If LSJL can physically deform the bone then perhaps it can deform the bone in such a way as to make it longer.

Creep of trabecular bone from the human proximal tibia

“Creep is the deformation that occurs under a prolonged, sustained load and can lead to permanent damage in bone{So to get creep with LSJL the duration of the loads should be longer}. Creep in bone is a complex phenomenon and varies with type of loading and local mechanical properties. Human trabecular bone samples from proximal tibia were harvested from a 71-year old female cadaver with osteoporosis. The samples were initially subjected to one cycle load up to 1% strain to determine the creep load. Samples were then loaded in compression under a constant stress for 2 h and immediately unloaded. All tests were conducted with the specimens soaked in phosphate buffered saline with proteinase inhibitors at 37 °C. Steady state creep rate and final creep strain were estimated from mechanical testing and compared with published data. The steady state creep rate correlated well with values obtained from bovine tibial and human vertebral trabecular bone, and was higher for lower density samples. Tissue architecture was analyzed by micro-computed tomography (μCT) both before and after creep testing to assess creep deformation and damage accumulated. Quantitative morphometric analysis indicated that creep induced changes in trabecular separation and the structural model index. A main mode of deformation was bending of trabeculae{stretchinig of the trabeculae would be what would make it longer although it’s possible that bending would make trabeculae longer if done in a certain way}.”

” One manifestation of creep damage is the decreased stature of elderly individuals due to the creep damage of vertebrae”

” trabeculae from vertebral areas are mostly rod-like, while in the metaphyses and epiphyses of long bones there is a more balanced mixture of plate-like and rod-like trabeculae. Furthermore, it was shown that these cellular structures degrade differently during the progression of osteoporosis, resulting in differences in the degree of anisotropy of mechanical properties”

” Creep occurs in three stages: primary, secondary and tertiary. Primary creep is the brief initial period during which the creep rate decreases and is accompanied with some material relaxation. In secondary creep, which is the longest and most studied regime, a steady state creep rate (dε/dt) is observed. Tertiary creep, occurring at the end of the secondary regime, is associated with an accelerated creep rate and more damage accumulation that results in eventual failure if the load is sustained. If the creep test is stopped during the secondary stage and the load removed, there is some elastic and viscoelastic strain recovery.”

“under a prolonged load, microcracking of the bone matrix (and not fracture of the whole trabeculae) was the primary mode of deformation during creep. On the other hand, it was shown that even a small damage, barely distinguished on radiographs, to older vertebrae accelerates creep, and leads to a visible contribution to a vertebra deformity”

Here’s a paper that shows possible positive benefits of creep deformation:

In vitro torsion-induced stress distribution changes in porcine intervertebral discs.

“A cadaveric porcine spine motion segment experiment was conducted.

To test the hypothesis that small vertebral rotations cause increased stress in the anulus while decreasing stress in the nucleus through stiffening of the anulus.

Stress profiles of the intervertebral disc reportedly depend on degeneration grade and external loading. Increased stress in the anulus was found during asymmetric loading. In addition, depressurization of the nucleus combined with an instantaneous disc height increase was found when small (<2 degrees ) axial vertebral rotations were applied{So twisting could increasing height?}.

Seven lumbar porcine cadaveric motion segments consisting of two vertebrae and the intervening disc with ligaments were loaded in the neutral position with 340 N of compression. Stress profiles were obtained in the neutral position, then after 0.5 degrees and 1 degrees axial rotation of the bottom vertebral body. The distribution of compressive stress in the disc matrix was measured by pulling a miniature pressure transducer through the disc along a straight path in the midfrontal plane. Stress profiles were measured in vertical (0 degrees ) and horizontal (90 degrees ) orientation.

Deformation of the anulus by small axial rotations of the lower vertebra instantaneously decreased the horizontally and vertically measured stress in the nucleus while increasing stress in the anulus. A 1-hour period of creep loading decreased the stresses in the nucleus and the anulus 20% to 30%, depending on the orientation, but the effect of an increasing stress in the anular region after axial rotation persisted.

The compressive Young’s modulus of the composite anulus tissue increases instantaneously when small axial rotations are applied to porcine spine motion segments. This is accompanied by decreased stress in the nucleus pulposus, increased stress in the anulus fibrosus, changes in the stress profile superimposed on and independent of prolonged viscoelastic creep and dehydration, and changes in stress distribution independent of horizontal and vertical orientation.”

“the nucleus acts as a sealed hydraulic system, in which the fluid pressure rises substantially when volume is increased (by fluid injection) and falls when volume is decreased (by surgical excision or endplate fracture). “Stress” peaks in the anulus reportedly are increased by prior loading and degeneration.”

“[The] pressure reduction in the nucleus pulposus under torsion coincided with an increase of disc height “

Magnitude of loads influences the site of failure of highly curved bones.

“The structure and material properties of bones along with applied boundary conditions determine the region of peak stresses, where fracture is expected to occur. As the site of peak stresses is not influenced by the magnitude of applied load, the fracture site is not expected to change during fatigue loading of whole bone at different loads. However, in a highly curved bone such as the rat ulna, the magnitude of applied loads was found to influence the fracture site. Fatigue loading was conducted under load control on intact rat forearms and on excised ulnae. The distance to the site of failure from the proximal olecranon process of ulnae was determined. In intact forearms, the site of failure demonstrated a linear progression distally, towards sites with lower moment of inertia (or sites exhibiting lower section modulus). Intact rat forearms and excised ulnae loaded to failure at low loads fractured 2-3mm distal to where they failed when applying high loads. This indicates a shift in the site of failure by approximately 10% of whole bone length just by varying the applied load magnitude. The site of failure in excised ulnae was similar when loading at 2Hz or at 4Hz, suggesting that this was frequency independent in this range and indicating that strain rate was not an important contributing factor. Creep loading of excised ulnae also demonstrated similar changes in the site of failure, indicating that magnitude of loads, and not type of loading were important in determining the site of failure.”

“the shape of whole bone can be such that failure occurs at sites other than the smallest cross-section and/or smallest moment of inertia. This is especially true for curved bones such as the ulnae and tibiae of commonly used rodent strains.”

“Loading was conducted by placing the excised ulnae between brass U-cups, with the load being applied in the direction parallel to the length of the ulna (left-to-right). During this loading, the natural curvature of the ulna causes bending induced tensile and compressive stresses on the lateral and medial surfaces, respectively”

“a gradual shift is observed as the site of failure of the ulna moves from 15.2 mm to 17.3 mm as the peak compressive load decreases from 26 N to 14 N”

“In excised ulnae, the site of failure shifted distally as the load was decreased, with failure occurring slightly distal to the mid-shaft at high loads and even more distally at lower loads, irrespective of the frequency of cyclic loading (2 Hz or 4 Hz) or the mode of loading (creep or cyclic).”

“Failure occurred at extremely short time scales at high loads, and at considerably longer time scales when loading at low loads. When loading at high loads, times to failure were not dependent on loading frequency or mode of loading (creep or cyclic). When loading at low loads, the time it took for the bones to fail decreased with increased frequency of cyclic loading  and was the shortest during creep loading. Dring cyclic loading, failure occurs in fewer cycles at greater loads, irrespective of the frequency of loading. At the same loads, loading at a higher frequency (2 Hz vs 4 Hz), there was no difference in the numbers of cycles to failure when loading was conducted at different frequencies (2 Hz or 4 Hz).”

“As expected, loading at high loads causes bones to fail in shorter times (within 30 s) as opposed to loading at low loads (periods of a week or two).”<-Loading for a week or two would be extreme.

Bone Creep can cause Progressive Vertebral Deformity

“Vertebral deformities in elderly people are conventionally termed “fractures”, but their onset is often insidious, suggesting that time-dependent (creep) processes may also be involved. Creep has been studied in small samples of bone, but nothing is known about creep deformity of whole vertebrae, or how it might be influenced by bone mineral density (BMD). We hypothesise that sustained compressive loading can cause progressive and measurable creep deformity in elderly human vertebrae.

27 thoracolumbar “motion segments” (two vertebrae and the intervening disc and ligaments) were dissected from 20 human cadavers aged 42–91 yrs. A constant compressive force of approximately 1.0 kN was applied to each specimen for either 0.5 h or 2 h{30 minutes is doable}, while the anterior, middle and posterior heights of each of the 54 vertebral bodies were measured at 1 Hz using a MacReflex 2D optical tracking system. This located 6 reflective markers attached to the lateral cortex of each vertebral body, with resolution better than 10 μm. Experiments were at laboratory temperature, and polythene film was used to minimise water loss. Volumetric BMD was calculated for each vertebral body, using DXA to measure mineral content, and water immersion for volume.

In the 0.5 h tests, creep deformation in the anterior, middle and posterior vertebral cortex averaged 4331, 1629 and 614 micro-strains respectively, where 10,000 micro-strains represents 1% loss in height. Anterior creep strains exceeded posterior (P < 0.01) so that anterior wedging of the vertebral bodies increased, by an average 0.08° (STD 0.14°). Similar results were obtained after 2 h, indicating that creep rate slowed considerably with time. Less than 40% of the creep strain was recovered after 2 h. Increases in anterior wedging during the 0.5 h creep test were inversely proportional to BMD, but only in a selected sub-set of 20 specimens with average BMD < 0.15 g/cm³ (P = 0.042). Creep deformation caused more than 5% height loss in four vertebrae{imagine if the reverse occurred}, three of which had radiographic signs of pre-existing damage.”

“Sustained loading can cause progressive anterior wedge deformity in elderly human vertebrae, even in the absence of fracture.”

“yield strain does not differ greater between cortical and trabecular bone”

they suggest the the change was due to microcracking of the bone matrix and relative gliding and rearrangement of microfibrils. This may be hard to mimic in a longitudinal direction but not impossible.

Vertebral deformity arising from an accelerated “creep” mechanism

“Vertebral body creep was measurable in specimens with BMD <0.5 g/cm². Creep was greater anteriorly than posteriorly (p < 0.001), so that vertebrae gradually developed a wedge deformity. Compressive overload reduced specimen height by 2.24 mm (STD 0.77 mm), and increased vertebral body creep by 800 % (anteriorly), 1,000 % (centrally) and 600 % (posteriorly). In 34 vertebrae with complete before-and-after data, anterior wedging occurring during the 1st creep test averaged 0.07° (STD 0.17°), and in the 2nd test (after minor damage) it averaged 0.79° (STD 1.03°). The increase was highly significant (P < 0.001). Vertebral body wedging during the 2nd creep test was proportional to the severity of damage, as quantified by specimen height loss during the overload event.”

“Mechanical experiments on small bone samples have reported residual deformation after [time-dependent] loading”

Analysis of creep strain during tensile fatigue of cortical bone

“Fatigue tests on 31 bone samples from four individuals showed strong correlations between creep strain rate and both stress and “normalised stress” (σ/E) during tensile fatigue testing (0–T)”

Bone creep-fatigue damage accumulation

“Bone displayed poor creep-fracture properties in both tension and compression. The fracture surfaces of the tensile creep specimens are distinctly different than those of the compressive specimens. The results suggest that tensile cyclic loading creates primarily time-dependent damage and compressive cyclic loading creates primarily cycle-dependent damage.”

Below I will submit evidence of LSJL.  It is not perfect proof but with the resources available it is not possible to generate perfect proof.

However, I will submit the following facts as evidence that there is a very strong possibility that LSJL works.

The basis on whether this is proof of LSJL depends on the answers to the following questions:

• What is the probability that every bone shaft on my left side of the body is longer than the right except for the one metacarpal which I performed LSJL?
• What is the probability that my LSJL loaded finger is longer likely due to lengthening of the metacarpal when everything on my left side is longer(can provide additional evidence of my left side being longer if needed)?

Is this not reasonable proof that LSJL works?

 

So the current hypothesis is that LSJL lengthened my right index finger metacarpal.  The right index finger metacarpal is about 1% longer than the left and since my left bones are almost universally longer than my right bones(at least for all the bones that I have identified) that probably means about a 2% growth(with 1% being a correction of the discrepency).  The remaining bones of the index finger may have grown as well but not beyond the initial discrepency.

Here are my two hand images.  If I could proof that the fourth and fifth metacarpals were longer on my left side on my right that would provide evidence that the fact the index finger metacarpal is longer on my right side is an outlier and is due to loading from LSJL.  The middle finger is not taking into account because it is close to where I loaded with LSJL so there might be some byproduct lengthening of the middle finger.

Here’s a labeling of the bones of the hand.  It would be easy to measure if it was like but the bones are not that organized.

Here’s a labeling of the bones on an actual skeleton.  You can see how the hamate mucks up with an accurate measurement.

 

From these images you can see how hard it is to get an accurate measurement of the 4th and 5th metacarpal.  The shaft of the fourth metacarpal is definitely longer on the left side and eyeballing the shaft of the the 5th metacarpal the left bone looks like a little bit longer.  In terms on the exact beginning and end of the bone it is hard to tell because of the hamate.

Here’s the left and right index finger:

 

The shaft of the right bone looks longer in addition to the overall bone being longer.

I submit that the fact that the fourth and fifth metacarpal all have the left shaft as longer than the right like all the other bones I have compared with the exception of the right and left metacarpals of the index finger of LSJL induced lengthening.

Update Nov 5,2014: Some people have commented that I am now monetizing the website. The negative reaction is a little surprising. The real reason I am putting everything in this book is because I am afraid of the possibility that all this knowledge which would be very helpful to humanity could be lost if something happened to me or something happened to the website. If hope the regular readers remember what happened to all that knowledge that was accumulated on the now dead GrowTallForum.com discussion boards. 5-6 years worth of information and ideas completely disappeared in 1 day after the admin decided to stop pushing forth with the endeavor. 

Every time I get on an airplane and feel turbulence, I start to wonder what I have contributed to the world. How would I be remembered if I went down with the airplane? Did I make a positive change?

Maybe the book I plan to write is a way for me to leave  something behind for the next generation of researchers, in case I suffer a horrible accident. This website has recently gone through at least 2 website technical problems, shutting down the website. I have come to realize that almost everything that is on the internet is just not on stable ground. At least if the information I will combine together is in PDF format and distributed to thousands of people around the world, the information would survive.

If the book was in real paperback or hardcover form, it could survive even the apocalypse, since the information and research I have gathered in the last 2 years will always be available.

I am currently working on writing a book that summarizes EVERYTHING that is on this website. All the important things will be added, and the extraneous information will not be. I will mention all the research and work that has been attempted in the last 15 years, from Sky, to Tyler, to Hakker, to Tim, and others who have tried to help out.

That is why I will not be posting on this website for at least another 4-6 months.

In addition, I have to focus on two other different businesses which are my primary sources of income.

• Most of my time in the day is devoted to my companies and earning money, and keeping fit.
• Most of my time at night will be devoted to finishing this book, as well as caring for my family members.

When the book is finally finished, probably in 2016, it will be released to the world, and this website will be transformed into something completely different.

I have decided to use the Natural Height Growth as one of the brand names under my primary umbrella corporation, and treat this website as a real asset. I will be coming back to make good on my promise to push the research much further.

This website will keep on going, and I will try to clean things up, and change dead links, and similar maintenance stuff now.

Anything new that comes out in the next few months will be from Tyler.

 Mimicking the Biochemical and Mechanical Extracellular Environment of the Endochondral Ossification Process to Enhance the In Vitro Mineralization Potential of Human Mesenchymal Stem Cells.

” Chondrogenesis and mechanical stimulation of the cartilage template are essential for bone formation through the endochondral ossification process in vivo. Recent studies have demonstrated that in vitro regeneration strategies that mimic these aspects separately, either chondrogenesis or mechanical stimulation, can promote mineralization to a certain extent both in vitro and in vivo. However, to date no study has sought to incorporate both the formation of the cartilage template and the application of mechanical stimulation simultaneously to induce osteogenesis. In this study, we test the hypothesis that mimicking both the biochemical and mechanical extracellular environment arising during endochondral ossification can enhance the in vitro mineralization potential of human mesenchymal stem cells (hMSCs). hMSC aggregates were cultured for 21 days under the following culture conditions; (1) Growth Medium – hydrostatic pressure (HP), (2) Chondrogenic Priming-HP, (3) Growth Medium + HP, and (4) Chondrogenic Priming +HP. Each group was then further cultured for another 21 days in the presence of osteogenic growth factors without HP. Biochemical (DNA, sulfate glycosaminoglycan, hydroxyproline, alkaline phosphatase activity, and calcium), histological (Alcian Blue and Alizarin Red), and immunohistological (Col I, II, and X, and BSP-2) analyses were conducted to investigate chondrogenic and osteogenic differentiation at various time points (14, 21, 35, and 42 days). Our results showed the application of HP-induced chondrogenesis similar to that of chondrogenic priming, but interestingly, there was a reduction in hypertrophy markers (collagen type X) by applying HP alone versus chondrogenic priming alone. Moreover, the results showed that both chondrogenic priming and HP in tandem during the priming period, followed by culture in osteogenic medium, accelerated the osteogenic potential of hMSCs.”

“application of hydrostatic pressure (0.1 MPa – 10 MPa) to human bone marrow stem cells aggregates  or those seeded on a collagen or agarose scaffold can significantly  enhance expression of chondrogenic markers (aggrecan, SOX‐9).  The highest amount of matrix deposition was found when a pressure of 10 MPa was applied for a  minimum of 5 days”

” the  application of HP without any external growth factors resulted in reduced hypertrophy,  whilst allowing for chondrogenesis, however once the HP was removed and the cells were  exposed to osteogenic growth factors the cells began to produce hypertrophic markers but  at a much slower rate than those exposed to chondrogenic growth factors alone”

In this study scientists are able to create growth plate-like chondrocytes from embryonic stem cells with a specific set of gene inductions.

Small molecule-directed specification of sclerotome-like chondroprogenitors and induction of a somitic chondrogenesis program from embryonic stem cells.

“Pluripotent embryonic stem cells (ESCs) generate rostral paraxial mesoderm-like progeny in 5-6 days of differentiation induced by Wnt3a and Noggin (Nog). canonical Wnt signaling introduced either by forced expression of activated β-catenin, or the small-molecule inhibitor of Gsk3, CHIR99021, satisfied the need for Wnt3a signaling, and that the small-molecule inhibitor of BMP type I receptors, LDN193189, was able to replace Nog{so abnormal methods are able to replicate the bodies processes}. Mesodermal progeny generated using such small molecules were chondrogenic in vitro, and expressed trunk paraxial mesoderm markers such as Tcf15 and Meox1, and somite markers such as Uncx, but failed to express sclerotome markers such as Pax1. Induction of the osteochondrogenically committed sclerotome from somite requires sonic hedgehog and Nog. Consistently, Pax1 and Bapx1 expression was induced when the isolated paraxial mesodermal progeny were treated with SAG1 (a hedgehog receptor agonist) and LDN193189, then Sox9 expression was induced, leading to cartilaginous nodules and particles in the presence of BMP, indicative of chondrogenesis via sclerotome specification. By contrast, treatment with TGFβ also supported chondrogenesis and stimulated Sox9 expression, but failed to induce the expression of Pax1{Pax1 is upregulated by LSJL} and Bapx1. On ectopic transplantation to immunocompromised mice, the cartilage particles developed under either condition became similarly mineralized and formed pieces of bone with marrow. Thus, the use of small molecules led to the effective generation from ESCs of paraxial mesodermal progeny, and to their further differentiation in vitro through sclerotome specification into growth plate-like chondrocytes, a mechanism resembling in vivo somitic chondrogenesis that is not recapitulated with TGFβ. ”

“The osteochondro-progenitors that develop during embryogenesis are limb bud mesenchyme (derived from lateral plate mesoderm) responsible for limb bone and cartilage generation, sclerotome (from somite/rostral paraxial mesoderm) responsible for rib, vertebral joint, intervertebral disc and vertebral body formation, and ectomesenchyme (from cranial neural crest) responsible for craniofacial bone and cartilage generation.”

“The Flk1−Pdgfrα+ rostral paraxial mesoderm from ESCs consistently show chondrogenic activity in vitro ”

“SAG+LDN (PSL) stimulation during the first 6 days of micromass culture was crucial for inducing Pax1 and Bapx1 expression from the isolated E-cadherin−Flk1−Pdgfrα+ rostral paraxial mesoderm, as was the Shh+Nog stimulation”

“BMP signaling counteracts Shh+Nog and inhibits sclerotome induction”