Growth plate regenaration has been covered before here and here.  Ultimately, this provides more evidence that the presence of germ immature cells are the key limiting factor in creating new growth plates.  Thus our primary focus should be on developing mechanical and supplemental methods that alter the structure of cells to be more like these growth plate chondrocyte precursor cells.

Regeneration of the Growth Plate

Pdf-growth plate regeneration

“The occurrence of growth plate regeneration has been doubted. However, in 5 different series of experiments reported between 1950 and 1986 regeneration of injured parts of growth plates in long bones of rabbits and pigs could be demonstrated. The 1st series implied partial X-ray injury of growth plates in rabbits aged 3–6 weeks.The 2nd series implied autotransplantation of the head of the fibula in rabbits aged 10–21 days. The 3rd, 4th and 5th series implied transplantation of autologous fat grafts into provoked defects of growth plates in rabbits and pigs. The findings show that regeneration of a growth plate occurs when a part of it is injured in such a manner that a bone bridge is not formed between the epiphysis and the metaphysis. Regeneration of a plate is much faster in relation to the growth in length of the bone in the rabbit than in the pig. The 1st and 2nd series suggest that regeneration takes place by interstitial proliferation of cells from the germinal layer of the uninjured parts of the plate. Signs of partial regeneration of growth plates have been seen in radiographs after operation for partial closure of growth plates in children. ”

Growth plate regeneration refers to the healing of damaged growth plates but if we learn the mechanisms by which growth plates are repaired we could potentially use those mechanisms to create new growth plates.

“Microscopic examination showed that injured portions of cartilage were pushed aside by the unirradiated carti­lage growing into the irradiated area transversely in rela­tion to the axis of the bone. In several experiments defor­mities and radiolucent foci appeared which showed similarity to those seen in dyschondroplasia{ectopic masses of cartilage}. When one  half of the distal  growth  plate  of the radius  had  been  irradiated then lagging  behind of  ossitication could  be demonstrated after 9 days.”  Part of the injured cartilage was left behind in the metaphysis as the bone was growing.  Another part adhered to the bony plate of epiphysis.  In between, there was what appeared to be normal growing regenerating cartilage.

2nd series. Another set of experiments describes growth plate regeneration via interstitial growth.  This type of growth would be very promising in terms of inducing adult height growth.  No perichondrium and no zone of ranvier ossification groove was present.  So there was no pool of typical growth plate progenitor cells.

“The regeneration seemed to take place from the viable parts of the germinal cell layer.”<-Bone and cartilage tends to come from the mesodermal layer.  But mesodermal cells implies the type of immature cells like embryonic stem cells.  But perhaps the right mechanical forces can still induce more adult mesenchymal stem cells into becoming more immature cells and into pre-chondrocyte growth plate cells.

“lt is generally accepted that interstitial latitudinal growth occurs in the very young animal, when the germinal zone cells of the growth plate are adjacent to a largely cartilaginous epiphysis as the tissues are plastic.”<-Plastic refers to irreversible deformation rather than elastic deformation where the object returns to normal.  You can get plastic deformation in adult bones it’s just much harder.

Later the study states that interstitial growth can still occur even against a more rigid epiphysis as long as the germ cells are present.

Occurding to Figure 16 area C, the germinal cells look much like resting zone cells.  We’ll have to study how much LSJL and other mechanical stimuli can induce mesenchymal stem cells to be more like mesodermal germinal cells.

A Mechanical Jack-like Mechanism Drives Spontaneous Fracture Healing in Neonatal Mice

“To study the mechanism underlying spontaneous regeneration of fractured bones, we left humeral fractures induced in newborn mice unstabilized, and rapid realignment of initially angulated bones was seen. This realignment was surprisingly not mediated by bone remodeling, but instead involved substantial movement of the two fragments prior to callus ossification. Analysis of gene expression profiles, cell proliferation, and bone growth revealed the formation of a functional, bidirectional growth plate at the concave side of the fracture. This growth plate acts like a mechanical jack, generating opposing forces that straighten the two fragments. Finally, we show that muscle force is important in this process, as blocking muscle contraction disrupts growth plate formation, leading to premature callus ossification and failed reduction.”

“The ossification of soft callus bares similarities to the process of endochondral ossification during skeletogenesis”

“another type of growth plate known as synchondrosis{these do fuse though} is located between the bones of the skull base. The synchondroses exhibit a remarkably organized structure, as each consists of two mirror-image growth plates facing opposite directions. These growth plates are fed by a shared resting zone located between them. The formation of double layers of prehypertrophic and hypertrophic chondrocytes drives growth in opposite directions, leading to expansion of the skull volume”

“the growth plate must also be able to generate considerable forces. Indeed, studies in various animal models as well as in humans suggest that the different growth plates can generate forces that range from the equivalent of 40% to 200% of body weight”

“an active bidirectional growth plate is formed at the concave side of the callus to mediate bone growth. This finding strongly supports our hypothesis that bone growth by the bidirectional growth plate generates the force required for the movement of the two fracture fragments during reduction, similar to a “mechanical jack” mechanism.”

“Expression analysis of SRY box containing gene 9 (Sox9), Col2a1, and Col10a1 revealed that the absence of muscle contraction led to symmetric chondrogenesis and loss of the bidirectional growth plate organization”

“in the absence of muscle contraction the callus fails to organize and act as a growth plate and undergoes early ossification”

“all of the characteristics of an active growth plate exist in the callus at the concave side of the fracture site, including gene expression profiles, cell proliferation, and bone growth. We therefore argue that the growth plate in the callus serves not only for intermediate stabilization, but also to actively promote bone reduction. However, unlike the epiphyseal growth plates and similar to the synchondroses that mediate cranial base expansion, the bidirectional growth plate at the fracture site drives growth in opposite directions. This generates force that moves the fragments toward straightening in a mechanical jack-like effect.”

Meclozine is available without a prescription: Meclizine Chewable Tablets – 25mg – Model 85207 – Btl of 100.  Open growth plates only though but it looks like it could be very effective as it is similar to CNP which has a pretty big impact on height.

Even if you don’t understand anything below.  Please spread the word about this study.  It looks like a quite promising OTC height increase supplement.

Unfortunately, there have been no studies on Meclizine and human height and as shown by the study below there is cell toxicity to Meclizine.  Since Meclizine is a well established supplement, anyone who is currently undergoing longitudinal growth and wants to grow taller should take Meclizine at dosages recommended on the bottle and following all other directions about directed use.

Meclozine Facilitates Proliferation and Differentiation of Chondrocytes by Attenuating Abnormally Activated FGFR3 Signaling in Achondroplasia.

“Achondroplasia (ACH) is one of the most common skeletal dysplasias with short stature caused by gain-of-function mutations in FGFR3 encoding the fibroblast growth factor receptor 3. We used the drug repositioning strategy to identify an FDA-approved drug that suppresses abnormally activated FGFR3 signaling in ACH. We found that meclozine, an anti-histamine drug that has long been used for motion sickness, facilitates chondrocyte proliferation and mitigates loss of extracellular matrix in FGF2-treated rat chondrosarcoma (RCS) cells. Meclozine also ameliorated abnormally suppressed proliferation of human chondrosarcoma (HCS-2/8) cells that were infected with lentivirus expressing constitutively active mutants of FGFR3-K650E causing thanatophoric dysplasia, FGFR3-K650M causing SADDAN, and FGFR3-G380R causing ACH. Similarly, meclozine alleviated abnormally suppressed differentiation of ATDC5 chondrogenic cells expressing FGFR3-K650E and -G380R in micromass culture. We also confirmed that meclozine alleviates FGF2-mediated longitudinal growth inhibition of embryonic tibia in bone explant culture. Interestingly, meclozine enhanced growth of embryonic tibia in explant culture even in the absence of FGF2 treatment!!!!!!!. Analyses of intracellular FGFR3 signaling disclosed that meclozine downregulates phosphorylation of ERK but not of MEK in FGF2-treated RCS cells. Similarly, meclozine enhanced proliferation of RCS cells expressing constitutively active mutants of MEK and RAF but not of ERK, which suggests that meclozine downregulates the FGFR3 signaling by possibly attenuating ERK phosphorylation{Since everything . We used the C-natriuretic peptide (CNP) as a potent inhibitor of the FGFR3 signaling throughout our experiments, and found that meclozine was as efficient as CNP in attenuating the abnormal FGFR3 signaling!!!!!!!!{And CNP is a huge height increase disease}. ”

Loss of function of FGFR3 leads to tall stature and Meclozine decreases FGFR3 function even in normal cells.

“CNP has a short half-life and continuous intravenous infusion is required for in vivo experiments. The CNP analog with an extended half-life, BMN 111, has recently been developed and significant recovery of bone growth was demonstrated in ACH mice by subcutaneous administration of BMN 111″

” 0, 1, 2, 5, 10, and 20 µM of meclozine exhibited dose-dependent increases in RCS[Rat Chondrosarcoma cells] proliferation. We did not observe dose-dependency at 50 µM, which was likely due to cell toxicity. We also confirmed that 10 and 20 µM of meclozine increased the number of RCS cells”

“treating RCS cells with FGF2 for four hours induced expressions of matrix metalloproteinase 10 (Mmp10), Mmp13, and a disintegrin-like and metalloproteinase with thrombospondin type 1 motif 1 (Adamts1) transcripts{LSJL upregulates Admts1 and MMP13 but still increases height, LSJL in conjunction with Meclozine could increase height more}. We found that meclozine and CNP significantly suppressed expressions of these matrix metalloproteinases. We also quantified expressions of Col2a1 and Acan transcripts, but FGF2 treatment for 72 hours did not reduce the expression levels of these genes in RCS cells”

The rightmost figure(the one with n=6) is the Meclozine solo group.  Eyeballing it, it looks like it could be about 5% increase in longitudinal growth.  Note that a 5% increase on 5’9″ is 6’0″.

FGFR3 signaling in chondrocytes.  LSJL does increase ERK phosphorylation.  Maybe that is a side effect of the boost of LSJL on longitudinal growth and not a cause of longitudinal growth.  And that both Meclozine and LSJL would have additive effects.

” a synthetic compound A31 is an inhibitor of the FGFR3 tyrosine kinase by in silico analysis. They demonstrated that A31 suppresses constitutive phosphorylation of FGFR3 and restores the size of embryonic femurs of Fgfr3Y367C/+ mice in organ culture. In addition, A31 potentiates chondrocyte differentiation in the Fgfr3Y367C/+ growth plate.  P3 has a high and specific binding affinity for the extracellular domain of FGFR3. They showed that P3 promotes proliferation and chondrogenic differentiation of cultured ATDC5 cells, alleviates the bone growth retardation in bone rudiments from TD mice (Fgfr3Neo-K644E/+ mice), and finally reversed the neonatal lethality of TD mice”

“These novel FGFR3 tyrosine kinase inhibitors, however, may inhibit tyrosine kinases other than FGFR3 and may exert unexpected toxic effects in humans. Meclozine may also inhibit unpredicted tyrosine kinase pathways, but we can predict that there will be no overt adverse effect, because meclozine has been safely used for more than 50 years.”

Here’s a study that will provide some insight into FGFR3 and why it inhibits growth in some cases but not in others:

The paradox of FGFR3 signaling in skeletal dysplasia: why chondrocytes growth arrest while other cells over proliferate.

“Somatic mutations in receptor tyrosine kinase FGFR3 cause excessive cell proliferation, leading to cancer or skin overgrowth. Remarkably, the same mutations inhibit chondrocyte proliferation and differentiation in developing bones, resulting in skeletal dysplasias, such as hypochondroplasia, achondroplasia, SADDAN and thanatophoric dysplasia{So maybe the longitudinal growth induced by LSJL is not produced by chondrocytes but rather by the stem cells which would be promising evidence for post LSJL-inducable height growth}. A similar phenotype is observed in Noonan syndrome, Leopard syndrome, hereditary gingival fibromatosis, neurofibromatosis type 1, Costello syndrome, Legius syndrome and cardiofaciocutaneous syndrome. Collectively termed RASopathies, the latter syndromes are caused by germline mutations in components of the RAS/ERK MAP kinase signaling pathway. This article considers the evidence suggesting that FGFR3 activation in chondrocytes mimics the activation of major oncogenes signaling via the ERK pathway. Subsequent inhibition of chondrocyte proliferation in FGFR3-related skeletal dysplasias and RASopathies is proposed to result from activation of defense mechanisms that originally evolved to safeguard mammalian organisms against cancer.”

“FGFR3 [inhibits] chondrocyte proliferation. FGFR3/ERK signaling triggers disintegration of the cyclin D3-cdk6 complex in the G1 phase of the cell cycle, followed by increased association of p21WAF1 and p27Kip1 cell cycle inhibitors (CKI) with cyclin-cdk2 and cyclin-cdk4 complexes, leading to inhibition of their kinase activities. Upon FGFR3 activation, CKIs accumulate at the protein level, due to the interaction with transcriptionally induced cyclin D1. cyclin D1 upregulation also mediates the pro-mitogenic effects of FGFR/ERK signaling. Duration, magnitude and timing of cyclin D1 and p21WAF1 induction in the G1 phase of a cell cycle determines the nature of the response to an ERK signal. A strong but transient ERK activation in the early G1 induces intermittent p21WAF1 accumulation and stable cyclin D1 expression, leading to cell proliferation. In contrast, robust and persistent ERK activation leads to stable p21WAF1 accumulation and growth inhibition despite the concomitant induction of cyclin D1.

In chondrocytes, unlike most other cell types, FGFR3 activation elicits highly prolonged ERK activation lasting for up to 24 h. This phenotype is likely to stem from the maintenance of ERK pathway activation within the protein complexes interacting directly with FGFR3. ”

So FGFR3 inhibits growth in chondrocytes but not other cell types is because FGFR3 activates ERK for too long which leads to growth inhibition due to excess levels of p21WAF1.

“In chondrocytes, the premature senescence caused by FGFR3 activation does not involve the p53 pathway but appears CKI-dependent as induction of several CKIs (p21WAF1, p27Kip1, p16INK4a, p18INK4c, and p19INK4d) accompanies FGFR3-mediated inhibition of chondrocyte proliferation in vitro and in vivo”

NEW:

Meclozine Promotes Longitudinal Skeletal Growth in Transgenic Mice with Achondroplasia Carrying a Gain-of-Function Mutation in the FGFR3 Gene.

“Achondroplasia (ACH) is one of the most common skeletal dysplasias causing short stature owing to a gain-of-function mutation in the FGFR3 gene, which encodes the fibroblast growth factor receptor 3. We found that meclozine, an over-the-counter drug for motion sickness, inhibited elevated FGFR3 signaling in chondrocytic cells. To examine the feasibility of meclozine administration in clinical settings, we investigated the effects of meclozine on ACH model mice carrying the heterozygous Fgfr3ach transgene. We quantified the effect of meclozine in bone explant cultures employing limb rudiments isolated from developing embryonic tibiae from Fgfr3ach mice. We found that meclozine significantly increased the full-length and cartilaginous primordia of embryonic tibiae isolated from Fgfr3ach mice. We next analyzed the skeletal phenotypes of growing Fgfr3ach mice and wild-type mice with or without meclozine treatment. In Fgfr3ach mice, meclozine significantly increased the body length after two weeks of administration. At skeletal maturity, the bone lengths, including the cranium, radius, ulna, femur, tibia, and vertebrae were significantly longer in meclozine-treated Fgfr3ach mice than in untreated Fgfr3ach mice. Interestingly, meclozine also increased bone growth in wild-type mice. The plasma concentration of meclozine during treatment was within the range that has been used in clinical settings for motion sickness. Increased longitudinal bone growth in Fgfr3ach mice by oral administration of meclozine in a growth period indicates potential clinical feasibility of meclozine for the improvement of short stature in ACH.”

“A CNP analog with an extended half-life, BMN-111, has recently been developed, and significant bone growth recovery was demonstrated in amouse model of ACH by subcutaneous administration of BMN-111”

“Meclozine was administrated to 2-week-old wild-type mice for 3 weeks. As wild-type mice were weaned at 2 weeks after birth, we started meclozine treatment 1 week earlier than that for Fgfr3ach mice.  The body length of meclozinetreated mice was significantly longer than that of untreated mice after 1 week”

“the plasma concentrations of meclozine used in the current study (0.2 or 0.4 g of meclozine per kilogram food).”

“Meclozine, an OTC H1 inhibitor, has been safely used for motion sickness for more than 50 years, and its optimal dose and adverse effects have already been established”

“in patients with ACH [given treatment with meclozine], the patients could be expected to increase 6.7 to 7.1 cm in height, based on the average height of adults with ACH.”

<-Treatment of mice with meclozine without FGFR3 deficiencies.  The meclozone treated mice are noticeably taller and lengthier.

“A-C, Wild-type mice were treated with meclozine 2 weeks after birth for 3 weeks. A, Visual images and soft X-ray images of wild-type female mice with or without meclozine. Meclozine-treated mice were larger than the untreated mice. B, Body and tail lengths of meclozinetreated
wild-type female mice were significantly longer than those of untreated wild-type female mice. Statistical significance analyzed by two-way ANOVA is shown on the right side of each graph. *P  .05 by Fisher’s LSD test for each pair. C, The lengths of the radius, ulna, femur, tibia, and vertebrae on the soft X-ray films were significantly increased by meclozine treatment by unpaired t test. D and E, Pregnant mice were treated with meclozine from embryonic day 14. D, Visual images and skeletons stained with Alizarin red and Alcian blue of wild-type mice at postnatal day 5, with or without meclozine. Meclozine-treated offspring were larger than untreated offspring. E, The lengths of the ulna, femur, and tibia measured using stained skeletons were significantly increased after meclozine treatment, as assessed by unpaired t test.”

The coloration of regions of an area in an xray reflect their density.  If a region of bone is grayer than normal that bone is less dense.  If a bone is less dense that could mean that it is a region of new growth or that the bone is naturally less dense.  But even though some regions of less density are natural, if these regions of decreased density are expanded it is very possible that this could be indicative of increased growth.  If this expansion occurs in the longitudinal direction then it is indicative of longitudinal bone growth.  If you compare my right and left lateral finger xrays below you can see that my right bone has much greater expansion of these gray regions than the left and the regions extend into the longitudinal direction thus being indicative of longitudinal bone growth.

I need your help to confirm or deny this theory.

I statement I found on white versus black regions in x=rays: “On x-ray, bone and dense materials such as barium are white. Black would be air (lungs or air in the GI tract). Other tissues are in shades of gray. You can see the outline or shadow of the kidneys or certain muscles, for example. But you cannot see these things in detail. X-ray does not show the difference between normal vs. “dead” tissue. A CT scan, or even better, a MRI would be better suited for that type of diagnosis. ”

The darker regions of the bones are more likely to be less dense or possibly new grown bone.  Some bones are naturally less dense than others.  So we have to compare the bones also to standard bones.  If there are more gray areas than normal then it’s likely that there was new bone growth.

Here’s one lateral index finger view:

Which my finger looks more like.  Here’s one that my left finger looks more like(this is also a right index finger):

Have to compare color intensity of areas of right versus left bone.

Here’s a finger with some gray areas.  There is a large gray region on the tip of the proximal finger and some on the bottom part of the distal region of the medial index finger.  Note this is a fractured finger so we’d expect there to be some anabolic growth.

So, it’s normal to have those regions of darker bone.

There are other potential reasons why one part of the bone can be much darker than the other but one strong possibility is that it is new LSJL induced bone growth.  Since LSJL involves lateral loading it makes sense that much of the growth can be better observed than a lateral angle(the differences in coloration can not be seen as well from an overhead view).  From the overhead view the right index finger looks to be whiter than the left index finger infact.  Click on the images below to enlarge them.

Each of the circled points A-D represents a region of bone that is much lighter than the other.  On the left side these regions are present but the are much lighter.  At point A it seems to blend better with the whiter region of the bone in contrast to the right side where it is more a bulbous head.  The bone at B looks totally different.  C and D are similar but the right(LSJL loaded side the darker region of the bone is much bigger).

Percentage growth based on darker area versus lighter area:

Proximal Head(Tip of dark region to tip of light): 23.4 pixels

(bottom of proximal index finger bone to top of light region): 170.4 pixels

13.7% growth.

However, I’d guess that my left bones are about 1% longer than my right.  If my right finger did grow longer than 10% my right proximal finger would measure longer than my left which is not the case.  You can see from the above images of other images that the normal finger has these darker regions, those regions are just expanded above normal.  So maybe the the proximal finger bone didn’t grow the entire gray region but the gray region just expanded in response to the stimulus.  In fact a study has shown that the finger bones naturally grow into adulthood.  So these darker regions of bone could be a sign of adult finger growth.  The same study stated that metacarpals tend to decrease in length so the fact that my right metacarpal grew longer is a good sign that this growth could extend to other bones.

What’s a bit unfortunate is that the growth plates are on the proximal(bottom) end of the finger bones and the gray regions are on the distal(top) ends of the finger bones.  However, the distal regions of my right finger bones do seem to be a bit more gray than the left bones so it is possible that the growth plate region was stimulated by LSJL.

Below is some more information about x-rays.

Here’s something I found describing xrays:

” The bone along the joint is usually whiter (called “sclerosis”) and may have little points of bone growing out (called “osteophytes”). There may be holes in the bone ( called “cysts”) and the bones may be starting to slide out of alignment (called “subluxation”).”<-None of these images quite explains the growth in LSJL.

Here’s a comment I found from Yahoo! Answers:

“Bones always appear as white images in regular xrays. However they arent really white because the film is clear, the plastic on the view box is white. But on xray film it is coated with a metalic layer. The xrays make the metalic layer stick to the film. So the black part of the film is where all the xrays reach the film. If the area on the xray is gray, then that means that some of the xrays are getting through implying that the structure is more dense than the black part. Soft tissue appears gray. The bone is a very dense structure allowing minimal to no xrays getting through. The film is then put through the processor and the film runs through chemicals that make the picture “stay” on the film. It is then rinsed and dried. Since the xrays make the metalic layer stick, none stick to the area of the bone because no radiation got through and the layer was washed off during processing. This is why bones appear white, they are the densest structure.”

Here’s another response from Yahoo! Answers regarding why one part of the bone is darker than the other:

“When a bone X-ray is taken, radiation is momentarily irradiated on the area being examined. X-rays pass through the body to produce an image on film. Structures like bone that are dense and have a high atomic number absorb a lot of X-rays, so less X-rays reach the film and the bone appears white on the film. Muscle, fat, tumour, and fluid absorb less X-ray than bone, and appear darker than bone on the film. Air distributed in various pockets within the body (usually due to an abnormality) has a low atomic number and density, and consequently appears black, because most X-rays pass through without being absorbed. You would be advised to consult the doctor or radiologist dealing with this matter and enquire as to the suspected cause of the description that you describe. You may find that further tests/examinations will result from the X-Ray result which will determine or assist the diagnosis.
The information provided here should not be used during any medical emergency or for the diagnosis or treatment of any medical condition. A licensed physician should be consulted for diagnosis and treatment of any and all medical conditions. “<-I don’t think air pockets could explain the larger gray area on the right side bone.

On this page is an image of tissue types in regard to whiteness: http://radiologymasterclass.co.uk/tutorials/physics/x-ray_physics_densities.html#top_first_img.  The coloration is consistent with soft tissue.

Here’s an image of a periosteal chondroma:

“In this x-ray of the wrist, the saucer-like hollow in the radius bone is a classic indication of a periosteal chondroma. “<-That’s not really consistant with what’s going on in my bone.

As for my ganglion cysts according to here, they are usually caused by myxoid(mucous) degeneration of collagen and usually lined with flattened mesothelium.

I can’t really find any adequate explanation as to the brighter regions of my finger.

Update by Michael:

From what I remember from being in some medical derivative courses back in my university days, I do remember the idea of X-rays penetrating into human tissue. White light means that the X-rays did not completely go through the tissue, while the black color is an indicator that the X-rays went through less dense tissue, like fat and tendons. 

I don’t have the enlarged X-rays pictures with me anymore but I don’t remember the left or right index fingers having any major differences in color. I think the important thing to remember is that we are looking for bone length differences, not bone density variations.

Now it is theoretically accurate to say that if we can show that LSJl caused bone density changes, causing the X-ray to cause a darker band on a metatarsal bone then LSJL might lead to bone longitudinal growth. However, on a much more practical level, even if the BMD is lowered, that doesn’t seem to translate to bone length increases, even after half a decade of doing joint loading on a consistent basis. I don’t think that it is worth trying to validate the LSJL theory based on a slight difference in color/density from comparing the left and right X-rays of the index fingers. That is too much of a stretch even for me.

As for the fingers growing longer, that actually makes a lot of sense. The human nose gets longer over time, the human ears droop lower and lower, and even the human mandibular joint area grows longitudinally if you have a pituitary problem.

For the old time regular readers, remember my study on why deer antlers can fall off, and regrow back in length every season? It is because of the occurrence of a laceration/osteonomy at the beginning, causing an open wound. A blastema develops in that region. That blastema eventually grows into a pseudo “growth plate”. The top part of the horn is where the mesenchyme is, and it is covered by a layer of perichondrium, NOT periosteum. That means that the top roof surface that is encapsulating the “rest zone’ type cells in the mesenchyme is flexible. It is only being pushed down by air and gravity, not an entire body, like the grow plates in the tibia of an adult human, which can be over 200 lbs of weight. Similarly, the human fingers have the same type of structure, a human anatomical peninsula, like the human tibia-knee area, which is more like an isthmus.

What I am trying to say is that fingers is similar to the horns on the deer. I have already shown a few times that some stem cell powder can regrow fingers. It is not that a big of a stretch to then conclude that human fingers, like noses, and ears, and pregnant female’s feet can grow throughout one’s life.

This study shows that the increase in spinal height after bed rest and space flight may be due to an increase in GAG content in the intervertebral disc.

Assessment of Lumbar Intervertebral Disc Glycosaminoglycan Content by Gadolinium-Enhanced MRI before and after 21-Days of Head-Down-Tilt Bedrest.

“During spaceflight, it has been shown that intervertebral discs (IVDs) increase in height, causing elongation of the spine up to several centimeters. Astronauts frequently report dull lower back pain that is most likely of discogenic origin and may result from IVD expansion. It is unknown whether disc volume solely increases by water influx, or if the content of glycosaminoglycans also changes in microgravity. Aim of this pilot study was to investigate effects of the spaceflight analog of bedrest on the glycosaminoglycan content of human lumbar IVDs. Five healthy, non-smoking, male human subjects of European descent were immobilized in 6° head-down-tilt bedrest for 21 days. Subjects remained in bed 24 h a day with at least one shoulder on the mattress. Magnetic Resonance Imaging (MRI) scans were taken according to the delayed gadolinium-enhanced magnetic resonance imaging (dGEMRIC) protocol before and after bedrest. The outcome measures were T1 and ΔT1. Scans were performed before and after administration of the contrast agent Gd-DOTA, and differences between T1-values of both scans (ΔT1) were computed. ΔT1 is the longitudinal relaxation time in the tissue and inversely related to the glycosaminoglycan-content. For data analysis, IVDs L1/2 to L4/5 were semi-automatically segmented. Zones were defined and analyzed separately. Results show a highly significant decrease in ΔT1 (p<0.001) after bedrest in all IVDs, and in all areas of the IVDs. The ΔT1-decrease was most prominent in the nucleus pulposus and in L4/5, and was expressed slightly more in the posterior than anterior IVD. Unexpected negative ΔT1-values were found in Pfirrmann-grade 2-discs after bedrest. Significantly lower T1 before contrast agent application was found after bedrest compared to before bedrest. According to the dGEMRIC-literature, the decrease in ΔT1 may be interpreted as an increase in glycosaminoglycans in healthy IVDs during bedrest. This interpretation seems contradictory to previous findings in IVD unloading.”

“Average ΔT1 value of all intervertebral discs was 104.87 ms (sd 7.64 ms) pre-bedrest and -20.20 ms (sd 4.70 ms) post-bedrest.”

“It seems to be well established that increased GAG concentration within the IVD will result in a decrease in ΔT1. A high GAG-concentration causes a small ΔT1 during dGEMRIC-measurements because only small amounts of contrast agent shift into the IVD. A low GAG-concentration in turn leads to a high ΔT1. Increased ΔT1 after an intervention (as compared to before) has been interpreted as degeneration process”<So T1 has nothing to do with the height it has to do with the GAG content.  So a decrease in deltaT1 means that GAG content likely increased.

I couldn’t find anything that showed that bone could grow taller in response to creep strain but it seems that other objects can get longer.  Creep Strain can cause a change in shape of bone at very low magnitudes of strain but at very high amounts of time which is important as the amount of load required to induce plastic deformation of bone is outside ordinary means.  The optimal load for creep strain may about half that of which is used to induce fracture.

I could only find studies that showed that creep strain compressed bone not that it could lengthen it.

However, if creep strain can lengthen other objects shouldn’t it be able to do the same to bone?

Here’s a high school science experiment that shows that creep strain can lengthen objects:

Do Materials Get Tired? Do Rubber Bands Get Longer During Use?

“Some materials will slowly deform when a constant force or displacement is applied to them. This time-dependent and permanent deformation is called creep.

If you have ever noticed that chewing gum gradually sags when it is stuck to something or watched a plastic grocery bag gradually tear apart when it is carrying too much weight, you have observed creep!”

The science experiment involves loading a rubber band with a weight for 24 hours to observe creep and then measuring the change in length.

Now rubber bands are much more elastic than bone which is a problem.

Another problem is that based on how the tensile creep strain is applied to the bone other soft tissues will be loaded which may fail first before the bone has undergone creep for an appropriate amount of time.  Another issue is that inducing creep failure in bone may cause loss of bone structural integrity may cause problems.

Methods of inducing creep strain in bone seem to lend itself to several common exercises:

Holding weights for extended periods of time to lengthen arms.  For creep strain it has to be for a significantly long amount of time and then there’s the issue of the soft tissues failing first.  Can anyone find any anecdotal evidence of people who do farmer’s walks(you don’t actually have to walk to induce creep strain just holding the weights is enough) having longer arms?

Hanging to lengthen arms.  And again there’s no guarantee that creep strain will be induced in the arms before soft tissue failure.  And you’d have to do it for quite a sustained amount of time although you can take breaks as creep train is based on fatigue loading so you can rest for brief intervals as long as total bone fatigue gradually increases.

Inversion to lengthen legs although more load than body weight is likely needed and it would be very hard to maintain the kind of duration for creep to take place.

Does anyone have any anecdotal evidence of these exercises increasing arm or leg height?  While common I’m not sure these exercises are best for creep strain based lengthening due to the likelihood of your joints giving out before your bones.

1) Stretching(on the spine)

Read this summation of the theory of spinal stretching.

Although one study indicates that a twisting motion can increase height in some cases, other human studies have suggested that twisting can only reduce height in human models.  This is due to the nucleus pulposus not being mechanically stable in contrast to the annulus fibrosus which can grow.  In response to mechanically strain, there was degeneration in the nucleus pulposus and there is a medical term for this caused degenerative disc disease.

Now, other joints do not have nucleus pulposus like the joints of the ankle and knee so those can potentially grow in size.  Interesting though is that one study found that wingspan decreased more with age than overall height.  Which is contrary to what we would believe with discs being prone to degeneration.  There is an increase in the hand phalanxes continuously throughout life.  Now I received an increase of 0.8%(at least) in my right index finger metacarpal.  So the normal hand phalanx growth does not explain my growth.  That study suggests that articular cartilage can undergo endochondral ossification which can add appositional bone growth to the longitudinal ends of the bone resulting in longitudinal bone growth.

Now one thing is that nucleus pulposus is so prone to degeneration and can reduce height so much is that we can reduce degeneration.  For example by living in zero gravity, by strengthening the muscles surrounding the spine to reduce spinal load, or via spinal tractors/inversion to reduce load allowing water to return to the nucleus pulposus.

This height increase method listed here(Aquatic Vertical Suspension) resulted in an immediate height increase of about 4mm.

2) HGH

People have supplemented with HGH at levels at or greater than those who have “suffered” from gigantism reported no height gain.  Gigantism does not merely involve elevated HGH levels but also resistance to HGH suppression.  Gigantism also involves a tumor.  Two factors that are not involved in HGH supplementation.

There has been no evidence as of yet that HGH can induce exogenous growth plates to induce new longitudinal bone growth.  Although some anecdotal evidence of HGH induced growth has been reported.

3) Microcracks

There hasn’t been any evidence to suggest that microcracks can lengthen bone.  And mineralized bone seems to be incapable of interstitial growth(growth from within ala growth plates) due to high ECM stiffness.  Thus there needs to be an intermediary tissue involved like cartilage in order to lengthen bone in a roundabout way.  So to lengthen bone via microfractures you’d have to reduce ECM stiffness to allow for interstitial growth.  Here’s one possible method to reducing ECM stiffness using acid that has been suggested.

4)Bone Stretching

For example via the Rack.  The amount of load required to induce a bone fracture is  usually a colossal figure like 25000-lbs.  And the amount of load to induce plastic deformation(bone stretching or negatively compression) is usually very close to the fracture point.  This makes the generation of such loads problematic.  That’s why the design of LSJL is to try to induce mesenchymal condensation and neo-growth plate formation.

Creep Strain can induce plastic deformation at much lower loads.  However, a considerable continuous amount of load is required to induce 1-2 weeks.  I could not find any evidence of creep strain inducing plastic deformation in a positive way(stretching), only a negative way(compression).  I couldn’t find any other studies where length was even considered as only damage to the bone was measured.