Note:  I’m still hard at work at finding a methodology of growing taller and am investigating non-LSJL method.

Finite-element analysis of the mouse proximal ulna in response to elbow loading.

“Bone is a mechano-sensitive tissue that alters its structure and properties in response to mechanical loading. We have previously shown that application of lateral dynamic loads to a synovial joint, such as the knee and elbow, suppresses degradation of cartilage{We also should investigate inducing endochondral ossification of the cartilage, perhaps Lateral Joint Loading could be involved in that} and prevents bone loss in arthritis and postmenopausal mouse models, respectively. While loading effects on pathophysiology have been reported, mechanical effects on the loaded joint are not fully understood. Because the direction of joint loading is non-axial, not commonly observed in daily activities{This is what’s so interesting about lateral joint loading, any height increase method has to be something that people do not do in ordinary activities as otherwise people would already have discovered that it makes you taller}, strain distributions in the laterally loaded joint are of great interest. Using elbow loading, we herein characterized mechanical responses in the loaded ulna focusing on the distribution of compressive strain. In response to 1-N peak-to-peak loads, which elevate bone mineral density and bone volume in the proximal ulna in vivo, we conducted finite-element analysis and evaluated strain magnitude in three loading conditions. The results revealed that strain of ~ 1000 μstrain (equivalent to 0.1% compression) or above was observed in the limited region near the loading site, indicating that the minimum effective strain for bone formation is smaller with elbow loading than axial loading{This is likely due to increases in fluid flow and/or hydrostatic pressure resulting in most of the adaptive response}. Calcein staining indicated that elbow loading increased bone formation in the regions predicted to undergo higher strain.”

“dynamic strain in bone matrix and strain-induced fluid flow in the lacuno-canalicular network are two of the major contributors to mechanotransduction in bone”

“Unlike axial loading, such as in ulna and tibia loading, joint loading employs lateral loads that sandwich a synovial joint, such as the knee, ankle, and elbow”<-I have not heard joint loading described this way before.  This description emphasizes the lateral compression force.

” we determined the strain distribution to the ulna in response to elbow loading using a mouse model and finite-element (FE) analysis. Daily loading with 1-N peak-topeak force at 1 Hz for 5 min was applied to ovariectomized (OVX){OVX mice simulates osteoperiosis} mice as well as sham-OVX mice (control mice){we are more interested in this group}, and bone mineral density (BMD) was measured at the site of loading after 4 weeks of loading. ”

” We employed three loading configurations: load and a single point of support, load and a three-point support, and load across soft tissues that may mimic surrounding skin and muscle”

” The lateral loads to the elbow were given 5 min per day for 5 weeks using 1-N force (peak-to-peak) at 5 Hz to the right arm, and left arm data were used as a contralateral control. ”

You can see the bone formation in the control group.  Definitely doesn’t indicate that it increases height but it indicates that it does something which is a start.  There seems to be an increase in bone width as well which is harder than just increasing the trabecular bone from within which is also very good although these mice are 12 week old female mice.  But the increase in bone width indicates the possibility of abnormal effects going on which would be needed to induce height growth.

” We employed three loading and boundary conditions in response to elbow loading with 1-N loads: lateral loads applied at two opposing locations; lateral loads applied at a single site on one side and three supporting sites on the other side; and lateral loads on a pair of soft disks that sandwiched the elbow.”<-it’ll be interesting to see which is best.  I think the soft disks would really diminish the load.

“Compression of a pair of soft-tissue disks induced multiple strain spots that were widely distributed from the proximal tip to the whole elbow joint ”

“Elbow loading generates artificial lateral forces that are rarely encountered during routine physical activity. Unlike axial or bending loads with ulna loading or tibia loading, the mechanical response of synovial joints, such as the elbow, to lateral loads has not been fully characterized”You can’t really see any abnormal bone formation here like you could in the earlier image and they look to be similar sites.  “Calcein-stained cross sections of the proximal ulna distal to the trochlear notch” whereas the earlier one is “c μCT images of the cross sections of the proximal ulna, ~ 1 mm distal to the edge of the trochlear notch”

” Compared to strain at the single loading site, three supporting sites significantly reduced
the maximum compressive strain by ~tenfold (from ~ 2% in the dark blue label to ~ 0.1% in the cyan level). “<-So maybe one loading site is best.  Multiple loading sites would counter the deformation and act as a sort of stabilizing force [cancel each other out].  “strains exceeding 0.1% (1000 μstrain) are confined to the vicinity of the loading site and supporting points”<-So maybe in someone that is growing we would we want to load directly near the growth plate or in an adult maybe near the articular cartilage.

Not very much height stuff but good to see it still being worked on.

{Tyler-This was a post by Michael John.  I am still very much working towards finding a way to grow taller.  Now I am focus on in inducing endochondral ossification of the articular cartilage.  I am growing through old studies.  It’s just a lot of studies are more of the same}

Note: The efficacy of this compound has been very controversial

I have been spending a ridiculous amount of time recently doing a LOT of research on the chemical compound known as Menaquinone-7, aka MK7, aka Vitamin K2. There has been a lot of research that I have found which confirms this idea that MK7 Supplements will lower the risk of hip femoral neck fractures in post menopausal women.

A recent PubMed Study “Three-year low-dose menaquinone-7 supplementation helps decrease bone loss in healthy postmenopausal women.” finally has admitted to the idea that it may not just be the Bone Mineral Density that can be dramatically reduced in its decreasing rate, but maybe the overall height of a person, at least slightly.

Let me quote the following…”MK-7 significantly decreased the loss in vertebral height of the lower thoracic region at the mid-site of the vertebrae.”

Something that has been worrying me for so long, from looking at so many claims of professional MDs is that since the most well known type of food source which has high concentrations of Vitamin K2 is Natto, was this “Why is it that if the Japanese are eating so much Natto (Since Natto is such a critical part of the Japanese diet, unlike any other country in the world) and soy based products relative to other ethnic groups, do Japanese women (or even Eastern Asian women in general) seem to have the highest rates of osteoporosis?”

Wouldn’t eating Natto have the opposite effect?

Is it just a racial thing, where different races actually have different levels  of BMD on average?

The Science behind Menaquinone-7

It seems that with MK7 at least, it can stimulate the level of osteocalcin and GLA in the body. the osteocalcin and GLA have a certain area of their molecular structure which allows them to chelate the Calcium atoms out of the soft tissue areas of the body, like the blood vessels. Remember that one of the things that happen as we get older is that there is a sort of plaque buildup in our blood vessels. 20% of the buildup in our vessels is calcium in nature. Somehow the K2 can cause the calcium buildup in the soft tissue area/blood vessels to reverse in ossification.{Tyler-obviously this would be very powerful if it happened in the bones}

What I am sure about

When the dentist Weston Price did his analysis on all those kids who didn’t seem to develop cavities back in the 30s or 50s (not sure what decade it was), he claimed that the compound was something he called Activator X. Recently people are saying that the activator X compound is just Vitamin K2, specifically the MK-7 version.

The K2 he managed to give to kids to reverse their cavities was some type of grass feed butter, combined with Cod Liver Oil. Remember what Dave Asprey has been asking the people who take his Bulletproof coffee to do? Put some grass-fed butter in it. It turns out that the Grass Feed Butter Oil has a higher than average concentration of K2 in it. Not only that, the entire idea of the possibility of reversing cavities was because I used to lurk in the Bulletproof Executive Forum , and heard other people who claim to have it happen to them. Dr. Pamela Smith has claimed in one Youtube video though that you would need a recommended 100 mcg of Menaquinone-7 to get a reasonable effect.

However, when Price did the X-rays to show that the teeth seemed to fill out, he didn’t consider the factor of Strontium, as well as the fact that to get the caries to reverse, you still need to at least put some filling on the cap of the teeth first. The hole in the center is supposed to be filled up over time from K2 supplementation.

{tyler}-

Here’s more about the effects of Vitamin K2 on GLA

Matrix Gla Protein Is a Developmental Regulator of Chondrocyte Mineralization And, When Constitutively Expressed, Blocks Endochondral and Intramembranous Ossification in the Limb

“Matrix GLA protein (MGP), a γ-carboxyglutamic acid (GLA)–rich, vitamin K–dependent and apatite-binding protein, is a regulator of hypertrophic cartilage mineralization during development. However, MGP is produced by both hypertrophic and immature chondrocytes, suggesting that MGP’s role in mineralization is cell stage–dependent, and that MGP may have other roles in immature cells. It is also unclear whether MGP regulates the quantity of mineral or mineral nature and quality as well. To address these issues, we determined the effects of manipulations of MGP synthesis and expression in (a) immature and hypertrophic chondrocyte cultures and (b) the chick limb bud in vivo. The two chondrocyte cultures displayed comparable levels of MGP gene expression. Yet, treatment with warfarin, a γ-carboxylase inhibitor and vitamin K antagonist, triggered mineralization in hypertrophic but not immature cultures. Warfarin effects on mineralization were highly selective, were accompanied by no appreciable changes in MGP expression, alkaline phosphatase activity, or cell number, and were counteracted by vitamin K cotreatment. Scanning electron microscopy, x-ray microanalysis, and Fourier-transform infrared spectroscopy revealed that mineral forming in control and warfarin-treated hypertrophic cell cultures was similar and represented stoichiometric apatite. Virally driven MGP overexpression in cultured chondrocytes greatly decreased mineralization. Surprisingly, MGP overexpression in the developing limb not only inhibited cartilage mineralization, but also delayed chondrocyte maturation and blocked endochondral ossification and formation of a diaphyseal intramembranous bone collar. The results show that MGP is a powerful but developmentally regulated inhibitor of cartilage mineralization, controls mineral quantity but not type, and appears to have a previously unsuspected role in regulating chondrocyte maturation and ossification processes.”

Understanding Growth Plate Fusion(and growth plate senescence) will help us understand if these processes can be reversed.  And just as a note I am still working on devices and methodology to grow taller.

A Computed Microtomography Method for Understanding Epiphyseal Growth Plate Fusion.

“The epiphyseal growth plate is a developmental region responsible for linear bone growth, in which chondrocytes undertake a tightly regulated series of biological processes. Concomitant with the cessation of growth and sexual maturation, the human growth plate undergoes progressive narrowing, and ultimately disappears. Despite the crucial role of this growth plate fusion “bridging” event, the precise mechanisms by which it is governed are complex and yet to be established. Progress is hindered by the current methods for growth plate visualization; these are invasive and largely rely on histological procedures. Here, we describe our non-invasive method utilizing synchrotron X-ray computed microtomography for the examination of growth plate bridging, which ultimately leads to its closure coincident with termination of further longitudinal bone growth. We then apply this method to a dataset obtained from a benchtop micro computed tomography scanner to highlight its potential for wide usage. Furthermore, we conduct finite element modeling at the micron-scale to reveal the effects of growth plate bridging on local tissue mechanics. Employment of these 3D analyses of growth plate bone bridging is likely to advance our understanding of the physiological mechanisms that control growth plate fusion.”

“It is the terminally differentiated hypertrophic chondrocyte, which mineralizes its surrounding extracellular matrix. This process, thought to involve membrane-limited matrix vesicles, is biphasic and tightly regulated by a number of enzymes and factors including alkaline phosphatase (Alpl), PHOSPHO1, the ankylosis protein (Ank), ecto-nucleotide pyrophosphatase/phosphodiesterase-1 (Enpp1) ”

“as growth slows, the human growth plate undergoes progressive narrowing as bony bridges form and span its width. This ultimately leads to complete growth plate closure and the cessation of human growth. These bone bridges are also known to form upon growth plate injury, thought to be through an intramembranous ossification mechanism”

“in two genetic mutations resulting in estrogen deficiency (in the estrogen-receptor gene, and in the CYP19 gene), the growth plate fails to fuse and growth persists, albeit rather slowly, into adulthood”

“Evidence from studies in both humans and rats revealed the cessation of growth long before any histological evidence of growth plate fusion, suggesting that epiphyseal fusion is a marker of growth cessation and not its cause “<-Thus it may be possible to renew growth plate growth by reversing cessation and not fusion.

“young (8 weeks old) CBA wild-type mice, growth plate bridging is associated with locations that contain high local von Mises stresses. Moreover, we reveal that with aging an increased number and density of growth plate bridges is observed”

” in wild-type mice, increased growth plate bridging translates into increased stresses in the bone directly beneath the growth plate.”<-So maybe these stresses contribute to growth plate closure.

“At 8 weeks, few bridges are detected and overall the growth plate is squeezed in a “sandwich” configuration. This suggests that compressive hydrostatic stresses are engendered across major volumes and that higher shear stresses are generated only at the peripheral edges of the growth plate. Yet, the results of numerous mechanobiological models support that growth and ossification is accelerated by tensile strain (or shear stresses) and that cartilage tends to be maintained by hydrostatic compressive stress“<-so for a longer growth period we need to encourage hydrostatic compressive stress.

A radical switch in clonality reveals a stem cell niche in the epiphyseal growth plate.

“Longitudinal bone growth in children is sustained by growth plates, narrow discs of cartilage that provide a continuous supply of chondrocytes for endochondral ossification. However, it remains unknown how this supply is maintained throughout childhood growth. Chondroprogenitors in the resting zone are thought to be gradually consumed as they supply cells for longitudinal growth, but this model has never been proved. Here, using clonal genetic tracing with multicolour reporters and functional perturbations, we demonstrate that longitudinal growth during the fetal and neonatal periods involves depletion of chondroprogenitors, whereas later in life, coinciding with the formation of the secondary ossification centre, chondroprogenitors acquire the capacity for self-renewal, resulting in the formation of large, stable monoclonal columns of chondrocytes{if these chondroprogenitors never become senescent then we can grow forever}. Simultaneously, chondroprogenitors begin to express stem cell markers and undergo symmetric cell division. Regulation of the pool of self-renewing progenitors involves the hedgehog and mammalian target of rapamycin complex 1 (mTORC1) signalling pathways. Our findings indicate that a stem cell niche develops postnatally in the epiphyseal growth plate, which provides a continuous supply of chondrocytes over a prolonged period.”

“CD73 (encoded by Nt5e) was among the most upregulated stem cell surface markers (4.9 ± 1.2-fold; P28 versus P2; P = 0.018) and immunohistochemical analysis confirmed de novo expression of CD73 at P28 (markers for cell proliferation (Ki67) and differentiation (MEF2C) were controls for developmental changes”

“Cells in the growth plate might also orient as a result of migration or stacking due to tissue polarization, which is reflected by the orientation of primary cilia. Cilia on flat chondrocytes, but not on chondroprogenitors, were polarized (with 61.3 ± 4.8% and 32.8 ± 2.2% of cilia, respectively, oriented longitudinally, P = 0.005, n = 3;”

3j is supposed to summarize it

LSJL is lateral loading of the synovial joints or possible the epiphysis of the bone to stimulate fluid flow to stimulate degradation(remodeling) of the cortical bone and creation of mesenchymal stem cell chondrogenesis through a favorable microenvironment.

Martial arts bone condition is another form of this as impact is a form of loading.  However impact loading would not stimulate the soft tissues surrounding the bone which are all connected to the bone this is an important distinction.  Axial loading does not really drive fluid flow so that elements punching as a studiable stimulus.  However, several martial artists do tapping of the bones of the leg and arm.

The different between this and an LSJL style tapping would be that the tapping would not necessarily be at the longitudinal ends of the bone so the bone would be more innervated and there would be less of a fluid pressure gradient than at the longitudinal ends of the bone.  The goal of martial arts bone conditioning is described as something like calcification or bone thickening which is not exactly what we want.

The other difference between LSJL and martial arts bone conditioning is the intensity of the load.  Short intense bursts is more osteogenic whereas longer less intense bursts of loading are more chondrogenic.  This is primarily because osteocytes respond to sudden changes in fluid flow but osteocytes(probably) cannot make you taller as osteocytes produce bone and bone is what blocks you from growing taller!  Soft tissue is what allows for interstitial growth.  So for LSJL style loading you would tap the longitudinal ends of the bone with more frequency and less intensity.

If the bones weren’t so innervated would you be able to grow via martial arts style loading?  Probably not by rolling a bottle up and down your leg.  But we know that martial artists fracture legs during kicks.

And fractures definitely result in longitudinal bone growth because the bone clot results in a lot of fluid stimulus and it removes the cortical bone impediment.

We also know that there’s a phenomenon known as stress fractures where bones can develop fracture over time to non-overly traumatic loads just as the bone is no longer able to recover.

But we want to know if it’s possible to induce the longitudinal bone growth stimulus without fracturing a bone.  And could it be possible with a tapping stimulus?  The key is to target a less innervated part of the bone which happens to be the epiphysis although there are some epiphysis where regions are fairly innervated.  Tapping the epiphysis also generates a fluid pressure gradient.

With these fluid pressures we want to stimulate bone degradation via osteoclasts(remodeling)[this process could be accelerated via HGH] but we don’t want bone deposition via osteocytes and osteoblasts we want cartilage deposition although it’s feasible that other fibrocartilage tissues could work so that’s why we want sustained loading pressures over time so consistent taps.  The stress fracture phenomenon is also beneficial for our purposes.  Microcracks are good at stimulating fluid forces.

Nerve issues are probably unavoidable but we want to choose the least nerved location.

Does anyone have any anecdotal evidence of martial artist effects on bone?

I know there’s not a lot of solid proof of anything here but basically I’m testing epiphyseal tapping over prolonged periods to generate bone degradation and creating a favorable microenvironment for replacement via soft tissues.  I wanted people to know what I’m working on as I haven’t posted here in a while.  I’m solely dependent on generating proof at this point so if anyone has any evidence of martial artists generating any kind of visible bone adaptation whatsoever that would be extremely helpful.

According to the study it only increases IGF-1, but it may have other effects that are not known about.  Red Clover flowers contain p-Coumaric Acid.  I could only find p-coumaric acid available for scientific use.

p-Coumaric acid stimulates longitudinal bone growth through increasing the serum production and expression levels of insulin-like growth factor 1 in rats.

“The aim of the present study was to examine the effects of p-coumaric acid on the longitudinal growth of the long bone in adolescent male rats. Teatment with p-coumaric acid significantly increased the tibial length and the height of each growth plate zone and the ratio of 5-bromo-2′-deoxyuridine-positive cells relative to total proliferative cells. Expression of insulin-like growth factor 1 and its receptor in the proliferative and hypertrophic zones, and serum levels of growth hormone and insulin-like growth factor 1 were significantly increased as well in the p-coumaric acid-treated group. Via increasing both the serum level of insulin-like growth factor 1 and its expression, p-coumaric acid could promote cell proliferation in growth plate zones. These results suggest that p-coumaric acid has the potential to increase height and may be a feasible alternative to growth hormone therapy.“<-the statement that this may be a feasible alternative to growth hormone therapy makes this seem more powerful than just your typical supplement.

The study also mentions other supplements that have beneficial effects on chondrogenesis.  If you look at figure 1 and 2 you can see that there are differences between p-Coumaric Acid and Growth Hormone growth plates.  The scientists suggest that p-Coumaric acid upregulates IGF-1 and IGF-1R.