Here is something that I recently found which will help a large percentage of people which will let them gain about half a centimeter in increase height quite quickly. Something which I have always believed is that getting exercise which can remove the load on our backs and vertebrate bone will lead to some height increases.

I was watching this Youtube video by Dr. Dror Paley when he mentioned the fact that one of the things he does when he is performing surgeon on his patients, but most especially the ones suffering from Dwarfism, or Achondroplasia, is to correct the hyperlordosis that is often most visible in people suffering from dwarfism.

Refer to the Youtube Video “Achondroplasia A Guide For Parents By Dr Dror Paley.mp4”. Notice how the lower back area is curved towards the posterior direction.

When the surgery is being doing, the femur is pushed backwards during the lengthening of the lower limb bones.  Somehow it straightens out the pelvis, and by doing that, it also straightens out the spine.

The surgical part probably doesn’t seem that interesting but the surgical methods doing in the OR doesn’t always have to be. The thing is that if we can look at our own vertebral curves in an X-Ray, almost all of us have the lower back area curved a little. We can do something in our normal lives to possibly correct for those things with some serious dedication.

The study that proves that this exercise would indeed increase height, at least temporarily  – Spine Height and Disc Height Changes As the Effect of Hyperextension Using Stadiometry and MRI

So there are 2 things you can do to correct for lordosis

Part 1

Before the first video, I would like to remind people that I wrote a post maybe a year ago showing that I had found another scientific article showing that the Supine Flexion Exercise would also work to help decrease the load in the back. Refer to the post “Restore Spinal Disk Height And Increase Height Temporarily Through Land Based Supine Flexion”

Part 2

You will need to go to the local gym and use the device which is above. It is known as the Hyperextension Exercises. The machine you will need is found in almost any local Gym. It has no moving parts. You just lie down on it, stomach facing the ground. You just use your lower back muscles or the core muscles to raise the upper torso/body upwards against gravity.

The benefit of these two types of exercises will be more than just a slight increase in height. You will also notice that your mid-section will become smaller, and if you are a guy, a 6-pack of abs. Having a strong back and core from repeated using this gym machine will over time give

I think it was more than 6 months ago when I found certain publications that Dr. Dror Paley had done research to find the effects of IGF-1 on lengthening of muscle. Refer to the post How Muscle Tissue Is Lengthened – Bone Lengthening Will Not Be Limited – Breakthrough!. In that post, I had revealed a Grant that Paley along with other limb lengthening surgery surgeons had proposed to study the effects of using IGF-1 during distraction osteogenesis surgery. (IGF-1 Gene Therapy of Muscle during Distraction Osteogenesis)

In that post, I had proven that the limitation that certain posters on the online forums have set forth, on the inability of muscle tissue to stretch, has also been worked out and had the technical problems resolved. The muscle factor has now been considered and worked around.

What I would propose fro Paley’s research is a personal theory. Here it is…

It might be that IGF-1 does not really help make the growth plates grow thicker and have the chondrocytes proliferate more. What might actually be happened is that the IGF-1 is having the most affect on the muscle tissue surrounding the growth plate, while it is still active.

If we assume that the IGF-1 which is injected into the leg close to the growth plate makes the muscle tissue in that area thicker, which I believe right now could translate to mean longer, then the tension on the bone in the center would decrease.

If we remember the studies which show that “periosteal stripping” would increase the rate of bone longitudinal growth, the surgeons who did those tests more than 100 years ago had suggested that if you just remove the elements that hold the growth plates in place (ie periosteum layer) then the inhibitory factors would be removed, allowing the functional growth plate to expand much more than expected.

If the periosteum is one of those factors, acting like a tough raincoat wrapped around the body which doesn’t allow the growth plate to push outwards, then the muscles which are bound in a certain length could be thought of as the other major factor (maybe also the ligaments and tendons that are connected to the bones might have also an effect).

Since the IGF-1 would increase the muscles, and thus make them longer, as Paley suggested, maybe the growth plates would feel less inhibited by that factor, and the bone in the middle of a limb grow longer as a result of the growth plate having the chance to push outwards a little more.

Comparing “races”: Based on the idea that different “races” have different levels of IGF-1 that is stimulated during puberty, I would even make the guess that the people who are African Americans have increased IGF-1 stimulation compared to the other race groups. (Refer to “Growth Hormone and Weight Gain in African-American Girls“) Studies show that the african american community have around a 15% increased rate for developing Diabetes Type II since the African American children have higher blood insulin levels.

From the study “Relationships Between IGF-1 and IGFBP-1 and Adiposity in Obese African-American and Latino Adolescents” I refer to the following passage…

” It has been shown that Latino and Caucasian prepubertal females have lower IGF-1 levels compared to African-American females (16,20). Other studies have reported positive correlations between total body fat and IGF-1 concentrations in Caucasian children (21,22) and our laboratory demonstrated a positive relationship between IGF-1 and body fat in African-American and Caucasian children that was not explained by diet, physical activity, socioeconomic status, or adiposity”

Does that mean then African American’s would end up taller than other races since the IGF-1 level is slightly higher? Not really, since we need to realize that the natural physiological way for IGF-1 to even be developed is for it to be converted from HGH in the pancreas. HGH does make the chondrocytes in the growth plate divide faster, but the HGH also speeds up the senescence and maturity of bone. Also, IGF-1 can also be sourced from other areas of the body besides just the organ where HGH had the transformation.

So at the same time IGF-1 would cause the muscles to “loosen up”, the elevated GH levels in the system would also speed the body towards ossification. This phenomena is noticed when we see the data showing that on average, African American Females start puberty about 0.5 years earlier than their Caucasian American counterpart. However, the age at which the body stops getting taller would also be earlier as well.

Mathematically speaking, if we say that the duration of puberty is the same for black and white adolescent, from 10.5-17.5, and 11-18 respectively, then it would mean that the ‘white’ groups would on average end up slightly taller, since they had about an extra 1/2 of a year to grow on average. Then when we add in the factor that elevated IGF-1 rates might give the growth plates more growing potential during a short duration of time (from having one of the inhibitory factors removed), in the peak puberty years, then it might turn out that on average, “white” and “black” americans would end up almost exactly the same in height when we average out the entire population and truncate the outliers.

The end result is that while the adult height for the two ethnic groups eventually end up to be almost the same, the adult African American ends up having a higher BMI from a higher adult weight, which is positively correlated with the levels of IGF-1 as detected when they were still an adolescent.

The more research I do on the possibility of getting the Lab grown cartilage implantation to work, the more and more it seems that the possibility is more and more true. I recently found another article showing how researchers in labs around the world have gotten the cartilage to be grown, and quite easily, using 90s printers. (source: http://www.nytimes.com/2013/08/20/science/next-out-of-the-printer-living-tissue.html?pagewanted=2&_r=4&ref=todayspaper&)

A Daryl D’Lima, who is the head of an orthopedic research lab at the Scripps Clinic, has already succeeded in getting bio-artificial cartilage from extracted bovine tissue.

First, he and his team succeeded from getting an old inkjet printer (a 1990s-era Hewlett-Packard printer, a Deskjet 500, with bigger nozzles, a thermal inkjet printer) to put on layer upon layer of a gel containing the cells that cartilages are composed of. The ideas was to replace the ink in the cartridges with their cartilage-making mixture, which consisted of a liquid called PEG-DMA and the chondrocytes. (This I am assuming is from bovine sources).

Second, he and his team have also gotten some bit of cartilage that have been extracted from people who have already gone through knee replaceent surgery.

Like any good researcher, he is cautious in his optimism, and the speed at which his research in the lab will be viable to be placed in the market for the general public to use. Technically speaking, the process might still need to be perfected a little, but it seems most of the challenges at this point is beauracratic in nature, (ie conduct clinical trials, and getting regulatory approval)

D’Lima’s hope is to have just a printer in the OR one day right next to the surgeons. It will… “custom-print new cartilage directly in the body to repair or replace tissue that is missing because of injury or arthritis…”

This device that D’Lima’s team have build is not really like the 3D Printers that are conventionally used in manufacturing companies like PLA and ABS. This bioprinters print cells, but what is actually extruded through the extruder head is a gel or liquid medium. The gel medium would eventually act like the extracellular matrix of the cell, and that eventually turns into living tissue.

When we look closer at the possibility of pushing the cells in the gel medium through the 3d bioprinter’s head without killing the cells, it seems that the cells did indeed survive. The heat pulse was so rapid that most cells survived the process. (Important thing to remember: There is actually two main ways to get the tissues made. The 2^nd approach on making living functional tissues involve starting with a scaffold first and then adding cells into it.)

The advantage of using a bioprinter to print layers of gel and cells on top of the previous layer is that with the bioprinter, it can control the placement of the cells to be similar to cell layout and overall cell structure and aligment of natural cell arrangements. Remember that to have a cartilage to work like a natural growth plate, the cells (chondrocytes) will need to be stacked on top of each other in a “column” like structural alignment.

What we do have in terms of bad news is that we probably will not have the bioprinters making functional hearts in a few years though. That might take more like 20-30 years. The company Organovo is mentioned again. Thomas Boland, a researcher at the University of Texas has still been able to say that the future is in regenerative medicine.

It does however say that when it comes to the cartilage tissue, it is much easier to bioprint than most other tissues. Dr D’Lima says the following “… cartilage might be the low-hanging fruit to get 3-D printing into the clinic”

The reason why cartilage tissue is easier than the others is because it is simpler. The chondrocytes in the ECM is actually quite low maintenance. The cells don’t get their nutrients through blood vessels, but through diffusion through the ECM.

Here at NHGH I will be the first person to acknowledge that what Dr. D’Lima is trying to create is articular cartilage for the ends of bones, not epiphyseal cartilage types, although at the structural level, they are the same thing. Articular and Epiphyseal cartilage are both hyaline cartilage. We want to get epiphyseal type hyaline cartilage created, which will be implanted between two bone segments.

The natural growth plate or epiphyseal cartilage does seem to get its main source of nutrients from blood vessels, that run to the epiphysis and the metaphysis. That might be a technical challenge if we tried to shift the expected functon of the cartilage we are bioprinting to not just stay in cartilage form (for treating articular cartilage damage due to osteoarthritis) but to eventually grow volumetrically and push overall to become longer and make bones longer.

What is good to know however is that the body naturally produces chemical signals that would cause the local area of an osteonomy (bone cut) to start to develop vascularization. Over time, blood vessels will automatically grow into the cartilage implant. This process is however slow.

I was driving home today and heard over the radio that there was news that a certain Dr. Karl Michaelsson in Sweden conducted a very large observational study to try to get the definitive answer on whether drinking milk does help make bones stronger or not. After looking at the carefully tabulated data of more than 100,000 subjects who took careful notes of their life over time, it seems that drinking more milk over a 20 year time span does NOT make the bones less likely to fracture.

This would seem to be going against what we were taught as little kids. The idea was that drinking milk was supposed to make young children taller and make the bones stronger. So far, we have proven that the correlation between young kids drinking milk and them ending up taller as adult is extremely weak. Now it seems that the claim that milk should make the bones stronger has also been sort of disproven.

Refer to the article written a month ago http://www.telegraph.co.uk/health/healthnews/11193329/Three-glasses-of-milk-a-day-can-lead-to-early-death-warn-scientists.html

Other Sources –  http://www.washingtonpost.com/news/to-your-health/wp/2014/10/31/study-milk-may-not-be-very-good-for-bones-or-the-body/

From what I could get out of the radio, drinking 3 glasses of milk a day doesn’t decrease the chances of fracture, and may in fact cause the person to die earlier. For women, the risk of fracture actually increases.

The theory proposed by Dr. Michaelsson on why this is is the following – The two types of sugar in milk, glucose and lactose, seem to cause the human body to go through even more oxidative stress. Oxidative stress is supposed to be one of the main causes for the human body to go through aging/senescence.

It turns out that when we were babies first coming out of our mothers, the first source of food was our mother’s breast milk. That breast milk had a lot of lactose in it. However, the new born baby as the lactase enzyme in the body to break down that lactose sugar. Over time, as the human develops and grows older, the level of lactase in their bodies seem to drop at a dramatic rate. In some countries like Asia, the level of the lactase enzyme is so low that people develop the condition “lactose intolerance”. The just don’t have enough of the enzyme in their body that is specifically used to break down the lactosse sugar found in milk and other dairy products.

What was shown was that instead of milk, hard cheese seemed to be able to decrease fractures. The difference between why hard cheese is effective and milk is not seems to come down to the fact that hard cheese has less levels and concentrations of lactose.

Conclusion

The first thing to realize is that drinking more than average milk does NOT decrease fracture incidences. In fact, it might have the opposite effect. This point is further validated by the PubMed Study “Milk, dietary calcium, and bone fractures in women: a 12-year prospective study.”

What has been traditionally believed is that calcium is something that is desired for a developing children who is still growing taller. In the medical textbook that I have been reading, it seems that to have a developing child to be growing at their optimum level, they should be adding around 0.5 grams of extra calcium into their body everyday, and most especially during the puberty years, when they get their huge growth spurts, which should be around 1 gram of extra calcium each day

The reason milk doesn’t work in strengthening the bone is guessed by the researchers to be the negation of the effects of the calcium by the fat content in the milk.

Based on what I do know, it would still not be a good idea to stop giving the developing human child milk. Getting a reasonable amount of milk into a child is still somewhat important.

It might be that bovine derived milk is not completely compatible with the human stomach bacterial ecosystem. However, it does have some type of negligible effect.

Final TIp: Based on our research for the last two years, I am happy to tell the person who is worried about or suffers from low bone mineral density that they should instead look into a much better BMD(Bone Mineral Density) stimulant. –  Sclerostin Inhibitors (Refer to study “Sclerostin inhibition for osteoporosis–a new approach.”)

After writing the recent long post about the fact that articular cartilage can go back into growth more from increased HGH stimulation after growth plate closure, I thought I would leave a real formulation which will definitely work to make the interested reader taller.

If the reader is rich enough, I would tell them to get the following three compounds.

1. Real Human Growth Hormone
2. Relaxin
3. Growth Differentiation Factor-5

The last 2 years of my life dedicated to the pursuit of this knowledge has made me realize that this formulation of 3 compounds, when you inject it into your feet area, will cause the bones in the feet to loosen up, and then grow wider through periosteal appositional growth. The end result is that the feet bones now have more layers of bone and when the patient stands back up again, the overall skeletal structure has been “lifted” up slightly.

In addition, one would also have to keep their feet elevated for more than 6 months, while at the same time stretching the feet from the ankle area in a physical therapy type of situation.

The result would be a noticeable few millimeters or even 1 centimeter of increase. This formulation would absolutely work.

As always, all 3 chemicals are extremely hard to obtain, being very expensive. The normal person might be able to get their hands on real HGH these days, but the other two, I have no idea.

This is probably the first really long post I have written in maybe 2 months. However, there have been an accumulation of new evidence suggesting that for some people even in their mid-20s, after full epiphyseal growth plate closure, could notice height increases, but at a smaller level.

So why do I now believe in this theory which goes against everything that the medical literature claims?

The first thing is that I have finally gotten around to reading this book “Bones and Bones, 2nd Edition” by Weinmann and Sicher for the last 4 months on my desk which I only cracked a few times. Tonight I took a really close look at what the medical authors wrote in the section on abnormal pituitary stimulation causing gigantism and acromegaly.

From page 210 to 228, the focus was on the overproduction of hGH from the pituitary gland. The stuff on Gigantism wasn’t too helpful, but the stuff written about Acromegaly was.

If the readers would ever buy the book, on page 214 I quote the following sentences….

“The elongation of the hands and feet is often first noted by the patient since he is forced to buy larger gloves and shoes….Probably the fact that each digit in the hand and foot consists of four segments (three in the thumb and big toe) is responsible for the considerable lengthening of the digits by small increments at the articular ends”

“Although increased endochondral ossification of the articular cartilages cannot contribute significantly to the length of the humerus, femur, or similar long bones, an accumulation of small increments on seven sites on the three-phalangeal digits will result in marked elongation…”

The authors would then go on to notice that the excess of HGH in adulthood would cause the thorax area of the chest to become distorted, since in the adult human, the thorax/chest area is still fibrocartilage. HGH can make even fibrocartilage get wider/go into hypertrophy.

As for the irregular vertebral bones, the HGH release causes the bones to grow thicker, growing periosteally, on the anterior and lateral sides.

Along with the bones, the discs between them also get wider.

However, the fibrocartilage next to the discs differentiates, especially at the periphery of the disc and adjacent to the bone, into hyaline cartilage!

As the author, says “Thus, a new site for endochondral ossification is established, which creates a spur and a shelflike hyperostosis at the edges of the vertebral bodies.” Of course, we need to realize that they are talking about bone growth in the horizontal direction, not vertical. However, that doesn’t mean that there is no stimulation for the hyaline cartilage to also push against gravity in the vertical direction.

The last thing to realize is that for people who suffer from acromegaly, their mandible jaw bone over time starts to grow and become longer. That is because of the synovial joint in the area which the zygomatic cheek bone bridge meets the temporal bone with the mandible That is known as the Temporal-Mandibular Joint, or the TMJ. On a related note, it seems that the surgery of limb lengthening is done quite often to the TMJ area to make it longer (why, I don’t know)

So here is what the reader should take away. The following points…

• Even after the long bones have no “growth plates”, growth will still be going on everywhere else, including even the organs inside the body.
• Acromegalic people notice that their fingers and feet seem to get wider and longer, similar to how pregnant females notice the same thing
• The fibrocartilage in their IVD area changes into hyaline cartilage!
• The slight bit of articular cartilage also starts to go into over-activity.
• When it comes to fingers, they will continue to get wider and longer
• The TMJ jaw area of the person which never ossifies slowly makes the person’s skull “longer”

What is most surprising to me is the statement made that the fibrocartilage tissue differentiates into hyaline cartilage! And also remember, that between the fibrous and collagenous type of tissue in the discs and the vertebrate bone, there will always be a very, VERY thin layer of hyaline cartilage tissue, usually only at the thickness of say 3-5 cells across.

Now, let’s take a look at a well known case of a person who became tall due to overactive pituitary gland function. Anthony Robbins. He recently did a video interview with Lewis Howes to promote his first new book in 25 years, dealing with Money, Investing, and how to take control of one’s finances. I clipped one picture from their interview (to see the interview, Click Here).

While I was listening to the interview, I couldn’t help noticing how much bigger Robbin’s head was compared to Lewis’s. Lewis is probably around 6’5″- 6’6″ and Tony is well known for being 6′ 7″. However, Tony doesn’t look proportional. His skull, his upper chest/torso area, and his hands are abnormally large, but the length of his femur/upper leg is disproportionally short. Lewis in comparison looks very proportional.

This reveals (and validates) something which I have theorized for a long time, but may never be proven.

I don’t know anything about Anthony Robbin’s biological father, but I would say that he was not genetically not pre-programmed to end up super-tall, unlike Yao Ming or Shaq, who had tall parents and grandparents. He said he was only 5′ 2″ as a 15 year old kid. The HGH that caused his body to grow seemed to really make his head, torso, and hands, and feet bigger.

That means that when it comes to the long bones, the effect they have didn’t do as much as to the irregular bones.

I remember once theorizing that the disproportionate torso/leg ratio of Michael Phelps was because of his eating habits. For a person who ate a lot as a kid, their torso/leg length ratio would increase.

Now, compare that to a person who was not a big eater as a kid, but still ended up tall, like most NBA players. NBA players are notoriously well known for being “long” which means that their legs, and their arms are super-long, compared to their height. If you look at an old interview with Yao Ming and Tracy McGrady together, you would notice that Yao is 1 foot taller than Tmac when sitting down. That means that for a person like Yao, his height came from his torso mostly, which explains why Yao was known for abnormally short arms, with a wingspan of only 7’4″-7’4.5″. For Yao, his limbs were short.

So I will reiterate my theory again.

• People who are genetically pre-programmed to be tall get their height from their long limbs (arms and legs)
• People can change their pre-programming a little to become taller as adult by eating a lot as a kid, to change the length of their torso relative to the length of their legs, which are more or less set by the height of their “genetics”

Now I am not saying that Robbins was a big eater when he was younger. He probably wasn’t since he lived in a very poor family. His height came from this “gift from god” or stupid luck.

Of course, when it comes to Gigantism, I could play Devil’s Advocate and show another case, Elisany Da Silva, who would attribute her height from the lengthening of her limbs, not her torso. However, I would counter-argue that the proportionality is determined by the age at which the onset of overactive HGH started.

Getting back to the subject, I once wrote a post here on Maurice Tillet, the French Angel, who was actually quite short (5’6″ maybe) but developed acromegaly. The argument I made back then was that Tillet didn’t get any taller even though HGH was overactive in his system, to show that HGH stimulation after growth plate closure was not possible. Now, I am reversing my opinions, but only to show that there are exceptions to the rule. However, I suspect that his acromegaly started later in his life. There is a time limit for when HGH is no longer effective, and it is not at the point of growth plate closure, but some time after it. 

Why would I claim this idea? Well, the body of a 30 year old and a 23 year old is very different. I suspect that even at the age of say 24 or 25, even after the growth plates are supposedly “closed” a person who gets a high enough HGH stimulation would find that they would be able to increase their height, but only by as much as 1-1.5 inch though.

The human body is not a fixed entity, similarly to a bone. It is possible to shake the body to made certain biochemical physiological processes to accelerate enough to cause dramatic changes in the body. The very fact that my own girlfriend of the last two years would say that she grew 1 cm makes me wonder whether the human body is capable of making much more dramatic changes in a short period of time.

If the person is young enough, a high enough HGH injection into the body would shock the body into vertical growth for the last time.

It would stimulate the following areas of the body to grow…

1. The fibrocartilage in the region of the IVDs would differentiate into hyaline cartilage.
2. The 2 very thin layers of hyaline cartilage sandwiched between the discs and the vertebrate bone will start to proliferate just a little.
3. The irregular shaped bones in the feet will grow periosteally, have the macroscopic effect of  pushing the overall skeletal system upwards, thus grow taller.
4. The layer of articular cartilage in the hip joint will increase as well, as well as the articular cartilage of the tibia and femur in the knee joint.

All of the following physiological processes would accumulate in millimeters until the person gets maybe an overall 1 inch of extra height. That is not a lot, but it does prove a concept. The articular cartilage layer will indeed start to get thicker if you get the growth hormone into the system. 

If the person needs even more indication that articular cartilage growth is going to contribute to bones lengthening, realize this…

The mandible grows by endochondral ossification at the condyle and by surface apposition in certain areas. The condylar growth increases the height of the ramus and the overall length of the mandible!!

What that means is that for the human who has his/her normal growth plates closed, and they are have GH overstimulated, thus develop the medical condition known as acromegaly, the condylar growth, which is only from an articular cartilage layer, is enough to increase the length of the ramus, which is just the outer posterior lateral section of the mandible!!

This would suggest that if we could get off of our feet, and into an environment of lower gravity, HGH would work in increasing the length of the much bigger long bones like the femur trough articular cartilage layer deposition. If we were able to lie down on a horizontal bed for 24 hours for maybe 3-4 years, or live in a spaceship with 0 G, our long bones would grow longitudinally, at least up to a noticeable amount.

Concluding statement – Finally, let me reference page 220 of the book, the first paragraph “In acromegaly, growth of the mandible can again be initiated and continued even at a time when growth has normally ceased because of the peculiar histologis structure of the condyle. Here, the bone in younger individuals is covered by a cap of hyaline cartilage, which in turn, is covered by a thick layer of fibrous tissue. Remnants of the hyaline cartilage, which serves as a site of growth in the same way as the epiphyseal cartilage of the long bones, persist even in old individuals. As long as this hyaline cartilage is present, its proliferation can again be set in motion by a hyperactive pituitary gland, and it will then assume its function as a growth center of the mandible where it left off at the termination of normal growth. But even in cases in which an eosinophil adenoma or the hypophysis develops after the disappearance of the cartilaginous cap, a differentiation of hyaline cartilage from the fibrous covering of the condyle is not only possible, but also highly probably. If a new layer of hyaline cartilage has developed, endochondral growth can again set in after resorption of the terminal plate. As in other bones, the periosteal appositional growth is stimulated by the growth hormone; but this growth does not keep pace with the endochondral condylar growth, and the effect is a gradual increase in the mandibular angle.”

What the above paragraph shows is that you can make a bone longer even with just a cap of articular hyaline cartilage, similarly to how the antlers of deers grow out, which I did research more than 2 years ago. The key is to not be pushing down on the cartilage cap, which is not possible since we humans must walk. If we were upside down or had our overall weight lifted from the knee cap cartilage, the tibia bone will most likely start to slowly get longer.

Tyler’s Notes:

Here’s some hand xrays from an acromegalic hand:

First, notice how white it is indicating very high levels of bone density.  The epiphysis is much wider than normal.

Here’s another acromegalic hand xray:

The bones are again much whiter than normal indicating increased density but the increase in epiphyseal width isn’t there.

Here is another acromegalic hand xray more like the first:

There is epiphyseal widening but not as extreme as the first xray.

Let’s look at some developing fingers:

You can see that not only is the growth plate region not fully developed but the articular end without the growth plate too.  It is possible that this development which could occur with physical stimulation or with elevated HGH due to acromegaly could continue into adulthood and contribute to longitudinal bone growth.