As I had stated in my last post, the discussion on the Make Me Taller boards seemed to have lead to me finding another rather revolutionary way to possibly increase a person’s height.

The original Discussion was started HERE but after a few extra clicks of linkes, I found myself on this discussion where one of the profiles started to talk about an idea that was very foreign to me, and seemed also very hopeful located HERE.

…..The spine is a very delicate and dynamic aspect of our body. The Call To Torsos is for a compilation of research that may help discover or advance methods for minimally-invasive or non-invasive methods for increasing Sitting Height via lengthening the Introvertebral Discs.

The major challenge is, to increase the spine length you would need a minimally-invasive or non-invasive method for increasing the height of the Vertebrae (Bone – not at all ideal) or of the Introvertebral Discs (Fibrocartilage – very ideal).

You do not want to increase the bone length because this is likely to be more difficult and there will be increased load on the Introvertebral Discs. The Introvertebral Discs provide critical cushioning and mobility between the Vertebrae and they degenerate with age. If you could increase the height of the Introvertebral Discs, you would be combating the degenerative effects of age which lead to spinal injury, you would have a healthier spine less prone to injury and you would increase height.

The optimistic aspect is 1: science has approached a period where it is trying to master growing Bone and Fibrocartilage among many other biological tissues and 2: 24 Vertebrae are not fused and thus 25 Discs have reasonable potential to be manipulated http://www.giantscientific.com/height_gain_exercise.html , which means that only a very small increase in height needs to be applied to each disc (e.g. 0.5cm or half of the width of your pinky nail Multiplied By 25 = 12.5cm = about 5 inches or 4.92 inches to be exact).

While some research is being applied to methods for manipulating the body in completely non-invasive ways such as systemic oral consumption or even approaches similar to magnetics or radio waves etc, my theory is that in order to specifically increase height of the discs in a practical manner which will not have negative side effects on the rest of the body one will likely need minimally-invasive injections directly to the disc. 

I imagine a solution such as Ultrasound-Guided Injections of some sort of growth agent, probably best administered while inverting on a specially designed Inversion Table. This also needs to be done in a manner where the disc does actually grow the correct amount in the correct direction and in a uniform/proportional manner so that there is no bulging and interference with the nerves.

Nothing would likely be permanent, since the discs degenerate with age or the agent that may be found to do this may simply “inflate” the disc rather than actually grow it. However, there could be varying degrees of maintenance depending on application. It would be Controlled Introvertebral Fibrocartilage Hypertrophy and/or Hyperplasia or something technically close to that – not a permanent implant or anything incredibly invasive.

While this may seem too extreme at first though, the reality is Leg Lengthening is accepted here and it is a violent breaking of the largest bones in the body followed by lengthening with a lot of tearing/stretching of soft tissues, consolidating and soft tissue healing and rehab for months and years; whereas this is simply injections that could be done in a single day and actually improve the quality/safety/mobility/health of your spine and possibly provide about 5 inches in height. This could be similar to women getting botox injections to inflate their lips or actors/models getting botox to compensate for indented scars etc. You could even observe which discs would benefit best from an increase via the Ultrasound and make sure to take care of them first.

Me: On the GrownGrowth’s next post, he goes even further to explain the method/ technique to increase torso height

So, let’s talk about the anatomy and method again in order to address this perspective of yours. 

Method:

Controlled Introvertebral Fibrocartilage Hypertrophy and/or Hyperplasia, which I theorize is to be done by Ultrasound-Guided Injections while inverted.

Methodological application on anatomy:

Introvertebral Fibrocartilage Hypertrophy and/or Hyperplasia means…

Controlled lengthening of the cartilage (type: Fibrocartilage), commonly referred to as Spinal Discs, in between the vertebrae (Introvertebral) by causing the Discs to grow in a controlled manner.

Essentially, we recognize that growth plates that help bones grow are also made of cartilage (type: Hyaline) before they become bone; and that the Spinal Discs could greatly benefit from reasonable addition in size for health and anti-degeneration while also increasing height (old people partly get shorter from Spinal Disc Degeneration, the Discs provide flexibility and shock absorbing …etc).

Real example of the direct dynamic effect of the method on anatomy:

24 Vertebrae are not fused and thus 25 Discs have reasonable potential to be manipulated http://www.giantscientific.com/height_gain_exercise.html , which means that only a very small increase in height needs to be applied to each disc (e.g. 0.5cm or half of the width of your pinky nail Multiplied By 25 = 12.5cm = about 5 inches or 4.92 inches to be exact).

*If you pay attention to the Sitting Height : Leg Height : Total Height Ratios, you’ll realize that 5 inches is going to be towards the rare extreme of maximum lengthening … much like only about 2 people on this forum have lengthened their legs 6 inches while most are thinking about 2-3 inches.

Real example put into perspective of the systemic or indirect effect on the anatomy:

With leg lengthening, there is usually 1 lateral cut in the bone per segment (rarely 2). This means that all of the lengthening is occurring at one “pressure point” or “load point” so to speak. So to compare LL of bones to the lengthening of the spine, like you were trying to do, this would be as if you only enlarged 1 of the 25 discs by 5 inches, whereas I am talking about enlarging each of the 25 discs a very small amount (again, even 5 inches is only 0.5cm lengthening per disc or the width of half of your pinky nail – think of how incredibly small that is for 5 inches of effect). While the overall increase is large, the “load dispersion” spread proportionally by only 0.5cm makes this very practical for 1: how much each disc can grow, 2: how much this effects surrounding anatomy because there is no large gap created in any one area rather the effect itself is so proportional that it is “almost systemic”.

(Common sense, plus see my skin experiment and rope analogy below!)

More importantly, is the very elaborate understanding of how each of those organs are secured to the body and/or secured to each other. 

So, let’s try to put the effect on the organs in perspective with all of this:

First, we’ll eliminate what we should:

These organs are in the fused section of the spine, and thus the only load that is going to be applied here is approximately 0.5cm for the 1 and only disc directly connected at the top and a similarly small load at the point where the intestine connects etc. It will not be the collective load, but the load in the specific area of connection.

So, we know for sure that the rib cage is firmly attached to the spine. We need to be incredibly concerned that when lengthening the spine the heart and lungs are still going to be as protected as they should be. What I do not understand, nor know how to certainly find out without dissecting a cadaver or talking with an experienced surgeon, is exactly how the heart and lungs are secured and thus how they would move in relation to the spine and ribs moving.

What is good to know is, a healthy body is already quite flexible. For example, when somebody performs a reverse arch type of pose:

….the spine is effectively lengthening in some respect by the angle it bends even though there isn’t a height increase – maybe 1-3+ inches total – because of the flexibility of the Introvertebral Discs – and the ribs are moving greatly, yet the lungs and heart are also moving with the ribs and they are still protected even though there is a better angle for a spear to enter the heart.

Now, it is important to remember that even though a total height increase in my example of 5inches, the “load dispersion” means that the ribs themselves are not elevated by 5 inches! The bottom rib will elevate approximately 0.5cm and the ribs gaps will be stretched approximately 0.5cm per rib as they are connected to each vertebrae and they still have connective tissue in the gaps for protection!

Regardless, as long as the heart and lungs are attached well enough – which I think/hope they are – they will simply move with the ribs (not need to grow or stretch at all) and be protected the same.

Again, I do not know how all of these are connected, but they are going to have a very small load of 0.5cm put on them very proportionately.

I’m quite sure this is not going to matter at all for the intestines. I bet it would make you a bit more regular because it would stretch them out a bit (don’t you notice how well your digest and dump after abdomen stretching?)! The small intestine is about 23 feet long  and the large intestine is about 5 feet long (plenty of room the lengthen 0.5cm proportionally along their surface area against the spine)!
Likewise, the rest of the organs could very possibly handle the proportional load covered only for their surface area in relation to the spine. 

So, what essentially remains is the skin and the muscles of the back and abdomen and their connective fascia/tissues. This, combined with gravity, should be the biggest resistance how I currently imagine. However, Hyperplasia and/or Hypertrophy can very logically potentially overcome this!

Now, to try to give an example of how easy the skin will surely adapt, do this:

Pinch the skin on your bicep between your thumb and index finger, grip it and pull it as far out from the arm as possible. You’ll probably get an inch of stretch easily. This is because the “load” is dispersed proportionally throughout the already-flexible skin.

However, let go. Now, think of only the small area of skin that your pinched for a grip and try to spread that small area of skin out the same inch or so that the skin collectively extended from you arm. You can’t because there is too much “load” on too small of an area, thus you have to tear the skin and cause it to grow new skin to stretch the same inch or so as the first experiment! However, you can stretch that small area about 0.5cm before the skin would have to tear, which helps make the point that each Introvertebral Disc could likely be manipulated by about 0.5cm!

In theory, the muscle and all connective tissue itself may adapt the same!

One other example by analogy is, imagine an old rope. Quality rope is usually made by 3 core strands interwoven, and each core strand has many micro strands of thread. An old rope loosens over time, with the core strands unweaving and the micro strands unweaving. The longer the rope is, the more the length difference. A very long and loosened rope, when pulled from each end, may increase in length by 5 inches; however, that is only because each micro strand and core strand is tightening proportionally throughout it’s entire length and no smaller segment of the rope could be lengthened 5 inches without cutting the rope.

I don’t think I am completely wrong. I may be completely correct. At worst I am partly correct. There certainly isn’t enough reason to be deterred based on this premise alone.

No, it is very possible with current technology. If we don’t already have all the pieces of the puzzle, we are very close. You still think stem cell progress is science fiction and you’re way off. HGH, IGF, MGF, BGH and Adult and Embryonic stem cells and more are all very well understood – though maybe not perfectly – and we are growing all sorts of tissues in vitro and directly on some animals and body builders are growing tissues on themselves etc.

I finally can get to editing and adding upon this section for the Gene Database after I found the GIANT collaborative project that was published back in one of the October editions in Nature magazine in 2010. This is the most comprehensive collection of gene that have at “significance” in height.

First, lets get through some terminology…

GIANT (Genetic Investigation of ANthropometric Traits consortium): is an international collaboration that seeks to identify genetic loci that modulate human body size and shape, including height and measures of obesity. The GIANT consortium is a collaboration between investigators from many different groups, institutions, countries, and studies, and the results represent their combined efforts. The primary approach has been meta-analysis of genome-wide association data and other large-scale genetic data sets. Anthropometric traits that have been studied by GIANT include body mass index (BMI), height, and traits related to waist circumference (such as waist-hip ratio adjusted for BMI, or WHRadjBMI). Thus far, the GIANT consortium has identified common genetic variants at hundreds of loci that are associated with anthropometric traits. (from Broad Institute website HERE)

SNP (Single Nucleotide Polymorphism): is a DNA sequence variation occurring when a single nucleotide — A, T, C or G — in the genome (or other shared sequence) differs between members of a biological species or paired chromosomes in an individual. (ie, two sequenced DNA fragments from different individuals, AAGCCTA to AAGCTTA, contain a difference in a single nucleotide. In this case we say that there are two alleles: C and T). Almost all common SNPs have only two alleles (from wikipedia article on SNP here)

GWAs (Genomic-Wide Association studies): In genetic epidemiology, a genome-wide association study (GWA study, or GWAS), also known as whole genome association study (WGA study, or WGAS), is an examination of many common genetic variants in different individuals to see if any variant is associated with a trait. GWAS typically focus on associations between single-nucleotide polymorphisms (SNPs) and traits like major diseases. These studies normally compare the DNA of two groups of participants: people with the disease (cases) and similar people without (controls). Each person gives a sample of DNA, from which millions of genetic variants are read using SNP arrays. If one type of the variant (one allele) is more frequent in people with the disease, the SNP is said to be “associated” with the disease. The associated SNPs are then considered to mark a region of the human genome which influences the risk of disease. (from wikipedia article on GWAs here)

Nucleotide: molecules that, when joined, make up the individual structural units of the nucleic acids RNA and DNA.

Gene variation: variation in alleles of genes, occurs both within and among populations. Genetic variation is important because it provides the “raw material” for natural selection. Genetic variation is brought about by mutation, which is a change in the chemical structure of a gene. (from wiki)

Allele: one of two or more forms of a gene or a genetic locus (generally a group of genes). Sometimes, different alleles can result in different observable phenotypic traits, such as different pigmentation. However, many variations at the genetic level result in little or no observable variation. Most multicellular organisms have two sets of chromosomes, that is, they are diploid. These chromosomes are referred to as homologous chromosomes. Diploid organisms have one copy of each gene (and therefore one allele) on each chromosome. If both alleles are the same, they are homozygotes. If the alleles are different, they are heterozygotes. A population or species of organisms typically includes multiple alleles at each locus among various individuals. Allelic variation at a locus is measurable as the number of alleles (polymorphism) present, or the proportion of heterozygotes in the population.  In many cases, genotypic interactions between the two alleles at a locus can be described as dominant or recessive, according to which of the two homozygous genotypes the phenotype of the heterozygote most resembles. Where the heterozygote is indistinguishable from one of the homozygotes, the allele involved is said to be dominant to the other, which is said to be recessive to the former. The degree and pattern of dominance varies among loci. For a further discussion see Dominance (genetics). This type of interaction was first formally described by Gregor Mendel. However, many traits defy this simple categorization and the phenotypes are modeled by polygenic inheritance. The term “wild type” allele is sometimes used to describe an allele that is thought to contribute to the typical phenotypic character as seen in “wild” populations of organisms…Such a “wild type” allele was historically regarded as dominant, common, and “normal”, in contrast to “mutant” alleles regarded as recessive, rare, and frequently deleterious. It was commonly thought that most individuals were homozygous for the “wild type” allele at most gene loci, and that any alternative ‘mutant’ allele was found in homozygous form in a small minority of “affected” individuals, often as genetic diseases, and more frequently in heterozygous form in “carriers” for the mutant allele. It is now appreciated that most or all gene loci are highly polymorphic, with multiple alleles, whose frequencies vary from population to population, and that a great deal of genetic variation is hidden in the form of alleles that do not produce obvious phenotypic differences. (from wikipedia article on allele HERE)

Loci (singular is Locus): is the specific location of a gene or DNA sequence on a chromosome. A variant of the DNA sequence at a given locus is called an allele. The ordered list of loci known for a particular genome is called a genetic map. Gene mapping is the procession of determining the locus for a particular biological trait. Diploid and polyploid cells whose chromosomes have the same allele of a given gene at some locus are called homozygous with respect to that gene, while those that have different alleles of a given gene at a locus, are called heterozygous with respect to that gene. (from wikipedia article on gene loci HERE)

Gene: is a molecular unit of heredity of a living organism. It is a name given to some stretches of DNA and RNA that code for a polypeptide or for an RNA chain that has a function in the organism. A modern working definition of a gene is “a locatable region of genomic sequence, corresponding to a unit of inheritance, which is associated with regulatory regions, transcribed regions, and or other functional sequence regions “. Colloquial usage of the term gene (e.g. “good genes”, “hair color gene”) may actually refer to an allele: a gene is the basic instruction—a sequence of nucleic acids (DNA or, in the case of certain viruses RNA), while anallele is one variant of that gene. Referring to having a gene for a trait is no longer the scientifically accepted usage. In most cases, all people would have a gene for the trait in question, but certain people will have a specific allele of that gene, which results in the trait variant. Further, genes code for proteins, which might result in identifiable traits, but it is the gene, not the trait, which is inherited. (from the wikipedia article on gene HERE)

Minor Allele Frequency (MAF): refers to the frequency at which the less common allele occurs in a given population. MAF is widely employed in Genome Wide Association studies for complex traits. (from wikipedia article on MAF HERE)

Now let’s get through how gene locus nomenclature is done… 

(the segment/pic clip posted below is taken from the wikipedia article on genetics loci above HERE)

Also Understand the Results And Measurements (specifically the P-value)…

What is P-value? – In statistical hypothesis testing, the p-value is the probability of obtaining a test statistic at least as extreme as the one that was actually observed, assuming that the null hypothesis is true. One often “rejects the null hypothesis” when the p-value is less than the significance level α (Greek alpha), which is often 0.05 or 0.01. When the null hypothesis is rejected, the result is said to be statistically significant. (from wikipedia)

Note: For a far better and more detailed explanation of what exactly is the P-value please refer to the notes from a University of Alberta Stats class located HERE.

What does it mean to be “statistically significant”?

It has become scientific convention to say that p-values exceeding 0.05 (one in twenty) just aren’t strong enough to be the sole evidence that two treatments
being studied really differ in their effect. When the term statistically signicant is used to describe the results from a clinical trial, it means that the p-value is less than this conventional reference point. It is possible to have very strong evidence to show that even a very small effect is nonetheless a real one. Consequently, it is possible to have a small p-value even though the size of the effect is not worth bothering with from the 5clinical standpoint. Thus, statistical signicance and clinical importance must be completely separate assessments.

Even when one treatment is superior to another in clinically important ways, it is possible for the study not to end in statistical signicance. The study may have been too small to detect any but the largest of dierences. And of coursechance can work against a treatment as easily as work in its favor. Consequently, not achieving statistical signicance must not be interpreted as having shown that the treatments studied are equally effective. (from University of Chicago Document HERE)

List Of Genes

[Note: This list of genes that have a “significant” influence on height variation was all taken from the Supplementary Material from the GIANT project.]

Analysis 1 (from GIANT article)

If you can see close enough, you can see that there was 42 single nucleotide polymorphisms associated in the circular diagram above. As stated in the original article found HERE…

“This analysis revealed 17 different biological pathways and 14 molecular functions nominally enriched (P<0.05) for associated genes, many of which lie within the validated height loci. These gene-sets include previously reported (e.g. Hedgehog signaling) and novel (e.g. TGF-beta signaling, histones, and growth and development-related) pathways and molecular functions (Supplementary Table 12). Several SNPs near genes in these pathways narrowly missed genome-wide significance, suggesting that these pathways likely contain additional associated variants.”

also

“Of 32 genes with highly correlated (r²>0.8) nsSNPs, several are newly identified strong candidates for playing a role in human growth. Some are in pathways enriched in our study (such as ECM2, implicated in extracellular matrix), while others have similar functions to known growth-related genes, including FGFR4 (FGFR3 underlies several classic skeletal dysplasias²³) and STAT2 (STAT5B mutations cause growth defects in humans²⁴). Interestingly, Fgfr4-/- Fgfr3-/- mice show severe growth retardation not seen in either single mutant²⁵, suggesting that the FGFR4 variant might modify FGFR3-mediated skeletal dysplasias. Other genes at associated loci, such as NPPC and NPR3 (encoding the C-type natriuretic peptide and its receptor), influence skeletal growth in mice and will likely also influence human growth¹⁷. Many of the remaining 180 loci have no genes with obvious connections to growth biology, but at some our data provide modest supporting evidence for particular genes…”

COMPLETE LISTING – 180 gene loci at present 

[Note: All the tables, graphs, and charts are edited and taken from the Supplementary Document for the GIANT article located HERE.]

Supplementary Table 1. Association results for Stage 1 (discovery GWAS), Stage 2 (in-silico replication), Stage 1+2 combined, and Stage 1+2 sex-specific meta-analyses, for the 180 independent signals that reached genome-wide significance (P<5×10^-8) in the combined Stage 1+2 analysis. I² represents the % heterogeneity of effect size between Stage 1 studies. P_het is the heterogeneity P-value.

• ^a SNPs most likely to be representing a previously published height locus are highlighted in green.
• ^b Gene regions are named after the gene nearest to the index SNP. A near-by (within 500kb from the index SNP) OMIM height gene (defined as a gene that when mutated results in a monogenic skeletal growth defect) is also included if it is not the nearest. All OMIM height genes are highlighted in blue.
• ^c Alleles are indexed to the forward strand of NCBI Build 36.
• ^d All p-values are based on the inverse-variance weighted meta-analysis model (fixed effects).