Thursday, October 20, 2011

Increase Bone Length by Stretching?

I'm not talking about ordinary stretching as in the Grow Taller 4 Idiot's Program, Yoga, or Pilates.  I'm talking more about Sky from Easy Height's new limb center.  Before my research stumbled upon the lateral synovial joint loading system, I believed that the best way to gain height was by stretching the bones.  You see bone is elastic, by the very definition of microstrain theory the bone is constantly changing in length. If the bone did not change in length then over time bone density would decrease.  One thousand units of microstrain is equivalent to 0.1% change in length.  If our bones did not lengthen or compress by 0.1% every day they would fall into disuse according to mechanostat theory

The problem with stretches like the medieval rack or sitting/sleeping with ankle weights is that they stretch more the cartilage and ligaments than the bones themselves.  Sky of easy height was working on a program that stretched the bone.  Unfortunately, Sky disappeared before sharing his data.

If your tie a rope around the top of your ankle and then load the bottom of the rope with iron plates, your leg is being stretched down and out(being lengthened).  If you then tie a rope around the bottom of the ankle and then tie the middle of the rope around a bar; and then load that rope with iron plates your leg is being stretched upwards and out.  If you do both of these at the same time with equal amounts of force then the up and down forces cancel out and your bone is only being lengthened outwards.

You could also alternate between pulling your ankle up and down which would proceed to lengthen your bone in a zig-zag motion.  We know that bone is elastic and that bone has the ability to microfracture.  If you stretch your bone and microfractures occur in a stretched state then the bone should maintain some of that elasticity.  Pull a pencil apart, when you do microscopic damage occurs in the length of the pencil.  The pencil is now longer than before.  Unlike a pencil however, bone has the ability to heal those microfractures.  So you distract the bone cause microfractures, the microfractures heal, and then you distract the bone again.  Gradually, becoming taller and taller over time.

One element of Sky's multitude of experiments that he has kept in his new Shinbone Version 2011 is cycling with ankle weights(with a raised saddle).  The hypothesis of why cycling with ankle weights would work is that you are stretching your leg bone forcing your leg bone to reach lower and lower. Now if Sky does have a method of performing cycling to properly put a stretching force on the leg bone then it could work.

There are a couple of problems involved with the heavy iron plates method however.  You are putting load on your tendons and ligaments.  You have to find some way to nullify the tendons and ligaments.  If you perform this method say around the ankle then you are probably only going to stretch the tibia and not the fibula.  The iron plates method would probably best be used in parts of the limb where there is only one bone such as the femur and humerus.

Essentially, a bone stretching method could work.  In contrast to LSJL, you would want the load slightly below the growth plate(you only want to stretch your cortical bone in contrast to LSJL where you are trying to deliver red bone marrow stem cells into your growth plate).  You would then have to find a way to perform it without putting all the strain on your tendons/ligaments.  You would then have to find a way to equally push the bone down from the top and the bottom.  You would have to make sure that you were causing microfractures during the process.  If you read the last study, you can see why it may be worth it to perform bone stretching while doing LSJL.

Osteodistraction of the maxilla in transverse deficiency in adults: Analysis of the literature and clinical case.

"Osteogenic distraction is a bone regeneration and reconstruction technique. [Osteogenic distraction is] "the process of creating new bone by stretching"[bone stretching can best be analyzed by tensile strain, however this seems to be a different form of stretching]. Disjunction entails separating two anatomical structures at their junction system and, therefore, at a suture[so they're not stretching the bone they're separating the junctions between the bone]. Usually, it involves separating two semi-maxillae in the transverse dimension by means of an osteotomy[osteotomy refers to bone cutting so they are cutting the bone but now it seems like they are separating two separate bones and not cutting the bones itself]. Transverse maxillary distraction appears to offer an alternative of choice to orthognathic surgery alone, which is frequently prone to relapse. The greatest benefit of osteogenic distraction lies in its greater potential for expansion and concurrent growth of the soft tissues. Among other things, this technique increases arch length, thus precluding tooth extractions in cases of maxillary crowding, and appears to provide more stable results than conventional surgical intermaxillary disjunction."

If osteodistraction does work by stretching between the bones then perhaps something that stretches the cartilagenous area of the knee could help you to grow taller.

Here's an image of the suture:

Effects of osteoinduction on bone regeneration in distraction: results of a pilot study.

"Rate and frequency of distraction as well as stimulatory effects transmitted by growth factors and local gene therapy have a decisive influence on bone regeneration. In a pilot study we tested the effect of four different morphogenetic and mitotic proteins and a genetically transferred vector system on bone healing in continuous osteodistraction in a large animal experiment on 24 Goettingen mini-pigs. For this purpose bone morphogenetic protein (BMP-2), BMP-7, TGF-beta, IGF-1 and a liposome vector were instilled into the distraction gap. The animals were killed after 1-4 weeks of consolidation. Histological and radiological evaluations showed maximum bone formation after the application of BMP-2/7, whereas the application of TGF-beta, IGF-1 and the liposomal vector had only a limited effect on bone regeneration. The quantitative analysis demonstrated an average amount of bone in the distraction gap of 50% and 61% after instillation of BMP-2 and 7, respectively. The BMP-2 expression, however, was maximal after induction with the non-viral vector. Only after BMP-2/7 application could physical, radiographic and histological evidence of bone union be detected. In bone distraction with a short observation period the application of morphogenetic proteins seems to enhance bone regeneration significantly. Before application in humans further studies are necessary to measure the dose-effect relationship, the mode of application and the efficacy of different inductive proteins. The combination of osteodistraction with osteoinduction, however, could shorten treatment times dramatically."

If you look in this picture you can see that the bone grew back without any compounds like BMP-2/7 or TGF-Beta1

A1 is one week after distraction A2 is two weeks.  So the bone does grow without chemicals and it also looks like there was no periosteum involved in contrast to distraction osteogenesis.  However the periosteal progenitor cells are capable of migration.

"Within the context of ossification, cellular elements with increased BMP-2 expression were found both in the distraction zone, and in the consolidated osseous area close to the osteotomy region. A reduced BMP-2 expression was found in the central distraction zones of those animals, where induction did not stimulate bone regeneration in the distraction region"<-so bone does not seem to form without BMP-2 in the distraction region in this study

"Labelled bone marrow stem cells are systematically mobilized and attracted to fracture sites from remote cell depots"<-Stem cells are still involved.  Also remember that a callus might generate hydrostatic pressure.

In the article on limb lengthening surgery, we learned that stretching Type I Collagen might cause a mechanotransduction based signal that results in the increase of the size of the micronuclei of bone cells thus causing bone hypertrophy.   This would mean that there would be no need for the fracture and that all you'd need is for tensile strain on Type I Collagen.

Limb bud mesenchyme cultured under tensile strain remodel collagen type I tubes to produce fibrillar collagen type II.

"In this work, we studied the effects of tensile strain on limb bud mesenchymal cells (MSC) cultured on a collagen type I tubular scaffold. A novel bioreactor was designed to culture the cells while subjecting the tubular scaffold to tensile stress and strain. Control samples included unseeded and MSC-seeded tubes cultured for 2 weeks under unloaded, no-strain conditions, and unseeded tubes subjected to prolonged tensile stress and strain. Mechanical properties of tube specimens were measured under oscillatory compressive stress. Following mechanical testing, scaffolds were fixed for immunohistochemistry or frozen for mRNA extraction. The storage modulii of both seeded/unstrained and seeded/strained tubes were significantly less than that of unseeded tubes, suggesting that MSC disrupted the structure and elasticity of the tubes' collagen type I. At a frequency of 1.0 Hz, the loss tangent of seeded/strained tubes was more than 2.5 times greater than that of seeded/unstrained tubes, and almost 6 times greater than that of unseeded tubes. Confocal microscopy and qRT-PCR results demonstrated that collagen type II and aggrecan expression was upregulated in the seeded/strained tubes.  Culture under tensile strain induces MSC to remodel the collagen type I tube with collagen type II and aggrecan expression into fibrils dispersed throughout the matrix[so basically tensile strain on the mesenchyme encourages removal of bone and the creation of cartilagenous, possibly growth plate like structures.  Note there is mesenchymal tissue in the bone marrow]. The seeded/unstrained tubes manifested less collagen type II with a more random expression pattern. Compared to seeded/unstrained tubes, qRT-PCR for collagen type II in the seeded/strained tubes showed a 4-fold increase in the message for collagen type II and a 13-fold increase in the message for aggrecan. These results demonstrate that MSC cultured for at least some period under tensile strain are able to remodel collagen type I scaffolds to produce a more viscous construct having many of the mechanical and biological features of engineered cartilage."

"In the knee, static compression of the joint creates hydrostatic stress, and movement of  the joint creates shear stresses. However, because the knee is a non-conformal surface, the cartilage will also experience a directional tensile stress and strain during use"<-We use static compression in LSJL to create hydrostatic pressure on the bone marrow of the epiphysis.

So tensile strain involved in limb lengthening surgery may stimulate cartilage formation by tensile strain on the mesenchymal tissue itself.  Here's the effects of tensile strain directly on the Type I Collagen.
Deformation-dependent enzyme mechanokinetic cleavage of type I collagen.

"Collagen is a key structural protein in the extracellular matrix of many tissues. It provides biological tissues with tensile mechanical strength and is enzymatically cleaved by a class of matrix metalloproteinases known as collagenases. Collagen enzymatic kinetics has been well characterized in solubilized, gel, and reconstituted forms. However, limited information exists on enzyme degradation of structurally intact collagen fibers and, more importantly, on the effect of mechanical deformation on collagen cleavage. We studied the degradation of native rat tail tendon fibers by collagenase after the fibers were mechanically elongated to strains of epsilon=1-10%. After the fibers were elongated and the stress was allowed to relax, the fiber was immersed in Clostridium histolyticum collagenase and the decrease in stress (sigma) was monitored as a means of calculating the rate of enzyme cleavage of the fiber. An enzyme mechanokinetic (EMK) relaxation function T(E)(epsilon) in s(-1) was calculated from the linear stress-time response during fiber cleavage, where T(E)(epsilon) corresponds to the zero order Michaelis-Menten enzyme-substrate kinetic response. The EMK relaxation function T(E)(epsilon) was found to decrease with applied strain at a rate of approximately 9% per percent strain, with complete inhibition of collagen cleavage predicted to occur at a strain of approximately 11%[but is inhibition of collagen cleavage good or bad for height growth?]. However, comparison of the EMK response (T(E) versus epsilon) to collagen's stress-strain response (sigma versus epsilon) suggested the possibility of three different EMK responses: (1) constant T(E)(epsilon) within the toe region (epsilon<3%), (2) a rapid decrease ( approximately 50%) in the transition of the toe-to-heel region (epsilon congruent with3%) followed by (3) a constant value throughout the heel (epsilon=3-5%) and linear (epsilon=5-10%) regions. This observation suggests that the mechanism for the strain-dependent inhibition of enzyme cleavage of the collagen triple helix may be by a conformational change in the triple helix since the decrease in T(E)(epsilon) appeared concomitant with stretching of the collagen molecule."

"Collagen degradation is a mechanism for extracellular matrix (ECM) remodeling and maintenance[the possibility for remodeling Type I Collagen into Type II Collagen which is the cartilage of the growth plate], and in response to trauma, disease and inflammation. Collagenases-1, 2 and 3 are the primary enzymes that act to degrade interstitial collagens (types I, II and III) in humans and animals. These collagenases are part of a larger family of enzymes (matrix metalloproteinases or MMPs) characterized by a zinc dependency for catalytic activity. MMPs are secreted by the cell as inert zymogens in response to the cell being activated by inflammatory cytokines, such as growth factors (interleukin-1) and mechanical loads. In order for collagen cleavage to occur, the collagenase (MMPs-1, 8 and 13, respectively) gains access to the collagen triple helix by binding to the enzyme’s attachment domain along the α-chains, followed by separation (unwinding) of the α-chains to expose the cleavage site, and then cleavage of the α-chain by the enzyme’s catalytic domain[tensile strain of 11% or greater(which means that the bone is stretched to 11% of it's original length) results in the in ability for collagen cleavage]. Collagenases contain two protein domains joined by a linker (hinge), a hemopexin C domain to which the collagen molecule attaches, and a catalytic domain responsible for the α-chain cleavage. MMP-1, 8 and 13 will cleave all three α-chains of interstitial collagens by a single scission at a specific site, located 3/4 from the N terminal and 1/4 from the C terminal, which is characterized by a Gly775-Ile776 or Gly775-Leu776 peptide bond, resulting in two fragments of the collagen molecule. Following this initial cleavage other MMPs (mainly gelatinases and stromelysins) can collectively further degrade the collagen fragments. However, the mechanism of the initial cleavage of the collagen molecule must originate with collagenase binding, triple helix unfolding and ¾-¼ scissoring."

"increasing tensile strain up to 4% (grip-to-grip) resulted in a decrease in the rate of enzymatic degradation, while strains above this (to 7%) caused an increase in the rate"<-Thus perhaps why limb lengthening surgery only stretches by 1mm a day which is well below 4%.

"mechanical deformation of type I collagen fibers caused by an axial strain (elongation) applied to the fiber will result in a significant decrease in the rate of collagen degradation by bacterial collagenase"<-This could cause height growth, if production of Type I Collagen outweighs degradation of Type I Collagen then bone could become longer.

It's possible that hydrostatic pressure is involved and that decreased cleavage results in increased hydrostatic pressure.

"Due to the self assembly nature of collagen, there appears to be a long range attraction which prevents molecules from coming too far apart and which induces the self assembly where hydrogen water bridges surrounding the molecule act as specific recognition sites for attracting other collagen molecules[So collagen attracts water to form water bridges]. More important, however, is that an exponential increase in the interaction energy (forces between triple helices) occurs as the α-chain separation distance decreases[as the Type I collagen fibers get farther apart the interaction cost increases]. Heightened hydration interaction forces are observed nearing the last 10-20 angstroms of α-chain separation (osmotic stress as high as 1000 MPa have been measured)[Increased hydration interaction forces due to increased distrace results in increased hydrostatic pressure]. This increased interaction force is [possibly] due to the energy required to rearrange the hydrogen bonding network near the molecular surfaces of macromolecules, such as might occur as the collagen molecule’s diameter is reduced as the molecule is stretched in response to an axial tensile load[tensile strain lowers the collagen molecule's diameter thus increasing the energy for hydrogen bond interaction]. Alterations in the ionic strength will also effect electrostatic interactions (<1 MPa at 15-60 Å). When the collagen molecules come into close proximity the van der Waals forces (<1 MPa at 10-25Å separation) result in an attraction or repulsion dynamic. Thus, a high concentration of repulsion ionic character will position the molecules further away from neighboring molecules creating a greater separation distance and ultimately a larger diameter. Conversely, attractive ionic character would link the molecules with a greater affinity, resulting in smaller diameters."

Stretching Type I Collagen lowers the diameter resulting in an increased energy required to rearrange the hydrogen bonding network.  This increases hydrostatic pressure.  So again it all leads to hydrostatic pressure.

So bone stretching may help during LSJL by lowering Type I Collagen fibril diameter thereby increasing hydrostatic pressure.

An exponential law for stretching–relaxation properties of bone piezovoltages

"Bone can change its mass, shape and density to adapt its external environment"

Ways to alter bone modeling include pizeoelectric potential, streaming potential, and fluid-generated shear stress.

"the piezoelectricity of bone arises from the organic components (mainly collagen)"

"Collagen molecules are filled and coated by platelet like tiny mineral crystals, which form the mineralized collagen fibril. A group of collagen fibrils embedded in the mineral crystals form a hierarchical structure of collagen fiber"

" Based on the hypothesis the deduced main reason for the stretching-exponential behavior is the triple helices structure of collagen fibrils distributed randomly in bone, which suffer relatively large deformation, under external loads, including self-deformations and relative slipping between molecule chains. The relative slipping movements may change the dielectric constants and resistances of bone, which leads to multiple relaxation time behaviors during deformation of bone."

Body height changes with hyperextension.

"The purpose of this study was to determine if the overall body height, as measured by a stadiometer, could be increased by brief episodes of hyperextension rather like a stretch that people frequently employ when arising. The subjects were loaded with 10 kg and the recovery with quiet sitting was compared to hyperextension 'stretches'. 15 s of hyperextension caused a significant temporary height increase [due to disc rehydration]."

"lifts up to 32 kg, and lateral bending with lifts up to 10 kg [were performed], the following parameters were estimated: lumbosacral angle and elongation, contribution of each lumbar segment to the lordosis reduction, relative pelvic/spine motion, and trunk velocity. "

-6.33mm was lost after 5 minutes of sitting.

"unloaded sitting with five hyperextensions resulted in an average height gain of +5.05 mm"

"[During Hyperextension] loads [may be] shifted to the facets and unload the discs."

Facet joints are synovial joints.

Here's how hyperextension may increase disc height

Facet joint is compressed whereas lumbar disc is stretched.

"facet overgrowth occurs as a result of arthritis and is the body’s response to bone-on-bone contact"

"the movement of bone on bone breaks down the subchondral surface and permanently damages the bone."<-Can this be used to help us grow taller?

Facet joint syndrome is facet joint overgrowth and it doesn't seem to have height benefits.
Exercise and the height of horses.

"The heights of 89 horses were measured at the withers before and after half a furlong of trotting exercise. The mean (+/- sd) height increase after exercise was 1.75 +/- 0.86 cm and the horses returned to their resting height within seven minutes. There was no linear relationship between gain in height and pre-exercise height."

Couldn't get this full study and it would be important before drawing conclusions.

The effect of mechanical stretch stress on the differentiation and apoptosis of human growth plate chondrocytes.

"The study is aimed to investigate the effect of stretch stress with different intensities on the differentiation and apoptosis of human plate chondrocytes. In the present study, the human epiphyseal plate chondrocytes were isolated and cultured in vitro. Toluidine blue staining and type II collagen immunohistochemical staining were used to identify the chondrocytes. Mechanical stretch stresses with different intensities were applied to intervene cells at 0-, 2000-, and 4000-μ strain for 6 h via a four-point bending system. The expression levels of COL2, COL10, Bax, Bcl-2, and PTHrp were detected by quantitative RT-PCR{Col10 could tell us what expression level induces endochondral ossification}. Under the intervention of 2000-μ strain, the expression levels of COL2, COL10, and PTHrp increased significantly compared with the control group (P < 0.05), and the expression level of PCNA was also increased, but the difference was not statistically significant (P > 0.05). Under 4000-μ strain, however, the expression levels of PCNA, COL2, and PTHrp decreased significantly compared with the control group (P < 0.05), and the expression level of COL10 decreased slightly (P > 0.05). The ratio of Bcl-2/Bax gradually increased with the increase of stimulus intensity; both of the differences were detected to be statistically significant (P < 0.05). In conclusion, the apoptosis of growth plate chondrocytes is regulated by mechanical stretch stress. Appropriate stretch stress can effectively promote the cells' proliferation and differentiation, while excessive stretch stress inhibits the cells' proliferation and differentiation, even promotes their apoptosis. PTHrp may play an important role in this process."

" At the end of the epiphyseal plate, the reserve zone, also known as stem cell zone, contains the resting chondrocytes. These cells, based on some trigger, enter into the proliferating zone. Then, the flattened chondrocytes undergo cell divisions in a longitudinal direction and organize in a typical column-wise orientation. In this zone, extracellular matrix (ECM) proteins, which are essential for the structure of the epiphyseal plate, have been synthesized by chondrocytes. In due course, either by a finite number of cell divisions or by alterations in exposure to a local growth facto chondrocytes are out of their capacity to divide and start to differentiate, accompanied by an increase in size.  The further progress of them in the differentiation pathway is to become hypertrophic chondrocytes, which possess a round appearance and secrete matrix proteins. And chondrocytes, at this stage, is characterized with an increase in intracellular calcium concentration, which is essential for the production of matrix vesicles "

"the rate of growth through endochondral ossification in epiphyseal plate is varied by the presence of sustained mechanical compression or tension and by cyclic compression, which indicate the effect of mechanical load on the growth rate "

"The chondrocytes of epiphyseal plates, in cytoplasm, were found to be plenteous shapes polygon, triangle, or short fusiform Nuclei of chondrocytes are precisely visible, and cells growth is monolayer. "

"Macro axis of chondrocytes was found to be trend in the direction of vertical tensile strain, and the phenomenon was most obvious in the group of 4000-μ strain "

" the cyclic tensile strain of 4000-μ strain has significantly contributed to the increase of cellapoptosisabout2-fold compared with corresponding ontrol and group of 2000-μ strain. The data indicates that the apoptosis of chondrocytes in epiphyseal plates may increase with increasing stretch stress. The result of apoptosis induction by cyclic tensile stress in growth plate chondrocyte illustrates that stretch stress can promote bone growth to some extent. Because stress stimulation may indirectly trigger a series of reaction and induce chondrocytes to undergo programmed cell death (apoptosis), then leave a scaffold for new bone formation{Thus more stretch may induce endochondral ossification}. "

Is bone’s response to mechanical signals dominated by muscle forces?

"Skeletal loading in vertebrates controls modeling drifts, modulated remodeling rates, and affects growth trajectories. It is unclear whether the majority of the mechanical stimulus detected by bone cells originates from muscle contraction forces, or from gravitational forces associated with substrate impact. A number of clinical and basic science reports indicate that muscle forces play a dominant role in generating the mechanical stimulus in exercise-induced bone gain. While it is in most cases difficult to separate the effects of gravitational forces acting on body mass from muscle contractions, several well-conceived experiments offer considerable insight into the propensity of muscle-derived forces per se to drive the adaptive response in bone. Load-induced osteogenesis requires that mechanical signals come packaged with particular characteristics, all of which can be generated from either gravitational or muscle forces. Neither of these two sources has been demonstrated empirically to be the source of bone’s adaptive response, but a convincing body of data suggests that muscle contractions are present, significant, and capable of accounting for a large majority of the adaptive responses."

"“Trauma excepted, muscles cause the largest loads and the largest bone strains, and these strains help to control the biological mechanisms that determine whole-bone strength.”"

"While it is widely accepted that bone adapts to the mechanical demands to which it is subjected, the origin of the mechanical demands that provide the driving stimulus for the tissue, i.e., muscle contraction or substrate reaction forces"

"It was commonly assumed that tissue deformation during loading (e.g., exercise) would stretch resident bone cells (e.g., osteocytes), and this stretching action would generate a cascade of signaling events that would eventually result in enhanced structural adaptation."

" fluid shear forces, and not mechanical stretch, were the driving stimulus behind load-induced osteogenesis in whole living bones."

"(1) stronger muscles pull with greater force on the skeleton, and consequently the bone must adapt; (2) larger, heavier bones require greater muscle force to move them, and consequently, the muscle must adapt to the greater bone mass; or (3) muscle mass and bone mass are controlled independently by the genetic program and/or the physical environment, and the associations between the two are spurious. "

For tennis players there is " there is a significant portion of the variation in bone size not explained by muscle mass."

" newborns suffering from intrauterine onset neuromuscular paralysis exhibit normal bone length but severely reduced cortical thickness and mass. These infants are frequently born with multiple fractures (e.g., humerus, radius, femur) that occurred prior to delivery. Considering that normal and paralyzed fetuses are both in a nearly “weightless” aqueous environment (bathed in amniotic fluid), it is unlikely that significant ground reaction forces are generated during the gestational period. Yet it is only when the muscle contractile forces are lost that the bones become pencil thin and fracture easily. These observations would argue for muscle-derived forces and against ground reaction/gravitational force as the primary stimulus driving the adaptive modeling response, at least in the developing skeleton."

"Greater than 70% of the forces generated within the femur during a normal gait cycle were found to result from muscle forces (which also were monitored via EMG), leaving less than 30% derived from body weight "

"The rats were trained to jump up to a platform, which precluded any impact loading (see text). Muscle-modulated jumping significantly enhanced periosteal growth."

"muscle forces per se are capable of providing a sufficient stimulus to drive bone adaptation. It is also clear that muscle forces normally provide a significant amount of force, and consequently strain, the axial bones."

" Mechanical signals must be of sufficient magnitude, be imposed at significant rates, and be dynamic in application in order for bone adaptation to occur. If physical activity generates ground reaction forces that meet those criteria, it is likely that the ground reaction forces will stimulate osteogenesis. Likewise, if muscular activity deforms the bone tissue in such a manner that those criteria are met, osteogenesis will occur."

Nordic Walking Increases Distal Radius Bone Mineral Content in Young Women

"Unlike the lumbar spine and femur, the radius does not bear a gravitational mechanical compression load during daily activities. The distal radius is a common fracture site, but few studies have addressed the effects of exercise on fracture risk. The aim of this study was to determine the effects of the pole push-off movement of Nordic walking (NW) on the bone mineral content (BMC) and areal bone mineral density (aBMD) of the distal radius and the muscle cross-sectional area (CSA) at the mid-humeral and mid-femoral levels. The participants were allocated to two groups: an NW group and a control group. The NW group walked at least 30 min with NW poles three times a week for six months. There were no significant changes in muscle CSA at the mid-humeral or mid-femoral levels between or within groups. There were also no significant changes in BMC or aBMD at 1/3 and 1/6 of the distance from the distal end of the radius in either group. However, the BMC and aBMD at 1/10 of the distance from the distal end of the radius were significantly increased by NW. The NW pole push-off movement provided effective loading to increase the osteogenic response in the ultra-distal radius. The ground reaction forces transmitted through the poles to the radius stimulated bone formation, particularly in the ultra-distal radius."

Mechanical loading effect to the functional bone adaptation

"Bone growth and bone loss are caused by mechanical elastic bone deformation. Muscles cause the highest loads and the largest deformations in bone and these deformations help to control biological mechanisms that determine the strength of entire bone."<-if other forces produced higher loads would they be the dominant force.

" in young rats who followed training program either jumping or running, tibia length as well as femur length and diameter increased"

"Muscle forces are able to promote bone response and functional adaptation. Muscle forces usually provide a significant amount of applied force, thus, they contribute to the deformation of long bones."


  1. You think doing both LSJL and bone stretching will be more effective or will they negate each other somehow..

  2. Your guide to lengthen the bone using a rope is a little bit confusing for me. Could you post some pictures or illustrations, that will help me to understand what do you mean. Thanks.

  3. I think doing LSJL is the best method right now period. I'm just speculating on Sky's method.

  4. sir i seriously wat to increase my height iam very dipress wid my height plz tell me how tod do micro fracture exercises i"ll be very thanksfull to u......................................plzzzzzz my id is

  5. Hi, Minigolfer, I am interested in this subject cuz i ve done some research regarding bone stretching. I learnt some successful ankle weight stories from Chinese website (Im chinese) and also compared the japanese non surgical method & the then I realized something in common among them and I now have some hypothesis which i believe will absolutely work on increasing bone length. I would like to share info and discuss with you. My email is Thanks

  6. what about having some kind of compact heavy miniclamp targeting the ankle bone all the day with you instead of ankle weights? wouldn't that have thesame effect as ankle weights with precise targeting ?

  7. Hey Minigolfer I don't really pass by your site much anymore but wanted to say thank you for helping me reach my height goal. I've been doing LSJL for 11 months year. I went from 5'8 to slightly over 5'11 and just turned 20!

    Went in for my checkup and my doctor could hardly believe it.

    Thank you and keep up your good work.

    1. Tyler have you tried contacting this guy

  8. also what do you think about using a tuning fork for height?

  9. What do you think about using injections to increase stem cells in the body and using lsjl to target growth plates

  10. the only possible way to increase bones are by the following two methods and both are heavily costly.

    1) Limb Strengthening Surgery - costs you $20000 or something like that. very painful.
    2) Ayurvedic Urea - its with no side effects but costs you $10000 or more


  11. can you really lengthen ligaments in legs through stretching