Neuropeptide Y: New Height increase supplement

It’s possible that a supplement for Neuropeptide Y may not be needed as cold exposure increases Neuropeptide Y levels. But it’s not clear if an increase in Neuropeptide Y will increase height.

Neuropeptide Y Promotes mTORC1 to Regulate Chondrocyte Proliferation and Hypertrophy 

“Peripheral neuropeptide Y (NPY) has been reported to regulate bone metabolism and homeostasis, however its potential roles in growth plate chondrogenesis remain unclear. Here, we found that NPY expression decreased during chondrocyte differentiation in vitro and in vivo. NPY was required for chondrocyte proliferation, while in contrast knockdown of NPY facilitated chondrocyte hypertrophic differentiation. {So maybe Neuropeptide Y can keep growth plates open for longer?} Administration of recombinant NPY in rat chondrocytes and metatarsal bones uncoupled the normal proliferation and hypertrophic differentiation during chondrogenesis and thereby inhibited growth plate chondrogenesis and longitudinal bone growth. Remarkably, NPY activated mTORC1 pathway in chondrocytes, whereas attenuation of mTORC1 activity by administration of rapamycin in vitro partially abrogated NPY-mediated effects on chondrocyte proliferation and hypertrophic differentiation. In addition, a combination of Y2R antagonist but not Y1R antagonist with NPY abolished NPY-mediated inhibition of metatarsal growth and growth plate chondrogenesis. Mechanistically, NPY activated Erk1/2 by NPY2R, then phosphorylated ERK1/2 activated mTORC1 to initiate PTHrP expression, which in turn promoted chondrocyte proliferation and inhibited chondrocyte hypertrophic differentiation. In conclusion, our data identified NPY as a crucial regulator of chondrogenesis and may provide a promising therapeutic strategy for skeletal diseases.”

You can potentially buy Neuropeptide Y for lab use. Couldn’t get the full study but here’s another paper on it.

Neuropeptide Y Acts Directly on Cartilage Homeostasis and Exacerbates Progression of Osteoarthritis Through NPY2R

“Neuropeptide Y (NPY) is known to regulate bone homeostasis; however, its functional role as a risk factor during osteoarthritis (OA) remains elusive. In this study, we aim to investigate the direct effect of NPY on degradation of cartilage and progression of OA and explore the molecular events involved. NPY was overexpressed in human OA cartilage accompanied with increased expression of NPY1 receptor (NPY1R) and NPY2 receptor (NPY2R). Stressors such as cold exposure resulted in the peripheral release of NPY from sympathetic nerves{This may explain why people in colder environments are taller}, which in turn promoted upregulation of NPY and NPY2R in articular cartilage in vivo. Intra-articular administration of NPY significantly promoted chondrocyte hypertrophy and cartilage matrix degradation, with a higher OARSI score than that of control mice, whereas inhibition of NPY2R but not NPY1R with its specific antagonist remarkably ameliorated NPY-mediated effects. Moreover, NPY activated mTORC1 pathway in articular chondrocytes, whereas the administration of rapamycin (an mTORC1 inhibitor) in vitro abrogated NPY-mediated effects. Mechanistically, mTORC1 downstream kinase S6K1 interacted with and phosphorylated SMAD1/5/8 and promoted SMAD4 nuclear translocation, resulting in upregulation of Runx2 expression to promote chondrocyte hypertrophy and cartilage degradation. In conclusion, our findings provided the direct evidence and the crucial role of NPY in cartilage homeostasis.”

“peripheral NPY can be also synthesized by osteoblasts, osteocytes, as well as chondrocytes both at embryonic and adult stage”

“the NPY-treated group exhibited more severe OA phenotypes than that of the control group as indicated by significant cartilage degradation and fibrillation together with a higher OARSI score”<-although we don’t know how that will translate to height.

“NPY activated mTORC1 signaling in articular cartilage, which in turn activated SMAD1/5/8 signaling and consequently promoted chondrocyte hypertrophy and cartilage degradation.”

“old exposure stimulates NPY release from sympathetic nerves, and then NPY could enter the blood since NPY-positive sympathetic nerve fibers have been found to be mostly distributed around and within blood vessels.  mice exposed in cold water increased circulating NPY.”

Skeletal phenotype of the neuropeptide Y knockout mouse

“lobal deletion of NPY results in a smaller femoral cortical cross-sectional area (-12%) and reduced bone strength (-18%) in male mice. In vitro, NPY-deficient bone marrow stromal cells (BMSCs) showed increase in osteogenic differentiation detected by increases in alkaline phosphatase staining and bone sialoprotein and osteocalcin expression. Despite both sexes presenting with increased adiposity, female mice had no alterations in bone mass, suggesting that NPY may have sex-specific effects on bone”

Neuropeptide Y Regulation of Energy Partitioning and Bone Mass During Cold Exposure

“wild-type (WT) mice at thermoneutral (29 °C) were compared to mice at room temperature (22 °C) conditions. Interestingly, bone mass was lower in cold-stressed WT mice with significant reductions in femoral bone mineral content (− 19%) and bone volume (− 13%).”

Magnitude and pattern of compensatory growth in rats after cold exposure 

“It is a common observation that normal growth is affected or suppressed in young individuals by environmental adversities and physical disturbances. On the other hand, when health or favorable conditions are restored, the tempo of growth promptly accelerates as if the individual is trying to make up for the growth debt incurred.”

“Growth retardation during the single cold exposure period, and prompt compensatory growth after return to the warm environment, occurred in both the tail and the body, and in the younger A as well as the older B rats. During the 2-week periods of cold exposure, tail gain of the A rats was only about 30 % of that of the warm controls (W2), while that of the B rats averaged about 50 %. Likewise, the rapid compensatory growth in tail length during the 2 weeks immediately after the end of cold exposure was more prominent in the A than in the B rats: the tail gain in the A
rats averaged around 145 % of that of the controls in contrast to 130 % in the B rats. Not only was the compensation greater in the A rats, but the compensatory period (period of significantly faster growth) was longer also, extending over 8 weeks (from 3rd to 10th), in contrast to 4 weeks (from 6th to 10th) in the B rats. By the end of the 10th week the tail length of A and B rats was not significantly shorter than that of the W2 group”

Uncoupling protein-1 is protective of bone mass under mild cold stress conditions

“UCP-1 is critical for protecting bone mass in mice under conditions of permanent mild cold stress for this species (22 °C). UCP-1−/− mice housed at 22 °C showed significantly lower cancellous bone mass, with lower trabecular number and thickness, a lower bone formation rate and mineralising surface, but unaltered osteoclast number, compared to wild type mice housed at the same temperature. UCP-1−/− mice also displayed shorter femurs than wild types, with smaller cortical periosteal and endocortical perimeters. Importantly, these altered bone phenotypes were not observed when UCP-1−/− and wild type mice were housed in thermo-neutral conditions (29 °C), indicating a UCP-1 dependent support of bone mass and bone formation at the lower temperature. Furthermore, at 22 °C UCP-1−/− mice showed elevated hypothalamic expression of neuropeptide Y (NPY) relative to wild type, which is consistent with the lower bone formation and mass of UCP-1−/− mice at 22 °C caused by the catabolic effects of hypothalamic NPY-induced SNS modulation.”

Devon Larratt grew longer arms as a result of arm wrestling

https://youtube.com/watch?v=E1DTwpRFcfk&feature=shares

Torsional stress like tennis, swimming, etc. tends to lengthen the arms. The reason for this is likely due to the fact that torsional stress is the most efficient way to drive fluid forces in the bone(think like wringing out a sponge).

Devon Larratt is 47 years old BTW. A 53.6cm to 54.1cm increase over two years is a pretty good growth rate. And that’s not accounting for the humerus. Also imagine if you grew the clavicle and other arm length too. That would be a solid increase in wingspan over two years.

There are many sports that cause torsional force on the arms but the only sport I could find that could really exert torsional force was on the legs and I did find some evidence of leg height increase however there is a high rate of selection bias towards shorter divers.

I am currently testing exercises that could potentially exert spiral/torsional/rotation forces in bone. There are many for the arms(think hammer curls for instance). For legs, I am trying things like split legged woodchop exercises. Something like kicking could potential work. The problem is that the kicks have to be sufficiently weighted and you still have to maintain momentum.

Breakthrough: type H blood vessels may be key to reversing growth plate loss

Knowing that H blood vessels are lost via aging is a breakthrough as it may indicate that restoring type H blood vessels may be key to restoring the growth plate.

Lateral Synovial Joint Loading has been linked to type H blood vessel formation. Type H vessels are key for transport of cells. If we can reverse the process of Type H vessels to type L vessels perhaps that would reinitiate a natural process of growing taller.

Mechanical forces couple bone matrix mineralization with inhibition of angiogenesis to limit adolescent bone growth

“Bone growth requires a specialised, highly angiogenic blood vessel subtype, so-called type H vessels, which pave the way for osteoblasts surrounding these vessels. At the end of adolescence, type H vessels differentiate into quiescent type L endothelium lacking the capacity to promote bone growth.{How do we reverse this process?} Until now, the signals that switch off type H vessel identity and thus limit adolescent bone growth have remained ill defined. Here we show that mechanical forces, associated with increased body weight at the end of adolescence, trigger the mechanoreceptor PIEZO1 and thereby mediate enhanced production of the kinase FAM20C in osteoblasts.{so if we are underweight type H blood vessels will stay around longer?} FAM20C, the major kinase of the secreted phosphoproteome, phosphorylates dentin matrix protein 1, previously identified as a key factor in bone mineralization. Thereupon, dentin matrix protein 1 is secreted from osteoblasts in a burst-like manner. Extracellular dentin matrix protein 1 inhibits vascular endothelial growth factor signalling by preventing phosphorylation of vascular endothelial growth factor receptor 2. Hence, secreted dentin matrix protein 1 transforms type H vessels into type L to limit bone growth activity and enhance bone mineralization.{so a dentin matrix protein 1 inhibitor may be a possible mechanism in which to grow taller?} The discovered mechanism may suggest new options for the treatment of diseases characterised by aberrant activity of bone and vessels such as osteoarthritis, osteoporosis and osteosarcoma.”

” Type H vessels are located exclusively at the sites of active bone growth, namely the ossification front (OF) and periosteum, and they are organised in columnar structure. Notch signalling, Hypoxia-inducible factor 1-alpha (HIF1α) activity, blood flow speed and slit guidance ligand 3 (SLIT3) were shown to support type H vessel formation”

“endothelial cells in bone require integrins for their proper functioning and maintenance, which highlights extracellular matrix (ECM) proteins as important factors for endothelium activity”

” we performed laser microdissection (LMD) of single capillary with associated surrounding cells in the OF of juvenile (4-week-old) and adult (12-week-old) mice.”

“Our detailed analysis of DMP1 protein localisation throughout postnatal bone development showed that until 5 weeks of age, the protein was mainly localised at the base of the zone of type H vessels in the [Ossification front]”

“DMP1 accumulation in the OF[Ossification Front] centre at 5.5–6 weeks correlated with a decrease in endomucin (EMCN) intensity and reduced amounts of MMP9 at the OF-GP border. This was associated with the disappearance of bulges and columnar structure of the vessels”

They found though that the DMP1 knockout femurs were shorter at a certain age point but perhaps a reduction in DMP1 would lead to slower more sustained growth.

“DMP1 secretion correlates positively with body weight and coincides spatiotemporally with FAM20C upregulation”

“mechanical loading through increasing body weight or/and muscle contractions, directly or indirectly, controls DMP1 secretion along with FAM20C upregulation.”

“, body weight-associated mechanical loading triggers the mechanoreceptor PIEZO1 to enhance the production of FAM20C kinase in osteoblasts, which induces a burst in DMP1 secretion into ECM. Second, large amounts of extracellular DMP1 inhibit VEGF signalling in the OF and transform highly angiogenic type H vessels into quiescent type L vasculature to limit bone growth activity. In parallel, extracellular DMP1 leads to rapid matrix mineralisation and strengthening of long bones”

Reducing the levels of human DMP1 or it’s receptors may be a way to grow taller in adolesence and possible allow for new bone growth post skeletal maturity but more testing has to be done.

Radial Shockwave Treatment may stimulate bone growth in the growth plate

It’s always exciting to see new possible treatments but this one may be pretty minor.  Extracorporeal shockwave treatment has been written about on the blog before.  Some more.  These studies found that extracorporeal shockwave treatment can stimulate growth.  Extracorporeal shockwave treatment can also stimulate the periosteum.

There are extracorporeal shockwave therapy machines for sale but they’re like $1,000.

Radial shockwave treatment promotes chondrogenesis in human growth plate and longitudinal bone growth in rabbits

“The process of longitudinal bone growth occurs at the growth plate where the chondrocytes undergo apparent structural and molecular changes to promote growth. Recent reports suggest that radial shockwave treatment (rSWT) stimulates bone length in cultured fetal rat metatarsals. Therefore, we investigated if rSWT has similar growth promoting effects on cultured human growth plate fragments and addressed the same in a preclinical in vivo rabbit model by subjecting their growth plates to rSWT.

Short-term effects of high-energy rSWT were evaluated in a unique model of cultured human growth plate cartilage (n = 5) wherein samples exposed to rSWT were assessed for chondrogenic markers at 24 h in comparison to unexposed samples obtained from the same limb.

Local in vivo effects were studied in six-week-old rabbits{6 week old rabbits are about equal to 42 week humans which is very young} who had their distal femurs exposed to four weekly sessions of rSWT at low- and high-energy levels (n = 4 each){weekly sessions are not that much}. At sacrifice, histomorphometric and immunohistochemistry analyses were performed. For effect on longitudinal growth, proximal tibiae of 22-week-old rabbits (n = 12) were asymmetrically exposed to rSWT; the contralateral side served as untreated controls. At sacrifice, the final bone length was measured.

In the ex vivo model of cultured human growth plate cartilage, rSWT exposure upregulated SOX9 and COL2A1 compared to control.

In the immature rabbit model, an increased number of proliferative chondrocytes and column density was seen for both the energy levels. In the adolescent rabbits, an increase in tibial length was observed after the fourth session of high-energy rSWT and until six-weeks after rSWT compared to the untreated limb.

Our preliminary experimental results suggest that rSWT may serve as a non-invasive treatment and possibly a safe strategy to stimulate longitudinal bone growth. However, further studies are needed to assess the in vivo effects of rSWT in models of disturbed bone growth.”

“22-week-old healthy rabbits (n = 12; 7 females, five males; weight 2.0–2.5 kg) was performed to document the effects of high-energy rSWT (3000 impulses, 180 mJ, 5 Hz) once weekly for four weeks on bone length. “

” Low-level laser beams and ultrasound are non-invasive modalities that have been investigated without success. Extracorporeal shockwave therapy (SWT) is a candidate for non-invasive modulation of growth plate activity as it has been successfully tested in fracture healing, nonunions, and other musculoskeletal disorders with minor complications in the clinic “

“After exposure to rSWT, gene expression analysis was performed after 24-h of culture. We observed increased expression of SOX9 (mean fold change: 3.0 ± 2.3) and COL2A1 (mean fold change: 19.0 ± 29.26) in treated samples when compared to untreated controls”

“he chondrocytes-column density (columns per mm growth plate width) in the proliferative zone was significantly increased in both the low-energy (low-energy rSWT: 40 ± 12 and control: 32 ± 9) and the high-energy rSWT groups (high-energy rSWT: 51 ± 13 and control: 37 ± 3)”

That looks like a pretty dramatic impact.  Although shockwave also increased chondrocyte apoptosis so it’s possible that it increases growth rate but not total growth plate assisted height.

“At 26 weeks of age, after four sessions (at weekly intervals) of high-energy rSWT, there was a significant increase in the differences between the lateral tibial length measured on radiographs when compared to untreated controls (mean difference: 0.28 cm; p = 0.008). Six-weeks after the last session of high-energy rSWT the difference in the lateral tibial length treated bones compared to untreated controls was 0.03 cm (p = 0.001)”  Rabbit tibial length may be about 10cm.  So 0.28cm is like a 2.8% increase. Which is kind of significant.

” it is challenging to maintain this significant increase in bone length when dealing with healthy animals as the bone lengths tend to equalize after treatment withdrawal”<-so it may only affect growth rate not growth capacity.

So basically it’s worth studying but we don’t know if it only increases growth rate.

 

In some cases it’s worth noting extracorporeal shockwave therapy reduced length as seen above but of course the incidents were growth was increased is greater.

“Previous studies that used fSWT, a device used for its osteogenic effects, showed no effect on the growth plate cartilage in rats and rabbits”

“The high-energy rSWT used in the histological study did not cause cell death as measured with apoptotic markers and was considered safe for longitudinal bone growth experimentation.”

“one of the animals that received high-energy rSWT showed excess bone formation in the medial femoral condyle proximal to the growth plate in the metaphyseal region. This could be an adverse consequence of rSWT on periosteal cells proximal to the growth plate reflecting either increased vascularity or traumatic detachment of the periosteum. Therefore, careful evaluation needs to be considered when translating rSWT to patients as it may cause unpredictable excess growth akin to a metaphyseal fracture.”<-this is huge for us! We want excess bone formation!

Here is the excess bone formation in question:

That is pretty significant. 22 rabbits were used.

“When investigating the effects of high-energy rSWT, we found up to 1% increase in the final bone length in treated adolescent rabbits when considering the observations as paired data. An earlier study in rabbits using (piezoelectric device) focal extracorporeal shockwave therapy (fSWT) supports the growth stimulatory effect . Our study is different from the previous one in three ways. First, we used rSWT, which is safer because it generates less energy with low penetration than piezoelectric fESWT. Second, we exposed adolescent animals to rSWT and followed them until growth plate fusion to know if the changes in bone growth were sustained until the end of growth. Thirdly, we performed molecular and histological studies to demonstrate effects at the growth plate level.”

“observed stimulation of growth following rSWT could be due to cellular changes within the growth plate. It is plausible that the stimulated resting chondrocytes may have augmented the propagation of daughter cells during their subsequent entry into the proliferative zone, thus contributing to an increased columnar density”

Here’s a study that shows that extracorporeal stimulation can add bone to the hip:

Acetabular augmentation induced by extracorporeal shock waves in rabbits

“We conducted this animal study to demonstrate whether exposing the acetabulum in immature rabbits to extracorporeal shock waves induces bone formation in the acetabulum. Five thousand shock waves of 100 MPa each were directed, from outside, at the acetabular roof of eight immature rabbits. At each of two time points (4 and 8 weeks) after treatment, the pelvises of four rabbits were removed and evaluated morphologically. Woven bone formation was observed on the lateral margin of the acetabular roof at 4 weeks after treatment, and the breadth of the acetabular roof in the coronal plane was significantly increased{coronal plane is basically length}. Eight weeks after treatment, the woven bone disappeared; the breadth of the acetabular roof, however, was significantly increased. These findings demonstrated that extracorporeal shock waves induced acetabular augmentation in rabbits. We conclude that extracorporeal shock waves, perhaps, could be applied clinically for the treatment of acetabular dysplasia.”

“No fracture was observed on the plain X- ray photo during the
monitoring period after irradiation.”

“Extracorporeal shock wave therapy, which was developed for lithotripsy, is thought to be also useful
to give dynamic loading to organs noninvasively. Shock wave demonstrates its physical action specific on bone as on calculus . It was reported that exposure to shock waves caused fracture of cancellous trabecula or periosteal lifting”

“Eight male New Zealand White rabbits aged 9 weeks weighing 1.0-1.2kg were used. Piezolith 2300 (Richard Wolf Inc., Germany) was used to produce extracorporeal shock waves. Ultrasonic waves were used for focusing. The focus was set in 3 mm cranial from superolateral edge of the acetabulum and 2 mm inside from lateral margin of the acetabular roof. Each 4 animals of the 8 animals were grouped into Group I and II. Shock waves were irradiated on the right acetabular roof from outside. The strength and the number of the shock wave were set to be 100 MPa and 5000 times respectively.”

The difference in bone growth is dramatic

WebMD article mentions microstrain to get taller

There’s an article on WEB MD called Best Exercises for Leg Length Discrepancy. It was reviewed by a medical doctor Dan Brennan.

From the article:

“Certain exercises and stretches may help minimize leg length discrepancy and ease any related symptoms.”

“Physical force can cause micro strains on your bones, which results in incremental changes in bone mass and length — especially if the exercise is repeated over time. “

I’ve studied microstrain in the past and I believe that microstrain is a tool that can be used to make people taller. Either by alterations in the fluid forces in the bone, by inducing plastic deformation, complete trabecular microfractures resulting in endochondral ossification one trabeculae at a time, or piezoelectric forces modifying osteoclast and osteoblast activity.

“One exercise that can put this kind of strain on your affected leg bones is side kicking into the air. To get the most out of this exercise, do multiple sets daily.”<-Is side kicking into the air going to cause the right forces to induce height growth? I’m not one to discount any potential height increase method. But I would at least like to see some anecdotal evidence for this if not some kind of study. I don’t know if you could get animals to side kick in the air. And I think it would be hard for humans to get the right technique as you’d want the right kind of microstrain. I assume the goal would be tensile plastic deformation gradually lengthening the bone one microstrain at a time or piezoelectric forces altering osteoblast and osteoclast activity such that the bone is remodeled in a more lengthened state.

The article also mentions a quadriceps left and hamstring stretch which I do not think are related to lengthening bones.

Here are the sources mentioned in the study:

Arthritis and Rheumatology: “Brief Report: Leg Length Inequality and Hip Osteoarthritis in the Multicenter Osteoarthritis Study and the Osteoarthritis Initiative.”

European Cells and Materials: “Mechanical Loading and How It Affects Bone Cells: The Role of the Osteocyte Cytoskeleton in Maintaining Our Skeleton.”

International Research Journal of Engineering, IT & Scientific Research: “Relationship between length of leg and strength of leg muscle to frequency of straight kicks.”

Journal of Athletic Training: “Standing and Supine Hamstring Stretching Are Equally Effective.”

Journal of International Medical Research: “Post-THA gait training to improve pelvic obliquity and decrease leg length discrepancy in DDH patients: a retrospective study.”

From Mechanical Loading and How It Affects Bone Cells: The Role of the Osteocyte Cytoskeleton in Maintaining Our Skeleton, “”1,000 microstrain equals a 0.01 % change in length of the bone compared to its original length. Vigorous exercise induces bone strains up to 1,000 microstrain in humans.”<-but this will only be a permanent increase in length if the 0.01% change in length is plastic. If the change in length is elastic it will return to it’s original length like a rubber band.

This study Relationship between length of leg and strength of leg muscle to frequency of straight kicks, I could not find anything that would suggest that kicking would increase legs.

This study Post-THA gait training to improve pelvic obliquity and decrease leg length discrepancy in DDH patients: a retrospective study, was more about functional limb lengthening discrepancy. “Gait training after surgery is one method to correct functional LLD.” i.e. limb lengthening discrepancy due to improper mechanics rather than actual bone length.

The other studies I can’t see how there would be any connection at all.

I found his email and sent him one if he wants to respond

Is it possible to use cardarine to grow taller?

Cardarine has been used by bodybuilders and is linked to height growth. Cardarine is a PPAR Delta agonist(activator).

PPARDelta has been linked to height. From A single nucleotide polymorphism on exon-4 of the gene encoding PPARdelta is associated with reduced height in adults and children.  “compelling evidence was found for this locus and its association with height (P = 10(-8)) with an overall effect size of about 0.5 cm per allele{1cm total}.” It’s possible that the effects of PPARdelta are biphasic where there is an equilibrium amount to maximize height and too little or too much reduces height or that there is a minimum amount of PPARDelta activation that is needed for height and that any further has no effect. The authors speculate that PPARDelta may affect height via metabolic efficiency or via affects on osteoclast function. Metabolic efficiency would have no effect on height as an adult but there is potential if it affects osteoclast function as degradation of bone would be a needed step to grow taller as an adult as it would both make the bone more susceptible to plastic deformation and allow for tissues that are capable of interstitial growth to take the place of bone.

Obviously, 1 cm in height is not going to break the bank in terms of increasing height while skeletally immature but if a PPARdelta agonist can increase osteoclast activity that can be used as part of a height increase routine.

Here’s the studies that says PPAR affects osteoclasts

Cloning and function of rabbit peroxisome proliferator-activated receptor delta/beta in mature osteoclasts

“Osteoclasts modulate bone resorption under physiological and pathological conditions. Previously, we showed that both estrogens and retinoids regulated osteoclastic bone resorption and postulated that such regulation was directly mediated through their cognate receptors expressed in mature osteoclasts. In this study, we searched for expression of other members of the nuclear hormone receptor superfamily in osteoclasts. Using the low stringency homologous hybridization method, we isolated the peroxisome proliferator-activated receptor delta/beta (PPARdelta/beta) cDNA from mature rabbit osteoclasts. Northern blot analysis showed that PPARdelta/beta mRNA was highly expressed in highly enriched rabbit osteoclasts. Carbaprostacyclin, a prostacyclin analogue known to be a ligand for PPARdelta/beta, significantly induced both bone-resorbing activities of isolated mature rabbit osteoclasts and mRNA expression of the cathepsin K, carbonic anhydrase type II, and tartrate-resistant acid phosphatase genes in these cells. Moreover, the carbaprostacyclin-induced bone resorption was completely blocked by an antisense phosphothiorate oligodeoxynucleotide of PPARdelta/beta but not by the sense phosphothiorate oligodeoxynucleotide of the same DNA sequence. Our results suggest that PPARdelta/beta may be involved in direct modulation of osteoclastic bone resorption.“

Here’s the other study:

PPAR agonists modulate human osteoclast formation and activity in vitro

“Peroxisome proliferator-activated receptors (PPARs) are members of the nuclear steroid hormone superfamily and exist in three isoforms: PPARalpha, beta and gamma, each with specific functions. In this study, we have investigated the expression of PPARs by human osteoclast precursors and osteoclasts generated in vitro. In addition, the effects of fibrates and isoform-specific PPAR agonists on osteoclast formation and resorption in vitro were determined. Human peripheral blood mononuclear cells (PBMCs) were stimulated with human recombinant RANKL and M-CSF to generate osteoclasts. RNA was extracted at days 0, 7, 14 and 21 and RT-PCR for all three PPAR isoforms demonstrated their expression throughout this culture period. To determine the effect on osteoclast formation, PPAR agonists (10(-8) M to 10(-5) M) were added from the beginning of the culture until day 14 and the number of multinucleated osteoclasts counted. The effect of PPAR agonists on osteoclast function was similarly determined by treating mature, multinucleated osteoclasts cultured on dentine wafers with PPAR agonists (10(-8) M to 10(-5) M) for 7 days and quantifying resorption. Bezafibrate and fenofibrate, which non-discriminately activate all PPAR isoforms, significantly inhibited the formation of multinucleated osteoclasts from PBMC in vitro. Bezafibrate treatment of mature osteoclast resulted in 50% inhibition (at 10(-8) M and 10(-7) M) of resorption, yet fenofibrate had no significant effect. Activation of individual PPARs with isoform-specific agonist (GW9578, L165041 and ciglitizone which preferentially activate PPARalpha, beta and gamma respectively) resulted in significant dose-dependent inhibition of multinucleated osteoclast formation. Divergent effects on osteoclast resorption were observed; GW9578 had no significant effect on resorption, whereas ciglitizone and L165041 dose-dependently inhibited and stimulated resorption, respectively. These data show for the first time expression of all three PPAR isoforms throughout the development and maturation period of osteoclasts generated from human PBMCs. In addition, we demonstrate that isoform-specific PPAR agonists have strong effects on multinucleation and highly variable effects on bone resorption. In conclusion, this study highlights the potential of PPARs as therapeutic targets in diseases with accelerated osteoclast formation and resorption.”

I couldn’t find any further studies linking PPARDelta to longitudinal bone growth nor can I find any anecdotal cases of people growing taller off of taking cardarine.