Does this study disprove LSJL and growth plate loading? No

Here’s a study that shows that growth plate loading can stunt growth but it also shows that it can enhance growth in one vertebrae which emphasizes the importance of developing the proper loading method.

In vivo dynamic loading reduces bone growth without histomorphometric changes of the growth plate

“This in vivo study aimed at investigating the effects of dynamic compression on the growth plate. Rats (28 days old) were divided into three dynamically loaded groups, compared with two groups (control, sham). A device was implanted on the 6th and 8th caudal vertebrae for 15 days{but note not on the 9th vertebrae which grows as we’ll see later}. Controls (n = 4) did not undergo surgery. Shams (n = 4) were operated but not loaded. Dynamic groups had sinusoidal compression with a mean value of 0.2 MPa: 1.0 Hz and ±0.06 MPa (group a, n = 4); 0.1 Hz and ±0.2 MPa (group b, n = 4); 1.0 Hz and ±0.14 MPa (group c, n = 3). Growth rates (µm/day) of dynamic groups (a) and (b) were lower than shams (p < 0.01). Growth plate heights, hypertrophic cell heights and proliferative cell counts per column did not change in dynamic (a) and (b) groups compared with shams (p > 0.01). Rats from dynamic group (c) had repeated inflammations damaging tissues{this group had the highest frequency of loading}; consequently, their analysis was unachievable. Increasing magnitude or frequency leads to growth reduction without histomorphometric changes. However, the combined augmentation of magnitude and frequency alter drastically growth plate integrity. Appropriate loading parameters could be leveraged for developing novel growth modulation implants to treat skeletal deformities{the authors themselves even allude to with this sentence that this does not disprove growth modulation but that it only suggests that it’s important to develop the appropriate growth modulation method}.”

“With the approval of the Institutional Animal Care Committee, 19 male Sprague–Dawley rats were received at the age of 21 days old. After 1-week of acclimatization, the protocol was conducted from 28 to 43 days old, corresponding to the rat pubertal growth spurt”

“The stress variation was chosen at a mean value of 0.2 MPa as it represents a wide physiological stress interval that is still retarding but not arresting bone growth (stress value over 0.6 MPa). The frequencies were either lower (0.1 Hz) or close to an average walking frequency (1.0 Hz) for humans. ”

“The loading device was adjusted daily at the same time of day for 10 min under isoflurane to compensate for longitudinal growth.”

“three caudal vertebrae (one loaded Cd7; two unloaded (Cd5, Cd9) used as intra-animal controls)”

Note how the CD9 vertebrae grew significantly faster than controls.  Also interestingly the sham group for both CD7 and CD9 vertebrae grew faster than controls.  “Shams (n = 4) were operated but no compression was applied.” <-so the operation itself could be stimulatory on the growth

“The ultimate dynamic (c) condition, combining an increase in both maximum magnitude and frequency, was tested only on three animals since severe inflammation occurred.”

CD9 has a significant increase in all growth plate parameters according to these figures.

Clearly the loading regime on CD7 had spillover reduction in growth in CD5 and stimulatory effect on growth in CD9.  It’s hard to say why that is without looking at say a stress strain analysis.  The device could be doing indirect tensile strain on CD9 and compressive strain on CD5.   But this study shows the importance of finding the right loading method in order to manipulate longitudinal bone growth.

Michael former admin of Natural Height Growth on Cyborg 4 Life’s Podcast

I think Micahel is too skeptical of non-surgical methods.  Weightlifting for example is far more effective than any surgical method to increase muscle(that I know) and CRIPSR technology to inhibit myostatin.  And weightlifting has life extension benefits over potential surgical technology.  As catabolism(fasting, temperature exposure, exercise) all increase life via autophogy and surgery once in a while cannot currently do that.  A regular way of stimulating longitudinal bone growth will have an exercise benefit over surgery and could lead to life extension.  Any form of marrow stimulation will potential have strong health benefits.

Also, I think Michael is too negative in regards to potential surgical/advanced methods of height increase.  Scientific progress is very inefficient.  I don’t think there’s anyone who’s saying that the way science is conducted is optimal.  It’s ultimately capitalism rewards people for doing the least amount of work for the most money.  And science has tons of failures which makes it more profitable to go into something with more guaranteed success like computers.  If science were done optimally then I think it would be more fair to criticize the snail like advancement in a lot scientific fields.

Will this finger stretcher work to increase hand size?

Finger stretcher

We know that the jaw bone can grow throughout adulthood via endochondral ossification of the articular cartilage. This may be why we see people with acromegaly have very large jaws. The reason that the jaw bone continues to grow at the articulations and the other bones don’t is because the jaw bone is less constrained by ligaments and is very moveable so the stress that the articular cartilage undergoes is enough to induce articular cartilage endochondral ossification and also the lateral pterygoid muscle is attached to the articular cartilage directly so if you stimulate the lateral pterygoid muscle in any way either via forced mouth opening or a bite jumping appliance you get the pull with if it’s sufficient results in articular cartilage endochondral ossification. You can literally see this in the histological slides in the above link. The problem is that this likely occurs very slowly unless cell turnover is highly accelerated like via HGH which occurs in acromegaly.

So there are two problems why we don’t see more development of the jaw in normal individuals:

1) The lateral pterygoid muscle isn’t stimulated enough because they don’t chew strong enough food or they don’t practice “mewing“(which does stimulate the lateral pterygoid muscle by the way and it’s slightly dynamic as while you are moving around your muscles have to adjust to keep your tongue to the roof of the mouth). And it’s possible that normal strength training exercise will also stimulate lateral pterygoid development. An exercise like the deadlift pulls on every muscle in the body but that pull won’t be as strong as if you train the lateral pterygoid muscle directly.

2) articular cartilage endochondral ossification is very slow unless again it’s accelerated by HGH.

One problem with the device is that you can’t really do anything else while using it. You might as well just pull on your fingers directly. The other problem I see is that the device doesn’t really look like it would stretch the articular cartilage directly. It looks like it would mostly stretch the skin.

We’d have to really look at the pull to see if it was pulling directly at the articular cartilage. The best bet in my mind to provide a sufficient stretch on the articular cartilage would be a twisting or bending motion of the joint. This would get around the issue of the ligaments limiting the potential stretch. The issue would be potential cartilage damage from improper joint movement. Also based on joint mechanics it may still not stretch the articular cartilage in a sufficient manner.

BREAKTHROUGH! Sea cucumber may boost longitudinal bone growth


Sea cucumber is available for sale but it is very expensive.  I found some sea cucumber tablets that were cheap however it’s not for certain that the tablets have all the benefits of eating sea cucumbers directly.

Novel Peptides from Sea Cucumber Intestine Hydrolysates Promotes Longitudinal Bone Growth in Adolescence Mice through Accelerating cell cycle progress by Regulating Glutamine Metabolism

“Sea cucumber intestines are recognized as a major by-product in sea cucumber processing industry and have been shown to have antioxidant properties. However, whether the sea cucumber intestine is beneficial to osteogenic remains unknown. In this study, low molecular weight rich in glutamate/glutamine peptides were obtained from sea cucumber intestines (SCIP) by enzymatic hydrolysis, and orally administered to adolescent mice to investigate the effects on longitudinal bone growth. The results showed that the SCIP supplement significantly increased the femur length and new bone formation rate by 9.6% and 56.3%, and elevated the serum levels of osteogenic markers ALP, Collagen I and OCN{this is pretty nuts.  I couldn’t find studies directly measuring what effect glutamine has on longitudinal bone growth directly}. Notably, H&E staining showed that SCIP significantly increased the height of the growth plate, in which the height of the proliferation zone was elevated by 97.4%. Glutamine is a major determinant of bone growth. We found that the SCIP supplement significantly increased glutamine levels in the growth plate by 44.2% and elevated the expression of glutamine metabolism-related enzymes Gls1 and GLUD1 in the growth plate{so it’s possible that sea cucumbers could have a benefit on glutamine in the growth plate due to some other ingredient in the cucumber other than the glutamine itself}. Further, SCIP upregulated growth plate acetyl coenzyme A levels to promote histone acetylation and accelerated cell cycle progression by upregulating Sox9 expression, thereby contributing to the rapid chondrocyte proliferation. To our best knowledge, this is the first report that SCIP could enhance longitudinal bone growth via promoting growth plate chondrocyte proliferation. Our present study will provide new ideas and a theoretical basis for high-value utilization of sea cucumber intestine.”

“the peptide from Euphausia superba promoted longitudinal bone growth in adolescent mice.  supplement with enzymatic hydrolysate of Stichopus japonicus could promote bone formation in vivo and in vitro.”

“the avascular nature of the growth plate makes glutamine a potential factor for regulating longitudinal bone growth”

“the SCIP supplement significantly increased femur length by 6.8% (SCIP-L{LOW DOSE}) and 9.6% (SCIP-H{High dose}) compared with the normal group”<-so we don’t know if even more is better than the doses mentioned.  The effect of growth plate height, proliferative height, and hypertrophic chondrocytes was also greater based on dose.

“the serum glutamine levels were gradually increased to a maximum between 0.25 h and 0.5 h and returned to baseline after 2 h. Conversely, as serum glutamine levels fell back, glutamine levels in muscle and femur peaked sequentially at 2 h and 3 h.”<-theoretically it could be worthwhile to take glutamine every 2 hours which would be very difficult to do.

“glutamine metabolism has been shown to upregulate chondrocyte proliferation genes (especially Sox9) by epigenetic modification”<-obviously epigenetic modification is very powerful.

“glutamine promoted the growth plate chondrocyte proliferation during endochondral ossification through acetylation modification of the histone 3K9”

So they did have a glutamine only group.  And the sea cucumber growth increased growth plate height further than that.  Also if you look at the growth plates, it’s a pretty dramatic difference.

Based on the information in this paper, it may be worthwhile for everyone growing to take a low cost sea cucumber supplement(i’d say actual sea cucumber is too expensive).  Not only for the growth plate but also joint cartilage.

This study Stichopus chloronotus aqueous extract as a chondroprotective agent for human chondrocytes isolated from osteoarthitis articular cartilage in vitro finds that sea cucumber has anabolic effects on articular cartilage.

Need help evaluating x-rays

I happened to get x-rays a year ago.  I was performing bone tapping at the time and was unable to get a copy of them because I couldn’t find any computer that would play a CD.  I found something that maybe an abnormality and evidence that bone tapping can induce changes in bone morphology but since I don’t have before and after I can’t be sure.  Like I said I just happened to have had xrays ordered.

Here’s the image of what may be an abnormality(if requested I can post full versions of all three xrays I have):

Here’s another tibia x-ray:

Above is a normal tibial x-ray.  Also here the x-rays of someone who performed LSJL.  Essentially the area circled in red looks clearer(less dense) than normal.  Is that indicative of neo-bone formation?  I can’t be sure.  So if someone could find an expert that would be helpful.  I can also provide copies of all the x-rays.  Please comment or email if you can help.

Study shows proof of concept that microfractures can increase bone length

“To investigate the effect of bone-marrow stimulation (BMS) on subchondral bone plate morphology and remodeling compared to untreated subchondral bone in a validated minipig model.
Three Göttingen minipigs received BMS with drilling as treatment for two chondral defects in each knee. The animals were euthanized after six months. Follow-up consisted of a histological semiquantitative evaluation using a novel subchondral bone scoring system and micro computed tomography (µCT) of the BMS subchondral bone. The histological and microstructural properties of the BMS-treated subchondral bone were compared to that of the adjacent healthy subchondral bone.  The µCT analysis showed that subchondral bone treated with BMS had significantly higher connectivity density compared to adjacent untreated subchondral bone (26 1/mm3 vs. 21 1/mm3, P = 0.048). This was the only microstructural parameter showing a significant difference. The histological semiquantitative score differed significantly between the subchondral bone treated with BMS and the adjacent untreated subchondral (8.0 vs. 10 P = < 0.001). Surface irregularities were seen in 43% and bone overgrowth in 27% of the histological sections. Only sparse formation of bone cysts was detected (1%).BMS with drilling does not cause extensive changes to the subchondral bone microarchitecture. Furthermore, the morphology of BMS subchondral bone resembled that of untreated subchondral bone with almost no formation of bone cyst, but some surface irregularities and bone overgrowth(!).”
And the bone bone overgrowth can be seen to be length as seen in the histological slides.
“The objective of BMS is to create canals in the subchondral bone to the underlying bone marrow, either by use of a drill(subchondral drilling) or an awl (microfracture).”<- an awl is a tool for piercing holes.  It’d be hard to mimic either a drill or awl safely using non-surgical methods but I don’t believe that it’s impossible.
The study mentions that other studies also showed bone overgrowth.
Bone overgrowth was defined as areas where the subchondral bone plate had grown into the cartilage.”<-this could be due to endochondral ossification or longitudinal appositional growth.
“Nine out of the 12 samples contained bone overgrowth corresponding to 27% of the sections.”
“Hematoxylin eosin staining, scale bars: 200 μm. Defects treated with BMS. (A) Shows irregularity of the subchondral bone plate (top arrow marks the beginning of the defect). (B) Bone cyst marked by arrows. (C) Remaining drill hole in the subchondral bone plate. (D) Overgrowth in the subchondral bone plate marked by to arrows, top arrow marks the beginning of the defect site. BMS = bone marrow stimulation.”<-so the overgrowth is very minor but if there was some way to reproduce it, it could add up to height over time.  The pigs used in the study were skeletally mature.