At this point in the research I would have to say that the prospect of being able to figure out a way to make a human body start to grow vertically again is actually very challenging. From doing more reading and achieving a better understanding on how the microscopic mechanisms and physiology of the growth plates, bones, and cartilage really work, I would say that I am starting to lean towards the side of most professional physicians and growth specialists in that there is no simple, easy to perform non-invasive way to make the body grow taller.

That however does NOT mean that we should give up toward figuring out an idea that would be better towards getting taller in a faster, less painful, less time consuming way. I would like to point out the fact that it wasn’t until the 1990s, just 20 years ago that physicians in the USA and the western nations like Great Britian, France, Germany realized that the idea of being able to slowly distract and pull human bones apart safely was even possible. The famous Gavriil Ilizarov spent 30 years studying in the former USSR perfecting his external fiaxtor method before he presented his finding in the late 1980s to the rest of the world. Even in the 90s most orthopedic surgeon’s did not know that lengthening of the bones was even possible without severe surgical complications. His legacy can be seen these days in Kurgan, Russia where there is a famous orthopedic surgery clinic named after him as well as his own statue, where he is depicted holding his famous external fixators. For more information about Gavriil Ilizarov, refer to the Wikipedia article on him

The research is reaching a plateau and the really detailed ways and process on how the signaling pathway in a growth plate really work is not even half understood. This means that we really don’t know how the growth plate cartilages in the human body really work at the finer details level.

There is one way that is absolutely sure to work, and that is to break the long bones that make up part of the overall height and then pull the two parts of the broken bone apart as the non-union is going through the healing process. This break is known by the general term Distraction Osteogenesis as well as the terms Callotasis or Callus Distraction. Refer to the studies and articles below…

• Study #1: Limb lengthening by callus distraction (callotasis).
• Study #2: The callotasis method of limb lengthening.

From the 2nd study…

“…Callotasis is a lengthening technique that involves slow, controlled distraction after subperiosteal-submetaphyseal osteotomy”

• Distraction is another term that being pulled apart. 
• Subperiosteal means situated or occurring beneath the periosteum, which is the layer of bone cells that surrounds the main bone layering.
• Metaphyseal (or the Metaphysis) means the growing part of a long bone between the diaphysis and the epiphysis
• Sub-Metaphyseal means going underneath or beneath the layer of the boen area known as metaphysis or metaphyseal.
• Osteotomy means cutting the bone which is not from some accidental fracture but due to a precise intentional surgical cut.

The break is not actually through the entire bone as is believed by some journalists who report on the surgery and say that people’s legs are sawed in half to make them grow taller. That is not completely true. All that is really needed is to break through the harder bone type, the cortical bone type for a chance to pull the bones apart. The trabecular bones themselves do have strength in themselves but they are much weaker. When the external fixators (or internal fixators) that is fixed onto the rods that are drilled through the limb is then pulled in a tensile direction, the trabecular bones will give way under the metal pulling which is how the bones are actually lengthened. Trabecular bones have a much higher porosity than cortical bones and have around only a fraction of the resistance towards plastic deformation.

The bones have a certain ability to start healing at a dramatic rate and the way that is done is through the flow of blood, marrow, and adult type stem cells to the region forming a cartilage-bone matrix material that is known as fibrocartilage, which will eventually turn into bone. The clogging nature of the mixture forms a emulsion-like coagulation known as the callus.

The other idea is what has been proposed for over 6 years on the Height Quest blog/website created by Tyler. He calls the method Lateral Synovial Joint Loading.

It would be easy to dismiss someone like Tyler as a quack or another internet marketer trying to sell a useless product but after 6 years of doing dedicated research and stating that he has grown upwards of 4 cms of height from applying the method as well as at least 3 other people claiming to gain a sizable height increase, the method can not be easily dismissed away. If he is a scam artist, he is one very dedicated scam artist in doing so much research, some of which has been rather enlightening.

Refer to the two posts I wrote months ago about how to do the technique for more details

• Post #1: A Simple Step By Step Guide For Lateral Synovial Joint Loading
• Post #2: Lateral Synovial Joint Loading Explained In Simple English

Or you can just read the original source which I created the posts/guides around…

• Height Increase Routine: LSJL FAQ

The entire method is basically a leap of faith on the efficacy over the idea of a biomedical technique performed on lab animals (mice) by a group of University Professors and Grad Students. This group in the biomedical engineering department at the University of Indiana did the experiments headed by two people…

• Hiroki Yokota –Website
• Ping Zhang – Website not found (or was taken down)

The two main studies that the entire technique is based on are…

• Study #1: Elbow loading promotes longitudinal bone growth of the ulna and the humerus
• Study #2: Lengthening of mouse hindlimbs with joint loading.

I don’t know whether this idea will ever catch on but it seems that there is a small group of researchers and experimenters who are trying it out taking around 10 minutes out of each day for up to a few years to see if there are any results.

This leaves actually only one other idea that has been shown to possibly work, but only at the theoretical level at this point. That is the idea of using the two areas of biomedical engineering of stem cell technology and tissue engineering to create functional growth plates which will eventually be implanted back into the adult human’s leg bone to start growth again. Of course, this idea will also require invasive surgery.

• Area #1: Stem Cell Research & Stem Cell Technology
• Area #2: Tissue Engineering, or more specifically Tissue Regenerative Medicine

These two areas of study are intertwined in many ways. All that we are trying to do is to regenerate a type of tissue that would cause bone tissue to expand volumetrically. That required cartilage tissue. So we are trying to make cartilage form. From multiple researchers over many decades, the overall conclusion reached is that due to the way the extracellular matrix in cartilage tissue works and how low in concentration the chondrocytes are in the cartilage, cartilage tissue is very hard to form at a fast proliferative rate.

From Source 1 “…Unlike bone and all other connective tissue types, cartilage is avascular,  lacking blood vessels.  For this reason alone, cartilage does not possess the regenerative capacity of bone or the other connective tissue types.  Remember, nutrient delivery is essential for tissue repair.  Blood vessels provide the nutrient delivery to most tissues.”

The best example is in the articualr cartilage seen in the knees and hips of older people. Over the years, from pounding and shocks from walking, the articular cartilage layer in the joints decrease in thickness, and eventually the layer is rubbed (or compressed) away leading to bone touching bone, causing the nerve endings in the joint area to signal pain signals to the brain. That cartilage layering is very hard to get back. Right now there are some proposed ideas on how to make the cartilage layer thicker.

So the main idea I am proposing in this post is that besides the ideas of callotasis and the scientific unproven (and experimental unproven at least on a high consistent level) loading of the lateral ends of long bone epiphysis, the last major idea that is reasonable to do at this point in technology is to create growth plates from scratch.

The Basic Science

From basic tissue engineering principles, we first need some type of cells from the subject or patient to start out with. This means that a possible biopsy is first done, more specifically a Bone Marrow Biopsy. Refer to the link on MedlinePlus for more information about Bone Marrow Biopsy.

From basic stem cell principles, we can’t just scrape the inner check of the subject to get ordinary cells. We need the stem cells because they still have a chance to change into the right type of cells we need in the beginning. We need stem cells to start out with, or at least the precursors to both the bone cells and the precursors to the cartilage cells.

In the study “Engineering Growing Tissues” which I would cite as the main reason I wrote the post “Engineering Growing Cartilage Tissue In Vivo Through Chondrocyte Transplantation (Big Breakthrough!)”, it was shown that to see from histological examination the phenomenon of actual bone tissue growing in size aka volumetrically, we would need both bone AND cartilage cells to begin with, not just cartilage cells or precursor (progenitor) cartilage cells.

Side Note: Theoretically we could just take a swab of the epithelial cells in the inner cheek of the subject and using the process of transdifferentiation turn them into the cartilage cells or stem cells needed to start the tissue engineering regeneration but the process of cell-cell transdifferentiation is just not well understood at this time. Currently the cell process of transdifferentiation has not even begun to be figured out yet so there is no way that we can figure out how to manipulate a fully differentiated cell to dedifferentiate back to its precursor form or into a another cell type. I would guess that it has to do with something in the microRNA of each cell, but it would require real professional researchers to figure that out. That could take many decades for anything to pan out.

Something I have been wondering is whether it is possible to just start out with not a pregenitor cell like a stem cell, but just some chondrocytes or cartilage taken from the subject’s/patient/s body. The easiest place I would guess is from the nose, or ears. The simplest idea would be to puncture a small hole in the earlobe to grab a piece of ear cartilage. However the type of cartilage that is found in the ear or nose may not have the right collagen type of chondrocyte concentration. It might be better to just take the cartilage sample, and then using chemical filtration techniques or purification techniques, separate using bioseparation principles the chondrocytes from the cartilage matrix.

So we need to get either of 3 types of cell types to start with from the subject…

• Stem Cells – Most likely way is using bone marrow biospy, which is EXTREMELY painful
• Progenitor cells – for Both the cartilage and bones cell types 
• Cartilage and Bone cells – Bone biopsy and clpping an ear or nose

Since stem cells are technical progenitor cells for all tissue types, it just makes sense that we go with a bone marrow biopsy to get the needed adult human stem cells in the beginning. I am not sure if the idea of using already differentiated, mature chondrocytes and osteoblasts would even work from the studies I have read, but it is a long shot.

From the marrow derived sample, we have to filter and purify the sample, removing the plasma, red blood cells, white blood cells, and whatever else is in the marrow from the stem cells.

These stem cells are not as powerful in their potential as say from the umbilical cord of a newborn baby or fetus, but they should be good enough. They are what some people call yellow in nature.

From the Wikipedia article on Adipose Tissue….

“…Recent advances in biotechnology have allowed for the harvesting of adult stem cells from adipose tissue, allowing stimulation of tissue regrowth using a patient’s own cells. In addition, adipose-derived stem cells from both human and animals reportedly can be efficiently reprogrammed into induced pluripotent stem cells without the need for feeder cells. The use of a patient’s own cells reduces the chance of tissue rejection and avoids ethical issues associated with the use of human embryonic stem cells.”The issue of tissue rejection is something that is also needed to be addressed for any type of implantation, explantation, or transplantation to work. The human body has its own natural resistance and defense system against foreign contaminants.

From the adult adipose derived stem cells (ASCs), we can get them into a type of medium, usually calf serum to help them grow and multiple in number. This is the proliferation stage.

Update June 21, 2013: It seems that my understanding of stem cells is somewhat wrong. I mistakenly believed that adipose derived stem cells and bone marrow stem cells are the same thing when new sources have come out to show that they are two different types of stem cells in adult humans. This post/article will need to be eventually rewritten to make the clear distinction between the adipose-derived stem cells (ASCs or ADSCs) and the bone marrow stem cells (MSCs or BDSCs). I will be reading over the studies…

• Morphological, molecular and functional differences of adult bone marrow- and adipose-derived stem cells isolated from rats of different ages.

• A comparison of bone marrow derived and adipose derived stem cells in point of care goat non-instrumented posterolateral intertransverse spinal fusion

• Mesenchymal Stem Cells Derived from Adipose Tissue vs Bone Marrow:In Vitro Comparison of Their Tropism towards Gliomas

I personally would say that it is better to take the stem cells from the bone marrow for our tissue engineering applications.

Once we have been able to get the stem cells to start differentiating into both the bone tissue cells and cartilage tissue cells that we want (because we want to have BOTH), we take the needed amount of concentration of cells, and embedd them into a scaffold. The scaffold is needed to act as a temporary holding structure for the cells to attach themselves to while they are still going through the proliferation stage.

The last major piece is the addition of certain types of growth factors to stimulate the bone and cartilage cells to start. At this stage, the best candidates I have found in research for the highest chondrogenic potential are a combination of TGF-Beta2 with BMP-7, and also the addition of GDF-5.

The scaffold with the growth factor mixture and the grown cell culture is what will be surgically implanted into the human body and let to naturally grow in vivo.

The result is the biotechnology of reinitiating the human body to grow taller again from getting a new growth plate added in. This is the idea on how to grow taller using stem cells technology and tissue engineering regenerative medicine. 

Things To Consider

This method will require the need to do a major surgical process. However, once the implant manages to fuse and be functional in parallel with the rest of the human bone, it will mean that we have been to get the human body to grow taller using new growth plates.

I don’t know just how far biotechnology will advance in the next 50 years. Some people have said that the 21st century will be the century of Biology and Breakthrough Biotechnology and Medicine from understanding Genetics and maybe there is still new fields and areas of medical study that has not even been invented yet. However at this point, this is what I think will be the best viable option for real continued height increase starting at the point of adulthood and bone maturity.

The idea of using stem cells and tissue engineering together to grow completely functional growth plates which can be implanted into the adult human body to make them grow taller again is not the dream that so many height increase seekers wish for but it is based on hard scientific fact and research. There are many studies showing how well stem cells work in growing tissues. There are many journalists who are claiming that one day tissuing engineering will be so advances that we will be able to replace individual organs and tissue parts like our body was a car.

I don’t want to focus on science fiction or make grand claims. This is what is possible, and I think this may be the other really big idea that will be here within a couple of decades helping people continue to grow taller when their first set of growth plates are gone.

 

Some people who comment on here say that I am crazy or obsessed with this issue and I can only agree with them. This subject on height and height increase is an obsession of mine. That is why I have been able to continue to do the type of research which I have found no where else on the internet, in terms of breadth, quantity, insight, and quality anywhere else beside maybe HeightQuest.com on the internet at least for English Language based websites. Maybe there are forums or websites or blogs which are even bigger then here like the old, now dead GrowTallForum.com forum or the GiantScientific.com forum which no one comments on anymore the last I checked.

If I was to be diagnosed by someone like Dr. Paley on why I am so preoccupied with this fixation on something which most people would say I have no control over and can’t change no matter what I do except short of limb lengthening surgery, he would say that I suffer from Body Dismorphia Disorder. Somehow I don’t like my body, but specifically the height aspect of it. This is abnormal for someone who is around the average USA height male, at around 5′ 11″. Most people who feel any type of short statured psychological disorders would more likely be on the short side. However, it would seem that Body Dysmorphia Disorder for the issue of height seems to affect many people who people would say is rather tall. The guy I interviewed recently Joey describes himself as 5′ 10″. The old researcher and contributor to the website Kazlina comes from a family of tall women, and she is aroudn the 5’8-5’9″ range. I read about this one guy from the old Impartial Height Increase Boards who was 6′ 4″ and was so intent on increasing his height that he was ready to go to China back in the mid 2000s for the surgery. I think he said that he wanted to be 7 feet for some reason, but after many years he stopped caring about this issue.

It would seem that no matter how tall or how much we have as humans, we never stop wanting and wishing we could get more or be more. My sister does. My dad does. My current gf does. Both of my female cousin wish that too. This desire is epidemic and affects so many people.

Something that would be very fitting to the same subject of being dissatisfied with our body would be where young adult males become preoccupied with the size of their penis or genitalia. I recently found a forum that is frequented quite a lot called Matters Of Size at MatterOfSize.com.

I took the time to read over the goal of the website and was very surprised that there were men who were so fixated on this area of life that they would devote many hours of a day for many months or years just for the possibility of increasing their penis length or width (girth).

I personally have no issues with the size of my own genitalia and I am confortable with that. These men who are on the website are. I would say that the same type of dissatisfaction we here have about our height, those guys on the forum have the same type of dissatisfaction for their genitalia size. People wish to be bigger. When subjects like whether Stretching or Jelqing I realize just how unique this area of the internet is. This type of forum about the male’s immense desire to feel better about themselves through getting a bigger penis size is very unique, but also very analogous to what we are doing. It is not wrong,  and I would never judge on how these guys want to spend their time to improve themselves in the way they think they need to to feel better about themselves and think they are good enough to love and be loved.

I think that we are doing the same thing, hoping, wishing, striving, working to become taller than what is given to us naturally. Both of the endeavors stem from at least a small degree of body dysmorphia disorder. Both of these areas of study and research are the human being way of trying to change something in their physical appearance to look better.

 

 

This is a theory that I am proposing which I have sort of reached after doing research for only less than 1 year. In this post I wanted to go deeper on the old mother’s tale of telling their children to drink their milk so that they will grow taller. The relationship between drinking milk and increasing one’s growth rate and ending up with a taller final height has been around at least as long as I have. I wrote about this connection a long time ago in the post “The Real Correlation Between Milk, Calcium, Bone Growth, And Height”

In that old post I had said that there is some evidence in showing that children who are malnourished in general will obviously lead to stunted growth. The fact is that height is correlated to how well calcium is absorbed into the body. The actual mineral that determines whether Calcium will be absorbed into the bone while the growth plates are still around and endochondral ossification is still going on is Vitamin D. Vitamin D is what will really determine whether the ossification will go faster and lead to more bones building on top of each other while the longitudinal growth was still going on.

The primary focus when mothers and nutritionists talk about is the calcium in the milk but they don’t tak much about the vitamin D. The truth is that in most diets in the developed world, Calcium deficiency is not a very big problem. The bigger issue could be Vitamin D. There is usually enough Calcium in the blood but if there is no way for the bone to absorb it, then the milk that is ingested will be wasted and will probably eventually be passed through the urinary tracts and expelled out of the body.

My theory is that drinking milk and getting calcium will only help increase the growth rate and height in pre-pubsecent girls. – due to low bone density in females and that fact that the effect of calcium is overtaken by the effect of estrogen when puberty does start.

From source #1 – “Height and Height Z-Score Are Related to Calcium Absorption in Five- to Fifteen-Year-Old Girls”

Clearly, an adaptive mechanism of increased calcium absorptive efficiency could be inadequate to meet the needs of very tall individuals or those with a severely deficient calcium intake, especially over a prolonged period of time (22). However, the results of recent controlled trials generally suggest that adequate mineralization of the skeleton does not require very high calcium intake levels during growth (11, 32). The ability to adapt calcium absorptive efficiency to biological needs for calcium is likely part of the reason that more moderate calcium intakes are adequate even during pubertal growth (9, 11, 32)

The section from this study shows that for even developing kids, they don’t need excess levels of Calcium concentration before they reach a level for optimum/highest growth rate of the bone.

From source #2 – “Calcium supplements in healthy children do not affect weight gain, height, or body composition.”

This 2nd article seems to show that if the developing kid tried to increase the calcium level in their blood from taking calcium supplements, they would see almost no increase in increased height. The value from this study was an increase of just 2 mm.

From source #3 – “Does a LOW Intake of CALCIUM Retard GROWTH or Conduce to STUNTEDNESS?”

Where calcium supplements have been fed for short periods to children and youths accustomed to intakes of calcium less than the recommended allowances, there appears to be no critical evidence that these additions have specifically produced increments in height beyond such observed in controls.

The conclusion is reached that it has not been established that calcium intake per se is of importance in regulating height. It is suggested that apart from gross undernutrition, the critical intake of calcium below which retardation of growth occurs, lies below the wide range of calcium contents of everyday diets consumed in different parts of the world.

The 3rd source shows that even when calcium supplements are given to kids who are accustomed to lower calcium rates, their growth rates and final height don’t increase much. They conclude that calcium intake is not that important in regulating height. Most diets around the world, besides malnutriton, already has enough calcium intake to not need to worry about deficiency calcium levels which would lead to stunted growth.

Source #4 – Calcium—Good for Teen Growth and Bone Building

This source was the first one that showed that adolescent males who take calcium supplements seem to show a final height on average 0.25 inches greater than a controlled group. However the researchers noted at the end stated that the 1/4 th of an inch greater height was only for the short term, and did not indicate whether the higher height was really for the boys’ ultimate final height.

As for girls, they state. “In a previous study, adolescent girls who were past puberty (ages 16 to 18) experienced an increase in bone-mineral density but did not increase in height more than girls who did not take calcium.” – The calcium supplements did help give them stronger bones by increasing the BMD but not their height.

Source #5 – “Effect of cow milk consumption on longitudinal height gain in children”

A section of the paper…

“Bonjour et al (6) found that prepubertal girls who consumed a diet including calcium-enriched foods grew in height in a randomized, double-blind, placebo-controlled study. In our longitudinal study, the mean height gain in the high-consumption group was higher than that in the low-consumption group, and the difference in height gain between the 2 groups was 2.5 cm/3 y.”

We could say that this source seems to suggest that girls who take high levels of calcium when they are still in the ages before puberty have on average 2 cm more in height for every 3 years of growth then girls who has low levels of calcium in their diet. The researchers concluded for this paper that drink large amounts of milk would be good for a person.

Source #6 – Adolescent height: relationship to exercise, milk intake and parents’ height.

The researchers here concluded that “Milk intake of female adolescents from Group I was significantly more than the other groups. It is concluded that parents’ height in both males and females and milk intake in females contribute to a greater adolescent height.”

Group 1 had the adolescents which were in the 97% percentile of height.

Conclusion:

These 6 sources which I had used before seem to point at the relationship that milk only has a reasonable effect on a child’s growth rate in kids who are in the pre puberty ages. There is evidence in the last 3 sources which seem to suggest that calcium intake from milk ingestion would help increase height, but the difference seems to be a couple of cms, not the 4-5 inches of difference those “Got Milk” commercial would make a parent believe. In most diets in the developed nations, Calcium and Vitamin D can be obtained from many other sources besides milk, cheese, or any other type of milk derivative. The calcium at moderate levels in girls seem to have the same rate of bone growth as high levels of calcium.

Source 5 and source 6 shows that girls who are still very young seem to have some benefit towards height from high milk consumption, and the result is just around 2 cms for every 3 years. Beyond the puberty stage, there is no more benefit towards height in girls. For boys, the increase is around .25 inches or a little less than 1 cm. The affect however was only for the short term, not the overall affect towards final height.

 

There has been many patents over the years that were filed by large and mid sized Biotech and Biomedical companies trying to protect their ideas and methods on how to regrow bones. This idea of using the TGF-Beta has been a very common and well understood concept. I list a few patents I have found from Google Patent which show exactly what concentrations of TGF-Beta would be needed to be injected into the human leg to cause bone growth in vivo. However this would not make the bone actually longer, but only make the bone mineral density increase.

Patent #1: Method of inducing bone growth using TGF-β – US 5158934 A

Abstract: A method is provided for generation of bone at a site of an animal where skeletal tissue is deficient comprising administering to the animal, locally at the bone site in the presence of a source of osteogenic cells, an effective amount of a composition comprising TGF-β in a pharmaceutically acceptable carrier, provided that such composition excludes a bone morphogenetic cofactor, the composition being administered in an amount effective to induce bone growth at the bone site. Also provided is a device for implantation into a site of an animal where skeletal tissue is deficient comprising a device treated with an effective amount of a composition comprising TGF-β and a source of osteogenic cells in a pharmaceutically acceptable carrier.

What is claimed is: A method for generation of bone at a site of an animal where skeletal tissue is deficient comprising administering to the animal, locally at the site in the presence of an osteogenic cell source, an effective amount of a composition consisting essentially of TGF-β in a pharmaceutically acceptable carrier, provided that such composition excludes a bone morphogenetic cofactor, the composition being administered to the animal in an amount effective to induce growth of morphologically normal, mature bone at the site.

Patent #2: TGF-β composition for inducing bone growth – US 5409896 A

Abstract: A method is provided for generation of bone at a site of an animal where skeletal tissue is deficient comprising administering to the animal, locally at the bone site in the presence of a source of osteogenic cells, an effective amount of a composition comprising TGF-β in a pharmaceutically acceptable carrier, provided that such composition excludes a bone morphogenetic cofactor, the composition being administered in an amount effective to induce bone growth at the bone site. Also provided is a device for implantation into a site of an animal where skeletal tissue is deficient comprising a device treated with an effective amount of a composition comprising TGF-β and a source of osteogenic cells in a pharmaceutically acceptable carrier.

What is claimed is:

1. A pharmaceutical composition for treatment of a site of an animal where skeletal tissue is deficient consisting essentially of about 1 to 100 ng/ml of TGF-β and an osteogenic cell source isolated from an animal, which composition is formulated in a pharmaceutically acceptable carrier and excludes a bone morphogenetic cofactor.

2. The composition of claim 1 wherein the osteogenic cell source is dispersed whole bone marrow, perichondrium, periosteum, or a cell line.

3. The composition of claim 1 wherein the TGF-β is TGF-β1 or TGF-β3.

Patent #3: TGF-β formulation for inducing bone growth – US 5422340 A

Abstract: A formulation suitable for inducing bone formation contains about 0.5 μg to about 5 mg of transforming growth factor-β and about 140 mg to about 50 g of tricalcium phosphate and excludes a bone morphogenetic cofactor. In another embodiment, the formulation contains about 0.5 μg to 5 mg transforming growth factor-β, about 140 mg to 50 g of tricalcium phosphate particles, and an amount of amylopectin ranging from about 01:1 to 1:1 amylopectin:tricalcium phosphate.

Field of the Invention: This invention relates to the use of transforming growth factor-beta (TGF-β) to induce bone growth in vivo and to formulations of TGF-β and tricalcium phosphate useful for this purpose.

What is claimed is: A bone-inducing formulation consisting essentially of about 0.5 μg to about 5 mg of transforming growth factor-β and about 140 mg to about 50 g of tricalcium phosphate.

2. The formulation of claim 1 wherein the tricalcium phosphate is particles.
3. The formulation of claim 2 wherein the particles are granules or a powder.
4. The formulation of claim 3 wherein the transforming growth factor-β is adsorbed on the granules or powder.
5. The formulation of claim 3 wherein the tricalcium phosphate is in the form of granules with a diameter of about 120 to 500 μm.
6. The formulation of claim 1 further comprising a polymer selected from amylopectin, gelatin, collagen, agarose, or a mixture of these polymers, in an amount effective to enhance consistency of the formulation.
7. The formulation of claim 6 wherein the polymer is lyophilized before use.

---

Analysis On The Patents: 

The first two patents are essentially the same one, since the patent inventors are the same people and they are from the same company, Genentch back in the mid 1990s. The Abstract or Introduction are the same thing. However there is just a slight change to the patents, which are separated by 2 years of patent filing. It seems that from the first two patents, there is 5 main parts to the patent…

1. A device used for implantation, like a syringe or something,
2. The TGF-Beta composition, which will have TGF-Beta1 and TGF-Beta3 (concentration is 1- 100 ng/mL of TGF-beta)
3. A carrier, probably like a gel or scaffold which the TGF-Beta will go into. 
4. A source of osteogenic cells – which is probably explanted out first. 
5. Excludes a bone morphogenetic cofactor.

These 3 parts (osteogenic cell source with TGF-Beta composition with the carrier) are combined and the device takes the mixture and puts it into an area of the human bone where there is no bone growth or bone. The mixture will cause bones to grow in the bone defect area. However that will not be enough to create the cartilage we need which will expand and grow out.

The third patent is very similar in its area of focus. The patent inventor is the same person. This time the TGF-Beta is used at a higher concetration, around 0.5 micrograms to 5 miligrams. There is a type of tricalcium phosphate which is in a granular, powder form. The TGF-Beta is absorbed into the granular powder and this mixture is added into bone defects to induce bone matrix formation. This patent also is excluding a certain bone morphogenetic cofactor. There is something called amylopectin which is used to make a polymer selected from amylopectin, gelatin, collagen, agarose, or a mixture of these polymers, in an amount effective to enhance consistency of the formulation.

Something that me and Tyler realize at this point is that intermittent mechanical loading may be one of the best approaches we have towards something that could work. However that chance is very small. The entire LSJL approach is based on short bursts of mechanical loading that is repeated maybe once or twice a day for a few days and then stopped, and then restarted a week later and have that cycle also repeated.

The reason why any type of stimuli that would be applied to the human body must be intermittent is that the human body (or any living organism’s body for that matter) has this ability to be able to react to stimuli from the external world and shift the way the systems in the body in how they work to a new set point of equilibrium.

The best example of this is when people who first start out trying weak drugs develop a tolerance for the weaker drugs and need to take stronger drugs to get the same type of effect they had when they first started out. Their body after continuous stimuli by the outside influence shifted the way the brain worked either upregulating or down regulating certain types of brain neurotransmitters and that resulting in a new place of physiological equilibirum.

The same principles apply to why Hakker and steroid researchers and users would talk about the need to cycle through the compounds. Cycling allows the body to re-set its equilibirum back to a state where the weaker stimuli would still have an effect.

Tyler talks about the fact that maybe the long bone epiphysis he has been loading for these years might have lost their sensitivity so he had to increase the dumb-bells he has been loading with. He had been able to theoretically increase the duration of the loading effectiveness by going off of the loading for a few days.

In my opinion, the mechano-sensitivity he is talking about is something that is unknown at this time.  I don’t believe Tyler can tell whether his epiphysis will still even respond to loading anymore. It could be that the loading he has done even from doing it intermittently has cause the area of bone to stop being able to respond at all to the loading anymore, whether electrically due to piezo nature of bone or any other type of Wolff’s Law bone remodeling patterns.

It could be that he needs to stop loading for an extended amount of time, maybe 2 months before starting again to give the bone area a chance to regenerate the osteogenic properties again.

This article I found seems to show that bone disorders where bone mineral density drops can be negated by doing mechanical loading

Method and device for treating bone disorders by applying preload and repetitive impacts

ABSTRACT

Bone disorders may be treated by applying a compressive preload and repetitive impacts. The patient may be maintained in a static position and the preload be provided by gravity or compression. The impact load, impact rate, and a number of impacts determined by a physician prior to treatment are chosen to generate electrical signals in the patient’s bone such that the majority of energy of the electrical signals lies between 0.1 Hz and 1 kHz, and the peak amplitude values of the electrical signals lie between 15 and 30 Hz.

Analysis & Interpretation

This shows that for bone growth, the compressive repetitive impacts do work. LSJL will work to promote bone growth. The values that is cited in this paper are very low actually at around 0.1-10,000 Hz. The amplitude of the loading is around 15-30 Hz.

Note: This is not an ordinary post, but a patent. There is more in the Description section of the patent.

To slow or reverse bone loss, doctors have focused their attention on estrogens, calcium, and exercise, used either together or individually. More recently, fluorides and thiazides have been tested as therapeutic agents, but none of these approaches has been successful in restoring a severely depleted skeletal bone mass to normal. In addition, many elderly individuals with advanced bone loss cannot participate in exercise programs due to poor reflexes, motor tone and balance, as well as stress pain and stress fractures.

Certain researchers have suggested an electrical intermediary in Wolff’s law. Wolff’s law states, in short, that bone adapts to the forces acting upon it. In other words, bone will increase in mass and remodel to relieve the applied stress.

Because bone is piezoelectric and electrokinetic, it generates an electrical signal in response to the applied force. That electrical signal then effects bone formation. This is explained in Bassett, “Effect of Force on Skeletal Tissues,” Physiological Basis of Rehabilitation Medicine, Downey and Darling eds., 1st ed., W. B. Saunders Co. (1971). On the basis of Wolff’s law and more recent investigations, two techniques have been developed for treatment of bone disorders. One involves mechanical forces and the other involves electrical forces.

Implications For Height Increase

The patent is an interesting read and shows that we can indeed grow bone mass at least from a short intense repetitive loading on bones so that the bones will induce electricity, which somehow stimulate some type of bone growth.

Overall, this patent is useful in showing that we have at least clear evidence that the LSJL method has already been proposed by some researchers before for bone mineral density problems. This is used to treat osteoporosis, not short stature.

There is supposed to be 2 techniques developed to treat bone disorders. One is mechanical and the other is electrical.

Mechanical –  periodical strain rates and cycling patterns generate maximal osteogenic response in avian bones….an experiment demonstrated that cyclically loading the bones at 0.5 Hz caused bone formation, although repetition of more than 36 cycles did not seem to increase bone formation.

Electrical – in vitro and in vivo measurements showed the electrical potentials developed due to bone deformation…. the development of products for the stimulation of bone tissue electromagnetically.

It seems that the end result for both of the techniques is that the bones being deformed create a electrical signal.

The main thing to get out of this is that LSJL has a very good chance of increasing growth rates in people with open growth rates. It might have a smaller chance of working on people with no growth plate cartilages if we can somehow get the bone layer underneath the articular cartilage to be slightly more osteogenic. LSJL might be able to do that in a small minority of people who try it.