Monthly Archives: June 2014

What 7 Feet Tall Isaiah Austin Having Marfan Syndrome Suggest To Professional Basketball Players

What 7 Feet Tall Isaiah Austin Having Marfan Syndrome Suggest To Professional Basketball Players

So I was not able to write much in the last 2 weeks due to a combination of issues: legal, technical, and health related. Hopefully most of those issues have been resolved.

The news that is making the rounds in the NBA and the basketball world in the last 2 days is that Current Baylor University’s Basketball Center and NBA Draft hopeful Isaiah Austin was diagnosed with Marfan’s Syndrome. It might be surprising news for some people but for people like me, it was almost sort of expected.

I became aware of Austin for a couple years now since I am a fan of basketball. It is always interesting to see what types of players are coming up in the annual NBA Drafts. Austin was a potential game changer for the NBA team who would draft him for his amazing length. When I first saw this kid, who was obviously tall, it did strike me as a little strange that a person would be as skinny as him, even for the ectomorphic body shape of most professional basketball players. Add in the fact that he always wore plastic goggles, and it just made him look slightly strange. It would turn out that he lost the use of one of his eyes in recent years due to a detached retina stem.

I have been aware of Marfan Syndrome for a long time, ever since I was doing research on the various genetic pathologies which can lead to tall stature like Klinefelter Syndrome, Ehlers Danlos Syndrome, Proteus Syndrome, the condition affecting the late Siah Khan and Zech Devits,  and Marfans and found pictures and threads on forums suggesting that Abraham Lincoln most likely had Marfan Syndrome. Lincoln was shown to have the average length of torso but his legs and arms were very disproportionally long. When Lincoln would sit down, his sitting height would be the same as most men of his time.

If I paid more attention to the videos on Isaiah Austin and how his body looked, I would have been able to diagnose him within a minute of having Marfan. However, since he is not playing professional sports yet, there was only a small handful of videos on this kid.

His body shape is similar to what we see in other super sized humans like Mamadou N’Diaye and Shagari Alleyne, who have more than just height but also unusually long wingspans. While N’Diaye has been diagnosed only this year with having an overactive pituitary gland condition, I am not sure if anyone has checked Alleyne yet. There are people who are tall from genetics and others who have become large due to a medical condition or genetic mutation.

It is a good thing that at least these days all prospects who want to play professional basketball are required to also get a full body physical and even blood work done to check for some hidden/unknown genetic predisposition towards some type of illness. Marfan Syndrome is one of those illnesses which are a type of silent killer. The syndrome causes connective tissue to be lossened, thus the extra height, but also the muscle tissue around the body.

The general medical concern is that the muscles that makes up the arteries and/or aorta is enlarged. If the body of the player playing a high intensity level physical stressful game gets pushed too much, that region of the heart can actually rupture, instantly killing the person from the loss of blood and internal bleeding.

Apparently Austin went to get an standard EKG (Electro Cardio Gram) and there seemed to have been some type of abnormality in the rhythm of the heartbeat noticed on the graph. Further tests showed he had marfan.

What all this news indicates is that there is a very good chance that a shocking high percentage of the people who player professional basketball have marfan syndrome, and they just don’t know it.

Generally, people who are above average in height are pushed into playing the sport. I would suspect that maybe even 1 out of 100 people who play professional basketball of any team in any country suffer from the disorder, but they just don’t realize it. This news that has come out should be a sign that people who notice that maybe their body is ectomorphic or have a very thin torso should get themselves checked out. They don’t have to be 7 feet tall like Austin but if they have that unique body shape, it would be a good sign to do something. The regular checkup with the GP (General Practitioner) is not enough since the family doctor and the nurses using even the best regular stethescope or Sphygmomanometer would be able to catch a heart murmur or rhythm irregularity.

new study from LSJL authors

Predicting and Validating the Pathway of Wnt3a-Driven Suppression of Osteoclastogenesis.

“we examined Wnt3a-driven regulation of osteoclast development. Mouse bone marrow-derived cells were incubated with RANKL in the presence and absence of Wnt3a. Using microarray mRNA expression data, we conducted a principal component analysis and predicted transcription factor binding sites (TFBS) that were potentially involved in the responses to RANKL and Wnt3a. The principal component analysis predicted potential Wnt3a responsive regulators that would reverse osteoclast development, and a TFBS prediction algorithm indicated that the AP1 binding site would be linked to Wnt3a-driven suppression. Since c-Fos was upregulated by RANKL and downregulated by Wnt3a in a dose-dependent manner, we examined its role using RNA interference. The partial silencing of c-Fos suppressed RANKL-driven osteoclastogenesis by downregulating NFATc1, a master transcription factor of osteoclast development. Although the involvement of c-Myc was predicted and partial silencing c-Myc slightly reduced the level of TRAP, c-Myc silencing did not alter expression of NFATc1. Collectively, the presented systems-biology approach demonstrates that Wnt3a attenuates RANKL-driven osteoclastogenesis by blocking c-Fos expression and suggests that mechanotransduction of bone alters the development of not only osteoblasts but also osteoclasts through Wnt signaling.”

LSJL upregulates c-Fos.  In all likelihood LSJL alters Wnt3a expression but there wasn’t any evidence in the LSJL gene expression studyFluid flow upregulates Wnt3a and LSJL does involve fluid flow although this was only in osteocytes and we’d want to know the effects on stem cells or chondrocytes for height growth purposes.  No evidence that LSJL alters Nfatc1 expression but it likely does and Salubrinal alters Nfatc1 expression.  According to a diagram, from that study LSJL would increase Nfactc1 expression but it reduces levels of phosphorylated eif2a.

“Wnt5a activates noncanonical Wnt signaling through a receptor tyrosine kinase-like orphan receptor and stimulates osteoclastogenesis. Wnt10b is required for maintenance of mesenchymal progenitors, and its deficiency leads to loss of bone mass. Wnt14 enhances endochondral ossification and accelerates chondrocyte maturation”<-Wnt14 may alter height.  However, Wnt14 does suppress chondrogenic genes and I couldn’t find any studies stating that Wnt14 transgenes or knockout causes overgrowth or undergrowth.  Genetic association study of WNT10B polymorphisms with BMD and adiposity parameters in Danish and Belgian males., says that Wnt10b may have an effect on height but more testing needs to be done.

“Mouse bone marrow cells isolated from long bones (femur and tibia) as well as RAW264.7 mouse pre-osteoclast cells [were used in the study]”.  If mouse bone marrow cells were used it may have ramifications for how stem cells are affected by stimuli and finding the right stimuli is the key for height growth.

“Administration of RANKL to bone marrow cells significantly increased the number of TRAP-positive multi-nucleated cells{osteoclast cells are trap-positive}. In response to 100 or 200 ng/ml of Wnt3a, the number of TRAP-positive cells was reduced in a dose-dependent manner. The observed suppression of osteoclast development by Wnt3a was associated with a decrease in the phosphorylated form of β-catenin (p-β-catenin) as well as NFATc1 ”

“Wnt3a-induced reduction of the relative mRNA expression levels of the genes (NFATc1, TRAP, OSCAR, MMP9, and cathepsin K) linked to osteoclastogenesis on days 1 and 2 in bone marrow cells”<-Note that none of these levels were lower than control(The cells that were not exposed to RANKL) and the reduction was dose dependent until at least 200ng/ml.

Wnt3a downregulates C-Fos and C-Fos may be an important part in LSJL induced growth.

Wnt3a upregulated Egr1, Notch1, and Tgif1 at greater levels than control so excess levels of Wnt3a may have an effect on stimulating on those genes even without altering cells exposed to RANKL.  It downregulated Hmga1, Smad3, Dnmt3a, and Bach1 versus control.  Smad3 is involved in TGF-Beta induced chondrogenesis.  Dnmt3a promotes DNA methylation.

Growth Plate Repair

RECENT RESEARCH ON THE GROWTH PLATE: Mechanisms for growth plate injury repair and potential cell-based therapies for regeneration

“[The growth plate] functions to produce a mineralised cartilaginous scaffold to which new trabecular bone is formed via a tightly controlled two-step process (called endochondral ossification) involving chondrogenesis and osteogenesis ”

“The resting zone has previously been thought to play a very minimal role during endochondral ossification as the pre-chondrocytes/cells within this zone proliferate minimally. However, studies have indicated the importance of the resting zone as it acts as a reservoir of stem cells/pre-chondrocytes for the chondrocytes in the adjacent proliferative zone”

“The proliferative zone is responsible for matrix production (including collagen-2 and aggrecan) and cellular division during endochondral ossification. The height of the proliferative zone directly correlates with the extent of longitudinal growth that can be achieved by the long bone. As regulated by various signalling pathways including parathyroid hormone-related protein, insulin-like growth factor (IGF1), bone morphogenic protein (BMP), Wnt/B-catenin, fibroblast growth factor (FGF) and others , chondrocytes cease to proliferate and become hypertrophic. The hypertrophic chondrocytes produce collagen-10 which is involved with matrix mineralisation. Together with the action of angiogenic factor vascular endothelial growth factor (VEGF) produced by hypertrophic chondrocytes and a low oxygen tension, the lower hypertrophic zone attracts blood vessel invasion from the adjacent metaphyseal bone, which brings along mineralised cartilage-resorptive cells (chondroclasts), bone-forming cells (osteoblasts) and bone-resorptive cells (osteoclasts) to convert the mineralised cartilage scaffold into trabecular bone in metaphysis.”

growth plate injury repair

“The initial inflammatory response involves an influx of key inflammatory cells into the growth plate injury site and up-regulation of inflammatory cytokines/mediators and some growth factors (A). The fibrogenic phase involves an influx of fibrogenic and progenitor cells containing MSC-like cells (B). The osteogenic phase involves the osteogenic and chondrogenic differentiation, formation of bony trabeculae together with angiogenesis within the injury site (C). The remodelling phase involves the maturation and active remodelling of the newly formed bony trabeculae as well as disappearance of cartilaginous repair tissue (D).”<-Cinc1 is also known as IL8 or CXCL1{Which is upregulated by LSJL}

“neutrophil-mediated inflammatory response was found to modulate downstream injury repair events. Following the depletion of neutrophils with a neutralising antibody, an increase in the undesirable bony repair tissue [occurred] with increased expression in bone-related genes such as Runx2 and osteocalcin, but decreased expression in cartilage-related genes Sox9 and collagen-2 ”

“Blocking TNFa resulted in a clear delay in the subsequent mesenchymal infiltration response and a reduction of the proliferation of these cells”

“At the growth plate injury site, some of these cells were found to express growth factors including BMPs, platelet-derived growth factor (PDGF) and FGF2 and receptors for BMPs and PDGF. In addition, some of these cells were found to be MSC like as they expressed the stem cell marker alpha-smooth muscle actin{acta2 which is upregulated by LSJL}”

“this influx of mesenchymal cells may contain a myriad of cells including MSC-like cells, osteoprogenitor cells, pre-osteoblasts, and/or pre-chondroblasts (either pre-existing or newly derived from the infiltrated MSCs).”

“significant peak in the mRNA expression of platelet-derived growth factor (Pdgf) and fibroblast growth factor 2 (Fgf2){up} following the initial inflammatory phase, suggesting a potential regulatory role for these two growth factors during this phase”

“In rats with growth plate injury, the inhibition of PDGF signalling caused a significant reduction in the amount of mesenchymal infiltrate, decreased amounts of bony and/or cartilage repair tissues, and thus an overall delay in bony repair 14 days post-injury”

“At the injured growth plate, bone formation has been observed to commence around day 7 with the appearance of bony trabeculae, and bone remodelling has been observed by day 14 with the appearance of bone marrow cells in between bony trabeculae”

“During the osteogenic phase of the growth plate injury repair process, the cells within the fibrogenic infiltrate differentiate into Runx2 and alkaline phosphatase-immunopositive osteoblasts and produce increased levels of bone matrix protein osteocalcin (both mRNA and protein) during days 8–14”

“after a ‘fibrous tissue’ is formed from the infiltrated stromal cells at an injured growth plate, its invasion by new blood vessels is a prerequisite for its osseous transformation”

“the absence of VEGF delayed bone formation by halting the initial soft callus from being converted into hard bony callus. ”

“osterix over-expression can induce bone healing”

“PKD up-regulates osterix and [is] important for osteoblast differentiation. Inhibition of PKD suppressed bony repair but induced more chondrogenic differentiation at the injury site”

“over-expression of osterix in osteochondroprogenitor cells resulted in a decrease in chondrogenic transcription factor Sox9.”

“In a rat tibial drill hole growth plate injury model, levels of Bmp2 mRNA expression were found notably increased in the early part of the fibrogenic phase and then again later during the osteogenic phase”

“synovium-derived MSCs in particular had the greatest capability to enhance the chondrogenic differentiation potential when compared with any other mesenchymal tissue-derived cells. However, other studies have reported that bone marrow-derived MSCs (BMMSCs) are most suitable for cartilage tissue engineering, as they possess higher proliferation rates and higher levels of expression of cartilage-specific genes, when compared with MSCs derived from other tissues”

“MSCs were successfully isolated directly from murine epiphysis.  This novel type of MSCs could potentially be better than BMMSCs as they have shown greater capacities in growth and differentiation potential as well as possessing immunosuppressive and anti-inflammatory properties”

LSJL Studies 3: Lengthening of mouse hindlimbs with joint loading

This is the most significant LSJL study to date.

Three key takeaways from this study:

1) LSJL increases bone length in existing growth plates via traditional mechanisms(chondrocyte hypertrophy)

2) LSJL increases bone length in non-traditional mechanisms as shown by the fact that LSJL also stimulates the reserve zone.  Reserve zone cells being the chondrocyte precursor cells and the ones able to form new growth plates.

3) LSJL dramatically alters the microenvironment of the bone(as shown by the histological slides).  It’s unclear exactly what changed but the decrease in bone trabeculae and the increase in bone marrow means that an LSJL loaded bone is more permissive to growth plate formation.  Osteomy is essential for renewed longitudinal bone growth.  As cartilage is capable of interstitial growth which induces longitudinal bone growth whereas bone is not.

Lengthening of mouse hindlimbs with joint loading

“Loads were applied to the left hindlimb (5-min bouts at 0.5 N[at 5Hz) of C57/BL/6 mice (21 mice, ~8 weeks old). Compared to the contralateral and age-matched control groups, knee loading increased the length of the femur by 2.3 and 3.5%, together with the tibia by 2.3 and 3.7%, respectively. In accordance with the length measurements, knee loading elevated BMD and BMC in both the femur and the tibia. Histological analysis of the proximal tibia revealed that the loaded growth plate elevated its height by 19.5% and the cross-sectional area by 30.7%. Particularly in the hypertrophic zone, knee loading increased the number of chondrocytes as well as their cellular height along the length of the tibia.”

3min/day for 5 days/week for 10 days total was LSJL applied.  Bone was harvested 18 days after the last loading.

“Femoral length was defined as the maximum distance from the distolateral condyle to the
most medial and proximal position on the femoral head. Tibial length was defined from the most proximal position of the tibial plateau to the most distal position of the medial malleolus.”<-this is important as changing where and how femoral length is measured would effect total femur length.  It is hard to tell the ramifications of this length setting for sure without more data though.

“The height of the growth plate (GP) was defined from the apical[apex] border of the reserve zone to the lower border of the mineralized cartilage”<-So the measurement of growth plate height would likely include not just growth plate chondrocytes but chondrocyte progenitor cells.  And you’d need chondrocyte progenitor cells to form new growth plates.

“the upper boundary of the hypertrophic zone was identified at the margin of the
chondrocytes that increased their size relative to those in the proliferative zone, whereas its lower boundary was at the terminal intact chondrocytes next to the metaphysis”

“At the cellular level, the numbers of proliferative and hypertrophic chondrocytes were counted and the total number of chondrocytes was calculated as their sum. The height of hypertrophic chondrocytes was determined using at least 20 cells in each slice”

“During knee loading, no apparent damage was detected at the site of loading or injection.”

“the longitudinal length of the femur was increased by 2.3% (14.19 ± 0.28 mm in contralateral control; 14.51 ± 0.28 mm in knee loading)”

“the longitudinal length of the tibia was increased by 2.3% (16.68 ± 0.23 mm in contralateral control; 17.06 ± 0.21 mm in knee loading)”<-interesting that the percent increase is so comparable(both 2.3%).

“Compared to the age matched control, knee loading increased the longitudinal length by 3.5% in the femur and by 3.7% in the tibia”<-Also a very similar percentage.

In the elbow loading study, “humerus was elongated by 1.2% compared to the contralateral and age-matched controls, while the ulna had become longer than the contralateral control (1.7%) and the age-match control (3.4%)”.  In 16 week mice(see same link above), the increase in length was 1.6% in the tibia.

Here is the growth plates under LSJL(I provide a more detailed analysis here):

LSJL growth plates

“H&E-stained sections of the growth plate in the proximal tibia. a Growth plate of the contralateral control. The bracket denotes the growth plate. b Growth plate (bracket)
of the loaded tibia. c Proliferative and hypertrophic zones of the contralateral control. d Proliferative and hypertrophic zones of the loaded tibia. Bars a, b 100 micro-m; c, d 200 micro-m”

Here’s a baseline growth plate with similar colors:


It’s difficult to say exactly what is going on in the growth plates of the control and LSJL-loaded version but what is clear is that the micro-environment of the two bones is dramatically different.  The LSJL loaded growth plate has much more bone marrow and many more osteoclasts(the white spots; although those spots could also be adipose tissue).  The increase in bone marrow and loss of bone trabeculae would be more enabling for micro-growth plates.  Thus, LSJL could create a more favorable microenvironment for micro-growth plates.

“Histological analysis revealed that knee loading increased the height and the cross-sectional area of the growth plate in the proximal tibia. First, the total growth plate height was increased by 19.5% (175 ± 25.6 micro-m in contralateral control; 210 ± 18.1 micro-m in loading) including the heights of the proliferative zone and the hypertrophic zone. In particular, the height of the hypertrophic zone was extended by 33.6% (48 ± 4.6 micro-m in contralateral control; 65 ± 3.4 micro-m in knee loading). Note that the height ratio of the hypertrophic zone to the growth plate (HZ/GP) was significantly increased, whereas the ratio for the proliferative zone (PZ/GP) was not altered”

“the cross-sectional area of the growth plate was increased by 30.7% (0.263 ± 0.108 mm2 in contralateral control; 0.344 ± 0.095 mm2 in knee loading)”

“At the cellular level, the numbers of chondrocytes were increased in the total growth plate and the hypertrophic zone by 28.5% and 46.3%, respectively. In the proliferative zone, however, no statistically significant difference in the numbers of cells was detected”

“the height of individual chondrocytes in the hypertrophic zone was elevated in the loaded side (16.3 ± 1.67 micro-m) compared to the control side (13.0 ± 1.45 micro-m)”

“oscillatory loads laterally applied to the knee not only induce anabolic responses but also lengthen the femur and the tibia.”<-Interesting that they do not state the necessity of an existing growth plate in this statement although admittedly this is not strong evidence.

The total length increase in the growth plate was more than the sum of the increases in the proliferative and hypertrophic zones, indicating that other regions such as the resting and calcifying zones were also affected“<-This is huge as the resting zone is where chondrocyte progenitor cells are derived.  If LSJL can induce mesenchymal stem cells to become chondrocyte progenitor cells than it can create new growth plates.

“Because the cross-sectional area of the growth plate is significantly increased with knee loading[the growth plate is wider], the data support that the bone-lengthening effects are not limited only to the lateral or medial loading site. At the cellular level, the number of chondrocytes in the hypertrophic zone was increased together with their cellular height. Our results are consistent with the notion that dynamic tensile and compressive loads stimulate and suppress longitudinal growth, respectively”

“In knee loading, the rate of lengthening with 0.5 N loads (peak-to-peak) was 0.1% per bout (femur) and 0.1% per bout (tibia) for 5-min loading per day.”

“both loaded and contralateral hindlimbs increased in length in the tibia.”

LSJL Studies 2: Effect of holes on LSJL

Not a lot on this study relating to longitudinal bone growth.  The important takeaway is evidence that LSJL can cause bone degradation which would be an important part of the process for neo-growth plate formation.

Effects of surgical holes in mouse tibiae on bone formation induced by knee loading.

“Loads applied directly to the knee (knee loading) have induce anabolic responses in femoral and tibial cortical bone. In order to examine the potential role of intramedullary pressure in generating those knee loading responses, we investigated the effects of drilling surgical holes that penetrated into the tibial medullary cavity and thereby modulated pressure alteration. Thirty-nine C57/BL/6 female mice in total were used with and without surgical holes, and the surgical holes were monitored. The left knee was loaded for 3 days[at 5Hz at 0.5N for 3 min a day], and the contralateral limb was treated as a sham-loaded control. Mice were sacrificed 2 weeks after the last loading. Although the surgical hole induced bone formation in both loaded and non-loaded tibiae, due to regional and systemic acceleratory phenomenon the anabolic effect of knee loading was substantially diminished. Without the holes, knee loading significantly elevated cross-sectional cortical area, cortical thickness, mineralizing surface, mineral apposition rate, and bone formation rate on the periosteal surface. For example, the rate of bone formation was elevated 2.1 fold (middle diaphysis–50% site from the knee along the length of tibiae) and 2.7 fold ( distal diaphysis–75% site). With the surgical holes  knee loading did not provide significant enhancement either at the 50% or 75% site in any of the histomorphometric measurements. Alteration of intramedullary pressure is necessary for knee loading to induce bone formation in the diaphysis{it may also be necessary to induce longitudinal bone growth} .”

Now they do say however that the drilling of the epiphysis did induce a response of the bone just not the same adaptations as it did without drilling.  Note that drilling was used rather than microfracture.  Although we can’t say for sure how surgical holes would affect LSJL’s effects on longitudinal bone growth.

“On days 2 and 6 after the last loading, the mice were given an intraperitoneal injection of calcein” and the results are shown below.  Calcein is used as a Ca2+ and Mg2+ indicator which are two proteins that are strong components of bone.

Without drilling:

Note that in group D which is the loaded group there is a huge hole in the middle of bone indicating that LSJL may in fact cause bone degradation which would allow for cartilagenous growth plates.  The fluid flow degrades bone and osteomy(removal of bone) may be necessary for new chondrogenesis.  It’s possible that this degradation of bone occurs in the epiphysis as well.  In group F the hole is smaller.  Group F was farther away from the site of loading than group.  Perhaps LSJL induces bone degradation more at sites closer to loading rather than farther away from loading.
  Slides were only taken from above so it’s possible that there would be bone degradation visible if the bone was horizontally sliced.  Bone degradation from a horizontal degradation would be ideal to allow for new growth plate formation for renewed longitudinal bone growth.
With drilling:
In this group both C and D have holes but in group F versus E the hole is much bigger in F.  In D the bone degradation is much more scattered than in C.  So LSJL can increase bone degradation in the body.
Unfortunately this study was performed before Yokota and Zhang realized that Lateral Synovial Joint Loading could be used to increase bone length so they didn’t measure the things that would interest us height seekers like if the tibia and femur had increased in length.

” knee loading induces alteration of intramedullary pressure in the femoral bone cavity and this alteration is synchronous to the loading frequency in Hz”<-The higher the frequency, the greater the intramedullary pressure.  I’m not sure exactly how to alter the frequency via LSJL but I believe that clamping/release from clamping/and then clamping again.

“cyclic deformation of the epiphysis alters pressure in the medullary cavity and the pressure gradient induces fluid flow in the diaphysis “<-Although fluid flow which can increase nutrient supply to chondrocytes, the number of changes induced to the growth plate via LSJL cannot be explained by just an increase in nutrient.

“In the presence of surgical holes, it is expected that the gradient is not adequately established because of incomplete pressure sealing.”

“A pressure gradient, elevated by venous ligation, was shown to increase interstitial fluid flow and this flow-mediated bone adaptation was considered to be independent of mechanical strain ”

“During knee loading no bruising or other damage was detected at the loading site, and after loading mice did not show a weight loss or a diminished food intake.”

“Osteoblast specific factor 2 (periostin) is preferentially expressed on periosteum and considered to play a role in the recruitment and attachment of osteoblast precursors in the periosteum”

“knee loading herein induces approximately 30 μstrain at the site of bone formation and the number of loading cycles per day is 900 for 3 days”

The Chemical That Would Make Adults Grow Taller Has Been Found – Game Changing Post!

The chemical that would make adults taller has been found – game changing post!

Grow TallerThis finding I had more than 3 months is what I had been alluding to when I told a few people that there was something big coming. The news about Teplyashin’s team was big, but this one seems to have a much more immediately, more practical effect. This post is what I was alluding to months ago. However, there are some key issues which we need to get cleared before we tell you guys what it is –


  1. It is not a pill or chemical you can take orally. It requires that you inject it into a certain area of the body.
  2. It is the main critical component, but one would need at least 2 other compounds combined with it, all injected using syringe and needle sequentially spaced out throughout a day to work.
  3. You can’t buy this compound easily, and I haven’t been able to find any places which sell it to regular non-lab people. – I am sure that here is some lab or factory in India or China which makes a synthetic version of this chemical but even the researchers working day after day with this chemical might not understand how effective it could be.
  4. A minority of adults will notice results (Just like always.) Most people will not notice results, except maybe just 1 cm of increase. However, that 1 cm is still enough to make a validation of the scientific theory/proof of concept.
  5. The results takes about 2-3 months total to really show.
  6. Expect on average about 2-3 cms of permanent height increase, but some people will get around 5-6 cm, depending on their skeletal structure.
  7. It works for a certain percentage of the population. I have not been able to find a sufficient reason why the chemical seems to increase only a small percentage of the human population.
  8. The amount of increase among adults has been reported to be as high as even 3-3.5 inches. (search on google for older posts I wrote where I tried to document every instance where some women mentioned it)
  9. It affects the body in a way which even I did not even consider or think of before. The body’s anatomy sure does interesting things. This claim is real, and it makes medical and anatomical sense.
  10. The chemicals (all 3) would need to be injected while at the same time another body contouring technique is being applied to the body.
  11. The increase in height would be permanent, at least in terms of a 20-30 year frame time, before people naturally start to shrink again at old age.

About two weeks ago I had been hinting at some type of discovery which I felt at the time was the biggest discovery that was made for our endeavor. I even wrote to Tyler saying that I had found something that was extremely close to our holy grail. Some people got curious and started to ask in the subsequent posts just what was this game changing post about. I alluded to it in the post about Calcium L-Threonate, and the posts about Russian Plastic Surgeon and Stem Cell Researcher Alexander Teplyashin’s research. When I wrote the two posts about the fact that his research team had succeeded in getting the stem cell technique to work successfully on lab sheep/ram leg bones, maybe some readers thought that the post was the big news. That was not it, even though it was just as earth shaking in its implications.

I wanted to post it now, because it was worth sharing to you guys. Like I always have said, I will share everything and let you guys in on all the secrets that I have found in the biomedical databases on the internet. I am a businessman but this thing, I figured that it was just not worth it to charge you guys.

I put this information public for the others. Some of you guys are young teenagers in the Philippines, India, Pakistan, who don’t have the type of money to pay for such information. Most probably didn’t come from a rich Singapore family who has millions to pay for limb lengthening surgery like Nick, who I interviews on the 11th pod cast episode. You want a miracle drug, which we can never give. This is the most effective chemical that I have ever found, even more effective than glucosamine sulphate, which had sort of gone viral in some ways (That post has already been viewed over 100,000 times)

So what is it?


So how can this chemical be validated to work on increasing height in people past complete epiphyseal cartilage ossification?

This was a compound which I and Tyler had both sort of conjectured about before but did not go deep into checking it out. The start of this saga started when I had made quite a few posts indicating that a small subset of women who went through pregnancy noticed that they started to notice other people becoming shorter. Tyler immediately guessed it was Relaxin and the citation by him on one PubMed study on how the pelvic bone structural alignment in cows which went through the 1st pregnancy did dramatically change seemed to only give slight proof. I agreed with him. However, more reports started to come in, maybe once every month with some mother or female writing in and giving the phenomena even more credibility.

I wrote another two full, detailed posts trying to explain the exact mechanisms on how the female body would end up longer even with relaxin, and the only explanation I could come up with was that the human female pelvic bone structural alignment also changed after the first or 2nd pregnancy just like heifers (female cows before ever going through their first pregnancy). If you just google the terms “pregnancy” and “height increase” into Google you would find those posts.

I decided to go back and really look at the compound after at least a dozen pregnant females came forth on online forums and claim that besides just the increase in feet and finger sizes during pregnancy, they noticed height increases, sometimes as much as even 3.5 inches in increases, over a span of 2-3 pregnancies.

That was when I stumbled upon a single Patent done, which hid from me and Tyler even after years of searching.

Refer to the patent below….

Method for remodeling bone and related sutures – Inventor: Dennis Stewart – Company: Bas Medical Inc.

Below are the other patent #s which are also associated with the idea/invention

The reason to have the patent filed multiple times is this. The practice of Patents is to file multiple patents for different countries for the same inventions. All the Patent numbers will essentially take you to the same patent.

In the abstract of the patent, the Inventors specifically says at the last sentence, and I quote…

“The invention further encompasses methods of modifying the height of a human subject”

It seems that this Dennis Stewart who has been researching the effects of Relaxin for over a decade (I checked his PubMed published papers) had filed the patent to protect the idea that Relaxin when administered to the bones can get them to grow. The bones have relaxin receptors.

So the million dollar questions is, “Why would this chemical work on human adults with fully fused growth plates?”

If people are hoping this compound can magically reopen their growth plates, it won’t do that. However, it has a very beneficial effect on all the tissue types we care about, epiphyseal cartilage, bone specific cells, and the ligaments that hold the bones together. In a certain context, the answer is yes it would work for even adults. How it works is much more interesting, which I will try to go into below.

My Personal Theory On Why Relaxin Can Make Adults Taller

In the last month, I have bought multiple books on joints and have been very lucky to find very cheap old textbooks in the local Salvation Army and GoodWill that is by my house. I picked up the Textbook “Joint Structure & Function – A Comprehensive Analysis – 4th Ed.” by Levangie and Norkin, which turns out to be one of those textbooks that people who go into Physical Therapy needs to read up on. I also started to read up on very old (early 20th century) medical textbooks and ideas which are now no longer practiced. In addition, I became very interested in the traditions of the practice known as Bone Setting, I remember seeing this documentary about this old Chinese Medical Practitioner in Singapore and/or Hong Kong who were able to fix and repair minor bone fractures and joint problems by moving bones and joints around. It reminds one of Rolfing and the Chiropractor practices today. After learning that the practice of bone setting is almost completely extinct, but used to be practiced by almost every single old civilization in the world, I asked the question whether the same bone setters who could fix bone breaks knew also ways to make joints more flexible. That is how I got into something known as Manipulation Therapy. I would purchase the old texts “Treatment by Manipulation” (by AG Tibrell FIsher) and further texts to increase my level of understanding on how joints work, and how they can be manipulated in a safe way.

By what I have read of so far, it seems that the modern form of Physical Therapy is derived from this early 20th century practice called Manipulation Therapy. When you start looking at what the authors say, they don’t base their massage/tissue manipulation techniques on chiropractor theory, which is subluxation theory. I haven’t gotten that far from reading the books but what I have been reading does seem to give the idea of using relaxing to increase the overall height of a person seem somewhat validated in theory. I do feel that my increased knowledge on the ways the joints are designed give me a more better understanding on how it is possible. Let me explain.

The Science Behind Relaxin

Relaxin ReceptorsThis is based on what is written in the patent by Stewart. Like so many other chemical compounds that is naturally produced in the body, Relaxin is an organic compound, a protein, specially a peptide hormone. It’s overall 3-Dimensional structure is similar to Insulin and Insulin like Growth Factor (IGF), which we know can be used in children who are still developing to grow bone size. It is actually in the same family as IGF. Historically, it has been known only as a hormone associated with pregnancy. It is supposed to make sure the uterus remain stable but makes the breasts in the pregnant female grow larger. The chemical seems to target mainly the brain, reproductive organs, and the heart. In the last decade, other researchers have found that it has an even greater effect than previously believed.

There seems to be 3 different types of Relaxin compounds, or more specifically there are three different relaxin expressing genes. H1, H2, and H3 Relaxin, which are all very specific to humans.

(Side Note: One researcher found that the biomolecular chemical pathway of relaxin (cAMP pathway) can be modulated by two G-protein-coupled receptors, LGR7 and LGR8. In the patent, the list of relaxin receptors are the following: LGR7, LGR8, GPCR135 and GPCR142.The pathway used by Relaxin is different from the Isulin ligands. In certain mammal species, during the actual act of labor in pregnancy, the relaxin is released to make the vaginal tissue relax aka expand for passage of the baby’s head. However, that does not seem to be relaxin’s role in cows and humans.)

I quote from the patent…

Another advantage of the present invention is that the target bone may be remodeled, repaired, removed or grown depending on the type and need of the bone

It seems that relaxin can be used to repair bone fractures, but we have already found multiple chemical compounds that can already do that. It’s pro-osteogenic effects however may mean it can have other uses than what we want it for.

In the next line, he writes “Similarly, a bone may be grown in size or height by administering relaxin

In the pictures of the patent, Stewart was able to identify the relaxing receptor in the epiphyseal plates (specifically the hypertrophic layer) through staining. Finding it not just in cartilage tissue, the chemical was found also in the bone cell types: osteoclasts, osteoblasts, and osteocytes.

He notes that the change in height when you administer the Relaxin can be as small as 0.2 cm to as much as even 30 cm, which is nearly a full feet in height increase, which I am not convinced is possible.

Here is where the inventor really shows something interesting. Supposedly the invention would work for people who range from 1-30 years old, although it is suggested to work on people in the 8-18 range. That makes sense since having growth plates would always work better. I am not going to put words into this person’s mouth but maybe his willingness to put the age range up to 30 means that he has speculated that the chemical would be good for people even at fully adulthood to make their bones bigger. Of course, I don’t think it is the long bones like the femur and the tibia he is referring to, but the non-long bone types in the skeletal structure. That is what I believe the increase in height will occur in.

The other amazing thing is that Dennis understood that beyond cartilage and bones, relaxing has beneficial effects on sutures, which is just another term used to describe the area where bones meet. Remember that besides the long bones in the human body, there is also the irregular bones (pelvic and vertebrate) which can grow.

This is where I think the holy grail lies. I believe that with the right relaxin formulation (H1, H2, and H3) administered to certain areas close to the sutures of the human body, ie the pelvic joints and the sutures on the sides of the intervertebral discs, you would be able to increase a person’s height by making the irregular bones in the skeletal structure grow larger volumetrically by adding more layers on the bones.

If we combine the intravenous injections of relaxin formulation with manipulation techniques aka physical therapy to straighten out the lumbar-pelvic area, what would be seen would be a permanent height increase in a large percentage of the patients.

I had tried to guess how the female body during pregnancy actually changes in standing skeletal posture to even allow for an overall height increase. I don’t want to go too deep and re-explain something I said before so please refer to the post “How Pregnant Women With Ossified Epiphyseal Cartilage Increase In Height” for more explanation. Remember, it is a huge leap in theory and basically just a personal, amateur level guess on what is happening underneath the skin.

The other big question to try to answer is…

“So why do most women during pregnancy not experience any height increase, but only a small minority of women do?”

That question, I can’t answer with a reasonable, scientific answer. 

Here is one guess: I once proposed before that it is possible that a small percentage of people, but most especially women never have fully fused growth plates. Those growth plates are only seen in X-Rays. You can’t look at an adult person and tell if they have any cartilage left at the ends of their long bones. We all have to assume that because they are an adult in their late 20s that they have fully finished growing taller, but no one except superman with his X-ray vision would be able to truly validate that idea by looking to see no more cartilage/growth plates. If that is true however, then it would then invalidate the entire premise of this post, which I am willing to accept. Logically, then all these claims made by women that they grew taller during pregnancy in their 20s and even 30s is just because their growth plates were never completely ossified. Of course, that would mean that we need to ask a completely different question, which is why it is that a minority of people seem to have unfused growth plates so late into their life.

If we assume that the first guess is not true, then the next guess on why only a select few women see any increase is that some women have irregular vertebrate alignment aka minor scoliosis which was never fixed until pregnancy, where the ligaments were relaxed enough to get the curved vertebrate to even out and become symmetrical.

I have noted that there does seem to be a weak positive correlation between above average females who notice that they grew taller during pregnancy. It might be that certain women who have already been suceptible to tall stature have bone relaxin receptors particularly sensitive to the relaxin, which is so similar in function and form as the insulin and the IGF types.

What a person should expect to really look for in terms of a signal is to see if their feet is getting bigger. The phenomena of pregnant women’s feet becoming bigger is well documented, which shoe sizes often increasing as much as by 2 shoe sizes. If the person taking the compound notices that their feet has started to increase in size, then it is a rather good physiological signal that the relaxin is working maybe also on the torso vertebrate bones and pelvic bones as well. So if we decide to start to inject our pelvic region and lower back with relaxin, we should be checking the size of our feet weekly for any changes.

How can a normal person obtain this chemical compound?

So far, I have not looked into how a person can get their hands on it yet, at least at a reasonable price. What I do know is that almost anything you want, some company in the world is willing to make it. (I know of one company based in Iran where the people there are chemists, CNC machinists, and 3D Modeling artists who can formulate any type of chemical or 3D Print any object that you want, as long as you can pay the upfront manufacturing costs to get the raw materials) For example, I was able to get modafinil from India and after just a quick search. On, I found that there is at least one company based in China which is selling Human Relaxin. For just 1 box which probably contains less than 10 mL, we are looking at $300-$500.

In comparison, during pregnancy the amount of relaxin that is produced in various parts of the body and then released through the system might be much more in magnitude. However, we could also make the case that when it comes to giving kids shots of growth hormone, which lasts even years, the amount of HGH that is injected is not that much, maybe just 10-20 mL if even that much. Remember that we did look at the amount of endogenous HGH released by the pituitary gland in growing kids even at the most optimal time, during deep REM sleep is still not that great in quantity.

That could mean that if the stuff we did buy from the Alibaba sellers of what is supposedly the synthesized relaxin is around the right amount, we would still be paying around $500 for each shot of the ligament loosening/bone increasing/growth plate increasing compound.

In Conclusion

I had always thought that the only ways to increase bones in length or by volume was by turning the bone tissue into cartilage, or getting whatever is left of the cartilage aka the articular cartilage surface to expand in thickness.

It seems that there is a third approach which I had not even considered, and that is by loosening the ligaments, tendons, and other connective tissue in the body. I understand that the ligaments are not structurally strong against gravity like bone or cartilage so it can’t provide the push to hold the body higher in elevation relative to the surface of the earth aka make the body become taller, but for a larger percentage of the population, a loosening of the ligaments around the lower back and pelvic region means that the bones will be readjusted in a way which will make any hidden skeletal abnormalities and angular bone alignment become aligned. The result is that those people will notice height increase. Remember, the patent’s title is Method for remodeling bone and related sutures, and when we actually look at how orthopedic surgeons define sutures, they refer the term “suture” to mean the spaces where bones meet. This compound has dramatic effects in the suture, which often means the space between the bones can be expanded.

I propose that along with this chemical (Relaxin Formulation), they should combine it with the following…

All of the chemicals have pro-chondrogenic capabilities. The idea is to get all of these compounds together and get the growth factors to be injected intravenously in series at the same time a physical therapist is using manipulation therapy on the lower torso region.

However, relaxin will be the real key to the entire process. It is relaxin which will make the pelvic region malleable enough for the modern day “bone setter” the physical therapists and maybe even the chiropractors to create a bone structural alignment that will result in permanent height gain. Since Relaxin has receptors in the cartilage as well as in all of the major bone cell types, it has a additive effect.

How Much Confidence Do I Have In This Chemical and It’s Effectiveness? Or, to put it another way, would it definitely work for permanent height gain that is noticeable, maybe 2 inches?

First, I am not a person who has studied the chemical for over a decade like the Inventor Dennis Stewart. I am also not him who decided to spent maybe even $2000-$4000 to pay to have this “invention” patented, which he did working for Bas Medical Inc. For a normal person/non-corporation to file a patent which would cost them thousands of dollars means that they are either extremely confident in what they have found/discovered/created or they have maybe too much money on their hands. As for myself, I am an amateur researcher who reads a lot of texts on joint mechanics and orthopaedics. Orthopaedics is sort of like a calling for me, which has allowed me to also study and read up on the cutting edge of research in cancer research, stem cells, and gene therapy, the biotech hot topics of the last few decades. If I could do things over again, I would have maybe chosen Pre-Med for my undergraduate studies, got into Med School, and tried to do really well in the Step 1 (USMLE Part 1) to get into the ultra-competitive orthopedic surgery route, which has been found to be the best paying medical sub-speciality where surgeons often earn around $700,000 per year in earnings.

I am not a doctor by training, but trained as a type of biochemical engineer who worked in labs looking for AIDS vaccines and Plastic Surgery techniques. Based on my personal research in the last 2 years doing this type of stuff, I have extreme confidence that using the relaxin formulation with other pro-chondrogenic growth factors combined with a bone & joint manipulation specialist (you can choose chiropractor, Asian bone setter, physical therapist, rolfing, or maybe even deep swedish masseuse) there would be a noticeable increase in height for the person which will be both permanent and noticeable. I am not going to say that everyone is going to get results, more like a minority, but I would guess that 10-20% of everyone who combines the chemical with the body manipulation will see results after 2-3 months.


Side Note: I was not not the first amateur height increase researcher to notice this phenomena. The person who back in the 2007-2010 time who created the or HeightFX grow taller formula (Website is now gone) also noticed the phenomena and made a post to some Mom forum asking for more information on how they grew taller but never got a response from them. I remember looking at the WayBack Machine at the content on the Height FX website and being amazed at just how clear and knowledgeable the person was on what would work. The guy who sold the bogus formulation understood all the easy, traditional paths on height increase and tried to figure out how pregnant women were getting taller but didn’t seem to push further into the research, so he never got as far as us.


For more information on the types of relaxin formulations that have already become patented, refer to the following patent #s.

  • 5,945,402
  • 5,451,872.
  • 6,200,953
  • 5,811,395
  • 5,911,997
  • patent application Ser. No. 09/846,149.
  • A process for producing relaxin is described in U.S. Pat. No. 5,759,807.
  • A process and compositions for the isolation of human relaxin is described in U.S. Pat. No. 5,464,756.
  • A method of chain combinations for human relaxin or analogs thereof are described in U.S. Pat. No. 4,835,251


I am reminded of this lecture given by Guy Kawasaki, one of the evangelists for the late Steve Jobs. He once said something which I still remember on how really great scientists find really breakthroughs in science.

When they see something in their experiments and data, which is not consistent with the other results or lays outside the trend line, instead of saying that the data point is due to normal error variance and removing it to make all of the other data points look smooth and linear, they say instead “hmmmm, that is interesting” and proceed to figure out why the outlier point in the data set does not agree with the others. That is the mark of a great scientific researcher. That is what happened in this case. The phenomena of pregnant women who end up taller was such a unique data set point, that I was forced to look into it and see why it was such an outlier. The outlier cases, as Malcom Gladwell states, is where the really interesting things lie.

Sure, there will always be some researchers who won’t be doing groundbreaking work, who are needed to repeat the experiments already done to validate the original researcher’s results, but it seems like these days, there are just too many Ph. Ds that are coming out of graduate school who is not doing any real research.

Is it because of all of the easy questions and obvious corollary conclusions have all been discovered, and all of the low hand fruit have been plucked?

Is it just too hard for a single person to figure out something revolutionary in nature anymore? Maybe there will never be another phenomena like how Einstein wrote 4 brilliant physics papers back in 1904, all of which would have been good enough to win a Physics Nobel Prize, which changed the very way we view the world.

It could be, since the sciences have become much more vast in scope and diverse. For example, we can look at the field of mathematics. Back in the late 19th century, the PolyMath Henri Poincare was probably the last mathematician who was skilled enough to work in all of the mathematica field of his time. Even the great John Von Neumann 30 years later when asked just how much of the current mathematical literature he was able to work on, he only said 26%.

It may be too hard for even the modern Fields Metalists to dig deep enough to find real gems, but for genetics, and biotechnology, I think even the amateur research like us can make some startling conclusions. So I say, be Alice and go down the rabbit hole, and see where it takes you.

You look at the results which don’t make any sense, because that is almost always where the real discoveries lie. Last year (or was it two years ago), when the French and European particle physicists were studying the resultant projectile pathways of all of the quarks, leptons, muons, and neutrinos that came about from smashing atoms together at the LHC (Large Hardon Collider), trying to find evidence for and validate the the work done more than 50 years ago by Peter Higgs, Stephen Hawking’s mused that he secretly hoped that they would NOT find the higgs boson. The thinking is that if they did not find it, it would mean that the current Standard Model of Physics on how the sub-atomic particle interact with each other was incomplete, which meant that nature and the universe had something else up its sleeve. The last time naturalist scientists tried to tie the loose ends of physics together, back in the 19th century, trying to integrate E&M and Newtonian Classical Mechanics together, they opened the new realm of reality and existence known as quantum mechanics and radiation. This time, there was no new startling discovery, which would open a new branch of physics research. Alas, the existence of the higgs boson was quite conclusive up to a high percentage so it seems like for at least the standard model, all of the particles have been accounted for.

I view this post as the result of noticing that not all the data and information was fully conclusive. It was only found by looking for what is inconsistent and different from everything else.