I do track the websites which link to this website. Some of the most common sites that come to this website are from some of the most negative areas on the internet. The level of anger, bitterness, and spite on these strange internet discussion boards means that you can’t tell the difference between a genuine poster who just wants to vent and rant onto an internet discussion board and a troll. I’ll just say a few messages for those guys who feel depressed, angry, resentful, or just mentally stuck over their short height. This is directed mainly towards reddit/r/short and places like sluthate.com

Guys, take it down a little. You may be 5’6″ and have some level of asperger’s syndrome but that does not mean that you can’t enjoy your life. If you are thinking of killing yourself or hurting another person Rodger Eliot style, then read the following message.

I would assume that most people believe that they are above average in intelligence. Well, two of the principle traits of people who are truly intelligent exhibit are that 1) they can make decisions based on long term goals and 2) have the ability to control their emotional impulses and states. You can may be really good at mathematics but you still can’t control your own emotional state with the behavior of an immature child. For those of you who read this message, you know who you are. Emotional Intelligence has been shown to be often a much better indicator of eventual success in life than any traditional IQ test.

Start of my message

I don’t do much these days for this website since I run my own business which now takes up so much of my time. However, let me assure the regular readers that based on what I have seen from being on the cutting edge of the tissue engineering & biomedical fields, there will be something that will come out in the coming decades that will be much better than the limb lengthening surgeries you see today, which means less pain, less invasive, and less possibility for surgical complications. I am talking about lab grown growth plate implantations and healing intervertebral discs compression. I personally don’t think it is possible to “reopen the growth plates” which so many people hope for. Some little bit of surgical incision will be needed to cut the bone slightly (osteonomy). I do dare to dream big, but I am also a realist on what is possible, and what is pure science fiction. There are no magic pills or silver bullets.

You guys should not be worrying how tall you are and how much the world discriminate against you. You can’t change the world, unless you feel like it is your life’s mission to combat heightism similar to MLK to black/white conflict and put in maybe 20 years of hard work to make slight social changes. I suggest that you should not waste your time and energy on fighting an uphill battle against this hard-wired instinctual pre-programming which most humans have which creates prejudice towards shorter humans.

It is there, heightism exists, shorter guys get less dating and romantic opportunities (and maybe also less respect from other guys in their work), yada yada yada. You can cry about how unfair people are to you all day but at the end of this year, you would realize that all this venting of frustrating you post onto reddit/other doesn’t improve your life overall by much. You did not move that needle of your life gauge even a little bit. For now, just swallow the hard reality of this unfair world and existence we live in, accept that you did not win the genetic lottery like a channing tatum, and go in a different direction.

If you dwell on this fact, about your short stature and how no matter how much you go the gym you can’t change your height, you are going to get stuck psychologically, and maybe spiral down to a psychological state which you can’t get out of.

A lot of guys might tell you to go to the gym to lift weights, work out, build confidence, dress better, have a great social life, etc. and they are only half right. Improving on the areas of life of what you can control helps somewhat, but it won’t help all the time. Sometimes no matter what you do to try to make up for your short stature, that girl you like still won’t move towards you. The reality is that there is probably over 100 Mil other guys in the world out there. They have their own standards, and if they are not willing to lower their height requirement for you, there is nothing you can do. You already did everything else to improve yourself. You did everything you can to make you have a better advantage in this game we call life for success, and maybe sometimes that is still not good enough. Sometimes the only thing that matters is how long your bones are.

Some of you will be depressed. Go outside to the beach and get some sun. Take up long distance running to get the dopamine receptors firing again. Stay off the computer.

Work on yourself on the cognitive level is the best place to start. Take some nootropics, do tDCS, experiment with sleep cycles, learn acupressure and deep tissue massage for stress relief, yoga, fishing, etc. to get your mind away from this sub-reddit and other negative areas on the internet.

Get an education to increase your level of intelligence first (since being smart and short is much better than being tall and stupid in the long run), go into business for yourself to increase your net worth and build real assets, make your money, enjoy life, and come back when you are maybe 15-20 years older. You will have the funds to then spend on the latest cosmetic biomedical treatments. Most of you I would assume don’t have a lot in the wealth area of life. Money is not the be-all,end-all but it is a tool to help you get what you want out of life.

Treat each dollar you have as your soldiers. Each day you send your soldiers out to capture more soldiers which can work for you. That is called using money to make more money (aka investing)

I lived in Gangnam, Seoul for 2 years so that type of exposure made me very accepting of the idea of cosmetic surgery to improve one’s appearance. It is okay, as long as it is empowering and can really improve your quality of life. Some people are against cosmetic surgery since they think that it will change who they think they are to make other people like them, but this world is a very competitive place. You need every little bit of advantage you can get.

Plus, one’s concept of who they are as a person is fluid. It is not static. As we go through life, our “self” evolves over time. Even our core values and belief system changes over time. Don’t be so stuck in your beliefs/value which cause you to miss out on not taking a chance on something great. It is very rare that we regret later in life for doing something instead of not doing something.

For something besides just a nice pep talk which can hopefully get the regular readers out of their heads and negative emotional states, just see how close we already are with the 3D Printed nose which is made from fibrocartilage, not the hyaline cartilage you would need. (https://www.youtube.com/watch?v=FuGZ-G0UCCY). Implantation, transplantation, vascularization problems, people are working on that.

{Tyler’s Comments:  I tend to avoid looking at the validity of the desire to grow taller.

You may say: “You need to accept your height.”

I say: “You need to accept my desire to increase my height.”

Does climbing mount everest make any sense?  What about getting the high score in a video game?

Human height has value.  We as humans should strive to further our value.

“If you set your mind to it, you can accomplish anything.”

ANYTHING………

ANYTHING……

Including growing taller and we should accept nothing less.}

As I recently got back into playing basketball at the local YMCA which I just gave up, I came to realize just how strange it is that so many basketball players have an unnatural obsession on their height.

Back in my college days, I would sometimes eat in the same dining hall as the college athletes and the one time I ever sat really close to a set of basketball players I could over hear their conversation. What struck me as really odd back then was that half of their conversation revolved around how tall they were, or how tall other people were. One guy would tell the other guy about this player from another school, and they would go into his height by picking at it. The strange thing was they they didn’t mention the skill level of that kid, but just how large the opposing athlete was.

To these guys, it seemed like the height of a person defined who they were as a person. It was not their GPA, or GMAT scores, or what they had done in their lives. It was just their height. Back then, I just didn’t understand.

Now that I have started to watch basketball again, professional basketball, the thing that is always brought up is the players height.

Just watch the old 90’s bulls intro. Why is it that the announcers have to list how tall their players are? How often do I need to be reminded that Michael Jordan is 6′ 6″? The LA Lakers announcers do it too. (refer to this link https://www.youtube.com/watch?v=ojHOO4qbE4s). Being tall is not a skill, but people in the basketball world treat it as a skill. Being bigger does not make the player better.

Here is a sick truth that I would need to reveal about the nature of the game today. For most black american guys who play this game today, like in the streets of the inner city, basketball is actually a game of posturing, and showing off. (Refer to here https://www.youtube.com/watch?v=OJixT7F-Vog) People don’t play the game for the fun, for the team effort, or for the personal skills that they develop. They play the game to exert their masculinity and express their dominance. In the African American community, the young males are told to be ultra-masculine in expression. The easiest way to exhibit their dominance and masculinity is being taller than other men. If they are taller than others, they are told to use their body to push through to the post. I can’t even begin to remember how many times I would be in a game where it felt like it was not 5-on-5 but 1-on-1. The ability to pass seems to have been lost on certain people.I personally love playing the game and hearing that swish as the ball goes through the hoop but I have decided to let go of playing this game, and stop all-together to get away from the game.

As I grow older, I realize just how many psychological hang-ups people have over their height when they are playing basketball.

Sometimes I start to question my own motives for even still watching this game. Do I really find this game where abnormally tall guys running (and jumping) up and down the court that mesmerizing? Could it be that at some level in my mind, I have an unhealthy obsession with height just like the fellow basketball players? How many other people in the world also seem to find their primary source of identity through their height?

I had decided long ago that the sport of American Football is a huge waste of time and resources, but now I am adding the sport of Basketball on that list. No more playing the game, and no more watching the game, either in real life or on the internet. Watching one more sports game or event is not going to improve my overall life in any way. Having the local hometown sports team win a national championship does not make my life better or even bring any real prestige to the city.

(I live in the greater Seattle/Pacific Northwest area and I saw the whole Superbowl phenomena happen two months ago. People would make sure to revolve their jobs and business around the football games. The local Whole Foods would announce over the air whether the Seahawks would win or not, and people would crowd around the TV in the local Costco. I am not sorry that the Seattle located team lost. Imagine the type of pressure the team would have been in if they had won a 2nd year. People would be forcing the guys on the team to win again for a 3-peat. )

When people say things like “We Won!” after the local sports team win, I always want to correct them in saying that it is NOT that ‘we won’ but that the team won, they just watched while sitting on their couches and drinking bear and eating chips. Somehow they are trying to find some way to feel good about themselves from the glory of other people’s accomplishments, through association. Maybe not everyone can have the god-given talent to play at the highest professional level and win in athletics, but in the long term, nobody in a hundred years will care about who won the 2014 American Football Superbowl Championship. I am happy that at least the professional athletes today can make millions of dollars, but in the long term, I pity them since everyone knows that the human body is bound to fail, and father time always wins last.

Can hanging out with tall people during development make you taller? One potential mechanism for how your communities genes may affect yours may be via biophotons.

The impact of physical connectedness on body height in Swiss conscripts.

“Human populations differ in height. Recent evidence suggests that social networks{who you hang out with} play an important role in the regulation of adolescent growth and adult height. We further investigated the effect of physical connectedness on height.
We considered Switzerland as a geographic network with 169 nodes (district capitals) and 335 edges (connecting roads) and studied effects of connectedness on height in Swiss conscript from 1884 – 1891, 1908 – 1910, and 2004 – 2009. We also created exponential-family random graph models to separate possible unspecific effects of geographic vicinity.
In 1884 – 1891, in 1908 – 1910, and in 2004 – 2009, 1(st), 2(nd) and 3(rd) order neighboring districts significantly correlate in height (p < 0.01). The correlations depend on the order of connectedness, they decline with increasing distance. Short stature districts tend to have short, tall stature districts tend to have tall neighbors. Random network analyses suggest direct road effects on height. Whereas in 1884 – 1891, direct road effects were only visible between 1(st) order neighbors, direct road effects extended to 2(nd) and 3(rd) in 1908 – 1910, and in 2004 – 2009, also to 4(th) order neighbors, and might reflect historic improvements in transportation. The spatial correlations did not significantly change when height was controlled for goiter (1884 – 1889) and for median per capita income (2006), suggesting direct road effects also in goiter-allowed-for height and income-allowed-for height.

Height in a district depends on height of physically connected neighboring districts. The association decreases with increasing distance in the net. The present data suggest that people can be short because their neighbors are short; or tall because their neighbors are tall (community effect on growth). Psycho-biological effects seem to control growth and development within communities that go far beyond our current understanding of growth regulation.”

Final height, target height and the community.

“Height varies with age, and it varies with historic time. Final height is determined by endocrine parameters and genetics, by nutrition and health, by environmental factors, by birth weight, early growth, BMI, and developmental tempo. European populations of the 19th century were short, but their shortness did not result from growth impairment at all ages. In those days, shortness was mainly due to a significantly blunted adolescent growth spurt. New modelling approaches suggest an independent regulation of adolescent growth and final height: the target for growth and final height appears to be set by the community{hanging around with probasketball players may make you taller?}. In order to test this hypothesis, we formed a geographic network of Switzerland consisting of 169 nodes (district capitals) and 335 connecting edges (roads), and investigated military conscript data obtained between 2004 and 2009. Average height of Swiss military conscripts was 178.2 cm (SD 6.5 cm). But conscripts from first order neighbouring districts were more similar in height than expected. Short stature districts have short, tall stature districts have tall neighbours. We found significant height correlations between 1st (r=0.58), 2nd (r=0.64), 3rd (r=0.45) and even 4th order neighbours (r=0.42). It appears that tall stature communities generate tall people, short stature communities generate short people, and migrants orientate towards the new height target of their host population (community effect on growth){So independent of genes from the community newborn migrants will be taller or shorter based on the community}. ”

Modeling determinants of growth: evidence for a community-based target in height?

“community-based target seeking in growth”

“adolescent height converges toward the average of the population. Height tends to cluster. The within-population variation of height is narrow.”

“Height differences are small throughout childhood but markedly increase during adolescence.”

“the smaller the adolescent is compared with past mean average height, the more the adolescent grows during puberty.”<-So according to this theory, if you are going through puberty and hang out with pro-basketball players you will grow taller than expected and at a faster rate.

“Short stature in cystic fibrosis results from tempo deceleration. Cystic fibrosis patients grow poorly at all ages (they have suboptimal peak height velocity and late pubertal growth, influenced by disease severity) but eventually achieve normal final height. ”

” tall communities generate tall people even in the presence of unfortunate living conditions”

According to Dose-dependent effect of growth hormone on final height in children with short stature without growth hormone deficiency.,exogenous administration of GH increased height by about 1 inch.  The authors of this study suggest that living around taller people could increase GH production as depression decreases GH production establishing a link between mental state and GH production.

Here’s a study that suggests that IGF-1 levels may play a role in the community effect on height.  Although it does not seem to be a strictly linear relationship between IGF-1 levels and height.  Height is more complex than that.

Sex, Sport, IGF-1 and the Community Effect in Height Hypothesis.

“We test the hypothesis that differences in social status between groups of people within a population may induce variation in insulin-like growth factor-1(IGF-1) levels and, by extension, growth in height{so “positive thinking” increases height via IGF-1 but again the relationship is more complex than IGF-1 increases height}. This is called the community effect in height hypothesis. The relationship between IGF-1, assessed via finger-prick dried blood spot, and elite level sport competition outcomes were analysed for a sample of 116 undergraduate men and women. There was a statistically significant difference between winners and losers of a competition. Winners, as a group, had higher average pre-game and post-game IGF-1 levels than losers. We proposed this type of difference as a proxy for social dominance. We found no evidence that winners increased in IGF-1 levels over losers or that members of the same team were more similar in IGF-1 levels than they were to players from other teams. These findings provide limited support toward the community effect in height hypothesis. The findings are discussed in relation to the action of the growth hormone/IGF-1 axis as a transducer of multiple bio-social influences into a coherent signal which allows the growing human to adjust and adapt to local ecological conditions.”

So it seems that the relationship as described here is that winners are more likely to have higher IGF-1 levels rather than winning increasing IGF-1 levels.

“Children and adolescents with pituitary gigantism have an excessive production of GH, and IGF-1 levels are elevated.”<-But again it seems as though there’s more to gigantism than excessive GH.

“the positive association between variation in IGF-1 levels and height, across the range from deficiency to excess, helps to explain differences in stature within and between human populations.”

” there is evidence for a new parameter that they define as ‘past relative height.’ This parameter operates during the adolescent growth period to adjust the growth rate of an individual toward the average height of her/his immediate community.”

“… the smaller the adolescent is compared with past mean average height [of the community], the more the adolescent grows during puberty”

Surprisingly the scientists found that women in sports tended to have higher IGF-1 levels than men in sports.

“Women, but not men, showed a significant association between their father’s social class and their own adult IGF-1 levels.”

Loading bones against each other also loads the ligaments against the growth plate.  One method of LSJL involves pushing bones against each other at the points of the epiphysis.

Mesenchymal stem cell characteristics of human anterior cruciate ligament outgrowth cells.

“When ruptured, the anterior cruciate ligament (ACL) of the human knee has limited regenerative potential. Cells that migrate out of the human ACL constitute a rich population of progenitor cells and we hypothesize that they display mesenchymal stem cell (MSC) characteristics when compared with adherent cells derived from bone marrow or collagenase digests from ACL. ACL outgrowth cells are adherent, fibroblastic cells with a surface immunophenotype strongly positive for cluster of differentiation (CD)29, CD44, CD49c, CD73, CD90, CD97, CD105, CD146, and CD166, weakly positive for CD106 and CD14, but negative for CD11c, CD31, CD34, CD40, CD45, CD53, CD74, CD133, CD144, and CD163. Staining for STRO-1 was seen by immunohistochemistry but not flow cytometry. Under suitable culture conditions, the ACL outgrowth-derived MSCs differentiated into chondrocytes, osteoblasts, and adipocytes and showed capacity to self-renew in an in vitro assay of ligamentogenesis. MSCs derived from collagenase digests of ACL tissue and human bone marrow were analyzed in parallel and displayed similar, but not identical, properties. In situ staining of the ACL suggests that the MSCs reside both aligned with the collagenous matrix of the ligament and adjacent to small blood vessels.  The cells that emigrate from damaged ACLs are MSCs have the potential to provide the basis for a superior, biological repair of this ligament.”

“mobile population of MSCs within the ACL”

“cells derived from both ACL sources and bone marrow underwent chondrogenic differentiation in the presence, but not absence, of TGF-β1”

“MSCs migrate to sites of injury”

So ligaments near the epiphysis can differentiate into chondrocytes.

Chondrocyte phenotype and ectopic ossification in collagenase-induced tendon degeneration.

“Chondrocyte phenotype and ectopic ossification in a collagenase-induced patellar tendon{in the new LSJL model the patella is a targetfor loading} injury model. Collagenase or saline was injected intratendinously in one limb. The patella tendon was harvested for assessment at different times. There was an increase in cellularity, vascularity, and loss of matrix organization with time after collagenase injection. The tendon did not heal histologically until week 32. Ectopic mineralization started from week 8. Tendon calcification was mediated by endochondral ossification, as shown by expression of type X collagen. viva CT imaging and polarization microscopy showed characteristic bony porous structures and collagen fiber arrangement, respectively, in the calcific regions. Marrow-like cells and blood vessels were observed inside calcific deposits. Chondrocyte-like cells as indicated by morphology, expression of type II collagen, and sox 9 were seen around and embedded inside the calcific deposits. Fibroblast-like cells expressed type II collagen and sox 9 at earlier times, suggesting that erroneous differentiation of healing tendon fibroblasts may account for failed healing and ossification in collagenase-induced tendon degeneration.”

“Chondrocyte markers were expressed in the clinical samples of calcific insertional Achilles tendinopathy”

“Chondrocyte-like cells as indicated by cellular morphology and expression of sox 9 and type II collagen were observed around the calcific deposits in collagenase-induced degenerative tendon injury”

“The differentiation of tendon progenitor cells into chondrocytes and bone cells was reported to be modulated by the expression of small leucine-rich repeat proteoglycans such as biglycan and fibromodulin, which control the differentiation process associated with BMP-2 activities ”

Tendons can differentiate into cells that undergo endochondral ossification.

The tendons are relatively close to the epiphysis as well.

The origin points of the knee collateral ligaments: an MRI study on paediatric patients during growth

“Different femoral origins for both the medial collateral ligament (MCL) and the lateral collateral ligament (LCL) have been reported in the growing skeleton (epiphyseal and metaphyseal). This study assesses the femoral origins of the knee collateral ligaments in skeletally immature individuals.
MRIs of 336 knee joints (median age 15 years (range 2–18 years)) were retrospectively analysed to assess the distances between the femoral origins of the MCL and LCL to the distal femoral growth plate.
Both MCL and LCL ligament origins were invariably located on the epiphysis. Mean MCL origin–growth plate distance was 9.6 mm (SD 2.1 mm; range 2.2–13.6 mm) in boys and 8.6 mm (SD 1.5 mm; range 3.4–12.0 mm) in girls{The MCL ligament is very close to the growth plate}. Mean LCL origin–growth plate distance was 9.3 mm (SD 1.8 mm; range 4.3–13.0 mm) in boys and 8.2 mm (SD 1.5 mm; range 3.4–11.8 mm) in girls{The LCL ligament is very close to the growth plate}. The distance between the growth plate and both collateral ligaments as well as the length of the LCL correlated positively with patients’ age and body size.
During growth, the femoral origins of the MCL and the LCL are constantly located on the distal femoral epiphysis. There is a linear increase in the distances from the ligaments’ origins to the growth plate according to age and body size.”

“The LCL attaches slightly closer to the growth plate than the MCL. The distances between the origins of the ligaments and the distal femoral growth plate increase in a nearly linear pattern until closure of the growth plate.”

Where tendons and ligaments meet bone: attachment sites (‘entheses’) in relation to exercise and/or mechanical load.

“Entheses (insertion sites, osteotendinous junctions, osteoligamentous junctions) are sites of stress concentration at the region where tendons and ligaments attach to bone.”

“Tendons and ligaments can be regarded as machines with multiple moving parts (fibrils, fibres and fascicles) that perform the basic function of force transfer to and from the skeleton. They distribute the loads applied to them dynamically in order to execute movement patterns. Their complex response to loading allows for multi-axis bending, and this adds to the stress concentration in the region where they attach to bone. This attachment site will be referred to in this review as an ‘enthesis’, but it is also known as an ‘insertion site’, or an ‘osteotendinous’ or ‘osteoligamentous’ junction.”

The tissue at the enthesis insertion site is either fibrous or fibrocartilagenous.

“chondral–apophyseal entheses are found at the ends of the long bones and periosteal–diaphyseal attachments occur on the shafts.”

“At fibrous entheses, the tendon or ligament attaches either directly to the bone or indirectly to it via the periosteum. In both cases, dense fibrous connective tissue connects the tendon/ligament to the periosteum and there is no evidence of (fibro)cartilage differentiation”

“Fibrocartilaginous entheses are sites where chondrogenesis has occurred and thus four zones of tissue are commonly present: pure dense fibrous connective tissue, uncalcified fibrocartilage, calcified fibrocartilage and bone”

“The inclusion of a zone of ‘pure dense fibrous connective tissue’ and a zone of ‘bone’ at a fibrocartilaginous enthesis highlight the difficulty of defining with any degree of precision where such an enthesis begins and ends.”<-Thus the ligament that attatches to the epiphysis near the growth plate line may extend partially into the bone itself.

“the proportion of the enthesis subchondral bone plate which consists of calcified fibrocartilage increases with age, because of a thinning of the cortical bone”

“Although tendons and ligaments are often viewed as non-distensible, they do have the ability to stretch and recoil by approximately 6% of their original length without any obvious signs of damage.”

“entheses can act as growth plates for apophyses at tendon and ligament attachment sites.”

“cartilage at the enthesis is initially derived from that of the embryonic bone rudiment.”

“this hyaline cartilage is eroded during endochondral ossification and replaced by enthesis fibrocartilage that develops within the adjacent ligament by fibroblast metaplasia.”

“Bony spurs (enthesophytes) are well documented at numerous entheses as bony outgrowths that extend from the skeleton into the soft tissue of a tendon or ligament at its enthesis”<-our goal is a cartilage ingrowth into the bone from the tendon/ligament.

Magnetic resonance imaging of entheses. Part 1.

“Achilles tendon, sagittal, histological section stained with Toluidine blue. Enthesis (EF) sesamoid (SF) and periosteal (PF) fibrocartilages are seen. The retrocalcaneal bursa (B) lies between the tendon and the bone and contains the tip of Kager’s retromalleolar fat pad (KP).”

“One of the interesting features of fibrocartilaginous entheses is the paucity[scarcity] of compact bone (often referred to as the cortical shell) immediately beneath the attachment site. The subchondral plate (i.e. the associated calcified fibrocartilage and cortical shell) is often very thin and in many fibrocartilaginous entheses, there are local areas where subchondral bone and calcified fibrocartilage are absent.“<-Thus, it would be easier for cells to migrate there.

“Fibrocartilage forms in tendons that are translocated around bony pulleys and regresses in tendons that are re-routed so that they are no longer subject to compression in the same region.”

Here’s the new LSJL routine I’m trying.  It’s not quite the same as LSJL as it’s not based on loading the synovial joints really, it’s more about loading groups of bones that are connected close to another bone by it’s growth plates.  It’s based on the observation that my arms gained in length relatively consistently but not the rest of my body.  The manner in which I clamp my elbow is relatively unchanged versus how I clamped it into LSJL.

For example, in LSJL you clamp the synovial joint on it’s side.

If you clamp the knee on it’s side you are pressing ligaments against the growth plate.

However by pressing the patella against the growth plate line you are not just pressing the ligament near the growth plate line(growth plate remnant), you are pressing the bone against the ligament which would generate a new stimulus.

The philosophy behind LSJL was to induce lateral compression of the bones to induce fluid flow in the bone to generate hydrostatic pressure to induce mesenchymal condensation to form neo-growth plates to grow taller.

Ligaments and other connective tissue have stem cells and coincedentally some run directly into the growth plate region.  Osteoclasts could theoretically eat away at bone and ligament stem cells could migrate and form neo growth plates within this growth plate line.  I’ll be posting some things to explore this theory.

Here’s where and how I’m clamping.  I know the pictures are bad but even if the pictures were better you’d still have to feel and experiment with the optimal clamping position.  But the idea is to clamp one bone against another bone.  So you clamp the fibula against the tibia or the patella against the femur.  Since bones often are connected to each other near the growth plate region this allows for the possibility of stimulating growth plate regeneration.

Now I haven’t tested this routine that long and ligaments and soft tissue are more fragile then bone.  So do this routine at your own risk especially something like the patella clamp.  I also have pretty minimal evidence so far as the only clamp that’s proved to be decently effective is the elbow clamp.  Most I’ve done for these clamps is a count of 120 but I get results for elbow clamping with about that much.  I’m going for several sessions a day though.

I might have to do a video as well for each to explain how I find the right clamping spots.

Patella clamp:

Fibula clamp:

Ankle(Tibia and Fibula) Clamp:

Cuneiforms and Metatarsals Clamp:

Elbow(humerus clamp):

Radius and Ulna(Wrist) Clamp:

Metacarpal bones(clamp):

Losartan may or may not affect height growth as occassionally suppresion of osteoclasts decreases height growth.

Losartan increases bone mass and accelerates chondrocyte hypertrophy in developing skeleton.

“Angiotensin receptor blockers (ARBs) are a group of anti-hypertensive drugs that are widely used to treat pediatric hypertension. ARBs treat diseases such as Marfan syndrome or Alport syndrome has shown positive outcomes in animal and human studies, suggesting a broader therapeutic potential for this class of drugs.  ARBs [effect] adult bone homeostasis; however, its effect on the growing skeleton in children is unknown. We investigated the effect of Losartan, an ARB, in regulating bone mass and cartilage during development in mice. Wild type mice were treated with Losartan from birth until 6weeks of age, after which bones were collected for microCT and histomorphometric analyses. Losartan increased trabecular bone volume vs. tissue volume (a 98% increase) and cortical thickness (a 9% increase) in 6-weeks old wild type mice. The bone changes were attributed to decreased osteoclastogenesis as demonstrated by reduced osteoclast number per bone surface in vivo and suppressed osteoclast differentiation in vitro. At the molecular level, Angiotensin II-induced ERK1/2 phosphorylation in RAW cells was attenuated by Losartan. RANKL-induced ERK1/2 phosphorylation was suppressed by Losartan, suggesting a convergence of RANKL and angiotensin signaling at the level of ERK1/2 regulation. To assess the effect of Losartan on cartilage development, we examined the cartilage phenotype of wild type mice treated with Losartan in utero from conception to 1day of age. Growth plates of these mice showed an elongated hypertrophic chondrocyte zone and increased Col10a1 expression level, with minimal changes in chondrocyte proliferation. Inhibition of the angiotensin pathway by Losartan increases bone mass and accelerates chondrocyte hypertrophy in growth plate during skeletal development.”

The images suggest that Losartan makes bones less porous.

“The growth plate is divided into four discrete zones defined by morphology: 1) the small round chondrocytes at the end of long bone constitute resting zone (RZ); 2) flattened chondrocytes with a typical columnar organization constitute proliferative zone (PZ); 3) the enlarged post-mitotic chondrocytes form the hypertrophic zone (HPZ); 4) the transitioning cells between proliferative and hypertrophic chondrocytes are referred to as pre-hypertrophic chondrocytes. Prominent Agtr1 signal in the hypertrophic chondrocytes (HPZ) ”

“Proliferative chondrocytes express a lower level of Agtr1 than hypertrophic chondrocytes do, while resting chondrocytes exhibit nearly absence of Agtr1expression”

“To evaluate how AngII signaling inhibition affects cartilage development in the long bone, we analyzed the growth plate of mice with or without Losartan treatment in utero from conception until P1. The total length of the growth plate did not show a significant difference between treated and untreated mice”