Monthly Archives: April 2013

The Values For The Magnitudes For The Forces And Loads Needed To Increase Epiphyseal Cartilages Thickness And Human Femur Bone Without Fracture (Important)

While we are usually talking about how it would be possible to distract and pull apart the extremely strong bone tissue for our height increase desires, it might be useful to first see how much of a weight would be required to pull the cartilage of a real growth plate apart.

Let’s see what some other PubMed studies have shown about at least distracting the cartilage in the growth plate for limb lengthening. It would seem that bones are considered brittle materials. For cartilage, they may not be that brittle, but they are also very strong. This means that there is probably a very small range of loading magnitude which will do the plastic deformation before the cartilage of the epiphyseal growth plate develops fractures.

Breaking force of the rabbit growth plate and its application to epiphyseal distraction.

Acta Orthop Scand. 1982 Feb;53(1):13-6.
Breaking force of the rabbit growth plate and its application to epiphyseal distraction.
Noble J, Diamond R, Stirrat CR, Sledge CB.
Abstract

The in vitro breaking forces of the distal femoral growth plates of young rabbits were measured as a background to the design of a bone lengthening method, using epiphyseal distraction. The mean breaking force in 16 femora was 12.98 +/- 3.48 kg and the mean strain was 0.91 +/- 0.33 mm. The mean stress in 10 femora was 14.51 +/- 3.88 kg/cm2. The procedure was repeated, after applying a 1.0 kg dead weight to 6 femora for 24 hours and the breaking force was then 15.01 +/- 4.70 kg, with a mean strain of 0.85 +/- 0.62 mm. A further 8 rabbits then underwent epiphyseal distraction for 2 days in vivo, with 1 or 2 kg forces delivered to two parallel K wires by a pair of spring devices, whereupon the femora were removed and tested as before. The breaking force on the distracted side was now only 8.91 +/- 3.71 kg, compared with 13.99 +/- 3.40 kg on the control side. Although not fractured, these plates had obviously been weakened. The clinical implication of this is discussed.

PMID: 7064671

Clin Orthop Relat Res. 1978 Oct;(136):111-9.
Sledge CB, Noble J.
Abstract

Kirshner wires were placed either side of the right distal femoral epiphysis and a constant tension device applied a distracting force across the plate in rabbits. Growth increase was measured between the wires and found to be about 150% greater than the concurrent normal growth between 2 control (undistracted) wires on the left; such growth increase can occur in the absence of fracturing. The forces required to do this were between 1/5 and 1/10 of those shown to cause fracturing in vitro. The growth increase was shown to be associated with hyperplasia and hypertrophy of the plate, as well as an increased rate of cell division and sulfated polysaccharide synthesis. This was in turn shown to be associated with an increase in new bone formation.

PMID: 729274

Clin Orthop Relat Res. 1990 Jan;(250):61-72.
Kenwright J, Spriggins AJ, Cunningham JL.
Source

Nuffield Orthopaedic Centre, Oxford, England.

Abstract

Axial force applied during epiphyseal distraction has been measured close to skeletal maturity in patients having leg lengthening, in a rabbit model, and in vitro from an amputation specimen. In the patient study, both slow distraction rates and low constant distraction loads were applied. For all the distraction regimens, it was not possible to lengthen the limb significantly without evidence of fracture as demonstrated by a sudden decrease in distraction force. Growth plate failure was observed from 600 to 800 N, these levels being lower than those recorded from the in vitro tests. In the animal study, three distraction regimens (0.13, 0.26, and 0.53 mm/day) were applied across the upper tibial growth plate of New Zealand white rabbits close to skeletal maturity. Distraction was applied and force measured using a strain-gauge dual-frame external fixator. The force-time results revealed two distinct patterns. One pattern, in which the forces rapidly increased to maximum values of approximately 25 N and then suddenly decreased, indicated fracture of the growth plate, which was confirmed histologically. In the other pattern, forces increased steadily throughout distraction, reaching maximum values at the end of distraction of approximately 16 N. Histologic observations indicated hyperplasia of the growth plate without fracture, however, only a small increase in limb length was detectable. Hence, if a significant increase in leg length is required close to skeletal maturity, then fracture of the growth plate must occur.

PMID: 2293946

Analysis & Interpretation

I have looked over my old post “Long Bone Tensile Strength, Loading Capacity, Compression Strength” and looked over the values which I had found back then. It seems that the values found for the bones were from a doctor from many decades ago taking the leg bones of already slaughtered cows and doing the tensile testing on them.

What we can gain in information from the old post is that the tensile strength in bones seem to be from collagenous fibers. However the collagenous fibers are more elastic than say the mineral calcium derived compressive strength. I note that one of the most basic elements that form the extracellular matrix of cartilage is Collagen Type 2. The stuff that is supposedly giving human long bones their strength in the tensile fashion is the exact same material as the element that makes up the majority of the cartilage in the growth plates.

Does this means that if we figure out what is the tensile loading capacity of the growth plate cartilage, we will be able to figure out the real tensile strength of human bone?

So cartilage might have around the same level of tensile strength as bones, but we have not ever really been able to figure out just how much of the overall material’s intrinsice resistance to the strain induced by tensile loading can be contributed to the calcium minerals.

So what does the results say from the abstract of these 3 PubMed studies?

From study #1, the testing was done on rabbit growth plate cartilage, is the results are not that easily translated into human growth plate cartilage values much less human bone tissue deformation values. The distal femoral growth plates were tested. The average magnitude of the force where the growth plate would “break” (whatever that means) was around 13 plus or minus 3.5 KG. The average real difference seen in the growth plate was around 0.90 plus or minus 0.33 mm. The average stress was around 14.50 plus or minus 3.90 kg. If the same growth plates had just 1 kg of a load was added on them for 24 hours, the average breaking force increased to 15 plus or minus 4.7 kgs. However after just the smallest epiphyseal distraction, the average force load needed dropped to 8.90 plus or minus 3.70 kg compared to the concurrent controlled growth plates which averaged around 14.0 plus or minus 3.4 kgs. For this study, the researchers didn’t see any type of fracturing but the growth plates were definitely weakened by just the smallest of distraction on the growth plate.

From study #2, two kirshner wires wrapped around the growth plate of the rabbits were pulled in opposite directions to simulate a tensile force in the axial direction. The tension force was constant and increased at a steady linear rate. The result is that the growth of the growth plates did increase by 150% which means that the growth plates increased in the thickness or rate of longitudinal increase by 2.5 X of the normal rates. It seems that the value of the tensile loading/ tension forces needed to push the growth rates up to this level is 10-20% of the amount of force needed to cause fracturing if the femur of the rabbits was instead removed from the rabbits body and done in vitro. The cause of the increase is determined to be from hyperplasia and hypertrophy

It seems that study #3 is the one that really reveals to us just how feasible is the idea of even trying out cartilage distraction would be for our endeavor let alone bone distraction. The results are not good. when the distraction forces are applied on just the cartilage when the rabbit or human reaches close to skeletal maturity shows that “…it was not possible to lengthen the limb significantly without evidence of fracture as demonstrated by a sudden decrease in distraction force”

The fact is that when we get close to the point where we loss the cartilage completely, it seems that any type of plastic deformation of even the cartilage seems to disappear, possibly due to the fact that the growth plate thickness becomes too small due to thinning and the creeping nature of the calcification layer moving upwards. The point where the distraction drops dramatically aka the point where fractures show up is around the 600-800 Newtons mark. This converts to around 135-180 lbs in american units. It seems that this is done in the body of the rabbit. However if the femur is taken out and have the tension testing done in vitro, the value of the breaking point is decrease. This is significant since most height increase seekers wish for something non-invasive. We would have to be able to stretch out the bones in vivo. With the cartilage testing from this study, it seems to suggest that cartilage stretching in vivo have higher values.

However there is some good results which suggest that the values we need to get distraction may not be that high. If we increase the loading magnitude at a much faster rate at just the 25 Newtons point, the growth plate cartilage will distract meaning that fractures will occur. The other option is to increase the load at a slower rate, but the results show that the cartilage had very little lengthening although there was no fractures in the cartilage, being only up to 16 Newtons.

The conclusion made by the researcher I feel is most revealing in that they state “Hence, if a significant increase in leg length is required close to skeletal maturity, then fracture of the growth plate must occur.”

Implications For Height Increase:

The biggest considerations we have to make about the results in the study and the ability to translate the results for human height increase applications are…

  • The studies were most performed on small laboratory rabbits, specifically New Zealand white rabbits.
  • In addition, the rabbits were also young, indicating that they might have had much more cartilage than one who was closer to bone maturity. We as human are not that young, and most of us don’t have growth plates anymore. 
  • The studies were done to see what are the values when the cartilage will distract and/or fracture, not for bones. This means that we have to account for the difference in different tissue types, and that may not be possible to do accurately without some serious “guesstimation”

The values were are finding are 13-15 KGs, 600-800 Newtons, and 25 Newtons if there is a sudden jerking motion done. So for what situations do these load values work in?

  • 13-15 kgs – To to induce cartilage fracture or distraction for young new zealand lab rabbits
  • 600-800 Newtons (135-180 lbs) – To induce fracture in the cartilage of old or adult new zealand lab rabbits that are about to reach full bone maturity.
  • 25 Newtons (5.6  lbs ) – To induce fracture in the cartilage of old or adult new zealand lab rabbits that are about to reach bone maturity through a very fast, quick increase in the tensile force loading aka a sudden jerk or “tug” on the long bone cartilage area. 

This shows that even for rabbits who are young with a lot of cartilage in their growth plate, the needed amount of load to get growth plate increased growth has to be as high as 30-35 lbs of force. For the ages rabbits who still have a little bit of cartilage left, the value increases to 135-180 lbs, and the researchers say that plastic deformation is not possible, but fractures has to occur.

Now, let’s remember that we are talking about RABBITS, NOT HUMANS. The human bone is at least around 10 times wider which means that the overall cross-sectional area of human long bones, minus the cavity from the intermedullary cavity, is around 50-100 more in area.

In addition, we are talking about rabbits with cartilage, and we want to translate these values to humans without cartilage!!

So let’s try to do a level by magnitude calculation.

  • Young rabbits with a lot of cartilage: 35 lbs
  • Older rabbits with very little cartilage and close to full cartilage ossification: 180 lbs

I had stated earlier from older posts that the main reason that human bones have their compressive strength is due to the calcium mineralization in the bone matrix and that the tensile strength is from the collagenous material.

So if the calcium minerals were removed from the huma bone, would the “bone” still have the same value of tensile strength? I mean, it is said that the tensile strength is from collagenous tissue.

I guess is that it would not.

Cartilage is also made from the same collageneous material.

I would guess that while the calcium minerals are not as dominant in being the real contributors to the bone strength in the tensile direction as the compressive direction, they still make up around a large percentage of the bone’s tensile strength. I would guess the calcium is 60-80% of the cause for high tensile strength too.

So we have to multiple the value of 180 lb by 5X. to get 900 lb. I really do think that it requires 900 lbs of force to cause fracture in the long bone of rabbits without cartilage. 

I am guessing the human femur bone is usually around 3 cms wide. The rabbit femur I would guess is maybe half a cm wide, 0.5 cms.

If we did an area difference between human femur and rabbit femur calculationg, assuming that the cavity in the middle of the femur is around 1/3rd the length.

  • For Rabbits: so 0.5 cm = 5 mm so radius 2.5 mm –> remove the 1/3rd in the middle of the femur to get a value of Area= 2.5^2*pi – 0.83^2*pi = 6.24*pi mm^2
  • For Adult Human Male: I assume diameter of human femur at 3 cm in thickness. 3 cm is 30 mm so radius is half, at 15 mm –>remove the 1/3rd in the middle of the femur to get a value of Area = 15^2*pi – 5^2*pi = 200*pi mm^2 

If I am to assume that my guess that 900 lb of force is needed to distract an adult rabbit’s femur bone to induce any type of elongation, whether through fracture or plastic deformation, then I have to somehow be able to extrapolate that already guessed value to a value for humans that is even further from hard data.

Calculation Style #1: Value for needed tensile force to elongate or “stretch” an adult human male’s femur bone 

Since the human bone is 6 times as wide as a rabbits bone, 3 cm in comparison to just 0.5 cms, the needed tensile load would be 36 times as much, since to calculate area, we have to square everything, and that would have to be applied to tensile force loading on bone. Sot the value for calculation style #1 is 36*900 = 32400 lbs of force needed.

Calculation Style #2: Value for needed tensile force to elongate or “stretch” an adult human male’s femur bone 

If we instead assume that strength is determined in terms of discrete quantities of area of bone, then he relative difference aka ratio of the human bone area to the rabbit bone area is the multiplicative factor we need. The values are human/rabbits = 200/6.24 = 32

So the value needed from Calculation Style #2 for adult human femur bones is 32*900 = 28800 lbs of force needed.

Previously, I had stated that the values of the breaking point of the human long bone was around 120-150 MPa which was found from Wikipedia and some very old studies done in the 19th century by amateur medical researchers. 150 MPA is around 21750 psi. Psi is pound per square inch. If we then multiple the area of the average adult male human femur bone, at around 3 cms thick, we get  

in terms of calculations, when the 3 cms is converted to inches, and then the area of the cortical bone is calculated, it is…

((1.18110236/2)^2-(1.18110236/6)^2)*pi = 0.9739 inches^2 = so the adult bone for tensile strength needs around 21750 pounds of tensile force to pull the bone apart. 

Conclusion: 

From the values found on a study looking at the breaking point of cartilage in lab rabbit legs, we reach 3 different values for how much tensile force would be needed to cause the bone lengthening in adult humans, 32000 lbs, 29,000 lbs, and 21,000 lbs, but all of them showing that the human bone can withstand more than an 2 – 5 elephants standing on a scale pulling the human bone apart.

It would seem that there is no hope in hell that height increase seekers would ever be able to even find a machine that can create that much tensile force.

However that might be something that I did not include from the results of the 3 studies. The fact is that when the cartilage of the rabbit experienced really fast increases in tensile load aka a “strong tug or pull”, the break point of the cartilage was just 25 Newtons, which is much smaller than the 600-800 Newtons needed if the tensile force was increased gradually. The ratio of 800/25 is 32.

If could be that if we took the value of the lowest value we have found or calculated, at 21,000 lbs and divided it by 32, it suggest that with just around 660 lb of tensile loading, maybe the human femur bone might be able to deform and elongate if we gave the bone a really strong, and really fast jerk or tug.

As an after thought to this post, I am not against the idea of pulling bone longitudinally for plastic deformation it since the idea can not be completely disapproved yet. If anyone can give me a single study or article which shows that bone itself can deform in the longitudinal direction, I would look into it further.

A List Of The Types Of Disorders And Pathologies Which Can Cause Overgrowth, Excessive Height, And Gigantism

Here is just a short post on the many types of conditions, disorders, and pathologies which can cause overgrowth, excessive height, and gigantism.

I took this information mainly from the article that was studying Siah Khan, entitled “Cranio-Spondylo-Tubular Dysostosis – A Unique Historic Iranian Giant “Siah-Khan Syndrome” – Report of an extremely rare or perhaps a unique case in the world from Iran”.

It was published in probably a scientific journal entitled “Genetics in the 3rd millennium, Vol. 8, No.2, Summer 2010”

In the article it is stated that these conditions lead to tall stature, but of course the tall stature is form a medical disorder.

1. The most common cause of pathologically tall stature is pituitary gigantism. – The excessive growth hormone, usually results from over- secretion by a group of somatotrope cells of anterior pituitary gland (somatotrope adenoma). The primary effect of the disease is excessive growth resulting in tallness (1, and 2). Tallness is accompanied by heavy, thick bones with large hands and feet and a heavy jaw. Once puberty is complete and adult height achieved, continued growth results in acromegaly. In this case diagnosis is not so difficult. By measuring blood growth hormone (GH) and insulin like growth factor 1 (IGF1), clinical impression can be confirmed.

2. There are some other very heterogeneous and very rare genetic and non-genetic conditions that overgrowth or tallness is a consistent finding in them (3, 4); such as

3. Precocious puberty

4. Extra sex chromosome syndromes (4),

5. Sotos syndrome (3, 5),

6. Beckwith-Wiedemann syndrome (3, 6),

7. Simpson- Golabi-Behmel syndrome (3, 7),

8. Marshal-Smith syndrome (3, 8),

9. …and some of the Craniotubular Dysostoses (3, 9, 14). 

If you are a height increase or genetic researcher, I will list the articles and studies for reference below for you to find off of PubMed.

Note: On a personal note, I would also add the fact that maybe Weaver’s Syndrome, Proteus Syndrome, and Marfan’s Syndrome also all seem to lead to tall stature. This implies that we should be doing even more studying on all of these syndromes and disorders to find out what are the main link that connects all of these syndromes to lead to tall stature. It could just be one main link and cause or it could be from a multiple of causes.

References

1. Daniels GH, Martin JB. Growth hormone excess: Acromegaly and gigantism. In: Isselbacher KJ, Marhn J13. Harrison’s Principles of Internal Medicine. Vol 2 13th ed. McGraw Hill; 1994.p.1989-91.

2. Cohen P. Hyperpituitarism, tallstature, and overgrowth syndromes. In: Behrman R, Kliegman R, Jenson HB. Nelson’s textbook of Pediatrics. 16th ed. WB Saunders; 2000.p.1685-7.

3. Jones KL. Early overgrowth with associated defects. Syndromes In: Smith’s recognizable patterns of human malformation. 5th ed. WB Saunders; 1997.p.150-68. 4. Graham JM. Rimion DL. Abnormal body size and proportion; generalized overgrowth disorders. In:

Rimon DL, Conner JM, Pyeritz RE, et al. Emery and Rimoin’s principles and practice of medical genetics. Vol. 4th ed. Churchill livingstone;2002.p.1075-77.
5. Sotos J F, Dodge P R, Muirhead D, et al. Cerebral gigantism in childhood: a syndrome of excessively rapid growth with acromegalic features and a nonprogressive neurologic disorder. New Eng J Med 1964;271:109-16.

6. Beckwith J B. Macroglossia, omphalocele, adrenal cytomegaly, gigantism, and hyperplastic visceromegaly. Beckwith J Birth Defects 1969;5:188- 96.

7. Savarirayan R, Bankier A. Simpson-Golabi-Behmel syndrome and attention deficit hyperactivity disorder in two brothers. J Med Genet 1999;36:574-6.
8. Johnson JP, Carey JC, Glassy FJ, et al. Marshall- Smith syndrome: two cases reports and a review of pulmonary manifestations. Pediatrics 1983;71(2); 219-23.

9. Sillence DO. Craniotubular remodelling disorders. In: Rimon DC, Conner JM, Pyeritz RE, et al. Emery’s and Rimoins principles and practice of medical genetics. 4th ed. Churchill Livingstone;2002.p:4130-5.

10. Ayuk J, Sheppard MC. Growth hormone and its disorders. Postgrad Med J 2006;82(963):24-30.
11. Viljoen D, Beighton P. Marfan syndrome: a diagnostic dilemma. Clin Genet 1999;37(6):417-22. 12. Faravelli F. NSD1 mutations in Sotos syndrome. Am J Med Genet Semin Med Genet 2005;137(1):24- 31.

13. Endo F. Berardinelli lipodystrophy syndrome. Ryoikibetsu Shikogun Shirizu 2000; (30pt5):143-4. Review. Japanese.
14. Lachman RS. Skeletal dysplasias. In: Taybi H, Lachman RS. Editors. Radiology of Syndromes, Metabolic disorders, and skeletal dysplasias. 4th ed. Mosby;1996.p.791-802.

For an even greater collection on Studies and papers on abnormal and unique cases on overgrowth and gigantism I would list the references I also found from the paper on Zech Devits below which was entitled “A Provisionally Unique Syndrome Of Macrosomia, Bone Overgrowth, Macrocephaly, and Tall Stature” which I had found from the TallestMan.com website.

reference

 

A Study Of Temperature Variation On Sea Slugs Can Explain Why People Are Taller In Colder Environments

While I was doing research for something else, I stumbled upon a nice study abstract which seems to make the connection between the effect of temperature on the growth rate and ultimate size of an organism to Bergmann’s Rule and why it seems that people from the Nordic Countries are taller than people from countries closer to the equator. The study is below…

Contemp Top Lab Anim Sci. 2005 May;44(3):31-5.
Temperature effects on growth, maturation, and lifespan of the california sea hare (Aplysia californica).
Stommes D, Fieber LA, Beno C, Gerdes R, Capo TR.
Source

Division of Marine Biology and Fisheries, National Resource for Aplysia, University of Miami Rosenstiel School of Marine and Atmospheric Science, Miami, Florida 33149, USA.

Abstract

We conducted a hatchery growth study to describe the variability in growth rates, spawning, and mortality of Aplysia californica in regard to rearing temperature. Animals were housed at a standard hatchery density of five animals per cage, at temperatures of 13, 15, 18, and 21 degrees Celsius. Animals reared at 13 or 15 degrees C grew as much as four times as large, lived twice as long, matured later, and spawned longer than did animals reared at 18 or 21 degrees C. At age 170 to 205 days the fastest growth rates occurred at 18 and 21 degrees C, and the slowest at 13 degrees C. As animals at 18 and 21 degrees C reached sexual maturity at ages 190 to 197 days, or approximately 60% through their lifespans, their growth rates slowed such that by age 260 days, the fastest growth rate was at 13 degrees C, and the slowest was at 21 degrees C. Animals reared at 13 and 15 degrees C reached sexual maturity at 242 and 208 days, respectively, or at approximately 40% of their life spans. Lifespan and maximum average animal weight were significantly inversely correlated with temperature (P </= 0.0001). However, there were no significant differences at any temperature in the age at which maximum animal weight was reached when this age was expressed as a percentage of the life span: animals reached their maximum weight at approximately 80% of their life span. Aging rate was highest for animals reared at 21 degrees C, while the mortality rate doubling time was lowest at this temperature. This would be expected for the accelerated lifecycle observed at higher temperatures.

PMID: 15934721

Analysis & Interpretation:

From a very quick glance at the abstract, it shows that when the sea slug is placed in an environment that is colder, their maximum size ends up being much bigger, and that they mature slower, and age slower, and might even live longer.

Many anecdotal evidence suggest that this type of phenomena which is called Bergmann’s Rule can be said about humans as well. People who are ethnically main from colder countries or nations like the Northern European countries are in general taller than people whose ethnicity come from places closer to the equator.

Common sense shows that land or countries closer to the equator get much more sunlight and heat than people who live further away from the equator. So their countries are generally warmer. I know from hearing people say that the Philippines can be very warm, even for the natives. This is also true in the Middle East and such.

Many people I know have suggested that Northern Chinese people are taller than Southern Chinese people. The application of the effect of temperature may explain why. Other people also anecdotally state that Koreans are taller than the Chinese on average, and this again can be explained from a geographically point of view. South Korea is situated further away from the equator, meaning that they get less sun and the temperature is lower, so they grow slightly longer and taller. Since the countries of Vietnam, Laos, Cambodia, and Thailand are closer to the equator,  the temperature is higher, so it would suggest that the national average height should be slightly lower. I have not checked the CIA national database for these numbers but it is something interesting to note.

So can we just make the sort of heuristic rule of thumb that people from nations and places further away from the equator tend to be taller? There is a weak correlation to back up that claim at this point.

It is interesting to note that the opposite is also true. There is also a Southern Hemisphere of Earth. And we know that the Southern most part of the world which has been hospitable for habitation for humans was in South America, in the Patagonia region in Chile and Argentina. Of course from my research in the past, I note that Patagonia is famous for the fact that European sailers saw that the humans living in this region were very tall, like giants. The name Patagonia even means something like the “land of the giants”.

We could also say that Australians are on average quite tall, but that could just be from the White European settlers which came there a hundred years ago. This South Hemisphere country/continent should also have tall native people, but there doesn’t seem to be much evidence of it.

So this little fact give even more credibility to the idea that the further your ethnicity are from the heat, to colder places in the world, the bigger your genetic lineage might become.

Of course, we I cam talking about is me trying to make connection and correlations in multiple unrelated areas of study and I could be completely wrong in my conclusion and will be proven wrong from some anthropological or sociological experiment a few decades from now.

Bone Growth Continues Throughout A Lifetime For Rat Species, So Is Tyler And The LSJL Theory Wrong?

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…

Contemp Top Lab Anim Sci. 2002 Sep;41(5):21-6.
Review of growth plate closure compared with age at sexual maturity and lifespan in laboratory animals.
Kilborn SH, Trudel G, Uhthoff H.
Source

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.

  1. 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
  2. This finding indicates that bone growth continues in the rat for a greater proportion of their lifespan than does that in other species.
  3. 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.

Update: Igor Vovkovinskiy Does Have Closed Growth Plates, At Least In The Distal Tibia

I wrote the last post a little too fast and never finished the full video on the 60 Minutes website entitled “Walking Tall” about Igor Vovkovinskiy. In the previous post, I had claimed that Igors own doctor is mistaken and wrong about stating that Igor can still grow. We as the height increase researchers and the licensed physician allowed to treat a pituitary giant is wrong in the science.

Now I am even more sure that the doctor was wrong about Igor. Igor can’t grow any taller. HIs height has stooped increasing. HIs tumor might make him wider, and given him a wider face, or hips, or thicker bones, but he should not be getting any taller.

The thing I was wondering about the previous post was whether the doctors had ever taken an X-ray of Igor’s body. Well I at the time did not watch the 2nd half of the 60 minutes video. It seems that they have. around the 9 minute mark the 60 minutes reporter meets Igor’s doctor to look at his leg bones.

You can clearly see that Igor’s lower limbs and the top of his feet has been X-rayed. I spent quite a few minutes to really check the X-ray.

Around 9:07 time, you can get a very clear view of Igor’s left leg. There is no cartilage or growth plates left. There is also no epiphyseal line either. Since the human body is more or less symmetrical, I would say it is reasonable to assume that if we saw the X-ray of his right leg and right feet, we would also find the same thing, no growth plates or epiphyseal lines.

So does this mean that Igor has no growth plates anymore? Not exactly, since in the human body, different areas and specific growth plates ossify at different times in development. I had written before in the past that even though the growth plates in the limbs may be gone, there might still be some cartilage left in the torso, in the vertebrate irregular bones.

If we look at one website MedHelp.com, a medical questions and answers site, we see that we do get sort of answer to our last question. A Dr. Vinod answers someone who calls themselves “shorty”.

Dr Vinod
Jul 12, 2009
To: shorty21841

We can give you the ossification of few of the important bones. It is difficult to write about primary, secondary and the total ossification of all the bones.

Femur:
The 3 epiphyses/growth plates at upper end fuse at 18years
The 1 epiphysis/growth plate at lower end fuse at 20 years

Tibia:
Upper end fuses at 16-18 years
Lower end fuses at 15-17 years

Humerus:
Upper end during 20th year
Lower end at about 16 years

Radius:
Upper end during 18th year
Lower end at 20 years

Take care!

Analysis:
So it does seem that of all the growth plates to go, the distal tibial ones may be one of the most early ones. It could imply then that Igor even at the age of 29 might have still a few cartilage left which might be the reason his doctor has claimed Igor can still grow taller. Maybe due to the difference in rates of growth plate closure, as seen from the chart of different regions above, it might be that igor does have some areas in his body which has been slower in ossifying than others.
If that is the case, then the next million dollar question is, “How is it that igor at the age of 29 could still have growth plate cartilage left?”
If that is not the case, then we can comfortably say that Igor is now past puberty, his growth plates are gone, and he is not getting any taller, and that his doctor is ignorant of how pituitary giantism really works.

Is This Doctor Wrong Or Are We As Height Increase Researchers Wrong About Growing After Puberty?

Today I was watching 60 minutes and I stumbled upon a short video segment talking about Igor Vovkovinskiy who almost everyone seems to know is the current tallest man in in the USA. Recently I was on Skype talking with Noel (will be the next podcast episode) and he mentioned that he lives in someplace close to Rochester, Minnesota, which is where Igor seems to be living right now. So this video was sort of interesting to see.

What is sort of frustrating to me and to so many other fellow height increase or grow taller researchers is what the professional doctor says in the video found from the 60 Minutes website entitled Walking Tall about Igor Vovkovinskiy. As I watched the video, the 60 minutes reporter and speaker, keeps saying that Igor is “still growing” which seems to imply that Igor’s height is still increasing.

We as researchers have always stated that once the growth plates are ossified, there is NO WAY you can grow taller, no matter how much natural or synthetic growth hormone (Somatotropin) you release into the system. So why could the reporters and journalist researchers at such a well established news channel as 60 MINUTES make such a big mistake on the science?

What makes me extremely angry or extremely confused is when Igor’s personal doctor, a Dr. Greg Garrison (might have spelled his name wrong) states around the 6:27 time area that “he continues to grow…” 60 minutes makes the suggestion that Igor’s personal doctor has become very knowledgeable on Igor’s situation and the tumor inside of him. Then The doctor makes the claim around the 6: 45 time area and says, “…but unfortunately, yes, he continues to add height, and he continues to add weight”. WHAT???

Again, you can watch the video by clicking HERE.

So this is the comment that was made which I completely disagree with. This guy who is supposed to know about endocrinology and graduate from Medical School should know more about pituitary tumors than people like us, but how can he as a medical professional claim that Igor is still growing in height? I am astounded at this doctor’s lack of knowledge on auxology like so many other doctors, as I have stated in a very recent post entitled “Why Most Doctors, Physicians And Medical Schools Don’t Teach Enough About The Skeletal System To Answer Questions Dealing With Auxology“. My point is that the doctor is either lying about Igor being able to grow taller or he is just doesn’t know enough about the human growth process and is giving false information to 60 Minutes.

As a side note, you can see that he actually makes a smile or a slight smirk around the time (6:45) when he says that Igor is still growing taller. Maybe he knows it is a lie or making some type of exaggerated joke, to make us believe in something that should not be possible, at least from our current understanding on auxology.

Igor was born in Sept 1982, which would make him 30 years old right, using the American way to measure age. In asia, he might be 31 years old, or maybe even 32. The segment on 60 minutes was aired in Sept 2012, which means Igor was 29 years old when 60 minutes did the excerpt on him. So his doctor claims that Igor was still growing taller at the age of 29 years old, because he has that pituitary gland condition? I think he is wrong, since we know that hGH can not make a person taller after the growth plates close.

I am of course always assuming that Igor being 29, is past puberty and has no more growth plates. I showed you guys recently in that YouTube video of my X-rays from when I was 25 and it shoed not even any epiphyseal lines left. That is what I am guessing Igor also went through. Having a tumour in the brain should not decrease the rate of bone maturity.

I wonder whether these doctors ever took the time to do an X-ray on Igor’s physeal plates. As smart people who made it through medical school, I would assume that they must have done those X-ray tests. Did they find that Igor’s plates were still open, maybe due to the pituitary  gland condition? I am guessing that they got the x-ray, saw no epiphyseal growth plates, but still are claiming that growing taller is still possible. That should not be working, even if you dump a gallon of Growth Hormones onto the human system, since there is no chondrocytes for the growth hormone to effect. All that is left are osteoblasts and hard nonliving tissue.

So who is wrong here, me and the other height increase researchers, or this doctor?

If the doctor is right, and igor is still growing, then we need to completely overthrow one of the fundamental axioms we have always operated on from our research.

What is fascinating to hear is that Igor was already 6 feet tall at the age of 6 years old! That is an insane growth rate