Monthly Archives: December 2013

LSJL Might Work

LSJL Might Work

The year 2014 is about to come and I wanted to write one last post for the year to cap it off. I wanted to write a quick post on my thoughts on LSJL after not looking at it for so long.

About 2 months ago Tyler finally came on the website to start writing here to help out the cause. He gave that announcement on his website Height Quest and so far he has produced around a dozen super informative articles, some of which helped piece together a few issues which I had been having questions about.

I have been at this research for just around a year and a half now, and I wanted to give some thoughts about the technique Tyler has been promoting for more than half a decade. When I first interviewed him in the 2nd podcast episode (Listen Here) he had stated that he had been interested in figuring this thing out for almost 5 years when he started writing about it back in 2008. That means for probably a decade now Tyler has been doing research on this issue.

That is what I call supreme dedication. Now, obviously the big question is “Is all this theoretical research going to pay off in the end?”

Obviously the hope by everyone who reads this website is that all this stuff if going to reach a happy ending at the end. Recently there have been a few comments made by people who said that there is too much theory and research going on with not enough experiments. They want so real stuff that they can do, like some pill they can take, or exercise they can do.

The most recent post about Running DC stimuli on Silver Acupuncture Needles was the one that made me realize that there is HUGE potential in using PEMF Devices. Using electric currents at a certain frequency and low intensity has a high correlation to bone ossification rates. There is also a anabolic effect on chondrogenesis on the chondrocytes in articular cartilage which is validated by certain studies.

My recent focus will be on the effects on bone and cartilage tissue from various types of electrical stimuli. That is what I plan to look at for the first 3-6 months of next year. There will be a few sporadic posts here and there but there is where I heading.

However, this post about LSJL. This post about my thoughts on why it just might work. Back in Sept 2012 I had wrote a rather infamous post entitled Sky’s Mistake, Why He Never Increased In Height“. Sky was a former height increase seeker who started a rather large movement back in the time frame of 2005-2010 to try the technique of induced microfractures to lengthen the shin bones. He started at 5′ 8″ and saw no gains after years of trials. He has since left the community and moved on with his life. I do hope the best for him in whatever he tries to accomplish. Looking at the way he did it, it was obvious it would not work.

If something as simple as hanging 30 LB weights on ones lower leg would increase height was effective, it would already been accomplished thousands of years ago. Throughout human history I would guess millions of people who were not happy with their height probably tried something similar. They tied some heavy to their feet or ankles, held on to a high bar, and tried to stretch their body out. That was too obvious. People before Sky would have tried it already. Thousands probably already had the same idea as him. The moral of this story is that there have probably been thousands of people before who tried the same thing he did and failed. Why would he think it would work for him?

Plus, I had calculated using simple tensile load (aka Pressure) over area calculations what it would take to possibly stretch out the bones beyond the elastic region in a stress-strain graph to the elastic region before reaching the Ultimate Yield Strength. I took tensile force values obtained from experiments done on young rabbits with healthy growth plate cartilage and mutipled those values by factors of 20X and 50X to reach a values of around 25,000-30,000 Lbs of force needed to strength the femur of an adult human male{Remember according to the definition of microstrain, bone is continuously changing in length throughout the entire day-Tyler}.

However, this post is about why LSJL just might work.

From a historical perspective, Sky’s method must have already been tried thousands of times before he came along. That didn’t work.

What Tyler proposed from the study “Lengthening of mouse hindlimbs with joint loading.” was a truly revolutionary idea. Sure, it may be true that even in aged rats/mice the growth plate cartilage never fully go away but the technique is unique because of the specified region he claims you should be pushing down on.

Thinking back on it, if Tyler had suggest any other place besides the synovial joints, I would have discounted the idea by now. However, based on the location and angle on which to load the bones, the technique is something which has probably never been attempted before, especially for any person trying to lengthen long bones.

Throughout human history, there have been people who have probably loaded almost every other area of their body. Every single military unit and group in history had their bodies trained to be strong and tough. It is especially well known that in certain Martial Arts like Karate and Kung fu that practitioners will purposely hit their bodies on hard surfaces to destroy nerves in the area and make that part of the body stronger. Just watch any video from YouTube where Master Ho Eng Hui breaks open a coconut with his finger, which has become thick and disfigured from years of finger loading. (Watch Here). {There’s a better image of the kung fu cocunut funger here in this video, it looks like there is some compression too which could explain why the finger doesn’t grow longer-Tyler} Spartan soldiers from thousands of years ago probably had every part of their body hit upon to be made tougher. Throughout the millenias it should not be too hard to suggest that other tough cultures and soldiers had unusual rituals where certain body parts were been hit over and over to be made tougher. However, we still have never heard any ancient society which had grown overly tall individuals.

Loading the fists, knuckles, feet heels was probably a major part of the regime of a person training in martial arts. Add in the fact that Muy Thai which involves using the shins, elbows and knees to hit in practice did not result in longer bones shows that loading in most of the major well known areas have never worked.

This suggest that Wolff’s Law (aka Bone Remodeling through Mechanical Loading) used on common body areas would NEVER result in ordinary long bones with NO growth plate cartilage becoming longer. They would however make the trabecular bones become more dense and possibly increase periosteal bone growth making the long bones thicker however. (Whether loading long bones w/ epiphyseal cartilage in certain ways to increase longitudinal growth is something which we think is totally possible)

I have looked at various articles and studies on the piezoelectric nature of the bones and what happens to the potential gradient in the bones as you push down on certain areas of the bones. The science that Tyler is showing can be validated if a person took the time to read over the studies he references. The hydrostatic pressure increase does have some type of effect on the differentiation, proliferation and hypertrophic rates of the MSCs in the epiphysis core.

The point from all this talk is to show that if you are going to try something like loading the bones in a place which other people possibly also loaded on, it would not work. That is why I don’t believe that loading the ankles would work. If it worked on the ankles, most people who have done yoga and pressed their full torso/body weight down on the ankles in the lotus position (or while meditating) would have noticed their lower legs becoming longer. Obviously that didn’t happen.

The unique approach of this bone loading method is to load the sides of the long bone at the epiphysis which is completely novel in approach. I can not think of why anyone in the past would ever want to try to load the sides of the epiphysis.

Based on this idea, on the fact that no one has probably ever done this technique purposefully in a diligent way, shows at least that it has not been completely disproven base on the trials and failures of thousands of people before us. If thousands and millions of desperate people have already tried this method before us, we would not need to be still discussing the efficacy of this method. I still have hope that for a small minority of people, the technique does have some chance.

I know the argument is not completely logical, but because very few people before recent years have probably ever been loading the sides of the epiphysis before (Why would any sane normal person who did not read the Zhang/Yokoto papers have any type of motive or incentive try something like that?) the technique has been at least NOT been proven wrong. 

(Note: I realize this type of strange logical argument is something people who believe on god would use when debating an atheist about the existence of god would also be using. Just because you can’t (or haven’t yet) disproved something yet does not mean it exists or is right. It is a sort of big leap of faith I am taking.)

So, Lateral Synovial Joint Loading just might Work.

Yokota LSJL MachineRead the post A Simple Step By Step Guide For Lateral Synovial Joint Loading to try it out.

In addition, I did want to tell the people that Yokota has gone into writing up a proposal to the building of the loading device. Check out the paper Development of a Portable Knee Rehabilitation Device That Uses Mechanical Loading

Have a good New Years guys and happy 2014.

Should You Tell A Person You Are Dating That You Had Limb Lengthening Surgery?

Should You Tell A Person You Are Dating That You Had Limb Lengthening Surgery?

Limb Lengthening SurgeryI recently found out that a new discussion board was created from former members of the Make Me Taller Community. They are now at

I haven’t given much time to looking over their discussions and threads but there was a sort of interesting little thread started. Apparently someone linked to another thread started on the Reddit website entitled I (M24) have had cosmetic leg lengthening to make me five inches taller. Is this something I should tell my girlfriend (F24)?” 

The guys’s situation is very interesting and seems to be a very valid issue that people who are considering the surgical method for increased height to consider. He went from an initial height of 5′ 7″ to 6′ 0″. The 12.7 cm of longitudinal increase in the person’s femur and tibia is something that is unheard of even among online community of people who actually pull the trigger and go through with the surgeries.

I took the liberty to upload the picture of his posting from the Reddit website.

Limb Lengthening Surgery

The thread has not been closed but there was over two dozen responses from all different types of people. Most of them did take the time to think over the issue and give them own biased opinions over what this person should do.

My Short Answer

Don’t tell the person you are dating. Who you were back then is no longer who you are now. If you are going to be spending so much money and time dedicated to reshaping your body, especially to change something that should NOT be malleable like height, then you might as well learn to accept your new body. It is absolutely true that due to genetic luck (or lack of it) your growth plates stopped maybe a little too early or you did not get the type of long bone longitudinal growth you might have wanted. That was what nature intended for you.

Of course, since we are very clever creatures which can create tools to make our lives better, we decided to defy nature and choose modern technology to give us something which nature would not give us.

If instead of surgery you somehow went through a dramatic growth spurt to give the same amount of height increase, would you feel any issue over the need to tell the person that you went through that growth spurt? Analogously, it would be the same as people who would rather let their own bodies fight off cancer using holistic herbal methods instead of give their bodies to the surgeons and chemotherapies which will cut into their bodies.

The reason you would ever even go through with Limb-Lengthening Surgery is because you could not accept the idea that you were going to stay at that height for the rest of your life. Your identification as a man who would be permanently below average in height was to you unacceptable so you decided to change that.

You have now gone through with the surgery, and become 5 inches taller, to become slightly above average in height. That is your new identity now. Forget about who you were once before, and live your life as who you are right now.

My Much Longer Answer

The only thing that would cause anyone to ask the question is over the emotion of guilt, and feeling bad over the idea of lying to another person. Of course the lying is not blatant, but through the omission of not telling the person something specific. Some people call it a half-lie. They are not being completely, fully honest to the other person.

Some things need to be kept to themselves. When it comes to the subject of sex and sex related topics people have a right to keep those things to themselves, and do whatever they want to do in the privacy of their own homes. That is what makes them happy. Why should they feel any type of social obligation to share their personal quest and endeavor with other people?

Cosmetic Surgery Considered From A Different Cultural Perspective

As I had said before, I live in the Gangnam area of Seoul. In terms of all the places in the world, this location I have been living in for almost a year and a half now has the highest concentration of people who have willingly gone under the knife for cosmetic surgery than any where else. Per Capita, it is extremely high. I can’t go outside of the street without seeing someone who have had Botox. My landlord who is a 50 years old female has gotten Botox multiple times and had her nose and eyebrow ridge done. Where I live, cosmetic surgery is normal and even promoted.

Of course, based on American standards we could say that the reason any person goes through with cosmetic surgery is because they are not happy with how they look. They have some type of hidden & strong insecurity which they can’t get over. We give them shame, gossip about them, and possibly make them feel worst about themselves when they “supposed” already feel bad about who they are already. Way to go us.

However, based on the modern Korean standard, many young kids who think getting cosmetic surgery is a positive thing think that it is a form of self improvement. In a culture which values on continuously improving oneself, similar to the Japanese concept of Kaizen, it might be argued that getting cosmetic surgery is just another way to improve oneself. In this case, improving one’s appearance.

I know plenty of people who go online to buy Nootropics to improve their cognitive abilities, and try different ways to biohack their bodies. They are trying to improve their bodies. Why is it that some people can accept almost all other forms of self improvement methods except cosmetic surgery? Why do people have something against the idea of using surgery to improve oneself cosmetically/appearance wise?

The Real Question Not Answered

Of course the other big question is “Are we lying to the person we are dating or in a relationship with by not telling them that we have had cosmetic surgery?”

At the most simplest level, if we were to be completely honest about the situation we are lying.

However, as anyone who has some level of awareness of the human creature & is mature through life experience would understand, we as humans with our flaws can not paint the world as black and white, 1s and 0s. There is a lot of gray zones and there have been century long debates about ethics and morality. The wise person would realize that morality is something that is relative. While most cultures might agree that there are big taboos like man-slaughter, rape, incest, and cannibalism (or even maybe homosexuality as recently stated in the Supreme Court of India), even our most sacred taboos and mores can be broken in unique cultures and countries which don’t practice our belief system. What 99 people out of 100 would say something is completely wrong, the other 1 person out of 100 would say it is okay.

We have these unique psychic tools known as Ego Defense Mechanisms, specifically Rationalization & Justification. Ultimately, if we were to be completely objective about it, it doesn’t matter matter if the person doesn’t tell the person they are with. If they do not tell the person, they will find a way to use Rationalization and Justification to make their decisions and actions acceptable to themselves.

We have to find a way to live with ourselves. We are going to be using Rationalization to justify our actions so that we can move on with our lives. The emotion called guilt may exist, and for a long time, but usually that guilt diminishes as we learn to maybe forget our past actions just long enough to make it to the next day. Most people want to believe that they are good people, but have weaknesses and flaws. We believe what we want to believe. We do the best that we can with the limited resources we do have.

As always, I want to here from the readers about what their personal opinions are. Leave a comment below and tell me your opinions

Does Inhibition Of FGFR3 Restore The Growth Plate Slightly – A Reply To Raja

Update August 1st, 2013: The conversation on this issue on whether inhibition of FGFR3 between Me and Raj continue with the following messages…

Raj —> Me

Unfortunately Michael, I don’t think you really got the point of my message.

You state: “We can not translate the chondrocyte dysplasia of rats to humans. The first reason is that dysplasia does not always equate to hyperplasia. The growth plates may go through dysplasia but that usually means that the subject is going to develop stunted growth instead of increased growth.”

In the two studies you looked at, about PD176076, it states that mice did have increased growth plate height, but with overall dysplasia. The dysplasia is caused by PD176076’s effect as a VEFGR inhibitor as well.

My point was that if FGFR3 inhibition will lead to hyperplasia, but ONLY if we target FGFR3, not VEGFR. The problem with current pharmaceuticals are the lack of specificity between different tyrosine kinases. As the study above states, PD176076 is also a VEGFR inhibitor. Inhibition of VEGFR will in fact lead to stunted growth (google this). Please, do some more research. Look at case studies were scientists have examined families with mutations in FGFR3. These people have tall stature caused by the hyperplasia of the growth plates.

But you are right, it does not say anything about the regeneration of growth plates. I specifically stated in my first message that this could be effective for individuals whose growths had just recently closed.

Again, you need to do more research. 

Me —> Raj

so how would the inhibition of FGFR3 and the prevention of the inhibition of VEGFR help a person who recently had their plates fused? I am already doing research on something else. help out.

take a look at calves with spider lamb syndrome. Their legs may be longer, but the limb will be bent/crooked.

Raj —> Me

Spider legs – a developmental defect.

Even if it does lead to spider legs, it should return to normal because our genes weren’t designed to cause spider legs.

And yeah, I’ll get cracking on that.

Most of the comments and emails I get to the website are not very helpful in the research. However, sometimes someone makes a comment or references of a study which causes a big change in our research. It seems that just recently a person named Raja wrote a comment stating that it might be possible for people who have had their growth plate close recently to reopen new plates slightly by inhibiting one of the Fibroblast Growth Factors, FGF3.

The Original Comment…

Growth plate regeneration may actually be possible for people between 17-21. Inhibition of FGFR3 may restore the growth plate, by a very small degree, as stated in the paper here: If we can regenerate the growth plate using FGFR3 inhibitors, we can use other kinase inhibitors (or pharmaceuticals) to increase the height of the growth plate, which can potentially increase final height as well. I am currently researching pharmaceuticals to achieve this and how to synthesis different FGFR3 inhibitors. Also, it has been PROVEN that FGFR3 inhibition causes skeletal overgrowth (just google this).

{Tyler’s Comments in Italics+Bold}

The Study – Cartilage Dysplasia and Tissue Mineralization in the Rat Following Administration of a FGF Receptor Tyrosine Kinase Inhibitor

Abstract – PD176067 is a reversible and selective inhibitor of fibroblast growth factor receptor tyrosine kinase, and was in preclinical development as an angiogenesis inhibitor for the treatment of solid tumors. A 14-day oral toxicity study of PD176067 in young female rats (7 weeks old) was conducted at doses of 2.5, 5, and 10 mg/kg/day (15, 30, and 60 mg/m2, respectively). Skeletal changes, and vascular and soft tissue mineralization were observed as primary drug-related toxicities. To determine if these changes are specific to young, rapidly growing animals with increased vascular and osseous development, PD176067 was administered to mature (11 months old) rats. Female rats received PD176067 by gavage for 14 days at doses of 2.5, 5, and 10 mg/kg/day and necropsied on day 15. Clinical signs of toxicity were seen at ≥5 mg/kg and one death occurred at 10 mg/kg. Physeal dysplasia{physeal dysplasia means that the growth plate grew and should result in longitudinal bone growth; 11 month old rats are pretty much growth plate senescent} (distal femur, proximal tibia, sternum) occurred in all drug-treated animals and was characterized by dose-related increased thickness of the zones of chondrocyte proliferation and hypertrophy, and marked thickening of the zone of ossification. Cartilage hyperplasia was characterized by proliferation of chondrocytes along margins of the synchondrosis and subperiosteum of sternebrae{if the origin of the growth plate chondrocytes was periosteum then it would mean that this FGFR1 inhibition could work on people without growth plates as older individuals could merely acquire new growth plates via the periosteum}. Serum phosphorus levels increased 47% and 166% at 5 and 10 mg/kg, respectively. Mineralization of cardiac myocytes, aorta, various arteries, renal tubules, and gastric mucosa and muscularis was seen at 10 mg/kg, and consistent with the presence of calcium-phosphorus deposition. Physeal changes occurred at similar plasma PD176067 exposures in young and mature rats (AUC ≥ 4.83 μg · hr/mL). PD176067 produced morphologically similar lesions in young and adult rats.

Initial Analysis – From doing only a reading of the abstract it seems that if we give this type of selective inhibitor of fibroblast growth factor receptor tyrosine kinase known as PD176067 to lab rats, the physis (growth plates) in its limbs goes through dysplasia. In the experiment, the lab rats were used to test the toxicity of the compound. Different dosages were used and young and old rats were tested. What is seen is that the zones of the growth plates did increase in thickness. There was signs of cartilage hyperplasia where the chondrocytes on the edges of the articular and epiphyseal cartilages replicated much faster. What is not good is that something else known as serum phosphorous increased. The bigger problem is that parts of the heart, aorta, and various arteries started to become mineralized. The effects were very similar in both the young and old rats.

From reading only the abstract I conclude that while it might be that this specific FGF receptor tyrosine kinase can cause the cartilage in joints to go through abnormal development and get thicker, there is no evidence that administering of any type of inhibitor of FGFR3 would lead to the reappareance of growth plates that might have been recently ossified.

Since Raja did say that I can just google the information about the link between inihibition of FGF3 and skeletal overgrowth, I did just that. The results are in the Further Research subsection

Deeper Analysis from Reading the Full Study PDF HERE – The first thing that is noted is that researchers have discovered that it is possible to stop cancer tumors from getting bigger by restricting the angiogenesis aka creation of blood flow to the tumor. Compounds like VEGF and FGFs actually can bind to receptors on cell surfaces with tyrosine kinase activity.

From the article “PD176067 is a reversible, selective ATP competitive inhibitor of FGF receptor tyrosine kinase, with in vitro IC50 values of 2–9 nM against human FGF receptor-1 (Parke-Davis, 2000)….inhibition of VEGF receptor tyrosine kinase is also observed, although at higher concentrations than for FGF receptor tyrosine kinase.”

The thing is that the researchers wanted to test just how toxic this inhibitor of FGF can be, young rats around 7 weeks old got various dosages twice a day. The result is that the growth plate in the young rats started to develop abnormally. In addition, many of the soft tissues started to mineralize and blood vessels also started to mineralize.

The section that would be most important to either validate or disprove the claim made by the commenter Raja that administering of a FGF Receptor Inhibitor is the section below, which I copy and pasted from the discussion section.

Abnormal endochondral ossification induced by PD176067 and classified as physeal dysplasia was present in the distal femur and proximal tibia growth plates in young rats at ≥5 mg/kg and mature rats at all doses. In young rats, progressive thickening of the physis was dose-related and severity of physeal dysplasia was minimal, mild, and mild to moderate at 2.5, 5, and 10 mg/kg, respectively. There was an approximately 4-fold increased thickness of cartilaginous growth plates in young rats at 10 mg/kg compared to agematched controls{That could be a pretty big increase in height} (Figure 3A and 3C). In young rats, the proliferating zone had increased numbers of flattened chondrocytes aligned in columns and was twice the thickness as compared to control rats{The increased number of flattened chondrocytes could be due FGFR1 resulting in disorganized flattened growth plates or it could be that FGFR1 inhibition results in chondrogenesis of subperiosteal cells resulting in possible new growth plate formation}. There was increased depth of the zone of chondrocyte hypertrophy, and marked thickening of the zone of ossification (primary spongiosa). Disorganization of the distal columns of hypertrophic chondrocytes, variable enlargement of the perichondrial lacunae, and increased numbers of primary spongiosa with retention of cartilaginous cores and thin rims of osteoid lining the trabeculae were present (Figure 3C). Capillary loops were present within the tubes of mineralized cartilage matrix (Figure 3E). However, there was decreased resorption or amalgamation of primary spongiosa into secondary spongiosa.

In mature control rats, the narrow, inactive physes were sealed by a layer of bone along the zone of ossification, and the metaphyses contained a few thick trabeculae (Figure 3B). With administration of PD176067 to mature rats, there was enhanced proliferation and maturation of chondrocytes. There was increased prominence of the stacks of proliferating chondrocytes and an approximately 2-fold increased thickness of the zone of hypertrophy (Figure 3D). The metaphysis contained irregular thick trabeculae with retention of chondrocytes and cartilage cores (Figure 3F). 

In both young and mature rats, the synchondroses of sternebrae were thickened by proliferating and hypertrophic chondrocytes (Figure 4A, 4B, and 4C). The cartilage hyperplasia elevated and extended along subperiosteal margins of the sternebral body with resemblance to endochondral ossification in young rats.

From the Results Section

Oral administration to rats of an inhibitor of VEGF receptor tyrosine kinase (AstraZeneca’s ZD4190) resulted in a marked increase in the femoral physeal zone of hypertrophy (Wedge et al., 2000). Administration of a recombinant humanized anti-VEGF monoclonal IgG antibody (rhuMabVEGF) to young adult cynomolgus monkeys produced physeal dysplasia characterized by increased hypertrophied chondrocytes, subchondral bony plate formation, and inhibition of vascular invasion of the growth plate (Ryan et al., 1999). 

Deletion of the murine FGF receptor-3 gene resulted in mice (FGFR-3−/−) that developed bone dysplasia characterized by expansion of proliferating and hypertrophic chondrocytes within the growth plate (Deng et al., 1996). The study by Deng et al. suggested that FGF receptor-3 regulates endochondral ossification by limiting chondrocyte proliferation in the growth plate; therefore, inhibition of receptor function results in chondrocyte proliferation.

PD176067 administration to rats resulted in chondrocyte proliferation and cartilage formation, characterized by increased thickness of both the zone of proliferation and the zone of hypertrophy. Although the mechanism by which this occurs in rats is unknown, inhibition of FGF and/or VEGF
dependent signaling pathways appears to be a component. In summary, the current and published data suggest that inhibition of growth factor signaling can lead to increases in chondrocyte proliferation and expansion of the hypertrophic zone, resulting in dysplastic growth of cartilage

From the Discussion Section

In conclusion, oral administration of PD176067 to female rats for 14 days resulted in physeal dysplasia and soft tissue mineralization. These lesions were morphologically similar in young and mature rats, and do not appear to be related to inhibition of angiogenesis. Tissue mineralization was associated with elevated serum phosphorus levels and was consistent with calcium phosphorus deposits.

Personal Conclusion – When I only analyze this specific type of FGF inhibitor, it shows that it can cause many sections of the growth plates in at least young rats to become expanded in thickness. When it is applied to older rats, who actually still have cartilage in their limb bones, the researchers write “With administration of PD176067 to mature rats, there was enhanced proliferation and maturation of chondrocytes. There was increased prominence of the stacks of proliferating chondrocytes and an approximately 2-fold increased thickness of the zone of hypertrophy

Now, let’s always remember that even in mature rats which might be many months old and don’t get their limbs growing longitudinally longer, their limbs are still cartilage tissue. When the researchers are saying that the chondrocytes did proliferate in mature rats, it is more likely that they are referring to the fact that mature rats still have chondrocytes in their long bones since the long bone still has cartilage in them. It seems that the growth plate never goes away for lab rats{The growth plate is still dysfunctional in older rats such that longitudinal bone growth stops so it is promising that growth begins a new; one possible method for growth beginning anew is the accumulation of new growth plate cells from the periosteal region which could potentially happen in older adults}. When the researchers are talking about the zone of hypertrophy in mature rats, that is what they are talking about.

Overall, after even read the entire PDF for the full study, there is no evidence that there can be growth plates can be be restored even slightly for humans. The reason is because old rats have cartilage in their long bones, and humans do not. We can not translate the chondrocyte dysplasia of rats to humans. The first reason is that dysplasia does not always equate to hyperplasia. The growth plates may go through dysplasia but that usually means that the subject is going to develop stunted growth instead of increased growth{While true that skeletal dysplasia doesn’t always result in increased height, it seems however that dysplasia’s relating to FGFR3 inhibition and/or CNP stimulation uniformly result in increased longitudinal bone growth, although in this study FGFR1 is inhibited and not FGFR3}.

I would say that the suggestion made by the commenter Raja is inaccurate and was a too big of a leap in scientific reasoning and logic. The studies never stated directly or implied that it would work in adult humans.

Tyler’s Comments:

It’s interesting that PD176067 is actually an FGFR1 and VEGFR2 inhibitor and not an FGFR3 inhibitor when FGFR1 is typically considered the good FGFR and FGFR3 the bad.  It should be noted that LSJL does result in upregulation of FGFR1 mRNA.  FGFR1 is involved in the commitment of stem cells to chondrocytes.  Maybe only downregulation of beta-catenin is required to commit stem cells to chondrocytes and FGFR1 merely plays an inhibitory role.

As a result of the FGFR1 inhibitor treatment there was increased incidence of hypocellularity bone marrow lesions(fewer cells than there should be) with increasing dose and increasing age.  It’s possible that the fewer cells are a result of these cells being used as growth plate cells.

As a result of FGFR1 inhibition there was also ectopic mineralization in the heart, kidneys, stomach, and arteries.  This could be the result of ectopic endochondral ossification in those areas thus the possibility that FGFR1 inhibition could in fact help form new growth plates.  It’s possible though that the ectopic mineralization is as a result of dysregulation of phosphorus and calcium as suggested in the study.

Figure 3A, C, and E are from young growth plates whereas A, D, and F are from mature growth plates.

“Growth plate of mature control rat is inactive and sealed by layer of bone (arrow).”<-so FGFR1 inhibition could possibly “unseal” the bone.

I also found another study which likes FGFR3 to BMP Type 1 receptor which is highly significant as BMPR1A may play a role in growth plate formation.

FGFR3 induces degradation of BMP type I receptor to regulate skeletal development.

chondrocyte-specific deletion of BMP type I receptor a (Bmpr1a) rescued the bone overgrowth phenotype observed in Fgfr3 deficient mice by reducing chondrocyte differentiation{for our purposes Bone overgrowth is a good thing}. FGFR3 inhibited BMPR1a-mediated chondrogenic differentiation. FGFR3 hyper-activation resulted in impaired BMP signaling in chondrocytes of mouse growth plates. FGFR3 inhibited BMP-2- or constitutively activated BMPR1-induced phosphorylation of Smads through a mechanism independent of its tyrosine kinase activity. FGFR3 facilitate BMPR1a to degradation through Smurf1-mediated ubiquitination pathway. Down-regulation of BMP signaling by BMPR1 inhibitor dorsomorphin led to the retardation of chondrogenic differentiation, which mimicks the effect of FGF-2 on chondrocytes and BMP-2 treatment partially rescued the retarded growth of cultured bone rudiments from thanatophoric dysplasia type II mice.”

“BMP-2 significantly promoted the hypertrophic zone length of embryonic metatarsals, but not the mineralized and proliferation zone length”

“Double Bmpr1a and Bmpr1b null mice have a phenotype of increased expression of FGFR1 in chondrocytes”

Thus inducing BMPr1a expression in stem cells could possibly aide in inducing neo growth plate formation.——————————————–

Further Research – I did google the term and the following studies were listed and I did read over the abstracts of these studies

Study #1: Fibroblast growth factor receptor 3 effects on proliferation and telomerase activity in sheep growth plate chondrocytes

Personal Interpretation – Researchers are in agreement that FGFR3 causes chondrocytes in growth plates to decrease in proliferation. It causes the decrease through down-regulating TERT expression and reducing telomerase activity indicating an important role for telomerase in sustaining chondrocyte proliferative capacity during bone elongation. From the researchers “The present study addressed whether reduced FGFR3 expression enhanced telomerase activity, mRNA expression of telomerase reverse transcriptase (TERT) and RNA component of telomerase (TR), and chondrocyte proliferation, and whether the stimulation of FGFR3 by T3 evoked the opposite response.”

Study #2: Enhanced skeletal growth of sheep heterozygous for an inactivated fibroblast growth factor receptor 3

Personal Interpretation – It seems that when the FGFR3 is inhibited in sheep, the condition is known as spider lamb syndrome. It was shown that lamb that had it, whether homozygous or heterozygous did end up with longer limbs and were taller than their counterparts. It did take longer for the lamb to reach the same weight as the normal ones but they did end up bigger in terms of the size/volume of the bones.

Study #3: Constitutive activation of MEK1 in chondrocytes causes Stat1-independent achondroplasia-like dwarfism and rescues the Fgfr 3-deficient mouse phenotype

From The Study –  “the MAPK pathway inhibits hypertrophic differentiation of chondrocytes and negatively regulates bone growth without inhibiting chondrocyte proliferation. Expression of a constitutively active mutant of MEK1 in chondrocytes of Fgfr3-deficient mice inhibited skeletal overgrowth, strongly suggesting that regulation of bone growth by FGFR3 is mediated at least in part by the MAPK pathway…a model in which Fgfr3 signaling inhibits bone growth by inhibiting chondrocyte differentiation through the MAPK pathway and by inhibiting chondrocyte proliferation through Stat1…FGF receptor 3 (FGFR3) is expressed in proliferating and prehypertrophic chondrocytes in the epiphyseal growth plates.

Study #4: A Lys644Glu Substitution in Fibroblast Growth Factor Receptor 3 (FGFR3) Causes Dwarfism in Mice by Activation of STATs and Ink4 Cell Cycle Inhibitors

Personal Interpretation – The researchers used genetic engineering to add a mutation into the chondrocytes of the growth plate in lab rats. The mutation is the substitution of something known as Lys644Glu. The result is increased FGFR3 expression, leading to mice that showed signs of dwarfism and small skeletal size.

Link #1: FGFR3 is a physiological negative regulator of bone growth

Link #2: Molecular mechanisms of FGFR3 signaling in cartilage

Related Information

It seems that for a long time there was a lot of studies which showed that this receptor for FGF3 have been very involved in skeletal growth.

Tyler wrote about the fact that FGFR3 was another idea that we should explore in an old post from backin October of 2011 entitled “FGFR3“. The most interesting thing that he showed was that there was some project by the NIH for a way to treat the stunted growth of FGFR3 using a soluble form of FGFR3 entitled “DELIVERY OF SOLUBLE FGFR3 AS A TREATMENT FOR ACHONDROPLASIA. The author is Steve Ghivizzani, Ph.D. with the University of Florido, Department of Orthopaedics and Rehabilitation at the College of Medicine.

The grant proposal writer notes that achondroplasia is almost always caused by the excess expression of FGFR3. They propose this idea to remove the stunting of growth due to excess FGFR3. “we hypothesized that systemic delivery of a soluble FGFR3 molecule would likewise titrate receptor-specific FGF ligands and thereby reduce aberrant FGFR3 signaling to rescue bone growth….We will address the following Specific Aims: 

  1. To determine the capacity of FGFR3?TM to bind FGF-ligand and thereby inhibit aberrant FGFR3G374R signaling in growth plate chondrocytes from transgenic and knock-in models of achondroplasia.
  2. To determine the effects of long-term delivery of FGFR3?TM on the skeletal growth and physiology of the FGR3G374R knock-in achondroplasia model.

On a related note on the subject of FGR3…

I was combing through the threads of the Make Me Taller boards and there was a post that noted that FGFR3 and the inhibition of it was one of the only ideas ever pursued by a real company to try to increase growth and height in humans. From the thread Starting up a biotech research/investment companysomeone (Harald Oberlander) writes this part….

Worldwide there is currently very few research activity concerning new height increase / limb lengthening therapy options. 

Children: To the best of our knowledge there is currently only one company worldwide, that researches an innovative height increase therapy: ProChon Biotech (, established in  Israel in 1997. ProChon is developing a monoclonal antibody for the treatment of achondroplasia. This antibody approach targets specifially the FGFR3-gene and hasn´t reached the stage of human clinical trials yet. If it is successful, it will only work for children with achondroplasia.

The fact is that Harald specifically named the name of a company that has been doing research to figure out how to make children taller beyond the traditional GH therapy.

It is ProChon Biotech, and it was using the type of technology that Raja is proposing, which is to target/inhibit the FGFR3 gene.

I would go to the ProChon website and read up more about this company. It seems that the company was created to find ways to regrow or regenerate cartilage tissue. The focus was on tissue regenerative technologies to relieve pain in knees from regenerating articular cartilage. The product that was created by ProChon and sold was something called the BioCart™ Cartilage Regeneration System. The system was a technology created to heal articular cartilage defects through microfractures. It was eventually bought out through stock options in May of 2011 by the company Histogenics Corporation, which also was in the cartilage regeneration and repair field.

One of the members on the board I became very interested in reading more about in terms of the research and the paper they have written, a Dr. Avner Yayon. I would try to search any research papers he had written in PubMed by typing in his name Avner Yayon. His papers may help further the research and might give a clue which direction the research should be going towards.

Conclusion – This shows that for children with growth plates at least, the possibility of increasing height is very likely using this other method, by finding a way to inhibit this specific FGF.

Plasma Discharge Treatment for Height

This treatment could potentially increase chondrogenic differentiation.  However, it involves free radicals and too many free radicals can be harmful to height growth.  Too much ROS accumulation can lead to MSC senescence.

Skeletal cell differentiation is enhanced by atmospheric dielectric barrier discharge plasma treatment.

“This study investigated the potential of non-thermal atmospheric dielectric barrier discharge plasma (NT-plasma) to enhance chondrocyte and osteoblast proliferation and differentiation. [The mechanism by which] NT-plasma interacts with cells [involves ionizing the atmosphere] generating extracellular reactive oxygen and nitrogen species (ROS and RNS) and an electric field. Appropriate NT-plasma conditions were determined to evaluate DNA damage and mitochondrial integrity.  Specific NT-plasma conditions were required to prevent cell death{How could we manipulate this in the growth plate?}, and that loss of pre-osteoblastic cell viability was dependent on intracellular ROS and RNS production. To further investigate the involvement of intracellular ROS, fluorescent intracellular dyes Mitosox (superoxide) and dihydrorhodamine (peroxide) were used to assess onset and duration after NT-plasma treatment. Both intracellular superoxide and peroxide were found to increase immediately post NT-plasma treatment. These increases were sustained for one hour but returned to control levels by 24 hr. Using the same treatment conditions, osteogenic differentiation by NT-plasma was assessed and compared to peroxide or osteogenic media containing β-glycerolphosphate. Although both NT-plasma and peroxide induced differentiation-specific gene expression, neither was as effective as the osteogenic media. However, treatment of cells with NT-plasma after 24 hr in osteogenic or chondrogenic media significantly enhanced differentiation as compared to differentiation media alone. NT-plasma can selectively initiate and amplify ROS signaling to enhance differentiation, and suggest this technology could be used to enhance bone fusion and improve healing after skeletal injury{healing after skeletal injury often involves endochondral ossification which is the mechanism by which you become taller}.”

“The NT-plasma discharge is generated by applying a high voltage, time-varying waveform between a dielectric covered electrode and the biological target. To prevent high temperature build-up and transition to arc, high voltage current is alternated between the two electrodes, one of which is covered with a dielectric. Within the NT-plasma discharge, the molecules present in air (O2, N2, H2O, CO2, etc) are ionized resulting in the direct formation of numerous reactive oxygen species (ROS) and reactive nitrogen species (RNS)”

” NT-plasma exposure promoted endothelial cell proliferation, which was abrogated by fibroblast growth factor (FGF)-2 neutralizing antibody. Proliferation and FGF-2 release were blocked by N-acetyl-cysteine (NAC), which prevented changes in intracellular redox. Mechanistically, these studies directly link NT-plasma effects to ROS or RNS generation.”<-FGF2 is involved in height growth.  However, elevated levels of FGFR3 which is an FGF2 receptor decrease height growth. Maybe a mechanism of inhibiting FGFR3, such as an over the counter pharmaceutical supplement, would be a solution to using NT-plasma.

“he Map5kinase Apoptosis signal-regulating kinase 1 (ASK1), is particularly sensitive to ROS as its activity is tightly regulated by four ROS sensitive proteins thioredoxin, glutaredoxin, Akt and 14-3-3. ROS activated ASK1 phosphorylates and activates both p38 and jnk kinases, which play key roles in cellular differentiation”<-LSJL activates Akt as well.

NT-Plasma increased ROS levels by 25-50% for about 1 hour.

“the N1511 chondrocyte cell line was subjected to the same NT-plasma treatment in the presence of BMP2 (200 ng/ml), a known inducer of chondrocyte differentiation. 24 hr after treatment, chondrocyte differentiation markers Runx2, ALKP were increased 3–6-fold above BMP-treated controls. By 56 hr, collagen type X (Col X) and another late marker, matrix metalloprotease 13 (MMP13) were both increased 20 and 4-fold, respectively above BMP-treated control.”<-Given the upregulation of Col X and MMP-13 NT-Plasma seems to encourage enchondral ossification.  Perhaps it could do so for the articular cartilage and we could grow taller that way?

Within the stem cell pool, quiescence and pluripotency is maintained by the repression of ROS generation. As such, mouse and human embryonic stem cells have immature mitochondria, reduced expression of OXPHOS enzymes, low metabolic activity, low oxygen consumption, decreased levels of ATP production, express modest levels of antioxidant enzymes and have a high glycolytic flux”

“chondrocyte differentiation in response to NT-plasma may be directly linked to ROS induced expression of SOX-9 and Runx2”

“laser irradiation induced intracellular ROS production and enhanced SOX-9 expression leading to chondrocyte differentiation and expression of collagen and aggrecan“<-One laser irradiation study to impact longitudinal bone growth was discussed here.

NT-Plasma Treatment was not tested directly on Mesenchymal Stem Cells but still could be useful if other factors are in the right place.

CRISPR Technique with Cas9 Enzyme To Alter Hereditary Traits Easily

CRISPR Technique with Cas9 Enzyme To Alter Hereditary Traits Easily

CRISPR Technique with Cas9 EnzymeNote: The original paper is found in the UK based magazine website for the Independent entitled “CRISPR gene therapy: Scientists call for more public debate around breakthrough technique

The technology to alter the human race is almost here and the newest technique in genetic engineering that is making waves is something known as the CRISPR Technique. The quotes says that it can “…be used to rewrite genetic defects to effectively cure diseases in mice and human stem cells”. It is able to correct the mutations in cells which lead to diseases. The acronym stands for “Clustered Regularly Interspaced Short Palindromic Repeats“. It is a type of RNA sequence that have traditionally only been in bacteria types but the genetic researchers have been able to take that unique genetic sequence and used it in the cells of other organisms with cells which might be more complex like mice and humans.

The sequence is a type of immune function and works as a guide. The enzyme/protein it guides is something known as the Cas9 protein to a very specific, target area in the DNA. Apparently this enzyme called Cas9 has the ability to “…cut the double strand, nick it, or even knock down gene expression“. Once the target DNA area had been cut or changed in some way by Cas9, then the double strand area can either be repaired or have a DNA segment inserted into the spacing. A group of Chinese researchers at the Shanghai Institute for Biological Sciences were able to use the CRISPR method to get the Cas9 to the right mutated allele and make a cut/cleavage. New alleles that were correct were added when the repairing process began. The method was tested on mice with hereditary mutation of cataracts and a large percentage of the zygotes that had the technique employed developed into baby mice without the cataracts. Another group tried it on the mutation causing cystic fibrosis. The overall opinion at this stage is that compared to other ways to cut, edit, and paste parts of the DNA around, this method compared with other gene editing techniques, it was straightforward.

One of the chinese researchers went on to even claim the following “…I think CRISPR/Cas9 system may be the easiest strategy to cure genetic disease than any other available gene-editing techniques,” – For more information we suggest looking at least over the abstract for the article “Cas9 as a versatile tool for engineering biology

Multiple high profile researchers have commented that it has the potential to “…revolutionise human gene therapy and genetic engineering”. The first group of people to get the process to even work was Professor George Church of Harvard. He is the director of the open access platform for people to share the data in their genomes known as the Personal Genome Project started back in 2005.

However, it was Jennifer Doudna & colleagues from Berkeley (at the Doudna Lab) in recent years were the first group of people to show that the technique can be effective in application on genetic engineering. It has worked on human cells and lab mice embryos.

It is noted that it might be maybe 1-2 decades before the technique can be implemented on IVF embryos (In Vitro Fertilization).


The following picture above was taken from the Next Big Future website.

So how would the method work?

Remember that there are three different types of RNA in the human cells. Besides the sex cells or gametes in humans, which would be the sperm and eggs, as well as the red blood cells which have no nucleus, every single cell that is in the human body has a nucleus with the necessary 23 pairs of chromosomes. The chromosomes are shaped either like an X or Y. they are actually just winded up chromatin loops which are winded up some more.

Within the chromatin are where the actual double strands of DNA wind around histones, creating something known as a nucleosome, which is further wrapped into solenoid shaped parts.

We are talking about it at the level of the actual double strands. The method guides a type of RNA sequence with the Cas9 to the exact area of the DNA with the genetic mutation. The Cas9 can come in, and cut the area of the mutation away. The double strand can then either just repair itself or an extra DNA segment is popped into the space that was created from the cleavage.

So how does this affect us, people who wish to become taller?

One of the main things I have always said is that even after all the research is done and every single possibility checked, we might reach the conclusion that there is nothing we can do for adult height increase that does not involve some type of invasive surgery. At this point, I would actually be willing to suggest that their is no alternative to the surgery method.

What I am willing to propose from the research being done is a faster, cheaper, less painful way to break the long bones (aka distraction) to height increase surgery. I am willing to make some type of compromise if the science has been completely exhausted and their is no clever way to elongate bones without using some type of chisel and hammer to at least cause the first break in bones.

If however, the readers of this website still refuse the method, then there is nothing we can do. The only option at that point is to hopefully find a way to help our children and offspring, the people who will carry out genetic lineage become taller. I will not be too selfish and hope that I would become taller as a adult. It if doesn’t work, that is okay as long as the research continues and I find a way to serve humanity. It would make more evolutionary sense to do everything in my power to help my future offspring to have the genetic advantage of extra height.

The most obvious area of our current modern lives where adult human height still means a lot is in the dating world. It might not mean a lot to women, but for men it means a lot. When young women in their 20s are asked directly at face value why they seems to always gravitate towards taller men no matter what the situation, the answer after some serious probing into their psyche and deep motives reveal that they just wish to produce offspring that are taller than they were. Maybe due to some warped low sense of self for being short themselves, they felt a need to overcompensate for their genetic “hindrances” by looking for a “genetically healthy” male. Obviously height is the easiest indicator of genetic fitness in human males and that is the measuring stick females of almost all human cultures have used to judge the worthiness of men at some level or another.

If we remember basic gene therapy information, there is two different ways that gene therapy can work. You have the 1) somatic gene therapy, and 2) the germ line gene therapy.

Whereas the somatic gene therapy would only have some type of medical benefit for the person, germ line gene therapy, which the CRISPR technique does, will mean the entire rest of the generations to come will have their hereditary trait.

If this new genetic technique is proven to work, that argument that females have been making since the beginning of human history over their biological/reptilian brain egocentric validation for their choice in taller men about worrying over having smaller offspring will no longer be valid. If we as genetic engineers can go into the human IVF embryo, using the CRISPR method, and alter the 5-6 most influential genes that affect human height, then our offspring will be able to grow upwards of maybe 4-5 inches taller than without the gene alternation. Obviously it has been shown in multiple genome-wide association studies (GWASs) meta-studies of the SNPs/genes that have some effect on human height that there is supposed to be around 200-500 or so genes that have some effect. We just need to target the top 5-6. Remember pareto’s principle and how uneven distributions work in nature.

In previous articles that I (and Tyler) have written about the exact genes in the genome which have a higher than average effect on the overall adult human height, we found elements like HMGA2 (source) (source 2), FGFR3, and GDF5 have a huge effect on human height from the way they regulate the rate of endochondral ossification and how fast the epiphyseal plates mature. Take a look at the study “A common variant of HMGA2 is associated with adult and childhood height in the general population

Of course in recently years at least 2 dozen new genes also seem to have some effect, but at a smaller degree. (source) Take a look at the study “Genome-wide association analysis identifies 20 loci that influence adult height

The other approach is to actually induce a type of slight matution into an average embryo with normal traits to give their abnormal body abilities. We learned from studying the genetics of families who have had the pituitary gigantism causing condition that the AIP gene (Aryl hydrocarbon receptor-interacting protein) has a slight mutation. (source) That is just one gene that has been mutated, and the result is familial genetic change where multiple members of the family become tall individuals. Why not use the CRISPR method to change the AIP gene? – For more information we suggest reading the article AIP-Related Familial Isolated Pituitary Adenomas”


Mamadou N’Diaye – Two Different Basketball Playing Sengalese 7 Feet Tall Men and One Footballer

Yesterday while I was looking over basketball related topic I came across an article entitled The Highest-Paid African Players in NBA History and I realized that there was a case of mistaken identity. There was a total of 10 different people listed who were from Africa over the years who have become very successful playing in the NBA. They are…

  1. Mamadou N’Diaye – Country: Senegal – Height: 7′ 0″ – Years in NBA: 2000-2005
  2. Manute Bol – Country: South Sudan – Height: 7′ 7″ – Years in NBA: 1985-1995
  3. Bismack Biyombo – Country: Democratic Republic of Congo – Height: 6′ 8.5″ – Years in NBA: 2012
  4. Luc Mbah a Moute – Country: Cameroon – Height: 6′ 8″ – Years in NBA: 2008 –
  5. Hasheem Thabeet – Country: Tanzania – Height: 7′ 1.5″ – Years in NBA: 2009 –
  6. Michael Olowokandi – Country: Nigeria – Height: 7′ 0″ – Years in NBA: 1999 – 2007
  7. DeSagana Diop – Country: Senegal – Height: 7′ 0″ – Years in NBA: 2001 – 2013
  8. Luol Deng – Country: South Sudan – Height: 6′ 7″ – Years in NBA:
  9. Hakeem Olajuwon – Country: Nigeria: Height: 6′ 10″ – 6′ 11″ – Years in NBA:
  10. Dikembe Mutombo – Country: Democratic Republic of Congo – Height: 7′ 1.5″ – 7′ 2″ – Years in NBA:

We realize that some of the information has not been added like what years were the players playing in the NBA. However, what I wanted to raise awareness for today is that there was a mistake made on that website, and it shows that there has been a case of mistaken identity. Of course there is a good reason why any journalist might make this easy to make mistake.

There are THREE different people named Mamadou N’Diaye (That is relatively well known)

The picture shown on the website is of the younger one while the player that was profiled was of the older one.  I have since given an email to the writer, a Mr. Nitin Bhandari to tell him the wrong picture was used. It is a small thing, but as a person who tabulates and collects data on very tall people and basketball players it is something that I wanted to point out.

So let’s do a complete comparison of the three (currently) people named Mamadou N’Diaye, all of whom are from Senegal.

Mamadou N’Diaye #1

From the Wikipedia article on him we find out the following information…

  • Born on June 16, 1975 (so currently around 38 years old)
  • He played in college basketball at Auburn
  • He was drafted by the Denver Nuggets back in 2000 in the 1st round as the 26th pick
  • He played for 10 years from 2000-2010
  • He was a part of the following teams –
  • Toronto Raptors
  • Dallas Mavericks
  • Atlanta Hawks
  • Los Angeles Clippers
  • Currently: Assistant men’s basketball coach at Coastal Carolina University for the 2013-2014 season
  • Other sources include the NBA Scouting Report and HoopsHype

mamadou n'diaye

Mamadou N’Diaye

Mamadou N’Diaye #2

Mamadou-Ndiaye 5This is the kid that is probably going to get the most coverage in recent years. What makes him standout is his insane height, which most people are citing to be 7′ 5″. That would make him one of the tallest college basketball players in the entire country. His name has also been spelled as Mamadou Ndiaye. He was at least 18 years old as a High School Junior back in Jan of 2012. That would make him about 19-20 currently. His shoe size is 19½.

Back in Jan of 2012 it was reported that the teenager was just a high school junior. He got VISA to stay in the USA from Simi Valley Stoneridge Prep (based in California). He arrived in the US back in 2010. After he did a physical, it was found out that he has an a tumor on his pituitary gland causing excess GH release into his system. The MRI done on his brain revealed a golfball-sized tumor on Ndiaye’s pituitary gland. The tumor was pressing up against Ndiaye’s optic nerve.

Mamadou N'Diaye HeightA lot of people are saying that this kid is going to be a player in the NBA but we here feel that the chances are extremely small.

Many pituitary giants who were young and playing in some D Level small college were written up by people who believed that they would become basketball legends. It is true that any young 7 footer who is playing basketball usually is written in the press as the next Kobe or Lebron like Thon Maker but the expectation is almost always too high for the young kids to live up to.

Not one has achieved that yet. Examples include…

  • The Chinese Sun Ming Ming
  • The UNC Asheville Kenny George
  • Satnam Singh Bhamara

The only exception we know is for Romanian Gheorghe Dumitru Mureșan who did have only a below average NBA Career.

As for who is really the tallest college player disputes, we realize that former Gonzaga Center Will Foster was also supposed to be 7′ 5″ although he might be closer to 7′ 4″ based on some websites and sources. There is also UK Paul Sturgess which seems to have moved on the the Harlem Globetrotters.

Mamadou N’Diaye #3

We only found out about this player also named Mamadou after looking on Wikipedia. It seems that currently he is a footballer aka soccer player playing for a team based in Portugal.