The Metal Fixator To Hold The Cut Bones In Place Is The Critical Element

Ever since I found out that the company EpiBone was working towards creating lab grown osteochondral tissue, it was obvious that they were working towards making bone tissue that will go through the natural process of chondrocyte formation, chondrocyte condensation, osteocyte differentiation, and eventual total ossification of the previously chondrogenic tissue. This process is called endochondral ossification.

The ultimate goal as claimed by the CEO is that they want to grow bone tissue that can be implanted into bone defects in a living human. Based on the claims made, the obvious corollary to this claim is that they will also be working on bone tissue that can expand and grow on their own.

The idea is like this specific situation.

A young child (8-10 years old) who still has developing and growing limbs develops cancer of the bones aka osteosarcoma. The surgeons realize that they have to remove that bone tissue that has the cancer. That bone part is taken out, which could be a rather large chunk, but the orthopedist realizes that the child has not finished growing. They need to now replace that piece of bone they took out with a new one, which can also grow in length and width along with the bone in the limbs of the kid.

Alsberg’s team as early as the early 2000 showed that it was possible to grow “growth plate like” tissue that grows  volumetrically. Using that research as a stepping stone, the research team at EpiBone would be able to use the same growth factors, scaffolds, and peptides to get a growing bone-cartilage tissue in the lab.

The surgical technique of then implanting that Pseudo-Epiphyseal Cartilage tissue into the area of bone that is missing is not hard. That part where you fuse the bone edge of the implant with the edge of the originally cancerous cut bone does not need to be that difficult, although it can be technically challenging right now.

It appears that the real, true critical part that is limiting the possibility of using just stem cells and tissue engineering techniques to lengthen bone is not in the research.

It comes down to the need to fix the cut bones into alignment with each other, and not move about.

This is the entire reason why the original creator of the limb lengthening method need to ever use the External Fixators. The Fixators were always there to hold the bones in place, so that they don’t become crooked, or bent.

If we now really sat down and thought about it like a Monday Morning Quarterback aka “hindsight is 20/20”, the 2 decades of research on lengthening of bones done by Gavriil Ilisarov in the Kurgan from the 1960s to 1980s to perfect the technique of bone lengthening was bound to be successful, as long at the rate of lengthening of bone was just slow enough to account for osteogenic healing and tissue/callus formation rates. Once you realized that the bones in our body is one of the tissues in our bones with have the highest rate of healing potential in terms of broken bones over time fusing together, on a very theoretical level, there was no doubt that bones that have an external fixator that can pulls bones slowly aka lengthening would eventually heal over, resulting after say 3-6 months of tensile pulling, would result in longer bones.

Ilizarov used the Circular External Fixator to hold the bones into place. The technique for bone lengthening eventually was learned by the Germans ie at Dr. Betz, who developed his own internal fixator technique. Dr. Dror Paley developed his own internal fixator way called PRECISE. You always need some type of really strong, non-biodegradable element to hold the cut bones into place, whether it is to be placed inside the bone or attached to the bone from the outside.

The most minimally invasive method for limb lengthening surgery was developed by Dr. Bai Helong in China as early as the early 2000s, which involved a very thin method rod that is screwed to the top cut bone and the bottom cut bone, which is elongated. The rod would run in parallel to the axis of the long bone. As the metal rod is elongated through a mechanical action, the bones that the metal rod is screwed into, would elongate with the rod.

The callus that is formed in the region where the bones meet is stretched out and then reformed. This is what really happens during distraction osteogenesis. This is, and has always been the way bone lengthening actually works. Tissue that is developed between the interface of two bones, in the form of some pre-chondrogenic tissue aka “callus”, is stretched, ossified slightly, and then stretched again, until the desired lengthening of the bones finally is reached.

Notice how you always need to screw metal rods into the bones. You need the metal rods to go through the bones to give the bones enough structural strength.

This is one of the biggest issues that critics of the current bone lengthening methods have. They don’t like the idea that not only do you break the bones, but you also have to drill into the already cut bones at least in 2 different locations of the long bone, just to hold the overall long bone into position.

If an alternative to the current bone lengthening methods is ever developed, the technique will still need to hold the bones into position, without the chance of the cut bones falling apart and the legs ending up bent, or never fully fused back.

In a previous talk I had with someone over Skype, I had believed that maybe it was possible to implant some really strong bio-degradable material as a replacement to the metal rods or metal fixators.

Another LSJL study shows bone length increase

I actually missed that this LSJL study showed height increase as it was a minor comment that joint loading increased height of the femoral head.  Since the femoral head is a diagonal offshoot of the femur it may not necessarily increase height but it is an increase in bone length all the same.  However, the osteonecrosis induced in the study may be a prerequisite to induce the femoral head growth.  However, it should be noted that the osteonecrosis decreased femoral head height but the degradation of existing bone may have allowed for new bone growth.

This is an LSJL related study published by Yokota and Zhang.  The primary author seems to be more Zhang who seems more into the lengthening effects than Yokota.  This study shows that joint loading increases fibrous differentiation.  And fibrous differentiation would be a potential intermediary step for neo-growth plate formation.  Knee loading increased vessel remodeling and osteoclast formation which would be needed to make room for a new growth plate but these levels were only slightly greater than control group and reduced from the osteonecrosis group so we can not say for sure whether this will happen in LSJL on a normal bone.

Overall this study shows that LSJL does at least one of the steps required for neo-growth plate formation: fibrous type tissue formation.  This fibrous tissue would then have to be further differentiated into more cartilagenous tissue.  The perichondrial ring(or ring of LaCroix) is fibrocartilagenous.

Knee loading protects against osteonecrosis of the femoral head

“Osteonecrosis[loss of blood to the bone] of the femoral head is a serious orthopedic problem. Moderate loads with knee loading promote bone formation.  Using a rat model, we examined a hypothesis that knee loading enhances vessel remodeling and bone healing through the modulation of the fate of bone marrow-derived cells. In this study, osteonecrosis was induced by transecting the ligamentum teres followed by a tight ligature around the femoral neck. For knee loading, 5 N loads were laterally applied to the knee at 15 Hz{this is pretty high frequency} for 5 min/day for 5 weeks. Changes in bone mineral density (BMD) and bone mineral content (BMC) of the femur were measured to evaluate vessel remodeling. Femoral heads were harvested, and bone marrow-derived cells were isolated to examine osteoclast development and osteoblast differentiation.  Osteonecrosis significantly induced bone loss, and knee loading stimulated both vessel remodeling{vessel remodeling shows promise as that would be very helpful for neo growth plate creation} and bone healing. The osteonecrosis group exhibited the lowest trabecular BV/TV in the femoral head, and lowest femoral BMD and BMC. Knee loading increased trabecular BV/TV as well as BMD and BMC. Osteonecrosis decreased the vessel volume, vessel number and VEGF expression, and knee loading increased them. Osteonecrosis activated osteoclast development, and knee loading reduced its formation, migration, adhesion and the level of “pit” formation{pit formation could potentially be beneficial though as that pit could where a neo-growth plate would go}. knee loading significantly increased osteoblast differentiation and CFU-F{An increase in CFU-F means an increase in mesenchymal stem cell proliferation which is a good for neo-growth plate formation but doesn’t guarantee that it will occur}. A significantly positive correlation was observed between vessel remodeling and bone healing. Knee loading could be effective in repair osteonecrosis of the femoral head in a rat model [by] promoting vessel remodeling, suppressing osteoclast development, and increasing osteoblast and fibroblast differentiation. “

“The mechanism of knee loading is considered to change intramedullary pressure of femoral and tibial bone cavities. The load driven pressure may generate fluid flow in a lacuna canalicular network in bone cortex. The pressure activates bone metabolism-related genes in femur and tibia”<-what we are interested in an increase in fluid flow and hydrostatic pressure to induce chondrogenic differentiation.  Hydrostatic pressure by itself isn’t likely to induce chondrogenic differentiation by itself as it is typically three orders of magnitude below the pressure needed to induce chondrogenic differentiation.  But the addition of bone deformation and fluid flow may bridge the gap and induce chondroinduction.

“Male Sprague–Dawley rats (~12weeks of age)”

“knee loading was achieved through dynamic loads applied to the left and right knee joints of rats in the lateral–medial direction, respectively. To position the knee properly, the lower end of the loading rod and the upper end of the stator were designed to form a pair of semispherical cups. The lateral and medial epicondyles of the femur together with the lateral and medial condyles of the tibia were confined in the cups.  The tip of the loader had a contact
area of 15 mm in diameter.”

See Figure 1 of the paper(first link on the page) for an image of the knee loader.

Loading increased vascular remodeling in the osteonecrosis + LSJL group but not versus control.  But there was no normal bone plus loading group.

Joint Loading actually seemed to reduce the number of mesenchymal stem cells but that could be due an increase in differentiation.  Mesenchymal condensation was more visible in the osteonecrosis group and mesenchymal condensation is a prerequisite for neo-growth plate formation.

Bone, Accepted manuscript. doi:10.1016/j.bone.2015.09.012

Knee Loading seemed to restore osteoclast adhesion and migration to slightly above control levels but that slightly above could indicate activity that would remodel the bone enough to allow for mesenchymal condensation.

Bone, Accepted manuscript. doi:10.1016/j.bone.2015.09.012

Knee loading greatly increased CFU-F and Osteoblast differentiation versus both osteonecrosis and control group. “Knee loading enhanced differentiation of osteoblasts and fibroblasts.” Fibroblastic tissue(marked by CFU-F) could potentially become chondrogenic tissue.  Fibrocartilage is a thing.  But to be a true growth plate, additional mechanical stimulation would be needed to turn that fibrocartilage into pure cartilage.

Bone, Accepted manuscript. doi:10.1016/j.bone.2015.09.012

Knee loading increased the height of the femoral head partially

Bone, Accepted manuscript. doi:10.1016/j.bone.2015.09.012

It’s a big breakthrough that LSJL increased height in the femoral head.  The osteonecrotic bone had far more marrow in B, thus under osteonecrosis LSJL may have had more room to induce growth.

The perichondrial ring of the growth plate is fibrocartilagenous in nature and may be the source to provide cells to the growth plate.

“The current histology and bone mineral density data are suggestive of the role of bone marrow-derived stem cells in load-driven bone healing, and they also establish a causal relationship between the observed vessel remodeling and bone healing effects with knee loading”<-This is huge because we want to induce stem cells to form neo-growth plates.

According to this LSJL would increase blood perfusion which would be the most interesting thing.  If the bone has more blood flowing through can create unique biological opportunities remember one of the key steps to distraction osteogenesis is a blood clot.

It was mentioned that LSJL upregulates bone metabolism related genes.  Here’s a study that lists bone metabolism related genes:

Association of osteoporosis susceptibility genes with bone mineral density and bone metabolism related markers in Koreans: the Chungju Metabolic Disease Cohort (CMC) study.

“bone metabolism-related markers, such as serum concentrations of calcium, phosphorus, PTH,
and 25(OH) D”

“genetic variants of MEF2C, ESR1, TNFRSF11B, and SOX6 were associated with bone metabolism-related markers”

Lowering Fbn1 levels may increase bone length

Even though it mainly seems like it’s an active growth plate thing, it’s possible that FBN1 deficiency could stimulate neo-growth plate activation as it does stimulate TGF Beta activation and there’s ectopic tendon calcification.

TENDON-DEPENDENT CONTROL OF LONGITUDINAL BONE GROWTH

“Skeletal abnormalities caused by disproportioned bone overgrowth (LBO), are a common trait in Marfan syndrome (MFS), a connective tissue disease caused by mutations in the extracellular matrix (ECM) protein and TGFβ regulator fibrillin-1 (Fbn1). The cause of LBO in MFS is unknown and therapies are not available. Fibrillin-1 hypomorphic mouse model (Fbn1mgR/mgR) faithfully replicates MFS skeletal manifestations including elongated bones however, its early demise due aortic rupture limit the magnitude of LBO investigation.

To circumvent Fbn1mgR/mgR lethality and investigate the contribution of specific skeletal tissues to LBO, Fbn1 gene expression was targeted in developing limbs by crossing Fbn1Lox/Lox mice with Prx1-Cre, in or bone with Osx-Cre, in cartilage and perichondrium with Col2-Cre, in skeletal muscles with Mef2c-Cre, and ligaments and tendons with Scx-Cre. Bones length of Fbn1 conditional mice KO was measured and relevant histological, cellular and biomechanical parameters were assessed.

Fbn1Prx1−/+ and Fbn1Prx1−/− mice had longer limbs bones compared to WT mice and amount of fibrillin-1 in the limb matrix was inversely proportional to bone length. Interestingly, Fbn1 gene targeting in ligaments/tendons resulted in LBO, altered tissues’ mechanics and TGFβ-induced switch of tendon stem cells to chondrocytes. Gene targeting in other limb’s anatomical locations did not result in LBO thus ruling out the participation of surrounding tissues to this bone phenotype.

Fbn1 gene inactivation in ligament/tendon is associated with increased local TGFβ, altered biomechanical properties and LBO. As previously reported, ligaments/tendons respond to changes in mechanical load by increasing the levels and/or the activity of TGF-β while bones undergo morphological adaptation in response to muscle loads transmitted by tendons. We hypothesize that dysregulation of local TGFβ signaling and altered biomechanical properties of fibrillin-1 deficient ligaments/tendons affect endochondral ossification by improper load transmission to bone. By showing ligament/tendon-dependent regulation of postnatal longitudinal bone growth this study provides a paradigm-shift in tendon biology and it shades a new light on LBO pathophysiology in MFS, thus providing the bases for new pharmacological interventions for this and related skeletal conditions.”

So lower levels of Fbn1 means longer bone length and FBN1 deficient tendons and ligaments alter endochdondral ossification by altering load transmission to bone.  We can alter load transmission without altering FBN1.

Here’s a grant(2016) related to the subject:

TENDON-DEPENDENT CONTROL OF LONGITUDINAL BONE GROWTH

“disproportionate increase of longitudinal bone growth that causes serious malformations of the limbs, anterior chest and Spine is the clinical hallmark of patients afflicted with Marfan syndrome (MFS), a connective tissue disease caused by mutations in the extracellular matrix (ECM) protein and TGFβ regulator fibrillin-1. Our preliminary studies of mice with tissue-specific ablated Fbn1 gene activity have revealed an unsuspected causal relationship between tendon/ligament (T/L) dysfunction and longitudinal bone overgrowth (LBO). Specifically, we found that (1) Fbn1 inactivation in T/L cells was necessary and sufficient to promote linear bone overgrowth associated with dysregulated growth plate (GP) gene expression; (2) fibrillin-1-deficient tendons displayed abnormal tissue architecture and impaired mechanical properties, particularly at bone- insertion sites; (3) the relative amount of fibrillin-1 correlated with discrete changes in tendon mechanics; (4) tendon-derived stem/progenitor cell (TSPC) cultures deficient for fibrillin-1 differentiated improperly as result of increased latent TGFβ activation; and (5) ectopic tendon calcification of fibrillin-1-deficient tendons was commonly observed. We therefore hypothesize that fibrillin-1 assemblies normally restrict GP-driven linear growth of neighboring bones by specifying the mechanical properties of tendons through the control of ECM organization and TGF-regulated TSPC differentiation. Accordingly, the scope of our proposal is two-fold; first, to characterize how fibrillin-1 deficiency translates into tendon dysfunction and tendon-associated LBO, and second, to establish how local TGF hyperactivity in tendons promote tissue degeneration thereby leading to excessive linear growth of the adjacent, structurally normal bones. To this end, we will characterize the expression of molecular and cellular determinants of tendon development and maturation in mice deficient for fibrillin-1 in T/L matrices, in addition to employing computational approaches to identify probable disease-causing molecular abnormalities in the GP of these tendon-defective animals (Aim 1); apply data-driven statistical models to determine how graded fibrillin-1 deficiencies correlate with tendon mechanics and associated LBO (Aim 2); and assess whether systemic TGFβ neutralization modifies tendon pathology and LBO severity in fibrillin-1-deficient mice (Aim 3). The results of these investigations are expected to substantially advance our limited understanding of tendon function in health and disease and implicitly, of the cellular, molecular and tissue factors that coordinate the postnatal growth of musculoskeletal tissues. ”

 

LSJL Update 12-7-2016

Here’s the last LSJL update.

The growth seems pretty solid from last update:

Current

20161206_162420

1 month earlier:

20161108_155418

So increasing the intensity and duration of clamping on the right foot seems to have worked.  I’ll keep trying to see if can get more growth.  I may have some growth in my right hand from clamping there but I’ll wait to see if the growth is more significant as I can always get x-rays there.

I’ll also try to get growth in the longer limbs but once I can prove growth in smaller limbs I can get more resources to use for the longer ones.  It does seem like the foot itself is growing more than the toes so maybe it’s easier to grow those bone shapes even though there’s a lot of the same obstacles for longitudinal bone growth for “short” bones there could be differences we don’t know about.  these bones are also surrounded by different tissues than long bones which could make a difference.

So I’ll try the same intensity/density of clamping on the foot and see if I can grow on the hands and other limbs and increase clamping intensity on those areas.

Changing The Gut Microbiome Definitely Causes People To Become Taller – Breakthrough!

Over the last 2 months I have definitely gone back into going deep into the research and I have made some quite startling connections and one of my theories on how it is possible to make people taller has definitely become validated by a study I found just a few days ago.

First, let me say that I have pored over hundreds of studies on the subject of pediatrics, growth, endocrinology, and biology. I have thousands of saved studies I still have not read in depth. When you spend this much time reading, analyzing and thinking about a subject, you start to see connections where maybe other people have not seen yet.

My initial theory on the link between the intestinal tract and the growth pattern of a person was started when I sat in at this thing called Mini-Medical School that the state school (University of Washington) close to my house. There was maybe a total of only 6-8 lectures, but 1 entire lecture was dedicated to a professor called about Fecal Transplantation.

Fecal transplantation is the medical process of taking a bit of the fecal matter from one person and putting it into the gut of another human, to change the microbiome, aka the bacteria composition. It sounds disgusting to the average person, but when I heard about the case where a obese female was turned permanently skinny (she could not gain weight afterwards no matter how much she ate) after she had the fecal sample of a skinny person implanted, my eyes were as big as saucers. Now I understood the power of fecal transplantation.

Since that time, I have looked for more studies which link gut bacteria composition to the person’s overall health. I have looked into probiotics, started drinking a lot of Kombucha tea, and looked for ways to optimize my gut health. One thing I have started to do is gone completely on the Soylent 2.0 diet (with avocado, garlic, aspirin, water, tea). I wonder what would happen to my overall health if I just stuck to really basic food elements.

If you think about it, it really does make sense. I once wrote about the possibility that babies will probably have better growth patterns when they stay on drinking their mothers milk than going on the formula too early, because of the colostrum and the casein content. Tyler proposed years ago in a blog post about the possibility of the link between taking casein and height increase but he did not consider colostrum as the other key active ingredient in human female milk.

We all know that the rate of growth is highest when we are just a baby. Our digestive tracts are still virgin, and not fully developed yet. Those critical component’s in the mother’s milk have antibodies and other active ingredients that basically gives the newborn all of the necessary stuff to grow their immune system fight pathogens (bacteria and virus) that will eventually come at the baby as it grows up and lives on as an adult. It is the mother’s milk that goes into the babies digestive tract, and this is probably the most important determinant of how well the baby will do later.

There are many studies which link the health of the digestive tract to onset of Alzheimers, Arthritis, and Periodontal disease even. To the average person trained in the traditional medical school, it wouldn’t make any sense how it is possible that there is any link between what is in our intestine and the health of our brain. They are two totally different organ systems, which rarely have any affect on the other.

That is actually true, for an adult, but if we reverse time, and put that person back as a baby, when they just came out of the womb, they are still begin developed neonatally, so it makes sense that you can change the overall health of the person as an adult with a few key actions when they are just a baby, since their fitness level and health potential can still be molded.

What I claim is possible is to basically take the fecal matter of another baby who has the genes for tall stature, and implant that fecal matter into the subject baby. Don’t do take the fecal matter of a human adult, because the fecal matter of a human adult is actually poisonous and potentially deadly, at least for the baby’s digestive system. There is a reason why we can use cow and bat fecal matter to use as fertilizer, but human fecal matter would just kill plants if you used it as fertilizer.

This will cause the still modifiable baby’s immune system to change to have the microbiome of a baby who is genetically predisposed towards tall stature. Think Shaq being 7′ 1”, whose mother was 6′ 2”, and how both of his grandfathers were supposedly 6′ 9” in height. There are definitely families in any population which have the genes for tall stature. The theory is that the baby who has the fecal implant will now became much bigger as an adult than if they didn’t get the transplant.

For further proof, I refer the reader to the study which validates this idea. “Gut microbiota induce IGF-1 and promote bone formation and growth”. The study is extremely new, just published Oct of 2016.

Abstract

Appreciation of the role of the gut microbiome in regulating vertebrate metabolism has exploded recently. However, the effects of gut microbiota on skeletal growth and homeostasis have only recently begun to be explored. Here, we report that colonization of sexually mature germ-free (GF) mice with conventional specific pathogen-free (SPF) gut microbiota increases both bone formation and resorption, with the net effect of colonization varying with the duration of colonization. Although colonization of adult mice acutely reduces bone mass, in long-term colonized mice, an increase in bone formation and growth plate activity predominates, resulting in equalization of bone mass and increased longitudinal and radial bone growth. Serum levels of insulin-like growth factor 1 (IGF-1), a hormone with known actions on skeletal growth, are substantially increased in response to microbial colonization, with significant increases in liver and adipose tissue IGF-1 production. Antibiotic treatment of conventional mice, in contrast, decreases serum IGF-1 and inhibits bone formation. Supplementation of antibiotic-treated mice with shortchain fatty acids (SCFAs), products of microbial metabolism, restores IGF-1 and bone mass to levels seen in non-antibiotic- treated mice. Thus, SCFA production may be one mechanism by which microbiota increase serum IGF-1. Our study demonstrates that gut microbiota provide a net anabolic stimulus to the skeleton, which is likely mediated by IGF-1. Manipulation of the microbiome or its metabolites may afford opportunities to optimize bone health and growth.

My Conclusion

This very study shows that if you can adjust the gut microbiome of a baby lab mice, the long term, net result is that the grown up adult mice will have much longer and bigger bones. The process is that the gut has some way to stimulate the Liver and Adrenal Glands to release much more IGF-1 into the body. IGF-1 as we know is what growth hormone breaks down into which goes to the growth plates to make bones longer and wider.

Of course we must always be aware of the possibility that many times, transplants are rejected by the subject’s/host’s body. But that is a discussion for another day.

A Simple Jaw Realignment Exercise Increased This Man’s Height Over 2 Inches.

A few months ago, I became aware of this website called ClaimingPower.com, written by this guy who said that his goal for the last half a decade was to change the overall shape of the face, by pulling the nose. The led to me getting in contact with other people who are working on the same type of project. This one guy shared to me that he found a much faster, more effective method to pull the face, to make the face more aesthetically pleasing.

We talked for about an hour on Skype and he said that it is possible to get this type of “facial realignment” change since the irregular bones that make up the human face (maxilla, mandible, occipital, etc.) are not fused. There are sutures between the bones which means that the bones can indeed move slightly. The last I heard from him, he had gotten a 6 figure initial investment and was trying to patent his technique.

So I wanted to understand and learn more about this interesting small world and who else has tried this bone remodeling idea. One name that came up a lot was Michael Mew, who has famously given talks at Men’s Self Improvement Conferences, specifically the 21 Convention, which used to be a convention were men in their 20s shared tips and techniques on how to pick up women.

A little more searching on Google revealed a few more relevant websites, but there was one website which caught my eye. Orgone Energy Products. This website is quite interesting and strange. What the website reminds me of is one of those really much older website designs you saw maybe back in the mid 2000s. Some products that are listed on there like CycloAstragenol are products which were really hot and talked about a lot by the media 5 years ago but has now died down. Could an extract from the Astragalus plant really help inhibit the shortening of telomeres and hold back aging? We are not sure.

There is one blog post entitled “Orgoneproducts Newsletter: New Hormone Enhanced Orgone Chembusters, (NCR) Nuero-Cranial Restructuring, and True Love.” writen back in Nov 2 (of 2015?) which made a strange claim.

Apparently from doing this simple jaw alignment exercise, this guy went from 6 2.5″ to almost 6′ 5″ in height.

Quote…

“The one natural solution for boosting testosterone levels in Men that I offer is TKO- Tongkat Ali an Indonesian herbal based formula that will raise testosterone levels. Hormones are a complete conversation in themselves, feel free to contact me for more info that I am hesitant to put into print…..The good news is even the worst case scenario can now be changed with consistent application of physical regenerative therapies, hormonal reset, continual immersion in high intensity life force fields. What types of physical regenerative therapies am I talking about? Three, specifically and a fourth to be talked about at a later date. First is Neuro-Cranial Restructuring, the short name is NCR, not to be confused with National Cash Register. NCR developed by Dr. Howell, is an advancement of endo-nasal therapy. It uses small nasal balloons to release connective tissue in the sphenoid bone. An NCR treatment is like unlocking a spring, allows for symmetry correction in the head, face, and spine. The balloon is inserted in one of the six nasal passages in the nose. There is a testing protocol to determine which nasal passage. The testing protocol is where the magic is found, diagnosing the correct nasal passage with each treatment allows for the least amount of force to be used to create the greatest movements without trauma. Each NCR treatment creates compound positive symmetry changes which results in correcting facial and spinal distortions over time. Incremental change leading to massive long term results. In my case, I have partially corrected a scoliosis in my spine that resulted in an increase in functional height of 2.5 inches. When I started I was 6′ 2″ and a half, I am now a shade under 6′ 5″. My head size increased as well as I my eyes became more level over a 5 year period. We now have a fulltime NCR practicioner, Plato Rosinke, in New York City. Plato has been trained by Dr. Howell and is one of the more proficient NCR practioners in the world.”

My Personal Interpretation – Now I don’t know how old this person is who writes the blog, or how bad his case of scoliosis is. However, he did claim that his height increased by almost 2.5 inches after this technique, which somehow straightened out his back. The truth is that most people have some level of curvature of the vertebrate. If this technique can somehow alleviate the level of curvature of the vertebrate, then this technique should work for the majority of the people in a population giving at least a fraction of a inch extra in height..

Not only that, he made another claim in a more recent post (June 24) that his shoe size also increased. “The Shoes Have It.. Starecta/Bite Block Changes: Shoe size jumps from 11-13.5

Quote…

“The starecta/bite block begins the reversal of the compensation process and the body unwinds and regains it’s natural symmetry. After three months on the Starecta, I was having almost daily headaches. I thought this was part of the correction process, but little did I know it was from shoes that were way too tight. I had naturally high arches the story goes, one day I got the epiphany that maybe I needed bigger shoes! I hobbled down to my favorite shoe store on St. Marks and First; the name escapes me, but it is my favorite. A small selection, but all the shoes are well thought out at this nameless shoe store that be my favorite of all-time. I got a new pair of sneakers size 12; I had jumped a full shoe size...About a month later, the headaches started up again, but this time I was wise and made a pre-emptive strike and ran to my favorite nameless shoe store to buy the next installment in this shoe saga. The headaches again subsided, there was peace in the land and all was well. This time I started to look more closely at my feet, I speculated based on the size of my arches, I was not quite done with the shoe expansion….They no longer had my Size! I had outgrown them, 13.5 apparently was too much of a man for them.”

My Personal Interpretation

This guy makes the claim that there is some type of biomechanical connection between the feet and the alignment of the jaw. He was using this device/technique called the Starecta for months and the headaches started. By some luck, he realized that maybe the headaches were caused from having the shoes being too tight. So he got a size higher. Later, the headaches came back so he got another size larger.

My Final Conclusion

Whoever writes those blog posts have gotten themselves into the area where scientists would never go into. Many things that this person says works is not based on real scientific data. However, this person is willing to try a lot of different healing methods to see which ones works for him. The efficacy of all of the techniques and ideas he throws out should always be questioned.

What I found suspicious is that he talks alot about heartbreak and hormonal issues. It is very possible that he is still a teenager, and this growth in height and feet size is just from natural growth of the body. Or maybe he is in his early 20s. Then we have to consider the possibility that this person actually suffers from a pituitary tumor, which is causing the excessive height growth and the increase in feet size. That would definitely explain those intermittent bouts of headaches. People who suffered from excessive GH in their body from their puberty years to adulthood, turning the gigantism to acromegaly talked about how they suffered through headaches.

If the person who runs the website is ever reading this, I strongly suggest they go check their hormone levels with an Endocrinologist and get a CT scan of their brain.