Monthly Archives: March 2014

Breakthrough: Another study shows mechanical loads can alter height growth

Previously, I wrote another study about how mechanical loading can shape and alter joint and growth plate development.

If mechanical loading can alter limb development, then not only can mechanical loading regimes be used to increase height during development but also possible after growth plate fusion by creating new growth plates. In fact one of the genes associated with the pre-growth plate cells in the zone of Ranvier is the mechanically sensitive to activation CMF608.

Mechanoadaptation of developing limbs: shaking a leg.

“The developing skeleton experiences mechanical loading as a result of embryonic muscle contraction. Embryos [may] coordinate the appearance of skeletal design with their expanding range of movements. Embryo movement [has a large role] in normal skeletal development; stage-specific in ovo immobilisation of embryonic chicks results in joint contractures and a reduction in longitudinal bone growth in the limbs. Epigenetic mechanisms allow for selective activation of genes in response to environmental signals, resulting in the production of phenotypic complexity in morphogenesis; mechanical loading of bone during movement appears to be one such signal. It may be that ‘mechanosensitive’ genes under regulation of mechanical input adjust proportionality along the bone’s proximo-distal axis, introducing a level of phenotypic plasticity{in other words it’s possible to alter how tall you will grow via mechanical factors}. If this hypothesis is upheld, species with more elongated distal limb elements will have a greater dependence on mechanical input for the differences in their growth, and mechanosensitive bone growth in the embryo may have evolved as an additional source of phenotypic diversity during skeletal development.”

“Cell movement-generated forces influence condensation of cartilage elements in developing limbs. There is also evidence that fundamental processes, including growth, differentiation, death and directional motility of cells, are likely guided by forces exerted by the cell cytoskeleton. This conforms with ‘tensegrity’ principles, with differential growth patterns producing local extracellular matrix distortion and the generation of tension in the cytoskeleton of associated cells.”<-LSJL would induce local extracellular matrix distortion and generate tension in the cytoskeleton of cells.

“dynamic loading in adult bones produces extracellular fluid flow within the bone’s lacunar-cannalicular system, which is detected by osteocytes”<-The idea is that LSJL goes further to induce MSCs to differentiate into growth plate plate chondrocytes.

“Embryonic muscle contraction appears to be necessary for the formation of bone ridges, which act as anchoring points for muscle attachment and are therefore important in the transduction of muscle-induced loading via tendons to the skeleton.”

“immobilisation of embryonic chicks alters cellular organisation of the interzone and results in changes in shape of the distal femur and proximal epiphysis of the tibiotarsus and fibula. After cavitation occurs, maintenance of joint cavities is also dependent on mechanical input. Post-cavitation induction of flaccid paralysis with pancuronium bromide, a non-depolarising neuromuscular blocker, also leads to loss of the joint cavities. Rigid paralysis induced with DMB, a depolarising neuromuscular blocking agent, causes muscle contraction and has been shown to partially maintain joint cavities “<-But there is there just a threshold of mechanical loading that is needed for proper development or can we enhance this development with enhanced mechanical loading.

“Detailed ‘targeting’ of specific temporal windows during development indicates that the effects of in ovo paralysis on bone length become significant at approximately E13 of development. This indicates that embryo bone growth is initially not sensitive to mechanical stimulus, but that mechanosensitivity is acquired later during development. This suggests that intrinsically regulated initial limb growth ‘switches’ later to regulation dominated by extrinsic factors such as mechanical signals. It remains to be determined whether this immobilisation-related skeletal growth retardation is due to deficient chondrocyte proliferation, differentiation, matrix synthesis or hypertrophy or due to insufficient replacement of calcified cartilage by bone during the endochondral ossification process. It has been suggested that mechanical loading regulates the elongation of chondrocyte columns during zebrafish craniofacial development”

“evidence for mechanosensitivity in skeletal development is provided by observations of increased limb bone length when the level of embryo motility is increased in chicks. Incubation temperature increases embryo movement, with a 1 °C increase in incubation temperature producing a significant increase in embryo motility. This is associated with an increase in the number of myonuclei in embryo limb muscles and increased limb element lengths“<-Now this is the kind of fact we’re looking for. So people can make their kids taller but what about us. But we’d have to find the equilibrium temperature.

“This increase in limb length with temperature did not become significant until E12.5, providing further evidence that mechanosensitivity in skeletal element growth is acquired at a relatively late stage of development. Treatment with 4-aminopyridine (4-AP), a drug which stimulates the release of acetylcholine, thereby increasing its availability at the synaptic cleft and resulting in skeletal muscle hyperactivity, also stimulates embryo movement. Increases in tibia and femur lengths have been reported in chick embryos treated with 4-AP at E15 and E16, but not E14 ”

” The expression of IHH and hypertrophic markers such as MMP13 have been shown to be regulated in chondrocytes in vitro by cyclic mechanical stress”<-Although these genes wouldn’t be able to form new growth plates except possible IHH. Mesenchymal Stem Cells transfected by IHH were induced to become chondrocytes in one study.

“In ovo immobilisation has been shown to alter expression patterns of COL X and IHH in embryonic limbs, suggesting that these genes are involved in linking mechanical stimuli from embryonic muscle contraction with regulation of bone formation in the limbs”

Unfortunately, this study only shows examples where longitudinal bone growth was altered in a very small window during embryonic development. But increases the amount of evidence provided that mechanical loading can alter longitudinal bone growth which will eventually lead to prove that a specific mechanical loading regime such as that of LSJL may induce mesenchymal stem cells to become growth plate chondrocyte pre-cursors and form micro-growth plates.

Why LSJL Could Work And What We Have Been Doing Wrong, Thank You Nixa Zizu – Big Breakthrough!

Just today a follower of the website who calls himself Nixa Zizu (who is one of our biggest supporters and contributors) uploaded information to the Natural Height Growth Facebook page which might have really cracked open the case on why it seems that LSJL might not be working so most of the people who have been doing it.

His results after just 2 weeks of doing the technique have resulted in almost half a centimeter of height gain. In my personal experience in getting accurate readings on height from using just rulers and stadiometers suggest that it is a large difference, which is unlikely due to just the normal diurnal variations we usually use as a reason to explain any differences in measured height.

The Message is below…

Nikola is sort of a famous Serbian YouTube celebrity that has a Serbo-Croatian audience. He has been in contact with us and promised me that he would start doing the LSJL routine consistently to see if he could get any real noticeable, results. (Click Here to Subscribe to his YouTube Channel Nixa Zizu)

Now that he has stated that he increased his height by 4 mm by doing what is known as Angular LSJL, it gives us a 2nd data point to work with.

Humans are creatures who have brains designed to notice any type of pattern, to make order and sense of the trillions of sensory input that reaches the brain every single moment. I am making a note that I see a pattern from just two data points, where both of the people have said that we need to actually correct (slightly adjust) the way we have been doing LSJL.

Nixa’s claim is just 1 of those data points. The other data point comes from the LSJL Forum in the thread “LSJL works… If Done This Way“. The post of the thread calling himself gr0wthnut claims to have gained 1.5 inches in height.

Whoever this gr0wthnut is, he also made the point that the location we are supposed to clamp down on is not exactly correct. I also suspect that the poster on the forums named Nixalsjl which exchanged a round of posts with gr0wthnut is Nicola of YouTube fame and he took the advice he got from Gr0wthnut and actually applied it in his own slightly modified LSJL routine. I am personally proud of this fact since we are now making real improvements on the original idea, which has not been improved upon for almost 5 years now.

You can see his video below…

This is the other 2nd data point. We can make a trend line using just 2 data points and jump maybe too quickly to seeing some type of pattern (which might not even be there). What would be nice is to get a 3rd or even 4th case of someone who noticed height gains after doing this modified approach.

So what did we learn and what do we take away from reading this post?

It seems that we have been wrong about the location about where to load/clamp. The standard theory that you clamp laterally on the side protruding bony part of the epiphysis may not be the best place. It is actually in the bony sloping/slanted bone area just below the epiphysis. This is the location on where gr0thnut and Nixalsjl are referring to.

I always had personal reservations against the method since it made no sense from a biological perspective how clamping laterally would make bone grow longitudinally in the axial direction. I’ve written almost half a dozen posts over the last 2 years going back and forth trying both to 1. prove or 2. disprove this idea that Tyler has been trying to prove for more than half a decade now. One of my first round of questions to him was over the idea on how the hell does induced chondrocytes from the MSCs manage to push outwards in all 5 directions (the 6th direction would be just pushing inwards) against the wall of the epiphysis made of cortical bone to make the epiphysis larger in volume.

I have never been able to fully swallow the idea of LSJL completely since it makes no sense from a materials or mechanical point of view. No matter how I try to wrap my head around it, it just makes no sense to me on an intuitive level (It just doesn’t seem right) , even after multiple times Tyler tried to clarify to me how the molecular mechanism would work. The bones are not thin and malleable like a balloon which would just puff up from a slight bit of pressure in some region. They are harder than stainless steel if you apply a load in the right direction.

However, this angular idea makes more sense.

While most scientific analysis requires a lot of lab experiments, mathematics and physics knowledge to comprehend what could happen if we change one variable in the system, to figure out how bones would react to say a clamp pressing down on them requires just intuition on how large objects work. You can use intuition to make many arguments.

Let’s look that the types of loading that has been traditionally defined from above. Most calculations you do in at least introductory civil engineering and mechanical engineering course gives you very simple diagrams to analyze, formulate, and solve for some variable. You have to deal with just forces that is tensile, compressive, shears, strains, or torsional.

What we are suggesting can not be easily modeled, because you are loading on the slanted part before the epiphysis head starts. I would suspect that the region we are going to be mechanically stimulating would be also the soft and most easily deformed area.

Imagine that the epiphysis is like a tube of toothpaste. Remember how most parents tell their kids to squeeze the toothpaste, to go from bottom up, squeezing not in the middle, as the original theory says, but to squeeze from the edges to push the entire content upwards. That is similar to what I am at least saying. In the process of squeezing the toothpaste from the bottom up, the upper part protrudes outwards, extending the volume on the upper side, which is what causes the little bit of bone volume change.

The last major point comes from the book The Body Electric by Dr. Robert Becker which I have referenced multiple times before. In one specific section, his research team tried to figure out what is the exact molecular mechanism to allow for Wolff’s law to be possible. How does the bones actually remodel themselves from a mechanical load? After bending the bones and noticing that the thickness of the bones increased in the opposite area where the bones were loaded, they came up with the theory that if you bend a long bone just like when you are trying to bend a wooden rod, the electrons pop out out of the side where you are bending them and move toward the side where the they are experiencing the most compressive load. The excessive in electrons causes certain molecules to move to that side to balance out the charge differences, adding more bone thickness in the process.

If we then use the simple principle that the thickness of bones increases in the opposite direction of a mechanical load, to make the upper area of the epiphysis thicker, we would need to load in the opposite direction. Obvious that would not be possible, since we prefer to view the bone as a cylinder with both ends attached axially to another long bone. There is no way to make the proximal epiphysis end of a tibia longer by loading the distal epiphysis end of the same tibia, unless we cut off the feet.

That means that the next best thing, to get as close to the opposite direction of the epiphysis top surface is to load in the direction of the slant/angular region of the epiphysis right before the protrusion begins. That is what I suggest we start to do and change towards.

So, again, do you see the picture to the upper right? See where the line/arrow that is showing the label “spongy bone” is point at in the part of the epiphysis ? Load there.

The Take-Away – Change the location to clamp on the Angular or Slanted Area just before the epiphysis protrusion area is most pronounced, which is almost opposite of the top of the epiphysis

{So you’re suggest to load below the epiphysis? That might be interesting as it would increase pressure within the epiphysis rather than the entire bone. I might have to try that and see if can get the immediate results I got with finger loading. With finger loading, I’m loading a much larger area which would include the area where the epiphysis meets the diaphysis.

Right now the current method suggests loading where the epiphysis meets the articular cartilage. This new method would suggest loading where the epiphysis would meet the diaphysis. A drawback would be no loading two bones and once. Another drawback would be that the end of the epiphysis is weaker and is more susceptible to deformation via mechanical load. I will still give it a shot.-Tyler}

Other Issues

There have been a few concerns within the community of people trying out the LSJL routine since Tyler did post an update to his height gains in the recent post “Height Increase Progress Update“ where he said that his recent visit to the doctor showed that he was 5′ 8.25″. This would suggest that maybe he never got any gains in all the years he has been trying. Other doctors offices have said that he is at 5′ 9.75″. For me, I am not sure what to make of this new information. A 1 and a half inch discrepancy in measured height from one doctor’s office to another is very extreme. Maybe the gains he did get for a few years was lost but I have no idea what to make of it at this time.

I am not that concerned with whatever his gains are, since he still does great work in research and contributing to the website. His effort and work has helped push the endeavor extremely far and revealed multiple new ideas on how we should proceed into the future.

Also, the recent thread on Miles Cordell from the UK claiming to disprove this idea has to be taken into consideration. So is Mr. Cordell’s claim valid? He says that he has never found one valid scientific paper to back up the idea His idea is that the knees or whatever synovial joints one would clamp down on would become swollen, which might cause a temporary illusion of height gain.

I can’t say much to this since he hasn’t looked over the study where older lab mice had their long bones increase in length from intermittent mechanical loading of the joints. (and yes, we all realize that in mice, the epiphyseal cartilage doesn’t really ever go away)

So You Are A Basketball Player and You Wish To Become Taller…

I’ve said in the past before that for a long time, I was a huge basketball fan. Growing up in the 90s and watching what is probably one of the most transcendent figures in professional sports establish his immortality gave me personal ideas on becoming a professional athlete. After years of practice and drills in the basketball courts of North Carolina, I realized that I couldn’t jump or be fast enough laterally. Now I live in Seattle. Being from Seattle and the Pacific Northwest, it was sort of sad that the Supersonics decided to leave to be in Oklahoma City.

Just yesterday my friend told me that the Seattle Seahawks had won the Superbowl from the Denver Broncos this year and how the streets of downtown Seattle was littered with hundreds of thousands of people. I had no idea since I don’t keep up with any other sports except basketball. That shows just how out of the loop I am with almost every other sport. Maybe that is why I’ve always had a unique fascination over height, or maybe just length in general. When a person is a basketball fanatic, they care about how big people are.

In basketball, one’s identity can be primarily defined by one’s size. In no other sport is innate god-given genetic luck more important than in basketball. With almost any other sport, one can be quite successful if they put all their effort into it. Even football can be something one can succeed in, since speed and bulk mass is important. For the wide receivers, being smaller can be a good thing since their center of gravity is lower, and speed and the ability to dodge players is critical. We can work on speed and muscle bulk. There is no way to work on making our bones longer or larger.

I don’t know many sports where a person can be drafted and given a multi-million dollar contract based on just “potential” alone. I’ve seen too many guys drafted and defined as “raw” or as “a project” because they are 7 feet tall and decided to start playing basketball only maybe a couple of years ago. To be drafted into professional basketball requires mainly three qualities…

Length – It turns out that height is not everything. The draft scouts now realize that you have to consider the wingspan of the players, and their maximum standing reach as well.
Jumping ability – combined with a person’s maximum vertical reach with their feet still on the ground, this shows what is the real maximum vertical jumping reach of a player.
Coordination – most people over a certain size have a really low coordination ability. I’ve known plenty of people who couldn’t even dribble a basketball properly or get their brain to process a normal jump shot.

Beyond these three qualities, there are obviously a few more qualities which are not as fundamental as those but if you have plenty of natural resources in the fundamentals, the basketball scouts will take a chance with you and just call you a “project”.

This is why in basketball, the main requirement to be considered is size of the player. If you are big enough, there will always be people who want to mold you into a basketball player.

So wishing to become taller is probably one of the most common desires in developing basketball players. Gaining even 2 extra inches can change one’s athletic career forever.

The first thing to realize is that probably 98% of all basketball players have at some point expressed the desire to be even bigger than where they are now. Even if they are already in the long tail/upper reaches of the height distribution curve, it is still not enough for them. Gaining more height and length only helps their game.

Is there something a person can do as a basketball player to get more size?

It depends mostly on how old a person is. If the player is 17 or younger, they still have a chance to grow more, on average. If the player is 18 or older, then there is probably very little chance they would ever again experience a natural growth spurt. While 1-2 inches in possible, a 19 year old basketball player should not expect that their height is going to explode upwards in one year.

In the few well known cases like David Robinson, Anthony Davis, or Dennis Rodman, their unique growth progression is something that happens to very few people. They are the 1 in a million case which no one who has even an average intelligence should expect for themselves. I have always said that one should not count on dumb luck and chance for god or randomness to do something nice for them. That is why I am willing to start a website like this one.

The best thing to do for any High School or Middle School player (male or female) who has dreams to become a professional basketball player, it is absolutely critical that they asses their own unique situation, and be practical in their choices. So let’s take a look at the most popular basketball player in the game today…

What Can Lebron James Tell Us About How To Grow Taller?

It turns out that there is not a lot that the basketball prodigy can tell us since he had no control over it when he was going through adolescence and puberty. Like most young guys in middle school and high school playing organized basketball, one of the key desires is to become bigger (taller and longer) so that they can be better at playing the game. Height is an attribute that is extremely valued in the particular sport where the general rule is “the more the better”. I remember Lebron once saying that his idol when he was growing up was Michael Jordan. He wanted to be tall like Mike and also wanted to get MJ”s shoes. Coming from a low class family, and being raised by a single mother, it was not possible at the time for him to afford the Air Jordan sneakers. However, the other desire was achieved. He did eventually reach 6′ 6″ like his idol but it seemed that nature (or maybe god?) gave him even more, and he outgrew his idol. The realization one day that he was even bigger than his basketball idol was probably something he did not expect.

Was he happy about that? He might have surpassed MJ in stature but will he surpass MJ in accomplishments and rings in his playing career?

We could guess that his height was due to genetics, but there doesn’t seem to be that much information about James’ father, only mother. From the interviews and talks with the mother, I suspect that she is of average height (5′ 4″-5′ 6″). The father who I have found very little information about we might guess could have been a good athlete at a young age too, and might have been just above average in height (6′ 1″-6′ 3″). Using those types of values, even at the upper limit, James’ height calculated using the standard formulae would have been around 6′ 2″, maybe. Based on the SD of height, he is at least 2 SD away from what is predicted of his height by the calculate values of his parents

So his height is listed at 6′ 8″ with a wingspan of 7′ 2″. Many people point out that his predraft measurements say that he is actually 6′ 7.25″ without shoes but after examining his pictures compared to other professional basketball players and standard height doors, we have enough confidence to say that Lebron James’ height is more likely 6′ 7.75″ for most of the day standing upwards. Based on the normal way height changes from diurnal variations of the intervertebral discs, his height after being decompressed from lying horizontally for a long time (aka sleep) would most likely exceed 6′ 8″. I personally suspect that him ending up so much bigger than what was expected of him from just the math shows how random and unique case he is.

If we look at the body shape of this “basketball player” we notice that he is much wider/ thicker than the average professional basketball player. He is described by sports analysts of having a NFL Linebacker type of body. Where most of the other players have an ectomorphic body type, his is a mesomorphic type. People with mesomorphic body types are not supposed to become too tall, because of the amount of weight that the growth plates would be subjected to. If there is too much weight on the cartilage, they will go through faster senescence. His listing of weight at 260 lbs says that he weighs more than many NBA centers, who are much taller than him. He supposedly can put on 20 lbs of pure muscle from doing almost nothing and eating just lean chicken.

We look at his strength next. This guy is strong. Unlike Kevin Durant, who has rather thin shoulders, skinny, but long, Lebron has slightly larger than proportion shoulders and a wider mid-section/core. Where Kevin Durant couldn’t even do 1 bench press of 185 lb in the predraft, Lebron is one of the only NBA players who have ever broken a backboard.

In terms of strength and weight, his body and natural abilities is much higher than the prototypical NBA player. How can we explain this phenomena? We suspect that what has happened to Lebron is the same as what happened to MJ, Michael Jordan. These basketball superstars who are supposed to be genetic freaks were never supposed to be as tall and long as they were supposed to be. Sure, we can say that all professional basketball players are supposed to be much shorter than they are supposed to be, since they are so many standard deviations away from what their genetics predicted, but the unique body shape of Lebron is a very extreme example. He has the strength and thickness of someone who is much shorter but just became taller from random chance.

The same can be said about MJ. MJ’s family genetic history shows no one that tall. His sister is just 5′ 5″ and his father is 6′ 0″. His brother Larry is around 5′ 9″. Michael’s height should have been just 5′ 11″-6′ 1″. His height as his late James Jordan said was maybe a sign from god that Michael would have to be an athlete or he would have starved due to lack of focus and good work ethic when he was younger. When we look at MJ’s sons, they are both closer to the average, at around 6’1″ – 6′ 2″. Michael was an anomaly in his size since no one in his family was that big. He has the strength and width of someone who is much shorter (he is also one of the only other people to ever break a backboard) but somehow through chance became much taller than what his genes had predetermined.

Looking at the numbers

There are supposed to be 370,000,000 people in the USA today. Guessing, out of those, maybe 2-3 mil of those people have played basketball in an organized fashion. Out of those people, about 1.5-2 mil are young enough between the ages of 12-18 to still have intact growth plates. Most of these kids, white, black, asian, hispanic, probably harbor some dream of becoming taller and playing basketball professionally for a career.

So you have the intent, and the desire, as well as some drive to get better at the game, which means these young middle school and high school kids practice drill in the basketball courts 5 times a week in their school basketball teams. The mental aspect is all there. That probably makes up half or more of those kids, or about 1 million secondary school basketball players.

Then the only thing that is really required is the physical. The main requirement would be size. Is the kid big enough to be selected by a team at the next level? For the majority of them, they are not.

Most of those kids trying to get into the NBA (or even college basketball) will never be taller than 6′ 3″, which I believe is the current established cutoff point, where a kid goes from “average” size to “worth the scout to consider” size. For example, Anthony Davis was a completely passed over average skilled 6′ 3″ point guard until he grew 7 inches which pushed him into the national spot light. A 6′ 10″ PF/4 with point guard handling skills is something which is very hard to come by. On average, most kids have already grown to 98% of their expected final adult height by 15-17. A 7 inch growth spurt within a 1 year time is something to definitely take notice to which changes almost everything in the basketball world. When you are too short/small, the scouts at the next level will not look at you, unless one has tremendous skills.

The problem there, is that those others “skills” are also sort of an innate talent which a person can’t really work on. The ability to jump high, go for an explosive first step to drive pass the defender, the “handles” and lateral quickness are something which is mostly innate talent which can not be learned. Sure, one “can’t teach height”, but the basketball monday morning QBs also forget to mention that you can’t teach athleticism either. Some people just have more fast trigger muscles which allow them to jump higher, no matter how much jumping practice the other person competing against them does. One might be able to get the drills in the gym every day to get faster, but the limitation will come down to the thickness of the nerve bundles running down their limbs and the number of neurons in the brain, which gives the hard working kid the ability to be coordinated, explosive, and/or be able to read the signals during the game correctly and instantly. Those anatomical traits are set at birth.

When our team and research goes away, the kids are left to the forces of chance and pure dumb luck. Of course, every one of those kids who messages us claims that they will make it, and will work hard everyday. We are sure they will, but there will also be a million other kids just like them going through the exact same drills, the same exercises, the same routines and strategies. What is going to make them unique and differentiate themselves from the million other kids in the exact same position?

There is no way to really get around it either. There is no cheat code one can use. This is not like a college admission test where being a legacy, having parents throwing money, or knowing someone is going to give them a shortcut way to be admitted into that exclusive club thousands of others are trying to get in. You can’t scam your way into becoming a professional athlete, since that is based on scouts looking at the raw skills of a person. Maybe 20-30 years ago a real talent might have been missed and they never got their shot in the NBA trials, but these days with the internet, it is almost impossible for the basketball scouts to miss out on what many people call a “touch diamond”. Big guys who have some type of coordination are often sent to basketball camps to be worked on as a “project” because they are too “raw”.

We often get bombarded by teenagers telling us that they are basketball players wanting to become taller. What can they do?

There are many things they can do, but we haven’t written any type of guide yet for them.

However, what we can suggest can only give them at most 2 inches and those are for the most extreme cases. We try to be very realistic on what we can control and have any type of affect on. If these kids are hoping for something to give them 4-5 inches, I can only tell them to pray that they are that lucky and be that 1 out of 100,000 kid who gets the mega-growth spurt. I would of course tell them to not put all their hopes into something so random and improbable and focus instead of looking for something that has better odds for success. Hedge their dreams of playing professional ball and stay in school to learn a useful skill to take with them.

The life of a professional athlete is short since the human body will eventually wear down. You have to have some type of backup plan after one’s playing days are over.

In the world, we only hear about the success stories and the winners, the people who got lucky. (Sure, they were focused, worked hard, focused on learning, and were persistent but there are plenty of examples I know of people who still did not reach the success they hoped for due to bad luck in some area of life, which they had no control over or could have predicted earlier in life.) We never hear about the losers, the ones who never made it, who were not big enough or talented enough. This tendency of people to constantly use as case study the few minority cases where the person had a happy ending is known as survivorship bias. We like to trick ourselves in believing that our life and case is somehow special. Not everyone can become a MJ or Lebron. .

In the long term, our physical accomplishments are most likely going to become surpassed by someone else. Like all the Olympic records, the newer generation of kids will shatter the older generation of athletic records. People thought MJ was the greatest 20 years ago but now it is supposed to be Lebron, which might be surpassed by KD in another 10 years. Who is next, who will be so physically imposing and dominant who will make Lebron, Shaq, and Dwight H. look weak and small in comparison?

The people in our generation seems to be so fixated on the size, and strength of Lebron, DH, and KD, because we don’t have footage showing how well Bird, Magic, and MJ played which was 20 years ago. The older generations knows full well the accomplishments of Wilt Chamberlain but we don’t know that. They talk about his strength and dominance but we think of Shaq when we think of overwhelming size and dominance. We just didn’t experience what they experienced. That is their reference point. We all are using our own reference point, our current time line and say that the person in our current time is the best of all time, when they are only the best of our particular time or generation.

However, our mental and intellectual accomplishments will stand for much longer. As long as something we created or discovered is shared with the world and the world fully accepts and acknowledges our contribution and effort, people will always remember our life’s work.

In the words of the late Los Alamos physicist Richard Feynman…

“From a long view of the history of mankind, seen from, say, ten thousand years from now, there can be little doubt that the most significant event of the 19th century will be judged as Maxwell’s discovery of the laws of electrodynamics. The American Civil War will pale into provincial insignificance in comparison with this important scientific event of the same decade.”

This Non-Available Prodrug Taken Orally Helps Older Adults Become Taller

I am very happy with the results of the former post “This Non-Prescription Supplement Has Been Scientifically Proven To Make You Grow Taller Even With Closed Growth Plates“. The reaction that it received was what I was sort of hoping for and so far, it has had over 50,000+ views already. Since that post was so popular, I wanted to do a 2nd post which shows them another compound which we have found which have a similar ability.

This compound is known as a prodrug, which I am not sure how to obtain, taken orally has been shown only on a theoretical basis to increase height in the lab animals. In rats, their body lengths increased in the ways which we desire. From what I personally have read about it, I have about a 60% confidence in its ability to increase height in people who can ever get it. It would work best on adults, those people who are in theirs 30s and beyond. This suggests that this compound would indeed work for people with closed growth plates, or even specifically intended for people with completely ossified epiphyseal cartilage tissue.

So what is 2nd chemical compound which has this ability?

It is called CPA-926.

I first was informed of this particular drug in an article I had cited in one of my previous posts. This particular compound is mentioned in both the books Dynamic Reconstruction of the Spine (by Daniel H. Kim & Frank P Cammisa on pg 384) and Nonfusion Technologies in Spine Surgery. (edited by Marek Szpalsk on pg 53). I will also be referencing the medical reference “Therapeutic Strategies for Modulating the Inflammatory Diseases” edited by Barry M. Weichman but not as much as the other two.

There was also a few articles I had to glance over (notice I used the word glance, and not study) which validated this idea that the prodrug could indeed work.

It seems that this compound is both anti-tumorogenic and anti-inflammatory, which are always positives for almost any compounds we ever intend to swallow.

The most important study is the one done by Okuma.

Okuma M, An HS, Nakagawa K, Akeda K, Muehleman C, Masuda K (2005) Oral administration of esculetin prodrug inhibits intervertebral disc degeneration in the rabbit annular needle puncture model. Orthopaedic research society meeting, (p 370)

This particular article was published in The Spine Journal back in Sept 10, 2004 (volume 4 or 5).

We are not sure if there is a PubMed study link to it but the title of the study is located and scattered around Google just from a quick search.

From a quick look, it seems that even one patent referenced this method on how to treat discs that are degenerating.

For more proof that this idea of inhibiting the loss of disc, we refer to the patent “Method for inhibiting fibrocartilage degradation (WO 2005091960 A2)“ by Koichi Masuda, a director of Orthopaedic Surgery. (His Curriculum VItae is Available Here). I never did look over the patent extensively but did glance over the document to mine a few interesting facts about CPA-926.

The compound is provided by Kureha Chemical Ind., Co. Ltd., Tokyo Japan or Kureha Chemical Corp
Following the lateral X-rays of the lumbar spine, the vertebral body height and disc height of the IVDs were measured
Oral administration of CPA-926 preserved disc height and the histological analyses of these tissues show that CPA- 926 protects against disc degenerative chances in a rabbit model

At this point, it might not be possible to call up the sales people at Kureha and get them to ship a few grams of this cartilage regenerative chemical compound. I haven’t tried it but is only providing evidence of its efficacy.

In terms of how effective this chemical compound could be, it could be similar to Harpagoside, which I wrote about in the old post “Increase Height and Grow Taller Using Harpagoside“

So does this mean that every single compound which has inhibitory effects on compounds which have catabolic effects on cartilage (aka treats osteoarthritis) is good?

If we were to be completely general, I would give a tentative yes to that question. While there is probably a few dozen compounds the drug synthesize makers know of which have abilities to treat diseases associated with articular cartilage degeneration, very few of them have shown the characteristic of doing more than just preventing degradation, but also anabolic effects, where cartilage is regrown back. This prodrug of the chemical compound 6,7-dihydroxycoumarin suggests that it has those anabolic effects besides just the usual inhibition of catabolic processes in the IVDs.

Is it however better than just popping Glucosamine Sulfate?

We are not sure about the comparison but it is obviously harder.

Is it safe to take orally?

From the 3-4 main studies that have talked about this compound, it has been found to be safe on the lab rats and lab rabbits it was tested on.

So we buy this from somewhere?

I have not searched to see whether the Keruha Chemical Corp in Tokyo sells this stuff.

The Inhibitory Effects Of CPA-926 On The MMPs

On multiple posts written by Tyler over the years, he mentions over and over again how the MMPs (aka Matrix Metalloproteinases) are not good for height increase, specifically MMP-9 and MMP-13. My own research supports this opinion. The study by Yamada and even Watanabe (Esculetin suppresses proteoglycan metabolism by inhibiting the production of matrix metalloproteinases in rabbit chondrocytes.) suggests that for esculetin at least and whatever derivatives that is made from it (or a precursor to the compound) shows that the main way these compounds work is by targeting the pathways of the MMPs.

For the Future

I am also looking into three other compounds called RO 32-3555 (aka Trocade), SKI 306X and KHBJ-9B, which seems to have similar properties in being anti-inflammatory and great for prevention of cartilage degeneration. Those reports will be delivered on another day.

Study shows feasability of micro-growth plates

The idea of LSJL is to create microgrowth plates via fluid shear strain on the mesenchymal stem cells in the bone marrow. This study shows that microgrowth plates can exist:

Growth Plate Regeneration Using Polymer-Based Scaffolds Releasing Growth Factor

“Depending on the type of growth plate fracture and the severity it can lead to stunted bone growth or bone growth deformation. The current treatment options for growth plate fracture are removal of the bony bar and replacing it with a filler substance, such as, bone cement or fat, but still yield poor results 60% of the time. In previous work, poly(lactic-co-glycolic acid) (PLGA) scaffolds were developed and studied in vivo for the purpose of growth plate regenerationDepending on the type of growth plate fracture and the severity it can lead to stunted bone growth or bone growth deformation. The current treatment options for growth plate fracture are removal of the bony bar and replacing it with a filler substance, such as, bone cement or fat, but still yield poor results 60% of the time. In previous work, poly(lactic-co-glycolic acid) (PLGA) scaffolds were developed and studied in vivo for the purpose of growth plate regeneration”

“Figure 6.7. Fat implant showed thin, continual line of cells across medial side that contained reserve (R), proliferative (P), hypertrophic (H) cartilage cells and calcification zones (C).”

Another micro growth plate:

“Blank scaffold on (A) the lateral side with columnar structure and (B) the medial side with the appearance of stacked (S), reserve (R), proliferative (P), and hypertrophic (H) cartilage cells.”

Here’s a growth plate but loaded with IGF-1 so it’s much more sophisticated:

“IGF-I loaded scaffold showed dispersed pockets of cartilage cells throughout the medial side with the appearance of reserve (R), proliferative (P), hypertrophic (H), and degenerative zones (D).”

“In this study, the attempt to regenerate the growth plate did not result in columnar structure to the degree that the native growth plate has, regardless of the treatment type. It appeared that the fat implant allowed for some cartilage regeneration, but it was only a cell wide at most points and most of the chondrocytes were in the calcification zone. The tissue surrounding the cartilage areas was woven bone, which has been known to appear after fractures{But would this still result in a longer bone?}. The blank scaffold treatment resulted in tissue having a similar structure to that for the fat implants with a couple exceptions. First, there were a few areas where blank scaffolds had been placed with some cellular stacking, and secondly, the lateral side retained more structure, resembling that of the native growth plate, compared to defects treated with fat graft. The blank scaffolds gave the epiphyseal region more structural support, preventing further collapse of the lateral growth plate, while the fat graft implant had a thinner growth plate region across the whole tibia.”

“The defects treated with IGF-I-loaded scaffolds, both with or without seeded cells, showed a similar appearance on the lateral side as that of the blank scaffold group, however the medial sides were quite different. Without cells, the IGF-I-loaded scaffold resulted in pockets of chondrocytes throughout the medial side along the epiphyseal line that contained cells in all zones of cartilage development. The addition of cells created a large vertical pocket (~3 mm long) of chondrocytes located in the upper epiphyseal region. Interpretation of the IGF-I loaded samples was limited because only one sample could be used for observation so it is difficult to say if this cellular organization would occur again. The cells were mostly in the hypertrophic state and had no columnar organization. Both types of IGF-I loaded scaffolds (with and without cells seeding) increased the density of hypertrophic chondrocytes compared to the fat, blank, and hybrid scaffolds. Cells seeded on scaffolds containing IGF-I created the largest population of chondrocytes”

“Though the results did not show total growth plate regeneration, the necessary cell types were present”

It should be noted the mesenchymal stem cells used in this study were harvested from the diaphysis thus providing evidence that MSCs needed to create growth plates do not necessarily have to be from the Zone of Ranvier.

The study did not display changes in length due to the various scaffolds. The fat scaffold and IGF-1 seeded scaffold did reduce the angular measurement resulting from part of the growth plate being damaged. The blank scaffold altered the angular measurement disparity but increased it in the tibia and decreased it in the femur. We can be fairly certain that microgrowth plates can alter longitudinal bone growth as the angular measurement is dependent on how tall one side of the bone grows versus the other.

Even though this study involves scaffolds and LSJL does not. The information about microgrowth plates altering height growth can be extrapolated to LSJL as MSCs could migrate to the epiphyseal region and use bone as a natural scaffold.

This study provides evidence that you don’t need to create a whole growth plate to increase height.

Can rest intervals make LSJL more effective?

Enabling bone formation in the aged skeleton via rest-inserted mechanical loading.

“The mild and moderate physical activity most successfully implemented in the elderly has proven ineffective in augmenting bone mass. We have recently reported that inserting 10 s of unloaded rest between load cycles transformed low-magnitude loading into a potent osteogenic regimen{but is it a chondrogenic regimen?} for both adolescent and adult animals. Here, we extended our observations and hypothesized that inserting rest between load cycles will initiate and enhance bone formation in the aged skeleton. Aged female C57BL/6 mice (21.5 months) were subject to 2-week mechanical loading protocols utilizing the noninvasive murine tibia loading device. We tested our hypothesis by examining whether (a) inserting 10 s of rest between low-magnitude load cycles can initiate bone formation in aged mice and (b) whether bone formation response in aged animals can be further enhanced by doubling strain magnitudes, inserting rest between these load cycles, and increasing the number of high-magnitude rest-inserted load cycles. We found that 50 cycles/day of low-magnitude cyclic loading (1200 microepsilon peak strain) did not influence bone formation rates in aged animals. In contrast, inserting 10 s of rest between each of these low-magnitude load cycles was sufficient to initiate and significantly increase periosteal bone formation (fivefold versus intact controls and twofold versus low-magnitude loading){we’re not looking for periosteal bone formation, we’re looking for neo-growth plate formation but the principles may be the same}. However, otherwise potent strategies of doubling induced strain magnitude (to 2400 microepsilon) and inserting rest (10 s, 20 s) and, lastly, utilizing fivefold the number of high-magnitude rest-inserted load cycles (2400 microepsilon, 250 cycles/day) were not effective in enhancing bone formation beyond that initiated via low-magnitude rest-inserted loading. We conclude that while rest-inserted loading was significantly more osteogenic in aged animals than the corresponding low-magnitude cyclic loading regimen, age-related osteoblastic deficits most likely diminished the ability to optimize this stimulus.”

“While the inability to perceive mild and moderate loading events as stimulatory may reflect potential deficits in numbers and/or viability of mechanosensory (e.g., osteocytic) cells, the inability to initiate and, especially, sustain bone formation more likely reflects potential for deficits in the numbers and/or function of osteoblastic cells. Additionally, the declining availability of biomolecules involved in coordinating and enhancing osteoblastic response to mechanical stimuli (e.g., TGF-β, IGF-1){these biomolecules are involved in chondrogenesis too so it’s important to monitor changes in these biomolecules due to aging} potentially compromises the ability of bone cells in aged tissue to perceive low and moderate magnitude loading events as being stimulatory. Last, the age-related decrease in the surface to volume ratio of bone mineral matrix and increased viscosity of interstitial fluids could decrease biophysical stimuli delivered to bone cells via standard exercise regimens{this could affect neo-growth plate formation too as the degree of biophysical stimuli delivered to cells would affect the ability to form new growth plates}”

“A total of 49 aged female C57BL/6 mice (mean ± SE; 21.5 ± 0.16 months)”

“The device fixes the proximal tibia (at the tuberosity) against motion and applies controlled loads to the distal tibia, thereby placing the tibia diaphysis under “cantilever” bending in the medial–lateral direction.”<-not quite like LSJL.

“a strain versus load calibration curve was determined and yielded peak strains in the range of 800–2400 με at the periosteal surface (and 600 to 1800 με peak strains at the endocortical surface) for loads of 0.4–1.2 N, respectively.”

“rest-inserted loading (particularly at low magnitudes) enhances rates of bone formation by primarily increasing mineral apposition rates compared to cyclic protocols”

“attempts at further enhancing the bone formation response to rest-inserted loading by doubling strain magnitude, inserting rest-intervals, and subjecting animals to five-fold the number of high-magnitude rest-inserted loading cycles were all ineffective in the aged skeleton.”