“Our goal was to study the role of mechanical loading (one of the components of ambulation) on endochondral ossification and longitudinal bone growth. Thus, we applied cyclical, biologically relevant strains for a prolonged time period (4 weeks) to one tibia of juvenile mice, while using the contralateral one as an internal control. By the end of the 4-week loading period, the mean tibial growth of the loaded tibiae was significantly greater than that of the unloaded tibiae. The mean height and the mean area of the loaded tibial growth plates were greater than those of the unloaded tibiae. In addition, in female mice we found a greater expression of PTHrP in the loaded tibial growth plates than in the unloaded ones.”
This suggests that possibly boosting PTHrP directly could induce additional longitudinal bone growth.
“Mechanical forces related to gravitational changes, ambulation, and exercise may contribute to modulate bone growth.”<-this suggests that exercises that invert and every may modulate longitudinal bone growth.
“daily physical activities transmit complex mechanical loads including tension, compression, torsion, and shear to the skeleton”<-there are many ways to load bones that are under explored.
“Seventy-five 4-week old TOPGAL mice were exposed to mechanical loading using a Bose ElectroForce 3220 dynamic loading system. Before each loading session, mice were anesthetized with 3.5% isoflurane. Each loading session included 100 compressive loading cycles of 5 Newton (N) force to the right tibia at the frequency of 2 Hz per cycle”<-the reason that cyclic loading is more effective than static loading is likely related to fluid flow.
“mean tibial growth of the loaded tibiae was significantly greater than that of the unloaded tibiae, in the whole sample of mice “
This is a pretty significant different in length.
“Gravity and physical activity generate mechanical forces on the long bones and on the growth plates that may be involved in the regulation of bone growth.”<-one of the reasons why lateral loads are so effective is that it applies loads in a different mannerism against gravity.
“Of note, the stimulatory effect of mechanical loading on tibial growth persisted in the 4 weeks following the cessation of loading.
In addition, at the end of the 4-week loading period the whole growth plate and the epiphyseal zone heights, as well as the overall area of the loaded tibial growth plates were significantly greater than those of the unloaded growth plates. Such finding suggests a loading-mediated enhanced growth plate chondrocyte formation”
The study mentions that too high load can suppress growth. So maybe lighter weights are better and applying it the right way is more important but that may be for growth plates and not bones. Higher loads may be needed to stimulate growth in adult bones as bones are tougher tissue than catilage.
“similar studies in rodents indicate that elevated loading forces tend to inhibit longitudinal growth, while strains of lower intensity (like ours) tend to stimulate it. “
“After 4 weeks of loading, we found a greater Pthrp gene expression in the growth plate chondrocytes of the female mouse loaded tibiae, while no difference was found in male mice” however male mice also had greater length. So this suggests that mechanical loading also influences length by mechanisms not related to PTHrP.
So I stalled out in the old method at 75 1/4” for a long time(several months), it wasn’t until I tried this method that I started increasing the measurement again. I also increased the duration and am moving the vibration device around the hand more. That could play a role.
The old method took me from about 75 to 75 1/4”. I don’t know why I stalled out. Could be over time the body adapts to this stimulus and with this method I too will need to add other modalities to make it more effective.
Here’s the video demo:
Essentially what I do is I grip some oddly shaped objects for torsional loading. The more oddly shaped and weird the objects the better. You could also use bands, etc. ideally you’d the want the bone to have as many areas of compression and tension as possible. Fluid flows from areas of compression to areas of tension so the more areas of compression and tension there are there. The more fluid is going to flow.
Vibration is another stimulus to enhance fluid flow. The closer the vibration is the target bone/cartilage the better.
As seen in the video I kind of stir the hammers as a way to get more torsional loading and activity in the muscles. Muscles pull on the bone via the tendons creating more elastic bone deformation
The reason for changing the bones axis in relation to gravity I explain below in a an email to Hiroki Yokota the pioneer of the Joint Loading Modality and an expert in fluid flow to stimulate anabolic responses in the bone:
“You mention that the reason why lateral loads in bone is so effective is because of the water bottle analogy in pressing to the side is more effective in moving fluid.
But inversion/eversion is even more effective in moving fluid in the water bottle analogy and the arms undergo rapid eversion/inversion much more frequently than the legs.”
Hiroki Yokota’s response : “
I think your idea may work but we need to think about a basic fluid motion. A Navier-Stokes equation has three major forces to alter the flow. They are:
Pressure change
viscosity
gravity
Since viscosity is to prevent the flow, two driving forces to generate flow are pressure change and gravity. Lateral loading induces pressure change, while inversion activates gravity. We need to evaluate quantitatively the effects of loading-driven pressure change and inversion-induced gravity on fluid low in a bone matrix.”
Below are some studies that show that gravity can alter fluid flow in the bone and can stimulate cellular activity:
According to Fifteen days of microgravity causes growth in calvaria of mice. , microgravity alters interstitial fluid flow. Inversion and eversion would mimic this.
The Effect of the Microgravity Rotating Culture System on the Chondrogenic Differentiation of Bone Marrow Mesenchymal Stem Cells., microgravity rotating culture increased the chondrogenic differentistion of mesenchymal stem cells. Inversion and eversion would mimic this.
That interstitial fluid flow can stimulate bone response is not controversial. That this response includes making the bones longer is controversial. However, baseball pitching, tennis, and arm wrestling all of which have anecdotal reports of increase in bone length all have changing the bones axis in relation to gravity. Diving is the closest thing for legs that I could find that increases bone length and it also has constant rotation inversion/eversion to change the bone’s axis in relation to gravity.
I believe that interstitial fluid flow can make bones longer if this stimulus is sufficient. The reason that arm bones are easier to grow than legs is because the hands can grip things so the arm bones get more direct loading.
Think of an hourglass:
You tip it over the sand moves from one to another but not all right away(the rate at which it flows is affected by vicosity). You could affect the rate by which the sand flows by compressing the sides of the hourglass or vibrating the hourglass to make the sands move faster.
Interstitial fluid flow has the ability to affect osteoblasts, osteoclasts, and stem cells all of which could potentially combine to make a bone longer. The exact mechanism of how this could happen is not yet known. But if interstitial fluid flow can affect all these cells and can affect gene expression then it suggest that there is potentially a method by which interstitial fluid flow can increase bone length is possible even if the exact mechanism is unknown.
The arms are subjected to much better loads than the legs are. Legs are not typically inverted. They femur is kind of inverted in a squat or deadlift but the weight is not close to the femur it’s on the back or in the hands. Standing hamstring curls are typically done on machines which are not as an effective a loading as actually gripping the weight and it’s hard to grip weight with the toes. Iron boots perhaps? Kicks are typically not loaded. I am trying leg swings with ankle weights but the ankle weights are only 20lbs more weight may be needed. reverse crunches also involve inversion of the legs but weight/torsion needs to be on the leg itself
Torso is typically only inverted in good mornings and decline sit-ups and cartilage is easier to stimulate than bone since it is a softer more easily deformable tissue but the issue is it has a poor blood supply so it grows slower.
Finding ways to apply this method if it works can be done for torso and the legs but it will be more challenging.
One other person has reported growth with this method but he was under 25 but over 18 so it may have been natural growth since arms grow longer for longer.
I was originally going to shoot for x-rays around 75 1/4” but that was before I stalled out originally. I want to see a rate of consistent and steady growth. I do have before x-rays. I want some experimenters to try and validate the method. I also think 1/4” is not strong enough above measurement error.
Most people want to move on to the legs already but the legs are harder it needs to be validated on arms first. Wingspan was chosen because it’s easy to see when wingspan begins and ends and I do get some variance in measurement but I go for the peak measurement.
So next phase is:
Try to gain more in wingspan at a steady rate and validate with X-rays
Try to get experimenters to validate. I have gained wrist thickness and muscle mass with this so it has other benefits too. Other experimenters will reduce personal bias.
Gut microbiome is the microorganisms like bacteria that live in your digestive tract. The gut microbiome is influenced by your diet. There is a lot of research into the gut microbiome so if it does affect child’s height significantly improvements in that area could lead to dramatic increases in height for a population. Parent microbiome is passed on to a child so there is the possibility to increase height of a child by manipulating parent’s diet. Microbiome could impact height via IGF-1. Antiobiotic dosing which affects the gut microbiome has been shown to influence height. Changing the gut microbiome is not easy however. ” the composition of the gut microbiota is partially heritable and, once established, does not change substantially without a large or prolonged stimulus.“
“Longitudinal bone growth in children is governed by different genetic, nutritional and other environmental factors acting systemically on the endocrine system and locally at the growth plate. Recent studies have shown that this intricate interplay between nutritional and hormonal regulation of the growth plate could involve the gut microbiota, highlighting the importance of a holistic approach in tackling childhood undernutrition. In this review, I focus on the mechanistic insights provided by these recent advances in gut microbiota research and discuss ongoing development of microbiota-based therapeutics in humans, which could be the missing link in solving undernutrition and childhood stunting.”
“Growth hormone stimulates production of IGF-I in the liver, which then acts as an endocrine factor to stimulate bone growth at the growth plate. Growth hormone also stimulates local IGF-I production in target tissues, such as the growth plate and the intestine, which acts as a paracrine/autocrine growth factor. Nutritional status positively regulates bone growth and maturation of the gut microbiota, which reciprocally promote nutritional intake. The gut microbiota also promotes bone growth, perhaps directly, by stimulating IGF-I production. Possible mechanisms for such stimulation might involve SCFAs and NOD2-mediated bacterial sensing pathways in the intestinal epithelial cells.”
“growth deceleration is associated with the gradual decline in growth plate function, also known as growth plate senescence. Importantly, growth plate senescence is characterized by a gradual depletion of chondrogenic stem cells, decreasing chondrocyte proliferation and hypertrophy in the growth plate. Although growth plate senescence is generally associated with age, it appears not to be driven by age per se but instead depends on how much growth potential has been ‘used up’. In other words, chondrocytes in the growth plate appear to have a finite amount of growth potential, which is depleted gradually as more bone growth occurs, leading to the gradual decline in growth rate and the associated changes of senescence. This is supported by the fact that growth-inhibiting conditions, such as undernutrition, can slow down growth plate senescence, allowing bone growth not only to resume but temporarily to accelerate faster than normal for chronological age once nutritional status improves, a clinical phenomenon known as catch-up growth”<-so height seekers should have the goal to reverse senescence.
“The signal by which the gut microbiota stimulates IGF-I might not even be a metabolite. bacterial cell walls isolated from L. plantarum were sufficient to stimulate IGF-I and bone growth in mice”
“NOD2-activating ligands, such as muramyl dipeptide or the synthetic NOD2-activating adjuvant mifamurtide, alone were sufficient to induce IGF-I and bone growth, suggesting that NOD2 agonists could be a new class of therapeutic agents for improving childhood stunting.”
“another major cause of growth inhibition comes from a local effect of cytokines, which are often elevated in inflammatory diseases. At a systemic level, pro-inflammatory cytokines can inhibit bone growth by suppressing IGF-I. For example, in mice overexpressing interleukin-6 (IL-6), body growth is significantly suppressed, with decreased IGF-I and IGFBP3 but with normal levels of GH”
“The gut microbiota has been shown to influence circulating levels of pro-inflammatory cytokines. Serum IL-1β and IL-6 levels were correlated with the presence of certain bacterial strains in the gut microbiome. Mechanistically, butyrate, one of the SCFAs produced by the gut microbiota, has been shown to inhibit the inflammatory response elicit by lipopolysaccharides, TNFα and interleukins via GRP41 and GRP43, both in endothelial cells and in chondrocytes, suggesting that the gut microbiota could stimulate bone growth by reducing inflammation”
So you can use prebiotics and gut transplants potentially.
“In addition to the bare minimum of improving nutritional status, mitigation of gut microbiota dysbiosis, either by introducing growth-stimulating bacterial strains or by promoting gut microbiota maturation, should be considered as coupling therapeutic strategies.”
According to Fasting challenges human gut microbiome resilience and reduces Fusobacterium, fasting can alter the gut microbiome. Perhaps this could be how fasting affects bone length. “Water-only fasting could have a profound and long-lasting effect on gut microbiome.”
“Microbiome changes due to water-only fasting remained in five subjects even after returning to their normal diet, indicating the resilience of gut microbiome was successfully challenged. “
“skeletal stem cells were shown to be present in the epiphyseal growth plate (epiphyseal skeletal stem cells, epSSCs). Here, we explore the possibility that modulating the number of epSSCs can correct differences in leg length. First, we examined regulation of the number and activity of epSSCs by Hedgehog (Hh) signaling. Both systemic activation of Hh pathway with Smoothened agonist (SAG) and genetic activation of Hh pathway by Patched1 (Ptch1) ablation in Pthrp-creERPtch1fl/fl tdTomato mice promoted proliferation of epSSCs and clonal enlargement. Transient intra-articular administration of SAG also elevated the number of epSSCs. When SAG-containing beads were implanted into the femoral secondary ossification center of 1 leg of rats, this leg was significantly longer 1 month later than the contralateral leg implanted with vehicle-containing beads, an effect that was even more pronounced 2 and 6 months after implantation. We conclude that Hh signaling activates growth plate epSSCs, which effectively leads to increased longitudinal growth of bones. This opens therapeutic possibilities for the treatment of differences in leg length.” According to this paper Mechanotransduction pathways in the regulation of cartilage chondrocyte homoeostasis, “Mechanical stress up‐regulates Indian hedgehog expression (IHH) and activates hedgehog (Hh) signaling” “cyclic tensile strain activates Hh signaling and promotes the expression of ADAMTS‐5 in a primary cilia‐dependent manner, but in a high strain environment, histone deacetylase 6 (HDAC6) causes cilial disassembly and blocks this response”<-So we could potential mimic some of the effects of this study with mechanical loading because it also activates the hedgehog pathway but not too much activation as it blocks the mechanical loading benefits to hedgehog. So potentially with the right mechanical loading we could mimic the benefits of this study.
From the above picture, any method of increasing hedgehog signaling will work including potentially mechanical loading.
“Morphologically and functionally, the growth plate can be divided into the resting, proliferative, and hypertrophic zones. The resting zone contains slowly cycling cells, which, upon recruitment into the underlying proliferative zone, begin proliferating rapidly and arrange themselves into longitudinal columns of flat chondrocytes. Thereafter, these flat chondrocytes undergo further differentiation along with hypertrophy, forming the hypertrophic zone. Thereafter, the hypertrophic chondrocytes die or transdifferentiate, leaving a cartilaginous template on which spongy bone is built.”
“The resting zone contains a unique population of stem cells that express the parathyroid hormone–related protein (PTHrP). Furthermore, these stem cells reside in a niche that governs their abilities of renewal and generation of transit-amplifying proliferative chondrocytes. Interestingly, this niche arises postnatally, probably in association with maturation of the SOC, and only then can the stem cells obtain self-maintaining capacity and the ability to produce stable, long-lasting clones”
“
The importance of the Hedgehog (Hh) signaling pathway in development of the skeleton is demonstrated by the observation that deletion of Indian hedgehog (Ihh) (normally expressed by prehypertrophic and hypertrophic chondrocytes), either globally or specifically in cartilage, virtually eliminates formation of the growth plate. Together with PTHrP, Ihh is involved in a negative-feedback loop that controls the rate of chondrocyte differentiation. More specifically, Ihh produced by prehypertrophic and hypertrophic chondrocytes diffuses to the resting zone, where it stimulates expression of PTHrP, which in turn inhibits the hypertrophic differentiation of chondrocytes.
In addition, if Hh signaling is inhibited either genetically within the growth plate or pharmacologically during postnatal growth, the growth plate fuses abruptly“<-can we manipulate hedgehog signaling to keep the growth plate open for longer?
” Hh signaling stimulates the proliferation and clonal activity of epSSCs independent of age.”<-this is very promising for being able to potentially get the skeletal stem cells and then stimulate Hh signaling in adults.
“Local temporal stimulation of Hh signaling lengthens the legs.”
You can see from F how dramatically Hedgehog signaling increased the growth plate(SAG).
“The bony epiphysis (which develops from the Secondary Ossification Center) appears to be an appropriate location for such intervention, allowing placement of the Hh pathway agonist in close proximity to the epSSCs.”
” In the experiments presented here, some compound is likely released into the bloodstream, since an increase not only in femoral length, where the SAG-containing beads were placed, but also in the tibia of the same leg was observed. The arterial blood flow in extremities goes in the proximo-distal direction, and it is plausible that some levels of SAG diffuse in the same direction as the blood flow.”<-therefore the compound could be put into the blood stream without the beads for overall height!
“Noriaki said he was surprised that the cells in the resting zone “weren’t just lazy and doing nothing, they’re very hardworking cells, they can occasionally wake up and keep making chondrocytes.””<-that is amazing that means that potentially they can form new growth plates.
“It’s been hypothesized for many years that chondrocytes at the bottom of the growth plate die, but these findings show definite evidence that they survive and continue to make bone, he said.”
“The hallmark of endochondral bone development is the presence of cartilaginous templates, in which osteoblasts and stromal cells are generated to form mineralized matrix and support bone marrow hematopoiesis. However, the ultimate source of these mesenchymal cells and the relationship between bone progenitors in fetal life and those in later life are unknown. Fate-mapping studies revealed that cells expressing cre-recombinases driven by the collagen II (Col2) promoter/enhancer and their descendants contributed to, in addition to chondrocytes, early perichondrial precursors prior to Runx2 expression and, subsequently, to a majority of osteoblasts, Cxcl12 (chemokine (C-X-C motif) ligand 12)-abundant stromal cells and bone marrow stromal/mesenchymal progenitor cells in postnatal life. Lineage-tracing experiments using a tamoxifen-inducible creER system further revealed that early postnatal cells marked by Col2-creER, as well as Sox9-creER and aggrecan (Acan)-creER, progressively contributed to multiple mesenchymal lineages and continued to provide descendants for over a year. These cells are distinct from adult mesenchymal progenitors and thus provide opportunities for regulating the explosive growth that occurs uniquely in growing mammals.”
Have to figure out what’s unique about these cells and if there is a way to make these cells reawaken
“Chondrocytes in the growth plate continue to proliferate well into adulthood in mice”
“ In the center of the developing cartilage mold, chondrocytes stop proliferating and become hypertrophic chondrocytes. These cells signal to induce the migration of mesenchymal cells into the marrow space; these cells then differentiate into osteoblasts that then form bone on top of the cartilaginous matrix. Perichondrial precursors expressing osterix (Osx) invade into the cartilage template along with blood vessels and eventually become both osteoblasts and stromal cells in the marrow space”
“growth-related mesenchymal progenitors identified here and adult mesenchymal precursors.” We have to get these back
This below study indicates that Myo-inositol can increase mandibular condylar cartilage growth but mandibular condylar cartilage can keep growing so we can’t be sure if this applies to long bones but it’s still promising. Myo-inosotol is available for purchase and it’s relatively cheap.
From WebMD “Inositol, also called myo-inositol, D-chiro-inositol, or hexaphosphate (IP6), plays a critical role in the body’s cellular growth. Though it used to be referred to as Vitamin B8, inositol is not actually a vitamin.”
Inositol is already in foods such as beans, bananas, nuts, raisins,and brown rice.
So the question is whether additional supplement is necessary and whether that additional supplementation can result in longitudinal bone growth.
Mandibular Endochondral Growth Is Specifically Augmented by Nutritional Supplementation with Myo-Inositol Even in Rabbits
“At present, functional orthodontic appliances are used for stimulating mandibular growth in pediatric cases{bite jumping appliance also has potential to work post skeletal maturity}. However, the effectiveness of functional appliances is not always stable in daily practices. A more effective, reliable, and safer therapeutic method for mandibular growth promotion would be helpful for growing mandibular retrognathism patients. As we previously discovered that nutritional supplementation of myo-inositol in growing mice specifically increases mandibular endochondral growth{maybe it could enhance growth of other cartilage} we performed preclinical animal experiments in rabbits in this study. Briefly, six-week-old male Japanese white rabbits were fed with or without myo-inositol supplementation in laboratory chow until 25 weeks old, and 3D image analysis using micro CT data and histological examinations was done. Myo- inositol had no systemic effect, such as femur length, though myo-inositol specifically augmented the mandibular growth{so we have to investigate why that is, perhaps myo-inositol could be combined with other supplements to grow taller}. Myo-inositol increased the thickness of mandibular condylar cartilage. We discovered that the nutritional supplementation of myo-inositol during the growth period specifically augmented mandibular growth without any systemic influence, even in rabbits. Our results suggest the possibility of clinical use of myo-inositol for augmentation of the mandibular growth in growing mandibular retrognathism patients in the future.”
The fact that they think there might be clinical use is promising as it again it is available in foods so it suggests that supraphysiological doses might be helpful.
“A functional appliance is reported to induce mandibular growth by augmentation of endochondral growth in mandibular condylar cartilage and remodeling of the temporomandibular joint”<-this would be amazing if we could get it to happen in other joints and could be the key to growing taller
“nutritional supplementation of myo-inositol in growing mice specifically increases mandibular endochondral growth”<-however mice may not have as diverse a diet as humans
They suggest that mayo-inositol likely did not have systemic effect on growth as there was no change in body weight but if you look at the image you see a slight increase versus control.
However this sentence is not promising “
e myo-inositol group was 90.6 ± 1.1 group was 45.0 ± 1.5 mm, and that of the myo-inositol group was 43.4 ± 1.6 mm, and no mm. There was no statistically significant difference between the groups in femur length. This result suggests that myo-inositol does not have any promotional effect on bone statistically significant difference between the groups was observed. As to the femur length, the control group was 91.3 ± 0.9 mm, and the myo-inositol group was 90.6 ± 1.1 mm.”
However the rabbits(Japanese white rabbits) were given the doses at 6 weeks old and sacrificed at 25 weeks old which is pretty young so it’s possible that growth was slowed but the growing period was elongated. Rabbits stop growing between 5-18months.
“discovered that Pik3cd is specifically strongly expressed in mandibular condylar cartilage”<-maybe we can increase this expression other cartilages to make them grow.
“growth augmentation of the mandible with myo-inositol requires no local injection but just simply needs to supplement the food.”
So the big takeaway here is to make sure you’re getting enough your diet but perhaps we have to find a way to upregulate Pik3cd to grow other joints.
“growth augmentation in the mandible by supplementation of myo- inositol, it was 4.7% induction in our experiments using rabbits. Our previous experiment revealed 8.4% induction in mice”
“inhibition of Pik3cd by a chemical inhibitor almost completely inhibited myo-inositol-mediated augmentation of chondrocyte proliferation in mice”
So next actions for height seekers are definitely to to see if we can increase Pik3cd in other joints to make them more like mandibular condylar cartilage.
“lithium chloride (LiCl) is known to induce cell renewal in various tissues”
“After 14 days of culture, the length of dexamethasone-treated fetal rat metatarsals increased by 1.4 ± 0.2 mm compared to 2.4 ± 0.3 mm in control bones (p< 0.001). The combination of LiCl and dexamethasone led to bone length increase of 1.9 ± 0.3 mm (p< 0.001 vs. dexamethasone alone). By adding lithium, genes for cell cycle and Wnt/β-catenin, Hedgehog and Notch signaling, were upregulated compared to dexamethasone alone group.”
But they also studied Lithium on its own.
“local side-effects of GCs is the induction of apoptosis in growth plate chondrocytes,5through an increase in the expression of the pro-apoptotic protein Bax”<-Lithium could help reduce cellular apoptosis.
“exogenous GCs have been also shown to impair osteoblast and chondrocyte differentiation via downregulating the Wnt/β-catenin pathway, another key signaling cascade implicated in bone development and local growth plate regulation”<- we know that Lithium affects this pathway.
“Lithium chloride (LiCl) is a known GSK3β inhibitor and the treatment with LiCl increases the proliferation of human mesenchymal stem cells and also rescues from glucocorticoid-induced apoptosis of spontaneously immortalized murine calvarial osteoblasts”
“Bones treated with LiCl alone grew similarly as control (2.55 ± 0.18 mm, 2.64 ± 0.28 mm and 2.59 ± 0.33 mm increase, for 0.1 mM, 1.0 mM and 10 mM LiCl concentration, respectively; versus 2.43 ± 0.25 mm increase for control bones” so you can see that lithium increased growth versus control by about 10% versus the control group! The medium dosage grew the most so Lithium is probably biphasic(there is an optimal equilibrium dose where more has either no effect or is detrimental)
Here’s of what Lithium treated metatarsal looks like via controls:
Here’s another image that shows how significant it is:
“Lithium influenced the expression of 184 genes, of which 98 were up-regulated and 86 were down-regulated”
“a surgical osteoarthritis in vivo model, LiCl provided both in drinking water and intra-articularly was shown to improve the osteoarthritis score and to reduce the severity of cartilage destruction”
“the longitudinal bone growth setting, the results obtained from our proof-of concept experiments are supported by a previous study where lithium carbonate administration increased the width of the proximal tibia growth plate in the domestic fowl. The growth-promoting effect of LiCl was only minor in our “healthy” fetal rat metatarsals, compared to the effect in dexamethasone-impaired metatarsals”
“LiCl upregulates Axin degradation, which leads to β-catenin-induced transcriptional activity, Wnt/β-catenin pathway seems to be a plausible target that could explain the growth-promoting effect of LiCl in the dexamethasone-impaired metatarsals.”
“higher doses of LiCl have clinically been associated with undesired side effects such as tremor, dizziness, nausea, polyuria, weight gain, hypercalcemia or hypothyroidism, which therefore limits the use of high-dose LiCl treatment”<-again Lithiun is biphasic
So looks Lithium could be a height increase supplement and it is available to people!
