This post is my rant against the unfairness of the Google Ranking system which puts SEO leveraged articles ahead of the real content websites on the internet.

My Google Keywords tool is telling me that apparently that there is over 5,000,000 monthly searches for the phrase “How Do I Get Taller” and the #1 link for the 1st page is from a very plain, non-scientific, weak content article on the Article Database website WikiHow entitled “How Do Grow Taller: 8 Steps“. This article has so far 157 authors with up to 812 Revisions (and counting). There is over 2300 Facebook Likes, 3 Pins on it to Pinterest, and 148 Connections by Google+ Members. This article is also filled with Google Adsense ads in a rather sneaky way.

Of the entire article, there is only 8 sections with some really, really general recommendations with very little actionable steps. Sure, there is some nice pictures and the points are bulleted and numbered with easy to read colored material which makes things easy to read. Why is it that people are always more interested in what looks better and has weak content over the stuff which has strong content and not as good of an outer appearance?

So there is a video from the Video Database site HowCast on the article and it gives the same level of weak content.

On the entire article webpage there is 7 very well placed Google Adsense Ads with the most irrelevant ads on the right side offering me the opportunity to “Meet and Date Russian Girls”. Whoever wrote that short article probably has 20 clicks and day and makes $15/ day from just this one well ranked and ads stuffed article. This website has no ads placed and I am not making any income using the methods. I think it is unfair that things are so screwed up. While Blogs and Sites like HeightQuest.com which offers incredibly original research and analysis on this niche of height increase gets so little traffic, articles like this is getting maybe 10X the amount of traffic.

Why is this website not ranked at least on the first page of Google for this heavily typed in phrase? We need a change.

While I was going through Digg today I came across another story written about the jellyfish which many biologists claim is “biologically immortal”. This is the Turritopsis Dohrnii. The story was written for the online website for The New York Times written by Nathaniel Rich entitled “Can a Jellyfish Unlock the Secret of Immortality?“. Now, I have already looked at this jelly fish before in a previous post entitled “An Immortal Animal Turritopsis Nutricula And How To Apply It For Height Increase“. With this post I was really guessing at what it could do. With this new article I’ve read, I think my understanding on how to use the unique ability of the Jellyfish for our endeavor to increase height has gotten a little better.

As of right now, I am not sure if these two jelly fish types with different names, one being Nutricula and the other being Dohrnii are two different species or maybe two different sub-species. But that is not the point.

Analysis: What this article shows is that overall, the number of genes in a organisms genome is almost the exactly the same for most of the species in an entire kingdom, ie Animal. Genetically, we are very similar to even small animals and the jellyfish. The key difference we see seems to be from two previous articles I have written before we saw that the human species has around only 25,000 genes that were found in the Human Genome Project. Given the amazing variety of size, shapes, and forms our animal cousins can turn and morph into, there must be far more to determining our phenotypes besides just the genes. This is why I found the articles on “Hidden DNA” a key point to make. It is similar to the concepts in astronomy known as “dark matter” and “dark energy”. We know so little of dark energy or dark matter but reent findings show that they seem to make up most of the what is really going on in the Universe. Similarly, what was common scientific dogma even 20 years ago is being changed with the discovery that there is more to determining what makes us Human is more than just the genes in our genomes. There is also the microRNA, which are tiny strands of genetic material that regulate gene expression. Remember from our previous research on trying to get the progenitor cells to differentiate correctly into the right types of cell type to allow for our own body to form new chondrocytes, cartilage, and growth plates. We saw also that there is a clear correlation between cancer and human growth or increased height. People who are taller generally have a higher chance of developing cancer, whether it is just from the statistical fact that there is more cell numbers in their body, or whether it is because from the individual’s intrinsice rate of cell replication and proliferation. One thing which I have already been concerned about is whether if we do take the gene therapy approach to reactivating the body’s natural ability to cause chondrocyte or osteocyte proliferation, that might also cause the cell proliferation to grow out of control causing tumors which become malignant. There is a clear reason why nature chose to put a limit to the size that humans can possibly reach, and it may not be just from the effects of the laws of physics, ie. gravitational force. We note from certain families and orders within the animal kingdom like fish and reptiles that they technically never stop growing, but go through a process called “indeterminant growth”  which I wrote in a previous post entitled “Indeterminate Growth And Mammals“. The growth in length and width never completely stop but does slow down over time. It would appear also that the  rate of growth is determined by the size of the creature too which means that as the creature got bigger, it took a lot more energy to maintain the same rate and level of growth. So the rate of growth HAVE TO decrease to fit within the law of mathematics which I wrote before can be modeled by the simplest form of Differential Equation delT/delt = A*T. Going back to the Jellyfish, the process it uses is the generally termed transdifferentiation where one type of cell that has already reached the usually accepted biological dogma of differentiation process turns into another end within a differentiation process. This means that an adipocyte can’t turn into a chondrocyte. We know that technically the human body does have to rejuvenate and replace all of it’s cells after some time cycle. Most laymen say the time is 7 years. I am not sure about that but we can assume that it is a set amount of time. It shows that the genes may actually be controlled by the microRNA (miRNA). If the real ability for the Turritopsis’s ability to transdifferentiate from one specialized cell type to another is because of these miRNA which I have thought is the real control behind the gene expression. Then it gives me hope to know that there might be another layer of scientific study which we have not even reached yet. Going off of the axiom that miRNA is what turns on and off the activation of certain types of genes in the nucleus (or mitochondria) of a organism, what we should be doing is not manipulating the genes, but manipulating the hidden genetic material, specifically these microRNA. I have stated before that for adults, gene therapy will not allow for complete body transformation and allow for growth plates to regrow back for natural height growth .Sam Snyder whom I emailed also agreed upon this fact. However, from the combined knowledge that there is an even finer more subtle level of genetic dynamics going on may signal the possibility within the next few decades that we may indeed be able to find the right combination of miRNA to stimulate and modulate to revert cells in certain parts of the body to turn into different types and cause complete body change like the spontaneous formation of natural growth plates again causing natural height growth. We might even be able to figure out the way to reverse the process of senescence as well, just like what the Japanese researcher believed was possible.

From the article…

“…how the species — at any stage of its development — could transform itself back to a polyp, the organism’s earliest stage of life…”

“…the rejuvenation of Turritopsis dohrnii and some other members of the genus is caused by environmental stress or physical assault. We know that, during rejuvenation, it undergoes cellular transdifferentiation, an unusual process by which one type of cell is converted into another — a skin cell into a nerve cell, for instance. (The same process occurs in human stem cells.)…”

“…But we still don’t understand how it ages in reverse…..the Small’s Rule: small-bodied organisms are poorly studied relative to larger-bodied organisms…”

“….Like most hydrozoans, Turritopsis passes through two main stages of life, polyp and medusa. A polyp resembles a sprig of dill, with spindly stalks that branch and fork and terminate in buds. When these buds swell, they sprout not flowers but medusas. A medusa has a bell-shaped dome and dangling tentacles…..An adult medusa produces eggs or sperm, which combine to create larvae that form new polyps. In other hydroid species, the medusa dies after it spawns. A Turritopsismedusa, however, sinks to the bottom of the ocean floor, where its body folds in on itself — assuming the jellyfish equivalent of the fetal position. The bell reabsorbs the tentacles, and then it degenerates further until it becomes a gelatinous blob. Over the course of several days, this blob forms an outer shell. Next it shoots out stolons, which resemble roots. The stolons lengthen and become a polyp. The new polyp produces new medusas, and the process begins again…”

“…But the Human Genome Project, completed in 2003, suggested otherwise. Though it had been estimated that our genome contained more than 100,000 protein-coding genes, it turned out that the number was closer to 21,000…..From a genetic perspective, apart from the fact that we have two genome duplications, “we look like a damn jellyfish.”

“….Peterson is now studying microRNAs (commonly denoted as miRNA), tiny strands of genetic material that regulate gene expression. MiRNA act as an on-off switch for genes. When the switch is off, the cell remains in its primitive, undifferentiated state. When the switch turns on, a cell assumes its mature form: it can become a skin cell, for instance, or a tentacle cell. MiRNA also serve a crucial role in stem-cell research — they are the mechanism by which stem cells differentiate. Most cancers, we have recently learned, are marked by alterations in miRNA. Researchers even suspect that alterations in miRNA may be a cause of cancer. If you turn a cell’s miRNA “off,” the cell loses its identity and begins acting chaotically — it becomes, in other words, cancerous….”

“…Hydrozoans provide an ideal opportunity to study the behavior of miRNA for two reasons. They are extremely simple organisms, and miRNA are crucial to their biological development….”

So after a long time figuring out the technical details, the Apple iTunes store has officially accepted and added the Natural Height Growth Podcast to their database. Everything is now linked and the process is now easier and more automated. The 3rd and subsequent episodes will be much easier and faster to edit and upload.

You should see as of today’s date Nov. 28, 2012 only 2 episodes so far where I introduce myself and my research in the 1st episode and then bring as a guest Tyler from HeighQuest on to discuss his research in the 2nd one.

If you go there right now, you might notice there is actually 3 podcast episodes. However one of them was an error I didn’t realize I made many months ago while I was creating another post for the website. There was an old podcast I didn’t realize I had uploaded (on the subject of Michael Jordan and hanging on a bar to increase height) but that issue will be taken care of within a few days when the iTunes store updates and makes the correction.

The symbol on the right will be from this point on will be the official Natural Height Growth website & podcast symbol. I had a graphic designer make it for only $5 using the Fiverr.com service. It is supposed to represent the fact that using scientific principles from a variety of areas of study like DNA, engineering, and biological principles, we can innovate and come up with new ideas to think about how to solve this scientific problem of height increase, hence the overall light bulb symbol.

Please leave a comment and review on how the podcast can be improved and added upon. What would you as the listener and reader like to hear me and the guest talk about in the future?

We saw in a previous post Increase Height and Grow Taller Using Chondromodulin that a new type of glycoprotein recently learned about that has the ability to inhibit the formation of blood vessels aka vascularization in the chondrocyte area which might mean that it can at least slow down the ossification process of the chondrocytes leading to possible height increase. Let’s go slightly further into the analysis and see what can be found.

From study 1….

Chondromodulin-I which is a glycoprotein was identified as an angiogenesis inhibitor (ie. prevents the formation of blood vessels). ChM-I stimulated growth and colony formation of cultured chondrocytes. It is specifically expressed in the avascular zone of cartilage in developing bone, but not present in the late hypertrophic and calcified zones that allow vascular invasion. The researchers conclude with “It is what causes the angiogenic switching of cartilage, and that the withdrawal of its expression allows capillary in-growth, which triggers the replacement of cartilage by bone during endochondral bone development”

From study 2…

The researchers managed to isolate Chondromodulin II from bovine epiphyseal cartilage. Chondromodulin II stimulated the proteoglycan synthesis in rabbit cultured growth plate chondrocytes, an expression of the differentiated phenotype of chondrocytes. They also found another growth promoting factor with a higher herapin affinity, Chondromodulin III. It also stimulated DNA synthesis in chondrocytes in both the absence and the presence of fibroblast growth factor-2.

Implications

This new learned protein chondromodulin has been shown to stimulate proteoglycan synthesis and prevent vascularization so it is definitely another very important growth factor we will have to consider in our searching. It definitely does something in the regulation of the epiphyseal cartilage conversion to bone so it indirectly affects the longitudinal growth patterns.

From PubMed study 1 link HERE…

Pediatr Nephrol. 2000 Jul;14(7):602-5.

Chondromodulin-I as a novel cartilage-specific growth-modulating factor.

From PubMed study 2 link HERE…

J Biol Chem. 1996 Sep 13;271(37):22657-62.

A novel growth-promoting factor derived from fetal bovine cartilage, chondromodulin II. Purification and amino acid sequence.

From the website PowerfulIntentions.Org, which seems to be a community focused around the Law Of Attraction concept, a wrtier posts this about the Dhatrumurgasiniy . That is one hard to spell word.

WHAT IS DHATRUMURGASINIY

From the previous post where a patent was being reviewed, one very interesting compound I found which seems to be able to inhibit the endochondral ossifciation process where the cartilage and chondrocytes are ossified into bone, seems to have some potential. From the PubMed study below, the researchers conclude that…

“Our findings indicate that the antiangiogenic factor chondromodulin 1 stabilizes the chondrocyte phenotype by supporting chondrogenesis but inhibiting chondrocyte hypertrophy and endochondral ossification.”

From PubMed study 2 below…

“Cartilage-generated matrix components chondromodulin-I (ChM-I) synergistically stimulates growth and differentiation of chondrocytes in the presence or absence of FGF-2. In contrast, ChM-I inhibits the proliferation of vascular endothelial cells and tube formation, thereby further stimulating cartilage growth and inhibiting replacing cartilage by bone in an early stage. Another cartilage-derived chondromodulin-II (ChM-II) also stimulates cartilage growth. However, ChM-II does not inhibit vascularization but stimulates osteoclast differentiation.”

From source, Chondromodulin, an endogenous anti-angiogenic factor expressed in cartilage, has been suggested to inhibit invasion of endothelial cells into cartilage. In addition, the ectopic administration of ChM1 has been reported to suppress tumorigenesis in vivo. From source, In TMJ (temporomandibular joint), ChM-1 was expressed in the proliferative and hypertrophic zone of condylar cartilage and chondrocyte-like cells in the disc. No expression of ChM-1 was observed in osteoblasts and subchondral bone. ChM-1 may play a role in the regulation of TMJ remodeling by preventing blood vessel invasion of the cartilage, thereby maintaining condylar cartilage and disc integrity.

It can be proposed that chondromodulin may actually have the exact opposite effect in causing height decrease since it is anti-angiogenic. human height can only increased if there is a stable hard bone structure to support the additional bone layered to allow for bone lengthening but maybe chondromodulin can be used instead to hold off the growth plates from completely ossifying and be kept in cartilage form long enough to get other types of bone modulators inside to cause mesenchymal differentiation, chondrocyte proliferation and hypertrophy, and growth factor expression in the cartilage.

From PubMed study link HERE…

Arthritis Rheum. 2011 Sep;63(9):2721-31. doi: 10.1002/art.30335.

Chondromodulin 1 stabilizes the chondrocyte phenotype and inhibits endochondral ossification of porcine cartilage repair tissue.

Klinger P, Surmann-Schmitt C, Brem M, Swoboda B, Distler JH, Carl HD, von der Mark K, Hennig FF, Gelse K.

Source

Department of Orthopaedic Trauma Surgery, University Erlangen-Nuremberg and University Hospital Erlangen, Erlangen, Germany.

Abstract

OBJECTIVE:

To investigate the effect of chondromodulin 1 on the phenotype of osteochondral progenitor cells in cartilage repair tissue.

METHODS:

Self-complementary adeno-associated virus (AAV) vectors carrying chondromodulin 1 complementary DNA (AAV-Chm-1) were applied to cartilage lesions in the knee joints of miniature pigs that were treated by the microfracture technique. Alternatively, isolated porcine osteochondral progenitor cells were infected with AAV-Chm-1 or with AAV-GFP control vectors ex vivo prior to being transplanted into cartilage lesions in which the subchondral bone plate was left intact. The quality of the repair tissue and the degree of endochondral ossification were assessed by histochemical and immunohistochemical methods. The effects of chondromodulin 1 overexpression were also analyzed by angiogenesis assays and quantitative reverse transcriptase-polymerase chain reaction.

RESULTS:

AAV-Chm-1-infected cells efficiently produced chondromodulin 1, which had strong antiangiogenic effects, as verified by the inhibition of tube formation of endothelial cells. Gene expression analyses in vitro revealed the cell cycle inhibitor p21WAF1/Cip1 as one target up-regulated by AAV-Chm-1. Direct application of AAV-Chm-1 vectors into microfractured porcine cartilage lesions stimulated chondrogenic differentiation of ingrowing progenitor cells, but significantly inhibited terminal chondrocyte hypertrophy, the invasion of vessel structures, and excessive endochondral ossification, which were otherwise observed in untreated lesions. Indirect gene transfer, with infection of porcine osteochondral progenitor cells by AAV-Chm-1 ex vivo, also supported chondrogenic differentiation of these transplanted cells. AAV-Chm-1-infected cells maintained a chondrocyte-like phenotype and formed a hyaline-like matrix that was superior to that formed by uninfected or AAV-GFP-infected cells.

CONCLUSION:

Our findings indicate that the antiangiogenic factor chondromodulin 1 stabilizes the chondrocyte phenotype by supporting chondrogenesis but inhibiting chondrocyte hypertrophy and endochondral ossification.

Copyright © 2011 by the American College of Rheumatology.

What makes the permanent articular cartilage permanent? [Arthritis Rheum. 2011]

PMID:  21391200   [PubMed – indexed for MEDLINE]  Free full text

From PubMed study 2 link HERE…Connect Tissue Res. 1996;35(1-4):303-7.

Roles of cartilage matrix proteins, chondromodulin-I and -II, in endochondral bone formation: a review.

Suzuki F.

Source

Department of Biochemistry, Faculty of Dentistry, Osaka University, Japan. fsuzuki@dent.osaka-u.ac.jp

Abstract

Insulin induces early chondrogenesis in cultures of a clonal cell-line, ATDC5, which was derived from mouse embryonal carcinoma line AT805. Cartilage-generated matrix components chondromodulin-I (ChM-I) synergistically stimulates growth and differentiation of chondrocytes in the presence or absence of FGF-2. In contrast, ChM-I inhibits the proliferation of vascular endothelial cells and tube formation, thereby further stimulating cartilage growth and inhibiting replacing cartilage by bone in an early stage. Another cartilage-derived chondromodulin-II (ChM-II) also stimulates cartilage growth. However, ChM-II does not inhibit vascularization but stimulates osteoclast differentiation. Therefore, endochondral bone formation is regulated sequentially by cartilage-derived multiple autocrine factors. This opens a new mechanism of regulation of endochondral bone formation.

PMID: 9084668    [PubMed – indexed for MEDLINE]