Tag Archives: LSJL

Huge news someone other than Yokota/Zhang use a joint loading device

This is huge that someone else is doing a LSJL like device it means that something could be close to being put into practice.

Micromechanical Loading Studies in Ex Vivo Cultured Embryonic Rat Bones Enabled by a Newly Developed Portable Loading Device

“Mechanical loading has been described as having the potential to affect bone growth{we want it to affect bone growth post skeletal maturity of couse}. In order to experimentally study the potential clinical applications of mechanical loading as a novel treatment to locally modulate bone growth, there is a need to develop a portable mechanical loading device enabling studies in small bones. Existing devices are bulky and challenging to transfer within and between laboratories and animal facilities, and they do not offer user-friendly mechanical testing across both ex vivo cultured small bones and in vivo animal models. To address this, we developed a portable loading device comprised of a linear actuator fixed within a stainless-steel frame equipped with suitable structures and interfaces. The actuator, along with the supplied control system, can achieve high-precision force control within the desired force and frequency range, allowing various load application scenarios{the potential would be to use the device to induce longitudinal bone growth on skeletally mature individuals}. To validate the functionality of this new device, proof-of-concept studies were performed in ex vivo cultured rat bones of varying sizes. First, very small fetal metatarsal bones were microdissected and exposed to 0.4 N loading applied at 0.77 Hz for 30 s. When bone lengths were measured after 5 days in culture, loaded bones had grown less than unloaded controls (p < 0.05). Next, fetal rat femur bones were periodically exposed to 0.4 N loading at 0.77 Hz while being cultured ex vivo for 12 days. Interestingly, this loading regimen had the opposite effect on bone growth, i.e., loaded femur bones grew significantly more than unloaded controls{femurs have different proportions than metarsal bones, one possibility is that femur bones shape makes it more susceptible to fluid based forces and pressure gradients, due to the femurs longer shape it is possibly more susceptible to deforming forces than metatarsals}. These findings suggest that complex relationships between longitudinal bone growth and mechanical loading can be determined using this device. We conclude that our new portable mechanical loading device allows experimental studies in small bones of varying sizes, which may facilitate further preclinical studies exploring the potential clinical applications of mechanical loading.”

“two use-cases were devised: repetitive impact loading of small force (0.05–0.5 N) at a range of 30–180 repetitions and continuous sinusoidal loading of medium force (0.5–5 N) at a frequency range of 5–20 Hz.”<-something like a massage gun does something similar of repetitive impact loading.

Above is the device used.

So unfortunately for metarsals it does look like yes the device suppressed growth. However, initially the 0.1N load enhanced growth. More studies would have to be done.

In contrast femur bones grew pretty uniformly and the difference is pretty significant. Again, I think it is possible that this could be due to the different shape of the femur bones or maybe the load was too strong for the smaller metatarsal bones.

“Its square shape securely covers the entire cartilage area on each side of the embryonic femur bone, allowing the indenter to apply mechanical loading specifically to the growth plate in a stable manner.”<-just because the growth plate was the thing that was loaded does not necessarily mean that the growth plate was solely responsible for the growth there could be effects elsewhere as well including that which induces longitudinal bone growth.

“we identified that the same load applied to bones of different dimensions has opposing effects on bone growth, suggesting that the effects of mechanical loading on growth are dependent on the magnitudes and relative dimensions of the bones.”<-so they too think that the shape of the bone has an impact on whether growth is induced or not. The fact that the shape of the bones matter also suggests that yes it is possible that not all of the growth is due to the growth plate.

“Embryonic metatarsal bones from Day 19.5 of gestation are approximately 1 mm in length, whereas femur bones are approximately 4 mm, indicating that the level of mechanical loading that stimulates or inhibits bone growth is likely dependent on bone size.”

This is the sentence where the cite Yokota/Zhang’s joint loading study: ” The device’s controller enables sinusoidal loading, which has been demonstrated to have a bone growth-promoting effect in mice “

Can Flexioss be used to to prove LSJL or Lateral Impact Loading?

Arthur Lazar is someone who has spoken about LSJL in the past on Quora. “Not really. There is 0 evidence for that. The original working experiment was performed on mice – mice growth plates never ossify. MAYBE if someone would develop a machine which can put perfect constant pressure, perfectly shaped for bone area where the pressure is supposed to be, then in theory it could work. But this is a bro-science, so it’s a big MAYBE. But as for now, using clamp, dumbelss or whatever you can use to press at bone would never work.”<-Mice growth plates don’t ossify but they become senescent which is just as bad for growth.

Here’s some more of his thoughts on LSJL: “Yes, I do work on a device for automatic long bone loading method as I believe that the standard lsjl loading (manual with clamps, weights, mpistols) is an invalid approach that lacks consistency, frequency and stability which all was provided with the original, successful experiment.”<-I don’t know what an mpistol is. I believe it is a typo. I don’t know what the original intent is.

“Thank you for your interest, but currently my team is complete and current priority of the projects puts the lsjl idea on the bottom of the list. When I am done with the prototype and IF it will have a desired affect on Flexioss structure (in the terms of force application on the structure) I will publish the design in order to expand the team and get potential investors interested.”

Here’s another set of communications someone had with him.

So the question is should we be using flexioss to try to find the best loading regime to induce the proper stimulation to induce new longitudinal bone growth. I believe personally that the best regime is some kind of lateral impact loading(I believe that tapping the epiphysis would be superior than the diaphysis now but I am trying both). Clamping has a slippage problem which impact does not have. The loads of direct lateral impact are stronger than that occur during normal physiological activities which are more axial.

Lateral impact does occur during boxing both to the hand and to the face and ribcage. Also, it occurs to the feet bones during running(but this depends on whether you are a heel or toe striker). It also happens to bones during muay thai kick boxing.

The problem is that this impact is often at irregular intervals and not targeted to specific areas of the bone such as the epiphysis. The epiphysis is where there is less cortical bone, is close to where the growth plates used to reside in skeletally mature individuals, and is close to the articular cartilage which if stimulated could potentially contribute to height growth. In muay thai you have no control over where you are kicked and if you do kick you are trying to use the strongest part of the bone.

Lateral impact has the potential in my opinion to drive the most fluid forces throughout the bone. Greater than any axial impact certainly due to the pressure gradient of the bone and the epiphysis is the weakest most porous part of the bone so impact to that area has the potential to drive fluid forces throughout the entire bone. Muscular contractions also have the ability to stimulate fluid forces throughout the bone but that is limited by muscular size and strength. Lateral impact also has the ability to gradually induce plastic deformation throughout the bone. Most plastic deformation occurs axially to shorten the bones such as in rickets/paget’s disease etc. Lateral impact loads have the potential to induce plastic deformation in a way such as to lengthen the bones.

Here is the flexioss.

So the question is can we use the flexioss to find the best way to induce lateral plastic deformation in such a way as to lengthen the bones or to induce fluid forces to either induce articular cartilage endochondral ossification or to cause denovo cartilagenous regions within the bone.

In the study Dose-dependent new bone formation by extracorporeal shock wave application on the intact femur of rabbits., they found trabecular bones heaving with cartilagenous tissue which would be huge as bone tissue is not capable of interstitial bone growth.

The manufacturers of flexioss claim that it has properties similar to that of cancellous bone so yes it can potentially be used to find the best loading regime to induce plastic deformation in such a way as to longitudinally lengthen the bone. Obviously, it can’t really be used to mimic the fluid properties of the bone.

Microcracks effect on fluid flow. Long term loading may be key for LSJL.

This study is important because it indicates that microcracks may be bad for fluid flow which stimulates bone growth but good for cartilage growth as if fluid is not flowing than it is building up pressure and pressure is more conducive to chondrogenesis. This indicates that a method to induce fluid flow such as clamping/tapping should be higher duration and more “fatigue loading” based to insure the induction of microcracks. Fatigue loading is the act of inducing bone damage not by a sudden large damage but by sustained bouts of loading over time.

Influence of interstitial bone microcracks on strain-induced fluid flow.

“microcracks act as a stimulus for bone remodelling, initiating resorption by osteoclasts and new bone formation by osteoblasts. Microcracks alter the fluid flow and convective transport through the bone tissue. [We evaluate] the strain-induced interstitial fluid velocities developing in osteons in presence of a microcrack in the interstitial bone tissue. Based on Biot theory in the low-frequency range, a poroelastic model is carried out to study the hydro-mechanical behaviour of cracked osteonal tissue. the presence of a microcrack in the interstitial osteonal tissue may drastically reduce the fluid velocity inside the neighbouring osteons{So maybe microcracks will increase hydrostatic pressure as hydrostatic pressure is the pressure exterted by a fluid at rest}. This fluid inactive zone inside osteons can cover up to 10% of their surface. Consequently, the fluid environment of bone mechano-sensitive cells is locally modified.”

“Cortical bone constitutes the outer shell of long bones. This live entity is continuously renewed by bone cells in response due to the loading generated by daily activity”

“microdamage occurring inside the osteonal volume may generate a cell-transducing mechanism based on ruptured osteocyte processes. Concomitantly, microcracks are likely to alter the fluid flow and convective transport through the bone tissue and thus modify the hydraulic vicinity of the sensitive cells”

“the drag force caused by the pericellular fibres is thought to activate the cellular biochemical response through the interactions with the cytoskeleton”

“the pressure inversely increases from its Haversian reference to reach its maximum in the interstitial tissues.”

“the presence of the microcrack strongly modifies the fluid flow velocities in the osteons located in the immediate vicinity of the damage. It may generate an “inactive zone” inside the osteon wherein the fluid velocities are relatively low and thus the osteocytes stimulation too”<-But even though fluid flow may be low hydrostatic pressure may be high which may be better for chondrogenesis.

Fatigue Loading may be important to LSJL

This paper shows that axial loading can induce an almost complete fracture line through the bone through one side to the other. But the break is on the wrong axis. If fatigue loading was induced via transverse loading (lsjl or lateral impact loading) it is very likely that the micorodamage would be along the right axis. But to induce bone fatigue in this way would likely require heavier loads than inducing sufficient hydrostatic pressure to induce chondrogenesis as the goal of increasing fluid forces in the bone is to encourage bone decay and induce differentiation of tissues that are capable of interstitial growth.

Role of Calcitonin Gene-Related Peptide in Bone Repair after Cyclic Fatigue Loading

“We used the rat ulna end-loading model to induce fatigue damage in the ulna unilaterally during cyclic loading. We postulated that CGRP would influence skeletal responses to cyclic fatigue loading. Rats were fatigue loaded and groups of rats were infused systemically with 0.9% saline, CGRP, or the receptor antagonist, CGRP8–37, for a 10 day study period. Ten days after fatigue loading, bone and serum CGRP concentrations, serum tartrate-resistant acid phosphatase 5b (TRAP5b) concentrations, and fatigue-induced skeletal responses were quantified. cyclic fatigue loading led to increased CGRP concentrations in both loaded and contralateral ulnae. Administration of CGRP8–37 was associated with increased targeted remodeling in the fatigue-loaded ulna. Administration of CGRP or CGRP8–37 both increased reparative bone formation over the study period. Plasma concentration of TRAP5b was not significantly influenced by either CGRP or CGRP8–37 administration.”

“sensory innervation of bone may have regulatory effects on skeletal responses to bone loading”

“Periosteum, endosteum, and bone tissue are all innervated by nerve fibers. This innervation exhibits plasticity in response to mechanical loading, in that a single loading event results in persistent changes in neuropeptide concentrations in both loaded and distant long bones, as well as changes in the neural circuits between limbs”

“Individual bone cells are directly connected to the nervous system via unmyelinated sensory neurons. Bone cells express a range of functional neurotransmitter receptors and transporters, including those for calcitonin gene related peptide (CGRP)”

“12 rats were fatigue loaded until 40% loss of stiffness was attained, using an initial peak strain of −3,000 µε (Fatigue group). ”

“To induce fatigue, the load applied to the ulna was incrementally increased until fatigue was initiated, as indicated by increasing displacement amplitude from a stable baseline. ”

The break extends all along the bone but is on the wrong axis.

“Increased bone blood flow precedes bone repair in response to fatigue loading, and remodeling in response to decreased mechanical loading . Systemic administration of CGRP also decreases blood pressure in a dose-dependent manner””

“”treatment with CGRP_8–37 may have increased intraosseus pressure, transcortical interstitial fluid flow, and associated bone formation””

New study shows LSJL induces Bone Deformation

Bone Deformation is change in the bone shape or structure. This deformation can be compression of various cavities, stretching of the bone, twisting, and so son. This is important as bone deformation is one way to increase hydrostatic pressure by decreasing the cavity size. Hydrostatic pressure is the pressure exerted by a fluid at rest. Compressing the bone laterally inhibits the fluids ability to move thus increasing hydrostatic pressure. If there is more fluid within a smaller space than it follows that hydrostatic pressure increases. Hydrostatic pressure has been consistently shown to induce chondrogenic differentiation. Chondrogenic tissue is the key for longitudinal bone growth as traditionally chondrogenic tissue is capable of interstitial(growth from within) whereas bone is not. Only interstitial bone growth has been shown traditionally to induce significant longitudinal bone growth but there are potentially other ways to stimulate longitudinal bone growth.

Knee loading inhibits osteoclast lineage in a mouse model of osteoarthritis.

“Osteoarthritis (OA) is a whole joint disorder that involves cartilage degradation and periarticular bone response. Changes of cartilage and subchondral bone are associated with development and activity of osteoclasts from subchondral bone{Since osteoarthritis does affect the subchondral bone that does affect our ability to say that LSJL affects bone deformation in a normal bone but there is no reason why it shouldn’t}. Knee loading promotes bone formation. Knee loading regulates subchondral bone remodeling by suppressing osteoclast development, and prevents degradation of cartilage through crosstalk of bone-cartilage in osteoarthritic mice{This “crosstalk” may stimulate chondral tissue within the bone as well}. Surgery-induced mouse model of OA was used. Two weeks application of daily dynamic knee loading significantly reduced OARSI scores and CC/TAC (calcified cartilage to total articular cartilage), but increased SBP (subchondral bone plate) and B.Ar/T.Ar (trabecular bone area to total tissue area). Bone resorption of osteoclasts from subchondral bone and the differentiation of osteoclasts from bone marrow-derived cells were completely suppressed by knee loading{Knee loading affects the differentiation of bone marrow-derived cells which is the first step in proving that it causes chondrogenic differentiation}. The osteoclast activity was positively correlated with OARSI scores and negatively correlated with SBP and B.Ar/T.Ar. Furthermore, knee loading exerted protective effects by suppressing osteoclastogenesis through Wnt signaling. Overall, osteoclast lineage is the hyper responsiveness of knee loading in osteoarthritic mice. Mechanical stimulation prevents OA-induced cartilage degeneration through crosstalk with subchondral bone. Knee loading might be a new potential therapy for osteoarthritis patients.”

“Daily dynamic knee loading was applied at 1 N, 5 Hz, 5 min/day for 2 weeks”

Compare the OA+ loading to the control bone. The subchondral bone plate looks much more dynamic. There are three bone marrow regions rather than two(bone marrow is the blue dots).

You’ll also note that loading+OA increased the ratio of calcified cartilage out of total articular cartilage(but not above statistic significance. It did not fully restore the thickness of the bone plate. Alendronate is an anti reobsorption agent. Given that the ALN and loading group is different we can say that change in subchondral bone shape is likely not related to inhibiting osteoclast activity and is something unique to the loading group.

Compare the joint capsule region of control and OA+loading group. The Joint Capsule is the region that’s not inside the bone. The cells are a lot more spread out. There’s a dense redness in the control group which is not present in the OA+Loading group

We can see that the loaded group again has distinct characteristics and we can also see the growth plate. The growth plate of the LSJL group is distinct and there does seem to be signs of cellular migration. I’ll have to blow it up.

Circled is the region of possible cell migration.

Similar signs of migration in earlier in LSJL studies(above taken from Lengthening of Mouse Hindlimbs with Joint Loading).

“the expression of Wnt3a was significantly increased by knee loading. However, the protein and mRNA levels of NFATc1, RANKL, TNF-α, and Cathepsin K were significantly suppressed by knee loading”

“Female C57BL/6 mice (~14 weeks of age)”

If you look at this image of bone marrow derived cells extracted from the loaded group and the other groups you can see that the cells are more condensed and condensation is a prerequisite for chondrogenic differentiation,

This is an image of what mesenchymal condensation looks like:

Why LSJL Could Work And What We Have Been Doing Wrong, Thank You Nixa Zizu – Big Breakthrough!

Just today a follower of the website who calls himself Nixa Zizu (who is one of our biggest supporters and contributors) uploaded information to the Natural Height Growth Facebook page which might have really cracked open the case on why it seems that LSJL might not be working so most of the people who have been doing it.

His results after just 2 weeks of doing the technique have resulted in almost half a centimeter of height gain. In my personal experience in getting accurate readings on height from using just rulers and stadiometers suggest that it is a large difference, which is unlikely due to just the normal diurnal variations we usually use as a reason to explain any differences in measured height.

The Message is below…

Nikola is sort of a famous Serbian YouTube celebrity that has a Serbo-Croatian audience. He has been in contact with us and promised me that he would start doing the LSJL routine consistently to see if he could get any real noticeable, results. (Click Here to Subscribe to his YouTube Channel Nixa Zizu)

Now that he has stated that he increased his height by 4 mm by doing what is known as Angular LSJL, it gives us a 2nd data point to work with.

Humans are creatures who have brains designed to notice any type of pattern, to make order and sense of the trillions of sensory input that reaches the brain every single moment. I am making a note that I see a pattern from just two data points, where both of the people have said that we need to actually correct (slightly adjust) the way we have been doing LSJL.

Nixa’s claim is just 1 of those data points. The other data point comes from the LSJL Forum in the thread “LSJL works… If Done This Way“. The post of the thread calling himself gr0wthnut claims to have gained 1.5 inches in height.

Whoever this gr0wthnut is, he also made the point that the location we are supposed to clamp down on is not exactly correct. I also suspect that the poster on the forums named Nixalsjl which exchanged a round of posts with gr0wthnut is Nicola of YouTube fame and he took the advice he got from Gr0wthnut and actually applied it in his own slightly modified LSJL routine. I am personally proud of this fact since we are now making real improvements on the original idea, which has not been improved upon for almost 5 years now.

You can see his video below…

This is the other 2nd data point. We can make a trend line using just 2 data points and jump maybe too quickly to seeing some type of pattern (which might not even be there). What would be nice is to get a 3rd or even 4th case of someone who noticed height gains after doing this modified approach.

So what did we learn and what do we take away from reading this post?

It seems that we have been wrong about the location about where to load/clamp. The standard theory that you clamp laterally on the side protruding bony part of the epiphysis may not be the best place. It is actually in the bony sloping/slanted bone area just below the epiphysis. This is the location on where gr0thnut and Nixalsjl are referring to.

I always had personal reservations against the method since it made no sense from a biological perspective how clamping laterally would make bone grow longitudinally in the axial direction. I’ve written almost half a dozen posts over the last 2 years going back and forth trying both to 1. prove or 2. disprove this idea that Tyler has been trying to prove for more than half a decade now. One of my first round of questions to him was over the idea on how the hell does induced chondrocytes from the MSCs manage to push outwards in all 5 directions (the 6th direction would be just pushing inwards) against the wall of the epiphysis made of cortical bone to make the epiphysis larger in volume.

I have never been able to fully swallow the idea of LSJL completely since it makes no sense from a materials or mechanical point of view. No matter how I try to wrap my head around it, it just makes no sense to me on an intuitive level (It just doesn’t seem right) , even after multiple times Tyler tried to clarify to me how the molecular mechanism would work. The bones are not thin and malleable like a balloon which would just puff up from a slight bit of pressure in some region. They are harder than stainless steel if you apply a load in the right direction.

However, this angular idea makes more sense.

While most scientific analysis requires a lot of lab experiments, mathematics and physics knowledge to comprehend what could happen if we change one variable in the system, to figure out how bones would react to say a clamp pressing down on them requires just intuition on how large objects work. You can use intuition to make many arguments.

Let’s look that the types of loading that has been traditionally defined from above. Most calculations you do in at least introductory civil engineering and mechanical engineering course gives you very simple diagrams to analyze, formulate, and solve for some variable. You have to deal with just forces that is tensile, compressive, shears, strains, or torsional.

What we are suggesting can not be easily modeled, because you are loading on the slanted part before the epiphysis head starts. I would suspect that the region we are going to be mechanically stimulating would be also the soft and most easily deformed area.

Imagine that the epiphysis is like a tube of toothpaste. Remember how most parents tell their kids to squeeze the toothpaste, to go from bottom up, squeezing not in the middle, as the original theory says, but to squeeze from the edges to push the entire content upwards. That is similar to what I am at least saying. In the process of squeezing the toothpaste from the bottom up, the upper part protrudes outwards, extending the volume on the upper side, which is what causes the little bit of bone volume change.

The last major point comes from the book The Body Electric by Dr. Robert Becker which I have referenced multiple times before. In one specific section, his research team tried to figure out what is the exact molecular mechanism to allow for Wolff’s law to be possible. How does the bones actually remodel themselves from a mechanical load? After bending the bones and noticing that the thickness of the bones increased in the opposite area where the bones were loaded, they came up with the theory that if you bend a long bone just like when you are trying to bend a wooden rod, the electrons pop out out of the side where you are bending them and move toward the side where the they are experiencing the most compressive load. The excessive in electrons causes certain molecules to move to that side to balance out the charge differences, adding more bone thickness in the process.

If we then use the simple principle that the thickness of bones increases in the opposite direction of a mechanical load, to make the upper area of the epiphysis thicker, we would need to load in the opposite direction. Obvious that would not be possible, since we prefer to view the bone as a cylinder with both ends attached axially to another long bone. There is no way to make the proximal epiphysis end of a tibia longer by loading the distal epiphysis end of the same tibia, unless we cut off the feet.

That means that the next best thing, to get as close to the opposite direction of the epiphysis top surface is to load in the direction of the slant/angular region of the epiphysis right before the protrusion begins. That is what I suggest we start to do and change towards.

So, again, do you see the picture to the upper right? See where the line/arrow that is showing the label “spongy bone” is point at in the part of the epiphysis ? Load there.

The Take-Away – Change the location to clamp on the Angular or Slanted Area just before the epiphysis protrusion area is most pronounced, which is almost opposite of the top of the epiphysis

{So you’re suggest to load below the epiphysis? That might be interesting as it would increase pressure within the epiphysis rather than the entire bone. I might have to try that and see if can get the immediate results I got with finger loading. With finger loading, I’m loading a much larger area which would include the area where the epiphysis meets the diaphysis.

Right now the current method suggests loading where the epiphysis meets the articular cartilage. This new method would suggest loading where the epiphysis would meet the diaphysis. A drawback would be no loading two bones and once. Another drawback would be that the end of the epiphysis is weaker and is more susceptible to deformation via mechanical load. I will still give it a shot.-Tyler}

Other Issues

There have been a few concerns within the community of people trying out the LSJL routine since Tyler did post an update to his height gains in the recent post “Height Increase Progress Update“ where he said that his recent visit to the doctor showed that he was 5′ 8.25″. This would suggest that maybe he never got any gains in all the years he has been trying. Other doctors offices have said that he is at 5′ 9.75″. For me, I am not sure what to make of this new information. A 1 and a half inch discrepancy in measured height from one doctor’s office to another is very extreme. Maybe the gains he did get for a few years was lost but I have no idea what to make of it at this time.

I am not that concerned with whatever his gains are, since he still does great work in research and contributing to the website. His effort and work has helped push the endeavor extremely far and revealed multiple new ideas on how we should proceed into the future.

Also, the recent thread on Miles Cordell from the UK claiming to disprove this idea has to be taken into consideration. So is Mr. Cordell’s claim valid? He says that he has never found one valid scientific paper to back up the idea His idea is that the knees or whatever synovial joints one would clamp down on would become swollen, which might cause a temporary illusion of height gain.

I can’t say much to this since he hasn’t looked over the study where older lab mice had their long bones increase in length from intermittent mechanical loading of the joints. (and yes, we all realize that in mice, the epiphyseal cartilage doesn’t really ever go away)