How to increase kids height?

Forgive me the somewhat broken English.  The title is intended to target people looking for ways to increase their child's height.  Some might consider that child abuse but you also have to consider that you have to factor in that most fields are highly competitive and you want to give your child the best opportunities you possibly can.

I read somewhere in Freakonomics I believe that children born in certain months tended to be more likely to be successful in sports because they tended to be relatively bigger than other children their age. Being more successful at lower age levels led to improved training which turned into success at the higher levels. Well, imagine if you could increase growth rate?  You could give your children an advantage in athletics regardless of what month they were born in.

Here's some tips to increase kids height or rather their growth rate as all that matters in giving children an athletic advantage is an increase in growth rate.

Number one of course is growth hormone.  Growth hormone has been shown to markedly improve growth rate if not increasing bone length.

Epiphyseal distraction is another method.  Although this method was developed to increase height but failed it's still a way to increase growth rate.  Any method to provide distraction forces on the growth plate including lateral synovial joint loading(which provides distraction forces on the growth plate in addition to stretching forces on the cortical bone) will increase growth rate.  Bed rest also releases compression on the growth plate.

Another "natural" way to increase your child's height is to increase the level of growth hormone via exercise.

Growth hormonal methods are most effective as you also want to increase your child's muscle mass in addition to accelerating bone growth.

Adult methods such as increasing periosteal width or articular cartilage growth via microfractures may also be effective.  However, growth hormone has been shown to have limited effect on increasing periosteal width pre-puberty.

Yoko Height increase - How do we nerf the scammers?

Yoko height increase products and kimi height increase products are two of the prevalent scam sites on the internet.  Yoko cannot be an effective height increaser because it supposedly works works by increasing growth hormone.  As I stated in my series on Gigantism:  Human Growth Hormone only has the potential to increase periosteal width so it could potentially increase the height of the irregular bones in the spinal column but HGH can't affect the height of the long bones unless it's mutated.  Articular cartilage growth is another one of the claims made by gainheight.com one of the Yoko height increasing sites.  As I said in my article on growing with articular cartilage that it is possible for articular cartilage growth but as a result of my microfractures which release bone marrow stem cells which stimulate articular cartilage growth(the bone marrow needs to be coupled with blood flow).

The kimi height increasing product again works by stimulating growth hormone(if it has that affect at all) but again it needs to be mutated growth hormone to have any affect other than increasing periosteal width!

So how do we beat the scammers at their game?  We rank for their keywords for SEO methods and inform people!  We answer questions on Yahoo Answers about why these products are scams!

And then we give people more informed information like the very promising lateral synovial joint loading routine(I know most of you are having trouble understanding it I will have some more pictures of how to perform it with dumbells up soon I know someone is performing it with 10 lbs textbooks!).  If you're trying yoga to increase height than you might as well give lateral synovial joint loading a shot!

Height increase surgery and height increase shoe inserts are not scams but surgery is always bad if you can avoid it and I'd rather grow taller with hard work than just wearing lifts.

You can increase height after 25!  There are height increasing tips that work!  We have to start by convincing people that they should be trying other methods than wearing height increase insoles and that the only height increase products that work are well thought out exercises to increase height(yes there may be chemical methods as well but chemicals are were scammers thrive!).

This post was stuffed with keywords that I got from reading google's free adwords tool.  I guess you can consider it another pre-April Fool's Joke?  Yeah, it's a pretty lame attempt to try to get more search traffic to my site but we gotta fight growtaller4idiots idiots with some of their own medicine don't they?  We can't rely solely on social traffic to get people to good decent height increase information like on giantscientific.com or easyheight.com.

Finding the right height increase program starts with you!

Gaining height via chiropractic, acupuncture, and massage?

Spinal alignment is a part of overall body height.  A misaligned spine can affect the alignment of several other bones as well.  It's not just the length of the bones that matters for height or how tall you are it's also the architecture and placement of your bones.

The problem is that the effects of chiropractic treatment are so temporary.  Yes, adjusting the spine can affect overall height but is chiropractic treatment that effective? 

The costs and benefits of nonoperative management for adult scoliosis. 

"A prospective cohort of adult scoliosis patients treated nonoperatively had a minimum of 2-year follow-up during which time data were collected on the type and quantity of nonoperative treatment used... A 2007 systematic review of nonsurgical treatment in adult scoliosis revealed minimal data, and concluded that evidence for nonoperative care was lacking. METHODS: Duration of use and frequency of visits were collected for 8 specific treatment methods: medication, physical therapy, exercise, injections/blocks, chiropractic care, pain management, bracing, and bed rest. Costs for each intervention were determined using the Medicare Fee schedule. Outcome measures were the SRS-22, SF-12, and ODI. Analysis was performed for the entire group, and for subsets of high (ODI, >40), mid (ODI = 21-40) and low (ODI, In 55 scoliosis patients who received no treatment, the only significant change in HRQOL measures over the 2-year period was in SRS satisfaction subscore (0.3 points, P = 0.014). Among the 68 adult scoliosis patients who used nonoperative resources, there was no significant change in any of the HRQOL outcome parameters... An important caveat is that treatment was not randomized and therefore the treatment group might have deteriorated if not for the treatment they received." 

It doesn't matter what HRQOL, SRS, SRS-22, or whatever is.  If scoliosis patients can't get improved spinal alignment from chiropractic care who the hell can?  Chiropractors state that fluid builds up in the joints and that their adjustment procedure helps release it.  Chiropractic adjustments also help adjust the discs back into alignment preventing disc degeneration.  It's much easier to prevent disc degeneration than to try to find methods to encourage disc regeneration.  So as a means to help increase height chiropractic care is more of a means to maintain height or not to cancel out any height gains you get from intervertebral disc growth.  Chiropractic treatment will do nothing to fix spinal alignment however(which would be very useful as almost everyone has scoliosis to some degree). 

The problem I have with chiropractic care is that it's incredibly expensive.  I emphasize with chiropractors because they face the same ridicule as height seekers do from the health community.  Surgery should be the alternative medicine not chiropractic care.  Chiropractic treatment is an essential service that is overpriced given that almost everyone could benefit from it.  The field of chiropractic care suffers from price gouging. 

Unfortunately, chiropractors are needed to at least adjust any spinal bones that are out of alignment.  You just can't have the proper leverage to perform such adjustments on yourself.  You can perform some self-adjustments but not as good as a chiropractor can or someone who copies their methods.  It's hard to find people willing to take the risk though.  Chiropractic treatment does suffer from diminishing returns.  If you go once in a while it makes it easier to perform self adjustments as the bones are already loosened. 

Acupuncture, rolfing, and massage all work the same way.  When your muscles are overstretched your golgi tendon goes "Oh my god!  I'm too tight!  I need to relax!"  Your body releases endorphins(that's why massages feel so good) and your muscles relax.  If your muscles were pulling on your bones a certain way then you will end up with a height increase.  This is again effective for temporary height gain.  Your muscles are tight for a reason. 

It's easy to perform self massage(or rather self overstretching).  You can stretch your tight muscles to the point where they begin to relax(see the hundreds of grow taller e-books or websites), pinch your tight muscles until they relax(like the kneading motion of a massage), or put tight focused pressure on your muscle such as with a finger(acupuncture).   

Massage, and Massage-likes are only effective for a temporary increase in height and are not an effective long term strategy like those that would affect the actual bone(such as lateral synovial joint loading).   

Rolfing might be examined further in the future as it is listed as a method on several height increase sites and it involves connective tissues so it is slightly different than massage.

Hypothesis: upregulation of a muscle-specific isoform of insulin-like growth factor-1 (IGF-1) by spinal manipulation.

"Spinal manipulation is a manual therapy approach commonly employed by chiropractors, osteopaths and manipulative physiotherapists in the treatment of back pain. It is characterised by a rapid high velocity, low amplitude thrust which commonly causes an audible 'pop' or 'cavitation' in the joint. Any beneficial effects are generally explained with reference to changes in vertebral joint movement. This paper looks at the process of spinal manipulation to see if there is reason to expect effects beyond simple changes in the biomechanics of the spine. It shows that during the process of spinal manipulation, rapid stretching of spinal muscles is inevitable. muscle stretch is a potent stimulus for the upregulation of a splice product of the insulin-like growth factor gene by the stretched muscle{this upregulation could promote chondrogenesis as well}. Evidence that the product of this gene (mechano-growth factor; MGF) promotes muscle growth and repair (myotrophism) is presented, together with evidence that MGF promotes the growth and repair of neurones (neurotrophism). Against this background the hypothesis is proposed that one of the effects of spinal manipulation is to stretch spinal muscles which will upregulate MGF{also known as IGF-1eC} and result in local myotrophic and neurotrophic effects."

" spinal manipulation involves taking joints (usually zygapophyseal joints) near to their physiological end range by gross twisting of the trunk. This is followed by application of a more specific directional force to the joint (‘preload’) to bring it very close to its physiological range of movement. This preload (20–180 N) is followed without any reduction in force by a high velocity, low amplitude thrust (220–550 N) to the joint. The latter force is delivered over 200–400 ms. It pushes the joint briefly beyond its normal physiological range of movement and this event may be associated with an audible ‘pop’ or ‘cavitation’. The process of twisting the spine to a position where the preload and thrust are most efficiently delivered is often referred to as the ‘set-up’. This clearly involves stretch of muscles associated with the vertebral column-it can be seen and patients are aware of it. In contrast to spinal mobilisation, however, the process of spinal manipulation has the capacity to cause brief stretching of already contracting vertebral muscles (eccentric stretch). The electrophysiological evidence for this is as follows: the dynamic thrust has been associated with increased surface electromyographic (SEMG) activity of paraspinal muscles that occurs within 50–200 ms of the thrust and it is likely that both intrinsic and paravertebral muscles are involved. The latency of the SEMG response, however, is too short to be a voluntary contraction. Instead it has a latency within the range for the human stretch reflex that has been determined with cross-correlation and signal averaging techniques. This is strong evidence that spinal manipulation elicits a stretch reflex. This view is supported by experimental studies in the anaesthetised cat, where dorsoventral impulses applied to the L6 vertebra to mimic spinal manipulation evoked reflex neural activity that was recorded in the L6 dorsal roots and identified as coming from primary and secondary afferents to muscle spindles. The short intrinsic spinal muscles have a much higher muscle spindle density than longer onesand this suggests that they are particularly sensitive to stretch. Taken together, this data indicates that spinal manipulation is likely to cause eccentric contraction of extrafusal muscles of the spine, since a myotatic reflex is stimulated within 50–200 ms of the thrust and this falls well within the timescale of the thrust, let alone any ‘follow-through’ force that may be delivered.."

Can we build our muscles in such a way as to make us taller?

Unfortunately, their are no muscles on the top of the head so we can't gain height via hypertrophy there.  Their are however several muscles in the feet so it could be possible to gain height by having your muscles act sort of like lifts making you taller.

Source: Southwest Orthopedics

The plantar surface refers to the bottom of the foot.  The feet do have an arch(unless you are flat footed) but as evidenced by high heels if any part if the feet is elevated the whole body is elevated.  If we can cause hypertrophy(muscle growth) in say our adductor hallicus and abductor hallicus we will be slightly taller!

The abductor hallicus moves our big toe away from the body so if we say wore toe weights and abducted our toes from side to side we would build up our abductor hallicus.  The foot is not as adapt as the hand(huge understatement) is at gripping but I have lifted a ten pound dumbell by placing it between my big toe and the toe next to my big toe.  This isn't quite as optimal as wearing toe weights and just moving your toes around but most exercises involve the usage of several muscles.

We all know that muscle mass correlates with bone mass but their are determinants of bone mass that are not accounted for by increased muscle masses(determinants that we try to create by say laterally loading the ends of the long bones).  Increasing muscle mass cannot hurt however...

And an increased muscle mass may have systematic effects that aid in bone building.

Muscle may also modulate myostatin activity which inhibits cellular proliferation.  Muscle also provides direct stimulation to the bone.

Is bone formation induced by high-frequency mechanical signals modulated by muscle activity?

"Bone formation and resorption are sensitive to both external loads arising from gravitational loading as well to internal loads generated by muscular activity. The question as to which of the two sources provides the dominant stimulus for bone homeostasis and new bone accretion is arguably tied to the specific type of activity and anatomical site but it is often assumed that, because of their purportedly greater magnitude, muscle loads modulate changes in bone morphology. High-frequency mechanical signals may provide benefits at low- (<1g) and high- (>1g) acceleration magnitudes[so a stimulus that occurs frequently and the peak point of the stimulus is achieved very rapidly]. While the mechanisms by which cells perceive high-frequency signals are largely unknown, higher magnitude vibrations can cause large muscle loads and may therefore be sensed by pathways similar to those associated with exercise. Here, we review experimental data to examine whether vibrations applied at very low magnitudes may be sensed directly by transmittance of the signal through the skeleton or whether muscle activity modulates, and perhaps amplifies, the externally applied mechanical stimulus. Current data indicate that the anabolic and anti-catabolic effects of whole body vibrations on the skeleton are unlikely to require muscular activity to become effective. Even high-frequency signals that induce bone matrix deformations of far less than five microstrain can promote bone formation in the absence of muscular activity[but these stimulus may generate a lot of hydrostatic pressure for instance]. This independence of cells on large strains suggests that mechanical interventions can be designed that are both safe and effective."

"Cortical surface bone strains generated in the proximal tibia during a 0.3g, 45Hz vibratory regime were measured in two adult BALB/cByJ mice16. Under isoflurane anesthesia, a miniature single-element strain gage (1mm gage length) was implanted on the antero-medial surface of the proximal tibia. Upon recovery from surgery and with the animal standing on the vibrating plate, strain data were collected at a resolution of approximately 0.5 microstrain (με). The vibratory oscillations induced peak bone strain oscillations at the antero-medial surface of the tibia on the order of approximately 10με. In the rat, decreasing the acceleration of the signal to 0.15g and increasing the frequency to 90Hz reduces the strain magnitude at the cortical surface to about 2με"<-the acceleration of the signal is more important than frequency.

"subjects subject to 10min/d low-level whole body vibrations (30Hz, 0.3g). A per protocol (PP) analysis demonstrated that women had to stand on the vibrating plate for at least 2 min/d to achieve a gain in bone mass, including a 3.9% net benefit in cancellous bone of the spine or a 3.0% net benefit in cortical bone of the femur. In this study and in contrast to the previous two, muscle was included as an outcome measure. The low-level mechanical signal elevated muscle mass, with a 7.2% net benefit in the total paraspinous musculature, a 5.2% net benefit in the psoas muscle and a 7.9% net benefit in the erector spinae"<-the increase in muscle mass was greater than that of the bone.

"the study which demonstrated anabolism in both muscle and bone of young women employed a frequency of 30Hz. Excitation frequencies of at least 400Hz are required for maximal power output when the muscle itself is stimulated. In contrast, when a muscle dynamically oscillates without any electrical stimulation, its natural frequency is between 10-50Hz"<-dynamic muscle contraction is within the range of frequencies to stimulate bone but we're not sure if this applies to stem cells and chondrocytes as well or just osteoblasts.

"Following a 28d protocol, bone formation rates in the metaphysis of the proximal tibia were 159% greater in 90Hz rats when compared to age-matched controls, but 45Hz rats were not significantly different from controls"<-so to induce bone formation with vibration the frequency has to be greater than that caused by normal muscle contraction 45Hz is less than 50.

"During treatment, mice were anesthesized and therefore, all muscle tone was removed. Mice were allowed to freely ambulate between treatments. After 3wk, trabecular metaphyseal bone formation rates were 88% greater in tibiae accelerated at 0.3g than in their contralateral control, similar to the 66% increase in formation rates of bones accelerated at 0.6g. Stimulated tibiae also displayed significantly greater cortical area (+8%) and thickness (+8%), together suggesting that tiny acceleratory motions – independent of direct loading of the matrix"<-So bone formation can occur independent of muscle activity but myostatin regulation by muscle could still potentially play a role.


Muscle contraction controls skeletal morphogenesis through regulation of chondrocyte convergent extension

"Convergent extension driven by mediolateral intercalation of chondrocytes is a key process that contributes to skeletal growth and morphogenesis. Using the zebrafish as a model system, we found abnormal pharyngeal cartilage morphology in both chemically and genetically paralyzed embryos, demonstrating the importance of muscle contraction for zebrafish skeletal development. The shortening of skeletal elements was accompanied by prominent changes in cell morphology and organization. While in control the cells were elongated, chondrocytes in paralyzed zebrafish were smaller and exhibited a more rounded shape, confirmed by a reduction in their length-to-width ratio. The typical columnar organization of cells was affected too, as chondrocytes in various skeletal elements exhibited abnormal stacking patterns, indicating aberrant intercalation. Finally, we demonstrate impaired chondrocyte intercalation in growth plates of muscle-less Spd mouse embryos, implying the evolutionary conservation of muscle force regulation of this essential morphogenetic process."

However, this doesn't provide evidence that enhanced muscular contration may further elongate chondrogenic cells.

"During endochondral ossification, the mediolateral intercalation of chondrocytes into columns is an important module that facilitates elongation and contributes to bone morphology"

"Cell intercalation is a morphogenetic process, which occurs in epithelial or mesenchymal cells and leads to tissue narrowing, known as convergence, and its elongation, or extension. During convergent extension, the intercalating cell moves to separate neighboring cells, while staying in the same plane. During intercalation, cells increase their length-to-width ratio, perpendicularly to the direction of tissue elongation"

" in mice, unlike in zebrafish, columns are formed in the absence of muscle contraction indicates that the first step of intercalation is mostly muscle independent."

Biomechanical aspects of the muscle-bone interaction.

"Muscle and bone are inextricably linked genetically, molecularly, and mechanically. The intertwining of the connections at the different organizational levels (subcellular, cellular, and supracellular) makes it difficult to tease out the relative contributions of each connection. For instance, a change in the molecular communication between the tissues on the cellular level will likely also change their mechanical linkage at the supracellular (i.e., tissue and organ) level and vice versa."

"oscillatory muscle stimulation to tail-suspended rats for 10 min per day for 4 weeks to show that stimulation at 20 or 50 Hz was able to maintain trabecular bone mass, whereas stimulation introduced at 1 Hz was ineffective. The stimulation at 20 Hz resulted in minimal matrix deformation (<100 microstrain), but resulted in a ninefold increase in oscillatory (peak-to-peak) intramedullary pressure (ImP)"

"IFF can result from bone matrix deformation (i.e., strain) associated with muscle forces during locomotion which give rise to local pressure gradients within the matrix and drive interstitial fluid through the lacunocanalicular system. Alternatively, IFF can be generated through elevations in ImP. Pressurization of the intramedullary cavity causes an outward pressure gradient from the intramedullary cavity to the periosteal surface to also induce IFF within the lacunocanicular system "

Stontium

Stontium is available for sale:
Doctor's Best Strontium Bone Maker (340mg Elemental), 120-Count

Effects of Strontium on Collagen Content and Expression of Related Genes in Rat Chondrocytes Cultured In Vitro.

"chondrocytes were isolated from rat articular cartilage by enzymatic digestion and cultured for 24-72 h with 1-5 mM strontium. We investigated the effects of different concentrations of strontium on collagen content, type II collagen, insulin-like growth factor (IGF-1) and matrix metalloproteinase (MMP)-13 expression in rat cultured articular chondrocytes in vitro. The collagen content of the chondrocytes, determined as hydroxyproline, was measured by a colorimetry method. collagen content from the chondrocytes extracellular matrix increased with increasing strontium concentration. 3 and 5 mM strontium strongly stimulated protein expression and mRNA levels of type II collagen and IGF-1. Conversely, MMP-13 expression in chondrocytes decreased dose-dependently with increasing strontium concentration."

The problem is that MMP13 is an important protein for endochondral ossification.  If the increase in IGF-1 or other pro-chondrogenic compounds is independent of the decrease in MMP13 then maybe there could be a net height increasing effect.

The study mentions that the chondrocyte cytoskeleton was normal between 0-5 mM stontium.



The increase in IGF-1 seems to correlate with the reduction in MMP13 unfortunately.  Although MMP13 seems to have less of a relationship with Type II Collagen.

"In the first 48 h, supplementation with final concentrations of 3 and 5 mM strontium in the culture medium resulted in significantly higher amounts of hydroxyproline [synonym for collagen] than that of the control group"<-Also at 72 hours but not 24 hours.

"1–5 mM strontium had no significant effect on chondrocyte proliferation. Strontium ranelate has no significant effect on the DNA content of chondrocytes"<-Another knock for strontium's height increase potential.

"strontium ranelate increases collagen and non-collagenic protein synthesis by mature osteoblast-enriched cells, and stimulates type II collagen synthesis via a direct ionic effect"<-so the increase in Col2a1 could be independent of the decrease in MMP13.

"in freshly isolated rat chondrocytes, SrCl2 (3.2 and 10 mM) inhibited the synthesis of GAG and collagen. SrCl2 (2 mM) stimulated PG production."

"Cleavage of type II collagen by MMP-13 is required for the differentiation of chondrocytes and matrix mineralization"<-hence it's importance in endochondral ossification.

COMP

Cartilage Oligomeric Matrix Protein Enhances Osteogenesis by Directly Binding and Activating Bone Morphogenetic Protein-2.

"COMP binds BMP-2, and characterized the biochemical nature of the binding interaction. COMP binding enhanced BMP-2-induced intracellular signaling through Smad proteins, increased the levels of BMP receptors, and up-regulated the luciferase activity from a BMP-2-responsive reporter construct. COMP binding enhanced BMP-2-dependent osteogenesis in vitro, in the C2C12 cell line and in primary human bone mesenchymal stem cells, as measured by alkaline phosphatase activity, matrix mineralization, and gene expression. COMP enhanced BMP-2-dependent ectopic bone formation in a rat model. COMP enhances the osteogenic activity of BMP-2, both in-vitro and in-vivo."

But can COMP enhance the chondrogenic activity of BMP-2?  "COMP prolongs BMP-2-dependent Smad activation and receptor levels."<-since BMP-2 Smad signaling can induce chondrogenesis it should.

COMP along with BMP-2 also increased Smad1/5/8 phosphorylation and increased the amount of BMP-2 receptors.

COMP did not affect TGF-Beta signaling.

"Histological analysis showed that BMP-2 application induced bone formation, as observed with the von Kossa positive mineralized matrix and a few cartilaginous masses. Co-administration of BMP-2 and COMP, enhanced the von Kossa positive areas. More Safranin-O positive chondrocytes with empty lacunae were found in BMP-2 plus COMP group, compared to the BMP-2 alone group."<-So BMP-2 and COMP did induce chondrogenesis.

"COMP interacts with aggrecan and collagens, which results in enhanced assembly and retention of the matrix during chondrogenesis in MSCs. COMP regulates endochondral bone growth via overcoming the inhibitory effect toward matrix mineralization, and endochondral bone formation by extracellular matrix protein 1 (ECM1), by interacting to ECM1."

Is it possible to grow taller by gaining more body fat?

Some people have asserted that fat people tend to be taller.  They have speculated that it may be due to an abundance of nutrients or that adipose tissue acts on the human body in such a way as to result in a taller individual.  Body fat can reduce insulin sensitivity and this may lead to an increase in height(likely through an IRS-1 related mechanism which controls chondrocyte differentiation).  Leptin which is produced by body fat has anabolic effects as well.

In humans, adipose tissue is located beneath the skin, around internal organs, in bone marrow(you can reduce these levels by supplements like Vitamin D), and in breast tissue.  Skin is located at both the top of the head and the bottom of the feet.  An increase in body fat in the head would result in an increase in body height(but we all know how body fat likes to be stored closer to the center of the body rather than in the extremities).  An increase in body fat in the skin in the feet would also result in an increase in height but it would likely be compressed as a result of your bodyweight pushing down.  It would, however, result in an increase of your laying down height(your height measurement taken from heel to top of your head when you are laying down eliminating compression forces).

Adipose tissue is also located in bone marrow.  How much is based on chemical and mechanical stimulatory factors.  Adiposal stem cells do have the potential to differentiate into height increasing cells.  

Fat mass is negatively associated with cortical bone size in young healthy male siblings. 

"Total and regional fat mass were found to be inversely associated with areal bone mass and bone size, independent from lean mass (radius periosteal circumference beta: -0.29 +/- 0.04). Lean mass was positively associated with bone size but inversely with cortical density at both tibia and radius. The negative association between total fat mass and bone size was independent from sex steroid concentrations. Leptin but not adiponectin was inversely associated with bone size[this goes against our previous results which show Leptin can have height increasing effect, adiponectin is a chemical that "burns" fat], but this was no longer significant after adjustment for body fat[so given the same body fat levels, the person with higher leptin will be shorter].
Increased fat mass is associated with smaller bone size, challenging the view of a high bone mass index as a protective factor for osteoporosis, whereas lean mass was a consistent positive determinant of bone size."

But this conclusion that fat mass is negatively associated with bone size is not made in this study...(and of course other studies show that leptin has positive benefits on bone size).  There are studies that show that Leptin can reverse the inhibitory effect of diet on growth.  What's interesting though is that fat mass has an effect on bone independent of hormones such as leptin.

How does body fat influence bone mass in childhood? A Mendelian randomization approach. 

"Fat mass may be a causal determinant of bone mass, but the evidence is conflicting, possibly reflecting the influence of confounding factors. The recent identification of common genetic variants related to obesity in children provides an opportunity to implement a Mendelian randomization study of obesity and bone outcomes, which is less subject to confounding and several biases than conventional approaches. Genotyping was retrieved for variants of two loci reliably associated with adiposity (the fat mass and obesity-related gene FTO and that upstream of the MC4R locus) within 7470 children from the Avon Longitudinal Study of Parents and Children (ALSPAC) who had undergone total body DXA scans at a mean of 9.9 yr. Relationships between both fat mass/genotypes and bone measures were assessed in efforts to determine evidence of causality between adiposity and bone mass. In conventional tests of association, both with and without height adjustment, total fat mass was strongly related to total body, spinal, and upper and lower limb BMC (ratio of geometric means [RGM]: 1.118 [95% CI: 1.112, 1.123], 1.110 [95% CI: 1.102, 1.119], 1.101 [95% CI: 1.093, 1.108], 1.146 [95% CI: 1.143, 1.155]; p < 10(-10) [adjusted for sex, height, and sitting height]). Equivalent or larger effects were obtained from instrumental variable (IV) regression including the same covariates (1.139 [95% CI: 1.064, 1.220], 1.090 [95% CI: 1.010, 1.177], 1.142 [95% CI: 1.049, 1.243], 1.176 [95% CI: 1.099, 1.257]; p = 0.0002, 0.03, 0.002, and 2.3(-6) respectively). Similar results were obtained after adjusting for puberty, when truncal fat mass was used in place of total fat, and when bone area was used instead of bone mass. In analyses where total body BMC adjusted for bone area (BA) was the outcome (reflecting volumetric BMD), linear regression with fat mass showed evidence for association (1.004 [95% CI: 1.002, 1.007]). IV regression also showed a positive effect (1.031 [95% CI: 1.000, 1.062]). When MC4R and FTO markers were used as instruments for fat mass, similar associations with BMC were seen to those with fat mass as measured by DXA. This suggests that fat mass is on the causal pathway for bone mass in children. In addition, both directly assessed and IV-assessed relationships between fat mass and volumetric density showed evidence for positive effects, supporting a hypothesis that fat effects on bone mass are not entirely accounted for by association with overall bone size." 

In the study they mention that neither genotype was shown to affect height.  Fat mass seems to have the greatest impact on periosteal growth(which could make you taller at the top of your head and soles of your feet).

So it seems as though adipose tissue cannot increase height except in a very minor fashion at the extremities of the body(both by increased periosteal deposition and by possible fat storage there).  Any adipose tissue effect is likely related to hormonal factors such as leptin.


Update on statural growth and pubertal development in obese children

"During pre-pubertal years, obese patients present higher growth velocity and that this pre-pubertal advantage tends to gradually decrease during puberty, leading to similar final heights between obese and non-obese children. Excess body weight might also influence pubertal onset, leading to earlier timing of puberty in girls."

"during pre-pubertal years, obese children present higher growth velocity and accelerated bone age compared to lean subjects. However, this pre-pubertal advantage in growth tends to gradually decrease during puberty, when obese children often show a reduced growth spurt compared to lean subjects. This latter effect, together with early pubertal maturation in obese children, determines similar final heights between obese and non-obese children."

"an increase in BMI of 1 unit led to an increase in height of 0.23 cm in boys and 0.29 cm in girls between ages 2 and 8 years. In addition, an increase in BMI of 1 unit reduced pubertal height gain of 0.88 cm in boys and 0.51 cm in girls, resulting in no beneficial effect on final height."

"Obese youth show a reduction in GH half-life, frequency of secretory bursts and daily production rate of GH.12 In particular, daily GH secretion and production rate have been calculated to fall by 6% for each unit increase in BMI, and 50% for an increase from 21 to 28 kg/m2. GH secretion is also impaired in response to all traditional stimuli acting at the hypothalamus. However, although GH secretion is blunted in obese children, their GH responsiveness appears to be increased compared to normal weight youth. At the peripheral level, increased GH binding protein (GHBP) values, corresponding to the extracellular domain of GH receptor, have been described in obesity"

Body fat in children does not adversely influence bone development: a 7-year longitudinal study (EarlyBird 18).

"A cohort of 307 children was measured biannually from 9-16 years for height and weight, and every 12 months for percent BF, bone area (BA), bone mineral content and areal bone mineral density (aBMD) by dual-energy X-ray absorptiometry. Pubertal tempo was determined quantitatively by age at peak height velocity.
Percent BF increased and then fell in the boys, but increased throughout in the girls. aBMD and BA increased in both genders. Greater BF was associated with higher aBMD and BA in girls, but only BA in boys. The extra aBMD associated with increased BF was greater in older girls. The rise in aBMD and BA was associated with earlier puberty in both genders. The impact of BF on aBMD was greater in later puberty in girls (0.0025 g cm-2 per 10% BF at 10 years versus 0.016 g cm-2 per 10% BF at 14 years).
Greater BF is associated with larger bones, but also denser bones in girls. The effects of fat and puberty are complex and gender specific, but BF of contemporary UK children does not appear to be deleterious to bone quality."

"On one hand, the extra mechanical load [of fat] leads to periosteal expansion and greater bone mass, while on the other the inflammation associated with obesity can lead to bone demineralization "<-both inflammation and periosteal expansion can affect height growth.

" In boys, the fall in BF noted [at age 15/16] occurred later in those whose growth spurt arrived later"

"the peak BF achieved was substantially greater among those whose APHV[Age where peak height velocity was achieved] was later"

Is it possible to grow taller via articular cartilage?

Unlike most bones which are totally covered by the periosteum, the long bones of the human body only contain periosteum on the sides of the bones while they have articular cartilage on the top.  If it were possible to increase the size of this articular cartilage, it would result in additional body height.

According to wikipedia: "Cartilage has limited repair capabilities, because chondrocytes are bound in lacunae, they cannot migrate to damaged areas "

But, "acute traumatic osteochondral lesions or surgically created lesions extending into subchondral bone by [for example] microfracture [causes] the release of pluripotent mesenchymal stem cells from the bone marrow, may heal with repair tissue consisting of fibrous tissue, fibrocartilage or hyaline-like cartilage."

"Blood and bone marrow (which contains stem cells) seep out of the fractures, creating a blood clot that releases cartilage-building cells."

This implies however that it is necessary to cause a microfracture severe enough to perforate the bone such that blood may flow out.  However, the key ingredient seems to be the stem cells and there is no reason that the blood cannot come from other sources(the body is filled with blood).  Even if the microfractures are not caused directly in the knee area as performed via the microfracture surgery it is still possible for any bone marrow release caused by a microfracture to be caught in the articular cartilage and through that build up to eventually stimulate cartilage growth.

It may be possible for this articular cartilage to be transformed into calcified cartilage and build up bone and height that way.

In Vitro Calcification of Immature Bovine Articular Cartilage Formation of a Functional Zone of Calcified Cartilage

"The zone of calcified cartilage (ZCC) anchors articular cartilage (AC) to subchondral bone through a layer of intermediate stiffness[So it may be possible to get some of that calcified cartilage to ossify into subchondral bone]. The regulation and functional consequences of cartilage calcification may vary with depth from the articular surface. The hypothesis of this study was that the in vitro calcification of immature AC occurs selectively in the deep region and is associated with a local increase in stiffness.
AC and growth plate cartilage (GPC) from calves were incubated in DMEM, 1% fetal bovine serum, 100 µg/mL ascorbate, and ±10 mM β-glycerophosphate (βGP) for up to 3 weeks. To assess the time course and effects of cell viability and βGP, full-depth strips of AC and GPC were analyzed by histology, indentation, and ⁴⁵Ca⁺⁺ uptake. To assess the effect of tissue zone, disks harvested from surface and deep zone AC and from reserve and hypertrophic zone of GPC were incubated independently and analyzed by compression and for ⁴⁵Ca⁺⁺ uptake and biochemical components.
The deep ~20% of immature AC calcified within 3 weeks, with calcification dependent on cell viability and βGP[B-Glycerophosphate may be something worth looking into in regards to height growh]. Mineral was deposited continuously around cells in AC but only between cell columns in GPC{The columnar nature of growth plate chondrocytes may be important, but also it could be dependent on the amount of extracellular matrix}. The deep zone of AC exhibited a compressive modulus of 0.53 MPa after βGP-induced calcification, ~4-fold stiffer than AC incubated without βGP.
Cartilage explants exhibit inherent zone-specific calcification processes, resulting in an increase in stiffness associated with cartilage calcification. Such properties may be useful for engineering a biomimetic ZCC tissue to integrate cartilaginous tissue to bone, thereby forming a mechanically functional osteochondral unit{If we can get this to happen naturally we can grow taller!}."

"The ZCC is 100- to 300-μm thick and is bound on one side by the tidemark, the gently undulating interface with uncalcified cartilage, and on the other side by the cement line, the highly interdigitated interface with subchondral bone."

"In the lower hypertrophic zone, calcification initiates in the territorial matrix close to chondrocytes and spreads throughout the matrix of the longitudinal septa between columns of lower hypertrophic chondrocytes."

"Chondrocytes from the superficial zone secrete soluble factors that can inhibit mineralization by deep zone chondrocytes during in vitro co-culture"<-manipulation of these soluble factors may be a way to manipulate height growth.

"In AC, enlarged chondrocytes and calcified matrix were localized to the deep ~25% of AC. "<-The calcification process may be important to chondrocyte hypertrophy.

Here's a picture compariing growth plate cartilage and articular cartilage:

The stacking of chondrocytes into columns is a key factor that proceeds ossification into bone and may be one of the reasons why articular cartilage doesn't fully ossify.  It also means that chondrocytes don't have to be wholly organized into later in the ossification process.

"Unlike monolayer chondrocyte cultures, which are subject to dedifferentiation and may have effects on cell hypertrophy and mineralization, explant cultures maintain the chondrocyte phenotype because the cells remain within their native extracellular matrix. "<-chondrocyte dedifferentiation may be a problem with LSJL unless sufficient extracellular matrix is secreted by the freshly differentiated chondrocytes.

Zone-specific gene expression patterns in articular cartilage.

"Articular cartilage was obtained from knees of 4 normal human donors[one female (age 23) and three male (age 24, 44 and 46) donors]. The cartilage zones were dissected on a microtome. RNA was analyzed on human genome arrays. Data obtained with human tissue were compared to bovine cartilage zone specific DNA arrays. Genes differentially expressed between zones were evaluated using direct annotation for structural or functional features, and by enrichment analysis for integrated pathways or functions. The greatest differences were observed between SZ and DZ in both human and bovine cartilage. The MZ was transitional between the SZ and DZ and thereby shared some of the same pathways as well as structural/functional features of the adjacent zones. Cellular functions and biological processes enriched in the SZ relative to the DZ, include most prominently ECM receptor interactions, cell adhesion molecules, regulation of actin cytoskeleton, ribosome-related functions and signaling aspects such as Interferon gamma, IL4, CDC42Rac and Jak-Stat. Two pathways were enriched in the DZ relative to the SZ, including PPARG and EGFR/SMRTE."

"The superficial zone (SZ) spans the first 10-20% of full thickness articular cartilage and contains densely packed collagen fibrils and low levels of aggrecan, although fibril associated decorin and biglycan are found in higher concentrations in the SZ. Chondrocytes in this zone produce little PCM, are elongated, flattened and are oriented parallel to the cartilage surface. Cells within the SZ synthesize and secrete the important joint lubricant superficial zone protein (SZP), which is also known as megakaryocyte-stimulating factor, lubricin, or PRG4"

"Clusterin, a glycoprotein that regulates complement activation and cell death is also exclusively expressed in SZ chondrocytes. Chondrocytes located in the SZ differ from DZ chondrocytes by their lower collagen type II gene expression levels, lower production of keratan sulfate and other proteoglycans. The SZ of mature articular cartilage contains cells with phenotypic and functional properties of mesenchymal stem or progenitor cell populations"  The stem cells there express CD105, CD166, Notch-1, STRO-1 and VCAM-1."

"SZ cells are strongly positive for alpha smooth muscle actin, a contractile actin isoform that is also present in progenitor cells"

"The middle zone (MZ) or transitional zone comprises the next 40-60% of cartilage thickness and contains randomly organized collagen fibrils, high concentrations of aggrecan, hyaluronic acid, dermatan sulfate and collagen type II"

"The deep or radial zone contains ellipsoid cells with an extensive PCM amongst radially orientated collagen fibrils that extend into the calcified zone to preserve cartilage and bone integration. In the calcified zone, which represents the boundary between cartilage and subchondral bone, cells are contained within a calcified matrix and express hypertrophic molecules such as collagen type X, alkaline phosphatase (ALP) and osteocalcin"

"increased turnover or activity of ribosomes [may occur] in SZ cells"

Genes upregulated in superficial zone(versus middle zone and deep zone) and in human cartilage also upregulated in LSJL{in italics if regulation differs in LSJL}:

VCAM1{down}

SULF1

MMP2

THBS4

MAMDC2

HHIP

DPT

CAPN6

CDH13

OGN{down}

DOK5

ASPN

SETBP1{down}

LAMA4

EGR2

TNC{down}

Genes downregulated in superficial zone:

Fat1{up}

MFAP3L

VAV3

BSP{up}

Genes upregulated in middle zone:

Genes upregulated in deep zone:

BSP

VAV3{down}

PDE7A{down}

Genes downregulated in deep zone versus other zones:

ASPN{up}

OGN

Col12a1{up}

LSJL gene expression shares the most gene expression similarities with the superficial zone of articular cartilage.

This next study suggests that remodeling of articular cartilage can occur via endochondral ossification into the subchondral bone.  However, why doesn't this remodeling increase height as in the growth plate?

The vascularity and remodelling of subchondrial bone and calcified cartilage in adult human femoral and humeral heads. An age- and stress-related phenomenon.

"A quantitative study of the vascularity and a qualitative study of the remodelling of the calcified cartilage and subchondral bone end-plate of adult human femoral and humeral heads were performed with respect to age. In the femoral head the number of vessels per unit area was found to fall 20% from adolescence until the seventh decade and in the humeral head 15% until the sixth decade. Thereafter an increase was noted in the femur but none in the humerus. More vessels were present at all ages in the more loaded areas of the articular surfaces: 25% more for the femur and 15% more for the humerus. The degree of active remodelling by endochondral ossification declined 50% from adolescence until the seventh decade in the femoral head, and 30% until the sixth decade in the humeral head, rising thereafter to levels comparable to those found at young ages. More remodeling was noted in the more loaded areas at all ages."

If you look at fig 5 you can see subchondral bone resorbing calcified cartilage so a kind of endochondral ossification does sort of occur.

"Lemper, who studied subchondral bone plate remodelling in rabbits by microradiography and tetracycline labelling, demonstrated that remodelling, which occurs at a very rapid rate in immature rabbits, continues at a slower rate after the termination of longitudinal growth. In a study of the adult human patella Green, Martin, Eanes, and Sokoloff (1970) concluded that “continuous growth activity goes on in the osteochondral region during the adult years”."

"the osteochondral ends of bone probably remodel as a result of vascular invasion and enchondral ossification of the calcified cartilage, "

"It can be seen that a group of cartilage-cells upon reaching the margin of the (subchondral) bone . . . becomes converted into one of (its) prominences"

Role of endochondral ossification of articular cartilage and functional adaptation of the subchondral plate in the development of fatigue microcracking of joints.

"Endochondral ossification of articular cartilage and modeling/remodeling of the subchondral plate and epiphyseal trabeculae are important components of the adaptive response. We performed a histologic study of the distal end of the third metacarpal/metatarsal bone of Thoroughbreds after bones were bulk-stained in basic fuchsin and calcified sections were prepared. The Thoroughbred racehorse is a model of an extreme athlete which experiences particularly high cyclic strains in distal limb bones. The following variables were quantified: microcrack boundary density in calcified cartilage (N.Cr/B.Bd); blood vessel boundary density in calcified cartilage (N.Ve/B.Bd); calcified cartilage width (Cl.Cg.Wi); duplication of the tidemark; and bone volume fraction of the subchondral plate (B.Ar/T.Ar). Measurements were made in five joint regions (lateral condyle and condylar groove; sagittal ridge; medial condylar and condylar groove). N.Cr/B.Bd was site-specific and was increased in the condylar groove region; this is the joint region from which parasagittal articular fatigue (condylar) fractures are typically propagated. Formation of resorption spaces in the subchondral plate was co-localized with microcracking. N.Ve/B.Bd was also site-specific. In the sagittal ridge region, N.Ve/B.Bd was increased, Cl.Cg.Wi was decreased, and B.Ar/T.Ar was decreased, when compared with the other joint regions. Multiple tidemarks were seen in all joint regions. Cumulative athletic activity was associated with a significant decrease in B.Ar/T.Ar in the condylar groove regions. N.Cr/B.Bd was positively correlated with B.Ar/T.Ar (P < 0.05, r(s) = 0.29) and N.Ve/B.Bd was negatively correlated with B.Ar/T.Ar (P < 0.005, r2 = 0.14) and Cl.Cg.Wi (P < 0.05, r2 = 0.07). endochondral ossification of articular cartilage and modeling/remodeling of the subchondral plate promote initiation and propagation of site-specific fatigue microcracking of the joint surface, respectively, in this model. Microcracking of articular calcified cartilage likely represents mechanical failure of the joint surface. Propagation of microcracks into the subchondral plate is a critical factor in the pathogenesis of articular condylar fatigue (stress) fracture. Functional adaptation of the joint likely protects hyaline cartilage from injury in the short-term but may promote joint degeneration and osteoarthritis with ongoing athleticism."

"Loading does not have to be great to induce microcracking, if it is rapidly applied"

"bone may not effectively resist propagation of microcracking, especially if abnormal or atypical loads are applied"

If you look at figure 4, you can see "In-growth of blood vessels into the calcified cartilage layer was a prominent feature seen in all joint regions but was increased in the sagittal ridge region"

"Microcracking always involved the calcified cartilage. Within the condylar grooves, short microcracks located within the calcified cartilage were typically co-localized with in-growth of a blood vessel into calcified cartilage. Longer microcracks extended proximally into the bone of the subchondral plate"

"Microcracking is co-localized with in-growth of blood vessels from the subchondral plate into the calcified cartilage"

"the subschondral bone spares cartilage from load done at the joint surface."  Remodeling of the subchondral may proceed changes to the articular cartilage.

"mechanisms that induce microcracking of calcified cartilage and in-growth of blood vessels into calcified cartilage are different. In-growth of blood vessels into the condylar groove calcified cartilage precedes and likely promotes initiation of microcracking of calcified cartilage in regions of the joint that experience particularly high stresses."

"Athleticism in racing Thoroughbreds commonly leads to premature failure of the hyaline articular cartilage, with development of full thickness erosions of the articular cartilage over the axial part of the condyles in the palmar/plantar region of the joint. Another common feature of active endochondral ossification of the joint surface is duplication of the tidemark. We identified duplication of the tidemark as a prominent feature in all regions of the joint. "

"Endochondral ossification of articular cartilage at the ends of long bones like represents functional adaptation to joint loading over time."

"mechanisms that induce microcracking of calcified articular cartilage and ingrowth of blood vessels are likely different"  In growth of blood vessels into calcified cartilage in the condylar groove proceeds and likely initiates calcified cartilage.  Blood vessel ingrowth in the calcified cartilage was associated with a reduction of width of the calcified cartilage layer.

"Microcracking of the articular surface likely represents early mechanical failure of the joint surface to high transarticular loads. In-growth of blood vessels into calcified cartilage promotes site-specific microcracking of calcified cartilage. Functional adaptation of the distal end of the Mc-III/Mt-III bone includes active endochondral ossification of the epiphyseal articular cartilage which may improve joint congruity, sclerosis of epiphyseal trabecular bone, and active remodeling and progressive loss of bone mass from the superficial region of the subchondral plate.  a common mechanism activates endochondral ossification of the joint surface and functional adaptation of the subchondral plate."

Type X collagen is upregulated by LSJL but not by axial loading.

The role of type X collagen in facilitating and regulating endochondral ossification of articular cartilage.

"There are spatial and temporal correlations between synthesis of type X collagen and occurrence of endochondral ossification. The expression of type X collagen is confined within hypertrophic condrocytes and precedes the embark of endochondral bone formation. Type X collagen facilitates endochondral ossification by regulating matrix mineralization and compartmentalizing matrix components.

Type X collagen is a reliable marker for new bone formation in articular cartilage. The future clinical application of this collagen in inducing or mediating endochondral ossification is perceived, e.g. the fracture healing of synovial joints and adaptive remodeling of madibular condyle."

"The peak of type X collagen mRNA and molecular expression in hypertrophic chondocytes of condylar cartilage occurred before the peak of new bone formation in the erosive cartilage. These finding are fully supportive to the statement that type X collagen expression is closely associated with endochondral ossification and invariably precedes the onset of ossification"

"Condylar cartilage, or the secondary cartilage growth starts with the mesenchymal-like tissue covering of the prenatal or postnatal condyle. The new members of the cartilage family therefore have been added without the mitosis of existing cartilage mother cells, but through mitosis of undifferentiated mesenchymal cells. This mode of growth in which new cells are added from the exterior is appositional growth"

How does articular cartilage differ from GP cartilage?

Early articular cartilage degeneration in a developmental dislocation of the hip model results from activation of β-catenin.

"Developmental dislocation or dysplasia of the hip (DDH) is one of the most common deformities in children. Osteoarthritis (OA) is the most frequent long-term complication. The molecular mechanism of early articular cartilage degeneration in DDH is still unclear. It is well known that β-catenin plays a crucial role in articular cartilage degeneration. The objective of this study was to verify the relationship between β-catenin and DDH cartilage degeneration. We used a DDH model that was established by modification of swaddling position in newborn Wistar rats. The hips were isolated from the DDH model rats and untreated control group at the age of 2, 4, 6 and 8 weeks. β-Catenin gene and protein were investigated by quantitative (q)RT-PCR and immunohistochemistry. Collagen X and matrix metalloproteinase (MMP)-13, markers of early cartilage degeneration, were assessed by qRT-PCR. Primary chondrocytes were cultured from cartilage of two groups at the age of 8 weeks. Expression of β-catenin, collagen X and MMP-13 was detected. Continued high expression of β-catenin was observed in cartilage from DDH model rats. mRNA and protein expression of β-catenin was significantly increased in primary chondrocytes of the DDH model compared with the control group. Collagen X and MMP-13 expression was higher in the cartilage and chondrocytes from DDH model rats than the control group. Our findings suggest that early cartilage degeneration in DDH may result from activation of β-catenin signaling."

"Expression of β-catenin in articular cartilage of control group at different ages. A. 2 weeks; B. 4 weeks; C. 6 weeks; D. 8 weeks. Expression of β-catenin protein decreased with age."

"morphology of articular cartilage in the DDH model differed from that in the control group. Loss of the smooth surface of articular cartilage and aggregates and clusters of articular chondrocytes were detected. "

The hip in DDH actually looks compressed which explains why it wouldn't result in height growth.

Comparison of gene expression profile between human chondrons and chondrocytes: a cDNA microarray study.

"The chondron is a basic unit of articular cartilage that includes the chondrocyte and its pericellular matrix (PCM). This current study was designed to investigate the effects of the chondron PCM on the gene expression profile of chondrocytes.

Chondrons and chondrocytes were enzymatically isolated from human articular cartilage, and maintained in pellet culture. Pellets of chondrons or chondrocytes were collected at days 1, 3 and 5 for cDNA microarray analysis.

In comparison with chondrocytes alone, chondrons had 258 genes, in a broad range of functional categories, either up- or downregulated at the three time points tested. At day 1, 26 genes were significantly upregulated in chondrons and four downregulated in comparison to chondrocytes. At day 3, the number of upregulated chondron genes was 97 and the number downregulated was 43. By day 5, there were more downregulated genes (56) than upregulated genes (32) in chondrons.  (HSPA1A, HSPA2 and HSPA8) [were upregulated] in chondrons. Genes related to chondrocyte hypertrophy and dedifferentiation such as SSP1 and DCN were downregulated in chondrons as compared to the expression in chondrocytes.

The presence of the PCM in chondrons has a profound influence on chondrocyte gene expression. Upregulation of the heat shock protein 70 may contribute to the robustness and active matrix production of chondrons. The intact PCM may further stabilize the phenotype of chondrocytes within chondrons."

"The pericellular “capsule” represents about 60% of the cross-sectional area of chondrons, and is an osmotic buffer zone to the enclosed chondrocytes"

Gene comparison to LSJL to be done.

"The influence of PCM on chondrocytes is continuous, but changes roles. At day 3, most of the significantly regulated genes in chondrons were in the functional categories of metabolism, protein assembly/transport and signaling. By day 5, the most prominent functional group was signaling."

"The upregulation of HSP genes (HSPA1A, HSPA2 and HSPA8) and BAG3, which is a cochaperone partner of HSP29, can be one of the mechanisms that protect chondrons from stresses. On the other hand, the decreased expression of SSP1, expressed by hypertrophic chondrocytes, in chondrons may suggest a reduction of terminal differentiation and apoptosis in the chondron population. "

Histology of epiphyseal cartilage calcification and endochondral ossification

"Cartilage calcification is carried out by chondrocytes as they hypertrophy and begin to secrete matrix vesicles. Calcification initiates when calcium phosphates appear inside these matrix vesicles, forming hydroxyapatite crystals that eventually break through the membrane to form calcifying globules, as in bone calcification. However, the extracellular environment in cartilage is different from that in bone: cartilage is abundant in proteoglycans but contains a small amount of osteopontin. Hypertrophic chondrocytes secrete vesicles in the cartilaginous matrix of intercolumnar septae only, forming well-calcified longitudinal septae and poorly-calcified transverse partitions. Such pattern of vesicle deposition permits the invasion of endothelial cells, which infiltrate into cartilage and induce migration of osteogenic and osteoclastic cells. Osteoclasts resorb the excess of calcified globules in the partitions, shaping calcified cartilage cores paralleling the longitudinal axis of long bones. After the formation of these calcified cartilage cores, endochondral ossification involves a series of well-defined events in which osteogenic cells deposit new bone onto the cartilage core and form primary trabecules.  "

"The extracellular matrices, as an ion reservoir, may constitute the adequate microenvironment for the initiation of calcification. Proteoglycans are complexes of various glycosaminoglycan (GAG) chains and core proteins. The GAG chains are highly negatively charged, which can attract free divalent cations such as Ca2+ . It seems likely that proteoglycans significantly impact the dynamics of the extracellular fluid's mineral ionic content. Since cartilage contains abundant proteoglycans, cartilage matrices may serve as a reservoir for free divalent cations. Especially, crystal ghosts appear to be rich in sulfated GAG chains , especially, chondroitin sulfate"<-So the ECM may signal when calcification occurs.

"proteoglycans in the extracellular matrix of the lower hypertrophic zone may be degraded by proteases and removed before calcification, and this seems to be the mechanism by which a matrix that does not possess the ability to calcify is transformed into one that has that capability. Interestingly, however, the concentration of sulfate or cartilage proteoglycans was not shown to change before and after cartilage calcification"

"epiphyseal chondrocytes may be able to transdifferentiate into osteoblasts, since terminally differentiated chondrocytes were biosynthetically active. These cells have been shown to synthesize osteogenic markers such as type I collagen, glycosaminoglycans, osteopontin, osteocalcin and osteonectin. Therefore, we assumed that chondrocytic apoptosis may depend on genetic programming such as Bcl2 expression, but may also be influenced by other conditions, i.e., intracellular concentration of Pi and nitric oxide generation. We also reported that parathyroid hormone-related peptide deficiency may stimulate chondrocytic apoptosis "

The tidemark of the chondro-osseous junction of the normal human knee joint

"The tidemark represents a calcification front, at which non-mineralised cartilage matrix comes to contain hydroxyapatite"

" though cells were often seen in close apposition to the tidemark, none were observed to be embedded within it. This is consistent with the ultrastructural observations of Bullough & Jagannath that chondrocytes were sometimes partially embedded in the mineralising face of the tidemark, but were not wholly sealed within it. In general, chondrocytes near the tidemark must maintain control over the local matrix and regulate the turnover of non-collagenous components of this matrix. During normal growth and development of diarthrodial joints the tidemark clearly represents a calcification front. In the normal adult joint, the tidemark is still a single structure, but the advance of mineral into the hyaline cartilage has ceased, though a residual ‘maintenance’ turnover of matrix may occur. Under these conditions the tidemark may have ceased to function as a calcification front, though it still contains some tightly bound calcium. It is possible that, at this stage, the tidemark has changed in function to one of inhibiting the formation or growth of microcrystals of hydroxyapatite and so protecting the hyaline cartilage from passive progressive mineralisation. "

Investigation of chondrocyte hypertrophy and cartilage calcification in a full-depth articular cartilage explants model

"Articular cartilage deterioration, which includes cartilage degradation and chondrocyte hypertrophy, is a hallmark of degenerative joint diseases (DJD). Chondrocyte hypertrophy is initiated in the deep layer of the cartilage; thus, a robust explants model for investigation of hypertrophy should include this zone. The aim of this study was to characterize and investigate the hypertrophy-promoting potential of different endogenous factors on an ex vivo articular cartilage model. The full-depth cartilage explants were harvested from bovine femoral condyle and cultured for 13 days in different conditions: 10 ng/ml oncostatin M + 20 ng/ml TNF-α; 100 ng/ml IGF1; 10–100 ng/ml bFGF; 10–100 ng/ml BMP2; 50 μg/ml ascorbic acid in combination with 10 mM β-glycerophosphate; and 20–100 ng/ml triiodothyronine. The cellular activity and morphology, degradation, formation and calcification, and expression level of hypertrophic markers were investigated. The hypertrophic factors tested all induced cellular activity and marked morphological changes starting at day 4, however, not in a synchronized manner. Both cartilage degradation and formation were induced by T3 (P < 0.05). Only T3 had a full hypertrophic gene expression profile (P < 0.05). We developed and characterized a novel model for investigation of chondrocyte hypertrophy. We speculated that this can become an important investigatory tool for investigation of matrix turnover, chondrocyte hypertrophy and cartilage calcification that are associated with DJD pathogenesis."

Finding out how to initiate chondrocyte hypertrophy could be a way to become taller.

" Cartilage calcification is initiated from the subchondral cartilage where chondrocytes undergo hypertrophic differentiation and apoptosis. "<-I'm not sure what is meant by subchondral cartilage.

"The full stage of chondrocyte hypertrophic phenotype was characterized by pre-hypertrophic chondrocytes produced by IHH, COLX synthesized by hypertrophic chondrocytes
and MMP13 related to mature hypertrophic chondrocytes, followed by ALP expression represented by chondrocyte hypertrophy and indicating matrix calcification. We found that several of the factors tested could induce morphological changes that resemble hypertrophy; however, only T3 (20 ng/ml) expressed a pre-hypertrophic and hypertrophic profile. "

Chondrocyte hypertrophy and osteoarthritis: role in initiation and progression of cartilage degeneration?

"Changes in chondrocyte behavior, such as expression of hypertrophy markers and matrix calcification, frequently resemble the phenomena observed in the hypertrophic layer of the growth plate of long bones"

"Temporary hyaline cartilage is found in the embryonic stages of endochondral bones and the growth plate and is finally replaced by bone. Permanent hyaline cartilage, present amongst others in articulating joints, does not undergo terminal differentiation under normal conditions."

"The cellular origin of both types of temporary and permanent cartilage is similar. As concluded from both in vivo and in vitro studies, the default route of chondrocyte differentiation is terminal differentiation (hypertrophy and apoptosis). An enlightening in vivo model of adult chondrocyte differentiation is osteophyte formation. Osteophytes are the result of chondrogenic differentiation of mesenchymal stem cells in the periosteum. Initially cartilage is formed but the final product is bone. Apparently, unrestricted differentiation of precursor cells into the chondrocyte lineage does not lead to permanent cartilage but to bone. In articular cartilage, this default route is somehow blocked to obtain permanent cartilage."

"A route that has been proposed[for OA] is that articular chondrocyte loose their differentiated phenotype and obtain a behavior with similarities to terminal differentiating chondrocytes (hypertrophy-like), as can be found in the growth plate of growing individuals"

"osteopontin, osteocalcin, Indian Hedgehog, Runx2, VEGF, HtrA1 and transglutaminase-2 (TG-2) are all shown to be associated with chondrocyte hypertrophy. However, one has to keep in mind that, although accepted as a hypertrophy marker, MMP13 synthesis is induced in chondrocytes by alternative routes, such as inflammation and mechanical stress"

"Calcification of articular cartilage and ossification as a result of terminal differentiation of chondrocytes might be different processes, but a number of studies have indicated overlapping phenomena. Studies in the sixties and seventies of the last century have shown that in human cartilage the number of tidemarks, the line bordering the calcified cartilage and the non-calcified cartilage, is increased above the age of 60. This movement of the tidemark to the cartilage surface should result in an increase in the thickness of the calcified cartilage, but it is shown that instead the calcified zone becomes thinner during aging. This indicates replacement of the lower calcified cartilage by bone because of endochondral ossification."

"OA is related to ossification processes in articular cartilage. Next to increased alkaline phosphates and pyrophosphate levels, calcification is a common observation in OA. Not only in large joints, but also degenerative changes in intervertebral discs have been associated with tissue calcification"

"Hypertrophic chondrocytes in the growth plate do not only express specific molecules such as type X collagen, but also undergo apoptosis to make bone deposition possible. Apoptosis can be considered as a marker for chondrocyte hypertrophy in OA cartilage"

Chondrocyte Extract

Differentiation of bone marrow-derived mesenchymal stem cells into chondrocytes using chondrocyte extract.

"[We] investigate the chondrogenic transdifferentiation potential of swine bone marrow-derived mesenchymal stem cells (BM-MSCs) by culturing with chondrocyte extract, using monolayer and micromass culture. Chondrogenic-specific markers were detected via reverse transcription-polymerase chain reaction (RT-PCR) and immunofluorescence. After 7 days of induction in monolayer culture, BM-MSCs reversibly permeabilized with streptolysin O (SLO), a bacterial exotoxin that is capable of forming large pores in the plasma membrane of mammalian cells, and expressed chondrocyte‑specific genes such as type II collagen (COL II) and aggrecan. A positive protein expression of COL II was also observed. However, BM-MSCs treated without SLO did not express the related genes and proteins. The transition of reprogrammed BM-MSCs was lost 14 days later. By using micromass culture, reprogrammed BM-MSCs were able to maintain the change until the 14th day. In summary, permeabilized BM-MSCs were transiently transdifferentiated into chondrocytes by co-culturing with the chondrocyte extract. Moreover, a high-density culture method was able to increase the time in which the phenotypic change was maintained."


Unfortunately I could not get the full study.

CHD4

Chd4 and associated proteins function as corepressors of Sox9 expression during BMP-2-induced chondrogenesis.

"Mouse embryonic fibroblasts (MEFs) differentiate into fully functional chondrocytes in response to bone morphogenetic protein-2 (BMP-2).  We identify proteins differentially expressed during BMP-2-induced chondrogenic differentiation of MEFs. We found 85 downregulated proteins, and Ingenuity Pathways Analysis (IPA) revealed a protein-protein network with chromodomain-helicase-DNA-binding protein 4 (Chd4) in the center. Chromatin immunoprecipitation (ChIP) and nuclease hypersensitivity assays showed that Chd4, interacting with Hdac1/2, cooperates with its related proteins Kap1 and Cbx1 to bind at -207/-148 of the Sox9 promoter. Let-7a targets the 3'UTR of Chd4 to promote chondrogenesis of MEFs. BMP-2 induced the upregulation of let-7a, targeting Chd4 and positively controlling the chondrogenic differentiation of MEFs."

"miR-199* might affect its target gene, Smad1, to regulate early chondrogenic differentiation"

"In hematopoietic stem cells, SNF2-like ATPase Mi-2beta is required for maintenance of multilineage differentiation in the early hematopoietic hierarchy"

"[Chd4 interacts with] Hdac1 and Hdac2 [which bind] to the promoter of Sox9 in vivo"

"BMP-2 induces the upregulation of let-7a, followed by the degradation of its target gene Chd4 and the separation of Hdac1/2 with Chd4. Subsequently, the competitive complex NF-Y-p-300 increasingly binds with the core promoter of Sox9, resulting in an open access for other positive transcription regulators of Sox9"

So inhibiting Chd4 may help in inducing chondrogenic differentiation.

POMC

POMC seems like a good candidate for height increase with knockout increasing height and overexpression decreasing height.

The melanocortin system in articular chondrocytes: melanocortin receptors, pro-opiomelanocortin, precursor proteases, and a regulatory effect of alpha-melanocyte-stimulating hormone on proinflammatory cytokines and extracellular matrix components.

"The pro-opiomelanocortin (POMC)-derived neuropeptide alpha-melanocyte-stimulating hormone (alpha-MSH) mediates its effects via melanocortin (MC) receptors. This study was carried out to investigate the expression patterns of the MC system and the effects of alpha-MSH in human articular chondrocytes.
Articular chondrocytes established from human osteoarthritic joint cartilage were analyzed by reverse transcription-polymerase chain reaction (RT-PCR) and Western blotting for the expression of MC receptors, POMC, and prohormone convertases (PCs). MC-1 receptor (MC-1R) expression in articular cartilage was further studied by immunohistochemistry. Ca(2+) and cAMP assays were used to monitor alpha-MSH signaling, while studies of alpha-MSH function were performed in cultures with chondrocyte micromass pellets stimulated with alpha-MSH. Expression of cytokines and extracellular matrix (ECM) components was determined by real-time RT-PCR, Western immunoblotting, and enzyme-linked immunosorbent assays.
MC-1R expression was detected in articular chondrocytes in vitro and in articular cartilage in situ. In addition, expression of transcripts for MC-2R, MC-5R, POMC, and PCs was detected in articular chondrocytes. Stimulation with alpha-MSH increased the levels of intracellular cAMP, but not Ca(2+), in chondrocytes. Both messenger RNA and protein expression of various proinflammatory cytokines, collagens, matrix metalloproteinases (MMPs), and SOX9 was modulated by alpha-MSH{So POMC can influence height by modulation all these genes}.
Human articular chondrocytes are target cells for alpha-MSH. The effects of alpha-MSH on expression of cytokines and MMPs suggest that this neuropeptide plays a role in inflammatory and degenerative processes in cartilage. It is conceivable that inflammatory reactions can be mitigated by the induction of endogenous MCs or administration of alpha-MSH to the affected joints. The induction pattern of regulatory and structural ECM components such as collagens as well as SOX9 and anabolic and catabolic cytokines points to a function of alpha-MSH as a trophic factor in skeletal development during endochondral ossification rather than as a factor in homeostasis of permanent cartilage."

"After 48 hours of stimulation with 10−6M α-MSH, the levels of mRNA for COL1A1, COL2A1, and, in particular, COL10A1 were profoundly elevated "<-It would seem like this would be good for height increase if POMC increasing a-MSH was regulating the height altering effects.

"Treatment with α-MSH significantly stimulated gene expression of MMPs 2, 7, and 9, while gene expression of MMP-13 displayed only a nonsignificant tendency for up-regulation."  Sox9, TGFB1, and IL6 also increased in expression.

"Processing of POMC by these PCs yields the MCs adrenocorticotropin (ACTH) and α-, β-, and γ-MSH, as well as the endogenous opioid β-endorphin (β-ED)."

"Since MC-2R selectively binds ACTH, human articular chondrocytes may respond to not only α-MSH but also ACTH."<-So a-MSH may compete with ACTH.  So ACTH may be better than a-MSH for height gain which is why POMC could decrease height by competing with the more pro-height ACTH.  If something other than POMC can upregulate ACTH.

" α-MSH might be a positive inducer of growth of the long bone, which has been described in earlier studies utilizing γ2-MSH. Administration of γ2-MSH elevates growth plate height in general, and augments the proliferating and hypertrophic zone in particular. ACTH induces expression of type II and type X collagens in bone marrow–derived stem cells and in costal chondrocytes, which are representative of committed resting chondrocytes in the growth plate. Presumably, ACTH promotes the development of the OA chondrocyte phenotype of progenitor cells and increases matrix production and differentiation of early committed chondrocytes"

Is it easier to grow taller via short, irregular, et al. bones than it is long bones?

According to Cliff Notes:

Here are the main features of a long bone:

• The diaphysis, or shaft, is the long tubular portion of long bones. It is composed of compact bone tissue.
  
• The epiphysis (plural, epiphyses) is the expanded end of a long bone.
  
• The metaphysis is the area where the diaphysis meets the epiphysis. It includes the epiphyseal line, a remnant of cartilage from growing bones.
  
• The medullary cavity, or marrow cavity, is the open area within the diaphysis. The adipose tissue inside the cavity stores lipids and forms the yellow marrow.
  
• Articular cartilage covers the epiphysis where joints occur.
  
• The periosteum is the membrane covering the outside of the diaphysis (and epiphyses where articular cartilage is absent). It contains osteoblasts (bone-forming cells), osteoclasts (bone-destroying cells), nerve fibers, and blood and lymphatic vessels. Ligaments and tendons attach to the periosteum.
  
• The endosteum is the membrane that lines the marrow cavity.
  

Here are the main features of short, flat, and irregular bones:

• In short and irregular bones, spongy bone tissue is encircled by a thin layer of compact bone tissue.
  
• In flat bones, the spongy bone tissue is sandwiched between two layers of compact bone tissue. The spongy bone tissue is called the diploe.
  
• Periosteum covers the outside layer of compact bone tissue.
  
• Endosteum covers the trabeculae that fill the inside of the bone.
  
• In certain bones (ribs, vertebrae, hip bones, sternum), the spaces between the trabeculae contain red marrow, which is active in hematopoiesis.
  
  
  We know it is possible to increase the width of the periosteum. The periosteal width increased by about 4% as a result of sprinting. And, we know that bone can model in the absence of microfractures. In addition to these two facts, sprinting also increased cortical bone area. In short and irregular bones, the periosteum covers the entire outside of the bone therefore any change in periosteal width should increase height.
  
   So the potential for height increase via increasing the periosteal width of the non-long bones is not very much at all.
  
  The vertebrae are irregular bones. If you increase the periosteal width of all your vertebral bones by 4% that would be quite a significant increase in overall body height. Flat bones include the skull and the pelvis which provides another opportunity to add 4% of height. Since flat bones consist of trabecular bone sandwiched between two pieces of cortical bone they are also sandwiched between two pieces of periosteum.
  
  Now, if you take all that together that would be a pretty significant increase in height. Let's say that the spine is 2 feet long, now we also have to consider that the pelvis and the skull can add to height too but we have to consider that the intervertebral discs don't. If you increase the bone width by 4% you get 0.96 inches. But consider that it's not 4% of the bone width that increased in the sprinting studies it's 4% of the periosteal width.
  
  However, if we could perform exercises that could increase the growth of the periosteum by more than 4% than that height increase could turn into something quite significant.
  
  So, until we find exercises that can really expand the size of the periosteum it's best to keep our experiments towards growing taller via distraction forces(lateral synovial joint loading) and microfractures(i.e. sprinting, jumping, weight exercises).
  

Can exercises designed to strengthen the intervertebral discs make you taller?

Many grow taller sites state that you can increase your height by increasing the size of your intervertebral discs.  For example, by hanging or by the cobra yoga stretch.  The question is:  Does the science support this? Of course, even if the science doesn't support it that may mean that effective exercises for increasing intervertebral disc size have not been tested yet.  However, it is unlikely that the intervertebral disc can stretch.  The chondrocytes within can proliferate and secrete more extracellular matrix and thereby expand.  But, I don't think stretching would accomplish that.


Effect of running exercise on proteoglycans and collagen content in the intervertebral disc of young dogs.  

"Collagen and proteoglycans in the intervertebral disc (LI-II) of young beagle dogs (age 55 weeks) were analyzed following a 15 weeks' daily 20 km running training on a treadmill with 15 degree uphill inclination. In nucleus pulposus no statistically significant alterations were found in the content of proteoglycans or collagen. In annulus fibrosus the total tissue wet weight and total amount of collagen (hydroxyproline) increased by 34-36% in the runners as compared to age-matched, untrained controls. Since the total amount of proteoglycans did not increase, the annulus fibrosus became relatively depleted of proteoglycans, as indicated by the 27% reduction in uronic acid concentration, expressed either per wet weight or hydroxyproline. The average molecular size of the remaining nonaggregating proteoglycans was larger, and there was also a trend towards increased proportion of proteoglycans aggregating with hyaluronan. Most of the chondroitin sulfate side chains were 6-sulfated (65-66%). Running did not alter the sulfation or length of the chondroitin sulfate chains. The decreased proteoglycan/collagen ratio in annulus fibrosus may result in altered mechanical properties of the tissue and reflects its adaptation to enhanced motion and stress."

The molecular size of the proteoglycans increased(indicating an increase in proteoglycan hypertrophy).  Total tissue weight and tissue wet weight increased indicating an increase in the secretion of extracellular matrix.  The number of proteoglycans did not increase.  This may be something interesting to study in the future the proliferation and differentiation of proteoglycans.

Now we need to study intervertebral disc anatomy to see if an increase in the total amount of collagen and the size of the proteogyclans would increase disc height.  Here's a picture from spine universe:

 

"The annulus fibrosus is a strong radial tire–like structure made up of lamellae; concentric sheets of collagen fibers connected to the vertebral end plates. The sheets are orientated at various angles. The annulus fibrosus encloses the nucleus pulposus.

Although both the annulus fibrosus and nucleus pulposus are composed of water, collagen, and proteoglycans (PGs), the amount of fluid (water and PGs) is greatest in the nucleus pulposus. PG molecules are important because they attract and retain water. The nucleus pulposus contains a hydrated gel–like matter that resists compression. The amount of water in the nucleus varies throughout the day depending on activity." 

In the dog exercise study,  the amount of collagen and proteoglycans increased in the annulus fibrosus but they did not increase in the nucleus pulposus.  And, it is the nucleus pulposus that resists compression therefore exercise(including stretching) probably cannot be used to help resist the compression forces that occur during day to day activity.   It was found that LIPUS was stimulatory on the nucleus pulposus and therefore LIPUS may increase disc height.

However, can an increase in the amount of collagen and the size of the proteoglycan molecules in the annulus fibrosus still be used to increase disc height? 

An increase in the size of proteoglycan molecules should not increase disc height as proteoglycans are proteins and do not contribute to the structure of the disc. 

Now, Marfan's Syndrome is a connective tissue disorder(collagen is a connective tissue) that increases height(Vincent Schievalli was 6'5" but remember correlation not equal to causation so Vincent Schievalli's height may have been a coincidence).  However, the exact manner in which Marfan's Syndrome can increase height is unknown. 

Is a collagen scaffold for a tissue engineered nucleus replacement capable of restoring disc height and stability in an animal model? 

"The idea of a tissue engineered nucleus implant is to seed cells in a three-dimensional collagen matrix. This matrix may serve as a scaffold for a tissue engineered nucleus implant. The aim of this study was to investigate whether implantation of the collagen matrix into a spinal segment after nucleotomy is able to restore disc height and flexibility. The implant basically consists of condensed collagen type-I matrix. For clinical use, this matrix will be used for reinforcing and supporting the culturing of nucleus cells. In experiments, matrixes were concentrated with barium sulfate for X-ray purposes and cell seeding was disclaimed in order to evaluate the biomechanical performance of the collagen material. Six bovine lumbar functional spinal units, aging between 5 and 6 months, were used for the biomechanical in-vitro test. In each specimen, an oblique incision was performed, the nucleus was removed and replaced by a collagen-type-I matrix. Specimens were mounted in a custom-built spine tester, and subsequently exposed to pure moments of 7.5 Nm to move within the three anatomical planes. Each tested stage (intact, nucleotomy and implanted) was evaluated for range of motion, neutral zone and change in disc height. Removal of the nucleus significantly reduced disc height by 0.84 mm in respect to the intact stage and caused an instability in the segment. Through the implantation of the tissue engineered nucleus it was possible to restore this height and stability loss, and even to increase slightly the disc height of 0.07 mm compared with the intact stage. There was no statistical difference between the stability provided by the implant and intact stage. Results of movements in lateral bending and axial rotation showed the same trend compared to flexion/extension. However, implant extrusions have been observed in three of six cases during the flexibility assessment. The results of this study directly reflect the efficacy of vital nucleus replacement to restore disc height and to provide stability to intervertebral discs. However, from a biomechanical point of view, the challenge is to employ an appropriate annulus fibrosus sealing method, which is capable to keep the nucleus implant in place over a long-time period. Securing the nucleus implant inside the disc is one of the most important biomechanical prerequisites if such a tissue engineered implant shall have a chance for clinical application." 

So collagen was able to increase height(thus maybe explaining the tall stature that individuals with Marfan's Syndrome tend to exhibit), however, this was collagen in the nucleus pulposus not the annulus fibrosus.  So the answer as to whether exercises can increase height via the intervertebral discs?  Maybe but the fact that the nucleus pulposus does not seem to be stimulated by exercise(LIPUS may have a stimulatory effect though) is a very limiting factor(removal of the nucleus decreased height very significantly by 0.84 mm).  So any height gained by the annulus fibrosus may not be able to be maintained by the nucleus pulposus however exercise may increase laying down height via intervertebral disc size which takes the nucleus pulposus' function to resist compression out of the equation. 

Elastin plays a role in the height of intervertebral discs too but only when the discs are loaded from the side and would therefore have no impact on overall body height. 

Typical height increase stretches are not likely to increase intervertebral disc height which can make you taller by 0.07mm a pop.  However, LIPUS may be able to if applied on the discs.