It may be possible to apply tensile strain to articular cartilage to induce endochondral ossification there thereby inducing height growth.

Effects of cyclic tensile strain on chondrocyte metabolism: a systematic review.

“Chondrocytes reorganize the extracellular matrix of articular cartilage in response to externally applied loads. Thereby, different loading characteristics lead to different biological responses. Despite of active research in this area, it is still unclear which parts of the extracellular matrix adapt in what ways, and how specific loading characteristics affect matrix changes. This review focuses on the influence of cyclic tensile strain on chondrocyte metabolism in vitro. It also aimed to identify anabolic or catabolic chondrocyte responses to different loading protocols. The key findings show that loading cells up to 3% strain, 0.17 Hz, and 2 h, resulted in weak or no biological responses. Loading between 3-10% strain, 0.17-0.5 Hz, and 2-12 h led to anabolic responses; and above 10% strain, 0.5 Hz, and 12 h catabolic events predominated{catabolic responses doesn’t necessarily mean bad for height growth}. However, this review also discusses that various other factors are involved in the remodeling of the extracellular matrix in response to loading, and that parameters like an inflammatory environment might influence the biological response.”<-3% strain is quite high but that’s for bone for cartilage it may be different.

“cartilage compression exposes the chondrocyte to compressive forces, to osmotic pressure, to fluid flows and also to tensile forces”<-lateral compression such as via lateral loading of the articular cartilage has potential to induce tensile forces.

“after loading with CTS, cells exhibited a more elongated cell shape and aligned perpendicular to the loading direction”

Collagen Type I was upregulated by CTS which could indicated endochondral ossification.

“Fibronectin connects collagen fibers and other ECM proteins. It is linked to the cell membrane through integrins and might transmit forces from the ECM to the chondrocyte. CTS at 7%, 0.33 Hz and 0.5 Hz, for 4, 12 and 24 h increased the fibronectin mRNA levels in comparison to non-loaded chondrocytes”

“7% CTS for 4 h at 0.33 Hz elevated the expression of IGF-1 and IGF-2. The mRNA expression of TGF-β1 was increased by several loading protocols ranging from strains of 5–12%, from 12–48 h and at frequencies of 0.05 and 0.5 Hz”

According to CYCLIC TENSILE STRAIN AND CYCLIC HYDROSTATIC PRESSURE DIFFERENTIALLY REGULATE EXPRESSION OF HYPERTROPHIC MARKERS IN PRIMARY CHONDROCYTES , tensile strain encourages endochondral ossification whereas hydrostatic pressure encourages chondrogenesis.

This study would only be relevant to people with existing growth plates as it only studies load effects on chondrocytes.  But, regardless, since we are studying mechanical loading methods to study height growth any mechanical loading study may be relevant.

Regional variations in growth plate chondrocyte deformation as predicted by three-dimensional multi-scale simulations.

“The physis, or growth plate, is a complex disc-shaped cartilage structure that is responsible for longitudinal bone growth. In this study, a multi-scale computational approach was undertaken to better understand how physiological loads are experienced by chondrocytes embedded inside chondrons when subjected to moderate strain under instantaneous compressive loading of the growth plate. Models of representative samples of compressed bone/growth-plate/bone from a 0.67 mm thick 4-month old bovine proximal tibial physis were subjected to a prescribed displacement equal to 20% of the growth plate thickness. At the macroscale level, the applied compressive deformation resulted in an overall compressive strain across the proliferative-hypertrophic zone of 17%. The microscale model predicted that chondrocytes sustained compressive height strains of 12% and 6% in the proliferative and hypertrophic zones, respectively, in the interior regions of the plate. This pattern was reversed within the outer 300 μm region at the free surface where cells were compressed by 10% in the proliferative and 26% in the hypertrophic zones, in agreement with experimental observations.  While the current model is relevant to fast dynamic events, such as heel strike in walking, we believe this approach provides new insight into the mechanical factors that regulate bone growth at the cell level and provides a basis for developing models to help interpret experimental results at varying time scales. ”

“The physis, or growth plate, is a complex disc-shaped cartilage structure that is responsible for longitudinal bone growth. This growth is modulated by many systemic and local factors including those arising from mechanical loading”

“Potential tissue level signals for modulating endochondral bone formation [include] hydrostatic and octahedral shear stresses and principal stresses”

“chondrocytes, are the active agents of growth and contribute to bone growth through cell proliferation, hypertrophy and extracellular matrix secretion in highly specialized, highly cellular and organized anatomic structures known as chondrons. It is likely that tissue level strains and stresses are experienced differently by chondrocytes embedded within such structures, possibly providing signals of varying intensity and type depending on location.”

“Mechanotransduction is more readily related to cell deformation than to tissue level stresses. In the context of bone growth, there is evidence that cell proliferation and differentiation can be regulated through activation of stretch-activated ion channels in the cell membrane following changes in cellular shape and size”

“Recent observational studies of physeal samples under compression have revealed regional variations in cellular strains and suggest that global physeal strains may be amplified at the cellular level”<-This statement may be applicable to other cells like the enthesis of ligament attachments or mesenchymal stem cells.

“The prescribed compressive displacement which was equivalent to 20% of the initial uncompressed combined initial thicknesses (0.67 mm) of RZ and P/H zones resulted in a -14.8% growth plate engineering strain across the combined layers of the reserve, proliferative and hypertrophic zones, while the combined proliferative and hypertrophic zone received -17.2% strain. The reserve zone experienced -9.5% and the calcified cartilage zone -3.3% compressive strain.”<-Effects on the reserve zone are interesting to us because those contain stem cells so would show any interesting effects on non-growth plate cells.

“Chondrons, the primary functional and structural units of the growth plate, deformed by buckling near the free surfaces where the cartilage bulged outward while remaining straight in the interior regions”

“chondrocytes in the interior of the growth plate undergo about 50% less strain than the prescribed overall growth plate strain.”

“Younger growth plates that are thicker (3 mm) also had thicker reserve zones, which may affect the transverse outward bulging at the free surface differently.”

“During compression of cells at short times scales (~0.5 s) intracellular water is redistributed within the cell[but not necessarily more compression]”

” At long time scales constant external pressure induces cell shrinkage, but cell shrinkage takes an order of magnitude (~10 s,) longer than the transient impact of heel strike or even the 0.2 s duration of the stance phase of a gait cycle and as long as an hour to reach equilibrium”

“growth plate stresses reached values of 0.1 to 0.6 MPa in compression during activities such as sitting. From the stress relaxation experiments on explants it may be estimated that 0.2 MPa corresponds to the stress levels attained after stress relaxation for displacements of the epiphysis equal to 20% of the initial growth plate thickness (defined as the combined thicknesses of the reserve, proliferative and hypertrophic zones).”

“Chondrons appear to be oriented along the minimum principal strain directions, becoming roughly perpendicular to the epiphyseal bone plate, whereas the hypertrophic portion along with the calcified cartilage bars and primary spongiosa align more with the primary compressive load direction along the tibial long axis”

Some interesting info but the significance is unclear yet.

To focus on the disadvantages of height is an unhealthy psychological pursuit.  To focus on striving to grow taller is a healthy psychological pursuit.

Here’s a typical conversation to someone about height:

A:  Don’t worry about height.  It’s what’s on the inside that counts.

B:  Why is it acceptable for height to be descriminated against?  Why is male height so associated with a male’s value?  Why is it acceptable to laugh at people because of their height?

A: You should accept who you are.  Play with the cards your dealt.

B:  If you have a losing hand, do you accept that or do you throw the cards off the table and start a fist fight?  If you can’t beat the game change the rules.

A: Life isn’t fair.  Sucks for you.

If you try to get into an argument with someone about height it usually begins with a lot of platitudes which are refuted until their opposing argument devolves into “too bad”.

The argument with the best reasoning often isn’t the argument that wins.  Short support sites shouldn’t exist.  Realistically, very little improvements can be made for the average or below against the tall.  And ultimately such sites serve as a means of perseverating on height.

You can try to forget your height.  You can play video games.  You can engage in an activity where height is of less importance such as a musical instrument.  Although even in those activities such as piano or guitar, finger length has an effect on playing.  You can get around it with techniques but it’s still a reminder that you’re just not as good.  Even playing pool, height can be an advantage in performing certain shots.

There’s acceptance but will you ever accept?  Ryan Seacrest complains about his height all the time.  There’s escapism but will you be satisfied with just escape?  Most forms of escapism lack the depth and complexity of real life.

The healthiest way to focus on height is to strive to find a way to grow taller.  Instead of dwelling on it.  Instead of comparing height with your friends.  Instead of realizing that you’re shorter than that other guy that you thought was really short.

The research I’ve done on entheses is intriguing and I’m trying to develop a new routine to explore it. What’s most intriguing about Entheses is that it resembles the Zone of Ranvier which contains the stem cells to contribute to the growth plate.  What if by pushing two bones together such as the fibula and the tibia on the epiphyseal region we can stimulate the entheses to form neo growth plates?

Don’t accept that there’s no way to grow taller.

Your height is mostly based on the length of your bones{The other determinants of height are opportunities to find new ways to grow taller}.  The length of the bones is determined mostly by your growth plate{The rest of the length is determined by other means but are difficult to get to contribute in significant ways but again is another way to pursue the quest for height}.  The growth plate goes away after puberty after the exhaustion of the stem cells that contribute to the growth plate.

To grow taller you could find:

1) Increase other minor determinants of height not involving growth plate growth

2) Induce the formation of neo growth plates

3) Induce plastic(permanent) deformation of the long bones.  Stretch the bones in such a way that they increase in length in a way that is instant and permanent(although this has never bone in done and the mechanisms of measurement are not accurate enough to best gauge the elastic and plastic range of a bone).

4) Other?  For you to determine.

Escapism and acceptance aren’t the only options for dealing with your height.  Don’t let people tell you that you should just accept your height.  Every time you think about dwelling on the negative effects of not being tall, focus instead on finding ways to grow taller.

You can get distraction osteogenesis surgery but it costs a lot of money and ideally you’d have multiple surgeries.

This field of science is entirely under researched(but most areas are due to how slowly science progresses).  And due to the complexity it is difficult for it to be Lorenzo’s Oiled(Homemade scientific discovery).  It’ll be hard to find a more efficient way of performing distraction osteogenesis but you could find a home made way of inducing new growth plate formation.  Cells do respond to mechanical and chemical stimulation after all.  And has every manner of mechanical stimulation already been performed?  No.  Especially methods that would appear counterintuitive like lateral joint loading(now adjusted to focus more on pushing two bones together near the entheses rather than clamping the synovial joint region).  And there are novel apparatus to create to generate forces that we couldn’t using our own muscular force.

Don’t dwell on how Dave France doesn’t get as good a roles as James Franco because he’s shorter.  Don’t dwell on how the third Hemsworth brother doesn’t get as many roles because he’s shorter.

Focus on researching methods to grow taller!  Even when I find a way to grow taller, it’s not going to be perfect right away.  I’m going to need your help.  You’re going to need my help.  The faster people stop dwelling on height and start growing taller the faster we can start getting taller.

Can hanging out with tall people during development make you taller? One potential mechanism for how your communities genes may affect yours may be via biophotons.

The impact of physical connectedness on body height in Swiss conscripts.

“Human populations differ in height. Recent evidence suggests that social networks{who you hang out with} play an important role in the regulation of adolescent growth and adult height. We further investigated the effect of physical connectedness on height.
We considered Switzerland as a geographic network with 169 nodes (district capitals) and 335 edges (connecting roads) and studied effects of connectedness on height in Swiss conscript from 1884 – 1891, 1908 – 1910, and 2004 – 2009. We also created exponential-family random graph models to separate possible unspecific effects of geographic vicinity.
In 1884 – 1891, in 1908 – 1910, and in 2004 – 2009, 1(st), 2(nd) and 3(rd) order neighboring districts significantly correlate in height (p < 0.01). The correlations depend on the order of connectedness, they decline with increasing distance. Short stature districts tend to have short, tall stature districts tend to have tall neighbors. Random network analyses suggest direct road effects on height. Whereas in 1884 – 1891, direct road effects were only visible between 1(st) order neighbors, direct road effects extended to 2(nd) and 3(rd) in 1908 – 1910, and in 2004 – 2009, also to 4(th) order neighbors, and might reflect historic improvements in transportation. The spatial correlations did not significantly change when height was controlled for goiter (1884 – 1889) and for median per capita income (2006), suggesting direct road effects also in goiter-allowed-for height and income-allowed-for height.

Height in a district depends on height of physically connected neighboring districts. The association decreases with increasing distance in the net. The present data suggest that people can be short because their neighbors are short; or tall because their neighbors are tall (community effect on growth). Psycho-biological effects seem to control growth and development within communities that go far beyond our current understanding of growth regulation.”

Final height, target height and the community.

“Height varies with age, and it varies with historic time. Final height is determined by endocrine parameters and genetics, by nutrition and health, by environmental factors, by birth weight, early growth, BMI, and developmental tempo. European populations of the 19th century were short, but their shortness did not result from growth impairment at all ages. In those days, shortness was mainly due to a significantly blunted adolescent growth spurt. New modelling approaches suggest an independent regulation of adolescent growth and final height: the target for growth and final height appears to be set by the community{hanging around with probasketball players may make you taller?}. In order to test this hypothesis, we formed a geographic network of Switzerland consisting of 169 nodes (district capitals) and 335 connecting edges (roads), and investigated military conscript data obtained between 2004 and 2009. Average height of Swiss military conscripts was 178.2 cm (SD 6.5 cm). But conscripts from first order neighbouring districts were more similar in height than expected. Short stature districts have short, tall stature districts have tall neighbours. We found significant height correlations between 1st (r=0.58), 2nd (r=0.64), 3rd (r=0.45) and even 4th order neighbours (r=0.42). It appears that tall stature communities generate tall people, short stature communities generate short people, and migrants orientate towards the new height target of their host population (community effect on growth){So independent of genes from the community newborn migrants will be taller or shorter based on the community}. ”

Modeling determinants of growth: evidence for a community-based target in height?

“community-based target seeking in growth”

“adolescent height converges toward the average of the population. Height tends to cluster. The within-population variation of height is narrow.”

“Height differences are small throughout childhood but markedly increase during adolescence.”

“the smaller the adolescent is compared with past mean average height, the more the adolescent grows during puberty.”<-So according to this theory, if you are going through puberty and hang out with pro-basketball players you will grow taller than expected and at a faster rate.

“Short stature in cystic fibrosis results from tempo deceleration. Cystic fibrosis patients grow poorly at all ages (they have suboptimal peak height velocity and late pubertal growth, influenced by disease severity) but eventually achieve normal final height. ”

” tall communities generate tall people even in the presence of unfortunate living conditions”

According to Dose-dependent effect of growth hormone on final height in children with short stature without growth hormone deficiency.,exogenous administration of GH increased height by about 1 inch.  The authors of this study suggest that living around taller people could increase GH production as depression decreases GH production establishing a link between mental state and GH production.

Here’s a study that suggests that IGF-1 levels may play a role in the community effect on height.  Although it does not seem to be a strictly linear relationship between IGF-1 levels and height.  Height is more complex than that.

Sex, Sport, IGF-1 and the Community Effect in Height Hypothesis.

“We test the hypothesis that differences in social status between groups of people within a population may induce variation in insulin-like growth factor-1(IGF-1) levels and, by extension, growth in height{so “positive thinking” increases height via IGF-1 but again the relationship is more complex than IGF-1 increases height}. This is called the community effect in height hypothesis. The relationship between IGF-1, assessed via finger-prick dried blood spot, and elite level sport competition outcomes were analysed for a sample of 116 undergraduate men and women. There was a statistically significant difference between winners and losers of a competition. Winners, as a group, had higher average pre-game and post-game IGF-1 levels than losers. We proposed this type of difference as a proxy for social dominance. We found no evidence that winners increased in IGF-1 levels over losers or that members of the same team were more similar in IGF-1 levels than they were to players from other teams. These findings provide limited support toward the community effect in height hypothesis. The findings are discussed in relation to the action of the growth hormone/IGF-1 axis as a transducer of multiple bio-social influences into a coherent signal which allows the growing human to adjust and adapt to local ecological conditions.”

So it seems that the relationship as described here is that winners are more likely to have higher IGF-1 levels rather than winning increasing IGF-1 levels.

“Children and adolescents with pituitary gigantism have an excessive production of GH, and IGF-1 levels are elevated.”<-But again it seems as though there’s more to gigantism than excessive GH.

“the positive association between variation in IGF-1 levels and height, across the range from deficiency to excess, helps to explain differences in stature within and between human populations.”

” there is evidence for a new parameter that they define as ‘past relative height.’ This parameter operates during the adolescent growth period to adjust the growth rate of an individual toward the average height of her/his immediate community.”

“… the smaller the adolescent is compared with past mean average height [of the community], the more the adolescent grows during puberty”

Surprisingly the scientists found that women in sports tended to have higher IGF-1 levels than men in sports.

“Women, but not men, showed a significant association between their father’s social class and their own adult IGF-1 levels.”

Loading bones against each other also loads the ligaments against the growth plate.  One method of LSJL involves pushing bones against each other at the points of the epiphysis.

Mesenchymal stem cell characteristics of human anterior cruciate ligament outgrowth cells.

“When ruptured, the anterior cruciate ligament (ACL) of the human knee has limited regenerative potential. Cells that migrate out of the human ACL constitute a rich population of progenitor cells and we hypothesize that they display mesenchymal stem cell (MSC) characteristics when compared with adherent cells derived from bone marrow or collagenase digests from ACL. ACL outgrowth cells are adherent, fibroblastic cells with a surface immunophenotype strongly positive for cluster of differentiation (CD)29, CD44, CD49c, CD73, CD90, CD97, CD105, CD146, and CD166, weakly positive for CD106 and CD14, but negative for CD11c, CD31, CD34, CD40, CD45, CD53, CD74, CD133, CD144, and CD163. Staining for STRO-1 was seen by immunohistochemistry but not flow cytometry. Under suitable culture conditions, the ACL outgrowth-derived MSCs differentiated into chondrocytes, osteoblasts, and adipocytes and showed capacity to self-renew in an in vitro assay of ligamentogenesis. MSCs derived from collagenase digests of ACL tissue and human bone marrow were analyzed in parallel and displayed similar, but not identical, properties. In situ staining of the ACL suggests that the MSCs reside both aligned with the collagenous matrix of the ligament and adjacent to small blood vessels.  The cells that emigrate from damaged ACLs are MSCs have the potential to provide the basis for a superior, biological repair of this ligament.”

“mobile population of MSCs within the ACL”

“cells derived from both ACL sources and bone marrow underwent chondrogenic differentiation in the presence, but not absence, of TGF-β1”

“MSCs migrate to sites of injury”

So ligaments near the epiphysis can differentiate into chondrocytes.

Chondrocyte phenotype and ectopic ossification in collagenase-induced tendon degeneration.

“Chondrocyte phenotype and ectopic ossification in a collagenase-induced patellar tendon{in the new LSJL model the patella is a targetfor loading} injury model. Collagenase or saline was injected intratendinously in one limb. The patella tendon was harvested for assessment at different times. There was an increase in cellularity, vascularity, and loss of matrix organization with time after collagenase injection. The tendon did not heal histologically until week 32. Ectopic mineralization started from week 8. Tendon calcification was mediated by endochondral ossification, as shown by expression of type X collagen. viva CT imaging and polarization microscopy showed characteristic bony porous structures and collagen fiber arrangement, respectively, in the calcific regions. Marrow-like cells and blood vessels were observed inside calcific deposits. Chondrocyte-like cells as indicated by morphology, expression of type II collagen, and sox 9 were seen around and embedded inside the calcific deposits. Fibroblast-like cells expressed type II collagen and sox 9 at earlier times, suggesting that erroneous differentiation of healing tendon fibroblasts may account for failed healing and ossification in collagenase-induced tendon degeneration.”

“Chondrocyte markers were expressed in the clinical samples of calcific insertional Achilles tendinopathy”

“Chondrocyte-like cells as indicated by cellular morphology and expression of sox 9 and type II collagen were observed around the calcific deposits in collagenase-induced degenerative tendon injury”

“The differentiation of tendon progenitor cells into chondrocytes and bone cells was reported to be modulated by the expression of small leucine-rich repeat proteoglycans such as biglycan and fibromodulin, which control the differentiation process associated with BMP-2 activities ”

Tendons can differentiate into cells that undergo endochondral ossification.

The tendons are relatively close to the epiphysis as well.

The origin points of the knee collateral ligaments: an MRI study on paediatric patients during growth

“Different femoral origins for both the medial collateral ligament (MCL) and the lateral collateral ligament (LCL) have been reported in the growing skeleton (epiphyseal and metaphyseal). This study assesses the femoral origins of the knee collateral ligaments in skeletally immature individuals.
MRIs of 336 knee joints (median age 15 years (range 2–18 years)) were retrospectively analysed to assess the distances between the femoral origins of the MCL and LCL to the distal femoral growth plate.
Both MCL and LCL ligament origins were invariably located on the epiphysis. Mean MCL origin–growth plate distance was 9.6 mm (SD 2.1 mm; range 2.2–13.6 mm) in boys and 8.6 mm (SD 1.5 mm; range 3.4–12.0 mm) in girls{The MCL ligament is very close to the growth plate}. Mean LCL origin–growth plate distance was 9.3 mm (SD 1.8 mm; range 4.3–13.0 mm) in boys and 8.2 mm (SD 1.5 mm; range 3.4–11.8 mm) in girls{The LCL ligament is very close to the growth plate}. The distance between the growth plate and both collateral ligaments as well as the length of the LCL correlated positively with patients’ age and body size.
During growth, the femoral origins of the MCL and the LCL are constantly located on the distal femoral epiphysis. There is a linear increase in the distances from the ligaments’ origins to the growth plate according to age and body size.”

“The LCL attaches slightly closer to the growth plate than the MCL. The distances between the origins of the ligaments and the distal femoral growth plate increase in a nearly linear pattern until closure of the growth plate.”

Where tendons and ligaments meet bone: attachment sites (‘entheses’) in relation to exercise and/or mechanical load.

“Entheses (insertion sites, osteotendinous junctions, osteoligamentous junctions) are sites of stress concentration at the region where tendons and ligaments attach to bone.”

“Tendons and ligaments can be regarded as machines with multiple moving parts (fibrils, fibres and fascicles) that perform the basic function of force transfer to and from the skeleton. They distribute the loads applied to them dynamically in order to execute movement patterns. Their complex response to loading allows for multi-axis bending, and this adds to the stress concentration in the region where they attach to bone. This attachment site will be referred to in this review as an ‘enthesis’, but it is also known as an ‘insertion site’, or an ‘osteotendinous’ or ‘osteoligamentous’ junction.”

The tissue at the enthesis insertion site is either fibrous or fibrocartilagenous.

“chondral–apophyseal entheses are found at the ends of the long bones and periosteal–diaphyseal attachments occur on the shafts.”

“At fibrous entheses, the tendon or ligament attaches either directly to the bone or indirectly to it via the periosteum. In both cases, dense fibrous connective tissue connects the tendon/ligament to the periosteum and there is no evidence of (fibro)cartilage differentiation”

“Fibrocartilaginous entheses are sites where chondrogenesis has occurred and thus four zones of tissue are commonly present: pure dense fibrous connective tissue, uncalcified fibrocartilage, calcified fibrocartilage and bone”

“The inclusion of a zone of ‘pure dense fibrous connective tissue’ and a zone of ‘bone’ at a fibrocartilaginous enthesis highlight the difficulty of defining with any degree of precision where such an enthesis begins and ends.”<-Thus the ligament that attatches to the epiphysis near the growth plate line may extend partially into the bone itself.

“the proportion of the enthesis subchondral bone plate which consists of calcified fibrocartilage increases with age, because of a thinning of the cortical bone”

“Although tendons and ligaments are often viewed as non-distensible, they do have the ability to stretch and recoil by approximately 6% of their original length without any obvious signs of damage.”

“entheses can act as growth plates for apophyses at tendon and ligament attachment sites.”

“cartilage at the enthesis is initially derived from that of the embryonic bone rudiment.”

“this hyaline cartilage is eroded during endochondral ossification and replaced by enthesis fibrocartilage that develops within the adjacent ligament by fibroblast metaplasia.”

“Bony spurs (enthesophytes) are well documented at numerous entheses as bony outgrowths that extend from the skeleton into the soft tissue of a tendon or ligament at its enthesis”<-our goal is a cartilage ingrowth into the bone from the tendon/ligament.

Magnetic resonance imaging of entheses. Part 1.

“Achilles tendon, sagittal, histological section stained with Toluidine blue. Enthesis (EF) sesamoid (SF) and periosteal (PF) fibrocartilages are seen. The retrocalcaneal bursa (B) lies between the tendon and the bone and contains the tip of Kager’s retromalleolar fat pad (KP).”

“One of the interesting features of fibrocartilaginous entheses is the paucity[scarcity] of compact bone (often referred to as the cortical shell) immediately beneath the attachment site. The subchondral plate (i.e. the associated calcified fibrocartilage and cortical shell) is often very thin and in many fibrocartilaginous entheses, there are local areas where subchondral bone and calcified fibrocartilage are absent.“<-Thus, it would be easier for cells to migrate there.

“Fibrocartilage forms in tendons that are translocated around bony pulleys and regresses in tendons that are re-routed so that they are no longer subject to compression in the same region.”

Here’s the new LSJL routine I’m trying.  It’s not quite the same as LSJL as it’s not based on loading the synovial joints really, it’s more about loading groups of bones that are connected close to another bone by it’s growth plates.  It’s based on the observation that my arms gained in length relatively consistently but not the rest of my body.  The manner in which I clamp my elbow is relatively unchanged versus how I clamped it into LSJL.

For example, in LSJL you clamp the synovial joint on it’s side.

If you clamp the knee on it’s side you are pressing ligaments against the growth plate.

However by pressing the patella against the growth plate line you are not just pressing the ligament near the growth plate line(growth plate remnant), you are pressing the bone against the ligament which would generate a new stimulus.

The philosophy behind LSJL was to induce lateral compression of the bones to induce fluid flow in the bone to generate hydrostatic pressure to induce mesenchymal condensation to form neo-growth plates to grow taller.

Ligaments and other connective tissue have stem cells and coincedentally some run directly into the growth plate region.  Osteoclasts could theoretically eat away at bone and ligament stem cells could migrate and form neo growth plates within this growth plate line.  I’ll be posting some things to explore this theory.

Here’s where and how I’m clamping.  I know the pictures are bad but even if the pictures were better you’d still have to feel and experiment with the optimal clamping position.  But the idea is to clamp one bone against another bone.  So you clamp the fibula against the tibia or the patella against the femur.  Since bones often are connected to each other near the growth plate region this allows for the possibility of stimulating growth plate regeneration.

Now I haven’t tested this routine that long and ligaments and soft tissue are more fragile then bone.  So do this routine at your own risk especially something like the patella clamp.  I also have pretty minimal evidence so far as the only clamp that’s proved to be decently effective is the elbow clamp.  Most I’ve done for these clamps is a count of 120 but I get results for elbow clamping with about that much.  I’m going for several sessions a day though.

I might have to do a video as well for each to explain how I find the right clamping spots.

Patella clamp:

Fibula clamp:

Ankle(Tibia and Fibula) Clamp:

Cuneiforms and Metatarsals Clamp:

Elbow(humerus clamp):

Radius and Ulna(Wrist) Clamp:

Metacarpal bones(clamp):