I wrote before in a post over the fact that for rats (and maybe also mice) that the cartilage that makes up the growth plate in their bodies never completely disappear due to ossification. This was entitled “A Clue To Why The LSJL Method Works In Rats And Not Humans”
In that post, I had found a study which showed that even though the limbs of rats may not be getting any longer, the cartilage in their long bones are still there. Since the LSJL method is just like a heavy load being pushed laterally on the cartilage, it would seem from just a common sense mechanical point of view that the cartilage would have enough elasticity to be pushed wider in thickness from the loading on the side.
I recently found another article which seems to put the LSJL theory further into question. Remember that the whole premise behind the LSJL method was that hind leg bones performed on even aged lab rats/mice/rodents saw that their bone length increased.
Since we have decided to translate the growth morphology and process of humans to rats, we assumed that the process and rate of ossification and bone maturity in rats is just like in humans. We are both mammals aren’t we?
Well this article I found from PubMed entitled “Review of growth plate closure compared with age at sexual maturity and lifespan in laboratory animals.” seems to suggest that the basic premise of the one study and article on why LSJL can even work on humans is put into deep scrutiny. The abstract is below…
Animal Care and Veterinary Service, Department of Medicine, University of Ottawa, Ontario, Canada K1H 8M5.
Abstract
Although it is assumed that most mammals experience growth plate closure and cessation of bone growth soon after sexual maturity, bone growth in rats continues throughout their lifespan. The rat was compared to other laboratory animals to assess differences in the duration of bone growth and its relationship to age at sexual maturity and lifespan. We reviewed the literature from 1966 to March 1999 by searching MEDLINE and other databases. Growth closure times and age at sexual maturity were retrieved for the mouse, rabbit, dog, cat, sheep, cow, horse, nonhuman primates, and human. For all species, we calculated the ratios of: 1) age at growth plate closure to lifespan, 2) age at growth plate closure to age at sexual maturity, and 3) age at sexual maturity to average lifespan. The ratio of age at physis closure to the average lifespan was large for the rat (22 to 35) and showed some overlap with that of humans (17 to 25); this ratio was comparatively small in all other nonhuman species (range, 4 to 17). This finding indicates that bone growth continues in the rat for a greater proportion of their lifespan than does that in other species. The ratio of age at physis closure to age at sexual maturity was larger for the rat (5 to 6) than that for other species, indicating that bone growth continues much longer after sexual maturity in rats than in other animals. The ratio of age at sexual maturity to average lifespan was largest for humans and nonhuman primates (13 to 14), indicating the increased time to reach puberty versus that in other species. These differences are important for studies in which animal models are used in research involving bone growth.
PMID: 12213043
Analysis & Interpretation:
The study and article suggest that even after sexual maturity, for rats at least, their bone does not reach full maturity ie. haven’t finished growing yet. We saw from the study “Knee loading promotes longitudinal bone growth in both young and adult mice” by Ping Zhang and Yokota that even for adult mice that the bone increased longitudinally. Previously I argued in the other post that the reason even “aged” or “old” rats can increase in long bone length was that there was still cartilage ie growth plates left. Now there is even more supporting evidence that the bone morphology and process in rats is just different from humans’ enough to show that maybe the LSJL theory does not have the scientific backing Tyler might think it really has.
Like I said before, this new study may put more evidence to show that at least in theory, LSJL should not work, at least not in humans. The abstract says 3 critical things.
- Although it is assumed that most mammals experience growth plate closure and cessation of bone growth soon after sexual maturity, bone growth in rats continues throughout their lifespan
- This finding indicates that bone growth continues in the rat for a greater proportion of their lifespan than does that in other species.
- bone growth continues much longer after sexual maturity in rats than in other animals
This shows that at least for humans with open growth plates with the cartilage, maybe LSJL would work on them, but for humans which don’t have any more cartilage, there is more evidence shouldn’t work on them.
So the question comes back again. How come Tyler has said that he grew by 4 cms from using the LSJL method? Plus, there are other people who also claim they have gain from 1-2 cm from doing it. Now for me, I am getting a lot of contradictory information.
The studies and articles published on PubMed shows that because rats have longer relative time after sexual maturity before full bone closure, if ever, that Tyler’s idea would work on rats, but probably not humans.
However there are quite a few testimonials not just from Tyler showing that clamping the knees do work in making a person grow taller from full ossification.
All I can say right now is that I am more confuse than ever, but I will also use the objectivity of science to cut through all the bullshit out there to arrive at the truth.
I grew half an inch with LSJL so I am certain that it works. It just takes a long time to see results.
How old are you jimmy?
19 atm
First, the oldest LSJL was done on is 16 week old rats. That rat breed experiences growth plate cessation at 6 months old.
That LSJL will work on adult humans is based on the gene expression patterns which show upregulation of mesenchymal condensation genes and pro-chondrogenic genes which would not require initial growth plates to induce chondrogenic differentiation.
Also, that hydrostatic pressure and tensile strain can induce chondrogenic differentiation.
Absence of proof is not proof of absence. And given so few studies of course the proof isn’t as good as it should be.
I am just being very careful not to jump on the bandwagon too quickly. We are in what I would say, beside the science of age reversal, the hardest and most difficult body modification research out there. Height increase science is something most people would laugh at. We need rock hard evidence before we start shouting anything from the rooftops.
It doesn’t matter, but wasn’t joint loading tested on mice and not rats? As far as I know, the growth plates in mice don’t close unless induced. Has anyone asked the original researchers if joint loading can somehow coincidentally lengthen mature bones, rather than just enhance growth in bones that are still developing? I’m still not sure how a bone can ever grow after the plates fuse. How is chondrogenesis going to elongate a mature bone? This seems really silly.