Can Forskolin help with increasing height?

Over at the Hakker forum, I saw that he was recommending Forskolin as a possible way of increasing height.  Forskolin is available for sale: Life Extension Forskolin 10mg Capsules, 60-Count. Can Forskolin help increase your height?  He lists the beneficial effects as boosting cAMP, GH, and lowering SOCS.  SOCS increases FGFR3 levels which have been implicated in dwarfism.  FGFR3 inhibits chondrocyte differentiation which means that high SOCS and/or FGFR3 levels may reduce LSJL effectiveness by making it harder for stem cells to differentiate into chondrocytes. That means that Forskolin can increase the effectiveness of LSJL by decreasing the minimum hydrostatic pressure required to induce chondrogenic differentiation.

Previously, we also learned that cAMP and in turn Forskolin helped regulate osteoblast adhesion to cell surfaces.  Hyaluronic Acid at a high molecular weight inhibits cAMP activity.  If cAMP does help with height increase then if you are taking Hyaluronic Acid you may wish to take Forskolin as well.  However, Hyaluronic Acid is usually not available at the 300 molecular weight that they found inhibits cAMP activity.

cAMP may be important to height growth by another mechanism than osteoblast adhesion and may enhance production of pro-chondrogenic molecules like aggrecan.

Forskolin Stimulates Aggrecan Gene Expression in Cultured Bovine Chondrocytes.

"Prostaglandins are autacoids that elevate intracellular 3prime prime or minute:5prime prime or minute-cyclic adenosine monophosphate (cAMP) levels in chondrocytes and other cells in culture. To facilitate intracellular cAMP accumulation, bovine chondrocytes were incubated with forskolin alone or forskolin and isobutylmethylxanthine. Both significantly increased proteoglycan synthesis, which was inhibited by the cAMP-dependent protein kinase inhibitor H89[meaning that the Forskolin enhancement of proteoglycan's is mediated by CAMP]. two large proteoglycan core proteins migrated more slowly than the 200-kDa marker protein and two small proteoglycan core proteins migrated slightly slower than the 46-kDa marker. aggrecan steady-state mRNA levels were increased by forskolin and isobutylmethylxanthine after 1 h and 5 h incubation. Decorin and type II collagen mRNA levels were not altered under these conditions. Link protein mRNA levels were slightly elevated, but only at the 5-h time point. These results indicated that stimulation of intracellular cAMP accumulation by forskolin or forskolin and isobutylmethylxanthine resulted in augmented proteoglycan synthesis via increased steady-state aggrecan mRNA levels. Suppression of proteoglycan synthesis by the cAMP-dependent protein kinase inhibitor H89 suggested that cAMP-dependent protein kinase may also play a role in regulating the synthesis and completion of newly synthesized proteoglycans."

Forskolin increases Aggrecan mRNA synthesis and this synthesis dependent on molecules related to cAMP.  Aggrecan in addition to Type II Collagen and Sox9 is a marker of chondrogenesis.

This study found that high doses of Forskolin inhibits proteoglycan synthesis:

Metabolic effects of forskolin in chick chondrocytes.

"chick embryo sternal chondrocyte cultures [were used]. After 8 h exposure to 100 microM forskolin, ATP levels and oxygen consumption were unaltered. Protein synthesis was unaffected up to 50 microM forskolin and protein degradation was unaffected by forskolin up to 100 microM. In contrast, incorporation of the proteoglycan precursors, 35SO4 and [3H]glucosamine, was more sensitive to forskolin. Inhibition was linear with dose between 10 and 100 microM, reaching 70% at 100 microM. Incorporation of 35SO4 into glycosaminoglycan chains initiated on an artificial beta-xyloside acceptor was inhibited in the same manner. cAMP accumulation was maximal at 10 microM forskolin, a concentration which did not alter proteoglycan synthesis.  A major, acute effect of forskolin is inhibition of proteoglycan synthesis in a cAMP-independent manner."

So for chicks at least you don't want more than 10 microM of forskolin.  Forskolin also slows down maturation of chondrocytes so it may help you grow taller for longer.

Extracellular calcium and parathyroid hormone-related peptide signaling modulate the pace of growth plate chondrocyte differentiation.

"An adequate supply of Ca2+ is critical for normal growth plate development. Changes in extracellular [Ca2+] ([Ca2+]e) modulate the function of chondrocytes with high [Ca2+]e promoting cell differentiation[calcium encourages chondrocytes to further hypertrophy until apoptosis]. signal transduction by the PTH/PTHrP type I receptor (PTH1R) slows down chondrocyte differentiation[Teriparatide has been shown to enhance chondrogenesis].
Raising [Ca2+]e from 0.5-3.0 mM dose-dependently promoted the development of mouse growth plate chondrocytes as indicated by decreases in proteoglycan accumulation and in the expression of early differentiation marker genes and by increases in mineral deposition and in the expression of markers of terminal differentiation[Forskolin by slowing the development of growth plate chondrocytes may enable for more division before terminal differentiation]. The effects of high [Ca2+]e on gene expression and matrix synthesis were blunted by incubating cells with PTHrP and vice versa. High [Ca2+]e also suppressed the expression of PTH1Rs. Chronic stimulation of PTHrP/PTH1R signaling by adenoviral expression of constitutively active human PTH1Rs (223hPTH1Rs) reduced the effects of high [Ca2+]e on proteoglycan synthesis and gene expression. Similar results were seen when we treated cells with forskolin[Forskolin reduces the effects of high calcium on inhibiting proteoglycan synthesis] or 8-bromo-cAMP.
The pace of chondrocyte differentiation depends on a balance of interactions between PTHrP/PTH1R and extracellular Ca2+ signaling and that high [Ca2+]e promote cell differentiation potentially by reducing the availability of PTH1Rs and the level of cAMP-dependent signal transduction."

"Maturing and upper hypertrophic chondrocytes express the type X collagen [α₁(X)] and alkaline phosphatase (ALP) as well as the PTH1R[So PTH1R would seem to counteract the effects of Type X collagen and alkaline phosphatase. Terminally differentiated chondrocytes in the lower hypertrophic zone (or mineralization zone) demonstrate high levels of the osteopontin (OP), osteonectin (ON), and osteocalcin (OC) expression and deposit Ca²⁺- and phosphate-containing mineral (i.e. hydroxyapatite) into the matrix"

"PTH (1–34), induced apoptosis in a dose-dependent manner. This observation supports our finding in mGPCs overexpressing hPTH1Rs that demonstrated increased apoptosis. We, however, did not observe apoptotic responses in uninfected cultures continuously treated with PTHrP with concentrations as high as 10⁻⁷ m. We think this is due to the ability of ligand to desensitize endogenous PTH1Rs"<-So too much Parathyroid Hormone may be bad by inducing too much apoptosis.  Continuous treatment of Teriparatide may not induce apoptosis but continuous treatment also means that the body has adapted to Teriparatide and no longer responding to Teriparatide.


Thus, Forskolin can help increase height during development by stimulating the cAMP pathway(which slows down terminal differentiation) and by inhibiting SOCS which stimulates FGFR3 which has been implicated in dwarfism.

Forskolin can help increase height with LSJL by encouraging stem cells to differentiate into chondrocytes.

Here's a study that states that Forskolin increases Testosterone levels:

Body composition and hormonal adaptations associated with forskolin consumption in overweightand obese men.

"Thirty subjects (forskolin, n = 15; placebo, n = 15) were studied in a randomized, double-blind, placebo-controlled study for 12 weeks.
Forskolin administration resulted in a change in bone mass[could the change in bone mass involve chondrogenesis?] for the 12-week trial compared with the placebo group. There was a trend toward a significant increase for lean body mass in the forskolin group compared with the placebo group (p = 0.097). Serum free testosterone levels were significantly increased in the forskolin group compared with the placebo group[testosterone inhibits myostatin which can inhibit chondrogenesis]. The actual change in serum total testosterone concentration was not significantly different among groups, but it increased 16.77 +/- 33.77% in the forskolin group compared with a decrease of 1.08 +/- 18.35% in the placebo group.
Oral ingestion of forskolin (250 mg of 10% forskolin extract twice a day) for a 12-week period was shown to favorably alter body composition while concurrently increasing bone mass and serum free testosterone levels in overweight and obese men."

However, this study was only on overweight and obese men.  Men with high lean body mass would also be considered overweight.  However, this study was only done on sedentary individuals.

According to the study Forskolin stimulates cAMP.

"Therefore, because of forskolin's ability to stimulate adenylate cyclase in a variety of tissues, the increase in bone mass that occurred during this study shows that forskolin can improve bone mass in overweight and obese men."<-Forskolin stimulates bone via the NO pathway and the NO pathway can stimulate chondrogenesis.

Forskolin- and dibutyryl cyclic AMP-mediated inhibition of chondrogenesis.

"Both the notochord and extracellular matrix materials (ECM) induce somite chrondrogenesis. ECM modulates the intracellular cAMP level during chondrogenic differentiation. Notochordal induction, which resulted in somite chondrogenesis (reflected by increased sulfated glycosaminoglycan synthesis) reduced the intracellular cAMP level in somites. Addition of forskolin and dibutyryl cAMP resulted in increased intracellular cAMP levels and decreased synthesis of sulfated glycosaminoglycans (decreased chondrogenesis). In the case of dibutyryl cAMP, the inhibition of sulfated glycosaminoglycan synthesis was related to the length of exposure time. Thus, the inverse relationship between cAMP content and enhanced chondrogenesis supports the theory that, in somites, a decrease in the intracellular cAMP level may be necessary to trigger chondrogenic differentiation."

Thus likely refers to further chondrocyte differentiation and not initial differentiation of stem cells into chondrocytes.