This grant by Jeffrey Baron has insights on the cessation of growth.

Regulation Of Childhood Growth

“Children grow taller because their bones get longer. This bone elongation occurs at the growth plate, a thin layer of cartilage within juvenile bones. The growth plate contains progenitor cells located within the resting zone. Children stop growing taller because the growth plate cartilage undergoes programmed senescence which involves extensive changes in gene expression, declining chonodrocyte proliferation, altered chonodrocyte differentiation, and involution of the growth plate{Note that this does not necessarily involve estrogen although estrogen may be a part of it}. Eventually growth plate senescence leads to cessation of bone elongation and epiphyseal fusion. Estrogen accelerates this developmental process, causing growth to stop earlier.  Senescence occurs because progenitor cells in the resting zone of the growth plate are depleted in number and that estrogen acts by accelerating this depletion. Body size varies enormously among mammalian species. In small mammals, body growth is typically suppressed rapidly, within weeks, whereas in large mammals, growth is suppressed slowly, over years, allowing for a greater adult size. Body growth suppression in rodents is caused in part by a juvenile genetic program that occurs in multiple tissues simultaneously and involves the downregulation of a large set of growth-promoting genes{If we can upregulate these genes via mechanical and dietary mechanisms can we reverse this body growth surpression?}. This genetic program is conserved among mammalian species but that its time course is evolutionarily modulated such that, in large mammals, it plays out more slowly, allowing for more prolonged growth and therefore greater body size. Epigenetic mechanisms may orchestrate this juvenile growth-regulating genetic program. Extensive genome-wide shifts in H3K4 and H3K27 histone methylation [occur] with age. Temporal changes in H3K4 trimethylation showed a strong, positive association with changes in gene expression whereas changes in H3K27 trimethylation showed a negative association. Genes with decreases in H3K4 trimethylation with age were strongly implicated in cell cycle and cell proliferation functions. The common core developmental program of gene expression which occurs in multiple organs during juvenile life is associated with a common core developmental program of histone methylation. In particular, declining H3K4 trimethylation is strongly associated with gene downregulation and occurs in the promoter regions of many growth-regulating genes, suggesting that this change in histone methylation may contribute to the component of the genetic program that drives juvenile body growth deceleration. In some children with subnormal linear growth, a cause can be identified, but in many the etiology remains unknown. This condition, idiopathic short stature (ISS), can sometimes be severe. We used whole-exome sequencing to study three families with autosomal dominant short stature, advanced bone age, and premature growth cessation. In these families, we identified novel heterozygous mutations in ACAN, which encodes aggrecan, a proteoglycan in the extracellular matrix of growth plate and other cartilaginous tissues. Our study demonstrated that heterozygous mutations in ACAN can cause a skeletal dysplasia which presents clinically as short stature with advanced bone age. The accelerating effect on skeletal maturation has not previously been noted in the few prior reports of human ACAN mutations. Our findings thus expand the spectrum of ACAN defects and provide a new molecular genetic etiology for the child who presents with short stature and accelerated skeletal maturation. ”

So we want to study H3K4 trimethylation and see if we can re-upregulate it during aging to find away to grow taller.  Although he only claims that H3K4 trimethylation downregulation is only associated with gene downregulation, he suggests that this H3K4 trimethylation downregulation may be a part of a larger program to cease growth.

Although it seems like it would be very difficult to manipulate H3K4 trimethylation and it would require something like a retrovirus.