This will be another one of those posts which a real breakthrough is made at least in my own research.

What I propose may be the first real way to increase height in physically mature adults in an almost proportional way. The evidence that has been mounting for this idea has been increasing for a long time and this will be the culmination of around 6 months of research.

The growth factor I am proposing now is that of the Growth Differentiation Factor 5. So far I have written a lot about this compound but recent research and development has pushed me over the fence on this compound and it’s possible affect on skeletal development. 

The study or evidence that really pushed this protein to the top of the most viable and feasible growth factors to use for even height increase in physically mature adults was a study I found when I was doing research for another post, “A Detailed Study And Analysis On Growth Differentiation Factors GDFs Which Influence Growth And Height“. From the paper “Mechanisms of GDF-5 action during skeletal development” I would find this amazing statement in the abstract.

“To investigate how GDF-5 controls skeletogenesis, we overexpressed GDF-5 during chick limb development using the retrovirus, RCASBP. This resulted in up to a 37.5% increase in length of the skeletal elements, which was predominantly due to an increase in the number of chondrocytes. By injecting virus at different stages of development, we show that GDF-5 can increase both the size of the early cartilage condensation and the later developing skeletal element. Using in vitro micromass cultures as a model system to study the early steps of chondrogenesis, we show that GDF-5 increases chondrogenesis in a dose-dependent manner.

We did not detect changes in proliferation. However, cell suspension cultures showed that GDF-5 might act at these stages by increasing cell adhesion, a critical determinant of early chondrogenesis. In contrast, pulse labelling experiments of GDF-5-infected limbs showed that at later stages of skeletal development GDF-5 can increase proliferation of chondrocytes. Thus, here we show two mechanisms of how GDF-5 may control different stages of skeletogenesis. Finally, our data show that levels of GDF-5 expression/activity are important in controlling the size of skeletal elements and provides a possible explanation for the variation in the severity of skeletal defects resulting from mutations in GDF-5.”

This shows the amazing affect the GDF can have on skeletal development. When I decided to go back into this website’s old records of posts, I found even more evidence that this compound was something I had researched before which I had stated had amazing potential. Back in October I had posted the article “Is Growth Differentiator Factor 5 GDF5 Gene The Most Influential Gene Towards Height?” In that post I had cited an article found from ScienceDaily.com and highlighted this statement found from it…

“The variants most strongly associated with height lie in a region of the human genome thought to influence expression of a gene for growth differentiation factor 5, called GDF5, which is a protein involved in the development of cartilage in the legs and other long bones.”

More evidence for the GDF-5 is found from the paper “When evolution hurts: height, arthritis risk, and the regulatory architecture of GDF5 function” which state that the GDF- controls epiphyseal chondrocyte maturation!! Remember that we also remember that the GDFs have the ability to control the direction of the differentiation, even reversing the differentiation process. The next phrase I would like to quote from the same abstract is…

“Recent studies have shown that high frequency genetic variants in GDF5 are significantly associated with both stature…”

From the website of the Broad Institute an article entitled “Genes linked to height no longer in short supply” they state that besides the better known HMGA2 gene, the GDF-5 gene may be the 2nd most influential gene that researchers have fonud so far which affects height. From another study “In vivo effects of recombinant human growth and differentiation factor 5 on the intervertebral disc“ the researchers only used just 1 injection of the GDF-5 on the degenerated intervertebral disk of lab rabbits. They conclude with…

“The study provided encouraging preliminary evidence that a single injection of GDF-5 induced recovery of disc height in the IVDs of rabbits with degenerative changes previously induced by annular needle puncture. Stimulation of the anabolic cascade by rhGDF-5 could therefore prove useful as a therapeutic approach to delay the progression of disc degeneration or to promote the repair of the degenerating human IVD”

It would seem that Tyler from HeightQuest.com has already had the same ideas and thoughts about the possibilities of using the GDF-5 to gain height from regenerating intervertebral disk space. The post he wrote about is “Increase disc height with GDF-5 and BMP-7” back in 2010. It would seem that even the most established medical professional all agree with us on this idea. From Google Books (or Google Scholar) I would find reference to the idea of using either or both the GDF-5 and the BMP-7 (aka OP-1) in increasing disk width/height at least for a extended temporary amount of time. The book is “The Lumbar Intervertebral Disc by Frank M. Phillips,Carl Lauryssen”, page 167. I myself have also written about the phenomena of using OP-1/BMP-7 for degenerated disk regeneration in the old post “Osteogenic Protein 1 OP-1 Or Bone Morphogenetic Protein 7 BMP-7 Can Increase Intervertebral Disk Height (Important)”

Even more evidence for the chondrogenic ability of GDF-5 comes from the study “Human Mesenchymal Stem Cells Induced by Growth Differentiation Factor 5: An Improved Self-Assembly Tissue Engineering Method for Cartilage Repair” . We see that the GDF-5 injected in mesenchymal stem cells cultures cause the right type of differentiation. From another source, this time a Ph.D Thesis Candidate named Bernhard Appel of the University of Rogensburg entitled “Cartilage Tissue Engineering: Controlled Release of Growth Factors. Effects of GDF-5, Sexual Steroid Hormons and Oxygen” he looked at the effect of using the GDF-5 and insulin in combination to increase the number of chondrocytes. From page 57-74, entitled “Synergistic effects of growth and development factor-5 (GDF-5) and insulin on primary and expanded chondrocytes in a 3-D environment” the GDF-5 and Insulin in synergy increase all the primary elements one would find in cartilage : extracellular matrix (ECM) composition, i.e., glycosaminoglycan, and collagen content.

Proposed Theory On Height Increase:

What I propose from all the research and studies we have found and my own guesses (yes, this theory is a big guess) is that if we just increase the GDF-5 expression in even physically mature adults we would find that we can gain increased height, but especially in the synovial joint areas. One source did say that the GDF-5 is found also along the surface of articular cartilage. If the GDF-5 increased in expression, then I would guess that the overall human height qoulc increase by at least a few inches just from cartilage thickening. As a supplement, we can take the Chondroitin Sulfate, Heparan Sulfate, and the Hyaluronic Acid which go into the extracellular matrix of cartilage. At this point, the GDF-5 is as important as the PTHrP , BMP-7, and the Chondromodulin Type-1 that I have seen so far. They are the top, most likely contenders in getting any real height increase in adulthood.

The only thing that really needs to be worked out is how we can increase the process of the rate of bone mineral resorption in the blood. This could obviously be as simple as tilting the PTH/PTHrP feedback loop on the Calcium and Vitamin D content in the blood stream, but it might be more complicated than previously believed.

This article was written 80 years ago so it is very old but I wanted to try to take some idea or clue from it since the results we find from it are so unique and strange. This paper was cited by the study which I have looked at extensively ““A PROCEDURE FOR STIMULATION OF LONGITUDINAL GROWTH OF BONE, AN EXPERIMENTAL STUDY“. The experiment is entitled “SURGICAL STIMULATION OF BONE GROWTH BY A NEW PROCEDURE – PRELIMINARY REPORT” by ALBERT B. FERGUSON, M.D.

An clip of excerpt of the study is below.

I think I need to resolve another common quoted fact or anecdote that so many other people who sell height increase products like to talk about. It has to do with the idea that you can see that baseball pitchers and other athletes who use their arm so much and stretch their arm through constant throwing develop longer arms and also longer fingers.

The argument obviously is that if you can find that adult baseball pitchers do have longer arms than their non-dominant, non pitching arm, then you can possibly increase your height through exercise and routine tensile bone stretching for lengthening as well.

Well today I am going to try to see whether the idea that is so commonly quoted is true or not. I would like to cite three studies I have found recently.

1. Analysis of the pitching arm of the professional baseball pitcher. – Author: King J, Brelsford HJ, Tullos HS. (other source)

2. Humeral hypertrophy in response to exercise – Author: HH Jones, JD Priest, WC Hayes, CC Tichenor and DA Nagel

3. Stimulation of Bone Growth Through Sports, A Radiologic Investigation of the Upper Extremities in Professional Tennis Players – Author: Hartmut Krahl, et. al.

Analysis & Interpretation:

The first study had no abstract and it would have cost money to get the study so I opted not to buy the study but went to another study.

For the 2nd study, we find that the study was on tennis players, not baseball pitchers. The study was done on both tennis players males and females. The men were on average 27 years old and the females were 24 years old. The average number of years the men have been playing was 18 years while the females were 14 years. The study was only on the humerus, not the ulna or the metacarpals. Roentgenograms were used to study the bone changes. The results showed that the humerus of the tennis players all showed hypertrophy, but the increase in size was in width. The thickness of the upper arm bone increased and the intermedullary bone cavity shrunk from the cortical bone increasing in thickness inward. For all 4 parameters used in analysis and recording, the posterior side, anterior side, the medial side, and the lateral side, which basically means that all 4 sides of the cardinal directions were measured.

What is nice is that the 2nd study did cite the first study I have listed and showed the King and associates found that the humerus of the baseball pitchers of the dominant arm were thicker than the arm that was not primarily used for pitching. Others things the 2nd study reveals is that other researcher found that the bone density in athletes for their distal femoral ends was higher than average people .Antoher group of researchers would find that the bone density in cross country runners was also higher with more trabecular bone. The researchers in the 2nd study would conclude by stating that exercise does induce bone hypertrophy.

As for the 3rd study, I post the abstract below…

Abstract

This contribution addresses the following questions: Does unilateral sports-specific strain affect the skeletal system of the athlete? Specifically, can any differences be found in longitudinal growth of the bones of the fore arm and hand in professional tennis players between the stroke arm and the contralateral arm? An investi gation was conducted involving 20 high-ranking profes sional tennis players (12 male and eight female players) between 13 and 26 years of age as well as 12 controls of the same age range. The radiologic examinations of the bones of the forearm and hand yielded an increase in density of bone substance and bone diameter as well as length in the stroke arm as compared with the contralateral arm. Whereas the first results confirm previous findings, the stimulation of longitudinal growth has never been reported. This change in bone structure and size can be attributed to two factors: mechanical stimulation and hyperemia of the constantly strained extremity. It may thus be regarded as a biopositive adaptation process.

Me: What we are finding is that the researchers are now looking at the longitudinal/length difference in the athletes, this time being tennis players. Full article is not available without me paying for it so I was not able to find the full study details. The key thing I can reveal from the study is that in the abstract, the sentence…”The radiologic examinations of the bones of the forearm and hand yielded an increase in density of bone substance and bone diameter as well as length in the stroke arm as compared with the contralateral arm.”

It does seem that at least from this 3rd study, the researchers have found that the forearm of the stroking arm to be longer than the contralateral arm.

This shows that the results indicate that there is indeed a bone density and bone thickness increase, but only again anecdotal evidence that the arm with more exercise and loading inducement would cause hypertrophy. So I would try to find 3 more studies to see what the evidence is…

1. Dimensions and estimated mechanical characteristics of the humerus after long-term tennis loading. – Author: Haapasalo H, Sievanen H, Kannus P, Heinonen A, Oja P, Vuori I

2. Effect of long-term impact-loading on mass, size, and estimated strength of humerus and radius of female racquet-sports players: a peripheral quantitative computed tomography study between young and old starters and controls. – Author: Kontulainen S, Sievänen H, Kannus P, Pasanen M, Vuori I.

3. Exercise-induced bone gain is due to enlargement in bone size without a change in volumetric bone density: a peripheral quantitative computed tomography study of the upper arms of male tennis players. – Author: Haapasalo H, Kontulainen S, Sievänen H, Kannus P, Järvinen M, Vuori I.

Analysis & Interpretation: 

From the first study, the researchers did indeed take into account the length of the humerus into measurement. What they did find was that there was indeed a small, but still noticeable increase in player’s humerus length. Quoted…”The playing-to-nonplaying or dominant-to-nondominant arm differences in humeral length ranged from +0.2 to +1.4%, the difference being significant in young male players (+1.4%), young female controls (+1.1%), and older female players (+0.7%). When comparing players’ relative side-to-side length differences with those of the controls, no significant differences were found.” They conclude with ” In conclusion, long-term intensive tennis playing, especially if started in childhood or adolescence, clearly increases thehumeral BMC, BMD, and CWT but seems to have only a minor effect on the width of this particular bone.” and “In older players, the relative side-to-side differences are at the same level or only slightly larger than those in their age-matched controls. This suggests that even intense physical loading of a mature bone is only marginally better in increasing the bone mass, bone density, and CWT of the target bone than the normal daily use of the dominant extremity.”

This shows with some real evidence that at least for young males that probably still had their growth plates, intense playing of tennis might have caused a slight increase in bone length. Even in older females, there was still a little bit of humeral difference between the playing arm and the control, but only at around 0.7%.

For the 2nd study, the measure variables for also young female tennis players on their humerus are

• Bone mineral content (BMC)
• Total cross-sectional area (TotA) of bone
• Cross-sectional area of the marrow cavity (CavA) and that of the cortical bone (CoA)
• Cortical wall thickness (CWT)
• Volumetric density of the cortical bone (CoD) and trabecular bone (TrD),
• Torsional bone strength index (BSIt) for the shaft,
• Compressional bone strength index (BSIc) for the bone end

The length of the bone was never analyzed but the thickness of the cortical bone was again noticed. The explanation was that “the structural adaptation of the humeral shaft to long-term loading seemed to be achieved through periosteal enlargement of the bone cortex“.

For the 3rd study, the researchers again found that the cortical wall increase in thickness for the males but that the overall bone density didn’t seem to increasem much. The volume of the bone did increase but the increase was in width from the inside where the inter-medullary wall cavity decreased

Conclusion:

It would seem that from the 6 studies I have looked at, 2 of the only studies which did look at humerus length did not a small different between the dominantly used arm and the non-dominant arm. Of course both of the studies were done on young developing tennis players, not baseball pitchers.

I would be more willing to guess that the throwing arm of the baseball pitcher may be longer but the most likely reason is that the longer arm could be from the shoulder joint or elbow joint being progressively moved and subjected to pulls. What I have found is that the baseball pitcher has a very high level of suffering elbow injuries.

What is absolutely clear is that the only way to even have a change to see a length difference between the two arms is for the athletes to start very early in life and age in the sport to have any chance of body modification. This is assuming and guessing that any arm length differences is from the use of the arm with the growth plate cartilage still in there. There is a small chance that frequent intense throwing of the base might indeed exert some effect on the thickness of the growth plates in the arms when the male athletes is still developing

What other height increase researchers like Sky tried to do would not have worked with their knee lunges and kicking because they were probably too old and had no cartilage for them to stretch out.

 

I have written many posts for the website but this post I feel may be one of the most important and possible breakthrough posts and insights so far in the research. 

In the last two recent posts I had been focused on this experiment done entitled “A PROCEDURE FOR STIMULATION OF LONGITUDINAL GROWTH OF BONE AN EXPERIMENTAL STUDY” which showed that apparently it is possible to increase height by stripping the periosteum in the region of the long bones close to the growth plates in people who still had their growth plates.

In the last two posts I had not been able to figure out any possible theoretical justification on why the experimental idea  would work until only a few minutes ago. The insight I reached is slightly startling and comes in a form of almost epiphany which makes me wonder whether I could be wrong in my thoughts or not. What I plan to  do now is get Minigolf’s/Tyler’s own thoughts on my new proposed explanation on why his idea on Lateral Synovial Joint Loading has eve been abel to even have any results.

In many posts before I had debated on the feasibility and effectiveness of the idea proposed by Tyler from HeightQuest.com. In some posts I had argued that the idea would not be effective with “Evidence That The LSJL Method Or Loading Is Ineffective In Post-Pubertal Adult Humans? (Important)” and “Why LSJL Might Not Work, An Explanation Using Bone Mechanics And Bone Bridge Studies“ while in other posts I had argued that it had potential of been effective with “New Proposed Height Increase Method Using LSJL Device WIth Chondrocyte Implants And Growth Factor Injections“ and “Growth Plate Physeal Longitudinal Growth May Actually Overcome Bone Bridges, New Evidence Showing LSJL May Work”

This post will be a completely new proposed alternative idea and explanation on why the LSJL method has been only sporadically effective and seem to only work for a small increment in height increase. I have always been in the school of scientists who believe that science must always be proved through real experimental facts and results. That is why I have always felt that ideas and theories that are too theoretical (but still logically consistent) like the string theory or M-Theory one finds in theoretical physicists attempt to reconcile the differing results of quantum theory and general relativity is not a good path to take.

I personally believe that for a decent theory to work, it must first be able to explain the data we find in our experiments. This theory I am proposing which I am excited in today is something which required the knowledge of almost all of the bone parts to take come up with.

It started from the article I have been looking at recently. The idea of periosteum removal for longtitudinal growth increase was unique but it got me wondering. Here is the proposed hypothesis I have been thinking about…

The LSJL method does work because it manages to induce incisions/fractures/ breaks into the long bone’s surface, past the periosteum causing an entire layer of the long bone to be lifted, thus turning the inner cambium proliferating layer of the periosteum to increase in size, thus adding the neccesary surface thickness increase ,thus height increase.

Let’s look at this hypothesis step by step.

1. You take some thing like a clamp or dumbbell and use a dynamic, alternating hitting/ loading motion on it.

2. On the rare clamp session, one does manage to clamp at just the right magnitude and angle to cause a clear crack in the outer bone layer.

3. Remember that the bone has on the outside a layer known as the periosteum. However, what is not well known is that the periosteum is actually a 2 layer part. There is the outer layer which is hard, protective, and non-proliferative. The inner layer of the periosteum is what is known as the cambium layer, (like the cambium tree layer cells) where the cells are proliferative.

4. If we read the Wikipedia article on the perichondrium, which is the layer which protects hyaline cartilage and the growth plates before being vascularized and then going through ossification, and also read the article on the periosteum, we can see that the the outer two layer are very similar. From the article on the periosteum, we would learn that the perichondrium would actually turn into the periosteum from vascularization. This could suggest that the inner layer of the adult mature human with long bones still would have a type of cell which can differentiate.

Note: At this point I have not done the research but I would guess that the cells we find in the inner layer of the adult human’s long bone of the periosteum is a type of stem cell, or at least a progenitor cell which has not been differentiated into bone cells, specifically the osteocytes/osteoblasts yet.

Update 2/5/2013: From the Wikipedia article on the periosteum, the issue for Note has been resolved. From the article, it specifically states…

The fibrous (inner) layer (of the periosteum) contains fibroblasts, while the cambium layer contains progenitor cells that develop into osteoblasts. These osteoblasts are responsible for increasing the width of a long bone and the overall size of the other bone types. After a bone fracture the progenitor cells develop into osteoblasts and chondroblasts, which are essential to the healing process.

5. From the article we had been looking at, the theory to explain why periosteum stripping would work is that the stripping caused the inner periosteum layer to be pushed out of the outer layer of the periosteum, giving it enough flexibility to differentiate into chondrocytes causing the entire upper layer or area of the long bone to be finally allowed to be pushed up.

6. I had always had a reservation over the LSJL idea because the theory is that chondrocytes induced inside the epiphysis has enough force from it’s hypertrphy to push in all 3 dimensions of space past the cortical bone holding it together. Remember that the cortical bone is as strong as steel tensile strength. This issue was raised in the post “Why LSJL Might Not Work, An Explanation Using Bone Mechanics And Bone Bridge Studies“. The problem was always that the chondrocytes induced can not push past the bones, especially since the bones are holding the chondrocytes inside intact in all 3 dimensions.

Note: This main issue over the fact that the chondrocytes have no direction to push in was rasised in the post “How Lateral Synovial Joint Loading Works To Increase Height From Non-Distraction: FAQs and Concerns Answered (Guest Post)”

The counter-arguement would be that in growing children, the chondrocytes does have to push upwards against the gravitionaly force and weight of the upper body of the person to increase the height. So any chondrocyte accumulation into cartilage would have to be strong, even if it has only 1 dimension or degree of freedom it can move and increase in size in, ie. longitudinally.

7. So we can say that the LSJL loading on certain people who have working inner periosteum cambium progenitor cells caused a fracture deep enough to allow the cells to be not fully, completely enclosed in by the hard bones. This means that the induced chondrocytes finally have 1 degree of freedom they can increase again. The 1 degree of freedom, with the contraint of not allowing the chondrocytes to push the long bones longitudinally to increase in length will finally be removed, means that the bones will have cells turned to chondrocytes can finally increase again.

Note: Just this last month I would write two critical posts “Local Growth Factor Injections In Aged Periosteum Result In Increased Cambium Proliferation And Cartilage Formation (Breakthrough)“ and “Increase Height And Grow Taller Using Local Subperiosteal Injection Of Growth Factors IGF-1 And TGF-Beta Percutaneously.” looking at the possible way of using the periosteum inner cells as a possible new alternative growth plate source. The study found yesterday shows that the periosteum inner cambium cells may indeed be used as a possible way to increase the long bone longitudinally.

8. Tyler would show from many protein pathway diagrams looking as multiple gene up-regulations that the technique of dynamically loading bone will cause many of the genes that cause chondrogenesis to be up-regulated. I don’t disagree with him on this fact, and at this point I do believe that the LSJL does cause chondrogenesis in some of the progenitor cells. However, I think he may be mistaken on which cells the loading actually have been having an effect on. Instead of the MSCs we have been thinking has been differentiating from the marrow inside the epiphysis, I propose in this post that the actual cells that are been turned into chondrocytes are actually the inner periosteum cells, the cambium cells. The loading like the stripping of the periosteum, causes the entire inner layer of the cambium layer to be able to push up the top layer of the bone easily,

9. This reasoning and thinking would completely resolve why it is that people like Tyler who has been doing it has seen results, but the results stop after say 3-4 cms. You have hit the bone for too much in the same area of the long bone. From too much hitting, the inner periosteum has become vascularized and completely turned to osteoblasts and calcified. From my own observation of the bones I have shown in video been disected which I have uploaded to YouTube HERE, I can say with complete confidence that even after just 1 day in normal room temperature with normal moisture, the articular cartilage that is exposed to air become extremely hardened to the level of bone-like very quickly. I would guess the process or action which caused this is diffusion of water or air molecules causing the cartilage to loose it’s elastic structure and properties.

10. If Tyler and other people who practice it has been getting results, they have essentially destroyed certain areas of the epiphysis in the periosteum which causes appositonal growth (width wise) for physically mature humans. They have managed to get results, but the results are only a 1 time thing. While it is believed that the bone from remodeling has become desensitized (from piezoelectric sensitivities)  to the loading and we need to increase the loading to get the bone to work again, my thinking at this point is that the loading can be done only once, and cause only a certain amount of real height increase.

The issue with this type of post is that only a few real serious height increase researchers would be able to understand that implications of this post but I feel that this post may be one of those which will dramatically change the direction of this website and the direction of the research we are doing.

Implications and how to solve this issue & Increase height:

What I propose now is that instead of only a blunt instrument to hit or rub the epiphysis like Tyler proposed in LSJL, it would be smarter to instead use 2 types of equipment in succession.

• First, use a rather sharp, edge instrument to cut/fracture the epiphysis on the side edges, creating effectively a circle of microfractures (aka a closed cloop of indents on the long bone ends which is mostly bone, lacking any muscle tissue tissue). The idea of microfractures is something many former height increase researchers have looked at and does have a high possibility to work. It doesn’t have to be very large or strong, just a few light tapping on the epiphysis close to the closed growth plate with a wedge and hammer like the picture on the right (but not that deep into the bone.

• Note: Remember that for the distraction osteogenesis of the ilizarov external method or limb lengthening method to happen, the surgeons actually do exactly the same thing. For the initial distraction to hammer, they use a chisel/wedge and hammer to create just a small , unifrom fracture. For our purposes, we do something every similar, but a weaker one creating smaller fractures.

• I would talk about the need to create a close path around the long bone in my recent post “A Proposed Height Increase Method Using Microfracture Surgery Techniques With Fibrocartilage Formation” and that is what I propose again. Find a small wedge with a long, slightly sharp edge and hammer and lightly tap at the surface of the distal tibial epiphysis to induce the microfractures needed around the entire long bone end.

• Now use the dynamic loading frequency and amount of size we have been previously doing for our LSJL. Follow the posts “Lateral Synovial Joint Loading Explained In Simple English” and “A Simple Step By Step Guide For Lateral Synovial Joint Loading“ or go to the HeightQuest.com website or use the LSJL forums or use the guide copied to GrowTallInfo.com for another guide on how to do the method/routine.

• The addition of the tapping would make the LSJL far more effective in getting results. After one sees results, the location of the tapping will have to be moved, further and further up (distally) up the distal tibial end. This is because after the induced microfracture of the periosteum is made, that region will become ossified into bone eventually, and the region will be dead for any chondrogenesis. To gain more height, the tapping will have to occur where there is still some cambium progenitor cells left, which means tapping closer to the top of the tibia, creating another layer and chance for the periosteum to increase in thickness.

In the last post I would reveal that I had found a study done years ago where a group of researchers found that if you strip the periosteum area close to (but not on) the epiphyseal cartilage area, there was a noticeable increase in longitudinal growth of the bone.

What I would suggest then in this post is an idea for increasing height for people who are still growing which I would say is very simple.

What I would suggest is that the individual would try to stimulate the areas close to the growth plates in their body, near the bone area to lead to increased longitudinal growth.

If we remember the application of the LSJL method using the dumbbells, I would suggest actually something very similar. We take a large, rather blunt heavy instrument, and apply a sliding force to the region of the lower leg/tibia in the epiphysis region, which would be close to the physis (growth plate).

While the rate/frequency of the rubbing has not been determined or optimized yet, I propose that the rubbing action of say a heavy, large surfaced dumbbell would be effective enough to possibly strip some of the periosteum level cells and possibly cause some increased growth.

What I have been thinking is to use a type of chisel that one finds from woodworking like a fishtail chisel which can evenly and accurately reach a more uniform compressive load action on the bone area.

The area to rub in the knee region is right on the bone area above where the growth plate would be located. Refer to the picture to the left where the arrow is point at. We would be wanting to rub and try to get the periosteum in the bone area above it.

The action I would suggest is to go with a scrapping or up and down motion on the bone above the tibial physis but the motion should be performed across the entire bone region.

If the study “A PROCEDURE FOR STIMULATION OF LONGITUDINAL GROWTH OF BONE” done on rabbits can be translated to humans even slightly, this method for increased longitudinal growth in growing children should work.

However it might be a better idea to move away from sharp tools that might have been traditionally for woodworking purposes and go with even the hard, but large area edge of a textbook to get the same type of movement and stimulating effect. Interesting, this idea was also proposed in the Book “School Of Height” which I had briefly talked about in the previous post “The School Of Height By A.S. Palko Book Arrived, Thanks Kazlina“, but the idea was instead to rub the knee or joint regions with a certain type of material.

 

The generation of loads in excess of the osteogenic threshold by physical movement.

“stresses in bones in excess of the osteogenic threshold will stimulate bone growth; however, protocols for the generation of these stresses had not been established. Two trial movements were examined in the study: the plié and a movement requiring the subject to move a leg sequentially to 45° displaced positions – the star excursion balance test. Using inverse dynamics and an optimisation approach, the loads in the muscles crossing the hip and knee joints and the corresponding joint contact forces were calculated. It was found that the osteogenic threshold was exceeded in both these trials identifying them as suitable exercises in the maintenance of bone health. In the order of increasing bone load at the hip, and hence increasing bone growth stimulation, are the following demi plié, star excursion balance test with maximum reach criterion, grande plié and star excursion balance test with maximum speed criterion. In the order of increasing bone load at the knee are demi plié, grande plié, star excursion balance test with maximum reach criterion and star excursion balance test with maximum speed criterion. However, due to the high loads encountered, these exercises are not recommended for subjects with advanced osteoporosis although the boundary between therapeutic bone loading leading to increase in bone mineral density and loads capable of causing fracture is unclear.”

“BMD fracture thresholds:110 mg/cm^3 in the distal femur and 70 mg/cm^3 in the proximal tibia”

“threshold of stress at which bone growth is stimulated corresponding to a stress of approximately 20MPa, which for a bone’s Young’s modulus of 20 GPa is 1000me.”

“As the lever arm at which the muscles act at the joint is typically relatively small compared to the segment length to which they are attached, the loads in the muscles and hence the compressive forces in the joint and bone can be very large”

“during a quasi-static rise from a deep squat, the tibio-femoral joint forces were 5.5–6.6 times the body weight.”

“a hip joint contact force of 2.38 times body weight occurred while walking at 4 km/h, 2.51 times body weight during stair ascent and 2.60 times body weight during stair descent.”

The star excursiion balance test generated a force around 6 times bodyweight in the knee.