I recently have found more evidence that a very old post I did may have more validity than I thought back then when I wrote about it. That old post is “The Connection Between Colostrum, Growth, and Height”. it seemed that Tyler would also immediately write about the possibility that Colostrum would work when he posted something similar “Increase longitudinal bone growth with Colostrum?”

Now there is this article I found written in 2009 entitled “Colostrum Functions Like Human Growth Hormone to Reverse the Aging Process”. The article is probably written for the page to gain traffic and get ad clicks but it is still rather informative. I wrote the old article about colostrum and its potential to help people grow taller when the website was still rather new but now I am a little better informed on what is going on. 

Tyler mentioned back in that post that we should figure out what type of cytokines are in the colostrum and whether the growth factor that get ingested make it to the blood stream or does the stomach just break down growth factors and they never manage to get to the areas where growth happens.

From the article above…

Research has shown that colostrum is the one supplement that can bring help to everyone that uses it, largely because of its ability to perform many of the functions of human growth hormone (HGH) in the body.

The colostrum also has some anti-inflammatory effects on intestiinal epithelial cells.

While human mothers produce a small amount of colostrum, cows produce approximately nine gallons during the first thirty-six hours after giving birth. Colostrum is produced by almost all mammals, and is not species specific…

This means that supplementing with colostrum provides many of the benefits of HGH without the high cost or need for daily injections. It is IGF-1 that is responsible for many of the benefits provided by colostrum. Studies indicating that bovine colostrum supplementation can increase levels of IGF-1 in the body date back to 1998.

Growth factors from colostrum:

IGF-1 is a truncated form of IGF that is 10 times more potent than IGF-2 in stimulating hypertrophy and cell regeneration. It is present in bovine colostrum. (International Journal of Cellular Biology, 1996)

Fibroblast growth factor, IGF-1 and epithelial growth factor are all important mitogens for healing the skin. They are all found in bovine colostrum. (Journal of Surgery Research, 1995)

Analysis & Interpretation:

It is not a good idea to believe everything you read from the internet but this article seems to have been written by someone who knew what they were talking about. If the facts are real, then we can say that colostrum seem to have very similar properties and effects as human growth hormon, HGH. IGF-1 is also found inside colostrum.

That initial bit of cream that mammal mothers produce after they give birth to babies seem to be colostrum and this has many anti-bacterial, anti-viral properties making sure the baby is well fed and protected when it is first born. This compound seem to be extremely good for humans and for protection from pathogens and illness which stunt growth for developing children.

If I was to suggest maybe a supplement to take for people who are still growing, getting real colostrum supplements is something that I would consider to use.

Something that I found today while I was reading over an old PDF I had downloaded and put in a big folder was lecture notes from a Upper Class (or even Graduate School) university Biology course from a California State University.

The Lecture notes were entitled “Chapter 10: Postnatal Growth of Fins and Limbs through Endochondral ossification Cornelia E. Farnum Review by Susan Lujan”

The link for the website if you check the URL seems to be from a Biology 680 course (and lecture #4) by a Dr. Stuart S. Sumida from the Laboratory for Vertebrate Paleontology at California State University, San Bernardino (CSUSB)

In the lecture notes, in the section that talks about growth strategies, there is a small part where notes on indeterminate is talked about. Now, I have looked at the idea of indeterminate growth before in previous posts and noted that some animal families or orders have this property where they never stop growing in size, in length, height, weight, and size. These included the usual suspects like fish, reptiles, amphibians, etc. However there was a part where I did not expect which is where the notes seem to suggest that the cartilage in elephants may not completely go away suggesting that elephants may experience a form of indeterminate growth…

I wanted to do more research to see whether this claim that the growth plates of elephants never close true or not. So I googled the term “elephant epiphyses” to see what would appear.

Source #1: From the article “How Elephants Grow: Heterochrony and the Calibration of Developmental Stages in Some Living and Fossil Species” – V. Louise Roth Journal of Vertebrate Paleontology -Vol. 4, No. 1 (Sep., 1984), pp. 126-145 – Published by: The Society of Vertebrate Paleontology

• It states that “In elephants, ontogeny is prolonged and the period of growth is lengthy.”
• Also, in the abstract, “limb bones that complete epiphyseal fusion late in ontogeny also grow more in absolute terms”

Source #2: From a PDF by a person named Gary Haynes in the Anthropology Department in the University of Nevada, Reno entitled “One way to understand mammoths: lessons from actualistic studies of modern elephants”

• Bottom left part of Page 83: Most fractures were created by elephants trampling on elements partly buried in the surface sediments or lying atop the ground. In a few cases, spotted hyenas had first gnawed off an epiphysis, especially common with bones from elephants whose epiphyses had not fused to the shafts at the time of their death.

Source #3: From the book “Mammoths, Mastodonts, and Elephants: Biology, Behavior and the Fossil Record” (Low-ball): Gary Haynes” : Page 350:

These sources show that maybe the reason elephants get so big is because they have epiphyseal cartilage that don’t fused together even at advanged age.

From a 4th source, “The Wild Elephant and the Method of Capturing and Taming it in Ceylon”

(Low-ball): Sir James Emerson Tennent – Sketches of the Natural History of Ceylon The epiphyses were still distinct Page 125 of 295

• The researcher seems to find mammoths that at the age of around 30 years old still had distinct, and rather well kept growth plates. This made the researcher suspect that the ancient mammoths could live to be up to 150 years or even more (300 years old).

“The only attempt which I know of to establish a period historically or physiologically is that of FLEURENS, who has advanced an ingenious theory on the subject in his treatise “_De la Longevite Humaine_.” He assumes the sum total of life in all animals to be equivalent to five times the number of years requisite to perfect their growth and development;–and he adopts as evidence of the period at which growth ceases, the final consolidation of the bones with their _epiphyses_; which in the young consist of cartilages; but in the adult become uniformly osseous and solid. So long as the epiphyses are distinct from the bones, the growth of the animal is proceeding, but it ceases so soon as the consolidation is complete. In man, according to FLEURENS, this consummation takes place at 20 years of age, in the horse at 5, in the dog at 2; so that conformably to this theory the respective normal age for each would be 100 years for man, 25 for the horse, and 10 for a dog. As a datum for his conclusion, FLEURENS cites the instance of one young elephant in which, at 26 years old, the epiphyses were still distinct, whereas in another, which died at 31, they were firm and adherent. Hence he draws the inference that the period of completed solidification is thirty years, and consequently that the normal age of the elephant is _one hundred and fifty_.[3]”

Implications For Height Increase:

There is some evidence like these stories and scientific article which suggest that even though the elephant is the biggest, heaviest animal on land, it still somehow manages to keep the growth plates in its legs around for decades.

Not only that, it seems that there ie vertebrate growth plates which don’t fuse until the 5th or 6th decade of the elephants life meaning that while their shoulder height might have stopped growing keeping their “height” stable, they are still growing anterior and posteriorly into a longer animal.

The evidence for mammoths, compared to the elephants of today is even more astonishing. Some paleontologists are stating from the resources that maybe the mammoths that are found may never stop growing since their bones don’t fuse in the growth plate area.

The evidence shows many times over that the elephants may still be able to grow their bones in terms of volume even into advanced age.

What we see here is something which I didn’t think was possible, especially with such a large in weight land mammal like an elephant. However it makes sense that elephants should have unfused growth plates for so long since they do end up growing to become almost the tallest animals on land.

I had previously believed that the tissue of cartilage would not be strong enough to be able to withstand even the compressive load from the weight of a 200 lb adult human male. The cartilage would not be thick enough or strong enough to hold up that much weight without it being compressed and squeezed to the point where it disappears. This felt like common sense.

The example with the elephant, which is probably the heaviest land animal on earth really makes me rethink about what the cartilage tissue is capable of handling. The biggest elephant ever shot was around 26,000 lbs and 14 feet tall. The mammoths from the ice ages were even bigger.

I guess maybe it might be important to rethink about just strong and durable growth plates really are from the example of how long elephants manage to keep growing.

What is inside the elephant’s DNA that allows them to grow in the vertebrate even in the 6th decade of their life? That is something that the height increase researcher would be interested in knowing.

Recently I got a message or comment to the website where someone would link to a study that Tyler from HeightQuest.com had written about in the post “Reverse Ossification”

The study or article was entitled “Growth Plate Reappearance after Closure in Ankle Radiography for Trauma“

Article abstract:

Bone growth plates or physis are present at the end of long bones and are responsible for longitudinal growth. These plates consist of 4 layers and are lucent in radiography as a line perpendicular to the longitudinal axis, Because of cartilage layer x-ray absorption is less than calcified bone. Gradually increases with age and bone maturity these line will be narrower and as longitudinal bone growth stops, the line disappears. This phenomenon occurs at different ages in different bones of the skeleton but with complete maturity at the age of 19, all growth plates are closed and sclerosed. Re-appearing after closing is uncommon. We introduce two young patients in this study due to trauma have been treated for an ankle cast and the growth plates of tibia and fibula in their control X-ray was re-appeared. Subchondrel Bone Resorbtion is a known phenomenon that will occur after 6 to 8 weeks immobility in any bone. The lucent line caused by imbalance in osteoblast and osteoclast activity and bone absorption. Re-appearing of growth plates can be caused by reversed ossification and bone absorption.

Analysis

Months ago Tyler had brought the article to my attention when he asked for my help in finding some way to translate the article written in Persian/Farsi since the article was written by medical researchers based in Iran. I tried using Google Translate and Yahoo’s Babel Fish technology without success.

After getting some extra time to looking back at the study and really think over what is really going on, I wanted to make some observations about what is going on. The first thing I see is that the doctors say that “Re-appearing after closing is uncommon”

The way they word the phrase makes a person who is really intent on finding a way to reverse the ossification think that maybe the reappearance of growth plates happen a lot more often then say “NEVER”.

Are these researchers saying that they have seen growth plate reappearance before in other cases? Because I have not in any studies, medical textbooks, or journals.

Here is what I guess is really going on. The cartilage is indeed there. The X-rays they see show that the absorption rate is lower. If we look at how X-rays turn out, we remember that the calcified bones will absorb more so the color on the X-rays is much lighter, or transparent. The less absorption on X-rays turn out darker and less transparent.

What you see in the article which Tyler copied to the Post is a series of X-rays but I would say even after looking at long bone X-rays before that I can’t really see what the growth plate is supposed to have regenerated.

The picture to the right is the only X-rays where I am noticing any type of mark or fracture in the bones. If we look at the way the dark line is on the bone, I would say that the line is very straight, and not curved and crooked like how the cartilage appears in young pig ankles, which I showed in one of the website’s YouTube video HERE

At this point, I would say that the darker shade of line on the tibia area is not the hyaline growth plate cartilage coming back but something else.

That something else I am proposing is actually fibrocartilage. Fibrocartilage is what would be formed if you managed to puncture or lacerate the bone deep enough to get below the subchondrel layer of the cortical bone.

When I was doing research on the subject of microfracture surgery I wrote a post about the possibility of using microfracture surgery to grow taller entitled “Increase Height And Grow Taller Using Microfracture Surgery, Part I”

From the Wikipedia article….

Through use of an awl, the surgeon creates tiny fractures in the subchondral bone plate.^[9] Blood and bone marrow (which contains stem cells) seep out of the fractures, creating a blood clot that releases cartilage-building cells

Analysis

The principle of microfracture surgery results in the fact that the cells in the bone marrow will seep out and the progenitor adult stem cells will first differentiate into the chondrogenic lineage, at least at first.

All the physicians are in agreement that when the surgeon uses the awl to drill a hole into articular cartilage, the cartilage that is formed is fibrocartilage, not hyaline cartilage. In the procedure section on how microfracture surgery is done, the awl is a drill tool that goes pass the hard cortical bone layer and reaches to the spongy, more porous cancellous bone area where the marrow and adult progenitor cells are.

And this is what I think is really showing up in the X-rays of this document that Tyler and the other person found. That straight dark line that slices horizontally across the X-ray I am saying is more likely a bone fracture that is mostly likely filled with progenitor cells which wil turn it into fibrocartilage, not the hyaline type of cartilage the Iranian researchers claim them to be.

I wrote about a proposed idea on how we could theoretically use the fibrocartilage that is formed to increase our height at “A Proposed Height Increase Method Using Microfracture Surgery Techniques With Fibrocartilage Formation”

Perhaps there might be a possibility to combine the propose method from the post above with trauma injury type os incidents which lead to X-rays showing fibrocartilage formation. I said in the recent post that to do reverse ossification properly, we would have to have at least two major stages that not only happen at the same time, but also happen sequentially. they are…

1. One step would be to somehow remove the hard inorganic, nonliving tissue between the bone cells (osteocytes) and lacunae in the extracellular matrix of the bones. 

2. The second step would be to be able to cause only chondrogenesis (to create cartilage) to occur in the area which lost the inorganic nonliving tissue. 

Remember that ossification is where either the chondrocytes turns into osteocytes and osteoblasts or they die leaving the spaces for the osteocytes to take up later in development.

This is like how life goes. You can either turn into something else through evolution or a transformation or you die out to be replaced by something else. If you want that process to go in reverse, you would either have to figure out how to do transdiferrentiation, which the immortal hydra had figured out how to do, or you have to figure out how to reverse in the aging process, which the immortal hydra also figured out.

Since we are not talking about the entire body as an organism, but also a section of our body to regenerate back the cartilage we lost from the natural growth process, it would be much easier to first remove the dead, non-organic, hard calcium miineral deposits first. After the deposits are removed, then you replace over the now empty space with cartilage forming chondrocytes with some type of injection or growth factor mixture.

I would conclude with two things.

1. The X-rays is not showing growth plate hyaline cartilage re-appearance, but actually some type of fracture that was made by the injury. The bone is cracked and maybe some other body tissue has gotten into the bone cracked region.

1. If the X-rays is not a fracture, but actually cartilage, then it is not the hyaline cartilage we are looking for, but actually fibrocartilage that has seeped out of the cavity and the trabecular bone from the inside.

Let’s look at what is stated in the beginning of the young kids who are getting their X-rays looked at.

In recent news for the last week, there was reports coming out about the fact that a team of researchers in Oregon (Oregon Health & Science University) managed to be able to produce stem cells from cloning human embryos for the first time.

NBC News: Cloning technique produces human stem cells for the first time

What I wanted to talk about in this post is just how this type of news, about the fascinating new branch of biomedical research, will possibly effect the height increase endeavor for the coming years and even decades.

First, what is the endeavor of even doing stem cells research in the first place, at least for this group of researchers?

Answer: “…use cloning technology to make human embryos and grow stem cells from them in the hopes of making perfectly matched grow-your-own tissue transplants.”

The article writer goes into a very superficial description of what the researchers did with….

“They used a human egg cell and parts of a human skin cell to grow a very early human embryo, then transformed cells from this ball of cells into beating heart cells and skin cells. The process may eventually help treat a range of diseases, from Parkinson’s to rare inherited conditions, they reported Wednesday…”

The scientific abstract they referenced to from the journal Cell was “Human Embryonic Stem Cells Derived by Somatic Cell Nuclear Transfer”

Cell, 15 May 2013
Copyright © 2013 Elsevier Inc. All rights reserved.
10.1016/j.cell.2013.05.006

Authors

What we are seeing is that

Something to note here is the term “Oocyte”. From the Wikipedia article on oocytes…

An oocyte, oöcyte, ovocyte, or rarely ocyte, is a female gametocyte or germ cell involved in reproduction. In other words, it is animmature ovum, or egg cell. An oocyte is produced in the ovary during female gametogenesis. The female germ cells produce a primordial germ cell (PGC) which undergoes mitosis to form an oogonium. During oogenesis the oogonium becomes a primary oocyte.

Analysis #2:

Let’s go back to the scientific article that was cited, Human Embryonic Stem Cells Derived by Somatic Cell Nuclear Transfer

Summary

Reprogramming somatic cells into pluripotent embryonic stem cells (ESCs) by somatic cell nuclear transfer (SCNT) has been envisioned as an approach for generating patient-matched nuclear transfer (NT)-ESCs for studies of disease mechanisms and for developing specific therapies. Past attempts to produce human NT-ESCs have failed secondary to early embryonic arrest of SCNT embryos. Here, we identified premature exit from meiosis in human oocytes and suboptimal activation as key factors that are responsible for these outcomes. Optimized SCNT approaches designed to circumvent these limitations allowed derivation of human NT-ESCs. When applied to premium quality human oocytes, NT-ESC lines were derived from as few as two oocytes. NT-ESCs displayed normal diploid karyotypes and inherited their nuclear genome exclusively from parental somatic cells. Gene expression and differentiation profiles in human NT-ESCs were similar to embryo-derived ESCs, suggesting efficient reprogramming of somatic cells to a pluripotent state.

Interpretation

What we see is that this experimental study somehow managed to figure out around the decade old problem on how to create stable human nuclear transfer-embryonic stem cells (NT-ESCs)

As states in the introduction of the article…

In humans, SCNT was envisioned as a means of generating personalized embryonic stem cells from patients’ somatic cells, which could be used to study disease mechanisms and ultimately for cell-based therapies (Lanza et al., 1999; Yang et al., 2007). However, the derivation of human nuclear transfer-embryonic stem cells (NT-ESCs) has not been achieved despite numerous attempts during the past decade. The roadblock responsible for failure is early embryonic arrest of human SCNT embryos precluding derivation of stable NT-ESCs. Typically, SCNT embryos fail to progress beyond the eight-cell stage, presumably due to an inability to activate critical embryonic genes from the somatic donor cell nucleus (Egli et al., 2011;Noggle et al., 2011)

After noticing in lab rhesus monkeys that their fibroblast skin cells could be reprogrammed into the NT-ESCs they were looking for so they state “…Therefore, we reasoned that, similar to other mammals, human MII oocytes must contain reprogramming activity.”

This is where they got the idea of using the very early stage of the ovum right before fertilization and removing the nucleus for its reprogramming activity.

For the researchers who are going to use the stem cells that make tissue for medical reasons , I agree with the general idea that the best option for people is to become their own donors since it seems that it is much harder for some people to find that perfect donor for them.

As stated in the article….

“…using a patient’s own cells offers potentially huge advantages. “A lot of patients don’t have an optimal donor,” he said. So bone marrow transplants are done only for the patients in the most dire need.

“If we could make every patient their own donor … we would bypass the transplant barrier,” he said. “Everyone could be a donor for themselves.””

Implications For Height Increase Research:

We found that from our bone marrow, which is what is inside the long bone intermedullary cavity, some types of stem cells which have limited differentiating ability. They can differentiate into chondrocytes if we really focused on just finding the right growth factors to induce them into the chondrogenic lineage, although it seems that most growth factors are both osteogenic and chondrogenic. If we can get the stem cells ,in say the epiphysis or diaphysis, to turn chondrogenic, there is still not enough time for them to form the cartilage tissue needed to expand and push the bones longitudinally before turning into the osteblasts and osteocytes. The recent news about this group of university researchers in oregon makes me think about the possibility of injecting the newly created stem cells using somatic cell nuclear transfer into human bone for to form cartilage tissue or growing the blastocytes derived into epiphyseal hyaline cartilage. This approach may be the easiest way to make real growth plates in the lab using non-controversial methods like taking the pluripotent stem cells from embryos.  

Sometimes it really surprises even me just how common the desire to become taller is, even among the best, most talented, most accomplished, and most beautiful humans on earth. I had written about the fact that the immensely popular, international Korean singer Boa had expressed constantly her regret in not drinking enough milk when she was younger and desiring to be taller in the post “Korean Singer Boa Is Dissatisfied Over Her Height”. I was reading the news on CNN and the story of this olympic medalist japanese figure skater named Daisuke Takahashi appeared which got me interested. It seems that for this Japanese young male, he really cares about how he looks and seems to have some type of insecurity over how he looks compared to other people, even after all he has accomplished.

I will be only taking a small section of the full article to show where he talks about his desire to become taller.

CNN Article: Daisuke Takahashi: Japan’s golden boy on the importance of being ‘gorgeous’

Despite his success — he also won silver at last year’s worlds — the 27-year-old admits he still looks up to his rivals.

“I never thought I have anything special. I’ve always thought about what I don’t have compared to other skaters,” he says.

“I tend to think like other skaters get more applause than I do. I constantly think about ways I can level up, and I’m often jealous of other skaters,” he adds, laughing. “When I see someone’s cool performance, it makes me want to be like them, and that’s what motivates me.”

A big part of figure skating is the outfits — often elaborate lycra creations that might otherwise seem more at home in a musical stage show.

“I don’t have long legs and arms, and I am … short,” quips Takahashi. “So I want something that makes me look taller and with longer legs and arms.

“I want something will make me a bit bigger, and so something with flaps that give my arms a little flow.”

I guess the thing to really understand is that maybe this desire to become taller is something that people wish for because they are constantly comparing themselves to other people and go through cycles of feeling inadequate, unattractive, jealousy, and competitiveness.

This innate desire to always be comparing ourselves to other humans to see who is better off, in terms of all the measurable (and non measurable) qualities that make life better may be something that can not be turned off. Insecurity runs in almost everyone expect the most secure people with the highest levels of self esteem. Maybe the reason why we all seem to want to be taller is because we can’t fully accept ourselves with who we are and when we look at our naked bodies in the mirror, we feel only disappoint.

However, would being taller solve all of our self esteem issues? If we did find an alternative solution to become taller than through limb lengthening surgery, and we had the procedure done to us to make us into the height we desired, would that stop our madness to want to improve ourselves and keep growing (figuratively)?

I don’t know what Daisuke Takahashi is thinking in his head, and can only guess at the possible reasons on why he wishes for his limbs to be longer. He says that with having longer limbs he would be better looking. All I wanted to say is that this young man who is loved by his nation and admired throughout the world still wishes to become better looking by being taller.

I guess height is something that will always be valued and strived for.

This is one of those articles which I realized that had to be written at some point to make sure I was complete and thorough in all of my research. At this point it is rather obvious for the long time visitor that if we had the ability to use the grow taller treatment when we still had open growth plates known as growth hormone injections of growth hormone therapy, most of us who tried would have ended up with a taller final height.

I have NOT written extensively about the possibility of using growth hormone therapy and treatments to make children who have short stature (below average stature in their age range) which is the result of growth hormone deficiency to make them taller. Instead, I have probably written more about growth hormone secretagogues than the actual growth hormones that are around. I have written about growth hormone segretagogues in the post “What Are Growth Hormone Secretagogues?”. It has been shown in many studies and experiments that not just growth hormones, but also the growth hormone secretagogues would also cause increased growth rates and adult height.

One thing that the general public doesn’t know is that the pituitary gland that is releasing the GH is also responsible for releasing a few other types of hormones that control the endocrine function of the body. The pituitary gland releases both the growth hormone, which is known as somatropins or somatotropins and also the compound known as somatostatins. Both of these seem to be from the anterior region of the pituitary gland.

Something to note is that there is both synthetic and natural growth hormones. The growth hormones that are taken from human cadavers is known as just hGH and the growth hormone made from recombinant DNA technology is known as rhGH.

There is probably over dozens of PubMed Studies which show that injecting growth hormones like Humatrope, Somatropin, Nutropin, and Genotropin in a young child who is still growing with open growth plates will lead to them developing a higher growth rate and end up taller when they finish growing vertically.

Only 5 studies are chosen to be listed below. The main point is that for some people, getting injected with growth hormones will make them taller.

1. Effect of growth hormone therapy on height in children with idiopathic short stature: a meta-analysis.
2. Effect of growth hormone treatment on adult height of children with idiopathic short stature. Genentech Collaborative Group.
3. Growth velocity, final height and bone mineral metabolism of short children treated long term with growth hormone.
4. Final height after combined growth hormone and gonadotrophin-releasing hormone analogue therapy in short healthy children entering into normally timed puberty.
5. Adult height in short normal girls treated with gonadotropin-releasing hormone analogs and growth hormone.

If the reader would prefer to read over the abstracts, they would also notice that growth hormone therapy can in improved upon by combining the injected growth hormone with another type known as gonadotropin-releasing hormone analogs (GnRHa). From the 5th source…

“…the combination of GH and GnRHa is significantly more effective in improving adult height than GH alone in girls with idiopathic short stature, early or normal onset of puberty…”

The values for final height increase is very noticeable.

• With GH alone – around 6 cms
• With GH and GnRHa together – around 10 cms

The amount of GH & GnRHa used is around 100 microg/kg or 10 g/L (for the GH standard dosage). The dosages were given around every 2 weeks for years, usually a 3-5 year range until the child is getting close to full bone maturity, which is when over 1 years time, their height increased only 1 cm or less with the bone age (BA) usually over 15 years of age.

The first paper was insightful in showing just how much more growth can be achieved by a child who is given the treatment over a controlled group without the therapy. On average, the increased growth was about 1 extra inch of height increase every year. On average, the total extra height gained was 2-2.5 inches of extra adult height from using the growth hormones. When the cost is calculated out, it is shown that extra inch of height gained from therapy is actually around an extra $35,000 each time.

However there are studies which seem to show that for these kids, the therapy does not mean that they will be able to push past what their body was genetically programmed to reach. The 3rd study seems to conclude with the opposite point.

The study concluded with “…We conclude that combined rhGH and GnRH analogue therapy in short adolescents with normally timed puberty does not contribute to increase their final height above their pretreatment predicted adult height…”

Some height increase researchers have argued citing research done like the study above that it is not that everyone will end up taller from getting excess GH release, but that only people who are already suffering from the genetic pathology of having the growth hormone deficiency disorder will have their height increased. The deficiency may not just be about growth hormones but other types. It would also include certain types of disorders that result in short stature like Turner’s Syndrome and IUGR.

I actually have to disagree with their point when we see what happens to people like Tanya Angus or Sultan Kosen. If the GH is not making these people taller from the pituitary gland suffering hyperplasia, then what is causing them to get taller?

We can see from Angus’s case that before she was suffering from the metastasizing pituitary tumor, she was already at a respectable 5′ 8″ tall, a good height to be at for the average statured American female. From an endocrinological point of view, she was not suffering from any type of growth retardation endocrine diseases when her abnormal grow started when she was around the age of 18. It was clear that she never suffered from any type of growth hormone deficiency. When her tumor pushed the pituitary gland into hyperplasia, GH was increased over 10X, and she grew. If a person who does not suffer from growth hormone deficiency develops a pituitary tumor, no matter how much the tumor is causing excess GH release, they should not be increasing in height, only maybe muscle mass and increased energy, since it is seen that GH is also touted as the hormone that is supposed to be good for anti-aging and age reversal properties.

However Tanya Angus did get taller around the age of 18, from the height of 5′ 8″ and her tumor kept pushing GH throughout her body.

It would be easy to rebuttal the conclusion of the last study with another study…

• Effects of combined gonadotropin-releasing hormone agonist and growth hormone therapy on adult height in precocious puberty: a further contribution.

This study noticed that for girls who don’t have growth hormone deficiencies but do notice precocious puberty, their height was increased up to 12 cms if they used a combination of growth hormones and GnRHa

Then again new findings like “High dose growth hormone treatment induces acceleration of skeletal maturation and an earlier onset of puberty in children with idiopathic short stature.” seem to shift the overall physician’s opinion back to the idea that maybe GH treatment is not as good as we think…

“…Long term growth hormone (GH) treatment in children with idiopathic short stature (ISS) results in a relatively small mean gain in final height of 3-9 cm, which may not justify the cost of treatment. As it is unknown whether GH treatment during puberty adds to final height gain…”

There is a gain, but the gain is around 1-3.5 inches in extra height. Is the height increase really worth that much money they ask? It would seem that if the child gets the GH therapy for too long, the bone age and bone maturity can be advanced so far that it can cause precocious puberty, meaning the amount of time left to grow is decrease.

Some articles are actually agreeing with this idea like “High-dose GH treatment limited to the prepubertal period in young children with idiopathic short stature does not increase adult height” confirm this new opinion. It seems that compared to controls, the GH therapy doesn’t really make the final adult height increase a lot, especially when the therapy is taken off. It would seem that the growth rate actually decreases to below average if the growth hormone is stopped being added.

So now I am fully confused. Does growth hormone help shorter kids really end up taller than if they didn’t use the therapy, or is the increase so little that the cost of the treatment is just not worth it?

The 3rd study seems to make a good overall conclusion about the results. “…We and others have demonstrated a clear increase in their growth velocity short term, but improvement of their final height remains unclear and controversial” The thing to really take away from this post is that maybe the GH and GnRHa is only good for the first few years, but then have no effect towards increased longitudinal growth of the bones, meaning that the overall final adult height is not really increased that much, if at all.

The entire point of all 5 studies can be summarized by the conclusion made in the 2nd study by the Genentech Collaborative Group which was published in 1999…

“Long-term administration of growth hormone to children with idiopathic short stature can increase adult height to a level above the predicted adult height and above the adult height of untreated historical control children.”

As for other applications and whether the growth hormone therapy would work to cure other causes for idiopathic short stature, there has been studies that say that they can. These include

• hypophosphatemic rickets
• osteogenesis imperfecta
• intrauterine growth retardation (IUGR)
• Turner’s syndrome

For some of these disorders, the increase in height can be as dramatic as 12 cms (or almost 5 inches!)