Mechanical Loading on Tendons(Some evidence for Entheses LSJL)

Considering the alternative LSJL method relies on pushing two bones against one other at ligament and tendon attachment sites, understanding how mechanical loading affects tendons is important.

The effects of mechanical loading on tendons–an in vivo and in vitro model study.

“Mechanical loading constantly acts on tendons. This study aims to investigate tendon mechanobiological responses through the use of mouse treadmill running as an in vivo model and mechanical stretching of tendon cells as an in vitro model. In the in vivo study, mice underwent moderate treadmill running (MTR) and intensive treadmill running (ITR) regimens. Treadmill running elevated the expression of mechanical growth factors (MGF) and enhanced the proliferative potential of tendon stem cells (TSCs) in both patellar and Achilles tendons. In both tendons, MTR upregulated tenocyte-related genes: collagen type I (Coll. I ∼10 fold) and tenomodulin (∼3-4 fold), but did not affect non-tenocyte-related genes: LPL (adipocyte), Sox9 (chondrocyte){this is the gene were are looking for}, Runx2 and Osterix (both osteocyte). However, ITR upregulated both tenocyte (Coll. I ∼7-11 fold; tenomodulin ∼4-5 fold) and non-tenocyte-related genes (∼3-8 fold){so the load has to be sufficient to affect the target gene}. In the in vitro study, TSCs and tenocytes were stretched to 4% and 8% using a custom made mechanical loading system. Low mechanical stretching (4%) of TSCs from both patellar and Achilles tendons increased the expression of only the tenocyte-related genes (Coll. I ∼5-6 fold; tenomodulin ∼6-13 fold), but high mechanical stretching (8%) increased the expression of both tenocyte (Coll. I ∼28-50 fold; tenomodulin ∼14-48 fold) and non-tenocyte-related genes (2-5-fold){Stretching has to be high to affect the target gene}. However, in tenocytes, non-tenocyte related gene expression was not altered by the application of either low or high mechanical stretching{So mechanical stretching likely cannot induce transdifferentiation}. Excessive mechanical loading caused anabolic changes in tendons, it also induced differentiation of TSCs into non-tenocytes.”

So we induce the differentiation of TSCs and Ligament Stem Cells(which are likely similar to tenocyte stem cells) into chondrocytes at the entheses which can then form new growth plates.

” IGF-1 is of interest because its Eb isoform, also known as mechano-growth factor (MGF), may be a key component of the mechanism that translates mechanical loads into cellular biological changes.”

“under mechanical loading conditions, TSC population in the tendon grows, providing progenitors”

““round tenocytes” were observed in the supraspinatus tendon after intensive treadmill running (16.7 m/min) for 12 weeks. Based on our findings in this study, we suspect that these “round tenocytes” could be chondrocytes differentiated from TSCs, because i) TSCs, not tenocytes, are able to undergo non-tenocyte differentiation under high mechanical loading conditions; ii) a round shape is a typical morphology of chondrocytes, and iii) these round cells produce abundant proteoglycans detected around the cells in the tendon”

This study provides evidence for the entheses method of LSJL loading(termed henceforth as entheses LSJL).  Where the bone is clamped at the site where two bones are connected by a ligament.  These ligaments contain entheses which attach to the bone and are similar in attachment to the Zone of Ranvier.  That tendons contain stem cells which can differentiate into chondrocytes suggests that it’s probably highly similar that ligaments contain ligament stem cells which can differentiate into chondrocytes.  The difference primarily being that tendons are constantly subjected to mechanical load by virtue of their attachment to muscle.  The issue now is proving that there are stem cells within the entheses of a ligament.


Knowledge about the attachment of ligaments and tendons to bone is important to the new method of LSJL loading.  This method involves clamping regions where two bones are attached to each other via ligaments.

According to Physical Therapies in Sport and Exercise there is no communication between tendons and bone however.  It describes the tendon enthesis as as an unmineralized bundle of rounded cell fibrocartilage wrapped in bundles of type II collagen.  It states though that these cells do not have connective arms to other cells so tendons and bones would have no communication.  We are interested in ligaments rather than tendons, as tendons would get  a lot of load from muscular activity but is still relevant as both tendons and ligaments have entheses.

Enthesis fibrocartilage cells originate from a population of Hedgehog-responsive cells modulated by the loading environment.

“Tendon attaches to bone across a specialized tissue called the enthesis. This tissue modulates the transfer of muscle forces between two materials, i.e. tendon and bone, with vastly different mechanical properties. The enthesis for many tendons consists of a mineralized graded fibrocartilage that develops postnatally, concurrent with epiphyseal mineralization.  By genetically demarcating cells expressing Gli1 in response to Hedgehog (Hh) signaling, we discovered a unique population of Hh-responsive cells in the developing murine enthesis that were distinct from tendon fibroblasts and epiphyseal chondrocytes. Lineage-tracing experiments revealed that the Gli1 lineage cells that originate in utero eventually populate the entire mature enthesis. Muscle paralysis increased the number of Hh-responsive cells in the enthesis, demonstrating that responsiveness to Hh is modulated in part by muscle loading{surprisingly lower muscle loading seems to increase responsiveness}. Ablation of the Hh-responsive cells during the first week of postnatal development resulted in a loss of mineralized fibrocartilage, with very little tissue remodeling 5 weeks after cell ablation. Conditional deletion of smoothened, a molecule necessary for responsiveness to Ihh, from the developing tendon and enthesis altered the differentiation of enthesis progenitor cells, resulting in significantly reduced fibrocartilage mineralization and decreased biomechanical function. Hh signaling within developing enthesis fibrocartilage cells is required for enthesis formation.”

“Fibrous entheses include a periosteal component and typically insert into the metaphyses or diaphyses of long bones. By contrast, fibrocartilagenous attachments typically insert into epiphyses or bone ridges. These attachments are characterized by a partially mineralized region of fibrocartilage at the tendon-bone interface, with a round cell morphology and increased proteoglycan content relative to tendon. Due to these characteristics, mature entheses have been likened to arrested growth plates

Since tendons at first glance do not have much communication between themselves and bones how about ligaments?

Establishing a Coculture System for Ligament-Bone Interface Tissue Engineering

“Ligament-bone interface (enthesis) is a complex structure which comprises of ligament, fibrocartilage and bone. The fibrocartilage transformation adds significant insertional strength to the interface and makes it highly resistant to avulsion forces. Many ACL grafts cannot generate native interfacial region, leading to their failure. Co-culture has proved to be an effective way to generate new tissues in tissue engineering. Studies have found important signaling molecules in transduction pathway of chondrogenesis to be transmitted via gap junctions. Stem cells cocultured between ligament and bone cells would enable transmission of chondrogenic factors from bone/ligament cells to bone marrow stem cells (BMSCs) via gap junctions, resulting in their differentiation into fibrocartilage.  In this study, two set of co-culture (BMSCs and ligament cells; BMSCs and bone cells) were established. Confocal microscopy showed efficient dye transfer from bone/ligament cells into BMSCs. This was further confirmed and quantified by FACS, which showed a gradual temporal increase in the percentage of BMSCs acquiring Calcein.”

This study also states that there is ligament and bone communication:

In vitro study of stem cell communication via gap junctions for fibrocartilage regeneration at entheses.

Entheses are fibrocartilaginous organs that bridge ligament with bone at their interface and add significant insertional strength. To replace a severely damaged ligament, a tissue-engineered graft preinstalled with interfacial fibrocartilage, which is being regenerated from stem cells, appears to be more promising than ligament-alone graft. Such a concept can be realized by a biomimetic approach of establishing a dynamic communication of stem cells with bone cells and/or ligament fibroblasts in vitro.

The current study has two objectives. The first objective is to demonstrate functional coculture of bone marrow-derived stem cells (BMSCs) with mature bone cells/ligament fibroblasts as evidenced by gap-junctional communication in vitro. The second objective is to investigate the role of BMSCs in the regeneration of fibrocartilage within the coculture.

Rabbit bone/ligament fibroblasts were dual-stained with DiI-Red and calcein (gap-junction permeable dye), and cocultured with unlabeled BMSCs at fixed ratio (1:10). The functional gap junction was demonstrated by the transfer of calcein from donor to recipient cells that was confirmed and quantified by flow cytometry. Type 2 collagen (cartilage extracellular matrix-specific protein) expressed by the mixed cell lines in the cocultures were estimated by real-time reverse transcription PCR and compared with that of the ligament-bone coculture (control).

Significant transfer of calcein into BMSCs was observed and flow cytometry analyses showed a gradual increase in the percentage of BMSCs acquiring calcein with time. Cocultures that included BMSCs expressed significantly more type 2 collagen compared with the control.

The current study, for the first time, reported the expression of gap-junctional communication of BMSCs with two adherent cell lines of musculoskeletal system in vitro and also confirmed that incorporation of stem cells augments fibrocartilage regeneration. The results open up a path to envisage a composite graft preinstalled with enthesial fibrocartilage using a stem cell-based coculture system.”

” Inside the embryo, tendons and ligaments appear as fibrous cellular outgrowths from the perichondrium of cartilaginous precursor to later bone. In the neonates, as the cartilaginous anlage ossifies, fibrocartilaginous elements of the ligament are cemented into the initial calcified cartilage, which is later replaced by mature bone. Only a thin layer of proliferative epiphyseal cartilage remains at the interface{this is a very promising fact as proliferative epiphyseal cartilage is a solid start in term of neo growth plate formation}. The resulting mature tendon or ligament insertion comprises four zones: collagenous ligament or tendon, nonmineralized fibrocartilage, mineralized fibrocartilage and cancellous bone”

The role of muscle loading on bone (Re)modeling at the developing enthesis.

“Muscle forces are necessary for the development and maintenance of a mineralized skeleton. Removal of loads leads to malformed bones and impaired musculoskeletal function due to changes in bone (re)modeling. In the current study, the development of a mineralized junction at the interface between muscle and bone was examined under normal and impaired loading conditions. Unilateral mouse rotator cuff muscles were paralyzed using botulinum toxin A at birth. Control groups consisted of contralateral shoulders injected with saline and a separate group of normal mice. It was hypothesized that muscle unloading would suppress bone formation and enhance bone resorption at the enthesis, and that the unloading-induced bony defects could be rescued by suppressing osteoclast activity. In order to modulate osteoclast activity, mice were injected with the bisphosphonate alendronate. Bone formation was measured at the tendon enthesis using alizarin and calcein fluorescent labeling of bone surfaces followed by quantitative histomorphometry of histologic sections. Bone volume and architecture was measured using micro computed tomography. Osteoclast surface was determined via quantitative histomorphometry of tartrate resistant acid phosphatase stained histologic sections. Muscle unloading resulted in delayed initiation of endochondral ossification at the enthesis, but did not impair bone formation rate. Unloading led to severe defects in bone volume and trabecular bone architecture. These defects were partially rescued by suppression of osteoclast activity through alendronate treatment, and the effect of alendronate was dose dependent. Similarly, bone formation rate was increased with increasing alendronate dose across loading groups. The bony defects caused by unloading were therefore likely due to maintained high osteoclast activity, which normally decreases from neonatal through mature timepoints. These results have important implications for the treatment of muscle unloading conditions such as neonatal brachial plexus palsy, which results in shoulder paralysis at birth and subsequent defects in the rotator cuff enthesis and humeral head. ”

This study only studied tendon and not ligament entheses though.

This site has a lot of into about entheses:

“The normal enthesis has a tendency to develop new bone formation with ageing. This manifests as incidental “bony spurs” that are visible on X-rays”

“Joint tissues under tension favours bone development and the outermost part of the enthesis is subject to predominant tension (pulling force).”

Here’s an entheses with neo-bone formation:
enthesesFc stands for fibrocartilage and the arrows are pointing at abnormal bone formation.  Not how the fibrocartilage is shaped into the bone like a zone of ranvier.
zone of ranvier

This website describes the groove of Ranvier:

“During the first year of life, the zone spreads over the adjacent metaphysis to form a fibrous circumferential ring bridging from the epiphysis to the diaphysis”

“This ring increases the mechanical strength of the physis and is responsible for appositional bone growths.  Supplies chondrocytes to periphery

The site also says that ligaments have rounder cell morphology than ligaments which is more consistent with a chondrocyte cell.  Interestingly it says that ligaments also do not plastically deform which means that they can not permanently increase in length as a result of pulling force.

Strategies to engineer tendon/ligament-to-bone interface: Biomaterials, cells and growth factors.

“The complex and heterogeneous structure of the enthesis is essential to ensure smooth mechanical stress transfer between bone and soft tissues. Following injury, the interface is not regenerated, resulting in high rupture recurrence rates. ”

“entheses exhibit gradients in tissue organization, composition and mechanical properties that serve to (1) effectively transfer stress between mechanically dissimilar materials and (2) sustain the heterotypic cellular communications required for interface function and homeostasis”

“the first part of the enthesis consists of fibrous connective tissue (tendon/ligament) characterized by the presence of parallel collagen fibers with interspaced elongated fibroblasts organized in arrays. The ECM primarily consists of collagen type I and small amounts of proteoglycans. The next zone is non-mineralized fibrocartilage, populated by round fibrochondrocytes arranged in rows. The ECM contains mostly collagen type II (typically characteristic of hyaline cartilage) as well as high levels of pericellular collagen type III, small amounts of collagen types I and X, and proteoglycans (mainly aggrecan) with associated chondroitin 4- and 6-sulfate glycosaminoglycans (GAGs). The third zone is mineralized fibrocartilage. This zone is populated by hypertrophic fibrochondrocytes, which are round and bigger than fibrochondrocytes. The ECM is composed mainly of collagen type II with significant amounts of collagen type X and aggrecan. Finally, the mineralized fibrocartilage merges into bone tissue containing osteoblasts, osteocytes and osteoclasts, together with collagen type I and high mineral content (69%) of which 99% is hydroxyapatite”<-Fibrocartilage may not be cartilage but it should should be capable of interestitial growth like growth plates.

“Enthesis fibrocartilage has been proposed to act as a barrier for cellular communication between tendon/ligament fibroblasts and osteocytes. This is due to the fact that fibrocartilage tissue is poorly vascularized and fibrochondrocytes do not express connexins and do not form gap junctions. Thus, intercellular communication needs to take place indirectly via cell–matrix interactions or soluble factors.”<-This will make getting stem cells from the enthesis into the bone slightly more challenging.

” the similarity in cellular and ECM composition between the fibrocartilage and the hyaline cartilage indicates an adaptation to compression. Consistently, mechanical loading plays an important role during enthesis maturation and contributes to the generation of a structural and cellular gradient at the insertion site. This gradation of structural composition turns into a gradation of mechanical properties that enables load transmission and reduces stress concentration”

enthesisgeneEnthesis cells express both Scx+ and Sox9+ progenitor cells.  We have to encourage the enthesis to express more Sox9.

“During murine development, a progenitor cell population expressing both scleraxis (Scx) and Sox9 differentiates into Sox9 + chondrocytes or Scx + tenocytes/ligamentocytes to form the tendon/ligament-to-cartilage junction. Interestingly, tenocytes are derived from both Scx +/Sox9 − and Scx +/Sox9 + progenitors, while ligamentocytes are derived exclusively from Scx +/Sox9 + progenitors[So ligaments always have chondrocyte differentiation capacity]. The closer the tendon is to the cartilaginous primordium, the more tenocytes arise from Scx +/Sox9 + progenitors. Similarly, enthesal chondrocytes located near the tendon/ligament-to-cartilage junction arise from Scx +/Sox9 + progenitors, while growth plate chondrocytes are derived from Scx −/Sox9 + progenitors. As development proceeds, the Scx +/Sox9 + progenitor cells upregulate either Scx expression, leading to cells of the tendon/ligament lineage, or Sox9 expression, leading to cells of the chondrocyte lineage. It has been proposed that TGF-β is necessary for Scx +/Sox9 + progenitor cell lineage specification, while the BMP-4/Scx axis determines its differentiation.”

“Fibrochondrocyte cells are expected to show a higher expression of collagen type II and lower expression of collagen type I when compared to fibroblasts. In addition, hypertrophic fibrochondrocytes synthetize higher levels of collagen type X. Chondrocytes, however, produce more collagen type II and less collagen type I than fibrochondrocytes.”

According to this paper, a crocodile may have a fibrocartilagenous growth plate which means that creating such a growth plate for humans is possible:

Crocodilian bone-tendon and bone-ligament interfaces

“We investigated bone-tendon (27 sites) and bone-ligament (12 sites) interfaces in six pairs of crocodile limbs and girdles under light microscopy. These crocodilian interfaces often included a direct, unmediated insertion in which the tendon or ligament fibers inserted directly into the bone itself without fibrocartilaginous mediation. This was quite different from the usual direct insertion known in mammals and lizards. Fibrocartilaginous tissue at the bone-tendon interface is generally believed to protect tendon fibers against shear stress. Other types of insertions were found in the crocodilian epiphyses, namely, hyaline cartilage and pseudofibrocartilaginous insertions. Notably, a thick periosteum/perichondrium and subchondral layer was involved at both interfaces. The thick periosteum/perichondrium seemed to form along the epiphyseal hyaline cartilage and might function in replacement of fibrocartilaginous tissues. Crocodilian thick periosterum/perichondrium would be expected to reinforce the limb and girdle bones — especially their epiphyses, in which secondary centers of ossification are absent. The subchondral layer — a kind of fibrocartila-ginous tissue — seemed to play the role of the growth plate in compensating for the absence of secondary centers of ossification. Therefore, we hypothesized that the crocodile-specific bone-tendon interfaces were the result of these specializations of bone development and growth. In crocodiles, the disadvantages of the single ossification center are effectively compensated for by specialized morphologies, including these interfaces. Specialized bone growth provides the crocodile with the largest body size of the recent reptiles and an extremely fast method of locomotion.”

Although according to the book Fins into Limbs: Evolution, Development, and Transformation avian growth plates become fibrocartilagenous when they are done growing.

The human tibial tubercle is formed by fibrous growth plates.

To Dwell on Height-Healthy or Unhealthy?

To focus on the disadvantages of height is an unhealthy psychological pursuit.  To focus on striving to grow taller is a healthy psychological pursuit.

Here’s a typical conversation to someone about height:

A:  Don’t worry about height.  It’s what’s on the inside that counts.

B:  Why is it acceptable for height to be descriminated against?  Why is male height so associated with a male’s value?  Why is it acceptable to laugh at people because of their height?

A: You should accept who you are.  Play with the cards your dealt.

B:  If you have a losing hand, do you accept that or do you throw the cards off the table and start a fist fight?  If you can’t beat the game change the rules.

A: Life isn’t fair.  Sucks for you.

If you try to get into an argument with someone about height it usually begins with a lot of platitudes which are refuted until their opposing argument devolves into “too bad”.

The argument with the best reasoning often isn’t the argument that wins.  Short support sites shouldn’t exist.  Realistically, very little improvements can be made for the average or below against the tall.  And ultimately such sites serve as a means of perseverating on height.

You can try to forget your height.  You can play video games.  You can engage in an activity where height is of less importance such as a musical instrument.  Although even in those activities such as piano or guitar, finger length has an effect on playing.  You can get around it with techniques but it’s still a reminder that you’re just not as good.  Even playing pool, height can be an advantage in performing certain shots.

There’s acceptance but will you ever accept?  Ryan Seacrest complains about his height all the time.  There’s escapism but will you be satisfied with just escape?  Most forms of escapism lack the depth and complexity of real life.

The healthiest way to focus on height is to strive to find a way to grow taller.  Instead of dwelling on it.  Instead of comparing height with your friends.  Instead of realizing that you’re shorter than that other guy that you thought was really short.

The research I’ve done on entheses is intriguing and I’m trying to develop a new routine to explore it. What’s most intriguing about Entheses is that it resembles the Zone of Ranvier which contains the stem cells to contribute to the growth plate.  What if by pushing two bones together such as the fibula and the tibia on the epiphyseal region we can stimulate the entheses to form neo growth plates?

Don’t accept that there’s no way to grow taller.

Your height is mostly based on the length of your bones{The other determinants of height are opportunities to find new ways to grow taller}.  The length of the bones is determined mostly by your growth plate{The rest of the length is determined by other means but are difficult to get to contribute in significant ways but again is another way to pursue the quest for height}.  The growth plate goes away after puberty after the exhaustion of the stem cells that contribute to the growth plate.

To grow taller you could find:

1) Increase other minor determinants of height not involving growth plate growth

2) Induce the formation of neo growth plates

3) Induce plastic(permanent) deformation of the long bones.  Stretch the bones in such a way that they increase in length in a way that is instant and permanent(although this has never bone in done and the mechanisms of measurement are not accurate enough to best gauge the elastic and plastic range of a bone).

4) Other?  For you to determine.

Escapism and acceptance aren’t the only options for dealing with your height.  Don’t let people tell you that you should just accept your height.  Every time you think about dwelling on the negative effects of not being tall, focus instead on finding ways to grow taller.

You can get distraction osteogenesis surgery but it costs a lot of money and ideally you’d have multiple surgeries.

This field of science is entirely under researched(but most areas are due to how slowly science progresses).  And due to the complexity it is difficult for it to be Lorenzo’s Oiled(Homemade scientific discovery).  It’ll be hard to find a more efficient way of performing distraction osteogenesis but you could find a home made way of inducing new growth plate formation.  Cells do respond to mechanical and chemical stimulation after all.  And has every manner of mechanical stimulation already been performed?  No.  Especially methods that would appear counterintuitive like lateral joint loading(now adjusted to focus more on pushing two bones together near the entheses rather than clamping the synovial joint region).  And there are novel apparatus to create to generate forces that we couldn’t using our own muscular force.

Don’t dwell on how Dave France doesn’t get as good a roles as James Franco because he’s shorter.  Don’t dwell on how the third Hemsworth brother doesn’t get as many roles because he’s shorter.

Focus on researching methods to grow taller!  Even when I find a way to grow taller, it’s not going to be perfect right away.  I’m going to need your help.  You’re going to need my help.  The faster people stop dwelling on height and start growing taller the faster we can start getting taller.

If You Feel Depressed Or Angry Over Your Short Height – For Reddit and Sluthate

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

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. ( 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.”



Including growing taller and we should accept nothing less.}

The Unhealthy Obsession Of Basketball Players Towards Height, Why I Am Giving Up Basketball and Football

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 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 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 your height growth be influenced by your community?

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.