Thus, during development it may be important to optimize your gut microbiome via possibly avoiding antibiotics, modifying diet, etc.  This also means that there is the possibility of modification of the microbiome via transfer, etc.  Although there doesn’t seem to be any clear degree of optimization as of yet.

The microbiome: A heritable contributor to bone morphology?

“Bone provides structure to the vertebrate body that allows for movement and mechanical stimuli that enable and the proper development of neighboring organs. Bone morphology and density is also highly heritable. In humans, heritability of bone mineral density has been estimated to be 50–80%. However, genome wide association studies have so far explained only 25% of the variation in bone mineral density, suggesting that a substantial portion of the heritability of bone mineral density may be due to environmental factors. Here we explore the idea that the gut microbiome is a heritable environmental factor that contributes to bone morphology and density. The vertebrae skeleton has evolved over the past ~500 million years in the presence of commensal microbial communities. The composition of the commensal microbial communities has co-evolved with the hosts resulting in species-specific microbial populations associated with vertebrate phylogeny. Furthermore, a substantial portion of the gut microbiome is acquired through familial transfer{so what the mother eats during pregenancy may affect a childs height}. Recent studies suggest that the gut microbiome also influences postnatal development. Here we review studies from the past decade in mice that have shown that the presence of the gut microbiome can influence postnatal bone growth regulating bone morphology and density. These studies indicate that the presence of the gut microbiome may increase longitudinal bone growth and appositional bone growth, resulting differences cortical bone morphology in long bones. More surprising, however are recent studies showing that transfer of the gut microbiota among inbred mouse strains with distinct bone phenotypes can alter postnatal development and adult bone morphology. Together these studies support the concept that the gut microbiome is a contributor to skeletal phenotype.”

“The majority of the mammalian microbiome is present in the gastrointestinal system. The mammalian gut microbiome consists of hundreds of distinct microbial species (bacteria, archea, viruses, single celled eukaryotes) interacting with one another and with host cells at the gut endothelial barrier. The body is first colonized by microbes soon after birth. Over the first few years of life the composition of the gut microbial community fluctuates considerably until achieving a relatively stable composition”

“The gut microbiome is also heritable: maternal transfer of the microbiome soon after birth is among the most influential contributors to the establishment of the gut microbiome; and later in life components of the gut microbiota are transferable through close contact such as that occurring within households and due to familial dietary habits. The composition of a mature gut microbiota can fluctuate on an hourly or daily basis due to variations in diet. However, the overall composition of an established gut microbiota are robust to perturbations; the vast majority of the microbial composition returns to its prior state following a mild or temporary perturbation. Hence, the composition of the gut microbiota is partially heritable and, once established, does not change substantially without a large or prolonged stimulus. That the gut microbiota is established at an early age suggests that heritable components of the gut microbiota may contribute to the patterns of bone mass accrual that determine adult bone morphology and density.”

“most bacteria associated with vertebrates reside in the gastrointestinal tract, where densities can reach ~10¹¹ cells per milliliter, yet relatively few of the constituents of this gut microbiota are known to cause disease in their hosts.”

“the composition of the gut microbiota can be influenced by environmental variation, including host diet, geography, and temperature ”

“transplantation of gut microbiota from Gairdner’s shrewmouse (Mus pahari) into germ-free house mice stunts host growth rate relative to transplantation of house-mouse gut microbiota”

“The ability of the gut microbiome to influence bone morphology has been recognized since the first animal studies of oral antibiotics in the 1920–30s which reported alterations in whole body growth as well as bone length and morphology following chronic oral antibiotic dosing”

According to Identifying Components of the Gut Microbiome that Regulate Bone Tissue Mechanical Properties, disruption in the gut microbione results in a femur length reduction.

“the absence or depletion of the gut microbiota, while potentially influencing the acquisition of trabecular bone at the growth plate, likely has little effect on the amounts of trabecular bone present at skeletal maturity.”

“Schwarzer and colleagues found that young (two month-old) germ-free mice were much smaller than conventionally raised mice in terms of whole body mass, whole body length, whole bone length and femoral cortical area”

“Yan and colleagues found that adult (10 month old) germ-free mice had smaller endosteal and periosteal diameter at the femur midshaft and shorter whole bone length in adulthood than mice that had been conventionalized at two months of age, in part leading to their conclusion that exposure to the gut microbiota leads to a net increase in bone acquisition during life. Guss and colleagues and Luna and colleagues found that disruption (but not decimation) of the gut microbiota in mice using narrow spectrum antibiotics from 1 to 4 months of age was associated with small but significant reductions in femur length “

Mewing is basically putting the tongue on the roof of the mouth.    Now does the force of the tongue actually push the maxilla forward advancing it over time?  It’s possible.  But I think the majority of the benefits of mewing are due to the fact that actively putting the tongue on the roof of the mouth achieves lateral pterygoid muscle activation.   You see it’s been shown in orthodontal work via forced mouth opening and bite jumping appliance that lateral pterygoid muscle activation can simulate cartilage and endochondral ossification of the mandibular condyle.

The lateral pterygoid muscle attaches directly to the cartilage and by stimulating and activating by placing the tongue on the roof of your mouth you’re constantly pulling on the cartilage throughout the day.  Now it’s possible that mewing also has other benefits.  But if a large portion of mewings benefits are due to the lateral pterygoid muscle activation then it doesn’t matter if you’re mewing if you’re instead doing something else that activates the lateral pterygoid muscle such as talking or chewing.  But placing the tongue on the roof of the mouth is is something that can be done during sleep and I have successfully done this during sleep.  Thus your cartilage can be stimulated more frequently.

So, to apply the mewing principle to the other parts of the body?   How do we make alterations in posture and position such we can stimulate cartilage and growth throughout the day?

Chest up, shoulders back.  Shoulders back activates the upper back muscles.  Chest up activates the lower back muscles.  Now you don’t have to do this in a ridiculous way.  You just have to do enough so that the muscles are activated.  If if you at the the above pictures you see that most of the back muscles are angled upward so if you achieve muscle contraction it will pull all the spinal components upward too.

Now you may think if I round my shoulders forward and round my back that will stretch the back components too?  But if you do that the back will be stretched in an an unnatural way and out of alignment?  ie. scoliosis.  Like I said the muscles are already slanted and will pull upward if activated and it will pull in proper alignment.

If you want better results than get stronger back muscles(stronger lateral pterygoid muscle for the jaw).   Unfortunately, the back muscles do not attach directly to the cartilage but they do attach to soft tissues that will indirectly pull on the spine.  You can’t really mimic this with a back device you really want to do it yourself to achieve back muscle activation.

Now height gains won’t be much but a lot of people sit down for a lot of the day and don’t have good posture.  On an individual level the height gains probably won’t be significant(unless you have incredibly strong back muscles) but if everyone did it there would probably be small significant height gains.

If you’re worried about looking ridiculous then just find the minimal amount to pull your shoulders back and your chest up to achieve back muscle activation,  Ideally you’d want to sleep in this posture so your muscles pull while you sleep to.  So you would sleep on your back with your shoulders back and your back slightly arched.  Now you’re trying to sleep so you want to find the minimal amount of effort you can do to do this.  It cannot be achieved with a device as that will reduce muscle activation.

So think tongue on the roof of your mouth, shoulders back, chest up(or back arched).  Ideally while you sleep too.

There a few possibilities as to why the height gain occurs:

1. Improvement in posture
2.  Increase in bone density reducing bone compression
3.  Longitudinal bone growth

High‐Intensity Resistance and Impact Training Improves Bone Mineral Density and Physical Function in Postmenopausal Women With Osteopenia and Osteoporosis: The LIFTMOR Randomized Controlled Trial

“Optimal osteogenic mechanical loading requires the application of high‐magnitude strains at high rates{I’m not sure this is the case given fluid flow models}. High‐intensity resistance and impact training (HiRIT) applies such loads but is not traditionally recommended for individuals with osteoporosis because of a perceived high risk of fracture. The purpose of the LIFTMOR trial was to determine the efficacy and to monitor adverse events of HiRIT to reduce parameters of risk for fracture in postmenopausal women with low bone mass. Postmenopausal women with low bone mass (T‐score < –1.0, screened for conditions and medications that influence bone and physical function) were recruited and randomized to either 8 months of twice‐weekly, 30‐minute, supervised HiRIT (5 sets of 5 repetitions, >85% 1 repetition maximum) or a home‐based, low‐intensity exercise program (CON). Pre‐ and post‐intervention testing included lumbar spine and proximal femur bone mineral density (BMD) and measures of functional performance (timed up‐and‐go, functional reach, 5 times sit‐to‐stand, back and leg strength). A total of 101 women (aged 65 ± 5 years, 161.8 ± 5.9 cm, 63.1 ± 10.4 kg) participated in the trial. HiRIT (n = 49) effects were superior to CON (n = 52) for lumbar spine (LS) BMD (2.9 ± 2.8% versus –1.2 ± 2.8%, p < 0.001), femoral neck (FN) BMD (0.3 ± 2.6% versus –1.9 ± 2.6%, p = 0.004), FN cortical thickness (13.6 ± 16.6% versus 6.3 ± 16.6%, p = 0.014), height (0.2 ± 0.5 cm versus –0.2 ± 0.5 cm, p = 0.004){0.2 cm is pretty significant.  If the gain is due to posture then wouldn’t the low intensity exercise program gain posture as the low intensity group would also build functional strength?}, and all functional performance measures (p < 0.001). Compliance was high (HiRIT 92 ± 11%; CON 85 ± 24%) in both groups, with only one adverse event reported (HiRIT: minor lower back spasm, 2/70 missed training sessions). Our novel, brief HiRIT program enhances indices of bone strength and functional performance in postmenopausal women with low bone mass. Contrary to current opinion, HiRIT was efficacious and induced no adverse events under highly supervised conditions for our sample of otherwise healthy postmenopausal women with low to very low bone mass.”

One thing to consider is that there may be a load threshold for bone strengthening.  Since the women were so weak 85% of 1RM was needed to get above the load but for a stronger individual a smaller percentage of the 1RM may theoretically be needed.

” Resistance exercises (deadlift, overhead press, and back squat) were performed for the remainder of the intervention period in 5 sets of 5 repetitions, maintaining an intensity of >80% to 85% 1 RM. Participants performed up to 2 sets of deadlifts at 50% to 70% of 1 RM to serve as a warm‐up, as required. Impact loading was applied via jumping chin‐ups with drop landings. Participants were instructed to grasp an overhead bar with their shoulders and elbows flexed to 90 degrees, and their hands shoulder width apart with an underhand grip. The participant then jumped as high as possible while simultaneously pulling themselves as high as possible with their arms. At the peak of the jump, the participant dropped to the floor, focusing on landing as heavily as comfortably possible. Each exercise session was performed in small groups with a maximum of 8 participants per instructor, who was an exercise scientist and physiotherapist.”

I’m not sure if impact loading would be superior to tapping.  Tapping applies the load directly to the bone and whole body impact can damage soft tissue(although so can tapping).  I feel it more in the bone when tapping than whole body impact.

“Participants allocated to CON undertook an 8‐month, twice‐weekly, 30‐minute, home‐based, low‐intensity (10 to 15 repetitions at <60% 1 RM) exercise program designed to improve balance and mobility but provide minimal stimulus to bone. The CON program consisted of walking for warm‐up (10 minutes) and cool down (5 minutes), low‐load resistance training (lunges, calf raises, standing forward raise, and shrugs) and stretches (side‐to‐side neck stretch, static calf stretch, shoulder stretch, and side‐to‐side lumbar spine stretch). The intensity of resistance exercises was progressed from body weight to a maximum of 3 kg hand weights for the final month of the program.”<-I think this exercise regime would improve posture.  But if you look at table 2 this group lose 0.2cm of height.  Although if you look at the back extensor strength increase in table 5 the amount is far more in the high intensity group which would look to posture.

“Although not originally a primary outcome measure, we observed that HiRIT improved stature compared with CON. The observed improvement in stature after HiRIT is likely to be a consequence of increased BES(back extensor strength), as BES is inversely associated with magnitude of kyphosis. Our results add support to the findings of other exercise intervention studies that have demonstrated improvements in BES by 21% and corresponding kyphosis reductions of 5° to 6° in postmenopausal hyperkyphotic women”

Now we don’t want the height gain to be due to back extensor strength.  We want the height to be due to longitudinal bone growth.

According to Short-term and long-term site-specific effects of tennis playing on trabecular and cortical bone at the distal radius, “In children, no significant difference was observed between the dominant and nondominant forearm lengths (21.6 cm on both sides). In adults, the respective values were 25.3 ± 1.6 cm and 25.0 ± 1.6 cm, with a significant side-to-side difference”.  So also a bone density increase correlates with about a .3cm gain and you can’t account for this gain in terms of posture.

More on tennis increasing bone length can be found here.

Whole-body morphological asymmetries in high-level female tennis players: A cross‑sectional study

“This cross-sectional study aimed to examine the degree of whole-body morphological asymmetries in female tennis players. Data were collected in 19 high-level female tennis players (21.3 ± 3.4 years). Based on anthropometric measurements (upper arm, lower arm, wrist, upper leg and lower leg circumferences as well as elbow and knee widths) and dual x-ray absorptiometry research scans (bone mineral density (BMD), bone mineral content (BMC), lean mass (LM), fat mass (FM) as well as humerus, radio-ulnar, femur and tibia bone lengths), within-subject morphological asymmetries for both upper (dominant vs. non-dominant) and lower (contralateral vs. ipsilateral) extremities were examined. Upper arm (p = 0.015), lower arm (p < 0.001) and wrist circumferences (p < 0.001), elbow width (p = 0.049), BMD (p < 0.001), BMC (p < 0.001), LM (p = 0.001), humerus (p = 0.003) and radio-ulnar bone length (p < 0.001) were all greater in the dominant upper extremity. BMC (p < 0.001) and LM (p < 0.001) were greater in the contralateral lower extremity, whereas FM (p = 0.028) was greater in the ipsilateral lower extremity.”

“Humerus bone length (cm) 27.6 ± 1.1(dominant)26.9 ± 1.2(non-dominant) Radio-ulnar bone length (cm) 25.0 ± 1.2(dominant)24.3 ± 1.3(non-dominant)”

I don’t think we can rule out that bone density can increase bone length.  It’s possible that since gains are typically small 0.2cm-1cm that they aren’t considered.  You’ll remember above that that the tennis study found the increase in bone length only in adult and not in children.  I don’t know if whole body impact is the best just based on personal testing I think direct impact is the best.  Tennis is pretty close to direct impact but the load is very inconsistent being based on how the game is going.  It may be possible to get larger increases with direct impact.  Whole body impact is skill dependent, runs risk of soft tissue injury, and you may land wrong.  It’d be interesting if a bone density regime like osteostrong has any impact on bone length or height parameters.

There’s lot of evidence that milk can help increase height during development.  The so called “dutch diet“.

This website has more info on extracellular vesicles and it’s own thoughts on the study.

Bovine milk extracellular vesicles induce the proliferation and differentiation of osteoblasts and promote osteogenesis in rats

“Bone is constantly balanced between the formation of new bone by osteoblasts and the absorption of old bone by osteoclasts. To promote bone growth and improve bone health, it is necessary to promote the proliferation and differentiation of osteoblasts. Although bovine milk is known to exert a beneficial effect on bone formation, the study on the effect of bovine milk extracellular vesicles (EVs) on osteogenesis in osteoblasts is limited. In this study, we demonstrated that bovine milk EVs promoted the proliferation of human osteogenic Saos‐2 cells by increasing the expression of cell cycle‐related proteins. In addition, bovine milk EVs also induced the differentiation of Saos‐2 cells by increasing the expression of RUNX2 and Osterix which are key transcription factors for osteoblast differentiation. Oral administration of milk EVs did not cause toxicity in Sprague‐Dawley rats. Furthermore, milk EVs promoted longitudinal bone growth and increased the bone mineral density of the tibia. Our findings suggest that milk EVs could be a safe and powerful applicant for enhancing osteogenesis.”

The medieval rack just makes sense right?  You pull on the bones and stretch them to become longer but there seems to be an emptiness of anecdotal cases where the medieval rack increases height.

Now stretching on object in the tensile direction in the plastic deformation range can make an object longer up until the failure point.  The problem is obviously the failure point but ideally a bone should adapt to each new point of plastic deformation.  So you rack in the plastic deformation range lengthen bone a tiny bit.  The bone adapts then you lengthen more and repeat.

The plastic deformation point for bone is smaller than that of tendons and ligaments therefore you should be able to get into the plastic deformation range for bone without worrying about tendon and ligament damage.  Although that does not factor in muscle fatigue.

The tendons attach to bone at the enthesis.

From Enthesis and Enthesopathy website:

The new bone formation that occurs in diseases such as Ankylosing Spondylitis and Psoriatic Arthritis is an exaggeration of the normal tendency to make bone on the outer surface of the enthesis.

So you see pulling on the bones does work to increase bone length the problem is the pulling that occurs is not in the longitudinal direction there is direct proof of those at the enthesis.

So the rack may not pull on the bones at all the way it is designed it may pull on the tendons which in turn pull on the enthesis.

Also it may be that the rack causes bone growth so slowly that it is not feasible.

So the two issues with the rack:

1. It may not generate sufficient tensile strain on the bone in a longitudinal direction
2. Since the body has to adapt to each new point of plastic deformation it may be too slow to generate feasible growth.

For a feasible plastic deformation strategy:

1. The object must constantly stretch the bone in a longitudinal direction in the plastic deformation range
2. The object must be such that the bone has time to adapt to avoid bone failure
3. The object must be applied enough to generate noticeable growth.