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.

http://www.pedorthpath.com/about.html

Aneurysmal Bone Cyst<-may cause enlargement of affected bone.  Sometimes contain cartilage like-matrix.

Aneurysmal bone cyst of the mandible: A case report and review of literature

“Aneurysmal bone cyst (ABC) is rare benign lesions of bone which are infrequent in craniofacial skeleton. ABC’s are characterized by rapid growth pattern with resultant bony expansion and facial asymmetry. We describe a case of ABC in a 25 year old male patient affecting the body of the mandible with expansion and thinning of the buccal and lingual cortical plates. Treatment consisted of surgical curettage of the lesion. A one year follow- up showed restoration of facial symmetry and complete healing of the involved site.”

“ABC is a benign cystic lesion of bone, composed of blood-filled spaces separated by connective tissue septa containing fibroblasts, osteoclast-type giant cells and reactive woven bone”

 Spontaneous healing of aneurysmal bone cysts. A report of three cases.

” We report three cases of spontaneous healing of aneurysmal bone cysts (ABC). In one case histological material was obtained after resection of the already ossified expansile mass discovered as a lytic lesion seven months previously. In the two other patients, spontaneous ossification of a radiologically presumed ABC in the lytic and expansile phase was observed after nine and seven months respectively. The healed lesions have remained stable at 12, 32, and 36 months respectively. These findings suggest that when the diagnosis can be made with confidence, and the lesion is in a location and at a stage that does not entail any risk of fracture or compression, expectant management should be considered. Our three patients were aged 22, 19 and 18 years, older than usual for developing ABC. This is also true for many of the few other reported cases of spontaneous or almost spontaneous healing and suggests that ABC has a greater tendency to stabilise in older patients.”

If you look at the results the bone expansion seems to be permanent.

Cortical bone blocks height growth so it’s erosion is beneficial but only if coupled with replacement tissue(ideally cartilage).

Bone erosion in rheumatoid arthritis: mechanisms, diagnosis and treatment

“Bone erosion is a central feature of rheumatoid arthritis and is associated with disease severity and poor functional outcome. Erosion of periarticular cortical bone, the typical feature observed on plain radiographs in patients with rheumatoid arthritis, results from excessive local bone resorption and inadequate bone formation[so bone erosion occurs in everyone the balance is just switched in RA]. The main triggers of articular bone erosion are synovitis, including the production of proinflammatory cytokines and receptor activator of nuclear factor κB ligand (RANKL), as well as antibodies directed against citrullinated proteins. Indeed, both cytokines and autoantibodies stimulate the differentiation of bone-resorbing osteoclasts, thereby stimulating local bone resorption. Although current antirheumatic therapy inhibits both bone erosion and inflammation, repair of existing bone lesions, albeit physiologically feasible, occurs rarely. Lack of repair is due, at least in part, to active suppression of bone formation by proinflammatory cytokines. This Review summarizes the substantial progress that has been made in understanding the pathophysiology of bone erosions and discusses the improvements in the diagnosis, monitoring and treatment of such lesions.”

“erosions can also be observed in forms of arthritis other than RA, such as gout, psoriatic arthritis, spondyloarthritis and even osteoarthritis,”

“bone erosions typically emerge at the site at which the synovium comes into direct contact with bone (known as bare areas), suggesting that anatomical factors render these areas of juxta-articular bone susceptible to erosion”

“Anatomical factors that predispose skeletal sites for erosions include: the presence of mineralized cartilage, a tissue particularly prone to destruction by bone-resorbing cells; the insertion sites of ligaments to the bone surface, which transduce mechanical forces to the bone and could induce microdamage; and inflamed tendon sheaths (termed tenosynovitis), which pass by the bone surface, and enable the spread of inflammation from the tendon to the articular synovium“<-maybe the transmission of mechanical forces via ligaments could be exploited to induce height gain.

“The small bone channels that penetrate cortical bone carry microvessels and bridge the outer synovial membrane and the inner bone marrow space; these channels are also prone to erosive change early in the course of RA. The microvessels located within these channels facilitate homing of osteoclast precursor cells to the bone, which, upon contact with bone and receipt of the appropriate molecular signals, differentiate into osteoclasts. Widening of cortical bone channels, as a result of osteoclast-mediated bone resorption, is a typical early change in animal models of arthritis”

“Osteoclasts, giant multinucleated cells derived from the monocyte lineage, are the only cells capable of resorbing bone in the body.^2,3 Osteoclasts are designed to resorb bone by adhering tightly to the bone surface through interactions with both integrins and extracellular matrix proteins, as well as by assembling junctions, which seal the bone surface and the osteoclast and thereby separate bone from the surrounding extracellular space. Proton pumps along the osteoclasts’ ruffled border then create an acidic milieu, enabling solubilization of calcium from bone. Matrix enzymes synthesized by the osteoclast, including cathepsin K, matrix metalloproteinase 9 and tartrate-resistant acid phosphatase type 5 (TRAP), degrade the bone matrix”

“Development of osteoclasts occurs locally in the synovial tissue as a result of expression of the two essential osteoclastogenic mediators, macrophage colony-stimulating factor 1 (M-CSF)and receptor activator of nuclear factor κB ligand (RANKL; also known as TNF ligand superfamily member 11). This process involves the migration of monocyte-lineage cells from the bone marrow into the secondary lymphatic organs and finally into the joints. The differentiation step at which monocytes enter the joint is unclear. Indeed, monocytes could be already committed to a certain monocyte lineage, such as M1 or M2 macrophages, dendritic cells or osteoclast precursor cells when they enter the joint. Some data suggest that TNF, a key proinflammatory cytokine expressed in RA synovial tissue, stimulates the migration of osteoclast precursor cells from the bone marrow into the periphery. In addition, TNF stimulates expression of surface receptors such as osteoclast-associated immunoglobulin-like receptor before the precursor cells enter the joint, and these receptors facilitate differentiation.  Once within the microenvironment of the joint, these cells are exposed to M-CSF and RANKL, and differentiate toward osteoclasts. Final differentiation into bone-resorbing osteoclasts is then achieved following contact with the bone surface.”

Inflammation plays a role in osteoclast formation.

Todd Dodge is a scientist who works at Hiroki Yokota’s lab which developed the beginnings of LSJL.  Most of the paper is not relevant to LSJL except for his data that compares the inside of the control bone and an axial loaded bone.  The difference in the cracks is not as dramatic as the control and LSJL loaded bone.    This indicates that LSJL may alter bone structure more dramatically than typical loading and hopefully in such a way that facilitates neo-growth plate formation.  The key takeaway is the sample LSJL device provided in the picture at the end of this article and in the appendix of Todd Dodge’s paper.

Experimental and Computational Analysis of Dynamic Loading for Bone Formation<-Link to thesis at end of article

This paper is written by Todd Dodge who works closely with Hiroki Yokota who was involved in the initial ideas behind LSJL.

“Curvature in the structure of bone was hypothesized to enhance its damping ability and lead to increased bone formation through bending. In addition, loading at frequencies near the resonant frequencies of bone was predicted to cause increased bone formation, specifically in areas that experienced high principal strains due to localized displacements during resonant vibration“<-Is there a specific frequency for cartilage formation?

“Many types of applied mechanical loading of the skeleton have been proposed as potential treatments for osteoporotic conditions, including whole body vibration, axial loading or bending of long bones, and lateral joint loading. Each mechanical loading modality is thought to strengthen bone by causing dynamic fluctuations in intramedullary fluid pressure in areas that experience enhanced stresses and strains due to the applied load. This dynamic pressure gradient{This dynamic pressure gradient may also lead to stem cells differentiating into chondrocytes to form neo-growth plates} may cause fluid flow through the lacunocanalicular network of pores in the bone, causing a shear stress to be applied to osteocytes that inhabit those pores and channels. This shear stress may excite the osteocytes, causing activation of osteoblast activity and initiation of the bone remodeling process. Mechanical loading may also lead to application of force directly to osteocytes as strain in the bone matrix changes the shape of the lacunae and canaliculae{plastic changes in the bone matrix could lead to permanent lengthening? But it is unlikely given that bone is known for not being capable of interestitial growth}, imposing deformations on the osteocyte and its processes”

Todd Dodge used lateral knee loading on OVX rats.  1N of load was used at 5Hz for 5 min for a group of rats that was tail suspended.  Loading was done once a day for five straight days.  For a group of rats that were OVX 15Hz for 3 min for 10 days(5 days on, then one off)  12 week-old female sprague dawley rats.  So sort of medium along in the growing process with it starting to taper off.

“The slight increase in BMD in hindlimb-suspended mice may be attributed to additional mechanical stress being applied to the lumbar section of the body, possibly increasing bone growth in that area.”

Unfortunately longitudinal growth was not measured.

Here’s the tibia response to axial loading:

Compare this to the LSJL holes which are much bigger between control and loaded and are larger.

“Future studies may incorporate not only cortical bone but also trabecular bone and growth plates, as well as surrounding tissues such as muscle, skin, and joints.”<-We may need to wait for further studies to get the results we need for LSJL.

“the effects of loading may not only be localized to nearby bones, but may have remote impacts in the spine.”

Here’s the knee loading device that he recommends, note though it is designed for BMD not for lengthening: