75% of normal, but chondrocyte growth remained disordered with cell clustering"

"Injected chondrocytes (group C) prevented bony bridge formation in all specimens, even in those
few where cell survival appeared to be minimal.  Increased thickness of physeal cartilage produced by distraction was not due to increased cell proliferation in the physis. On the contrary, cell division appeared to be reduced with zonal separation. In 7 of 8 animals with injected chondrocytes, the cells continued to maintain a proteoglycan-rich cartilage matrix for the duration of the experimental period and in some cases showed ordered maturation. Evaluation at longer postoperative intervals showed an increase in vascularity at the distraction site, as fibrous stroma extending into the defects was replaced
with calcified tissue."

"the injected cells attached to the bottom of the separated physis and behaved as hypertrophic chondrocytes to delay premature physeal closure. The enlargement of the hypertrophic chondrocyte region was similar to that seen after slow distraction"

"this proliferation of hypertrophic chondrocytes is derived partly from the injected cells and partly from the tension effect on the physis."