Me: This is the biggest collaborative project geneticists and scientists have ever done looking at what are the hundreds of genes which do affect height which is a polygenic trait. For me, this article is a VERY BIG DEAL. Right here is the sum of the hard work done by hundreds of researchers who have all been studying to find out the genes that cause the variation in human height.

Note: If you really are serious about finding a solution I would say it is critical to look through the supplementary material which is cited at the bottom of the article. but you can click HERE for a copy of the .DOC file.

From the Nature website source link HERE.

From PubMed website source link HERE. for the actual link that I got the Full Text from click HERE.

Nature. 2010 Oct 14;467(7317):832-8. Epub 2010 Sep 29.

Hundreds of variants clustered in genomic loci and biological pathways affect human height.

Abstract

Most common human traits and diseases have a polygenic pattern of inheritance: DNA sequence variants at many genetic loci influence the phenotype. Genome-wide association (GWA) studies have identified more than 600 variants associated with human traits, but these typically explain small fractions of phenotypic variation, raising questions about the use of further studies. Here, using 183,727 individuals, we show that hundreds of genetic variants, in at least 180 loci, influence adult height, a highly heritable and classic polygenic trait. The large number of loci reveals patterns with important implications for genetic studies of common human diseases and traits. First, the 180 loci are not random, but instead are enriched for genes that are connected in biological pathways (P = 0.016) and that underlie skeletal growth defects (P < 0.001). Second, the likely causal gene is often located near the most strongly associated variant: in 13 of 21 loci containing a known skeletal growth gene, that gene was closest to the associated variant. Third, at least 19 loci have multiple independently associated variants, suggesting that allelic heterogeneity is a frequent feature of polygenic traits, that comprehensive explorations of already-discovered loci should discover additional variants and that an appreciable fraction of associated loci may have been identified. Fourth, associated variants are enriched for likely functional effects on genes, being over-represented among variants that alter amino-acid structure of proteins and expression levels of nearby genes. Our data explain approximately 10% of the phenotypic variation in height, and we estimate that unidentified common variants of similar effect sizes would increase this figure to approximately 16% of phenotypic variation (approximately 20% of heritable variation). Although additional approaches are needed to dissect the genetic architecture of polygenic human traits fully, our findings indicate that GWA studies can identify large numbers of loci that implicate biologically relevant genes and pathways.

In Stage 1 of our study, we performed a meta-analysis of GWA data from 46 studies, comprising 133,653 individuals of recent European ancestry, to identify common genetic variation associated with adult height. To enable meta-analysis of studies across different genotyping platforms, we performed imputation of 2,834,208 single nucleotide polymorphisms (SNPs) present in the HapMap Phase 2 European-American reference panel⁴. After applying quality control filters, each individual study tested the association of adult height with each SNP using an additive model (Supplementary Methods). The individual study statistics were corrected using the genomic control (GC) method^5,6 and then combined in a fixed effects based meta-analysis. We then applied a second GC correction on the meta-analysis statistics, although this approach may be overly conservative when there are many real signals of association (Supplementary Methods). We detected 207 loci (defined as 1Mb on either side of the most strongly associated SNP) as potentially associated with adult height (P<5×10^-6).

To identify loci robustly associated with adult height, we took forward at least one SNP (Supplementary Methods) from each of the 207 loci reaching P<5×10^-6 into an additional 50,074 samples (Stage 2) that became available after completion of our initial meta-analysis. In the joint analysis of our Stage 1 and Stage 2 studies, SNPs representing 180 loci reached genome-wide significance (P<5×10^-8;Supplementary Figures 1 and 2, Supplementary Table 1). Additional tests, including genotyping of a randomly-selected subset of 33 SNPs in an independent sample of individuals from the 5^th-10^th and 90^th-95^th percentiles of the height distribution (N=3,190)⁷, provided further validation of our results, with all but two SNPs showing consistent direction of effect (sign test P<7×10^-8) (Supplementary Methods, Supplementary Table 2).

Genome wide association studies can be susceptible to false positive associations from population stratification⁷. We therefore performed a family-based analysis, which is immune to population stratification in 7,336 individuals from two cohorts with pedigree information. Alleles representing 150 of the 180 genome-wide significant loci were associated in the expected direction (sign test P<6×10^-20;Supplementary Table 3). The estimated effects on height were essentially identical in the overall meta-analysis and the family-based sample. Together with several other lines of evidence (Supplementary Methods), this indicates that stratification is not substantially inflating the test statistics in our meta-analysis.

Common genetic variants have typically explained only a small proportion of the heritable component of phenotypic variation⁸. This is particularly true for height, where >80% of the variation within a given population is estimated to be attributable to additive genetic factors⁹, but over 40 previously published variants explain <5% of the variance^10–17. One possible explanation is that many common variants of small effects contribute to phenotypic variation, and current GWA studies remain underpowered to detect the majority of common variants. Using five studies not included in Stage 1, we found that the 180 associated SNPs explained on average 10.5% (range 7.9-11.2%) of the variance in adult height (Supplementary Methods). Including SNPs associated with height at lower significance levels (0.05>P>5×10^-8) increased the variance explained to 13.3% (range 9.7-16.8%) (Figure 1a)¹⁸. In addition, we found no evidence that non-additive effects including gene-gene interaction would increase the proportion of the phenotypic variance explained (Supplementary Methods, Supplementary Tables 5 and 6).

Figure 1

Phenotypic variance explained by common variants

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

As a separate approach, we used a recently developed method¹⁹ to estimate the total number of independent height-associated variants with effect sizes similar to the ones identified. We obtained this estimate using the distribution of effect sizes observed in Stage 2 and the power to detect an association in Stage 1, given these effect sizes (Supplementary Methods). The cumulative distribution of height loci, including those we identified and others as yet undetected, is shown in Figure 1b. We estimate that there are 697 loci (95% confidence interval (CI): 483-1040) with effects equal or greater than those identified, which together would explain approximately 15.7% of the phenotypic variation in height or 19.6% (95% CI: 16.2-25.6) of height heritability (Supplementary Table 4). We estimated that a sample size of 500,000 would detect 99.6% of these loci at P<5×10^-8. This figure does not account for variants that have effect sizes smaller than those observed in the current study and, therefore, underestimates the contribution of undiscovered common loci to phenotypic variation.

A further possible source of missing heritability is allelic heterogeneity – the presence of multiple, independent variants influencing a trait at the same locus. We performed genome-wide conditional analyses in a subset of Stage 1 studies, including a total of 106,336 individuals. Each study repeated the primary GWA analysis but additionally adjusted for SNPs representing the 180 loci associated atP<5×10^-6 (Supplementary Methods). We then meta-analysed these studies in the same way as for the primary GWA study meta-analysis. Nineteen SNPs within the 180 loci were associated with height atP<3.3×10^-7 (a Bonferroni-corrected significance threshold calculated from the ~15% of the genome covered by the conditioned 2Mb loci; Supplementary Methods, Table 1, Figure 2, Supplementary Figure 3). The distances of the second signals to the lead SNPs suggested that both are likely to be affecting the same gene, rather than being coincidentally in close proximity. At 17 of 17 loci (excluding two contiguous loci in the HMGA1 region), the second signal occurred within 500kb, rather than between 500kb and 1 Mb, of this lead SNP (binomial test P=2×10^-5). Further analyses of allelic heterogeneity may identify additional variants that increase the proportion of variance explained. For example, within the 180 2Mb loci, a total of 45 independent SNPs reached P<1×10^-5 when we would expect <2 by chance.

Table 1

Secondary signals at associated loci after conditional analysis

Figure 2

Example of a locus with a secondary signal before (a) and after (b) conditioning

Whilst GWA studies have identified many variants robustly associated with common human diseases and traits, the biological significance of these variants, and the genes on which they act, is often unclear. We first tested the overlap between the 180 height-associated variants and two types of putatively functional variants, nonsynonymous (ns) SNPs and cis-eQTLs (variants strongly associated with expression of nearby genes). Height variants were 2.4-fold more likely to overlap with cis-eQTLs in lymphocytes than expected by chance (47 variants: P=4.7×10^-11) (Supplementary Table 7) and 1.7-fold more likely to be closely correlated (r²≥0.8 in HapMap CEU) with nsSNPs (24 variants P=0.004) (Supplementary Methods, Supplementary Table 8). Although the presence of a correlated eQTL or nsSNP at an individual locus does not establish the causality of any particular variant, this enrichment shows that common functional variants contribute to the causal variants at height-associated loci. We also noted five loci where the height associated variant was strongly correlated (r²>0.8) with variants associated with other traits and diseases (P<5×10^-8), including bone mineral density, rheumatoid arthritis, type 1 diabetes, psoriasis and obesity, suggesting that these variants have pleiotropic effects on human phenotypes (Supplementary Methods; Supplementary Table 9).

We next addressed the extent to which height variants cluster near biologically relevant genes; specifically, genes mutated in human syndromes characterized by abnormal skeletal growth. We limited this analysis to the 652 genes occurring within the recombination hotspot-bounded regions surrounding each of the 180 index SNPs. We showed that the 180 loci associated with variation in normal height contained 21 of 241 genes (8.7%) found to underlie such syndromes (Supplementary Table 10), compared to a median of 8 (range 1-19) genes identified in 1,000 matched control sets of regions (P<0.001: 0 observations of 21 or more skeletal growth genes among 1,000 sets of matched SNPs). In 13 of these 21 loci the closest gene to the most associated height SNP in the region is the growth disorder gene, and in 9 of these cases, the most strongly associated height SNP is located within the growth disorder gene itself (Supplementary Methods, Supplementary Table 11). These results suggest that GWA studies may provide more clues about the identity of the functional genes at each locus than previously suspected.

We also investigated whether significant and relevant biological connections exist between the genes within the 180 loci, using two different computational approaches. We used the GRAIL text-mining algorithm to search for connectivity between genes near the associated SNPs, based on existing literature²⁰. Of the 180 loci, 42 contained genes that were connected by existing literature to genes in the other associated loci (the pair of connected genes appear in articles that share scientific terms more often than expected at P<0.01). For comparison, when we used GRAIL to score 1,000 sets of 180 SNPs not associated with height (but matched for number of nearby genes, gene proximity, and allele frequency), we only observed 16 sets with 42 or more loci with a connectivity P<0.01, thus providing strong statistical evidence that the height loci are functionally related (P=0.016) (Figure 3a). For the 42 regions with GRAIL connectivity P<0.01, the implicated genes and SNPs are highlighted in Figure 3b. The most strongly connected genes include those in the Hedgehog, TGF-beta, and growth hormone pathways.

Figure 3

Loci associated with height contain genes related to each other

As a second approach to find biological connections, we applied a novel implementation of gene set enrichment analysis (GSEA) (Meta-Analysis Gene-set Enrichment of variaNT Associations, MAGENTA²¹) to perform pathway analysis (Supplementary Methods). 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^11,13 (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. These results provide complementary evidence for some of the genes and pathways highlighted in the GRAIL analysis. For instance, genes such as TGFB2 andLTBP1-3 highlight a role for the TGF-beta signaling pathway in regulating human height, consistent with the implication of this pathway in Marfan syndrome²².

Finally, to examine the evidence for the potential involvement of specific genes at individual loci, we aggregated evidence from our data (eQTLs, proximity to the associated variant, pathway-based analyses), and human and mouse genetic databases (Supplementary Table 13). 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, including C3orf63, PML, CCDC91, ZNFX1, ID4, RYBP, SEPT2,ANKRD13B, FOLH1, LRRC37B, MFAP2, SLBP, SOCS5, and ZBTB24 (Supplementary Table 13).

We have identified >100 novel loci that influence the classic polygenic trait of normal variation in human height, bringing the total to 180. Our results have potential general implications for genetic studies of complex traits. We show that loci identified by GWA studies highlight relevant genes: the 180 loci associated with height are non-randomly clustered within biologically relevant pathways and are enriched for genes that are involved in growth-related processes, that underlie syndromes of abnormal skeletal growth, and that are directly relevant to growth-modulating therapies (GH1, IGF1R, CYP19A1,ESR1). The large number of loci with clearly relevant genes suggests that the remaining loci could provide potential clues to important and novel biology.

We provide the strongest evidence yet that the causal gene will often be located near the most strongly associated DNA sequence variant. At the 21 loci containing a known growth disorder gene, that gene was on average 81 kb from the associated variant, and in over half of the loci it was the closest gene to the associated variant. Despite recent doubts about the benefits of GWA studies²⁶, this finding suggests that GWA studies are useful mapping tools to highlight genes that merit further study. The presence of multiple variants within associated loci could help localize the relevant genes within these loci.

By increasing our sample size to >100,000 individuals, we identified common variants that account for approximately 10% of phenotypic variation. Although larger than predicted by some models²⁶, this figure suggests that GWA studies, as currently implemented, will not explain a majority of the estimated 80% contribution of genetic factors to variation in height. This conclusion supports the idea that biological insights, rather than predictive power, will be the main outcome of this initial wave of GWA studies, and that new approaches, which could include sequencing studies or GWA studies targeting variants of lower frequency, will be needed to account for more of the “missing” heritability. Our finding that many loci exhibit allelic heterogeneity suggests that many as yet unidentified causal variants, including common variants, will map to the loci already identified in GWA studies, and that the fraction of causal loci that have been identified could be substantially greater than the fraction of causal variantsthat have been identified.

In our study, many associated variants are tightly correlated with common nsSNPs, which would not be expected if these associated common variants were proxies for collections of rare causal variants, as has been proposed²⁷. Although a substantial contribution to heritability by less common and/or quite rare variants may be more plausible, our data are not inconsistent with the recent suggestion²⁸ that a large number of common variants of very small effect mostly explain the regulation of height.

In summary, our findings indicate that additional approaches, including those aimed at less common variants, will likely be needed to dissect more completely the genetic component to complex human traits. Our results also strongly demonstrate that GWA studies can identify large numbers of loci that together implicate biologically relevant pathways and mechanisms. We envision that thorough exploration of the genes at associated loci through additional genetic, functional, and computational studies will lead to novel insights into human height and other polygenic traits and diseases.

Methods summary

The primary meta-analysis (Stage 1) included 46 GWA studies of 133,653 individuals. The in-silico follow up (Stage 2) included 15 studies of 50,074 individuals. All individuals were of European ancestry and >99.8% were adults. Details of genotyping, quality control, and imputation methods of each study are given in Supplementary Methods Table 1-2. Each study provided summary results of a linear regression of age-adjusted, within-sex Z scores of height against the imputed SNPs, and an inverse-variance meta-analysis was performed in METAL (http://www.sph.umich.edu/csg/abecasis/METAL/). Validation of selected SNPs was performed through direct genotyping in an extreme height panel (N=3,190) using Sequenom iPLeX, and in 492 Stage 1 samples using the KASPar SNP System. Family-based testing was performed using QFAM, a linear regression-based approach that uses permutation to account for dependency between related individuals²⁹, and FBAT, which uses a linear combination of offspring genotypes and traits to determine the test statistic³⁰. We used a previously described method to estimate the amount of genetic variance explained by the nominally associated loci (using significance threshold increments from P<5×10^-8 to P<0.05)¹⁸. To predict the number of height susceptibility loci, we took the height loci that reached a significance level of P<5×10^-8 in Stage 1 and estimated the number of height loci that are likely to exist based on the distribution of their effect sizes observed in Stage 2 and the power to detect their association in Stage 1. Gene-by-gene interaction, dominant, recessive and conditional analyses are described in Supplementary Methods. Empirical assessment of enrichment for coding SNPs used permutations of random sets of SNPs matched to the 180 height-associated SNPs on the number of nearby genes, gene proximity, and minor allele frequency. GRAIL and GSEA methods have been described previously^20,21. To assess possible enrichment for genes known to be mutated in severe growth defects, we identified such genes in the OMIM database (Supplementary Table 10), and evaluated the extent of their overlap with the 180 height-associated regions through comparisons with 1000 random sets of regions with similar gene content (±10%).

Go to:

Scientists stack up new genes for height    (source link HERE, September 2010)

NOTE: We have to find that article!! (comes online on Sept. 29, 2010 in the journal Nature)

Update: I have decided to use the internet to look up the term” Genetic Investigation of ANthropometric Traits”

Filed under: Announcement, Research

Wednesday, September 29, 2010 — Competitors become collaborators to achieve a common goal: the discovery of genes that influence height.

CHAPEL HILL, NC — An international team of researchers, including a number from the University of North Carolina at Chapel Hill schools of medicine and public health, have discovered hundreds of genes that influence human height.

Their findings confirm that the combination of a large number of genes in any given individual, rather than a simple “tall” gene or “short” gene, helps to determine a person’s stature. It also points the way to future studies exploring how these genes combine into biological pathways to impact human growth.

“While we haven’t explained all of the heritability of height with this study, we have confidence that these genes play a role in height and now can begin to learn about the pathways in which these genes play a role,” said study co-author Karen L. Mohlke, PhD, associate professor of genetics in the UNC School of Medicine.

The study, which appears online Sept. 29, 2010, in the journal Nature, is the result of the largest consortium of researchers to ever study the trait. The consortium, aptly named GIANT for Genetic Investigation of ANthropometric Traits.

Traits, brought together hundreds of investigators from dozens of countries, to identify which genes affect height in almost two hundred thousand different individuals.

“These investigators had once been competing with each other to find height genes, but then realized that the next step was to combine their samples and see what else could be found,” said Mohlke. “The competitors became collaborators to achieve a common scientific goal.”

That pooling of resources was necessary because the scientists knew that height was a complex genetic trait, with possibly a number of genes of small effect each adding up to influence whether a person would be taller or shorter. In this large study, forty-six smaller genome-wide association studies of height were combined and then analyzed statistically, yielding 180 different regions or genetic loci that influence the trait. “These common gene variants could explain as much as sixteen percent of the variation in height,” said study co-author Kari North, PhD, associate professor of epidemiology in the UNC Gillings School of Global Public Health.

The researchers looked to see whether the 180 regions contained more genes that underlie skeletal growth defects than would be expected if those regions were just chosen randomly across the genome. They found that the genes were not random and could in fact point to functional pathways important in influencing height.

Members of the consortium are working to uncover the “missing heritability” – the proportion of inherited variation in height that is still unexplained. Because this study looked for common genetic variants, the researchers are now going after rare genetic variants that may also play a role.

“This work is giving the field important insights into skeletal growth, height and growth defects,” said Mohlke. “And it is also showing us how similar approaches can be taken to look for genes underlying other common traits and diseases relevant to body size, like type 2 diabetes.”

Also from UNC is co-author Keri L. Monda, PhD, research assistant professor in epidemiology in the Gillings School of Global Public Health. The research was funded by the National Institutes of Health.

Media contact: Les Lang, (919) 966-9366 or llang@med.unc.edu

Me: I was very surprised to find this article on inforbarrel.com located HERE written by an individual who went by the name of Tarin. It seems that this Tarin person is very knowledgeable on the subject of height, and the scientific research involved with possible height increase. It is not written by me and I am not sure if it is Tyler’s writing but it is spot on many of the ideas that I have looked into. If it is Tyler’s work and he wants me to take it down, I will. I know that infobarrel used to be a very big website which used to pay writers a reasonably high rate to write very content strong and detailed websites. Pat Flynn of Smart Passive Income was the person who introduced me to Infobarrel. He used to write articles for the website and has been paid a high 3 figure sum every month for stuff he wrote years ago. Pat, me , and Tyler (also Sky) have all at one point being in the internet marketing niche so I would guess a lot of guys who read the article post would realize it is actually an internet marketing strategy.

I think for the very beginner who is just starting to learn about the science of possible height increase beyond the stuff one can find in an E-product, this article is a great starting post to read and to get caught up on the ideas floating around. 

Scientific Methods of Height Increase

By Tarin Oct 6, 2010  0  0

Read more at http://www.infobarrel.com/Scientific_Methods_of_Height_Increase#GsTV0oGEsPTXE9Tu.99

Personal Message: I wanted to write this post as a final message to my own doubts of the effectiveness and feasibility of the LSJL method. After this, I will move away from talking about the method too much because I don’t feel I am qualified or knowledgeable enough on the subject to really study it in depth.

From this previous post HERE, Tyler and I had an exchange of emails back and forth with me trying to fully understand why the Lateral Synovial Joint Loading technique would or could ever even work. The main concerns I had were never put to rest and I wanted to make a clear statement for the readers now that there is quite a bit of data showing that by theory alone, the method should not work, at least at the level of understanding on how bone mechanics work at this point.

The reason is because of a type of effect from growth fractures known as bone bridges. I wanted to show the studies that have been done which showed growth plate fractures which caused what are known as ” bony bridge” which is a sort of like a real bridge that connects the bone epiphyseal end with the bone metaphyseal ends of the long bone together and they lead to almost completely stunted linear growth from just that small piece of bone connection. Before that they were technically separated by cartilage. It is also important to remember that even though the two bones are connected with bone, there is still an entire rest of growth plate surrounding the bone bridge, which doesn’t work well anymore,

The bony bridge effectively completely stopped the long bone from ever being able to lengthen, at least in that specific area where the epiphysis and metaphysis is attached.

What I am trying to say is that the LSJL method is effectively trying to push against bone that has completly surrounded it, in all 3 dimensions. Just from a broad general analysis point of view, I was arguing in the previous post with Tyler that the reasons growth plates work is that they completely seperate two pieces of bone. From a mathematically topological viewpoint I could say that the bones are solid in the radial direction but in the axial direction, they are completely separated by the growth plate. surrounding the 3 parts radially is the muscles and ligaments that go around it, but they are elastic and can stretch.

If we now look at how the method of LSJL is supposed  work (from my understanding after having the discussion with Tyler in the pervious post), chondrocytes proliferated and expanded in the epiphysis internal region of the long bone should be able to push the thick bone sorrounding it in the epiphysis in all directions 3 dimensionally out thus expanding out the  entire bone, but the LSJL method is hoping the epiphyseal bone will be the main parts that are suppose to be expanded. This means that the overall bone structure surroundin the chondrocyte and cartilage that is supposed to have developed has fundamentally changed, from not just 2 dimensionally anymore but 3 dimensionally Where there was once muscle which was elastic allowing for longitudinal stretching thus growth there is not bone, which is not as aleastic as muscle. That was my original concern.

For studies showing evidence that even a slight bone bridge between the two bone ends separated by the cartilage starts to get connected by the bone, growth is almost completely stunted. Topologically (and using some physics lingo) speaking the one direction the chondrocytes can expand in has been fixed with a constraint. If the originally perfectly aligned system of chondrocytes can’t even push past and beyond a bony bridge that has formed on just one side of the natural gorwth plates, what hope and effect does producing chondorcytes inside the epiphysis using LSJL can possibly have then where the bones are completely surrounding it?

As for the claim that Tyler has grown 1.5 inches from the Lateral Synovial Joint Loading, LSJL technique I really can’t explain that away. I could make the argument that there are plenty of stories of people who have gone through a slight or mini growth spurt really late in their 20s or even in their 30s. There are obviously some documented cases in the medical literature. One guy on a bodybuilding/ steroids internet forum/board talked about his mother who grew a little (1-2 inches) when she was in her mid to late 20s (can’t find the link at this time). If someone asked me to explain his (tyler’s) claim, another logical explanation to explain away the claim is to say that he is a liar and lying to you, but I would assume that Tyler is a honest person who would not lie about this type of thing, especially since he has been so dedicated for so long in finding a solution using real science and theory. I will just say that he is not lying to you. He is telling the truth about his height increase claim.

This reminds me of my claim behind the story of the Grow Taller Guru Lance Ward. He claims to be able to help you grow up to 6 inches within 90 days. I don’t know about that but in my review on him, I just guessed that when he was in his 20s, say 20 or 21, he felt dissatisfied with his height, he decided to do some streching and excercised and happend to go through an amazing growth spurt of 6 inches in a very short amount of time. If that really happened to him, then I would just curtly proclaim that he was just really lucky. He happened to be one of those people who wants to be taller, tried something out, was not supposed to grow anymore, but did grow and not just a little bit, but a lot in a really short time frame. If that is NOT the case, then I would say Lance lied about his story and did not increase in the 6 inches he claimed since he is really marketing his services in traditional internet marketing fashion which makes me distrust him.

I woudl guess that there are probably millions of below average height adolescent and teeenagers who secretly desire to be taller and try all sorts of exercises and stretching to increase in height. For some of them who are lucky and still have some growth left, they might be able to incerase by quite a bit of height. Michael Jordan desperately wanted to be taller (actually 7 foot) when he was a sophomore in high school being only 5′ 11″. He would hang on a bar in the house backyard and he grew 5 inches in 1 year but mostly in the summer. Dennis Rodman was said to have grown 10 inches in around 1 years time from the age of 20-22. Without that height he deinitely wouldn’t have been ever a NBA player .The 2012 NBA #1 draft pick Anthony Davis was a nobody in early high school being a 6’2 or 6′ 3″ point guard but his enormous and extremely lucky growth spurt of 7-8 inches shot him up to the best of the basketball world. Without the growth spurt, David might not have even been able to play college basketball. What I am trying to say is that maybe, just maybe that the growth that Tyler that has gotten is from just luck. There is always the arguement that life happens in strange ways. Sometimes strange things happen which look like miracles.

Now to play the devil’s advocate position against my previous argument…

Obviously the strange thing about his growth at such a later life is that unlike other people who might be in their late 20 s who have wanted to grown taller and did grow taller, he just happened to be one of the only people in the world who writes a Height Increase and Grow Taller blog/website and uses real science to find a solution. Not only that, he found a science and experiment backed possible height increase method and has been using it for years. If I was a betting man, I would say that the coincedence is too high. He has gotten something right, always assuming he has not been lying about his increase the entire time.

What are the chances that a guy who wants to be taller, does exercises to be taller and really tries, was in his middle to late 20s when he started doing the exercies, who also writes one of the only blogs or websites on the entire internet looking for a height increase solution, is knowledgeable on the real science of human growth, who also has found, claimed, and documented that he has growth in height which is beyond the range of measurement error, and if he is also being completely honest nad not lying about his claim, did actually grow???

How is it possible to just say that all of this was just by pure chance, only randomness. Randomness is the 25 year old women who is happy with her height, never searchs for any height increase information, barely exercises much, and find that she has grown 1-2 inches in her mid to late 20s. That is randomness.

What is supposed to happen with him is too improbable to be just chance or random luck (again, obviously assuming that he is not lying about his increase). He definitely has something which I can’t explain away. I want to prove that the technique/ method doesn’t work but I can’t and I don’t want to disprove it if I can help it. The method gives real hope to people out there who are already physically mature but want to increase their height without the incredible complications that is involved with limb lengthening surgery.

From source link HERE…

Premature Partial Closure and Other Deformities of the Growth Plate: MR Imaging and Three-dimensional Modeling

Growth arrest followed physeal injury at the knee and ankle in 1.4% of the large series of patients studied by Mizuto et al (1). The occurrence of arrest following Salter-Harris fractures at the knee and ankle is related to many factors, including the type of physeal fracture, the age of the patient, the physis involved, and the amount of energy applied to the bone (2,3). The knee is the most common site of growth arrest (4,5), with the ankle second (4). The development of bone bridges at these sites results in interference with longitudinal growth (4,5).

Physeal fracture is the most common cause of bone bridging across the growth plate, but growth arrest may also be due to other insults, as reported by Ogden (5,6). Such insults include infection, therapeutic irradiation, metabolic or hematologic abnormality, tumor, burn, frostbite, electrical injury, sensory neuropathy, microvascular ischemia, or insertion of metal. Pease (7) reports premature fusion of the growth plate in patients with hypervitaminosis A. Caffey (8) describes cupping of metaphyses following trauma, osteomyelitis, poliomyelitis, vitamin A toxicity, sickle cell anemia, achondroplasia, or osteopetrosis.

If the growth plate is affected eccentrically, tethering will cause angular deformity. If the growth plate is affected centrally, growth at the periphery causes cupping of the metaphysis with shortening of the bone (5). The younger the child, the more severe the complications.

Plain radiography remains the initial imaging approach. Interpretation problems arise if part of the physis is not parallel to the x-ray beam. The presence of growth arrest lines is helpful; if a growth arrest line extends across the entire metaphysis and is parallel to the physis, physeal bridge formation is unlikely (9). As needed, results can be compared with the normal appearance of the growth plate (10,11).

If surgical excision of a physeal bridge is considered, accurate knowledge of its size and position is necessary. Conventional tomography with grid mapping (12), bone scintigraphy (13), and computed tomography with reformatting (14–16) have been used for this purpose. MR has been used to image the growth plate (3,17) and has now become the imaging method of choice (18).

We present our findings in children at high risk for bone bridging in whom we obtained one or more MR studies and 3D models of the growth plate to determine the need for intervention.

From the Ortho Facts Website HERE…

Long-Term Outcome

Growth plate fractures must be watched carefully to ensure proper long-term results.

In some cases, a bony bridge will form across the fracture line that prevents the bone from getting longer or causes the bone to curve. Orthopaedic surgeons have developed techniques to remove the bony bar and insert fat, cartilage, or other materials to prevent it from reforming.

In other cases, the fracture actually stimulates growth so that the injured bone is longer than the uninjured bone. Surgical techniques can help achieve a more even length.

Regular follow-up visits to the doctor should continue for at least a year after the fracture. Complicated fractures (types III, IV, and V) as well as fractures to the thighbone (femur) and shinbone (tibia) may need to be followed until the child reaches skeletal maturity.

From the website for Wheeless Textbook For Orthopaedics on the subject of Physeal Bone-Bridge…

Physeal Bone-Bridge

I found this story about Christy Ruhe who had achondrosplasia which made her just 4′ 3″. It is from the website limb lengtheningdoc.com which is one of the websites that is for Dr. Dror Paley. I looked a little further and found the LA Times sotry from 2004 from this link HERE.
THE NATION

It’s now late September of 2001. Christy is focused on the changes unfolding in her own life, and the anticipation of her first limb-lengthening surgery is thrilling.

Her hospital gown drags on the floor as she slides off the bed onto a stepstool. She smiles widely at her nervous parents.

In the operating room, Paley’s plan is to break the thigh and shin bones of her left leg and stretch the bones for three or four months as they’re healing. A year later, he’ll lengthen the right leg.

Limb lengthening works by taking advantage of the body’s natural tendency to heal itself. The shin bones and femurs are broken and automatically begin to generate new bone. As they heal, they’re pulled apart to elongate them. The surgeries, which typically cost about $200,000 for both legs, are covered by insurance.

Paley cuts holes in Christy’s leg so that he can screw rods into the bone: seven in her thigh and five in her shin. Each is a foot long. Half the length protrudes from her skin, so Paley can attach them to a graphite brace that Christy will crank.

Paley bores the pins deep into the thick whiteness he sees on the X-rays.

Finding a good place to crack the bone, he first drills a tight chain of small holes. He puts a chisel to the perforation and pounds it hard with a mallet. The whirring and hammering make it sound like a construction site.

The pain is like an ocean that sucks her under again and again.

Christy lies on her stomach, and a physical therapist bends her knee as far as it will go. Muscles and nerves are stretching to meet the length of the new, soft bone.

The therapist pushes until she feels the soft tissue become elastic. It’s been only a few days since the first surgery.

Christy’s face reddens, and she rides the wave of pain with short breaths. She tries not to scream but can’t stop herself.

She wonders if the therapist knows what she’s doing. “This cannot be right!” she thinks.

(Page 2 of 2)

There’s little blood and not a lot of cutting in limb-lengthening surgery. But recovery is an extended test of mettle and will.

Christy will go through the agony twice. She knows that if she survives even the worst day, there will be another just like it a year from now.

Each day brings a monotony she comes to dread: therapy, broken up by hours of MTV and talk shows. She gets around in a wheelchair. Four times a day, she uses an Allen wrench to turn the brace and stretch her leg.

The growth of bone and muscle tissue is measured in millimeters — 1 mm a day — but Christy doesn’t feel it.

She smiles less these days, snaps at her parents and then regrets it.

She can’t sleep. The steel rods sticking out of her legs keep her from rolling over. She worries about jarring them, which sends slivers of pain up through the sore muscles.

Quitting is not an option.

“You have those moments when you say, ‘I can’t do it anymore. I can’t stand it,’ ” she said. “You have to look back at why you’re doing this. It’s for my health, my well-being.”

Before the surgeries, she talked herself into being resigned to a hard life. Now, the change in her body seems like an extraordinary gift. She reminds herself that the pain is temporary.

Gradually, she realizes how different her life will be. She even dreams differently now, seeing the world from her new height, as a person who blends into a crowd.

Most of Paley’s patients are children, and they crowd into the waiting room at the International Center for Limb Lengthening.

They come from nearly every continent. Little girls, with one shorter leg wrapped in a pink or purple cast, bring their Barbie dolls. Adult patients sit with their afflicted legs propped on a seat, rods penetrating the skin, machinery that looks misplaced inside healthy, smooth flesh.

It is spring of 2003, a year and a half after Christy’s first surgery, Her left leg, the one already lengthened, is straight and muscular. The leg is a promise to her that the surgeries will be successful.

But a chronic infection has developed in the skin around one rod in the right leg, which was operated on six months ago. Christy knows the rod must be removed.

The procedure will be done without general anesthesia, which always makes Christy’s stomach roil. The doctor expects this to be a quick procedure anyway, hardly worth administering even local anesthesia.

Paley attaches a T-shaped handle to the troubled rod. With the first turn, Christy begins to shriek. As the rod twists through bone, muscle and infected skin, she lets out short, piercing screams.

With one arm, John Ruhe tries to immobilize his daughter’s good leg and wraps his other arm around her shoulders. Her fist slams his chest as the pin turns.

Three minutes later, the end of the 12-inch pin appears. The hole in her thigh looks like a gunshot wound. Hot, red blood starts to roll out.

Christy’s back slumps. Her eyes are closed.

It’s two months later, and Christy is undergoing what she thinks will be her final surgery. The hardware that has become her second skin is to be removed.

But on an X-ray, Paley examines a hazy, white patch on the right thigh bone. Eight months of therapy should have left it solid — healed — but it isn’t.

Christy is unconscious a few feet away in the operating room when Paley makes the decision. If he takes the pins out now, the leg will break when she walks on it. They will have to wait at least two more months.

A banner at the party reads, “Congratulations Christy.”

It is a 25th birthday celebration, but the occasion also marks the end of her surgeries and crutches.

Friends and family who have supported her through an ordeal they can barely fathom write messages on a plastic sign.

“Good luck, and have a wonderful rest of your life,” says one.

“In my eyes, you’ve always been tall,” says the only note that hints at her physical transformation.

“You are my hero,” her sister writes.

All eyes are on Christy as she arrives. She steps carefully on her new legs. The right leg is still weak, but growing stronger.

Later, she says she doesn’t remember all of the pain she endured. Time has dulled the memory, and she prefers to look forward — to a life that she hopes will be easier, now that she’s in an adult-sized body.

She takes a second to place the faces before flashing her hundred-watt smile, a picture of self-assurance. “To me, I am tall,” she said. “I am a tall person now. That’s all that matters.”

This is a 7 minutes video that is a documentary on limb lengthening with one of the leading experts on the surgical method Dr. S. Robert Rozbruch and his associate. He is the Director of the Institute For Limb Lengthening and Reconstruction

The youtube source link this video was found from is HERE