Here’s a paper from Korea about a new longitudinal bone growth supplement that may be promising:

Effect of KH-BaRoKer-SeongJangTang based on traditional medicine theory on longitudinal bone growth

“KH-BaRoKer-SeongJangTang (KBS) is a recently developed formulation by using traditional drugs considering traditional medical theory of Oriental books such as ShinNongBonChoGyeong and JuRye, which has been used to improve the growth of child in Korea. Although KBS is usually prescribed to many children who are in retard for their age, its pharmacological effects have not been fully understood in experimental models. The aim of this study was to evaluate the effects of KBS on bone growth. Growth plate thickness and bone parameters such as bone volume/tissue volume (BV/TV), trabecular thickness (Tb.Th), trabecular number (Tb.N), connection density (Conn.D), and total porosity were analyzed by means of microcomputed tomography. Serum insulin-like growth factor-I (IGF-I) levels were measured by enzyme-linked immunosorbent assay. Hepatic IGF-I mRNA expression was analyzed by real-time polymerase chain reaction. Phosphorylation of signal transducer and activator of transcription5 (STAT5) was investigated using Western blot analysis and immunohistochemistry. The thickness of growth plate was increased by KBS. BV/TV, Tb.Th, TbN, Conn.D, and total porosity were improved by KBS. Hepatic IGF-I mRNA and serum IGF-I levels were elevated by KBS. Phosphorylation of STAT5 was increased with administration of KBS. These results suggest that KBS would be helpful to children who are in retard for their age through the elevation of IGF-I.”

Increase in Stat5 phosphorylation, increase in IGF-1, and increase in growth plate thickness could be indicative that the supplement could increase growth.

“Male ICR mice (4 weeks old) and diets were purchased from Dae-Han Experimental Animal Center (Eumsung, Republic of Korea), acclimated for 7 days, and then randomly assigned for 2 weeks to adequate protein (CON, 20% protein) or low protein diet (PEM, 4% protein) . The protein source used was casein. Except for the protein content, the two diets were identical and isocaloric. After 2 weeks, mice were divided into five groups, CON (adequate protein diet + distilled water (DW)-administered group); PEM (low protein diet + DW-administered group); KBS (low protein diet + KBSadministered group); Arg (low protein diet + Arg-administered group); Glu (low protein diet + Glu-administered group). The mice were fed indicated diet, administered each material three times a week for 12 weeks, housed four to six per cage in a laminar air-flow room, and maintained at a temperature of 22 ± 1℃, a relative humidity of 55 ± 1% throughout the study.”

So it seems that this supplement is an IGF-1 mimetic.  Whether this can increase height in children with normal IGF-1 levels depends on the bodies negative feedback mechanisms.

“Binding of GH to GHR activates receptor-associated intracellular tyrosine protein kinase Janus kinase 2 (JAK2), which phosphorylates signal transducer and activator of transcription 5 (STAT5). The phosphorylated STAT proteins translocate to the nucleus, where they bind to specific DNA sequences and regulate gene transcription. Among the signal cascades from the GHR, the JAK2-STAT5 pathway is regarded as a major pathway that mediates the action of GH on gene transcription in the liver. This pathway was shown to be responsible for the transcriptional action of GH on IGF-I. IGF-I is a mitogenic factor for various cells and plays an important role in cell growth and survival, and the majority of plasma IGF-I is biosynthesized in the liver”

Two of the ingredients of the supplement are listed to be arginine and glutamine which aren’t exactly game changing.  A detailed list of the ingredients are given in Table 2 of the paper(link provided).

The kbs growth plate and the general bone architecture does look a little bit better than the Arginine group.

“Effect of KBS on tibial growth plate thickness. (A) Representative 3D CT images of knee joint showing growth plate. (B) The thickness of excised bone growth plate was determined on five points. CON, adequate protein diet + DW-administered group; PEM, low protein diet + DW-administered group; KBS, low protein diet + KBS-administered group; Arg, low protein diet + Arg-administered group; Glu, low protein diet + Glu-administered group”

So the supplement didn’t have much more benefit over arginine.

“The lengths of proximal tibia growth plate in the CON and PEM groups were 112.82+/- 4.18 and 86.43+/-1.47, respectively. The growth plate lengths in the KBS, Arg, and Glu groups were 119.05+/- 6.48, 118.75+/- 4.81, and 87.82+/- 6.38, respectively. KBS and Arg significantly enhanced the longitudinal bone growth, whereas Glu did not”

Interestingly, the serum IGF-1 levels were lower than the contAnother major ingredient was a variation on the Hominis Placenta Extract.  Given that the source is the human placenta which is very powerful, it is possible that this extract has of yet undocumented effects.  And many species eat the placenta.rol group in the KBS group and lower than that in the Arginine group.

“Carthami Tinctorii Fructus increased the level of serum IGF-I and lengths of femur and tibia, however, its effect was very small and transient”

Something we can ascertain is that maybe excess IGF-1 levels don’t have that large of a benefit on height.  As the excess IGF-1 levels of KBS versus arginine groups did not result in increased height.

KBS and Arginine increased growth plate thickness by about the same amount so it’s hard tell whether KBS has additional effects beyond arginine.  The difference between KBS and Arginine growth plates are so small and the variance is so large that it’s hard to attribute the difference to anything other than normal variation.

It’s possible that KBS could increase longitudinal bone growth but whether that affect is greater than Arginine is unknown

Here’s the study on Carthami Tinctorii Fructus:

Determination of mineral content in methanolic safflower (Carthamus tinctorius L.) seed extract and its effect on osteoblast markers.

“Safflower (Carthamus tinctorius L.) seeds are used as a folk medicine to enhance bone formation or to prevent osteoporosis in Korea. Therefore, the methanolic extract of safflower seeds (MESS) containing high mineral content, such as calcium (Ca), potassium (K) and phosphorous (P), was evaluated for the role on osteoblast (Ob) markers of Sprague-Dawley rats. In serum of 3 to 11 weeks (wks) old rats, both osteocalcin (OC) content and bone-specific alkaline phosphatase (B-ALP) activity increased to their maximum levels in 4-7 wks. Hence, 3 wks old rats were selected for 8 wks oral treatment of MESS, resulted in the significant increase of Ob markers in serum such as OC content (4-8 wks), B-ALP activity (1-2 wks) and insulin-like growth factor I (IGF-I) level (1 wk), and the growth parameter such as the length of femur (2-8 wks) and tibia (4 wks). On the basis of Pearson’s correlation coefficient, there were a moderate correlation between OC and B-ALP at 8 wks, a low correlation between OC and IGF-I at 1, 4 and 8 wks, a moderate correlation between OC and femur length at 1, 2 and 8 wks, and a moderate correlations between OC and tibia length at 1 and 8 wks of MESS-treated groups. The result reveals that the changes of OC correlated at low to moderate level with the changes of B-ALP activity, IGF-I content and femur and tibia length in the MESS-treatment period. On the other hand, there were a strong correlation between IGF-I and femur length at 2 wks and moderate correlation between IGF-I and tibia length at 1, 2 and 8 wks of MESS-treated groups.”

“A Korean herbal formulation, Gami-Honghwain, is comprised of crude ingredients from safflower seeds and hominis placenta.”

“There are reports about chemical components of the safflower. Its leaves contain eight flavonoids, some of which showed potent antioxidant activities. Its seeds also contain numerous polyphenolic compounds such as lignans, glucosides, flavonoids and serotonins”

The increase in tibia and femur length ranged from 3-5%.  Note though that a 3% increase of someone who’s 5’9″ brings them to 5’11”.  And at all data points the treated group had longer bones than the control group.

“. In the aqueous extract from safflower seeds, there are K (2.306 μg/g), P (1.043 μg/g), Mg (0.474 μg/g), Al (0.175 μg/g), Fe (0.100 μg/g), Ca (0.075 μg/g), Zn (0.070 μg/g), Na (0.066 μg/g), Cu (0.055 μg/g) and Sr (0.022 μg/g). In the MESS, there are Ca (3.752 μg/g), K (1.313 μg/g), P (1.161 μg/g), Na (0.177 μg/g), Fe (0.170 μg/g), Zn (0.042 μg/g), Mg (0.023 μg/g), Al (0.019 μg/g), Cu (0.015 μg/g) and Sr (0.002 μg/g).”<-None of these seem to be novel compounds except for Strontium which is found in small amounts in normal human food.  Since Strontium amounts are so small it would be possible to be deficient in it and extra dietary strontium may increase longitudinal bone growth.

An interesting article appeared in the online website The Daily UK today which made me think about the issue of height from a perspective which I never put any effort into before. I refer to the story of Lena Dunham standing next to Taylor Swift Here.

In certain parts of the internet, where men talk about the post-modern version of dating and relationships, a concept has come out called “The Red Pill”, which promotes this idea that what men today think women want and what women really want are very different. These men believe that at the most basic, instinctual level, each heterosexual female wants a dominant, strong, masculine men as based on our savage animal origins.

A central public celebrity which is brought up often to portray the stereotypical image of what is wrong with the American and/or Westernized women of today is Lena Dunham.

Lena Dunham has been vilified by many of these internet blogging men for being too self-accepting of the changes in the female figure. Weight has been traditional the issue/factor that the post-modern men and the post-modern female has the most contention over.

In this day and age where young girls are being constantly being exposed to images of strong powerful women who proclaim to be feminist, they are taught that it is okay to be overweight and not have the type of figure that men desire. Self-acceptance and being fully comfortable with one’s body is very important. In retaliation, the young heterosexual males find these type of women who prefer to stay “overweight” or “full-figured” difficult to find a relationship with stating that they want the old more traditional feminine type of women, which is obviously just a glorified fantasy of something which never really existed. .

Anger, Spite, and Venom has been spewed on both sides, sometimes going as far as threats of sexual assault and bodily harm. Of course, anyone can be sort of a problem as long as they hide behind a screen and stay in anonymity. A sense of self-entitled runs high on both sides.

However, now the issue of height has been brought up. This is where things get interesting. Lena Dunham has been branded a feminism of this modern age, which she seems to be comfortable with that label. When it comes to weight, she has almost no problems. She had taken pictures of herself naked squatting down holding a piece of cake before. She was being overly expressive in showing of the excess of her body to the world.

This recent story that has appeared suggests that she has to content with the other anthropometric measurement which is making her realize that maybe this whole movement of body acceptance is a little harder than believed.

Remember the basic tenet of trying to compare weight and height.

• Weight is something you can change with a little bit of effort, work and discipline
• Height is something that is almost impossible to change

What my point is that when people like Lena Dunham and other feminists are talking about weight issues, and body acceptance, they are focusing on the wrong thing.

There is no need to argue for or against any topic dealing with weight, because weight can be changed and molded to whatever level we desire. 

It is height that is what most important. Your level of stature is what is most important, which is what someone like Lena Dunham realizes she will always be inferior to. With her brand of feminism, she chooses to not wear high heeled shoes, which just makes her look even shorter to her female counterparts, who are trying to accentuate their “tallness”.

It is not the fat-shaming guy online that Lena has to content with (since she can easily dismiss those guy as losers) but another female, who happened to be taller than her, who chooses to dress in a classy way, with her tall female friends.

Suddenly you are put on the spot and realize just how “different” you look compared to the others, your own peers,, who you thought before was at the same level as you, only to see from a more objective point of view that they are much higher than you, literally. The other thing that you realize is that there is nothing that you can do about this factor, unlike weight which you can work on.

What do you do when you realize that you have been fighting the easy fight but have always shied away from the hard fight?

• To gain acceptance of weight is easy.
• To gain acceptance of height is near impossible.

If this girl was to really want body acceptance, she should have focused on height first and foremost and not even consider dealing with the issue of weight. I find it tragic that many modern feminists seem to be putting too much energy and focusing on the wrong thing in life. They should instead be working towards women and men finding body acceptance over their height, not weight.

In evaluating potential height increase routines, there are questions that have to be answered true to potentially be effective.  Asking these questions before attempting a routine or supplement, will help to determine if that supplement or routine could possibly be effective although there are many supplements that can be synergestic.

1a.  Does the method increase longitudinal bone growth?

b. Or does the method stimulate an increase the thickness of the bone in a longitudinal direction(top of head or bottom of heel)?

c.  Or does the method target another tissue that is a determinant in height(for example: cartilage or skin at the top of the head)?

d. Does the method alter alignment(posture or loosening of ligaments via relaxin)?

The rest of these questions will involve assuming that 1a was the question that was answered yes to as b-d would have different follow up questions. Note that GH and IGF-1 are a maybe in terms of answering question 1a.  They tend to encourage tissue growth but do not necessarily encourage chondrogenic differentiation(although IGF-1 may).  Something like IGF-2 is something more likely to increase height as it is involved in an earlier development state.  And the growth plate is at an earlier development state than full bones.  GH and IGF-1 are present at all developmental states whereas something like IGF-2 is not.

2.  Does the method involve degradation of cortical bone?

b. Does the method stretch cortical bone(plastic deformation which requires extreme loads)?

This likely has to be an important criteria in the success of a height increase routine.  The end of growth involves the fusion of cortical bone between the diaphysis and the epiphysis.  Distraction osteogenesis involves the cracking of cortical bone.  Cortical bone is likely like a large constraint on longitudinal bone growth.  Note: LSJL likely degrades cortical bone via an increase in fluid flow.

D is the LSJL loaded bone and C is not.  There’s definitely degration of the trabecular bone in D and F.  In D the LSJL cortical bone looks thicker and stronger which would make it harder to grow taller.  However in F there are some signs of degradation.  First, note that in E, that the inner bone is a fairly solid circular object but in F there is a part that juts outward on the upper lateral region of F this could be a sign of cortical bone degradation.    And note that 50% is the dead center of the bone which is not a likely target for increasing bone length.  75% is much closer to the epiphysis and since most longitudinal bone growth occurs at the epiphysis this is very promising that the necessary cortical bone degradation can occur to enable bone elongation to occur.

The bone loading only occurred for 3 days.  If bone loading had occurred longer it is possible that the protrusion of the inner bone would extend far enough to reach the outer point of bone enabling a neo-growth plate to form.  The mice were 14 weeks old which is fairly fair along the skeletal maturity process.  Mice growth plates don’t fuse but they do become dysfunctional and this is the time when growth cessation occurs.  So a potential protrusion caused by cortical bone degradation at a late skeletal maturity state is promising for the possible effectiveness of LSJL on adults.

3.  Does the method stimulate chondrogenic differentiation?

Bones have not yet been shown to be capable of interstitial growth and only through an intermediary tissue(cartilage) are they able to grow longer.  It would be possible to grow taller through the articular cartilage(which is capable of endochondral ossification) at the longitudinal ends of the bones but there does not as of yet seem to be an effective way of doing that.

The creating of an intermediary tissue like cartilage within the bone seems to be necessary to make the bones grow longer.  LSJL upregulates chondrogenic genes.

In addition, the chondrogenic intermediary must progress through the various stages and undergo hypertrophy to push the bone apart.  But it appears that endochondral ossification tends to be the standard procedure for chondrogenic tissue.

I went to this conference for two main reasons. The first was to talk with a company that was selling a 3D Bioprinter. The 2nd was to listen to the lectures and presentations by the leading edge researchers in this field to see if anything that they are working on can be applied to what we are doing here.

Here is what I can say.

Every single industry, field, or niche has a few people who become very important in their chosen area of expertise. From this one conference, I did find out who are the main people we should be focusing on and following.

• Dr. Lawrence (Larry) Bonassar
• Dr. Anthony Atala
• Dr. Warren Grayson

It turns out that a Dr. Jason Spector who was a speaker at the conference giving his talk  “Tissue Engineering, Bioprinting, and the “Reconstructive Ladder”” alluded to the fact that he was working with Dr. Bonassar on research with MSCs (Mesenchymal Stem Cells) to develop cartilage, whether it be fibrocartilage or hyaline cartilage. When I was listening to him, the name sounded very familiar until I realized that I saw the name before and actually wrote a big post on the work being done by Dr. Bonassar’s team in Cornell where they grew an implantable spinal disc. Refer to the post “This Researcher Succeeded In 3D-Printing Spinal Discs Allowing Adults With Closed Growth Plates To Grow Taller If They Desired – Big Breakthrough“. Dr Bonassar’s work and his Lab should be one of the primary focuses for us.

The other speaker that spoke about relevant information was a Dr. Paul Gatenholm (talk was “3D Bioprinting of Human Cartilage and Skin with Novel Bioink”, who apparently was a protege/student of Dr. Atala. He has a company CellLink where his son works at which has produced a type of bioink that is used in 3D Bioprinters. This bioink acts as the medium that stem cells would go into which is something similar to Hydrogel/Alginate/Extracellular Matrix/Scaffold. It is made from a derivative of cellulose.

Dr. Atala is sort of a super-star in the field of tissue engineering, regenerative medicine, and cartilage generation. He has been alluded to multiple times in the conference and I had referenced his research before as well on this website. Refer to the post ” Increase Height And Grow Taller Through Bioprinting And Electrospinning“. If you read this previous post, you would see that there was a Youtube video of Gabor Forgacs, who explained the revolution in regenerative medicine. He was the speaker at this recent conference which started everything off.

There was a third speaker Rahul Tare (talk was  “Application of Custom-Built Acousto-fluidic Perfusion Bioreactor for Cartilage Tissue Engineering” who revealed that he was also working with MSCs to engineer cartilage tissue.

It turns out that this conference I went to has people associated with the big players in this field. Most people there already knew each other.

In terms of the technical, I realized that bioprinting cartilage tissue that can be implanted back into the body is an endeavor which is probably impossible. In a discussion with Dr. Michael Gelinsky, he did not think that bioprinting a hyaline cartilage was viable at least for a long time. However, the idea of slowly developing chondrogenic tissue from implanted autologous chondrocytes and/or MSCs into a scaffold is probable, if not very doable. If Dr. Teplyashin’s group’s results are any indication, this step has already been done.

The problem which the researchers were trying to solve was over vascularization. Vascularization was the main problem that people who want to bioprint organs need to figure out. It was the bottleneck.

The other problem is over regulations. It turns out that many of the most scientifically advanced countries who are working in tissue engineering and regenerative medicine will not allow organs be implanted into the patients body.

Here are the list of 3D Bioprinters that I found out about.

1. BioBots (3d Bioprinter)
2. RegenHu 3d Bioprinter
3. EnvisionTec Bioprinter
4. Organovo’s 3D Printer
5. Regenovo (China based)
6. Qingdao Unique Products 3D Bioprinter
7. Izumi International Inc (Deposition Machine turned into 3D Printer)

Some of the models were cheap but some were extraordinarily expensive.

Some others things I realized that I made a mistake on was to forget about the step of bioreactor. You need a bioreactor for the implanted cells into a culture or scaffold, with the growth factors, to proliferate in numbers. Dr. Spector revealed that to get the MSCs to differentiated into a tissue that is actually worth something, you need at least 200 million cells to work with. Anything less and the tissue that has been formed is not really enough.

So to make a correction on the steps, it would be

• 1. Biopsy of bone marrow to get MSCs/ Extract part of the iliac crest for chondrocytes
• 2. Use collagenase to dissolve the ECM around your desired cells
• 3. Spin the solution to separate the cells from the other compounds
• 4. Get the right type of cell medium (alginate, hydrogel, etc.) to put the cells in.
• 5. Instead of medium, it could be a scaffold shaped in whatever way you want.
• 6. Add some type of growth factor into the scaffold to help the cells differentiate or proliferate.
• 7. Put it into a bioreactor to make the cells proliferate.
• 8. Induce vascularization in the tissue (this is the tough part)
• 9. Take the scaffold/medium out and implant the grown  tissue back into the person’s body. Wait until vascularization occurs to connect the new implant with the rest of the patient’s body.

Notice how I did not say bioprinting anywhere. Remember that there is more than 1 way to get the stem cells/chondrocyte implantation to work.

There is actually 2 ways to do this.

1. You can use a 3D Bioprinter to bioprint a fully functional growth plate, with the chondrocytes inside in columnar structure form
2. You can put extracted MSCs or chondrocytes into a scaffold (hard structure) and grow it into a bioreactor. You eventually implant the scaffold between the bones and wait for the scaffold to slowly turn into a hyaline cartilage layer of tissue ala pseudo-epiphyseal plate cartilage.

The 1st way is going to be very difficult, but not impossible. The 2nd way is not as “clean” but it should work.

There will be more conferences in the coming months worth looking into. They are….

• 2015 4th Termis Tissue Engineering World Conference – Dr. Atala will be a keynote speaker there.
• Biomaterials & Tissue Engineering Gordon Research Conference – Dr. Warren Grayson will be a speaker there.
• Tissue Engineering, Synthetic Biology & Bioprinting (2016) – by SelectBio
• Innovations in Cell-Based Regenerative Therapies Conference (MSC 2015) –

What you sort of realize as you go down the list of speakers and attendees is that the same people was at this conference too. Eventually after so many conferences you meet the same 300 people over and over again.

Prx1 seems to be a very promising target for height increase as it seems to have targets early in development.  Unfortunately, I couldn’t find any Prx1 stimulating substances but hopefully you can?  Srx1 is involved in the repair of Prx1 so that could be another target as well.

Regulatory divergence modifies limb length between mammals

“Natural selection acts on variation within populations, resulting in modified organ morphology, physiology, and ultimately the formation of new species. Although variation in orthologous proteins can contribute to these modifications, differences in DNA sequences regulating gene expression may be a primary source of variation. We replaced a limb-specific transcriptional enhancer of the mouse Prx1 locus with the orthologous sequence from a bat. Prx1 expression directed by the bat enhancer results in elevated transcript levels in developing forelimb bones and forelimbs that are significantly longer than controls because of endochondral bone formation alterations. Surprisingly, deletion of the mouse Prx1 limb enhancer results in normal forelimb length and Prx1 expression, revealing regulatory redundancy. These findings suggest that mutations accumulating in pre-existing noncoding regulatory sequences within a population are a source of variation for the evolution of morphological differences between species and that cis-regulatory redundancy may facilitate accumulation of such mutations.”

“One developmental control gene known to promote limb skeletal elongation is Prx1, also called MHox or Prrx1. Prx1 is a paired-related homeobox gene expressed in somites, craniofacial mesenchyme, and limb mesoderm during mouse development”

“the forelimbs of Prx1BatE/BatE mutants are on average ∼6% longer than their wild-type littermates at E18.5 ”

“The forelimbs of Prx1-null homozygotes are ∼12.5% shorter than controls at E18.5”

“average mutant long bones express ∼70% more Prx1 than wild-type siblings”

“Long bone chondrocyte proliferation is elevated by ∼6% at E15.5 in Prx1BatE/BatE mutants.”

“[The Prx1 induced] limb elongation arises at stages of mouse gestation when Prx1 expression is limited to the perichondrium of the developing limb skeletal elements. It is known that the perichondrium is an important regulator of endochondrial bone growth”<-Could this be related to the zone of Ranvier which should be connected to the perichondrium?  Since the zone of Ranvier is linked to an earlier developmental state of the growth plate it could mean that Prx1 could be helpful in inducing neo growth plates.

According to this grant, Prx1 inhibits bone formation so it favors an earlier developmental state overall.

Prx1-Expressing Progenitor Primary Cilia Mediate Bone Formation in response to Mechanical Loading in Mice

“Increases in mechanical loading can enhance the addition of new bone, altering geometry and density such that bones better withstand higher forces. Bone-forming osteoblasts have long been thought to originate from progenitors, but the exact source is yet to be identified. Previous studies indicate osteogenic precursors arise from Prx1-expressing progenitors during embryonic development and adult fracture repair. However, it is unknown whether this cell population is also a source for mechanically induced active osteoblasts. We first identified that Prx1 is expressed in skeletally mature mouse periosteum, a thin tissue covering the surface of the bone that is rich in osteoprogenitors. We then traced Prx1 progenitor lineage using a transgenic mouse model carrying both a Prx1-driven tamoxifen-inducible Cre and a ROSA-driven lacZ reporter gene. Cells that expressed Prx1 when compressive axial loading was applied were detected within the cortical bone days after stimulation, indicating osteocytes are of Prx1-expressing cell origin. In addition, we evaluated how these cells sense and respond to physical stimulation in vivo by disrupting their primary cilia, which are antenna-like sensory organelles known to enhance mechanical and chemical signaling kinetics. Although Prx1-driven primary cilium disruption did not affect osteoblast recruitment to the bone surface, the relative mineral apposition and bone formation rates were decreased by 53% and 34%, respectively. Thus, this cell population contributes to load-induced bone formation, and primary cilia are needed for a complete response. Interestingly, Prx1-expressing progenitors are easily extracted from periosteum and are perhaps an attractive alternative to marrow stem cells for bone tissue regeneration strategies.”

“periosteum, which surrounds bones and is rich in progenitor cells known to preferentially differentiate towards the osteogenic lineage”

“physical stimulation activates and encourages osteogenic differentiation of progenitors within the periosteum.”

“One potential mechanism by which progenitor cells may become mechanically activated is through the primary cilium. Primary cilia are antenna-like organelles that extend from the cell surface and serve as signaling microdomains.”

“osteogenic response to fluid shear is lost when periosteal progenitor primary cilia are disrupted in vitro”

“Prx1-expressing cells become embedded osteocytes in response to physical loading and this mechanism requires the primary cilium.”<-if Prx1 enhances longitudinal bone growth and Prx1 mainly effects on chondrogenic cells maybe there are non chondrogenic ways to enhance longitudinal bone growth.

It seems that there was another legitimate program that was developed back in the early 90s by a Russian doctor who claimed that he could help people stretch their back and body to make them taller. It is very similar to the A-Grow-Bics program that came out by the French Trainer a few years back. There was even a few interviews and media coverage that came out with his claims. Based on what Michael Goldreyer (Goldreer) said, the clinic seemed to have gone bankrupt very quickly after it opened up back in the early 90s. However it is still interesting to see that the rumors that was coming out of russia of a doctor who developed a program which the book “School of Height” (PDF available for free download in the free section) was based on real events.

This will be the first of maybe a dozen videos that will be uploaded, almost all in Russian (a few will be in armenian and arabic). I plan to release the rest over time in the coming months.

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