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Metacarpal growth to prove LSJL

Below I will submit evidence of LSJL.  It is not perfect proof but with the resources available it is not possible to generate perfect proof.

However, I will submit the following facts as evidence that there is a very strong possibility that LSJL works.

The basis on whether this is proof of LSJL depends on the answers to the following questions:

    • What is the probability that every bone shaft on my left side of the body is longer than the right except for the one metacarpal which I performed LSJL?
    • What is the probability that my LSJL loaded finger is longer likely due to lengthening of the metacarpal when everything on my left side is longer(can provide additional evidence of my left side being longer if needed)?


Is this not reasonable proof that LSJL works?


So the current hypothesis is that LSJL lengthened my right index finger metacarpal.  The right index finger metacarpal is about 1% longer than the left and since my left bones are almost universally longer than my right bones(at least for all the bones that I have identified) that probably means about a 2% growth(with 1% being a correction of the discrepency).  The remaining bones of the index finger may have grown as well but not beyond the initial discrepency.


Here are my two hand images.  If I could proof that the fourth and fifth metacarpals were longer on my left side on my right that would provide evidence that the fact the index finger metacarpal is longer on my right side is an outlier and is due to loading from LSJL.  The middle finger is not taking into account because it is close to where I loaded with LSJL so there might be some byproduct lengthening of the middle finger.

hand bones

Here’s a labeling of the bones of the hand.  It would be easy to measure if it was like but the bones are not that organized.


Here’s a labeling of the bones on an actual skeleton.  You can see how the hamate mucks up with an accurate measurement.


4th metacarpal5th metacarpal

From these images you can see how hard it is to get an accurate measurement of the 4th and 5th metacarpal.  The shaft of the fourth metacarpal is definitely longer on the left side and eyeballing the shaft of the the 5th metacarpal the left bone looks like a little bit longer.  In terms on the exact beginning and end of the bone it is hard to tell because of the hamate.

Here’s the left and right index finger:


frontal index metacarpals

The shaft of the right bone looks longer in addition to the overall bone being longer.

I submit that the fact that the fourth and fifth metacarpal all have the left shaft as longer than the right like all the other bones I have compared with the exception of the right and left metacarpals of the index finger of LSJL induced lengthening.

I’m Writing A Book

I am currently working on writing a book that summarizes EVERYTHING that is on this website. All the important things will be added, and the extraneous information will not be. I will mention all the research and work that has been attempted in the last 15 years, from Sky, to Tyler, to Hakker, to Tim, and others who have tried to help out.

That is why I will not be posting on this website for at least another 4-6 months.

In addition, I have to focus on two other different businesses which are my primary sources of income.

  • Most of my time in the day is devoted to my companies and earning money, and keeping fit.
  • Most of my time at night will be devoted to finishing this book, as well as caring for my family members.

When the book is finally finished, probably in 2016, it will be released to the world, and this website will be transformed into something completely different.

I have decided to use the Natural Height Growth as one of the brand names under my primary umbrella corporation, and treat this website as a real asset. I will be coming back to make good on my promise to push the research much further.

This website will keep on going, and I will try to clean things up, and change dead links, and similar maintenance stuff now.

Anything new that comes out in the next few months will be from Tyler.

Resveratrol for height growth

I wrote about Resveratrol before and it is available for sale.

Resveratrol Supplementation Affects Bone Acquisition and Osteoporosis: Pre-Clinical Evidence Towards Translational Diet Therapy.

“Osteoporosis is a major public health issue that is expected to rise as the global population ages. Resveratrol (RES) is a plant polyphenol with various anti-aging properties. RES treatment of bone cells results in protective effects, but dose translation from in vitro studies to clinically relevant doses is limited since bioavailability is not taken into account. The aims of this review is to evaluate in vivo evidence for a role of RES supplementation in promoting bone health to reduced osteoporosis risk and potential mechanisms of action. Due to multiple actions on both osteoblasts and osteoclasts, RES has potential to attenuate bone loss resulting from different etiologies and pathologies. Several animal models have investigated the bone protective effects of RES supplementation. Ovariectomized rodent models of rapid bone loss due to estrogen-deficiency reported that RES supplementation improved bone mass and trabecular bone without stimulating other estrogen-sensitive tissues. RES supplementation prior to age-related bone loss was beneficial. The hindlimb unloaded rat model used to investigate bone loss due to mechanical unloading showed RES supplementation attenuated bone loss in old rats, but had inconsistent bone effects in mature rats. In growing rodents, RES increased longitudinal bone growth, but had no other effects on bone. In the absence of human clinical trials, evidence for a role of RES on bone heath relies on evidence generated by animal studies.”

“Resveratrol (RES) is a polyphenolic (3,4’,5-trihydroxystilbene) compound naturally present in red wine and a variety of plant foods such as grapes, cranberries, and nuts”

” human bone marrow-derived MSC with RES increased gene expression of the key osteogenic transcription factors, Runx2 and Osterix. RES was also demonstrated in vitro to act on various signal transduction pathways. RES activated the estrogen-mediated extracellular signal-regulated kinase 1/2 (ERK) signaling pathway regulating osteoblast differentiation and proliferation.  RES activated AMP-activated protein kinase (AMPK) which regulates osteoblast differentiation and inhibits bone resorption by acting as a negative regulator of RANKL. RES augmented Wnt signaling which stimulated osteoblastogenesis and bone formation. Treating human bone marrow-derived MSC with RES promoted differentiation of MSC towards osteoblasts by up-regulating Runx2 gene expression through the activation of Sirt1. Also, activation of Sirt1 by RES was shown to promote binding to PPARγ which repressed MSC differentiation into adipocytes. Additionally, RES suppresses osteoclastogenesis by acting through Sirt1 to bind to RANK which inhibited binding to RANKL”<-many of these processes should impact longitudinal bone growth as well.

Resveratrol stimulated tibial and vertabral length in new zealand white rabbits that were 12 weeks old.  200mg per kg of bodyweight were given.  Increased the amount of chondrocytes in the tibia and stimulated growth plate area while reducing fusion.  Decreased vascularization indicated by lower VEGF and laminin levels.

“RES supplementation delayed growth plate fusion by suppressing the replacement of avascular cartilage with vascularized bone indicated by the down-regulated gene expression of vascular endothelial growth factor, a signaling molecule in vascularization, and laminin, a cartilage protein.”

In 6 month old Fisher-Brown Norway rats, it increased tibia length and width.  Dosage was 12.5mg per kg of bodyweight.

“In vitro, RES treatment of chondrocytes obtained from an adult rat femur protected against the catabolic effect of pro-inflammatory cytokine, interleukin-1β”


Why Airborne Transmission Of The Ebola Virus Is Real – The CDC Is Not Telling The Full Truth

Airborne Transmission Of The EbolaNote: This post has nothing to do with the usual stuff we write about on this website. It is a post I wrote to express my own personal opinions on a recent medical topic and give the general public some extra information on the developments of the Ebola virus that is causing massive panic in the developed nations. I want the readers to make up their own minds on what they think the Ebola virus is capable of after reading this post. Am I right or am I wrong?

A few days ago I was having a nice talk with a friend of mine and the subject switched to the news about Ebola. All this recent talk about the disease made me realize that people need to be informed on the facts about Ebola, and not what just the media outlets and the news websites on the internet are telling them. Here is the truth.

The Ebola virus can be transmitted through the air. It is airborne.

This is my personal opinion, based on some initial research on the medical research, and scouring through the PubMed articles. Let me explain. I first became aware of the Ebola virus more than 2 decades ago, in 1997 in a middle school science class. The teacher in a rather unusual change of pace decided to show the class a documentary on the Ebola virus, to show us why biology was important and why we needed to understand this medical school course known as Epidemiology. (For those who might not know, the way modern medical school curriculum is broken down, 2 of the 4 school years are actually devoted to real textbook learning, which included courses on immunology, virology, pharmacology, physiology, and epidemiology. Refer to Stanford Med’s Curriculum here).

The first incident of an Ebola outbreak occurred in Zaire back in 1976. Almost 20 years after the first incident, Ebola broke out again in Zaire in 1995. It has around a 90-95% mortality rate for people who contract the virus. In that incident almost 400 people were killed.

It turns out that under some military/government order, the Ebola virus was brought into the USA back in 1989. A few dozen laboratory monkeys in a lab in Virginia started to die. Under orders, all the 60+ monkeys in a lab room were all killed to stop the contanmination. However, that did not stop the monkeys from dying. After the first room was cleaned and all the monkey’s killed, a second room that was not connected to the first room started to also have the monkeys inside drop dead. It turned out that the Ebola Virus was being transmitted through the air duct/ventilation shafts. This shows that more than 2 and a half decades ago, the virus was already airborne for monkeys.

To say the least I was scared to my core after finishing that little science lesson. (Ironically, I would be shown another Virus Outbreak Documentary, this time on the 1918 Spanish Influenza in 9th grade science class. Using science to scare young kids seems to be a common tactic in my school days.) Back then, the scientists and researchers studying up on this virus still weren’t sure about how the particular virus was being transmitted. However, here is what is known about it back then.

What was known back then was that the Ebola virus can be transmitted through the tears, the blood, and the surface of the skin. Since this virus is not like a flea which can jump from one host to the next using its legs, the only other way it can go to another host is if there is sweat as a medium on the surface of the skin. Viruses also are not like bacteria, which might have legs, known as flagella or cilia, which let them crawl around. The second person touches the skin with the finger surface touching the wet sweat and that goes to them. So now we know that the Ebola virus can be transmitted through 1. tears, 2. blood, and 3. sweat.

Pandemics comes from one of three different types of micro-organisms, 1. bacteria, 2. viruses, and 3. parasites. The Ebola is a type of virus, scientific name Ebolavirus zaire. Parasites are usually transmitted through the body by the intestinal tract, and the blood (ie Tapeworm). Bacteria usually are not transmitted through the blood because the White T-Cells would find them and kill them. That comes down to viruses. The question then becomes “How can a virus be transmitted through sweat, blood, and tears?” Sweat and tears makes sense, but blood as well? The most obvious common denominator would be water, since all fluid coming out of a human are predominantly composed of water, even urine which has a lot of urea/ammonia. I think it is safe to assume that this type of virus survives and is transmitted through water based fluids.

For humans at least, the way that the virus was being transmitted 2 decades ago was from one healthcare worker to the next. Let’s say that the first person gets sick and is lying in a hospital bed. They are too sick to do the basic functions so they have a caretaker who is right next to them to bring them food and take them to the bathroom. Over time the caretaker gets sick. Like a domino effect, that caretaker is then put into bed, and the caretaker’s caretaker gets sick as well, and the cycle continues.

Dr. William Close, who wrote the book “Ebola” showed that one cough is enough to transmit it. If I remember correctly, a cough is releasing one’s internal body liquid into the air in the form of liquid droplet, like the vapor you would find in a steam room/sauna.

We could even use influenza as a good example, to describe the way ebola would behave, since they are both virus based. When we look at the wikipedia article for the Flu/Influenza, “...Half of flu cases arise when people inhale tiny particles that float in the air, ” The Flu has multiple ways for transmission. If you look at the Wikipedia article on “Influenza Prevention”, it defines one of three ways to prevent Influenza “….the airborne route (when someone inhales the aerosols produced by an infected person coughing, sneezing or spitting)”  (Refer to http://www.journalofinfection.com/article/S0163-4453(08)00292-2/abstract)

If we look at this article “Influenza in the Hospital: Droplet or Airborne?” It seems that the difference between Droplet and Airborne is based on the 5 micrometer particle diameter cutoff point.

  • Large Droplet = greater than 5 micrometers
  • Airborne = less than 5 micrometers

If we then look at this article “Flu spreads via airborne droplets” we learn that the flu virus apparently is trapped in water droplets that are usually less than 5 micrometers on average, so  the illness is considered to be “airborne”. Hand washing would do nothing for the common Flu, since handwashing only removes the large sized droplets but not get the smaller airborne particles.

To further validate this point, If you refer to this study (http://cid.oxfordjournals.org/content/45/3/353.full), it shows that the definition on what constitutes an  “airborne” virus is based on the size of the microscopic parts, the AED, which is the diameter of the particles.

Also from the same study, “…At present, 3 major means of transmission of infectious organisms are generally recognized and form the basis of current recommendations for infection control. These differing sojourns and the survival of particles in aerosols have been better elucidated recently by new technology and help explain their capricious nature as effective vectors of infectious agents. of prime importance are the size of the particle, usually described as the particle’s aerodynamic equivalent diameter (AED), and its settling velocity. Particles of large AED settle quickly and, thus, are hazards primarily to those in close vicinity to an infected person. On the other hand, small particles are likely to remain airborne and destined for further spread. For example, particles with AEDs of 100 have settling times of 6.7 s (seconds), compared with 18.5 h (hours) for particles with an AED of 1

So the smaller the particle, the more time it will stay up in the air, since heavier particle will fall down on the ground due to gravity instead of get picked up by a draft of wind. What we need to do is scour through the PubMed database to find the AED (Particle diameter) of the ebolavirus zaire (scientific name) or the common flu virus, Influenza A.

Here was the first idea I had. – The Marburg Virus incident was like a precursor event which happened years before any of these nationally televised incidents, back in the 1960s in some town in Germany. The Marburg Virus was the first appearance of the Ebola virus, being very similar. Since they are similar in physiological function, we can assume that they would have similar mass, body shape, and form.

If you refer to the Wikipedia article on the virus, http://en.wikipedia.org/wiki/Marburg_virus, it says the following… “In general, the median particle length of marburg viruses ranges from 795–828 nm (in contrast to ebolavirions, whose median particle length was measured to be 974–1,086 nm” Source is http://www.sciencedirect.com/science/article/pii/0168170295000801.

I am not sure yet what the term “ebolavirions” mean, but if it means the individual virus unit, measured at around 1 micrometer each, then does it mean that the Ebola’s AED is also 1 AED? which would mean that it can stay in the air for up to 18 hours, which would definitely put it in the category of being “Airborne”.

Sure, we could say that the individual virus units, are likely would be clumped together, so maybe the AED of the virus might be much larger than we believe, but do they really clump together?

2nd Idea – Another way is if we can just compare the size of the influenza virus particle to the ebola virus particle, and if they are about the same size, then we will find out whether Ebola virus is airborne or not. The recent articles that have come out in recent years showed the Influenza A is airborne since the droplets that contain the virus is usually less than 5 micrometers in diameter.

From this John’s Hopkins’s Medical School’s Course PDF (http://ocw.jhsph.edu/courses/PrinciplesIndustrialHygiene/PDFs/Lecture4.pdf) , for the exact definition of AED, “The Aerodynamic Equivalent Diameter (AED) of a particle is the diameter of a unit density sphere that would have the identical settling velocity as the particle

It seems to calculate for AED, you have to take the particle, and use a droplet of water as the actual reference point. As it says in page 15 of the PDF, “…Referenced to spherical drop of water with identical settling velocity” – What we are actually calculating for when we are calculating the AED is to get the diameter for the droplet of water which would be falling at the same speed/velocity as this particle. So a micrometer diameter of lead (Pb) would have a truly large AED, since the drag force would do nearly nothing to slow it down as it is dropping and it has a high density. The ebolavirions may be 1 micrometer on average in size, but we have to account for the density, surface properties, drag force, and slip factor to get the “Settling Velocity” to be correct.

What I can say is that almost all microscopic living organic compounds are made from polymers, proteins, and RNA (collagen or amino acids), which are elastic, flexible, and have a lower density (specific gravity) than any type of sand/dust/solid particle, which would drop to the ground. It might be that the AED would be 1 magnitude larger (10X) than the actual diameter, but that would still make the AED around 10-20. If it is around that value, then the virus only reached the upper nasopharyngeal area, and not the tracheobronchial area, which is the lower respiratory area. (http://ocw.jhsph.edu/courses/PrinciplesIndustrialHygiene/PDFs/Lecture4.pdf) However, that is also a bad thing, since it would mean that coughing would be a very easy way to transmit what is in the upper tract area.

Based on that conjecture, if the medical definition of Influenza says it is technically a type of virus that can be transmitted through airborne pathways, then the Ebola virus must also based on medical technicality also be defined to be a type which can also be carried through airborne transmission, via microscopic water droplets, which is what causes the mist in saunas and water vaporizers. To validate this idea, we can just compare the size/diameter of the Ebola to the Influenza virus.

Concluding Thoughts

How can a virus spread so effectively among any local tribe/community if the natural automatic reaction among humans when there is a local outbreak is to stay indoors, and avoid contact with other humans in the area?

It can’t only be from human contact, and if we rule out it being airborne, as the CDC has claimed, then is it through the water. Maybe the low level of sanitation in Sierra Leone means that the entire village or area would be sharing/drinking from the same water source, but that would not explain why the doctors and helpers who treat the patients would develop them, since these are Western trained physicians. They would be drinking from bottles who were imported from other countries to make sure that the water supply is not contaminated.

Could it be that the virus is being transmitted through the skin surface, from sweat? Possible, but the medical staff is supposed to keep those gloves on at all times.

I personally hope that someone would be able to prove me wrong on all these main points, because I am just an amateur level researcher. If I am wrong, then this virus would be much less scary. If I am right though, god help us all.

You can refer to Nova’s Documentary on Ebola which is the source of half of the information that I present here

Proof that LSJL lengthened my finger

Go to this page to see the original x-rays.  Here’s a picture that shows that my right finger is longer than my left. However, what’s interesting is that the phalanx bones of the left index finger are actually longer than the right index finger.  So, I turned to the metacarpal bone of the index fingers and it turns out that the right metacarpal of the index finger is longer than the left and a longer metacarpal would explain the increased finger length in the image in the second link below.

LSJL may have lengthened all the bones of my right finger but because my left finger was always longer it may have only reduced the discrepancy.  If every single bone on the left side of body is longer than the right except for those that I performed LSJL on I submit that as proof of LSJL.  A possible reason that all my left bones are longer than my right bones but all my right bones are thicker could be related to FGFR3 and CNP.  My left side could have had less of the FGFR3 receptors or more of the CNP receptors.

I didn’t know that all my left sided bones were longer than my right until recently.  I just assumed it was due to my scoliosis or it was just an illusion because my right side was thicker.  So unfortunately, I did not account for it when designing to the experiment.  But again, if every single bone on my hands is longer on my left than my right metacarpal which is where I performed LSJL then we can take that as evidence that LSJL works.

Here’s a video with my right finger before any loading.:

Here’s the left hand before video:

My right index finger metacarpal did grow longer but it would appear that my other bones did not.  I say appear because it turns out that all my bones on the left side of my body are longer than the left.  Thus, any growth may actually just be shown by decreasing the gap between the right and left finger bones.  The right finger bones may have grown but that would not show up because the left finger bones were still longer.  If every single bone has the version on the left side be longer, but the one bone that had LSJL on it can we say that LSJL induced growth?

Here are the metacarpals of my right and left index fingers:

frontal index metacarpals


The lines are very straight.  I got pretty close to measuring out straight lines.  I measured the right metacarpal as being 1383.0 pixels long.  I got 1372.0 pixels long for the left metacarpal.  The left metacarpal might extend a little below the line but I zoomed in so I could get things accurate.  Right metacarpal is 0.8% longer.  Now here’s thing about the right finger being 0.8% longer.  All my left bones in my body are longer than the right bones but the right bones are thicker.  Thus, the right metacarpal may have grown to catch up to the left metacarpal and then grown further.  So actual growth may be larger than that.

I performed LSJL only on my right finger. Here’s an analysis of the other bones of the index finger:

Frontal 2 (1)


The slope of the line may be off by about 0.11 degrees or so which is very minor.  The left finger actually measures out longer.

Here’s an image of my proximal index fingers:Frontal 2This is a cut out of the proximal index fingers of the right and left finger bones from the x-ray from the link provided above.  Click on the image as the image shows flipped for some reason.  The right bone is the one labeled with the R.  The measurements were done by adjusting the two bones until they were as long as possible.  This insures that both bones were given the same advantages and the angle at which I put my finger is not a factor.  Measurements were done by someone else.

The lines on the graph are slightly off the vertical lines sloping down at a 1.2 degree angle towards the right side of the computer screen(using the image if you click on the image not the inverted one here).  This images slope favors the right side so the right side will appear longer if you don’t correct for the one degree.

Here’s another image:

Frontal 1This one slopes to the right only at about .80 degrees(measuring the straight line downwards it is .80 off from 90 degrees.  This images slope favors the right as well but not nearly as much.  The left bone is longer.

Here’s the cutout of the lateral view:

lateralYou can see here the the epiphysis of the right index finger are much larger but the left finger is longer overall.

How I’m changing my performance of LSJL now:
Next step is to confirm that all my left handed bones are longer except for that metacarpal.

Now since I have the x-rays, I’m going to be performing LSJL on both my right and left index finger.  Since I have x-ray images, I have those as a control using one of the fingers as a contralateral control is less important.

Previously, I was limiting my clamping based on my left side since my right side is stronger and thicker but since my left side is longer I’m not going to be clamping with whatever I can handle safely for my right side and whatever I can handle safely with the left side and not worrying about clamping them with the same intensity or amount of time.  Since my right side is so much stronger it should be able to withstand more clamping.  Thus, it was my goal with this to correct for the discrepancy between the right and left side in addition to increasing bone length overall.

Hoxd11 and the growth plate

This study supports that altering gene expression of Hoxa11 and Hoxd11 may be a way to grow taller as those genes can turn short bones into long bones.  Unfortunately, the genes that are known to interact with these genes are small in number and not known to be manipulatible by exercise or nutrition.  So it is more likely that in the future the Hoxa11 and Hoxd11 genes may contribute to height growth by manipulating the expression of these genes via an adenovirus.

The pisiform growth plate is lost in humans and supports a role for Hox in growth plate formation.

“The human pisiform is a small, nodular, although functionally significant, bone of the wrist. In most other mammals, including apes and Australopithecus afarensis, pisiforms are elongate. An underappreciated fact is that the typical mammalian pisiform forms from two ossification centers. We hypothesize that: (i) the presence of a secondary ossification center in mammalian pisiforms indicates the existence of a growth plate; and (ii) human pisiform reduction results from growth plate loss. To address these hypotheses, we surveyed African ape pisiform ossification and confirmed the presence of a late-forming secondary ossification center in chimpanzees and gorillas. Identification of the initial ossification center occurs substantially earlier in apes relative to humans, raising questions concerning the homology of the human pisiform and the two mammalian ossification centers. Second, we conducted histological and immunohistochemical analyses of pisiform ossification in mice. We confirm the presence of two ossification centers separated by organized columnar and hypertrophic chondrocyte zones. Flattened chondrocytes were highly mitotic, indicating the presence of a growth plate. Hox genes have been proposed to play a fundamental role in growth plate patterning. The existence of a pisiform growth plate presents an interesting test case for the association between Hox expression and growth plate formation, and could explain the severe effects on the pisiform observed in Hoxa11 and Hoxd11 knockout mice. Consistent with this hypothesis, we show that Hoxd11 is expressed adjacent to the pisiform in late-stage embryonic mouse limbs supporting a role for Hox genes in growth plate specification.”

“Compared with humans, the pisiform of most other mammals, including primates, is substantially enlarged and elongated”

Here’s a good visual of growth plate formation:growth plate formation

“a) At birth (P0) the pisiform largely consists of undifferentiated hyaline cartilage. Note the future articular surfaces adjacent to the triquetral (right) and the transitional region near the insertion of the FCU (left). Each of these is distinct from the fibrous periosteal layers that surround the future pisiform shaft. (b) At P4 the cartilage has undergone differentiation to flattened columnar and hypertrophic chondrocytes. It is the calcified hypertrophic matrix that is staining red in Fig. 3(a). (c) By P7 the primary center of ossification begins to be replaced by bone. A broad region of flattened columnar and hypertrophic chondrocytes is preserved at the palmar end (right). (d) At P9 the preserved strip of cartilage displays all of the hallmarks of a growth plate: organized columnar and hypertrophic zones and a perichondrial ring (yellow arrowhead) adjacent to the bone collar. (e) A transverse section through the carpal tunnel demonstrates the unique ossification of the pisiform (left). Note the preserved region of red stained cartilage at the palmar end. In contrast the scapholunate (right) has ossified as a single primary center extending into the projecting tubercle. (f) At P17 the growth plate appears to be losing its activity, as there is no longer an identifiable hypertrophic zone underlying the columnar chondrocytes.”<-so if via LSJL we can induce regions of hyaline cartilage they could potentially become growth plates.

“Full deletion of Hoxa11 or Hoxd11 results in a highly penetrant phenotype with shortened pisiforms that often fuse to the triquetral (ulnare) or less commonly to the scapholunate and triquetral ”

” ‘no Hoxd land’ for short bone morphology”<-Maybe we could upregulate Hoxd in short bones to make them become long bones?

“In short bones and epiphyses, the initial process of chondrocyte differentiation is similar. However, expanded cartilaginous growth plates or active perichondrial rings do not form. Instead, the periphery of these regions largely consists of a narrow three to four cell layer of round chondrocytes that anticipate the future articular zone. In each of these respects (organized chondrocyte zones, active perichondrial ring and deposition of the bone collar), the pisiform is more similar to long bones”<-The organized chondrocyte zones, active perichondrial ring and deposition of the bone collar could be related to Hoxd.

“mice with reduced Hoxa11/Hoxd11 expression display decreased proliferation within mesenchymal condensations and dramatic shortening of the radius and ulna such that they also resemble short bones”

If we can induce Hoxd11 expression in short bones we can make those bones longer and thus ourselves taller.

Looking at the String Embl gene interaction reveals a problem in that very few genes directly interact with Hoxd11.  Although LSJL upregulates the related gene Hoxd10:


Similarly with Hoxa11: