Limb lengthening surgery is only for the legs and people state that without torso lengthening people will be unproportionate(unless they already have long torso to height). So any method to increase torso length via surgery could potential be of interest to those people. Also, it could be possible to replicate a surgical method with some kind of mechanical loading or mechanical stimulation. So that makes it of interest to. But we’d have to see how exactly the mechanism by which the height increase works.

Lumbar vertebral canal stenosis due to marked bone overgrowth after routine hemilaminectomy in a dog

Stenosis is narrowing of the spinal canal which would be bad but possibly we could find ways around that. A hemilaminectomy is a surgical procedure that aims to enlarge the space in the spinal canal to reduce nerve compression or pressure. Based on how effective we believe this method could be we’d have to really understand how a hemilaminectomy works.

“Bone overgrowth after decompressive surgery for lumbar stenosis”

“A 13-month-old entire female dog{this is a pretty young dog}, a crossbreed between a Springer Spaniel and a Border Collie, weighing 24 kg, was referred with a 5-day history of progressive spastic paraplegia, indicative of a T3-L3 myelopathy. Magnetic resonance (MR) imaging revealed a right-sided L2-L3 compressive extradural lesion, compatible with epidural haemorrhage, which was confirmed by histopathology. The lesion was approached via right-sided L2-L3 hemilaminectomy and was successfully removed. One-year postoperatively the dog re-presented with pelvic limb ataxia. MR and computed tomography (CT) images demonstrated excessive vertebral bone formation affecting the right articular processes, ventral aspect of the spinous process of L2-L3, and contiguous vertebral laminae, causing spinal cord compression. Revision surgery was performed, and histopathology revealed normal or reactive osseous tissue with a possible chondroid metaplasia and endochondral ossification, failing to identify a definitive reason for the bone overgrowth. Nine-month postoperatively, imaging studies showed a similar vertebral overgrowth, resulting in minimal spinal cord compression. The patient remained stable with mild proprioceptive ataxia up until the last follow-up 18 months post-revision surgery.”<-unexplained bone overgrowth is good because it could indicate that there’s a possible height growth mechanism that we’re not aware of yet.

“Bone healing depends on the initial inflammatory phase, both local and systemic, in response to the injury. The repair phase is characterised by the formation of a soft callus, consisting of fibroblasts, chondrocytes, and osteoprogenitor cells. The new extracellular matrix produced by these cells serve as a temporary scaffold for bone formation. This phase involves the recruitment and differentiation of mesenchymal stromal cells (MSCs), which have the potential to differentiate into osteoblasts, promoting bone regeneration and bridging the fracture site. The remodelling phase is the final stage of bone healing, where the newly formed bone undergoes structural and functional modifications, restoring the bone’s normal architecture”

“In human medicine, bone overgrowth is an uncommon but important cause of relapse of neurological signs after decompressive surgery in elderly patients undergoing treatment for lumbar spinal stenosis, most performed at the L4-L5 level”

“factors such as segmental instability, micromotion, and abnormalities in mechano-signalling have been hypothesised to contribute to the excessive bone regrowth”<-we could potentially mimic things like segmental instability

IF you look at the next set of slides however

“[bone overgrowh] is commonly observed at the L4-L5 level, known to be the most mobile intervertebral level in humans”<-this is interesting because it potentially means that movement can influence growth but it could also indicate that cartilage degeneration is what initiates growth.

“Histopathological evaluation showed the presence of normal or reactive osseous tissue, rather than new bone and immature woven bone. This finding may be similar to heterotopic ossification reported in humans following trauma or injury. The presence of chondrocytes in some fragments could indicate a possible chondroid metaplasia and endochondral ossification, which are necessary for bone regrowth“<-the dogs were young so initiation of endochondral ossification is not terribly exciting but similar processes seem to occur in the elderly as mentioned in the study which makes it more exciting.

Overall this paper may hold something for the future but it is not really anything to write home about now.

So I’m revising the LSJL method to explore what I was doing when my medical records show I grew.

Is it still LSJL if you’re using impact and not loading the synovial joint region?  I’m trying to use impact ball pein hammer as an alternative to clamping as clamping as always had slipping problems.  In Hiroki Yokota’s methods, they could use advanced devices to avoid slipping.

Here’s the study that shows the LSJL worked on adult mice.  Although the mice in that study did not have senescent growth plates as the control group adult group grew as well.  The difference between mice and humans is that when mice growth plates become senescent they don’t seem to fuse.  This may lead to better force transduction between the epiphysis and the diaphysis.

Thus, new LSJL may be tapping on the longitudinal ends of the diaphysis of the bone.  The diaphysis is the core of the bone.  The epiphysis of the bone is highly load bearing so force may dissipate before it ever reaches the diaphysis which contains a lot of core bone materials.  Distraction osteogenesis works by fracturing the diaphysis not the epiphysis.  By tapping the diaphysis you can feel the force transmit throughout the entire bone.

The issue is that there are people who already apply force to the diaphysis of the bone.  Muay thai kick boxers who kick their shin’s.  Rolling a bar over your shin is not the same as the force won’t be the transmitted deeply and throughout the entirety of the bone.    Kicking an object with your shins will be in the center of the shin and not near the end of the shin thus there would be as an effective pressure gradient throughout the entire bone.    Muay Thai fighters have also broken their shins this way which is a step for lengthening bone in distraction osteogenesis….But unless the break is in a controlled manner it won’t result in bone growth.

So the difference between this and muay thai is the site that the impact occurs(at the starting points of the diaphysis rather than the middle), that it occurs in a more controlled fashion(although there are probably some muay thai fighters that can kick very precisely), that the impact loading is smaller and more rapid(frequency is an important factor in stimulating bone growth), and that the bone is the object being hit rather than the object doing the hitting(this may affect how the force is transmitted throughout the bone).  In addition, a ball pein hammer as a smaller surface area which increases the pressure transmitted to the bone rather than a larger object

It’s easy enough to do this for the radius, ulna, and tibia as those bones are well exposed.  The humerus and femur are covered by muscle but I seem to have potential sites.  But I can always just grow from the tibia and forearm bones and then use that proof to develop methods.  So I’ll see if I can grow and then share the method…

I’d argue that it still uses the principles of LJSL as it involves loading one site of loading to stimulate growth throughout the entire bone.  It involves stimulating the same principles: interstitial fluid flow, hydrostatic pressure, and pressure gradients.

Here’s the LSJL study, unfortunately not on longitudinal bone growth but there are some growth plate pictures:

Mechanical stimulations can inhibit local and remote tumor progression by downregulating WISP1

“Mechanical stimulations can prevent bone loss, but their effects on the tumor‐invaded bone or solid tumors are elusive. Here, we evaluated the effect of knee loading, dynamic loads applied to the knee, on metastasized bone and mammary tumors. In a mouse model, tumor cells were inoculated to the mammary fat pad or the proximal tibia. Daily knee loading was then applied and metabolic changes were monitored mainly through urine. Urine samples were also collected from human subjects before and after step aerobics. The result showed that knee loading inhibited tumor progression in the loaded tibia. Notably, it also reduced remotely the growth of mammary tumors. In the urine, an altered level of cholesterol was observed with an increase in calcitriol, which is synthesized from a cholesterol derivative. In urinary proteins, knee loading in mice and step aerobics in humans markedly reduced WNT1‐inducible signaling pathway protein 1, WISP1, which leads to poor survival among patients with breast cancer. In the ex vivo breast cancer tissue assay, WISP1 promoted the growth of cancer fragments and upregulated tumor‐promoting genes, such as Runx2, MMP9, and Snail. Collectively, the present preclinical and human study demonstrated that mechanical stimulations, such as knee loading and step aerobics, altered urinary metabolism and downregulated WISP1. The study supports the benefit of mechanical stimulations for locally and remotely suppressing tumor progression. It also indicated the role of WISP1 downregulation as a potential mechanism of loading‐driven tumor suppression.”

You can see the growth plate in figure 1F.  The growth plate looks thicker as does the articular cartilage.  The tumor of course plays a confounding variable.  You can also see that the entire bone of the loaded group looks different….

“As a mouse model of skeletal loading with C57BL/6 female mice, we conducted knee loading that applied sinusoidal compressive loads to the knee (Figure S1A). Dynamic loads of 0.5, 1, and 2 N at 2 Hz induced loading magnitude-dependent strain. Loads of 0.5 N (peak-to-peak), which will be used hereafter, induced approximately 100 με (axial compression) and 50 με (lateral tension), with a phase shift of ~180° between these two strains”

So the paper shows more promise that joint loading or methods that use it’s principles can induce longitudinal bone growth.

You can see the consistency so we can safely rule out measurement error.  I was also well in my 20’s so natural growth can be ruled out.  Either there was microgrowth throughout all years or there was a method used between 2012 and 2014.  I didn’t realize such a thing recently because I’ve never gone through my records before.

If it was in a method that I used between 2012 and 2014 and not incremental growth then it was the chisel and hammer method that I was looking at the time.

Here’s the method explained.  So I’m going to try to do this method again.

Indirubin has shown promise before as a CXXC5 inhibitor. ” elongated tibial length through delayed senescence and further activation of the growth plate in adolescent mice.”<-further activation of the growth plate is what is most interesting.

We have to be on the lookout for indirubin derivative, KY19382.

Here’s a patent PHARMACEUTICAL COMPOSITION CONTAINING INDIRUBIN DERIVATIVE AS ACTIVE INGREDIENT

Interesting parts of the patent:

“The composition of claim 7, wherein the compound promotes bone growth and/or increases bone thickness.

12. The composition of claim 7, wherein the compound promotes chondrocyte proliferation, induces differentiation of osteoblasts, and/or activates β-catenin stabilization and nuclear translocation of β-catenin.”

“The composition for promoting bone length growth in accordance with the present invention has the promoting effects on both proliferation of chondrocytes and differentiation of osteoblasts, thereby increasing both bone length and thickness (bone density). Therefore, because it has the advantages of a wide range of prescriptions for various age groups, it can be usefully used as a pharmaceutical composition that can promote the growth of bone length and thickness.”

“The food compositions of invention, if manufactured as a beverage, is essential at the rate indicated, and there is no specific restriction on the liquid composition, such as ordinary drinks, and may contain several flavoring agents or natural carbohydrates as an additional ingredient. Examples of natural carbohydrates described above are monosaccharides (e.g. glucose, fructose and the like), disaccharides (e.g. maltose, sucrose and the like), and polysaccharides (e.g. dextrin and cyclodextrin, as well as common sugars such as xylitol, sorbitol and erythritol). As flavoring agents other than those described above, natural flavoring agents (e.g. taumatine, stevia extracts, such as fume-based A and glycirrhizine, and synthetic flavoring agents, such as sakarin, aspartame) can be advantageously used. The ratio of the above natural carbohydrates is generally about 1 to 20 g per 100 ml of the composition of this invention and, preferably, about 5 to 12 g.”

So seems like it will be a beverage which could mean it’s for everyone!!!!!!!!!!

Here’s another interesting study:

Indirubin-3′-oxime stimulates chondrocyte maturation and longitudinal bone growth via activation of the Wnt/β-catenin pathway

“we identified indirubin-3′-oxime (I3O) as a compound capable of enhancing longitudinal bone growth. I3O promoted chondrocyte proliferation and differentiation via activation of the Wnt/β-catenin pathway in vitro. Intraperitoneal injection of I3O in adolescent mice increased growth plate height along with incremental chondrocyte maturation. I3O promoted tibial growth without significant adverse effects on bone thickness and articular cartilage. Therefore, I3O could be a potential therapeutic agent for increasing height in children with growth retardation.”

Look at the tibia growth in fig2 at 5uM it is sick!  Although a bit curved.  If you look at 2a it looks fairly normal though.

“I3O significantly increased the mRNA levels of early chondrogenesis markers, such as Col2a1 and Sox9. In addition, I3O treatment increased the mRNA levels of fully differentiated hypertrophic chondrocyte markers, such as Col10a1, Vegfa, Alp, and Mmp13, as well as prehypertrophic chondrocyte markers, such as Runx2 and Mmp9. Transcriptional induction of these genes by I3O treatment was suppressed by knockdown of Ctnnb1″

“The practical usage of I3O is advantageous because it is an indirubin derivative that is the main active ingredient in a traditional Chinese medicine, Danggui Longhui Wan”<-even if indirubin is in the Danggui Longhui Wan we still don’t know if it’s effective.

All height seekers should be monitoring Indirubin

Here’s a biohacker thread on indirubin.  One interesting comment: “The issue seems to be that the drug has not been studied in humans, nor in vivo for this application. With the current understanding of hormono-dynamics, GH secretagogues + antidiabetic compounds (metformin) seem to be the best bet to enhance height safely in adolescents.”  On metformin “Metformin in this case would mediate any deleterious effects on glucose metabolism exerted by the gh secretagogues which are known to mess up glucose tolerance.”

Here’s some studies with updates on Indirubin:

ERα/β/DMP1 axis promotes trans-differentiation of chondrocytes to bone cells through GSK-3β/β-catenin pathway

On the LSJL forums someone mentioned an anecdotal case where an individual supplementing with C60 fullerene got taller.  Does mentioned was about 50-100mg/year.  Several supplements were used though.  But in our quest to go taller it is worth to look at every single compound in existence to see if it could potentially have height increase improvements.  This page says C60 fullerene has been found to improve longevity, promote cartilage and bone strength, and result in less stiffer joints.  Since bone growth cessation is a form of aging we want to look at any anti-aging compound.  Obviously, anything that affects cartilage and bone is of interest to us.

Here’s the original post on the height increase.  The author speculates the the height increase may be due to “C60 is used with stearic acid to increase the pool of stem cells.”  “C60 stimulates mitochondria, and mitochondrial activity drives the activity of stem cells.”

According to this

Water-soluble C60-(OH)24 fullerene hydroxide as a therapeutic agent against the degeneration of articular cartilage in osteoarthritis

“During the development of osteoarthritis (OA), mechanical stress on articular cartilage downregulates the stable cellular activities of chondrocytes and induce the production of catabolic factors, such as proinflammatory cytokines and chemokines. In addition, it is well known that chondrocytes produce excess amounts of reactive oxygen species (ROS; superoxide, nitric oxide, hydrogen peroxide and peroxynitrite) in response to mechanical stress. Recent reports have demonstrated that mechanical stress to articular cartilage stimulates excess production of ROS from chondrocytes, consequently resulting in the depolymerization of hyaluronic acid and chondrocyte death. It has been suggested that the generation of ROS and the depletion of cellular antioxidants may be involved in the pathogenesis of OA.”

Since fullerene is an anti-oxidant it could potentially reduce height loss as a result of aging by preventing height loss due to Reactive Oxygen Species.  Since the individual mentioned in the forum is 60 years old that is a possibility.

“IL-1β significantly inhibited the production of proteoglycan and the glucose uptake in chondrocytes, and accelerated the secretion of MMP-3 from chondrocytes. Even in the presence of IL-1β (1.0 ng/ml, but not 10.0 ng/ml), C60(OH)24 inhibited the IL-1β-induced production of MMP-3, the IL-1β-induced down-regulation of proteoglycan production and glucose metabolism in OA chondrocytes. C60(OH)24 fullerene hydroxide also reduced the OA-relating catabolic factor-induced up-regulation of DNA repair enzyme, Apex 2, in OA chondrocytes.”

C60 is also used as a matrix for cartilage transplants according to Biodegradable polymers in chondrogenesis of human articular chondrocytes,

According to

Biological functions of fullerene

“A mixed aqueous solution of C60 and poly(vinyl pyrrolidone) is reported to induce differentiation of chondrocytes”<-this is a potential height increasing application if it can occur just by taking it naturally in the human body.

There are several studies that study that fullerene can induce cartilage differentiation and prevent cartilage destruction.

A Novel Promoting Action of Fullerene C60 on the Chondrogenesis in Rat Embryonic Limb Bud Cell Culture System

“Fullerene C60 was solubilized with polyvinylpyrrolidone (PVP) in water, and the aqueous solution was applied to the rat limb bud cell differentiation system. By the incubation with various concentrations of C60 with poly(vinylpyrrolidone) , cell differentiation was extremely promoted,up to the levels of a 3.2-fold increase of the controls. Although poly (vinylpyrrolidone) alone inhibited the cell differentiation in proportion to the concentration, the observed promoting action by C60 surpassed the action of poly(vinylpyrrolidone). This specific promoting action on the chondrogenesis is the novel significant activity of C60.”

The study speculates that C60 may promote chondrogenesis by resulting in the condensation of chondroitin sulfate which in turn promotes chondrogenesis.

The results on fullerene are inconclusive as we can’t be sure how the individual got the height(articular cartilage growth or increase in bone length?) and whether the height was due to reduced cartilage catabolism or due to stem cell proliferation.  And there’s not enough human studies.  One inch isn’t a lot to get excited about either.

Any loading study with pictures can provide insight on the possibility of ectopic chondrogenesis/endochondral ossification even if they do not directly study longitudinal bone growth as long as there are images.

One method to grow taller as adult:

1)Induce bone degradation allowing space for new growth plates to form(one way this could be induced is by inducing fluid flow flow in the bone via joint loading)

2) stimulate new growth plate formation via mesenchymal condensation(this would be induced by hyrostatic pressure via joint loading)

3) induce endochondral ossification of the ectopic cartilage.  This would happen naturally due to the bone microenvironment.

Knee loading repairs osteoporotic osteoarthritis by relieving abnormal remodeling of subchondral bone via Wnt/β‐catenin signaling

“Osteoporotic osteoarthritis (OPOA) is a common bone disease mostly in the elderly, but the relationship between Osteoporotic (OP) and osteoarthritis (OA) is complex. It has been shown that knee loading can mitigate OA symptoms. However, its effects on OPOA remain unclear. In this study, we characterized pathological linkage of OP to OA, and evaluated the effect of knee loading on OPOA. We employed two mouse models (OA and OPOA), and conducted histology, cytology, and molecular analyses. In the OA and OPOA groups, articular cartilage was degenerated and Osteoarthritis Research Society International score was increased. Subchondral bone underwent abnormal remodeling, the differentiation of bone marrow mesenchymal stem cells (BMSCs) to osteoblasts and chondrocytes was reduced, and migration and adhesion of pre‐osteoclasts were enhanced. Compared to the OA group, the pathological changes of OA in the OPOA group were considerably aggravated. After knee loading, however, cartilage degradation was effectively prevented, and the abnormal remodeling of subchondral bone was significantly inhibited. The differentiation of BMSCs was also improved{this is the kind of thing we would be looking for}, and the expression of Wnt/β‐catenin was elevated. Collectively, this study demonstrates that osteoporosis aggravates OA symptoms. Knee loading restores OPOA by regulating subchondral bone remodeling{subchondral bone remodeling could potentially increase height by increasing bone deposition at the longitudinal ends of bone}, and may provide an effective method for repairing OPOA.”

“Since bone is a mechano‐sensitive organ, moderate pulsating loading, oscillatory compressive loads, can be applied to various synovial joints in a form of elbow loading, knee loading and ankle loading. Joint loading can change intramedullary pressure of bone cavities. The moderately changing pressure may generate fluid flow in a lacuna canalicular network in bone cortex, and activate anabolic genes in bone{the goal would that a change in hydrostatic pressure in the bone would stimulate ectopic chondrogenesis/endochondral ossification}. In our previous studies, we have shown that knee loading is effective in …promoting longitudinal bone growth…”

“Dynamic loads were sinusoidal at 1 N (peak‐to‐peak) and the frequency was 5 Hz for 6 min/day (each knee, 3 min).”

It’s here that we’d look for signs for ectopic chondrogenesis.  It’s hard to tell for sure as there’s no loading group for normal bone.  In the the loading groups(OAL, OPOAL) there are clear differences in the subchondral bone plate.  Although the loading groups, all seem to have differences in the bone but the differences seem stronger in the trabecular bone.  The growth plate is different in the loaded groups but that’s not going to make a difference to adults.

In this it looks like there may be more cellular condensation in the OAL group and the OPOAL group(there are more cells and they’re closer together).  This is a precursor to mesenchymal chondrogenesis.  We’d need signs of bone degradation as well to prove that growing taller as an adult is possible.  And it’s hard to say that without seeing a normal bone.