Author Archives: Senior Researcher

Electromagnetic Stimuli and Resonance Frequency Vibrations For Tissue Transdifferentiation

Electromagnetic Stimuli and Resonance Frequency Vibrations For Tissue Transdifferentiation

Tissue TransdifferentiationI was recently listening to this episode where a person went on the radio to talk about how the late Nikola Tesla proclaimed that most of the universe’s hidden secrets can be found if a person would approach his analysis through the lens of looking at the world from a perspective of it being electromagnetic stimuli, energy, frequencies, and vibrations. The most famous quote to this claim was “If you want to find the secrets of the universe, think in terms of energy, frequency and vibration” – Nikola Tesla.

When I think back to this claim, I feel that there is probably more and more evidence that the proclamation is right. I remember back during my undergraduate days studying the higher level of classical mechanics. Beyond say the introductory physics course where we are asked to solve for different variables using the ideas of forces and momentums, it is possible to be much more mathematically elegant to solve the same problems using the principle of just energy alone.

For example, the Lagrangian formulation/interpretation of solving the problems of classical mechanics can be done on the principle of finding the path for the state or motion of least action. At the core of this entirely new approach on calculating say the motion of movement of a system being studied is the Langrangian Function which is really just the sum of the kinetic energy and the potential energy, either from a set initial point to an end point, or a set initial time point to a end time point. The function is L=T+V. The letter T represents the total kinetic energy of the system and the letter V represents the total potential energy of the system. What you get eventually is a large 2nd order differential equation you have to simply and solve for the value you are looking for. We obviously are not going to get into the mathematics of any physics in this post, but just explain the principles using words.

In addition, here is something known as the action of the system (S), which is defined in words to be “The summation of the Langragian function over time from an initial time point to an end time point” aka calculus integral function. The goal when you are solving a system is to figure out which path or state of the system would minimize that S.

One of the main reasons why this way of calculating motions, states, and other variables of the system is that by using just the principle of energy (Kinetic plus Potential) we don’t have to worry about the transition from one cartesian coordinate system into another. Remember that the original Newtonian way to calculate forces and motion required that you use the concept of vectors, which had a standard 3 parts to it. With this way, you can calculate out a single value with a single numerical value or symbol instead of having it in 3 parts.  For more information on what the hell I am talking about Click Here.

Getting back to the Main Point…

Beyond just giving a short explanation on physics, what I am hoping to show the reader is that the principle of energy can often be used to explain away phenomena as well as be used as a tool to solve problems which might be too hard in another approach.

In the same way, we can use the idea of waves, vibrations, frequency, and vibrations to explain certain phenomena that say using the traditional approach. Remember what happened in the Double Slit Experiment. A light source was shined through some type of solid pain with two parallel slits. You are looking at the wall or the surface behind the pane and if you see interference then the phenomena that is first reaches the pane has characteristics of a wave. The ramifications of the experiment showed that wave phenomena has properties of both wave and particles. This implied that particles (at least the very small ones) have characteristics of waves as well. Since we are using principles of frequency, wavelength, etc. to describe what could be considered another area of physics, we could use intuitive reasoning to extrapolate this idea that all phenomena could be explained using a waves and vibrations view of the dynamics of the universe. If that is the case, then maybe we could use waves and vibration stimuli to solve many engineering problems as well as medical problems.

What I am overall trying to get at is that maybe the simplest way to induce a statistically impossible biological process to happen, all we need to do is figure out what is the optimum level of energy or frequency, what is the right type of energy or stimuli to use, and what location we need to use it on.

When I look back at all of the ideas I have proposed over the last two years on how we might be able to get bones to grow again, I have gone through almost every single idea. Here is a list of most the types of stimuli I have looked into.

In my most recent seminal post about using a combination of silver acupuncture needles as a form of electrode to transmit a very small intensity level of Direct Current to stimulate cartilage and the periosteum to increase their size, I had used over a dozen old studies and citations of experiments done by researchers from back in the 80s to validate the concept. The PEMF technology I described would work with around 95% confidence in over its efficacy.

That post was “Electromagnetic Stimuli Will Increase Ossification and Make Bones Longer, Big Breakthrough!“

Function GeneratorI had previous showed that it might be possible to induce the bones to increase the rate of endochondral ossification with something as simple as a Function Generator or even a TENS Unit which often cost less than $100.

Take a look at the older post “Do We Use A TENS Electronic Pulse Massager or A Function Generator?“

At this point I have no clue what could be the biomolecular reason why sending something as simple as a pulsed electrical signal at a signal could induce human tissue of all varieties to have some type of effect. If we actually think about it, it should make perfect sense. Just think about what actually makes the human brain (or any brain) work anyway. The fundamental unit of the nervous system is the neuron, a nerve cell. (Sure you have stuff like the Ganglia but that is not the point.) The whole point of the neuron is to have the dendrites on the neuron cell body to integrate (add up over the surface) all of the biochemical signal into a type of voltage potential. When all the built up potential reached in the neuron to a certain threshold, an electrical current is fired from the cell down the axon, to the tips, which are close to the dendrites of other neurons.

The same can be said for the human heart. If we remember our introductory CPR class, the whole reason for pushing in a rhythmic fashion on the chest is to get the heart to beat again, so that the heart can act as a type of biological pump to push the blood through the vessels around the entire body to feed the tissues who always need ATP. When the Paramedics (or EMT) first gets to a body of a person who is not responding and/or unconscious, they check to see if they are breathing and has a pulse. The indication of a pulse, means that the heart in the person’s body is at least doing its job of pumping the blood, nutrients, minerals, and oxygen around to sustain the cells and tissues. If the heart stops, there is no pulse.

ElectrocardiographyThe heart operates actually on a very clear rhythm of electrical signal. For the people who have ever had an ECG (Electrocardiography) done, they have probably been told that what is being measured is the electrical signal that is coming from the heart beating. If there is some type of irregularity in the heartbeats, this is known as arrhythmia. To correct for it most people get some type of internal Implantable Cardioverter Defibrillator. If however the person is already on the ground, most emergency rescue personnel with some type of advanced life support (ALS) or basic life support training (BLS) will use some type of portable external defibrillators to reset the rhythm of the heart beating. What we are trying to say is that at the most basic level, our most important internal organs, the brain and heart, both operate on electrical current.

In one of my most recent posts Tyler said that what I was proposing, the changing of the bone tissue into cartilage tissue would be cell transdifferentiation. I countered to point out that if we are trying to regenerate epiphyseal growth plate cartilage tissue from bone tissue, it would not be enough. Even if we could do the transdifferentiation step, we still have to figure out what to do about the other biological, molecular, organic, and nonorganic material in the extracellular matrix of the bone. We might not need to worry about some organic and biological compounds like the collagen and proteins but we do have to worry about the inorganic compounds and minerals. The most common problem would be the Calcium Hydroxyapatite crystals which is the mineral that is causing the bones to become so strong and have such a high level of compression strength.

There are two things we have to induce.

  1. Changing the terminally differentiated osteoblasts and osteoclasts into chondrocytes
  2. Removing the minerals and inorganic compounds in the bone composition that causes the defining characteristic and properties of bone tissue.

However, it would probably be much easier to do the 2nd process. We have already shown in previous posts that using something as simple as Vinegar (Ascetic Acid) covering bone would be enough to chelate the hard minerals. This is known as bone decalcification. The hard part would be the first part.

How do we turn one type of cell into another?

The basic idea proposed by Dr. Robert Becker from his book (which I am still reading) shows that besides say the red blood cells which have no nucleus and the gametes which have just have the number of chromosomes, most cells in the human body does have dormant genes which are no longer turned on beyond a certain stage in prenatal development of child growth. How and why those genes are not turned on has not been figured out yet. What this suggest to some of us hopefuls is that idea that maybe using some type of stimuli, which I propose in this post to be electromagnetic or vibrational wave in nature, targeted in the right way could reactivate those genes again. If the same gene or microRNA in enough cells are activated, it might mean that we can get transdifferentiation to work and get one cell to possibility turn of the trigger causing them to become bone cells and turn on the one causing them to directly turn into cartilage cells aka chondrocytes.

I suspect that we might be able to use pulsing electrical stimuli or some type of ultrasonic high frequency, low intensity waves to stimulate the cells to go through transdifferentiation in an non-invasive approach similar to how using the MR Guided Focused Ultrasound Surgery works.

The Correlation Between Male Adult Height and Nasal Width and Ear Size

The Correlation Between Male Adult Height and Nasal Width and Ear Size

Ear SizeWhat I wanted to propose in this post is a hypothetical correlation which is from a lifetime of observation. I personally believe that there is a positive correlation between the width of the adult male and their ear size and their overall adult height.

I would suspect that if we were a primatologist and did a measurement of the nose widths of each male gorilla’s nose in a pack in the jungles of Eastern Africa, we would find that the alpha male who would have more testosterone would have on average a slightly wider nose and/or larger ears than the beta males which traditionally have thinner noses and smaller ears.

Of course it is easy to dismiss this by some people as common sense. Alpha males in gorilla packs tend to be bigger and taller than the beta males. That is from a slightly higher level of testosterone than the average level. Just from a proportionally of body parts perspectively, it would make sense that alpha male would thus have larger noses (as well as larger jaws, crane sizes, hands, etc)

However, I wanted to take the hypothesis and use it to as a sort of heuristic trick to help people determine which pre-pubescent young males still in elementary school before the growth spurt/puberty phase is most likely to get the largest growth spurts and end up the tallest.

If you measured the widths of each boy’s nose and the width of their ears and averaged out the boys of one class, it can be used to tell which males would end up taller than their peers as adults when their schooling is over

The same can be said about the ears. I propose the hypothesis that if we looked at the width of a young male’s ears compared to their male peers before they start puberty, we would have an accurate chance in predicting which boys would end up taller than the others.

We have found from at least 3 sources, including PubMed studies that the ears and noses actually never stop growing throughout a person’s life. It is said that over a 50 year span (after the normal growth phase has ended through complete bone maturity) a person will have their ears grow 1 cm overall.

In one of the references we have listed, it was claimed that because the ears and nose are cartilage, which never harden, they have the ability to expand. Unfortunately they are not hyaline cartilage, but fibrocartilage. Fibrocartilage is one of 3 different types of cartilages found in the human body. It does not have the orderly laminar layer hyaline cartilage structure so it doesn’t expand in some type of specific direction like the way the long bones growth during the normal endochondral ossification process. The fibrocartilage does grow and expand as the collagen in the extracellular matrix expands but it is very slowly.

So how does the fact that our ears and nose can still grow into old age (our 60s-70s) help us?

It shows that as long as there is some cartilage tissue, there is some chances for the cartilage to expand, even if the cartilage is fibrocartilage. Since the bones for most adults past normal growth phases (ei 20-50) still have a layer of articular cartilage, which is hyaline cartilage, then we can theoretically stimulate whatever cartilage we have left in the joints between our bones to increase slightly in size.

If our noses and ears can grow bigger, then we can make our bodies get bigger vertically if we can get the cartilage to increase in thickness in certain directions.

Again, I suspect that one can measure how tall a young boy will be relative to his male peers by comparing the width of their ears and noses before they hit puberty.

Update #10 – Thinking Of The Big Picture – January 1, 2014

Update #10 – Thinking Of The Big Picture – January 1, 2014

The Big PictureIt has been almost a year and a half since I first began documenting all of the information and ideas I have accumulated in this journey. There have been many things I have learned. This post that will be starting the year 2014 will be some of my thoughts on where this website will be heading. I am thinking of the big picture.

The posts we have been posting for the last few months have been getting more coverage and more and more people are coming to the website. Along with the comments have been a few people who have made some critical comments which we do indeed have to take into consideration.

Issue #1: All this writing about theory and medical facts don’t seem to go anywhere. The people want some real action steps they can do to get results.

Issue #2: We have ideas for people who have growth plates but non for people without them

Issue #3: The ideas we propose needs to be tested and have real people try them out.

Of course, I understand that these are the only two possible critical issues anyone would have with this website. This website’s main goal is to help people increase their height. We have not achieved that to any extent. There has been a lot of medical research in the form of reading study after study but nothing actively done. I am not willing to apologize for whatever action I have not been taking. This endeavor is not going to be something I can accomplish in a year, or even a few years.

In one of the most seminal posts I wrote about why it is so difficult to achieve what we are hoping to achieve, I had stated that the simplest, most logical route to take is to figure out how to convert the bone tissue of our long bones into hyaline cartilage

{Well, that would be what’s known as transdifferentiation.  I think it would be easier to induce mesenchymal stem cells into growth plate chondrocytes.  The pre-chondrogenic cells in the Zone of Ranvier are the cells that are used for growth plates.  Create a microenvironment that makes stem cells more like these zone of Raniver cells. Cells in the Zone of Ranvier are positive for BMPR1a.  So BMPR1a could be key for this.-Tyler}. That is unknown.

In Response To Tyler: I don’t think transdifferentiation is the way, since not even the real researchers with the best equipment have figured that out. There have been only a few cases showing that fibroblasts can be some type of proxy connecting the osteoblasts to the chondrocytes through reversing the natural biochemical processes/de-differentiation. What I suggest is first removing the calcium crystals from a small band of the bone that is causing the bone hardness. Calcification is the problem in my opinion. Decalcifying the crystals inside the extracellular matrix of the bones leaves just the collagen.

Look guys, I’ll just make this post update much shorter. A lot of the recent comments have been complaints that we have too much theory on this website and not enough actionable steps people can take. The other major complaint is that there is no proof that this stuff works.

That is all true. However, that is the nature of this endeavor. From a biologically perspective, there is probably nothing harder than what we are trying to do, save for finding a cure for cancer or reversing the aging process. We are doing the best we can, with the resources we do have.

However realize that we are probably the only hope you guys have. The guys who was doing serious research on GrowTallForum.com got far with the research, which took them years but they didn’t get anything and the website was brought down.

Unless one of you guys is willing to take up the mantle, and put skin into the game, then stop making all the critical points because we understand perfectly well the limits of what we can do. We all have lives, and other obligations. Me and whoever posts here have our own lives. We have no obligation to help anyone, but we choose to put our time and effort into it.

To put years and years of effort into doing the research, going through the history, figuring out how to create a website, and doing regular updates, as well as bringing all of the important information into one central website, as well as find all of the books out there provided free of charge, at the risk of civil law suits and DMSAs, we hope people realize that we are doing what we can. Back off and let us do the research our way.

I will give a time line on how fast this thing might take. This endeavor will probably take at least 10 years, but I would put the time closer to 15-20 years. I am in the game for the long term.

Height Progression

For the last 3 months I have not been able to get an accurate measurement of my height because my hair had grown too long. There was too much deviations of the measurements from each other.

The thing that has changed however has been my supplementation, which has been a daily intake of 1000 mg of Glucosamine Sulfate to see if there would be any changes.

Here is the good news. The intake of Glucosamine at 1000 mg has resulted in a decreased loss of height over the day time. Where before I would drop from almost 183 cm (around 182.8 cm) right out of bed to less than 181 cm at night, the measurement I am noticing at night has been around 181 cm at night. What this shows is that the glucosamine has been able to reduce the effects of gravity on the overall bone structure at a minimal level. The reduction of lost height has been around 2 mm.

This was only visible just yesterday after I went to get my head shaved. The decrease in the height of the hair let me compare notes of my height from 3 months ago, which was the last time my height was measured at a consistent level. As for any increases in height, I have noticed a very small increase in height for the measurement after waking up in bed. So as for the supplementation, it does have some effect.

In addition, my joints feel better. Where I used to feel pain in my left knee from an old injury from college sports, the pain has almost disappears. I guess that claim about the effects of Chondroitin and/or Glucosamine is sort of accurate.

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 LimbLengtheningForum.com

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: http://tpx.sagepub.com/content/33/4/449.abstract. 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 company” someone (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 (http://www.prochon.com), 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.