AC Electrical Signals Differentiates MSCS Into Bone and Cartilage Tissue Versus Adipose (Breakthrough)

These days I don’t get to do too much research on this website anymore. My duties are now more towards making money and proving a stable living for my future wife (yes, I am supposed to be getting married in the Summer of next year if everything goes to plan). I had once said that the main reason people give up on this endeavor is if they get have children. Life takes over and this dream of figuring out how to become taller takes a sort of backseat. I am not sure how this website and the research will continue once I do get married. I don’t plan to have kids anytime soon so maybe I still can push through a little more research.

I did want to give you guys a little bit of good news though, which is from a patent I found. It is entitled “Alternating electric current directs, enhances, and accelerates mesenchymal stem cell differentiation into osteoblasts and chondrocytes but not adipocytes – Patent #: WO 2013049598 A1″. I actually found the patent when I was trying to find which patents from Google referenced Dr. Robert O. Becker’s research that was done 20-30 years ago.

The 2nd reference: HRONIK-TUPAJ MARIE ET AL: “Osteoblastic differentiation and stress response of human mesenchymal stem cells exposed to alternating current electric fields“, BIOMEDICAL ENGINEERING ONLINE, BIOMED CENTRAL LTD, LONDON, GB, vol. 10, no. 1, 26 January 2011 (2011-01-26), page 9, XP021088361, ISSN: 1475-925X, DOI: 10.1186/1475-925X-10-9

The patent just got published in the last few months from what I would guess are a bunch of professors, post-docs, and graduate students from the University of Texas System.

The quick abstract – A method for directing, enhancing, and accelerating mesenchymal stem cell functions using alternating electric current. Mesenchymal stem cells are preferentially directed to either osteoblast or chondrocyte lineages, but not to the adipocyte lineage, when exposed to alternating electric current.

So why is this patent such a breakthrough?

I haven’t taken the time to dissect the patent but this is what I do know. The bone marrow of humans change as they get older. When the human is young, their bone marrow is more of a red color, which signifies healthy hematopeietic cells. I think I will let Wikipedia explain it a little better than me…

From the Wikipedia article on Bone Marrow – The two types of bone marrow are medulla ossium rubra (red marrow), which consists mainly of hematopoietic tissue, and medulla ossium flava (yellow marrow), which is mainly made up of fat cells. Red blood cells, platelets, and most white blood cells arise in red marrow…. At birth, all bone marrow is red. With age, more and more of it is converted to the yellow type; only around half of adult bone marrow is red. Red marrow is found mainly in the flat bones… and in the cancellous (“spongy”) material at the epiphyseal ends of long bones such as the femur and humerus. Yellow marrow is found in the medullary cavity, the hollow interior of the middle portion of long bones.

Anyone who has ever done research extensively on adult height increase would know that it is critical that one can get the MSCS that are still inside the epiphysis outer cortical bone tissue to turn into the right type of tissue. Most of us are already adults, so the MSCS that are left in the long bone ends/epiphysis, in the marrow, already are surrounded by yellow type bone marrow , which is just fat tissue or adipocyte.

I had reference Dr. Carl Brighton multiple times in this website, and his patent about using Capacitative Direct Current Electrical Signals to stimulate Epiphyseal Plate Increase growth was the find that sparked this idea inside of my head that maybe electrical stimuli is one of the major keys.

However, my engineering background from taking multiple Electrical Engineering courses and the Electrodynamics course from Junior level undergraduate physics programs made me always felt that Alternating Current (AC) was probably much better than DC (Direct Current) Emission.

I had found from other patents that Dr. Brighton had to his name published in the late 1980s showed that he kept on talking about these potential ways to up-regulate the expression of a lot of genes who go on to make proteins that are found in the extracellular matrix of hyaline cartilage. All of these involved setting some type of electrical emitting device to a specific frequency,

Examples:

• Up-regulation of bone morphogenetic protein (bmp) gene expression in bone cells by electromagnetic signals – WO 2005070136 A3
• Regulation of matrix metalloproteinase gene expression using specific and selective electrical and electromagnetic signals – WO 2004112708 A3
• Resolution of aggrecan gene expression using specific and selective electrical and electromagnetic signals – WO 2004029210 A3
• Regulation of type ii collagen gene expression using specific and selective electrical and electromagnetic signals – WO 2004033644 A3

From our 4th example, these are the exact figures on what he claims are the set points for the numerical values…

• …the generating step comprises the step of generating a specific and selective electric field having an amplitude of approximately 20 mV/cm, a sine wave configuration, a duty cycle of approximately 1/12, and a frequency of approximately 60 kHz.
• …the step of applying the specific and selective electric field to the cartilage tissue for a duration of approximately 30 minutes every 24 hours.
• …the generating step comprises the steps of selectively varying the amplitude, duration, duty cycle, frequency, and waveform of the specific and selective signal until the up-regulation of the gene expression of type II collagen mRNA in the cartilage tissue by the generated field is substantially optimized.

This shows that Brighton went away from the idea of applying DC Currents, and moved on to AC Currents. If he was not using AC Current, then he was using pulsing electrical currents. This was the other proposed idea which I had predicted in one of my last breakthrough posts “Using An Electrical Pulse Massager Physiotherapy Device To Increase Longitudinal Growth In Vivo For Open Growth Plates (Big Breakthrough)”

So either one of two things to control gene expression of specific cartilage protein stimulation…

1. He is using AC Current Signals
2. He is using pulsing electrical signals.

There is a difference between the function shape of the two types of electrical signals.

The Implication

I think we have found very good evidence that instead of using a DC signal to stimulate cartilage regrowth, we should be trying either Pulsing Electrical Signals or AC Electrical Signals. That is what is going to keep the few Mesenchymal stems cells still left in the bone marrow of the medullary cavity which already consists of half of adipocyte/fat tissue cells to differentiate specifically into cartilage and bone tissue.

Of course now there are two questions that develops.

• Is it better to be emitting AC Electrical signals or Pulsing Electrical signals?

• Which values for the following parameters (1. amplitude, 2. duration, 3. duty cycle, 4. frequency, and 5. waveform of the specific and selective signal) should we have to set the device (whether function generator, pulse generator, TENS Unit, Pulse Massager, etc. ) to to get the MSCS to differentiate specifically towards the chondrogenic line?

Cartilage-Specific Overexpression of ERRγ Results in Chondrodysplasia and Reduced Chondrocyte Proliferation.

“To assess the effect of increased ERRγ activity on cartilage development in vivo, we generated two transgenic (Tg) lines overexpressing ERRγ2 via a chondrocyte-specific promoter; the two lines exhibited ∼3 and ∼5 fold increased ERRγ2 protein expression respectively in E14.5 Tg versus wild type (WT) limbs. On postnatal day seven (P7), we observed a 4-10% reduction in the size of the craniofacial, axial and appendicular skeletons in Tg versus WT mice. The reduction in bone length was already present at birth and did not appear to involve bones that are derived via intramembranous bone formation as the bones of the calvaria, clavicle, and the mandible developed normally. Histological analysis of P7 growth plates revealed a reduction in the length of the Tg versus WT growth plate, the majority of which was attributable to a reduced proliferative zone. The reduced proliferative zone paralleled a decrease in the number of Ki67-positive proliferating cells, with no significant change in apoptosis, and was accompanied by large cell-free swaths of cartilage matrix, which extended through multiple zones of the growth plate. We identified known chondrogenesis-associated genes with at least one predicted ERR binding site in their proximal promoters, as well as cell cycle regulators known to be regulated by ERRγ. Of the genes identified, Col2al, Agg, Pth1r, and Cdkn1b (p27) were significantly upregulated, suggesting that ERRγ2 negatively regulates chondrocyte proliferation and positively regulates matrix synthesis to coordinate growth plate height and organization. ”

” in a cartilage-specific ERα-deleted mouse, appendicular bones developed normally, but exposure to high levels of estrogen failed to reduce bone length as it did in wild type (WT) mice, indicating that ERα was required for the natural deceleration of bone growth that occurs in mice upon sexual maturity”

Ironically, ERR-lambda decreased FGFR3 expression despite reducing height.

“Overexpression of ERRγ2 in a cartilage-specific manner leads to dose-dependent abnormalities in the axial and appendicular skeletons due to alterations in Cdkn1b expression and chondrocyte proliferation as well as differentiation-maturation- matrix synthesis”<-This is despite that ERRy2 results in overexpression of many anabolic chondrogenic genes.  Thus, it only takes one misexpressed gene to ruin longitudinal bone growth.

Click on the image for a better view.  IGF2 is a strong candidate for increasing height including adults giving it’s role for inspiring progenitor cells that form new growth plates.  The problem is how to increase it.

Target genes for height increase are as follows, for KO genes supplements or activities that inhibit these genes will increase height.  For OE genes supplements or activities that upregulate these genes will increase height.  For biphasic genes both overexpression and knockout decrease height.  There are many biphasic genes but they are not listed.

KO(inhibit these)(Black):
FANCC
NOG
NPR3
RNF135
SOCS2
STC2
GPC3
IGF2R
GPR30
POMC

OE(stimulate these)(Red):
NPPC
PLAG1
SHOX2
Twist1
CNP
IGF2
IGF1
Akt1
CTGF(CCN2)

Notice how close four genes are in proximity to IGF2: IGF2R, GPC3, POMC, GPER.  NPPC has a direct relationship with NPR3 with NPPC increasing height and NPR3 decreasing height.  IGF2 is a strong central locus for increasing height also being connected to IGF1 and Akt1.  LSJL increases Akt-phosphorylation by the way.

It turns out that the growth plate will regrow as long as their are progenitor cells, this area is called the zone of Ranvier.  IGF2 could play a role in making these growth plate progenitor cells.

Since IGF2 is such a strong target for height growth how can we increase IGF2 levels for height?

Loss of imprinting of IGF2 and the epigenetic progenitor model of cancer.

“While IGF2 usually supports normal cellular growth, LOI of IGF2 may lead to overexpression of the gene and moreover global chromatin instability.”

“differentiated cells present in adult tissue that can acquire the ability to become undifferentiated and behave like stem cells, or progenitor cells”

” In contrast to mutations in the genetic sequence of DNA, epigenetic changes occur beyond the level of DNA and alter the protein-DNA complex that forms chromosomes. One such epigenetic factor is parental imprinting”

“Insulin-like growth factor 2 (IGF2), a gene whose end action is to stimulate general growth, is usually imprinted such that only the paternal allele is expressed. When LOI occurs, the maternal allele may also be expressed and some studies have, indeed, correlated LOI of IGF2 with increases in expression“<-So we can cause Loss of imprinting in adults to increase IGF2 expression in adults.

“The ICR for the IGF2/H19 locus is located in the 5’ flanking region of the H19 gene and 90kb downstream of IGF2. The ICR on the maternal allele is unmethylated, while the ICR on the paternal allele is methylated. This methylation of the paternal allele ICR blocks the transcription factor CCCTC-binding factor (CTCF) from binding and creating a physical barrier that stops downstream enhancers from augmenting IGF2 promoters. This effectively silences the maternal allele”

“Mouse models have shown that CTCF binds to regions near the IGF2 promoter, as well as the ICR, and subsequently forms CTCF-CTCF dimers, creating an intrachromosomal loop. The CTCF dimer then interacts with the SUZ12 (suppressor of zeste 12 homolog) domain of polycomb repressive complex 2 (PRC2) which methylates histone H3 lysine residue 27 (H3K27) causing silencing of the maternal allele.  CTCF [synthesizes] decoy CTCF proteins. When introduced to cells, the decoys bind to the unmethylated ICR and IGF2 promoter but do not interact with SUZ12, thereby rendering Enhancer of zeste homolog 2 (EZH2), another part of PRC2, unable to methylate histone H3K27, resulting in reactivation of the imprinted allele{so the decoy CTCF are key to causing loss of imprinting of IGF2}. Neither intact CTCF sites nor hypermethylation at the ICR is sufficient for maintaining paternal allele silencing, and sequences outside of the CTCF binding sites at the ICR are needed for silencing”

“Thus, LOI of IGF2 may result from a variety of causes including: aberrant ICR methylation, a decreased expression of PRC2, a mutation of the ICR, or altered PRC2 H3K27 methylation. In contrast to the maternal allele, the paternal ICR is methylated, thereby blocking CTCF and PRC2 binding”

“A two-fold increase in IGF2 expression results in a 131% increase in offspring growth. Circulating IGF2 ligand has been shown to regulate crosstalk between the WNT and IGF1R pathways, which can lead to activation of either the phosphoinositide 3-kinase (PI3K)-AKT or the Ras-MAPK (mitogen-activated protein kinase) pathways that control metabolism, growth, differentiation, and apoptosis ”

“IGF2 expression levels thirty fold higher than wild type were not sufficient to develop tumors until senescence.”<-Elevated IGF2 levels do not directly cause cancer.  Just more cells = more opportunities for malfunction=increased likelihood for cancer.

“LOI of IGF2 causes a bi-allelic expression of the gene, resulting in the overexpression of the IGF2 protein”

” a diet lacking synthetic methyl donors, including folic acid, vitamin B12, choline, and methionine, could cause LOI of IGF2 in murine models”<-Not really something you want to do however.

IGF2 injections were shown to induce height growth in an LSJL related study.

There are no known supplements that increase IGF2 in humans and I don’t know of any therapies involving injections.

Using CTCF decoy proteins may be a way though:

Interruption of intrachromosomal looping by CCCTC binding factor decoy proteins abrogates genomic imprinting of human insulin-like growth factor II.

“Monoallelic expression of IGF2 is regulated by CCCTC binding factor (CTCF) binding to the imprinting control region (ICR) on the maternal allele, with subsequent formation of an intrachromosomal loop to the promoter region. The N-terminal domain of CTCF interacts with SUZ12, part of the polycomb repressive complex-2 (PRC2), to silence the maternal allele. We synthesized decoy CTCF proteins, fusing the CTCF deoxyribonucleic acid-binding zinc finger domain to CpG methyltransferase Sss1{not an easy thing to do homemade} or to enhanced green fluorescent protein. In normal human fibroblasts and breast cancer MCF7 cell lines, the CTCF decoy proteins bound to the unmethylated ICR and to the IGF2 promoter region but did not interact with SUZ12. EZH2, another part of PRC2, was unable to methylate histone H3-K27 in the IGF2 promoter region, resulting in reactivation of the imprinted allele. The intrachromosomal loop between the maternal ICR and the IGF2 promoters was not observed when IGF2 imprinting was lost. CTCF epigenetically governs allelic gene expression of IGF2 by orchestrating chromatin loop structures involving PRC2.”

” A maternally transmitted microdeletion of two CTCF binding sites in the ICR results in biallelic IGF2 expression and H19 silencing in Beckwith-Wiedemann syndrome”<-A syndrome that results in increased height.

Here’s a paper that states that Paxillin could be involved in IGF2 related growth:

Paxillin-dependent regulation of IGF2 and H19 gene cluster expression.

“Paxillin (PXN) is a focal adhesion protein that has been implicated in signal transduction from the extracellular matrix. Recently, it has been shown to shuttle between the cytoplasm and the nucleus. When inside the nucleus, paxillin promotes cell proliferation. Here, we introduce paxillin as a transcriptional regulator of IGF2 and H19 genes. It does not affect the allelic expression of the two genes; rather, it regulates long-range chromosomal interactions between the IGF2 or H19 promoter and a shared distal enhancer on an active allele. Specifically, paxillin stimulates the interaction between the enhancer and the IGF2 promoter, thus activating IGF2 gene transcription, whereas it restrains the interaction between the enhancer and the H19 promoter, downregulating the H19 gene. We found that paxillin interacts with cohesin and the mediator complex, which have been shown to mediate long-range chromosomal looping. We propose that these interactions occur at the IGF2 and H19 gene cluster and are involved in the formation of loops between the IGF2 and H19 promoters and the enhancer, and thus the expression of the corresponding genes. These observations contribute to a mechanistic explanation of the role of paxillin in proliferation and fetal development.”

“focal adhesion proteins can be found not only at focal adhesion contacts but also inside the nucleus and they can shuttle out of it and back in”

” The block of CRM1-dependent export pathway causes accumulation of paxillin inside the nucleus ”

“reactivation of IGF2 expression on the maternal allele has been previously reported in a number of human tumors and tumor cell lines”<-controlled reactivation could help us grow taller.

“SMC1A and MED23 play a role in paxillin-dependent regulation of the H19–IGF2 gene cluster. ”

 An essential role for IGF2 in cartilage development and glucose metabolism during postnatal long bone growth.

“Postnatal bone growth involves a dramatic increase in length and girth. Intriguingly, this period of growth is independent of growth hormone and the underlying mechanism is poorly understood. Recently, an IGF2 mutation was identified in humans with early postnatal growth restriction. Here, we show that IGF2 is essential for longitudinal and appositional murine postnatal bone development, which involves proper timing of chondrocyte maturation and perichondrial cell differentiation and survival. Importantly, the Igf2 null mouse model does not represent a simple delay of growth but instead uncoordinated growth plate development. Furthermore, biochemical and two-photon imaging analyses identified elevated and imbalanced glucose metabolism in the Igf2 null mouse. Attenuation of glycolysis rescued the mutant phenotype of premature cartilage maturation, thereby indicating that IGF2 controls bone growth by regulating glucose metabolism in chondrocytes. This work links glucose metabolism with cartilage development and provides insight into the fundamental understanding of human growth abnormalities.”

“Newly formed chondrocytes are proliferative and morphologically round, but eventually become flat chondrocytes to form the ‘columnar zone’”

“the Igf2 null growth plate cartilage was shorter and disproportionally thinner than the WT.  The mutant growth plate was generally well formed, but its hypertrophic zone was disproportionally larger and the epiphyseal zone shorter. In addition, there was a clear delay in SOC formation in the mutant, which contributed to the shortened cartilage template ”

“IGF2 deficiency caused a shortening of the prehypertrophic zone ”

” Our prior study on human adult articular chondrocytes also failed to detect Akt activation by IGF2, suggesting that IGF2 may act differently than IGF1 in chondrocytes ”

“the regulatory role of IGF2 on chondrocyte maturation and matrix production in endochondral ossification is mediated by its activity on glucose metabolism in chondrocytes.”

“TheIgf1r null mouse has shorter bones, but the IR null mouse has a normal bone length.  However, both knockouts had a reduced hypertrophic zone which is consistent with the phenotype of the Igf1 knockout.  Igf2 null bones, on the other hand, exhibit a disproportionally larger hypertrophic zone. These data indicate different roles of IGF1 and IGF2 on cartilage development. Consistent with this notion, although IGF2 overexpression promoted postnatal growth, it failed to compensate the phenotype caused by the loss of IGF1 ”

“IGF2 is unique in its ability to bind to IGF2R, and it has been shown that the direct binding of IGF2 to IGF2R stimulated proteoglycan synthesis and induced calcium influx in chondrocytes, as it occurs even in the presence of an antiIGF-IR antibody.On the other hand, knockout of Igf2r exhibits increased skeletal growth{Maybe because this encourages IGF2 to bind to different receptors? Thus,none of the single knockout of the potential receptors exhibits the same phenotype as that of the Igf2 null mouse. However, it is possible that the phenotype of the Igf2 null mouse is a result of its binding to multiple receptors, together with interaction of multiple IGF-binding proteins and subsequent complex downstream signaling”

Inhibiting Phd2 may be a potential drug target to help people grow taller.

Conditional Deletion of Prolyl Hydroxylase Domain-containing Protein 2 (Phd2) Gene Reveals its Essential Role in Chondrocyte Function and Endochondral Bone Formation.

“The hypoxic growth plate cartilage requires hypoxia-inducible factors (HIFs)-mediated pathways to maintain chondrocyte survival and differentiation. HIF proteins are tightly regulated by prolyl hydroxylase domain-containing protein 2 (Phd2) mediated proteosomal degradation. We conditionally disrupted the Phd2 gene in chondrocytes by crossing Phd2 floxed mice with Col2α1-Cre transgenic mice, and found massive increases (>50%) in the trabecular bone mass of long bones and lumbar vertebra of the Phd2 conditional knockout (cKO) mice caused by significant increases in trabecular number and thickness and reductions in trabecular separation. Cortical thickness and tissue mineral density at the femoral mid-diaphysis of the cKO mice were also significantly increased. Dynamic histomorphometric analyses revealed increased longitudinal length and osteoid surface per bone surface (OS/BS) in the primary spongiosa of the cKO mice, suggesting elevated conversion rate from hypertrophic chondrocytes to mineralized bone matrix as well as increased bone formation in the primary spongiosa. In the secondary spongiosa, bone formation measured by MS/BS and MAR were not changed but resorption was slightly reduced. Increases in the mRNA levels of Sox9, Osterix (Osx), Col2, Aggrecan, ALP, Bsp, VEGF, Epo, and glycolytic enzymes in the growth plate of cKO mice were detected by quantitative RT-PCR. Immunohistochemistry revealed an increased HIF-1α protein level in the hypertrophic chondrocytes of cKO mice. Infection of chondrocytes isolated from Phd2 floxed mice with adenoviral Cre resulted in similar gene expression patterns as observed in the cKO growth plate chondrocytes. Our findings indicate that Phd2 suppresses endochondral bone formation, in part, via HIF-dependent mechanisms in mice.”

“hypertrophic chondrocytes can transdifferentiate into osteoblasts and contribute to trabecular, endosteal, and cortical bone formation”

“In chondrocytes, HIF-1 increases the expression of VEGF and promotes angiogenesis in the
surrounding perichondrium ”

Only deletion of Phd2 in chondrocytes seems to increase height.  Deletion of Phd2 in say osteoblasts seems to decrease height.  Also Phd2 cKo seems to result in shorter overall body length. It’s just the primary spongosia that’s increased in length.

Sometimes I find new information from links that are made to this website and today was one of those days. It seems that there is a website called Good Looking Loser (which focuses on dating, fitness, making money, and lifestyle) has this forum where a person asked whether there was any other options besides Limb Lengthening Surgery which can lead to height increase after a person reaches adulthood and full bone maturity.

The link to the forum article is Topic: Limb lengthening surgery. Only way to get tall??

The guy was 26 years old, 5′ 10″, and wanted to be at least 1 inch taller.

It seems that as a response, two people did leave a reply which sort of made me think about the scientific implications when they mentioned that someone did seem to increase in height after HGH injections.

I took the liberty of clipping a pic and pasting his post below

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A Little Bit Of History To Put Things Into Context:

I remember seeing this guy and finding the website Good Looking Loser maybe 6 months ago from clicking on a link where people were talking about fitness. From what I remember, this guy, the one who posted, is one of the founders of the website. This website is sort of like a No Nonsense Approach for American guys in their 20s who want to chase after the typical dreams of meeting and having sex with as many beautiful girls as possible, becoming physically fit and ripped, making money quickly, enhancing one’s mind cognitively through taking nootropics (which I talked about using Provigil), and living the sort of location independent lifestyle promoted by Tim Ferris in his book “The 4 Hour Work Week“.

I am fully aware of these types of guys who are trying to live the life that they want. I was one of them a few years back. My whole point is that, this guy is not one of those people who is going to lie about this type of strange medical anomaly. I personally believe in his unique story. I can’t find any motive or reason why this guy would lie about something like that. He seems like a genuinely honest, no bullshit type of guy who just tells it like it is, sort of like how he designed his personal website (and his personal brand) to be like.

The guy (don’t know his name) is obviously very big in terms of muscles but I have no idea what his current height is. He just says that he did notice his height increasing to over 5′ 8” after he started to use HGH Injections as prescribed by his doctor for treating some sports injury.

Now, this growth in height happened in the span of 3.5 months in the Summer of 2006. That was 7.5 years ago. If we were to assume that this guy is maybe 31 currently, then those increase in height happened when he was 23-24, which is quite late in development.

If this guy is anything younger, like even in the age range of 29-30, we should not take too much note in his story. He would have been 21-23. That is still a reasonable young age for a small percentage of men to still have active growth plates.

Note: We realize also after reading about diurnal variations in the longitudinal growth in lower leg bones (tibia) that most men and women experience the greatest amount of growth spurt in the Summer season and at night time during sleep, . (read the PubMed article “Is longitudinal bone growth influenced by diurnal variation in the mitotic activity of chondrocytes of the growth plate?“. That might further disprove this guys point, since maybe what really happened was that he experience one last growth spurt in his early 20s in those summer months, which would coincide with his point that the entire thing happened through 3.5 months. That would suggest his growth plate cartilage was still intact.

The 2nd thing we note is that Tyler also mentioned in my 2nd Podcast Episode (Listen Here) that he was doing bodybuilding and weightlifting in his mid 20s and after he stopped weightlifting, he noticed that his own height increased by about 1 inch (from 5′ 8″ to 5′ 9″) after he stopped. It might be that this guy who was doing a lot of weight lifting took some time off from his routine of weight lifting to heal his knee and that gave his body time to readjust and get back to its normal height.

The next questions we should be asking ourselves (or him) are…

• How old was he when the thing happened?
• How much HGH was he injecting?
• How much of a gain did he achieve?

Can we explain away this single case of height increase through HGH injections as a case of a guy going through a late stage growth spurt in his early 20s during the summer months?

Or does this show that some HGH usages, in at least the initial stages when the body is first adjusting to recombinant growth hormone, might lead to the articular cartilage or the tissue in the intervertebral discs to somehow go into hypertrophy and lead to maybe 1 extra inch of height for adults with epiphyseal growth plate closure?

[Tyler’s Notes: Well I believe that IGF2 is one of the key proteins to induce new growth plates.

You can see in this image that GH1(human Growth Hormone) is linked somewhat to IGF2 but far more closely to IGF1.

My current theory is IGF2 is key to forming the mesenchymal progenitor cell layer that forms the resting zone layer and that CNP is key to the other stages of growth plate formation.

More on IGF2 and GH1:

Molecular genetics of human growth hormone, insulin-like growth factors and their pathways in common disease.

“The human growth hormone gene (GH1) and the insulin-like growth factor 1 and 2 genes (IGF1 and IGF2) encode the central elements of a key pathway influencing growth in humans. This “growth pathway” also includes transcription factors, agonists, antagonists, receptors, binding proteins, and endocrine factors that constitute an intrincate network of feedback loops. GH1 is evolutionarily coupled with other genes in linkage disequilibrium in 17q24.2, and the same applies to IGF2 in 11p15.5. In contrast, IGF1 in 12q22-24.1 is not in strong linkage disequilibrium with neighbouring genes.”

“Both IGF2 and H19 are well-known imprinted genes with opposite behaviours: IGF2 is expressed only from the paternally inherited chromosome, while H19 is transcribed only from the maternal chromosome. This is because both genes share the same set of enhancers (which are located downstream of H19, about 100 kb from the IGF2 promoters) and, while H19 gene uses the enhancers on the maternal chromosome, on the paternal chromosome, the enhancers are used by IGF2”

In adults IGF2 is normally imprinted so the gene is silenced.  But as in some cancers it is possible for loss of imprinting of these genes.  Maybe somehow this person experienced loss of imprinting of IGF2 which allowed HGH to stimulate IGF2 signaling and induce mesenchymal stem cells into growth plate progenitor cells for neo-growth plate formation.]

In the last post we had stated that we can use spinal decompression therapy using a strange expensive machine like the DRX9000 for disk height increase. This device has been promoted by Chiropractors as a way to treat many forms of pain derived from the back. One of the main functions of the device was to stretch out the torso by stretching out the dorsal side.

Note: The DRX9000 has been a very controversial product where chiropractors and medical doctors with MDs are almost exactly divided on their opinion on the efficacy and legitimacy of the product. There are a lot of people who claim that the device is a scam product which does not work in treating lower back pain and sciatica symptoms. (source)

This issue of decompressing the spine got me thinking back to an old YouTube video I watched years ago showing this Chinese-Malaysian Bone Setting Doctor based from either Singapore or Kuala Lumpur who used the principles of Traditional Chinese Medicine (which some people just call TCM) to “straighten out” his patient’s backs by popping bones into place and fixing bone fractures. I realized that these bone setters might be just as good as any of these modern devices in spinal manipulation, with purposes for pain relief and maybe also the additional benefit of height increase.

From the Wikipedia article on Bone Setters, it seems that these more holistic, homeopathic healers were the predecessors to the modern chiropractors, osteopaths, and physical therapists. They were the people who would pop your shoulder or hips back in place if you twisted the joints and they popped out by accident.

Apparently from the Wikipedia article, it says that this form of bone manipulation is not just from the Far East Asian countries.

It is also practiced in the following countries (source)…

• Ghana
• Mexico
• the Balinese 2 of Indonesia
• the Lomi-Lomi of Hawaii 3–5
• in areas of Japan – In Japan, it is called Sekkotsu, which is also called JudoTherapy. From one source, “Judotherapists can treat injuries such as fracture,
  dislocation, bruise, and sprain in the Sekkotsu clinic”
• China
• India 3
• by the shamans of Central Asia 6
• by sabodors in Mexico 7
• by bone setters of Nepal 8,9
• bone setters in Russia and Norway 10.
• Nigeria (source)
• Ancient Greece
• there is no clear evidence that bone setting, which is also known as manipulation therapy might have also happened in Mesopotamia, Babylon, Assyria, and possibly also Egypt.

The point is that if we are looking for some height increase, it might be reasonable to suggest that instead of going to see a chiropractor, we could also try to see a bone setting doctor. The practice is almost never practiced in the USA or most Western Countries. The closest we might come to these things is if we took a trip to southern Mexico.

Based on what we see of the listing of countries we find, I am note willing to recommend that people go to some of these countries due to concerns over a person’s health.

I personally don’t think that the bones setters one might find in Malaysia or China is somehow better or safer for a person but there seems to be a lot more documentation and at least anecdotal stories of people having medical benefits from going to these Oriental Practices of Medicine.

These Malaysian Bone Setters you might find in Singapore uses something called Nei Gong Tuina. Tik Dah, Zhenggushu, Zheng gushu, or Dit Da. We note that Dit Da might be a Hong Kong variation or Cantonese translation of a much more general form of Chinese Osteopathy (aka Chinese Bone Setting) different from the modern Mandarin way of pronouncing stuff.

From the article on Chinese Zhenggushu Bone Setters, there is supposed to be some orthopedic clinic called Luoyang Orthopedics Hospital, the largest of its kind in China, which treats patients with at least small fractures using non-invasive approaches. We quote the following below…

“Doctor Zhang, with the help of two assistants, gently manipulates the angle of the fractured bone with his hands and then suddenly pushes the bone. In the X-ray room, it is clearly seen that the fragment has been relocated to its normal place, and this was done in a flash of push.”

What is really amazing is that you can actually see how effective this bone setters are. They flash this X-Ray (or some type of medical radiological device) on the doctor’s hands and the patients area of the body with the broken bone. As the doctor readjusts the body right in front of you, you can see in real time through the X-ray the bones being popped back into place.

From the article….

“The practitioners refused to give up the time-honored therapy without a fight. They decided to operate the therapy by exposing their hands under X-rays and replacing the bones with the guidance of images. They believed this was the most direct way to improve the accuracy and effect of the ancient therapy. To protect the doctors from strong radiation, the hospital offered special lead gloves to them….”

The article mentions two very old bone setters named Guo Zongzheng and Guo Weihuai who were among the last of a long line of bone setters. I guess if we are going to be seeing any more really well qualified bone setting doctors, we should go now before that practice is lost.

Currently these special doctors seems to only be found in either Hong Kong or Singapore.

My personal opinion is that these bone setters are probably slightly more effective in spinal manipulation that the most chiropractors we meet. If they are better and more effective in spinal manipulation, they probably adjust the spine for a greater amount of height increase than a trip to the chiropractor.

I am not familiar with Oriental Derived Medicine and have never tried acupuncture myself although my Korean girlfriend seems to really enjoy Chinese Foot Massages which is known as Reflexology. I don’t doubt in the efficacy of certain Oriental Medicine in treating certain illnesses.