I actually missed that this LSJL study showed height increase as it was a minor comment that joint loading increased height of the femoral head.  Since the femoral head is a diagonal offshoot of the femur it may not necessarily increase height but it is an increase in bone length all the same.  However, the osteonecrosis induced in the study may be a prerequisite to induce the femoral head growth.  However, it should be noted that the osteonecrosis decreased femoral head height but the degradation of existing bone may have allowed for new bone growth.

This is an LSJL related study published by Yokota and Zhang.  The primary author seems to be more Zhang who seems more into the lengthening effects than Yokota.  This study shows that joint loading increases fibrous differentiation.  And fibrous differentiation would be a potential intermediary step for neo-growth plate formation.  Knee loading increased vessel remodeling and osteoclast formation which would be needed to make room for a new growth plate but these levels were only slightly greater than control group and reduced from the osteonecrosis group so we can not say for sure whether this will happen in LSJL on a normal bone.

Overall this study shows that LSJL does at least one of the steps required for neo-growth plate formation: fibrous type tissue formation.  This fibrous tissue would then have to be further differentiated into more cartilagenous tissue.  The perichondrial ring(or ring of LaCroix) is fibrocartilagenous.

Knee loading protects against osteonecrosis of the femoral head

“Osteonecrosis[loss of blood to the bone] of the femoral head is a serious orthopedic problem. Moderate loads with knee loading promote bone formation.  Using a rat model, we examined a hypothesis that knee loading enhances vessel remodeling and bone healing through the modulation of the fate of bone marrow-derived cells. Osteonecrosis was induced by transecting the ligamentum teres followed by a tight ligature around the femoral neck. For knee loading, 5 N loads were laterally applied to the knee at 15 Hz{this is pretty high frequency} for 5 min/day for 5 weeks. Changes in bone mineral density (BMD) and bone mineral content (BMC) of the femur were measured to evaluate vessel remodeling. Femoral heads were harvested, and bone marrow-derived cells were isolated to examine osteoclast development and osteoblast differentiation.  Osteonecrosis significantly induced bone loss, and knee loading stimulated both vessel remodeling{vessel remodeling shows promise as that would be very helpful for neo growth plate creation} and bone healing. The osteonecrosis group exhibited the lowest trabecular BV/TV in the femoral head, and lowest femoral BMD and BMC. Knee loading increased trabecular BV/TV as well as BMD and BMC. Osteonecrosis decreased the vessel volume, vessel number and VEGF expression, and knee loading increased them. Osteonecrosis activated osteoclast development, and knee loading reduced its formation, migration, adhesion and the level of “pit” formation{pit formation could potentially be beneficial though as that pit could where a neo-growth plate would go}. knee loading significantly increased osteoblast differentiation and CFU-F{An increase in CFU-F means an increase in mesenchymal stem cell proliferation which is a good for neo-growth plate formation but doesn’t guarantee that it will occur}. A significantly positive correlation was observed between vessel remodeling and bone healing. Knee loading could be effective in repair osteonecrosis of the femoral head in a rat model [by] promoting vessel remodeling, suppressing osteoclast development, and increasing osteoblast and fibroblast differentiation. “

“The mechanism of knee loading is considered to change intramedullary pressure of femoral and tibial bone cavities. The load driven pressure may generate fluid flow in a lacuna canalicular network in bone cortex. The pressure activates bone metabolism-related genes in femur and tibia”<-what we are interested in an increase in fluid flow and hydrostatic pressure to induce chondrogenic differentiation.  Hydrostatic pressure by itself isn’t likely to induce chondrogenic differentiation by itself as it is typically three orders of magnitude below the pressure needed to induce chondrogenic differentiation.  But the addition of bone deformation and fluid flow may bridge the gap and induce chondroinduction.

“Male Sprague–Dawley rats (~12weeks of age)”

“knee loading was achieved through dynamic loads applied to the left and right knee joints of rats in the lateral–medial direction, respectively. To position the knee properly, the lower end of the loading rod and the upper end of the stator were designed to form a pair of semispherical cups. The lateral and medial epicondyles of the femur together with the lateral and medial condyles of the tibia were confined in the cups.  The tip of the loader had a contact area of 15 mm in diameter.”

See Figure 1 of the paper(first link on the page) for an image of the knee loader.

Loading increased vascular remodeling in the osteonecrosis + LSJL group but not versus control.  But there was no normal bone plus loading group.

Joint Loading actually seemed to reduce the number of mesenchymal stem cells but that could be due an increase in differentiation.  Mesenchymal condensation was more visible in the osteonecrosis group and mesenchymal condensation is a prerequisite for neo-growth plate formation.

Knee Loading seemed to restore osteoclast adhesion and migration to slightly above control levels but that slightly above could indicate activity that would remodel the bone enough to allow for mesenchymal condensation.

Knee loading greatly increased CFU-F and Osteoblast differentiation versus both osteonecrosis and control group. “Knee loading enhanced differentiation of osteoblasts and fibroblasts.” Fibroblastic tissue(marked by CFU-F) could potentially become chondrogenic tissue.  Fibrocartilage is a thing.  But to be a true growth plate, additional mechanical stimulation would be needed to turn that fibrocartilage into pure cartilage.

” Knee loading increased the height of the femoral head partially”

It’s a big breakthrough that LSJL increased height in the femoral head.  The osteonecrotic bone had far more marrow in B, thus under osteonecrosis LSJL may have had more room to induce growth.

The perichondrial ring of the growth plate is fibrocartilagenous in nature and may be the source to provide cells to the growth plate.

“The current histology and bone mineral density data are suggestive of the role of bone marrow-derived stem cells in load-driven bone healing, and they also establish a causal relationship between the observed vessel remodeling and bone healing effects with knee loading”<-This is huge because we want to induce stem cells to form neo-growth plates.

According to this LSJL would increase blood perfusion which would be the most interesting thing.  If the bone has more blood flowing through can create unique biological opportunities remember one of the key steps to distraction osteogenesis is a blood clot.

It was mentioned that LSJL upregulates bone metabolism related genes.  Here’s a study that lists bone metabolism related genes:

Association of osteoporosis susceptibility genes with bone mineral density and bone metabolism related markers in Koreans: the Chungju Metabolic Disease Cohort (CMC) study.

“bone metabolism-related markers, such as serum concentrations of calcium, phosphorus, PTH,
and 25(OH) D”

“genetic variants of MEF2C, ESR1, TNFRSF11B, and SOX6 were associated with bone metabolism-related markers”

Here’s the last LSJL update.

The growth seems pretty solid from last update:

Current

1 month earlier:

So increasing the intensity and duration of clamping on the right foot seems to have worked.  I’ll keep trying to see if can get more growth.  I may have some growth in my right hand from clamping there but I’ll wait to see if the growth is more significant as I can always get x-rays there.

I’ll also try to get growth in the longer limbs but once I can prove growth in smaller limbs I can get more resources to use for the longer ones.  It does seem like the foot itself is growing more than the toes so maybe it’s easier to grow those bone shapes even though there’s a lot of the same obstacles for longitudinal bone growth for “short” bones there could be differences we don’t know about.  these bones are also surrounded by different tissues than long bones which could make a difference.

So I’ll try the same intensity/density of clamping on the foot and see if I can grow on the hands and other limbs and increase clamping intensity on those areas.

Sometimes it’s frustrating to be part of a rank of people so few who are working on to height increase methods.

It’s by all means possible to discover the Lorenzo’s Oil that increases height but increasing height is a lot more complicated than affecting fatty acid buildup.  Unless there’s a study that shows that a chemical directly increases height like maybe IGF2 or CNP is that chemical.  But there have been tons of cases where a chemical you think may increase height by delaying maturating or increasing chondrocyte proliferation actually decrease height growth.  With chemicals it’s a case of that a chemical doesn’t increase height until it actually shows that it increases height.  So with chemicals you have to settle for a lot of duds and just hope that you stumble upon something that works.  And there’s also things like the digestive system blocking chemicals from taking their desired action.

For mechanical methods, there’s far more that you can do.  Axial(top to bottom) loading, tensile(stretching), and impact loading are probably not going to produce height increase as they have all been performed at very high levels physiologically.  Axial loading has been done at over 1000lbs in squats and leg press with no reported height gain.  Tensile(stretching) has been performed at very high levels with the rack with no height gain the issue with tensile loading is that cartilage, tendons, ligaments, and muscles will fail far more easily than bone will.  Impact loading has been done in running with no reported height gain.

Lateral and twisting loading have happened far less physiologically.  In the case of twisting, it has in times produced height increase as a result of fracture.  The twisting strength of the bone is less than that of the soft tissues so it’s more likely to fail before the soft tissues.  And twisting is also highly stimulatory to the bone marrow which is what could create a new growth plate like wringing out a sponge moves the water.  Twisting also could cause damage to the bone architecture.  Lateral loading also moves and stimulates the bone marrow and could cause torsional(twisting forces).  You could also perform lateral loading on a twisted bone.

So there’s several ways you can help.  Head on over to the LSJL forum or post in the comments a good height increase forum and suggest better ways to induce lateral or twisting loading.  You can post a stretching routine but make sure it includes a lot of twisting forces.  Or suggest a new novel form of loading.  A ton of mechanical stimuli has been shown to pro-chondrogenic it probably just isn’t strong enough and there are blocks from it getting strength for example muscle/tendon failure.

No major scientific background is needed to help just a basic understanding of the body and lets start building a community to find a way to grow taller.

Here’s the last update.

Here’s the feet length progress pic:

Here’s the pic from about 6 months ago:

Yeah the distance is wrong so here’s one from about 2 months ago:

I can’t really tell how much growth I’ve had but it seems like some.  So not really proof right now.  Anyways, growth is disappointing considering that I got some significant growth initially in that the shoe started being tighter.  Already I’ve started clamping other areas of the feet in the hopes of spillover growth as clamping the big toe has seemed to induce growth in the other toes.

I’m going to clamp for longer and more intensely.  We’ll see if that gets me some good solid growth

Here’s the link to the last LSJL update.

It seems like my feet have continued to grow from clamping.

Actually there seems to be rather remarkable growth of the 2nd phalanx/phalange bone.  Right foot is loaded with LSJL and left foot is unloaded.  It’s hard to tell if my big toe has grown anymore.  I’ve changed my clamping strategy rather than trying to specifically clamp the epiphysis of the bone.  I’m clamping a part of the bone close to the epiphysis where I can avoid slippage.  This change in clamping strategy may be the cause of the second phalanx growth too. By focusing more on the force rather than location I notice a rush of blood/fluid flow to regions when I release the clamp this may be a beneficial stimulus towards longitudinal bone growth.

My hands look like they’re growing too but there’s no need for pics all I need to is get an xray of one hand and compare them to the existing ones I have.  I may be growing in height again too but until it’s more definitive it’s better to focus on things that are easier to measure.

LSJL does upregulate MATN3.  A rosette is a hexameric disc shaped aggregate.
Here’s what a rosette Nanotube looks like.  The novel aspect of this is that it can be injected as a liquid.

GROWTH PLATE CARTILAGE REPAIR VIA NOVEL MATRILIN3/ROSETTE NANOTUBE HYBRID MATRIX

“Approximately 15% to 30% of all childhood fractures are growth plate fractures. Because the growth plate determines the length and shape of a mature bone, this type of fracture may result in severe growth abnormalities in children. Pathologically, the growth abnormality is caused by the formation of a bony bridge in the injured growth plate cartilage. Currently, the clinical treatment of growth plate fractures includes the surgical removal of the bony bridge and insertion of autologous fat or cartilage tissue into the empty space to discourage bony bridge reformation. Such surgical procedures are invasive and result in unsatisfactory outcomes. In addition, this treatment is only useful after the bony bridge has formed. Our long-term goal is to understand how to prevent bony bridge formation and improve growth plate cartilage regeneration at cellular and molecular levels and develop the first preventive and therapeutic approach for growth plate fracture. Specifically, the primary objective of this proposal is to evaluate the therapeutic effects of a nano-matrix assembled from matrilin-3 (MATN3) and rosette nanotube (RNT) in a preclinical growth plate fracture model. Our central hypothesis is that the MATN3/RNT nano-matrix specifically promotes chondrocyte growth and enhances chondrogenesis of mesenchymal stem cells (MSCs), while it also inhibits vascularization and osteogenesis at the fracture site{these two things may increase growth plate generation especially since this is supposed to be used for growth plate fracture}. This is the cellular basis for such nano-matrix to improve growth plate cartilage regeneration and prevent bony bridge formation. We will test our central hypothesis and achieve the objective of the proposal by pursuing two specific aims: 1) to determine the ability of MATN3/RNT to prevent bony bridge formation; and 2) to determine the ability of MATN3/RNT to deliver growth factors for further improvement of chondrogenesis and growth plate cartilage regeneration. To achieve the two aims, our overall research strategy includes: 1) optimization of the ratio and dose of MATN3/RNT and its ability and bioactivity for loading growth factors in vitro; and 2) determination of the therapeutic efficay of the nano-matrix in our established growth plate fracture model in rats in long term. The proposed research is innovative: 1) biologically, it simultaneously promotes cartilage regeneration and inhibits bony bridge formation; 2) therapeutically, MATN3 and RNT can be injected as a liquid in a minimally invasive manner, and form a nano- matrix at the fracture site; 3) structurally, the nano-matrix concentrates bioactive MATN3 locally at the fracture site as well as binds TGF-β1 and IGF-1 to achieve multi-functional delivery. With the results of the two specific aims, we expect to 1) realize a synergistic strategy to specifically promote chondrogenesis while inhibiting osteogenesis and vascularization; and 2) develop an injectable approach for the localized delivery of cartilage growth factors. These outcomes have an important positive impact in developing novel, perhaps the first, preventive and therapeutic approach for growth plate cartilage repair. ”

Here’s more info about nanotubes:

Helical rosette nanotubes: a more effective orthopaedic implant material

“Due to the nanometric properties of some physiological components of bone, nanomaterials have been proposed as the next generation of improved orthopaedic implant materials. Yet current efforts in the design of orthopaedic materials such as titanium (Ti) are not aimed at tailoring their nanoscale features, which is now believed to be one reason why Ti sometimes fails clinically as a bone implant material. Much effort is thus being dedicated to developing improved bioactive nanometric surfaces and nanomaterials for biospecificity. Helical rosette nanotubes (HRN) are a new class of self-assembled organic nanotubes possessing biologically-inspired nanoscale dimensions. Because of their chemical and structural similarity with naturally-occurring nanostructured constituent components in bone such as collagen and hydroxyapatite, we anticipated that an HRN-coated surface may simulate an environment that bone cells are accustomed to interacting with. The objective of the present in vitro study is therefore to determine the efficacy of HRN as a bone prosthetic material. Results of this study clearly show that both HRN-K1 and HRN-Arg coated Ti displayed enhanced cell adhesion when compared to uncoated Ti. Enhanced cell adhesion was observed even at concentrations as low as 0.005 mg ml⁻¹. These results point towards new possibilities in bone tissue engineering as they serve as a starting point for further mechanistic studies as well as future manipulation of the outer chemistries of HRN to improve the results beyond those presented here. One such effort is the incorporation of peptide sequences on the outer surface of HRN and/or growth factors known to enhance bone functions. “