Author Archives: Senior Researcher

Can We Change Our Genes And DNA So That Our Children Can Be Taller And Tall Height Becomes Hereditary Within Our Family?

Something that I am sure any person who thinks a lot about height and how to grow taller eventually reaches is to wonder whether our children will end up short or tall, or hopefully wishing that our current or future children will end up to the type of stature we expect them to be at.

I know that personally, due to how obsessive I am with this endeavor, I may have some emotional difficulty if I eventually have a son who somehow doesn’t get even to the average height. I worry about this type of thing and wonder just how reasonable is it to worry already about something which hasn’t even happened yet and might be a decade into the future.

If I look at the direction and speed at which I am approaching any type of fatherhood, it is possible I will not be procreating at all in my life. I guess now that I am in another serious relationship, considering marriage, and settling down, I would not be too out of line to think about how well my future children with go through growth. Will they also worry as much about height and how tall they are as their dad?

I know that in my family, my mother, cousins, and my sisters all seem to have personal deep quirks and issues over their height, even though they would not be considered “short” by most people. It could be that I developed this strange obsession from being around my family. All I know is that every person in my family has expressed at some point their desire to be taller or regret that they are not taller than where they are now. What a strange family I am from.

So the original question is “Can We Change Our Genes And DNA So That Our Children Can Be Taller And Tall Height Becomes Hereditary Within Our Family?”

I would say that in the current genetics theory we are told, there is a small possibility we can.

geneticengineering

In genetic engineering, the most general idea is that before the human (or any living organism) is ever even born, before even conception, when the sex cells/gametes, the male sperm and the female egg have not been integrated together to form the zygote, we can do some genetic “editing” on the dna in the individualistic cells like adding additional dna or replacing a section of the genome by clipping it and replacing the section with something slightly altered. We can use vectors to do this job. From the blog “Designed Babies” post “How a Designer Baby Can be Produced” we learn that there seems to be two types of effect when we change DNA.

You have Somatic Modification and Germline Modification. So Let’s see what these two types are…

From the website for The Association of Reproductive Health Professionals, there are definitions given for the two types.

HUMAN GENETIC ENGINEERING: A CRITICAL DISTINCTION BETWEEN TWO APPLICATIONS

1. “Somatic” genetic engineering is genetic engineering that targets the genes in specific organs and tissues of the body of a single existing person without affecting genes in their eggs or sperm. Somatic gene transfer experiments are currently undergoing clinical trials, with mixed results to date. But they may someday be effective. Diagram 5 above shows how somatic genetic engineering works.

2. “Germline” genetic engineering is genetic engineering that targets the genes in eggs, sperm, or very early embryos. The alterations affect every cell in the body of the resulting individual, and are passed on to all future generations. Germline engineering is banned in many countries but not in the U.S. Diagram 5 shows how germline genetic engineering works.

genetic engineering

Implications For Height Increase: This post was to discuss the feasibility of being able to genetically change our children to make them taller. Obviously it is clear that of the two main ways to make people taller, the more effective approach is to do it before the child is even conceived. The effect is that all subsequent generations will also have the same traits and characteristics that you assigned to the genetic engineer.

What is interesting is that the websites and literature sort of suggest that even embryos can be altered genetically with a vector to change the DNA. I guess the key is to make sure the embryo is not too large or to far in it’s development to alter it’s DNA.

As for people who are already born, the effectiveness of genetic engineering is clearly decreased. We might wish for our 5 year old who is still growing to be even taller than what they are programmed to be and there might be a way to use somatic genetic engineering to achieve that. Somatic Engineering is still a very young area of study and there is little in this area in terms of concrete results. I know that at least a few biohackers in China and the USA who are already injecting themselves with certain types of vectors with growth factors inside to make themselves gain muscle muscle and loss weight faster.

I recently was reading the personal blog of the Professor, Researcher, and Multi-Millionaire Stephen Hsu at Information Processing and he would talk about the fact that at least one major private Chinese Research company has been trying to figure out how to engineer “genius babies”. In Hsu’s March 27th post, entitled “On the radio: NPR’s on the point” there is an audio file which you can play where he is being questioned on NPR about the details about China’s work in trying to create smarter babies. In the talk, Hsu would mention at least 4-5 times about the fact that besides intelligence, geneticists would also be trying to change other genotypes in the genome of the prenatal embryo. The first thing he brings up is the fact that height would clearly be the next big thing parents would probably secretly wish and love to change about their child.

Like I said before: Every single normal parent would want the best for their children to they would do everything they can to give the children, who might not even be born yet, every single physical advantage that money can buy.

Height would clearly be something that parents would ask to be manipulated. I would also then postulate that every single parent, if they had the chance would ask the child to be above average in height, or at least “tall” in description in comparison to other children ie the kids’s peers. However, what if then every single rich parent asks that their kid’s be tall?

The average height of boys and girls born to rich people with the money would shoot up in bamboo. Then it would turn into a sort of one-up-manship where each parent will try to make their kids at least slightly taller, maybe by 1 cm, then their friends’ or rival’s kids. After 3-4 generations, you’d have people who are programmed to be 8 feet tall. We’d look like midgets standing next to these genetically enhanced people.

So I guess the big thing we have to ask ourselves before we more further in the direction of creating “enhanced” babies is to ask what type of future do we really want to create and what are the odds that the super-humans we create in our children will turn into something ugly? Will they look at us and think that we are inferior creatures because we never got genetically enhanced?

I leave the reader with the quote from the website…

“The only situation in which germline engineering would be required over pre-implantation selection is one in which a couple would like to endow their child with genes that neither member of the couple possesses. This is the “enhancement” scenario, which we believe would lead to a dystopic human future if it were allowed”

Natural Height Growth Podcast, Episode 7 – Guest Tyler Comes Back To Discuss More About LSJL, Gene Expression, Periosteum Manipulation, And Much More

Logo1This episode is the biggest, longest podcast episode that I’ve done so far at a little less than 50 minutes to discussion on the deep technical science behind the artcles we have found in our research.

Episode #7: Guest Tyler Comes Back To Discuss More About LSJL, Gene Expression, Periosteum Manipulation, And Much More

Me and Tyler from HeightQuest.com would delve into the subjects of…

  • The recent findings of certain genes that have large roles in the regulating and determining final adult height.
  • Deer Antlers and their unique epimorphic growth potential
  • Further explanation of the molecular and genetic mechanisms on of the LSJL method on why it is feasible and effective
  • The recent finding of the issue of periosteum stripping and transverse cutting leading to increased longitudinal growth.
  • The reason why studying gene charts and expression is important for this research.
  • The recent finding of the disruption of vascularity in the inter-medullary cavity in the metaphysis leads to at least temporary increased longitudinal growth
  • The use of extracorporeal shockwaves (ESW) to increase periosteum thickness.
  • The major growth factors that have been shown to be most important in the research
  • Many more subjects that I can’t remember right now but are worth listening to.

Click Here to Subscribe via iTunes and/or leave a review for the podcast!

Length of time: 50 min

Beginning of actual interview: ~ 1:15

Listen Here – (to download, right click and ‘save’)

Natural Height Growth Podcast, Episode 6 – Details On Updates Of The Website Operations And Concerns That Has Been Raised

Logo1It has been over 3 months but a few new podcast episodes have been made and will be put up very soon. From looking at the statistics of the podcasting numbers, it seems that I haven’t put up a podcast episode in over 2 months now. This episode will be the first to clear up issues that I wanted to address earlier so we won’t have to talk about them in episodes which will be dedicated more towards talking about the science.

Episode #6: Details On Updates Of The Website Operations And Concerns That Has Been Raised

For this episode I will be talking alone about details on the updates which are going on with the website, personal changes and how they will affect the evolution of the website, and projects and ideas which I want to combine with the website. A lot of comments and emails have come to the website email and they have raised a few concerns which I felt was reasonable and important enough to talk about.

There is little technical/science talk here since it is just me alone. Wait until the next episode where I will get Tyler on to talk more about the research and the breakthroughs we have been finding, if any. Some ideas will be brought up.

Click Here to Subscribe via iTunes and/or leave a review for the podcast!

Length of time: 16 min

Listen Here – (to download, right click and ‘save’)

A Chart Of The Genes And Proteins Shown To Help Pluripotent Progenitor Stem Cells Differentiate Towards The Chondrogenic Lineage And Inhibit The Osteogenic Lineage

Note: I seem to remember that I might have already done a post on this diagram I have pasted below in this post before months before. Given the large number of posts I have written, my memory is not clear on which post that was. So I guess it is okay if I decided to redo an old post all over again, just so that it can be a review for me on the concepts and results.

This is one of those chart, tables, or diagrams which show that the research we have been doing is on the right track ,or at least that we are finally being good enough in our readings to know that what we have been hypothesizing is validated by other scientific works.

From the PubMed study & article “Concepts in Gene Therapy for Cartilage Repair“…

Analysis & Interpretation

I note that the growth factors in the chart are only for chondrogenesis and cartilage generation. This is good because so often when we are talking about the skeletal structure, we only are focused on the growth factors which will be best for osteogenesis, since most studies on bones and cartilage are for chronic, old age issues like osteoperosis and rheumatic arthritis, which are caused by bone mineral density decreases and cartilage degeneration. Nobody has done any research to see the research of cartilage generation from the lens towards height increase.

The chart below is rather big and complicated but the main point is that almost everything listed below has anabolic aka growth potential to make cartilage grow from at least progenitor mesenchyme cells if they are there.

So let’s go down the list.

We have seen the TGF-Betas before, type 1 and 2. Type 3 I am not familiar with.

We have the BMPs, 2, 4, and 7 which we have done extensive research on and they seem to be better at getting multipotent stem cells to differentiate into the chondrogenic lineage than the ostegenic lineage.

The CDMP stands for Cartilage Derived Morphogenic Protein. It seems that they go by a more familiar names, the Growth Differentiation Factors, and I have stated in at least two previous posts, (Is Growth Differentiator Factor 5 GDF5 Gene The Most Influential Gene Towards Height?” and A New Proposed Theory To Increase Height And Grow Taller Using GDF-5 (Breakthrough!)) that GDF-5 has potential to be huge in our goals to become taller. As for GDF-6 and GDF-7, I did a post about the whole group of GDFs many month ago entitled “A Detailed Study And Analysis On Growth Differentiation Factors GDFs Which Influence Growth And Height” and I seem to remember that only 2 of the many GDFs had potential to be used as a growth factor for chondrogenesis.  However I will look into the reference studies listed.

We have Smad which is both the gene that creates the protein, and the protein, but I have not done any research on it yet.

The Sox9 gene was shown to be critical in the post “Why Does The Epiphyseal Cartilage Disappear But The Articular Cartilage Remain? (Breakthrough!)” which shows that for Chondromodulin Type I to work and the area of the articular cartilage to not get vascularized, we need the Sox9 gene to be turned on.

The IGF-1 is very well known by researchers to have chondrogenic effects since it seems to be able to directly effect the receptors on the surface of chondrocytes.

Everything else, like the Brachyury, mLAP1, PDGF, EGF, HGF, Comp, etc. I have never even heard of.

What might be better for me to relearn the growth factors and proteins that help in cartilage regeneration is to look at the sections the chart is broken into,

Stimulation of Chondrogenic Differentiation

  • Anabolic Growth Factors
  • Signal Transduction Molecules
  • Transcription Factors

Stimulation of Cartilage Matrix Synthesis and/or Cell Proliferation

  • Anabolic growth factors
  • ECM Component
  • Enzymes for GAG synthesis

Inhibition of Osteogenesis & Hypertrophy

  • Growth factors – 1. Inhibiting TGF-Beta & BMP action, 2. Inhibiting terminal differentiation
  • Signal Transduction Molecules

Anti-Inflammatory 

  • IL-1 blockage (cytokine antagonist)
  • TNF-2 inhibition (Cytokine antagonist)
  • MMP inhibitory (Proteinase inhibitor)
  • cytokines
  • Enzymes for glucosamine derivatives (IL-1 inhibition)

Senescence Inhibition

  • Inhibition of telomere erosion
  • Free radical antagonist

Apoptosis Inhibition

  • Caspase inhibition
  • Fas-L blockage
  • NO – induced apoptosis
  • TNF-alpha, TRAIL inhibition

From a process point of view, we can see that multiple studies have been done to show that you can try to manipulate each stage of the cartilage or chondrocyte’s life. You can trying to inhibit apoptosis, inhibit senescence, decrease inflammation, inhibit hypertrophy and differentiation into bone cells. The more anabolic strategy is to stimulate cartilage cell division and create more of the extracellular cartilage matrix.

If we were just to look at the side of trying to make more cartilage and chondrocytes, we could just use Table 3, and use  the BMP-2,7, the TGF-Beta, GDF-5, and IGF-1 to stimulate more cartilage growth. However it is clear from the first table that we must somehow also get the other half of the process working too so that we can prevent the cells from aging or dying too quickly, as wells keeping them from going the bone cell direction in transformations.

It seems that there are at least a dozen ways that the cartilage cells get evolved to a point which makes them none functioning. Many of the proteins and cytokines I have seen before but with little research. This table is sort of an introductory way for the researchers to see which types of PubMed studies they should be look for to understand the types of molecular mechanism which control the chondrocyte.

Implications For Height Increase

The two tables below shows us that beyond just stimulation of chondrogeniic differentiation and cartilage matrix synthesis, and cell proliferation, we would have to also consider the other side, which is how to keep them from aging and dying so we have more time to manipulate the cartilage tissue to expand and multiple in the direction which we want to lengthen long bones.


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2

3

How To Read A Chart Describing The Growth Factors That Regulate The Sections Of The Epiphyseal Growth Plate (For The Researcher)

I recently found a nice diagram of the signaling pathways of the various proteins in a study (the 1st link below cited). I felt that it would be appropriate right now to look at the diagram since I feel confident now that I am sufficiently prepared to be able to look at the diagram and be reasonable well versed in knowledge to be able to dissect and really do some real analysis on the pathways.

From PubMed study “Mechanisms of Growth Plate Maturation and Epiphyseal Fusion

Authors: Joyce Emonsa Andrei S. Chaginc Lars Sävendahlc Marcel Karperienb Jan M. Wita

2nd resource : “LOCAL REGULATION OF GROWTH PLATE CHONDROCYTES: Molecular PLATE CHONDROCYTES: Molecular Mechanisms and Implications for Longitudinal Bone Growth” -Author: Anenisia Coelho de Andrade – Thesis for Doctoral Degree (Ph D) 2010

Analysis of the Chart to the right:

growthplatepathwaysWhat we are seeing right here is that the growth plates are controlled in each section by certain growth factors we have already seen before many times. However the fact is that we never fully tried to at least summarize all the growth factors together to make a better, more general understanding of the local regulation patterns and pathways that are involved.

Here is what we already know from our studies:

There is basically 3 main areas in the growth plate, the resting zone, the proliferative zone, and the hypertrophic zone. Some authors and medical professionals might even put a zone between the proliferative and hypertrophic zone called the pre-hypertrophic zone, as well as put the layer of ossification and calcification in, but the main idea can be summarized in three zones. The number of chondrocytes we have as the raw material is from the resting zone. From what I have gathered, that area seems to have a finite number of chondrocytes there which does not proliferate. The multiplication in number through cell division seems to happen when it gets to the proliferative zone.

The Legend or Map: All arrow heads indicate that the protein signal is promoting or up-regulating the protein is is pointed to.

The main pathway for the growth factor regulations is one which we have looked at a few times before, on posts like “The Connection Between Regenerating Deer Antlers and The PTHrP, PTH And IHH pathway for Cartilage Regulation, PTHrP Seems To Be The Answer (Big Breakthrough!)”

This is what I would call the IHH-PTHrP negative feedback loop pathway. It shows that the PThrP does two main things. The PTHrP is found mainly in the proliferative zone, as indicated by the diagram of how pathways work in the growth plate above.

  • Help stimulate, cause, or increase chondrocyte proliferation
  • Help inhibit, down-regulate, or decrease chondrocyte hypertrophy

As for the IHH, it has multiple functions and connections with other growth factors. It seems to be found in both the proliferative and hypertrophic zone, although the diagram suggest that is might be more in the proliferative zone.

It stimulates, up-regulates, and/or increases BMPs in both the proliferative and hypertrophic zones as well as PTHrP

  • Runx2 seems to stimulate the production of IHH
  • The FGFs however seems to inhibit or down-regulate the protein IHH

One compound in the diagram that has sort of caught my attention is the Runx2 protein/gene. It seems to modulate and maybe help increase the IHH, TGF-Betas, and the chondrocyte hypertrophy.

As for the BMPs, they are multiple types of BMPs, found in both the hypertrophic zone and the proliferative zone. It seems that BMPs in general help increase chondrocyte proliferation, decrease hypertrophy, and has some type of controlling role on the IHH.

In the end, we could try to describe all of the diagram in two major segments by asking the question “Which growth factors stimulate or inihibit the proliferation and hypertrophic zones?

So let’s do a listing of the two main zones.

Proliferation Zone

Stimulating/Increases:

  • IHH
  • BMPs
  • PTHrP

Inhibiting/Decreases:

  • Vitamin D
  • FGFs

Hypertrophic Zone

Stimulating/Increases:

  • Vitamin D
  • VEGF
  • Runx2

Inhibiting/Decreases:

  • Notch
  • BMPs
  • PThrP

Conclusions:

It is interesting to note that one of the posts which I felt was pivotal in the evolution of this website was the one where I initially suggested that PTHrP was probably the key growth factor we should be trying to get into our bone material to stimulate cartilage regeneration. I came to that conclusion after reading about the fact that abnormal overgrowth after study was shown to be from a high level of PTHrP expression, which happens in cancers.

What I have always believed in my personal opinion was that chondrocyte proliferation was always more important that chondrocyte hypertrophy towards longitudinal growth. Maybe Tyler would believe the opposite, since technically you grow taller in the bones only through hypertrophy of the chondrocytes, where they expand in volume multiple times. It was shown in one study that the rate of the longitudinal increase was proportional to the rate of volume increase in the chondrocytes in hypertrophy.

However I have found enough evidence to show that the real process limiting step in this multiple step process was the fact that you eventually run out of chondrocytes. From the Thesis “LOCAL REGULATION OF GROWTH PLATE CHONDROCYTES: Molecular PLATE CHONDROCYTES: Molecular Mechanisms and Implications for Longitudinal Bone GrowthThe Ph. D candidate seems to reference a study “Growth Plate Senescence Is Not a Function of Time per se but of Growth” which I would google and come up with the study “Growth-inhibiting conditions slow growth plate senescence.”

The abstract is pasted below…

J Endocrinol. 2011 Jan;208(1):59-67. doi: 10.1677/JOE-10-0302. Epub 2010 Oct 25.
Growth-inhibiting conditions slow growth plate senescence.
Forcinito P, Andrade AC, Finkielstain GP, Baron J, Nilsson O, Lui JC.
Source

Developmental Endocrinology Branch, Program in Developmental Endocrinology and Genetics, Eunice Kennedy Shriver National Institute of Child Health and Human Development, National Institutes of Health, CRC, Room 1-3330, 10 Center Drive, MSC-1103, Bethesda, Maryland 20892-1103, USA.

Abstract

The mammalian growth plate undergoes programmed senescence during juvenile life, causing skeletal growth to slow with age. We previously found that hypothyroidism in rats slowed both growth plate chondrocyte proliferation and growth plate senescence, suggesting that senescence is not dependent on age per se but rather on chondrocyte proliferation. However, one alternative explanation is that the observed slowing of growth plate senescence is a specific consequence of hypothyroidism. We reasoned that, if delayed senescence is a general consequence of growth inhibition, rather than a specific result of hypothyroidism, then senescence would also be slowed by other growth-inhibiting conditions. In this study, we therefore used tryptophan deficiency to temporarily inhibit growth in newborn rats for 4 weeks. We then allowed the animals to recover and studied the effects on growth plate senescence. We found that structural, functional, and molecular markers of growth plate senescence were delayed by prior tryptophan deficiency, indicating that the developmental program of senescence had occurred more slowly during the period of growth inhibition. Taken together with previous studies in hypothyroid rats, our findings support the hypothesis that delayed senescence is a general consequence of growth inhibition and hence that growth plate senescence is not simply a function of time per se but rather depends on growth.

This abstract thus suggest that the reason growth plates develop senescence,or aging is because they run out of chondrocytes. So this means that the step of chondrocyte proliferation or the number of chondrocytes in the resting zone are the limiting steps in the multi-step process. The reason why chondrocyte numbers in the resting zone is another rate limiting step is because of the study “Depletion of resting zone chondrocytes during growth plate senescence.”

And that is why I have felt that PTHrP is more important than IHH, since IHH promotes hypertrophy and PTHrP promotes proliferation.

Indirectly, the IHH stimulates BMPs in both zones which increase proliferation and decrease hypertrophy so maybe after more research, I may have to reverse my conclusion in this (and previous posts) but it is well known that IHH can negatively regulate PTHrP while PTHrP have always been about stimulating cell proliferation and there are no studies which show that PTHrP has any function like inhibiting anything.

As a final parting message, I would like to paste two clippings from the Medical Reference Book “Handbook of Growth and Growth Monitoring in Health and Disease” by Victor R. Preed, pge 940-941.

growthplate101growthplate102

The 32 Absolute Worst Parts About Being Tall

Taken from the media and entertainment website BuzzFeed.com.

I thought it was funny, and maybe something to think about for us who wish to be taller and think we are too short. It helps put some things into perspective and gives us the opposite side to think about. Taller people have many problems as well due to their stature, just as short people have problems due to their stature.

Tall people are literally giants among men, walking around with near total impunity, being given every advantage along the way. But sometimes the blessing can also be a curse.

by Tanner Ringerud @ BuzzFeed Staff – posted on February 18, 2013 at 11:08am EST

1. Every hug is awkward.

2. “I need someone tall to grab something!”

3. Low ceilings.

4. Beds are way too small.

5. Everyone hates you at shows.

6. You don’t fit in foreign cars.

7. People think it’s socially acceptable to jump on your back without asking.

8. Everyone expects you to be good at sports (but you’re not).

9. You’ve never actually seen your face in a mirror before.

10. Long legs means naturally outpacing anyone you walk with.

11. The deep end of the pool always leaves something to be desired.

12. Long sleeves are never long enough.

13. And pants are always way too short.

14. People ALWAYS insist you’ve grown since you last saw them.

15. One size fits all never fits.

16. Everyone asks how tall you are.

17. You haven’t been able to relax in a bathtub since you were 10.

18. Airplane seats are knee destroyers.

19. Your knees don’t fit under your desk.

20. You can never hear people at parties.

21. Getting called “Jolly Green Giant” when you wear green.

22. Everyone uses you as a beacon in crowds.

23. You’re always picked to be the goalie.

24. You always have to stand in the back of group pictures.

25. Or awkwardly crouch to get in frame.

26. “What’s the weather like up there?”

27. Public transportation wasn’t built for you.

28. You can’t swing on swings.

29. People use you for shade or to block wind.

30. Your legs are always in the way on trains, buses, and airplanes.

31. It’s always unnerving to meet people who are taller.

32. The points of open umbrellas are always right at eye level.