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Does Using Steroids While Still Growing Lead To Stunted Growth, Shorter Height, And Premature Early Growth Plate Closure

I had in a recent post “Grow Taller With Steroids And Steroid Derivatives, Part II” had suggested the idea that there is a weak but positive correlation with the usage of steroids and developing stunted growth and shorter final height in males.

It would seem that this subject of believing that premature usage of steroids will lead to shorter final height and stunted growth should be something that must be resolved once and for all.

From what I took from the MedlinePlus website which is linked to the National Library of Medicine and the National Institute of Health…

Anabolic Steroids

(aka Anabolic-androgenic steroids, Performance-enhancing drugs)

Anabolic steroids are man-made substances related to male sex hormones. Medical uses of anabolic steroids include some hormone problems in men, late puberty and muscle loss from some diseases.

Bodybuilders and athletes often use anabolic steroids to build muscles and improve athletic performance. But using them this way is not legal or safe. Abuse of anabolic steroids has been linked with many health problems. They range from unattractive to life threatening and include

  • Acne and cysts
  • Breast growth and shrinking of testicles in men
  • Voice deepening and growth of body hair in women
  • Heart problems, including heart attack
  • Liver disease, including cancer
  • Aggressive behavior

The main thing I wanted to take from the definition of this government sponsored website is that when the general public hears the word “steroids” they are actually thinking of a very specific type of steroids, which are known as anabolic steroids.

I personally had defined the term “steroids” to refer to more than just synthetic male androgens (aka synthetic testosterone) but also included synthetic growth hormones as “steroids”. I am probably wrong in the way I had defined it in the previous post since I had used it to mean two different synthetic compounds used by many people.

It would appear that not only are steroids used to increase muscle mass and definition, but the synthetic growth hormones like genotropin and somatotropin are also used by bodybuilders and professional athletes to gain muscle mass, increase strength, and increase stamina.

It seems that at least one type of synthetic compound which is not defined by the government can be legally defined as not being considered steroids.

So If we do define the term “steroids” in the way the popular general public views it, then we must say that steroids are just manufactured, synthetic male androgens aka testosterone.

If the anabolic steroids then are supposed to function exactly like testosterone, it might be smarter to ask the question, “would the natural increase of testosterone from like eating certain foods like brazil nuts cause the developing male teenager with open growth plates to lead to premature epiphyseal growth plate closure, shorter height, and stunted growth?” Would a 13 year old male who decides to eat food which would lead to increased testosterone into his system cause him to end up shorter?

If we were to go back to the list of negative effects of taking anabolic steroids, I would say that increased testosterone in the developing male’s system would lead to only half of those symptoms.  Anabolic Steroids should not lead to breast growth and shrinking testicles in males since testosterone does not do that, even in high levels.

High levels of testosterone will lead aggressive behavior, hair growth in females, deeper voices, and maybe a higher incidence of prostate cancer in males so steroids would do that, but all the other negative effects of steroids is not based on the evidence.

To answer the original question, the first answer I would give is that it depends on two major factors.

  • The specific individual
  • The stage of development when the steroids is being taken, ie at what age they start.

Since testosterone does convert to the female androgen estrogen, is too much testosterone is release into the male body very early, it could trigger puberty at an earlier stage, which means that the time and duration for height increase/growth is decreased so the final height is decreased.

Since most males start puberty around the age of 10-12, a male would have to start taking the anabolic steroids at the age of 10-11 to have any real evidence that the steroids can decrease their final height by any noticeable amount.

If the steroids is taken after puberty sets in while the person is still growing, the testosterone might still have an effect, but they result would be minimal. The number of chondrocytes are already decreasing and limited in the resting zone to begin with. An influx of testosterone aromatized into estrogen is more likely to saturate the system since there is only so many estrogen receptors on the growth plate to begin with.

Remember that males in general have less estrogen in their system than females. So in proportion they probably also have less estrogen receptors on their growth plates.

The 2nd major factor is that depending on the individual, like the type who has low levels of estrogen receptors, an increase in testosterone might actually increase their growth rate and their final height. Remember that the androgen estrogen is not only the hormone that closes the growth plate, but is also the hormone that initiates the puberty stage.

During the initial stage of puberty and during puberty, the growth rate of height is increased. If the male takes steroids during the early age, and actually stop around the end stages of puberty, they might be able to increase the already high rate of height increase. The extra testosterone would actually make the growth rate increase.

Plus some males have a low level of testosterone and estrogen receptors. The increase in testosterone results in the chondrocytes being proliferated faster at one stage. Since the number of estrogen receptors is limited and small, there is a constraint held on how fast the chondrocytes are bing used up. This means that the steroids can cause the male to increase his growth rate when he is growing the most while keeping the growth plate senescence at a low rate. This results in them developing a higher final height.

There have been studies which showed that decreased estrogen levels in early stages of male development ie around the early puberty stages means less longitudinal growth rates and less chondrocyte proliferation resulting in less early height.

The main point to understand is that steroids, if we are to define them as synthetic testosterone, might not stunt growth as so many people claim. Depending on the individual, at what stage in their development they take it, at how much estrogen receptors they have, and whether they use the anabolic steroids continuously or not, it could stunt or accelerate growth. However, in general and in most cases, the increased intake of testosterone is more likely to stunt growth than accelerate it. It is in the minority of situations and individuals where increased testosterone would lead to taller height.

 

 

Further Study On Robert Wadlow And The Hyperpituitarism Which Made Him The Tallest Record Person In History

In this post, I wanted to go back to look at the case of Robert Wadlow, who is documented as the tallest human in history verified by medical records.

In one of my older posts where I had looked at the unique case of Robert Wadlow entitled ”
Robert Wadlow, How Did He Grow So Tall?” I was not able to really understand the deeper physiological mechanics on why it seemed that he never even reached puberty which would have caused the process which would lead to his growth being eventually stopped.

I recently managed to find a PubMed study which looked at his case in a more scientific perpective entitled “HYPERPITUITARISM BEGINNING IN INFANCY THE ALTON GIANT“

From TheTallestMan.com forum Hyperpituitarism beginning in infancy. The Alton Giant 1932, the ENTIRE ARTICLE can be found on that thread.

From another TheTallestMan.com forum thread, here is Robert Wadlow’s height growth progression chart. I have copy and pasted the numbers below. (source is Robert Wadlow over the years (pictures and growth chart))

Growth chart:

  • Birth: Height not recorded.
  • Weight of 8.5 lbs. Perfectly normal.
  • 6 months old: Height not recorded. Weight of 30 lbs. Very heavy for a kid his age, I’m guessing he was hitting the 2′ mark at the time.
  • 1 year old: 45 lbs.
  • 5 years old: 5’4″ frame and 105 lbs. Apparently he was already taller than his grandmother by that age. Pics at the time further back him up. Damn.
  • 8 years old: 6′ and 169 lbs. Huge!
  • 9 years old: 6’2″. About 195 lbs, based on mixed sources.
  • 10 years old: This is where it starts getting really scary. He was about 6’5″ at the time, and weighed 210 lbs.
  • 12 years old: Neared 7 feet, with a 6’11” frame and a 241 lbs body! Taller than a modern basketball player.
  • 14 years old: 7’5″. Tallest Boy Scout ever recorded.
  • 16 years old: 7’10”. 374 lbs.
  • 18: 8’4″ and over 400 lbs.
  • 20: 8’7″ and 488 lbs. Heavy.
  • 21: 8’8″ and 492 lbs. A significant drop in weight followed the next year, possibly due to a health deterioration. This was the heaviest point in his life.
  • 22.4: 8’11.1″ (2.72m) frame and 439 lbs. His death point. Tallest man ever recorded.

About a 3-5 in. growth rate per year! Mad tall, no wonder.

Pictures give us a more in-depth insight. His later years send a chill up my spine at how tall he is.

To get a bigger version of the study in PDF format, you can click HERE for the link to Scribd.

Analysis & Interpretation:

I think it is time to really see what the medical physicians who tested him say on the cause for his very unique case.

The first thing that is noted is that it seems that pituitary giants not only seem to have excess HGH being release, but that the mechanism might even cause them to delay the growth plate closure. This idea is something that I had in the early part of my research thought was not possible, but a few message from Tyler (of HeightQuest.com) seems to suggest that maybe the physiological phenomena of pituitary release of the somatropin somehow negatively regulates the estrogens from reaching the estrogen receptors contributing to the decrease of the chondrocytes in the resting zone of the growth plate, which is the real cause of growth plate senescence.

I had argued in previous posts like “Tanya Angus Is Proof That Height Increase Is Possible After Epiphyseal Plate Ossification” and “Sultan Kosen Is Proof That Height Increase Is Possible After Growth Plate Ossification” that these acromegalic giants somehow still seemed to be able to add at least 1-2 extra inches even in their late 20s and since most people have their growth plates close in the early 20s, that was clear evidence that somehow the excess HGH in their system was able to allow them to overcome the limitation of now cartilage to hypertrophize. It seems that I might be wrong about those early premature assumptions from the article I have clipped and pasted below.

Even very recently a regular reader of the website/blog named bdbuilder has the same argument for why adult height increase might be possible . How is it that these giants are still able to grow into their late 20s? are their bodies different or the body maturity rate different than normal people?

So what is the analysis on Robert Wadlow? What does the medical study on him reveal about his cause for his abnormal growth which might give us some possible clues?

The first thing is that there is no recorded instances of any body in Wadlow’s family being of extremely large stature. Everyone in his family was average sized. His father might have been slightly taller than the average height of the time, being in the early 1900s, at 5′ 11″ but that is still within normal range of height.

Robert was born of average weight, but his accelerated started almost immediately. By the time he was 9 years old he was already around 6′ 1″ with enough strength to carry his father around. He had bad vision suffering myopia, but glasses corrected for that. He did get headaches but wearing the glasses seemed to stop the headaches. He drank a lot of water which could signify a thyroid problem. There was no sign of him having diabetes.

At the first time he was taken to the doctors for examination at the age of 11 years old, he was already 6 feet 10 inches (2.08 meters). His face features were also noted. The spacing between his eyes were rather large. He showed to sign of mandibular prognathism. The hair on his body did show very little pubic hair, which might mean that he was going through puberty, which is normal for boys around the age of 10-12 which is when puberty usually starts for boys. However his genitalia was rather small in comparison to other 11 year old male adolescents. That means that the previous assumption made by me on the idea that Wadlow never went through puberty which means that he had unlimited height growth potential may be wrong. Maybe Wadlow did have a normal growth curve, and he would have stopped growing if he had lived past the 22 years of life he did have. 

The X-Rays of his skull shows a lot of indications that he had the overdeveloped or tumour pressing on his pituitary gland. The sella turcica was being pushed to a large size. There seems to be evidence that a Rathke pouch still existed in the subject.

When an X-ray was done on his hands, it showed that his hands were very proportional compared to average hands, just everything being bigger. The growth plate cartilage in his hands and the rate of calcification aka the rate of bone maturity seems to be normal for the development.

After 13 months, Robert came back for another examination. His personality became more outgoing, his genitalia showed to be bigger, and the amount of pubic hair around his genitalia seems to have increased. At this age of 13, Robert was measured slightly less than 7 feet 3 inches tall. It is noted that his genitalia might still be smaller than usual, including his testicles. Hair had not really developed to his thighs or other areas between the legs and he didn’t have a beard. This could indicate that his rate of testosterone release into the system may be slower than average.

When he was tested on his heart, lungs, and blood tests, everything came out normal. It seemed that he did have a very low basal metabolic rate, a subnormal temperature, and cold hands and feet. His skin was very delicate with fine hair. The doctors guess that Wadlow most likely suffered from hypothyroidism due to the pituitary gland. The O2 consumption was lower than usual. His extremities, but especially his feet were abnormally large, which is usually a way to diagnose large stature or pituitary gigantism. His shoulder width seems to be proportionally small. From 1 year difference in comparison, his clavicle didn’t seem to increase in length. His sexual development seems to be slightly slow, but not too abnormal. He did show recent sexual consciousness as stated by his father at the age of 13.

The physicians note that wadlow seemed to be big from infancy, and grew at a very steady rate, with no growth spurts or times where growth slowed down dramatically. From my own diagnosis, it seems that Wadlow suffered from three main reasons why he grew so big.

  1. He did indeed have an overactive pituitary gland, from a very early age. 
  2. His basal metabolic rate is very low with a low body temperature. This means the process of puberty and growth was not accelerated, meaning the senescence of the growth plates was very low.
  3. His genitalia is proportionally small suggesting testosterone was not being pumped into his system at even the average rate and then being aromatized and converted into estrogen which would lead to full growth plate closure eventually. 

What is even more fascinating is that idea that the medical examiners say that there have been at least two cases where even lesions on the pineal gland can lead to gigantism. One of the articles seem to be in German and the other study is entitled “Preadolescent gigantism with precocious growth in brothers”

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Increase Height And Grow Taller Through Epiphyseal Distraction And Epiphysiolysis

Something that we as researchers have to admit at this point if we are up to date with the amount of research we have already done is that people with growth plates can achieve increased height and being taller much easier than people without their growth plates. Another word to describe the growth plates is the medical term “Physis” and when we are describing anything that is related to the term “physis” we say it is “physeal” or “epiphyseal”.

The 2nd thing the research has almost shown with definite conclusiveness is that distraction will help make the epiphyseal plates increase in thickness faster which translates to the overall human body to make them taller. Distraction, or even wounds in terms of fractures themselves give the bones a chance to either heal or develop pieces of mesenchyme progenitor cells which can lead to the chondrogenic lineage and develop into longitudinal growth.

This post is to see what we have available at this time from studies done to see how effective or feasible is the idea of doing distraction or by applying a tensile load on growth plate cartilage or just the epiphyseal ends of long bones to make them longer, thus make the person taller.

Study #1: Experimental limb lengthening by epiphyseal distraction.

  • Clin Orthop Relat Res. 1978 Oct;(136):111-9.
  • Sledge CB, Noble J.
  • PMID: 729274
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.

Study #2: Response of the growth plate to distraction close to skeletal maturity. Is fracture necessary?

  • Clin Orthop Relat Res. 1990 Jan;(250):61-72.
  • Kenwright J, Spriggins AJ, Cunningham JL.
  • Source: Nuffield Orthopaedic Centre, Oxford, England.
  • PMID: 2293946

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.

Study #3: Limb lengthening by epiphyseal distraction. An experimental study in the caprine femur.

  • J Orthop Res. 1987;5(4):592-9.
  • Steen H, Fjeld TO, Rønningen H, Langeland N, Gjerdet NR, Bjerkreim I.
  • Source: Sophies Minde Orthopaedic Hospital, University of Oslo, Norway.
  • PMID: 3681532

Abstract

Epiphyseal distraction of the left distal femur was accomplished in 10 goats (aged 3-4.5 months). A modified Hoffmann external fixation device was used as a unilateral distraction frame. A distraction rate of 1.5 mm/day was applied for 5.5 weeks. Epiphysiolysis occurred after 3-7 days of distraction. After the lengthening procedure, the growth plate had reduced in height in eight animals on radiographic examination. In two animals the growth plate was fused. Three animals were killed at 4 (Group 1) and 8 (Group 2) weeks and four animals at 16 (Group 3) weeks after the end of the distraction period. The gain in leg length obtained by distraction was reduced owing to growth retardation in the distal femur of the operated limb. The average final lengthening was 24.9, 19.4, and 13.4% in Groups 1, 2, and 3, respectively. Femur and tibia from both sides were tested mechanically in torsion. Only one femur fractured in the elongation area. All but one elongated femur fractured in the area of the diaphysis subjected to distractional force. The torsional strength of the elongated femur compared with control was reduced to approximately 50% in all groups. The corresponding torsional strength of the tibia on the elongated extremity compared with control was reduced to approximately 75% in all groups. The difference in relative strength of femur compared with that of tibia was statistically significant. This finding can be explained by a stress-protective effect on the femur in the distraction area caused by the external device.

Study #4: Epiphysiolysis as a method of limb lengthening.

  • Clin Orthop Relat Res. 1978 Jun;(133):230-7.
  • Letts RM, Meadows L.
  • PMID: 688713

Abstract

Epiphysiolysis followed by distraction was performed at the proximal tibial growth plates in 18 young rabbits. Union across the distracted plate occurred in all animals. In 12 rabbits skeletally immature at operation, premature fusion of the separated plate resulted in growth arrest of the operated limb. The contralateral control limb was longer at maturity by an average 1.10 cm. In 6 rabbits near skeletal maturity at epiphysiolysis, the operated limb was the longer at maturity by the amount distracted, an average of 0.62 cm. In all animals a permanent loss of joint motion resulted. Epiphyseal distraction in the very young rabbit does not appear to be practical due to consistent premature fusion of the distracted growth plate. It is possible to lengthen the limbs of rabbits near skeletal maturity with this procedure. An added advantage is that union between the epiphysis and the metaphysis always occurred, eliminated the problem of delayed ana non union found in diaphyseal lengthening. However, at this time, until the effects of distraction and compression on the adjacent joint can be minimized, epiphysiolysis as a method of limb lengthening is not recommended in children.

Analysis & Interpretation:

Study #1 seems to show that at least in lab rabbits, when you use steel wires wrapped around the distal epiphysis end of the femur and pull with the force/area or load that is just 1/5th of the amount needed to cause the bone to fracture, you can get the cartilage of the growth plate to increase its growth rate by 150%. The cause of the increased growth is from chondrocyte hypertrophy, hyperplasia, increased cell proliferation, and sulfated polysaccharide synthesis. What is important to note for this study is that the load was increased gradually in tension fashion.

Study #2 is one of the most significant studies yet to show what will probably happen with bone tissue if we tried to stretch out the bones for bone lengthening. However the study was done where the cartilage in growth plates were stretched out, not bones. The researchers were testing the behavior of growth plates for people or lab animals who were close to bone maturity. What is noticed for both situations where either the slow distraction rates and low constant distraction loads were applied, the researchers noticed that if one tried to lengthen the bone significantly the distraction force will reach a certain point before decreasing dramatically. The sudden decrease in the needed distraction force indicates that the pulling motion had caused a fracture in the growth plate. The failure of the growth plate in being able to continue doing plastic or elastic deformation is seen around the 600 Newtons to 800 Newtons level, which I don’t think is all that high in value for a load. It seems that the in vivo results are lower than the in vitro results.

In lab animals, specifically New Zealand rabbits of the 2nd study, the equipment used is a strain-gauge dual-frame external fixator. The rabbits were also close to bone maturity. When the results are graphed in terms of force vs. time, there seems to be two possible patterns seen in the results. Either the process of slowly increasing the tension load up to 16 Newtons while the distraction is done slowly or the process is increased to 25 Newtons rapidly and there is a sudden drop in the load force indicating fracture. The researchers note for a conclusion…

Hence, if a significant increase in leg length is required close to skeletal maturity, then fracture of the growth plate must occur.

If these results can be translated to human subjects, then we can say that the idea of using tension forces to slowly stretch out the growth plate cartilage in teenagers with plates that are almost closed may not be the best idea since it could result in the fracture of the cartilage. It seems that plastic or elastic deformation is a very low possibility, unless there is special equipment that can make the distraction very slow, in terms of maybe only 0.1 mm/day in bone lengthening.

In the 3rd study, the experiment was done on very young goats. There was only 10 goats used in the experiment. I am not sure at this time whether the goats of only 3-4 months years old would have open or closed growth plates but I would assume now that the growth plates were open since the goats were less than 1 years old. There was an unilateral distraction frame used. The rate of lengthening was 1.5 mm/day for 5.5 weeks (or around 40 days). What seems to happen is that the growth plates seem to decrease in length from the distraction. two of the goats actually had the growth plates completely fuse from the distraction.

After the experiment the goats were killed either 4, 8, or 16 weeks after in groups of 1,2, and 3 respectively. It seems that if one waited later to kill the goats, the measured increase in bone length actually decreased from some type of growth stunting. The goats that were killed later showed less bone lengthening. The long bones that were lengthening were also put in a device that would twist the bone to see how much weaker the torsional load strength had become. For most of the goats, the torsion strength after distraction of the femur had decreased to just 50% of what it was before. For the tibia who was put to the torsion load, the torsion strength dropped to just 75% of what it was before. This study is useful to see what would happen to the growth plates and overall bone strength if we tried to lengthen the femur or tibia in people with open growth plates.

In study #4, the long bones in rabbits are first cut at the section between the epiphysis and the growth plates. Then the entire long bone is stretched apart. What is evident from most of the rabbits is that from the epiphysiolysis, if it is done to young subjects, it will lead to premature fusion of the growth plate leading to growth stunting. If the epiphysiolysis is done on subjects which are close to skeletal maturity, the distraction would lead to longer bones compared to control subjects which didn’t have the epiphysis cut apart from the metaphysis. It seems that overall, there is a reducing in the bone joint mobility in all subjects if the cut is done. The researchers note…

“Epiphyseal distraction in the very young rabbit does not appear to be practical due to consistent premature fusion of the distracted growth plate.”

However they do say that the idea of bone lengthening right before the cartilage is completely ossified might be possible but anything before the time of skeletal maturity will only stunt the longitudinal growth of the full long bone.

It is important to note what the researchers say at the very end of the abstract for any orthopedic surgeons who wants to do limb lengthening on children…

“However, at this time, until the effects of distraction and compression on the adjacent joint can be minimized, epiphysiolysis as a method of limb lengthening is not recommended in children.”

 

Growth Acceleration For Children With Open Epiphyseal Plates From Electric Field Application Is Due To Voltage Gradients

In one of the biggest discoveries ever made on our endeavor, I and many other height increase seekers and researchers before me found a Patent “Method for non-invasive electrical stimulation of epiphyseal plate growth” (US 4467809 A) and the PubMed research article which was written with the patent “In vivo growth plate stimulation in various Capacitively Coupled Electrical Fields“. In this post, we go back to the patent and the PubMed article to see if we can look deeper into the references and the related articles associated with Dr. Brighton’s work to see whether there is more information we might be able to gain from studying the published works.

I wanted to go to 3 related studies he had published back in the 70s & 80s which all sort of involved the same basic idea. You apply a constant electrical current and put it close to cartilage or chondrocytes and see what will happen as a result.

Study #1: In vitro epiphyseal-plate growth in various constant electrical fields.

  • Brighton CT, Cronkey JE, Osterman AL.
  • J Bone Joint Surg Am. 1976 Oct;58(7):971-8.
  • PMID: 185224
Abstract

An in vitro epiphyseal-plate model was subjected to various electrical fields. At a voltage gradient of 1500 volts per centimeter, a consistent, highly significant acceleration of growth of the epiphyseal plate occurred as measured from photomacrographs and as indicated by incorporation of 45Ca, 35S, and 3H-thymidine. The growth acceleration was due to voltage gradients and not to current flow. Although the mechanism of action of the electrical field is not known, it is obvious that the voltage gradient, either directly or indirectly, incites a physiological response of the growth-plate chondrocyte.

Study #2: Increased cAMP production after short-term capacitively coupled stimulation in bovine growth plate chondrocytes.

  • J Orthop Res. 1988;6(4):552-8.
  • Brighton CT, Townsend PF.
  • Source: Department of Orthopaedic Surgery, University of Pennsylvania School of Medicine, Philadelphia 19104.

  • PMID: 2837556

Abstract

Growth plate chondrocytes from newborn calf costochondral junctions grown in monolayer were subjected to a capacitive AC signal of 500 V peak to peak (P-P) at 60 kHz for 48 h and were analyzed for [3H]thymidine uptake. The stimulated chondrocytes showed a 130% greater uptake over unstimulated controls. Other newborn calf growth plate chondrocytes were stimulated at 500 V P-P at 60 kHz for 2.5, 5.0, 10.0, and 20.0 min and were analyzed for cAMP. Chondrocytes stimulated for 2.5 and 5.0 min showed a 142.8% (p less than 0.05) and 394.5% (p less than 0.01) increase over controls, respectively. The chondrocytes stimulated for 10.0 and 20.0 min showed no significant difference from the controls. It is concluded that short-term exposure of growth plate chondrocytes to an appropriate capacitively coupled field stimulates cAMP production, but longer-term application of the electrical field is ineffective.

Study #3: In vitro growth of bovine articular cartilage chondrocytes in various capacitively coupled electrical fields.

  • J Orthop Res. 1984;2(1):15-22.
  • Brighton CT, Unger AS, Stambough JL.
  • PMID: 6491794

Abstract

Isolated articular cartilage chondrocytes from 1- to 3-week-old male Holstein calf knee joints were formed into pellets containing 4 X 10(6) isolated cells and were grown in tissue culture medium (minimum essential medium/NCTC 135) containing either 1 or 10% newborn calf serum (NBCS) in plastic Petri dishes in 5% CO2 and air at 37 degrees C in saturation humidity. On the 4th postisolation day either [35S]sulfate or [3H]thymidine was added to the medium, and the pellets were exposed for 24 h to capacitively coupled electrical fields (10, 100, 250, and 1,000 V peak-to-peak, 60 kHz, sine wave signals). The pellets were then harvested, dialyzed, hydrolyzed, and assayed for DNA, protein, [35S]sulfate incorporation, and [3H]thymidine incorporation. Results indicated that at 250 V peak-to-peak there was a statistically significant increase in [35S]sulfate in 1% NBCS and a statistically significant increase in [3H]thymidine in 10% NBCS. At potentials above or below 250 V no changes were noted. Thus, articular cartilage chondrocytes grown in pellet form can be stimulated to increase glycosaminoglycan synthesis or to increase cell proliferation by an appropriate capacitively coupled electrical field. The importance of the serum concentration in the medium in evaluation of biosynthesis in vitro is noted.

Analysis & Interpretation:

I had already used these studies before in previous posts but they were from many months ago when my knowledge on the subject and the research was still very superficial in nature. This time around I am going to try to go deeper on the details and understand at a deeper level what the implications and applications would be for the results of the studies.

Study #1 is the one that we see has the most interesting of results, at least in the abstract. When we apply a voltage gradient, then the epiphyseal plate cartilage seems to increase in its growth. Since the set up is in vitro, I do wonder just how one tests growth plates in an in vitro setup. Is the growth plate explanted from the test animal?

It is important to note that the growth of the cartilage is from the voltage difference, not from current flow. The optimum gradient they found was 1500 Volts/cm. The term “gradient” refers to differences between two points of some unit in concentration. A Voltage gradient means that if one measured the voltage with two electrodes with one of the electrodes kept in one place, and the other electrodes measured at difference lengths of the growth plate thickness or length, the voltage values relative to the set point would be changing. The growth plate’s increased growth is found through testing using Calcium, Sulfur, and Thymidine, and a type of imaging technique known as photomacrographs. The actual mechanism of how the applied electrical field actually works to increase growth plate increased growth is not known but the conclusion made by Brighton is that the voltage gradient created when the electrical field is generated is what will directly o indirect stimulate the chondrocytes.

In Study #2 we see that instead a DC current created a steady state electrical signal, Brighton tried to use an AC signal instead to see what would happen. The researchers took growth plate cartilage from a newborn calf’s ribcage area and put the chondrocytes in a monolayer structure. The AC electrical signal is induced at 500 Volts for the amplitude and the frequency being 60 Hz. The field is applied for 2 days (48 hours) and the chondrocyte concentration was tested by using thymidine uptake. There was a 130% increase over unstimulated chondrocyte controls. So the researchers tried the AC electrical field stimulation to test to see whether the chondrocytes would show increased cAMP production. When the 500 Volt amplitude, 60 Hz signal was applied, the 10 min & 20 min duration showed to increased cAMP production increase, but the 5 min and 2 min did show increased cAMP increase. This shows like so many other stimulants, if we want to make the chondrocytes in growth plates increase in cAMP production, which is one of the things we will need to do to make chondrocytes go faster, we have to have a optimum duration time for electrical signal stimulation. The optimum seems to be just a short term, 5 min. round which would increase the cAMP production by over 4 times.

In study #3 brighton ans other researcher took chondrocytes from newborn calf knee joints. The chondrocytes were put in pellets with the concentration of chondrocytes around 4,000,000 in each pellet. The pellets were grown in a tissue culture medium with different concentrations of calf serum in petri dishes. In 4 days after the chondrocytes were separated from the calf, the thymidine and/or the sulfate was injected into the culture. Then the capacitative electrical field was applied. The variable that was changed was the amplitude of the sinusoidal signals, which ranged from 10 volts to 1000 volts. The frequency was 10 kHz and the duration was 24 hours. Afterwards the pellets were taken, and treated to test to see how much DNA, proteins, sulfate uptake, and thymidine uptake the chondrocytes had done. With the 1% newborn calf serum in the culture, the 250 Volts led to a high sulfate uptake by the chondrocytes while the 10% newborn calf serum in the culture had the 250 volts cause a very high uptake of the thymidine. The researchers conclude with…

Thus, articular cartilage chondrocytes grown in pellet form can be stimulated to increase glycosaminoglycan synthesis or to increase cell proliferation by an appropriate capacitively coupled electrical field.

The implications and main things we should take away from the studies we just took at is the idea that we can easily create a device that can produce either the DC or AC electrical signals we need at the high voltage amplitudes and the frequencies we need to stimulate either the articular cartilage chondrocytes or the epiphyseal growth plate chondrocytes. If we can get any type of mesenchyme in the bone to differentiate into chondrocytes, the application of the right duration and voltage gradient of capacitative electrical signal would mean that the chondrocytes might start proliferating, which could result in even adults with no growth plate cartilage to develop cartilage again.

The Principles On Using FGF-2 To Induce Articular Cartilage Regeneration

The idea of using the growth factor FGF-2 and the need to understand how we can induce articular cartilage regeneration has been a couple of consistent topics I have brought up over and over again in this website. The FGF-2 aka Fibroblast Growth Factor has been one of the best candidates that is known at this time which can help the human body in vivo generate some type of cartilage-like tissue which we would definitely need to be added into the bone to remodel it in any way longitudinally. I wanted to summarize 4 PubMed studies I’ve found which show in either a direct or indirect way how effective using the FGF-2 growth factor is in getting cartilage to be formed.

Study #1: Differentiation of chondrogenic precursor cells during the regeneration of articular cartilage

  • Y. Hirakif1, C. Shukunami, K. Iyama, H. Mizuta
  • Department of Molecular Interaction and Tissue Engineering, Institute for Frontier Medical Sciences, Kyoto University, Kyoto; Departments of Surgical Pathology and Orthopedic Surgery, Kumamoto University School of Medicine, Kumamoto, Japan

Abstract

Objective: Full-thickness defects that penetrate articular cartilage are filled by fibrous, or fibrocartilaginous tissue and, to a very limited extent, also by hyaline cartilage. In rabbits, small full-thickness defects (to ≤53 mm in diameter) are capable of regenerating surfacing hyaline cartilage. However, chondrogenic differentiation does not occur in larger defects (≥5 mm in diameter). We studied the involvement of fibroblast growth factor-2 (FGF-2) in the cartilaginous repair response in full-thickness defects of articular cartilage in vivo, and attempted to facilitate cartilaginous repair of the defects by the local administration of FGF-2.

Design: The right knee joint of male adolescent Japanese white rabbits was entered through a medial parapatellan approach, and the patella was dislocated laterally to expose the articular surface of the femoral trochlea. Full-thickness defects were created in the weight-bearing area of the femoral trochlea with a hand-drill (the 5-mm diameter defects in 80 rabbits and the 3-mm diameter defects in 40 rabbits). The animals were fitted with an osmotic pump connected to silastic medical grade tubing, and a length of the tubing about 5 mm long was introduced into the articular knee cavity. The 5-mm-diameter defects received FGF-2 (50 pg/h) or sterile saline via an osmotic pump for the initial 2 weeks. Five animals each were sacrificed after 1, 2, 4, 8, or 24 weeks after creation of defects. The 3-mm diameter defects received a neutralizing monoclonal antibody against FGF-2 (50 nglh) or pre-immune mouse IgG (50 nglh) for the initial 2 weeks. Five animals each were sacrificed after 2, 3, or 4 weeks after creation of defects. The distal portion of each femur was removed, fixed, decalcified, and embedded in paraffin for the subsequent histological analysis. Sections were cut in the transverse plane, and histologically examined.

Results: The administration of FGF-2 (50 pg/h) resulted in successful regeneration of articular cartilage and the subchondral bone within 8 weeks after creation of 5-mm diameter defects. In these defects, undifferentiated mesenchymal cells initiated chondrogenic differentiation coupled with replacement by subchondral bone, resulting in the resurfacing of the defects by hyaline cartilage and the recovery of subchondral bone up to the original bone-articular cartilage junction. In contrast, the administration of a neutralizing monoclonal antibody against FGF-2 clearly interfered with the action of endogenous FGF-2 in 3-mm diameter defects, which were filled with fibrous tissue. None of the antibody-treated defects were covered with cartilage. We then assessed the proliferative capacity of the undifferentiated mesenchymal cells in the defects by immunostaining the proliferating cell nuclear antigen (PCNA) at 1 week after creation of defects. The capacity of reparative tissue to form cartilage was well correlated with the occurrence in the defects of a cell population that was PCNA-positive, undifferentiated, and capable of self-renewal.

Conclusions The local administration of FGF-2 resulted in the successful resurfacing of large (5 mm in diameter) defects by hyaline cartilage. Prechondrogenic mesenchymal cells were the likely targets of FGF-2, which probably promoted the formation of cartilage by stimulating a selective expansion of chondroprogenitor cells. Thus, activation of FGF-2 signalling is critically important for the induction of cartilaginous repair response in full-thickness articular cartilage.

Study #2: One day exposure to FGF-2 was sufficient for the regenerative repair of full-thickness defects of articular cartilage in rabbits

  • H. Chuma, M.D.†,  H. Mizuta, M.D., Ph.D.†, S. Kudo, M.D., Ph.D.†, K. Takagi, M.D., Ph.D.†, Y. Hiraki,Ph.D.‡
  • † Department of Orthopaedic and Neuro-Musculoskeletal Surgery, Faculty of Medical and Pharmaceutical Sciences, Kumamoto University, Kumamoto 860-8556, Japan
  • ‡ Department of Cellular Differentiation, Institute for Frontier Medical Sciences, Kyoto University, Kyoto 606-8507, Japan

Summary

Objectives

Administration of fibroblast growth factor (FGF)-2 for 2 weeks induces a successful cartilaginous repair response in 5-mm full-thickness articular cartilage defects in rabbits. The purpose of this study was to investigate the effects of a short time exposure to FGF-2 on the repair of the defects.

Methods

Five-mm-diameter cylindrical defects, which do not repair spontaneously, were created in the femoral trochlea of the rabbit knees. The defects were administered sterile saline or FGF-2 (150 pg/h) via an osmotic pump for the initial 1 day, 3 days, or 2 weeks, and we assessed the FGF-2 action on the proliferation and migration of mesenchymal cells in the reparative tissue. Using a total of 126 rabbits, we performed three sets of experiments. We also studied the effect of FGF-2 on migration of marrow-derived mesenchymal cells in vitro.

Results

FGF-2 treatment for 1 day or 3 days induced the sequential chondrogenic repair responses that led to successful cartilaginous resurfacing of defects within 8 weeks as well as the 2-week treatment did. We confirmed by a radioisotope study that FGF-2 injected was rapidly eliminated from the defects (a residual ratio of 50% within 30 min). The effect of FGF-2 on cultured marrow-derived cells suggested that FGF-2 facilitated the mobilization and migration of replicating mesenchymal cells from bone marrow.

Conclusions

Only 1 day exposure to FGF-2 is sufficient for induction of the chondrogenic repair response in 5-mm-diameter full-thickness defects of articular cartilage in rabbits. FGF-2 stimulated the recruitment of mesenchymal cells into the defects, which was a limiting step for the induction of cartilage.

Study #3: Fibroblast growth factor-2 promotes the repair of partial thickness defects of articular cartilage in immature rabbits but not in mature rabbits

  • Tetsuya Yamamoto†, Shigeyuki Wakitani‡, Kazuhiko Imoto†, Takako Hattori§, Hiroyuki Nakaya§,Masanobu Saito†, Kazuo Yonenobu†
  • † Department of Orthopaedic Surgery, Osaka-Minami National Hospital, Kawachinagano, Japan
  • ‡ Department of Orthopaedic Surgery, Shinshu University School of Medicine, Matsumoto, Japan
  • § Department of Orthopaedic Surgery, Osaka University Graduate School of Medicine, Suita, Japan

Abstract

Objective

To investigate cartilage response to fibroblast growth factor-2 (FGF-2) with increasing age in vivo, we examined the effect of FGF-2 on partial thickness defects of immature and mature rabbits.

Design

Sixty-nine Japanese white rabbits (34 immature rabbits, 35 mature rabbits) were examined. We made experimental partial thickness defects in articular cartilage of the knees. Then, we injected FGF-2 into the knees eight times, immediately after surgery and every 2 days for 2 weeks. A single dose of FGF-2 was 10 ng/0.1 ml or 100 ng/0.1 ml. In the control group, 0.1 ml saline was injected on the same time schedule. The rabbits were sacrificed at intervals following surgery that ranged from 2 to 48 weeks. The specimens were stained with toluidine blue and examined microscopically. We used a modified semiquantitative scale for evaluating the histological appearance of repair.

Results

In immature rabbits, the cartilage repair in the FGF-2 (100 ng)-treated group was significantly better than that of the other groups. The defects were almost completely repaired with chondrocytes that showed a round to polygonal morphology, and large amounts of extracellular matrix with intense metachromatic staining.

In mature rabbits, however, there was apparently no effect from FGF-2 in either group.

Conclusions

Application of FGF-2 facilitated cartilage repair in partial thickness defects in immature rabbits, but not in mature ones.

Study #4: Regeneration of articular cartilage defects in the temporomandibular joint of rabbits by fibroblast growth factor-2: a pilot study

  • H. Takafuji, T. Suzuki, Y. Okubo, K. Fujimura, K. Bessho
  • Department of Oral and Maxillofacial Surgery, Graduate School of Medicine, Kyoto University, 54 Syogoin, Kawahara-cho, Sakyo-ku, Kyoto-shi 606-8507, Japan

Abstract

The purpose of this study was to investigate the therapeutic usefulness of fibroblast growth factor-2 (FGF-2) in rabbit temporomandibular joints (TMJ) with osteoarthritis. A 10-mm3 defect was bored in the surface of the mandibular condyle head. The animals were divided into four groups: two test groups in which the defect was filled with lyophilized collagen containing 0.1 or 1.0 μg of FGF-2, and two control groups, in which the defects were filled with lyophilized collagen without FGF-2 or left empty. The defective sites were examined under a light microscope 3 weeks after surgery. Initiation of cartilage formation was observed in the defects filled with 0.1 μg of FGF-2, but only a small amount of cartilage was found in the defects of the 1.0-μg FGF-2- treated group. In the control groups, soft-tissue repair only or no tissue repair was found. In vivo, a dose of 0.1 μg of FGF-2 can stimulate articular cartilage restoration in defects of the TMJ in rabbits, although determining the effective concentration range of FGF-2 may be difficult. The present results suggest that an optimum concentration of FGF-2 could restore defects of TMJ articular cartilage clinically.

Analysis & Interpretation:

From studies 2 & 1, we see that the FGF-2 application on induced articular cartilage defects even up to 5 mm in diameter in area can lead to some type of cartilage repair. Study 1 suggest that not just fibrocartilage can be generated, but even the hyaline cartilage which articular cartilage is made of can be restored back. Not only that, the prochondrogenic progenitor mesenchymal cells seem to be the ones that are really affected by the FGF-2 and they only seem to differentiate in the chondrogenic lineage. The subchondral layer underneath the articular cartilage is also healed as well, and any mesenchymal stem cells that leak from the bone’s intermedullary cavity seem to be pushed towards the chondrogenic lineage. Study #2 agrees with the stimulating ability and function of the FGF-2 but also adds that even one administration of FGF-2 is enough to see chondrogenic results. The FGF-2 seems to be able to stimulate the mesenchymal stem cells to even start moving towards the defect in some mobile fashion.

Study #3 only states that when young test subjects are given the FGF-2 for cartilage repair in comparison to older subjects, the FGF-2 has a far more effect ability in cartilage regeneration ability. Older subjects had almost no cartilage regeneration response but younger testing animals had a much better result. This study was important in showing that like so many other treatments for medical repair or cosmetic enhancement, older test subjects have a far less chance of getting the benefits of treatments.

Study #4 shows that when the FGF-2 was used in application on lab rabbits on the temporomandibular joints (TMJ) area, it seems to show that there might be an optmum amonut of FGF-2 administration for highest level of articular cartilage repair. This study is important to show that the idea of using more FGF-2 is not always better. When the 4 groups were divided with two groups being the controls, it was seen that 0.1 micrograms of FGF-2 was better than 1.0 micrograms of FGF-2 in repairing the articular cartilage in the temporomandibular joint (TMJ) of the rabbits.

Does Praying Or Wishing To Grow Taller Really Increase Height And Make You Taller?

I remember Sky (from EasyHeight.com) once saying in a post of how his daily schedule goes that he would pray each night to his personal God for the strength and power to make the next day better and I wondered whether the power of prayer or wishing would have any influence on a person’s growth. Did Sky also wish for his body to transform to make himself taller?

I have looked through the updates on the website that is now no longer available and it seems that after 4-5 years of trials and doing bone lengthening stretches and pulling using weights, sprinting, and jumping he never increased at all in height. For all the desiring, wishing, and personal determination, dedication, and persistence, he never increased his height by even 1 inch.

I have thought about the issue of whether a person can use will or desire to make their bodies longer. There are some interesting cases we have found where the mental powers seemed to have some effect but the majority of people who express a desire, or even a strong obsession sees nothing results.

I would say that maybe when we still have our growth plates’ cartilage, we might be able to change our state or emotions to become slightly more positive and better to optimize the natural growth rate our genetic pre-programmed. There is already some studies which show that having a negative outlook on life will affect the immunity and health of a person who is still growing and possibly lead to more incidents of illness, which results in stunted growth and increased bone mineral density.

If we can use wishful thinking and praying, we might be able to increase our immune system, and nervous system to relax more, decrease stress, decrease illness, and optimize the natural growth rate. However, I don’t think it is possibly after the cartilage in our growth plates are gone to be able to use just our minds in terms of praying and wishing to increase our height.

There has been no documented cases which showed that through mental exertion or mental manipulation alone can the individual change or remodel the bones in their body, even in terms of increasing the bone mineral density. A female in her 50s can not wish to decrease her chances towards osteoporosis and bone fractures, but needs to implement some type of exercise program and eat more vitamin D based foods to strengthen and remodel her bones internally to be healthier.

There is a case to be said for the strange fact that Dr. Milton Erickson famously had a patient which supposedly increased their height by 12 inches in one year after therapy sessions with him. I wrote about this case in one of the earliest posts entitled “Milton Erickson’s Legend of 12 Inch Height Increase”.

It involved Dr. Erickson making the guy change his perception on how he viewed the world. However this case is well documented and has been going around the internet space and NLP community for the last 5 decades ever since the case was documented in one of his written books. At this point, I would guess instead that the person who was said to be 20 years ld when Dr. Erickson treated him still had the cartilage in his bones and through some relaxation method, he experience a rare case of “catch-up growth” which I wrote about in the post ”
Catch Up Growth Explained, Can We Use It To Increase In Height And Grow Taller?”

So it might be possible with a very good hypnotherapist or NLP expert to get a person to change their state or perception of the world to help increase the growth rate of a person who still have their growth plates, but there powers to change the mind would not work on a person who doesn’t have their growth plates.