Monthly Archives: November 2012

What I Learned From Tim Ferriss – Gene Therapy Is Already Being Used Illegally And Successfully To Increase Muscle Mass, So Why Can It Not Work To Increase Height?

One of the podcast I have been listening to for the last 2 years has been Pickup Podcast which I found years ago when I was going through the phase where I was absorbing Personal Development and Self Help material like a sponge. The podcast has been traditionally focused on teaching men how to better their social skills and mindsets to improve their dating life and romantic relationships. In recent times it has moved more in the direction of how to build a stronger core and self image so it has also encompassed “self help”. About 3 years ago, I needed that skills and knowledge base because I realized my own social skills were deficient.

In the most recent “Podcast Episode” where the guys interview the infamous Tim Ferris, who wrote the insanely popular lifestyle design book “The 4 Hour Work Week”, they were discussing Tim’s latest book where he talks about how to find the simplest way to mastery the science (or art) of cooking, using only a few basic elements (ie. Knife, Spices, Cookware, etc.) and also about other ways to hack life to optimize effectiveness, productivity, and time management, something I am a junkie on. If there is one thing I am addicted to still, it is listening to interviews and podcasts where really successful people come on to discuss their strategies and methods on optimizing their life.

If you follow this episode, around the 1:04-1:06 (that is hours btw) mark Tim mentions that he has a friend who has went to China to perform gene therapy testing (or what Dave Asprey would call Bio-Hacking) on himself to see what would be the effects. Tim claims that his friend has managed to increase his weight which was already at 240 lb by another 30 lbs of muscle in 28 days! This seems to be from using gene vectors which I have only begun to get into.

Here are the 3 main genes that the friend has been experimenting on and manipulating.

  1. Actin III – For fast twitching muscle fibers
  2. Interleukin
  3. Myostatin

So far I have already proposed at least 2 possible ways to increase height using gene therapy from changing the DNA of chondrocytes and progenitor mesenchymal stem cells. However what Ferriss’s friend is doing is something I didn’t think was even possible from using gene therapy (or at least legal).

From the Wikipedia article on Gene Therapy we realize that there are actually two types of gene therapy, 1. Somatic Gene Therapy and 2. Germ Line Gene Therapy. Somatic gene therapy is where the effects and modifications happen only on the person which was subjected to the treatment while germ line gene therapy is where the effects also has an effect and modify’s the subject’s offspring too. We are going to only focus on the first type right now and see if we can change our own bodies and not worry about what our kids and descendants will be like.

Getting back to the subject, (as the story goes) this friend went to China and somehow got his hands on some vectors from some supplier in a non-legal way and has managed to change his body at such a dramatic way in a very short time. As far as I know, there is no muscle mass increasing drugs in the market right now that can have this dramatic of an effect, even the most intense ones. Body builders who I have researched because of the link between steroid usage and potential height increase have consistently talked about the effects of some of the craziest stuff. This is at another level.

For me, this type of claim by Tim Ferriss seems to show to me that there are already people who have been successful in using illegal supplies and tried using gene therapy on themselves and gotten results. Since this happened in China (and we know that in China, anything can happen… like in Vegas) we sort of have to take this story with at least some bit of reservation. This story shows that if I (and Tyler and other genetics knowledgeable height increase seeker enthusiasts around the world) can figure out a more complete map on which genes affect the human height development (besides just HMGA2 and LIN28B), we might be able to manipulate our height by causing specific cell differentiation (and maybe even transdifferentiation) from gene vectors in less than 10 years of dedicated research.

A Complete Collection Of All The “Height Increase” And “Grow Taller” Books

This will be another one of those posts which will eventually turn into a section/webpage of the website which will be occasionally edited and added upon. I was not aware of just how big and many books of this type there are. When I was first doing my research, I had no idea that there was this many books all devoted to this topic. The Primary source where I found this list of books was from the “Grow Taller Step” website store section (HERE).

If you want to try out your luck and buy one of the books from the links, then that is your choice. I am not promoting these books on Amazon, only to say that they do exist. The good news for you the website visitor is that a nice number of the books below are already uploaded to the “Downloads” section of this website for you to take for free.

[Note: These books are NOT in alphabetical order, yet]

  1. How to Get Taller – Grow Taller By 4 Inches In 8 Weeks, Even After Puberty! – David Taylor – (Amazon Link)
  2. How to Get Taller – The Complete Exercise Guide (Grow Taller) – David Taylor – (Amazon Link)
  3. How To Grow Taller: Guaranteed Increase Your Height Within 8 Weeks – Peter Douglas (Amazon Link)
  4. Growing Taller Secrets: Journey Into The World Of Human Growth And Development, or How To Grow Taller Naturally And Safely. Second Edition – Robert Grand (No Amazon Link)
  5. How to Naturally Increase your Height (Grow Taller Guide) – Russian Sports Authority (Amazon Link)
  6. How to Grow Taller — The Amazing Secrets to Quickly and Easily Grow Taller! — Get the Respect of Being Stronger, Confident, Taller and More Attractive Today! – Mike Summers (Amazon Link)
  7. Grow Taller book – Hayden Carter (Amazon Link)
  8. How Can I Grow Taller: Learn How To Increase Height And How To Grow Taller Naturally And Artificially. Height Increase Tips, How To Get Taller With Yoko And More. So Is There A Way To Get Taller? Yes! – Jared D. Carlson (Amazon Link)
  9. Increasing Height Through Exercise – Steven C. Cummings (Amazon Link)
  10. Increase Your Height – Krishna Gopal Vikal (No Amazon Link)
  11. Grow Taller – Statton, Burk, Cunningham Serrano
  12. How to Grow Taller “Master Secrets to Growing at Least 4 Inches in 2 Months! – Monica Heart (Amazon Link)
  13. This Tall Grow Taller and Taller – The Answer to the Fear of Height [In Japanese Language] – Aiyoshi Kawahata (Amazon Link)
  14. How To Grow Taller: A Comprehensive Guide And Revolutionary Exercise Program To Make You Grow – Kanwaljit Singh Kalsi (Amazon Link)
  15. Grow Taller Proven Insider Secret Tips and Techniques That Will Help You Grow (Body Image Solutions) – Dr. Jesus Serrano (Amazon Link)
  16. The Most Effective Way to Grow Taller (Chinese Edition) – Yang Shu Wen (No Amazon Link)
  17. Small Children, Children Grow Taller Quiz – SHI DING PING BIAN ZHU (Amazon Link)
  18. Children Naturally Grow Taller (Chinese Edition) – PU XIU SHENG CAO FANG (Amazon Link)
  19. How Quickly Children Grow Taller 10 cm (Chinese Edition) – GONG SUI (Amazon Link)
  20. You Will Grow Taller at 23 (Chinese Edition) – Jin Yang Xiu (Amazon Link)
  21. Natural Human Growing Taller Method (Modul) – Jorge Garcia (Amazon Link)
  22. Gaining Height Through Exercise : 100 Straightening and Stretching Exercises to Make You Grow – Pierre Berthelet (Amazon Link)
  23. How to Grow Taller Naturally with the Power of Your Mind – Joan M Rivera (No Amazon Link)
  24. Grow Taller Now – Unknown (No Amazon link, source link)

Composition And Method For The Repair And Regeneration Of Cartilage And Other Tissues

Me: There is two patents I found that has the proposed ideas on how we can possibly inject dna mutated chondrocytes into the epiphysis of the femur and tibia to stimulate mesenchymal stem cells to differentiate into chondrocytes correctly.

Analysis:

For Patent 1 – Only a picture of the idea below was used. The idea as always to combine a type of gel system with growth factors in it and have extracted and regrown chondrocytes implanted in it. Then the entire piece is then implanted into a bone defect or fracture or cartilage to heal it.

For Patent 2 – we have a mixture to heal articular cartilage defects comprising of these components through implantation. There are two main pieces. In essence, it is a proliferating chondrocyte cell structure having phenotypic capability embedded in a vehicle or gel.

The first peice is the extracted and cultured chondrocytes of a certain packing density. This is bone marrow derived chondrocytes or osteoblasts of autologous or homologous origin, or homologous committed chondrocytes, or autologous or homologous muscle fibroblast derived chondrocytes or any other progenital cells from mesenchymal origin

The second part is a a biodegradable, biocompatible, biological resorbable immobilization vehicle (BRIV) adhesive glue. This is made of the following compounds

  • fibrinogen (100-150 mg/ml)
  • thrombin (60-90 units/ml)
  • CaCl₂ (an excess of 60 mM CaCl₂.)
  • protease inhibitor (selected from the group consisting of polysaccharide inhibitors, plasma protease inhibitors, and synthetic and natural non-plasma protease inhibitors)
  • about 10-30% serum (selected from fetal calf serum or umbilical cord serum from the second trimester or horse serum or any combination of such serums. may optionally contain growth factors such as IGFI, IGFII, TGFB, PDGF, or any other growth factors that will be found to facilitate the proliferation of the cells)

The chondrocyte population is embedded in the biological glue at a concentration of between from 100,000 to 500,000 cells per milliliter of glue.

For Patent 3 – Patent #3 was written by the same guy who wrote up patent #2 and he wrote it because it turns out patent #2 had a few limitations that was later found out from experiments. It was believed that for the greatest ability in chondrocyte proliferation the best type was embryonic. However this meant the right type of cells was hard to get and there was also the problem with immune system reactions. It would turn out that the concentration limits for the chondrocyte density in gel, the thrombin, and the fibrinogen were not good in actual experimental testing. The compositions and procedures were changed. I have decided just to slip the sections of the patent to the right and left. We can see that overall, the Patent #3 is an improved version to Patent #2 where this has been shown to be more experimentally feasible in causing more chondrocyte proliferation.

Implications: These patents show what exactly would have to go into a gel/resin and cultured cell pellet combination to make any idea of implanted chondrocytes to work out. The way to administer it would be relatively non-invasive through a small syringe with the loaded material going through the knee

Patent #1: Composition and method for the repair and regeneration of cartilage and other tissues (US8258117 B2) (Patent #1 link)

Patent Information:

Issue No. US8258117B2
Application Number 12/901, 293
Public date September 4, 2012
Filing Date October 8, 2010
Inventor
Michael D. Buschmann

2 more »
Applicants
Piramal Healthcare (Canada) Ltd

5 more »
United States Patent and Trademark Office patent classification 514/54

Patent #2: Composition for repair of cartilage and bone and method for their preparation as skeletal tissue implant (EP0339607 B1) (Patent #2 link)

A composition for the regeneration of articular cartilage and bones by implantation comprising bone marrow derived chondrocytes or osteoblasts of autologous or homologous origin, or homologous committed chondrocytes, or autologous or homologous muscle fibroblast derived chondrocytes or any other progenital cells from mesenchymal origin and a biodegradable, biocompatible, biological resorbable immobilization vehicle (BRIV) adhesive glue consisiting of fibrinogen, thrombin, CaCl₂, protease inhibitor, and about 10-30% serum, characterized in that said composition contains from 80-160 x 10⁶ cells/ml of BRIV. (From Patent)

Me: Also from the same Inventor Dr. Sam Itay…

Patent #3: Compositions for repair of cartilage and bone (Patent #3 link) [Note: I have already talked about this invention in a previous post]

A defect is provided in cartilage or bone, or both, to excize damaged or pathological tissue, and it is filled with an implant having capability for complete regeneration of the skeletal tissue as a chondrogenic or osteogenic phenotype. The implant comprises cells expressing a chondrocyte phenotype (80.times.10.sup.6 cells/ml) embedded in a biocompatible matrix having about 20% serum, which provides a permissive environment for maturation and transformation of the implant to a fully integrated state with the surrounding tissue. A portion of the implant may comprise a bone segment or a bone substitute.

This is a picture of the patent idea from patent #1.

Growth Hormones Exert A Direct Stimulatory Effect On Epiphyseal Cartilage And Stimulates Longitudinal Bone Growth Directly

Me: I think it is time to put the questioning of whether the hGH in the human body directly stimulated the epiphyseal plate for longitudinal growth to be answered conclusively. It does.

From article 1…

We see that chondrocytes from the tested rat’s epiphyseal plates are removed and cultured using calf serum. The thing to note is that to make the condrocyte colonies one needs the serum. There is also a strong correlation in terms that the number of colonies formed is directly proportional to the concentration of the calf serum. Overall we see that we need all three factors of

  1. Number of initial seeded chondrocytes
  2. Have enough 10-15% newborn calf serum
  3. Having around 10-40 ng/ml of hGH
They will allow for the best formation of chondrocyte colonies. The researchers conclude that “These results show that GH potentiates colony formation in chondrocytes of the epiphyseal growth plate, providing further support for the contention that GH exert a direct stimulatory effect on epiphyseal cartilage and thus stimulates longitudinal bone growth directly.” also…”The finding that GH preferentially potentiated the formation of large size colonies suggests that GH promoted the differentiation of early proliferative chondrocytes or stem cell chondrocytes with an inherent high capacity to proliferate.” This seems to suggest that the GH also has two really big functions to progenitor cells and proliferative chondrocytes, first in differentiating the progenitor cells into chondrocytes and then in helping lead to to chondrocyte proliferation.

From article 2…

We see that both hGH and IGF-1 both lead to increased cloning efficiency. What is even more interesting is that IGF-1 when used after the pretreatment of the chondrocytes by GH lead to a far greater effect of cloning efficiency. The researchers concluded that …” The results of the present study show that pretreatment of hypophysectomized rats with GH, but not with IGF-I, promotes the formation of chondrocyte colonies and make the chondrocytes susceptible to IGF-I in vitro. The results suggest that GH induces colony formation by IGF-I-independent mechanisms and that IGF-I is a second effector in GH action as previously shown”

From article 3…

This study was designed to investigate whether growth hormone (GH) influences the expression of its own receptor in chondrocytes. To investigate this possibility GH-receptor mRNA was measured in cultured rat epiphyseal chondrocytes in the absence or presence of GH under various experimental conditions. The researchers concluded that “GH specifically regulates mRNA levels for its own receptor in rat epiphyseal chondrocytes by interacting with somatogenic binding sites. These findings also suggest a transcription-dependent regulatory system between the GH-receptor and the GH-receptor gene.”

Implications: It seems that GH can be used to cause cell colony formation and is the first hormone that is usually used to stimulate epiphyseal plate chondrocytes. THe IFG-1 pathway is independent of it’s pathway. It seems that the GH causes it’s own receptors to form by turning it’s own receptor genes on.

From PubMed article 1 link HERE…

Endocrinology. 1986 May;118(5):1843-8.

Growth hormone potentiates colony formation of epiphyseal chondrocytes in suspension culture.

Lindahl A, Isgaard J, Nilsson A, Isaksson OG.

Abstract

The effect of human GH (hGH) on colony formation of rat epiphyseal plate chondrocytes was studied in suspension culture. Chondrocytes were isolated enzymatically from epiphyseal plates of the proximal tibia of 28-day-old normal male rats, and were cultured in a suspension stabilized with 0.5% agarose. After approximately 7 days of culture in the presence of 10% newborn calf serum (NCS), chondrocyte colonies developed consisting of varying numbers of cells in matrix. No colonies developed in the absence of NCS, and the number of formed colonies was proportional to the concentration of NCS (5-20%) in the medium. hGH potentiated the formation of large size colonies (diameter greater than 90 microns) after a culture period of 10 or 14 days. The lowest effective concentration of hGH was 10 ng/ml, while 40 ng/ml hGH gave a maximal stimulatory effect (40-50%). Higher concentrations of hGH (80 and 160 ng/ml) showed reduced potentiation of colony formation. The stimulatory effect of hGH was expressed at 10-15% of NCS at 14 days of culture. There was a linear relation between the number of seeded cells and the number of colonies formed, both in the absence and presence of hGH. These results show that GH potentiates colony formation in chondrocytes of the epiphyseal growth plate, providing further support for the contention that GH exert a direct stimulatory effect on epiphyseal cartilage and thus stimulates longitudinal bone growth directly. The finding that GH preferentially potentiated the formation of large size colonies suggests that GH promoted the differentiation of early proliferative chondrocytes or stem cell chondrocytes with an inherent high capacity to proliferate.

PMID: 3698898     [PubMed – indexed for MEDLINE]

From PubMed article 2 link HERE…

Endocrinology. 1987 Sep;121(3):1070-5.

Growth hormone in vivo potentiates the stimulatory effect of insulin-like growth factor-1 in vitro on colony formation of epiphyseal chondrocytes isolated from hypophysectomized rats.

Lindahl A, Isgaard J, Isaksson OG.

Abstract

The effect of GH pretreatment in vivo on the colony formation of epiphyseal chondrocytes from hypophysectomized rats and the subsequent responsiveness to insulin-like growth factor (IGF-I) was studied in vitro. Chondrocytes from epiphyseal growth plates of the proximal tibia of 36-day-old hypophysectomized rats were enzymatically isolated and cultured in suspension, stabilized with agarose (0.5%) in Ham’s F-12 medium and serum supplement. After 14 days the cultures were terminated and screened for cloning efficiency (number of colonies with a diameter greater than 56 microns/1000 seeded cells) and for distribution of cloning efficiency as a function of colony size. Pretreatment with human GH in vivo for 24 h (10 micrograms X 3) increased the cloning efficiency during the subsequent culture period (control, 1.5 +/- 0.1; human GH, 4.4 +/- 0.3). Addition of IGF-I to the chondrocyte cultures from control rats caused a slight increase in cloning efficiency (control, 1.5 +/- 0.1; IGF-I, 2.2 +/- 0.3) but caused a marked increase in chondrocyte cultures from GH-pretreated rats (control, 4.4 +/- 0.4; IGF-I, 8.2 +/- 0.9). The cloning efficiency was increased 12 and 24 h, but not 4 h, after start of GH-treatment in vivo. The increased responsiveness to IGF-I in vivo showed a similar time course after GH pretreatment. The distribution of cloning efficiency was altered in cultures of chondrocytes isolated from the GH-pretreated rats; large colonies were overrepresented in the GH-treated group. Colonies with a diameter exceeding 180 microns were only seen in cultures of chondrocytes isolated from the GH-pretreated animals. Addition of IGF-I in vitro did not alter the distribution of cloning efficiency, but increased the mean colony size of all colonies. Pretreatment of the rats with two different doses of IGF-I in vivo for 24 h (5 micrograms X 3 or 50 micrograms X 3) had a slight stimulatory effect on subsequent colony formation, but no potentiation of IGF-I in vitro was demonstrated. The results of the present study show that pretreatment of hypophysectomized rats with GH, but not with IGF-I, promotes the formation of chondrocyte colonies and make the chondrocytes susceptible to IGF-I in vitro. The results suggest that GH induces colony formation by IGF-I-independent mechanisms and that IGF-I is a second effector in GH action as previously shown for cultured 3T3-preadipose cells.(ABSTRACT TRUNCATED AT 400 WORDS)

PMID: 3622376    [PubMed – indexed for MEDLINE]
From PubMed article 3 link HERE…

Mol Cell Endocrinol. 1990 May 7;70(3):237-46.

Growth hormone regulation of the growth hormone receptor mRNA in cultured rat epiphyseal chondrocytes.

Nilsson A, Carlsson B, Mathews L, Isaksson OG.

Source

Department of Physiology, University of Göteborg, Sweden.

Abstract

This study was designed to investigate whether growth hormone (GH) influences the expression of its own receptor in chondrocytes. To investigate this possibility GH-receptor mRNA was measured in cultured rat epiphyseal chondrocytes in the absence or presence of GH under various experimental conditions. Chondrocytes were isolated enzymatically from epiphyseal growth plates of the proximal tibia of 20-day-old male rats and cultured in monolayer in Ham’s F-12 medium supplemented with 10% calf serum and 1% of a serum substitute. The cells were seeded at various densities (100,000-1,000,000 cells per flask) and cultured for 14 days. Subsequently, the calf serum-containing medium and the cells cultured for various periods of time (0-24 h) before total nucleic acid preparation. GH-receptor mRNA was measured with a solution hybridization technique using [35S]UTP-labeled RNA growth hormone receptor cloned from rat liver cDNA. Human GH (hGH; 50 ng/ml) increased GH-receptor mRNA after 3 h and maximal levels were seen 12 h after GH addition. This effect of hGH was time and dose dependent with a significant effect of hGH at a concentration of 0.5 ng/ml and a maximal effect at 50 ng/ml. The hGH-stimulated increase of GH-receptor mRNA was completely blocked by actinomycin-C1 (1.0-0.1 micrograms/ml), while cycloheximide (10 micrograms/ml) only slightly counteracted the hGH effect. Rat and human GH were equally potent, and ovine prolactin was effective at 500 ng/ml but not 5 and 50 ng/ml. A high dose of insulin-like growth factor-I (IGF-I; 1 microgram/ml) caused a small stimulatory effect and addition of 10% calf serum caused a marked increase in GH-receptor mRNA. The level of GH receptor mRNA after 14 days of culture was inversely proportional to the cell density at the start of culture. These results show that GH specifically regulates mRNA levels for its own receptor in rat epiphyseal chondrocytes by interacting with somatogenic binding sites. These findings also suggest a transcription-dependent regulatory system between the GH-receptor and the GH-receptor gene.

PMID: 1694505    [PubMed – indexed for MEDLINE]

Epiphyseal Plate Transplantation Through Vascularization (Breakthrough!)

Me: This is one of those posts that puts ideas into one’s head on what is possible biomedically. The study shows that one can transplant epiphyseal plates into host bodies as long as it is kept vascularized. The term vascularized just means that it has blood vessels going in and out of it keeping it feed with incoming nutrients and has a way to remove the waste. One big question I have had since reading Dr. Brighton’s detailed description of the plates was exactly how the blood vessels are distributed along the layers of the plate. We know that the resting zone is the most critical since it is where everything starts and is also the true determining area for how much longitudinal growth is possible. It also has at least 2 growth factors which determine the chondrocytes to start stacking in columns when they get to the proliferative zone.

There was 4 ways the researchers were testing to see the longitudinal growth.

  1. Serial roentgenograms – a time distribution of photographs made with x-rays
  2. Histological examination – using microscope to analyze the cells
  3. Fluorescent bone-labeling – sounds just like what it is
  4. Microangiography – Radiography of the minute blood vessels of an organ obtained by injection of a contrast medium and enlargement of the resulting radiograph

Implications: This study has proved that growth plate transplantation is completely possible, as long as you keep the chondrocytes fed through vascularization.

From PubMed study link HERE… (For a copy of the Full Text PDF click HERE)

J Bone Joint Surg Am. 1984 Dec;66(9):1421-30.

Free microvascular epiphyseal-plate transplantation. An experimental study in dogs.

Nettelblad H, Randolph MA, Weiland AJ.

Abstract

To evaluate the feasibility of transplanting vascularized epiphyseal plates while maintaining normal growth in the recipient site, twenty-two puppies from known, large breeds were divided into one control and three experimental groups of four animals each and one long-term group of six animals. The control group underwent insertion of a radiopaque marker in the fibular metaphysis bilaterally, and, in addition, a fibular osteotomy was performed on one side. In the experimental groups, a fibular switch was carried out, selecting one fibula as a vascularized graft and the other as a non-vascularized graft. Both the controls and the experimental groups were evaluated using serial roentgenograms, histological examination, fluorescent bone-labeling, and microangiography. One week, six weeks, three months, and seven months postoperatively, animals from each group were killed. Continuous growth was observed in the vascularized epiphyseal transplants and in the controls, with no statistical difference noted, whereas the non-vascularized transplants exhibited considerably less or no growth. Vascularized transplants demonstrated an average 21.2-millimeter increase in length while non-vascularized transplants showed a 6.6-millimeter increase. Histological examination, fluorochrome bone-labeling, and microangiography confirmed the continued viability of the vascularized epiphyseal transplants in contrast to the non-vascularized transplants.

PMID: 6501338    [PubMed – indexed for MEDLINE]

Former Tallest Women In The World Yao Defen Died

I was not aware of this news until a few minutes ago. I am a frequent visitor to the site TheTallestMan.com and I found out from visiting the forum that the tallest female in the world had died about a week ago at the age of 41 from some “acute ailment” as the posters claimed (source HERE).

I got the news from this story article HERE. I can’t read Chinese but the people at the Tallest Man website confirmed her passing.

This for me is really, really sad news because I really felt her pain from seeing how her life was going in recent years being subjected to brain surgery. I was able to look past her face and I realized that if you can look past the Acromegaly enhanced face features, she was a very beautiful women. The pictures of her when she was younger showed that she was very pretty.

It just goes to show you that sometimes being tall is not a good thing but can lead to great misery and pain. If we going to chase this dream for increased height, I hope we are chasing for this dream for the right reasons.

As for who can claim the title of “World’s Tallest Women” now we see that Margo Dydek passed away in recent years. So the title goes to either Maria Feliciana dos Santos or Sun Fang. I’d think Maria is probably 1 inch taller from the listings on the website.