Bodybuilders didn’t wait for scientists

It’s frustrating how much bodybuilding research there is in terms of sets, reps, and all sorts of factors to build up muscle and how little there is in terms of height.  Note that most of this research does not come from science it comes from tons of independent bodybuilders.

With muscle building we know that stressing the muscles in general increases their size.  Bodybuilders don’t wait for calf and pec implants to get bigger muscles.

We don’t know though how to lengthen bone?  We don’t know what stimulus to apply?  Actually we have a pretty good idea.

To induce chondrogenic differentiation(chondrocytes are the basis for the growth plate) one method is to induce a hydrostatic pressure of at least 0.1 MPa.  A blood pressure cuff during a heart beat generates about 120mmHg which is about 0.015MPa an order of magnitude of what we need.  To get 0.1MPa we’d need a blood pressure of about 750mmHg which would probably cause death.  There has to be a way for the body to safely induce hydrostatic pressure of 0.1MPa-10MPa’s to induce chondrogenic differentiation.  HP levels of the articular cartilage can vary between 1-5MPa in response to physiological(occurs normally) stress.  There are two possible ways to make up the difference in the hydrostatic pressure deficit(0.015MPa versus 0.1MPa or ideally higher) fluid flow and bone deformation.

Ultrasound levels of 30–200 mW/cm2, Frequency=1–1.5 MHz are one possibility(you’d target in the epiphysis).  Note I have not tested this so attempt at your own risk!  Muscular contraction can also increase marrow hydrostatic pressure.  You’d probably need to use external electrical stimuli to generate the muscular contraction needed to induce significant hydrostatic pressure.  Again I can not say whether or not this is safe or not!

An increase in hydrostatic pressure also results in an increase in fluid flow which may be the primary inducer of chondrogenic differentiation rather than the HP itself.  Thus you could find ways to induce fluid flow directly and in conjunction with an increase in hydrostatic pressure to get the needed stimulus to induce chondrogenic differentiation.

The growth plate is exposed to high hydrostatic pressure via the bone pressing down on it.  If we create a fibrous layer in a neo-growth plate region maybe the hydrostatic pressure to encourage a growth plate will occur naturally.  Note that LSJL does encourage fibrous tissue differentiation.  If we can create a fibrous tissue layer, the compression force of the bone itself will create the hydrostatic pressure and induce chondroinduction.

Fluid flow induces recruitment of integrins to focal adhesions.  This alteration in cell signaling by fluid flow directly could induce chondrogenic differentiation.

So we know the key to growing taller is to induce a new growth plate in the bone as bone tissue is not mechanically suited for interstitial growth.  We know that this can happen at around 0.1MPa hydrostatic pressure in the bone epiphysis.  It’s possible to make up for a deficit in hydrostatic pressure levels via other factors like fluid flow via dynamic lateral compression.  There’s also the possibility of using ultrasound and electrical muscle stimulation.  Such levels would have to be supranormal as no muscle stimulation of longitudinal bone growth has yet to be reported.  Since it is supranormal all the effects are not known so it would have to be tested somewhat for safety first.

New LSJL related study shows fibrous differentiation

This is an LSJL related study published by Yokota and Zhang.  The link to the study is provided and I was not able to copy the images here but you can read the study and click on the images.  Unfortunately, it does not relate directly to height growth.  However, it does show that joint loading increases fibrous differentiation.  And fibrous differentiation would be a potential intermediary step for neo-growth plate formation.  Knee loading increased vessel remodeling and osteoclast formation which would be needed to make room for a new growth plate but these levels were only slightly greater than control group and reduced from the osteonecrosis group so we can not say for sure whether this will happen in LSJL on a normal bone.

Overall this study shows that LSJL does at least one of the steps required for neo-growth plate formation: fibrous type tissue formation.  This fibrous tissue would then have to be further differentiated into more cartilagenous tissue.  The perichondrial ring(or ring of LaCroix) is fibrocartilagenous.

Knee loading protects against osteonecrosis of the femoral head

“Osteonecrosis of the femoral head is a serious orthopedic problem. Moderate loads with knee loading promote bone formation, but their effects on osteonecrosis have not been investigated. Using a rat model, we examined a hypothesis that knee loading enhances vessel remodeling and bone healing through the modulation of the fate of bone marrow-derived cells. In this study, osteonecrosis was induced by transecting the ligamentum teres followed by a tight ligature around the femoral neck. For knee loading, 5 N loads were laterally applied to the knee at 15 Hz{this is pretty high frequency} for 5 min/day for 5 weeks. Changes in bone mineral density (BMD) and bone mineral content (BMC) of the femur were measured by pDEXA, and ink infusion was performed to evaluate vessel remodeling. Femoral heads were harvested for histomorphometry, and bone marrow-derived cells were isolated to examine osteoclast development and osteoblast differentiation. The results showed that osteonecrosis significantly induced bone loss, and knee loading stimulated both vessel remodeling{vessel remodeling shows promise as that would be very helpful for neo growth plate creation} and bone healing. The osteonecrosis group exhibited the lowest trabecular BV/TV (p < 0.001) in the femoral head, and lowest femoral BMD and BMC (both p < 0.01). However, knee loading increased trabecular BV/TV (p < 0.05) as well as BMD and BMC (both p < 0.05). Osteonecrosis decreased the vessel volume, vessel number and VEGF expression (all p < 0.01), and knee loading increased them (all p < 0.01). Osteonecrosis activated osteoclast development, and knee loading reduced its formation, migration, adhesion and the level of “pit” formation (all p < 0.001). Furthermore, knee loading significantly increased osteoblast differentiation and CFU-F (both p < 0.001){An increase in CFU-F means an increase in mesenchymal stem cell proliferation which is a good for neo-growth plate formation but doesn’t guarantee that it will occur}. A significantly positive correlation was observed between vessel remodeling and bone healing (both p < 0.01). These results indicate that knee loading could be effective in repair osteonecrosis of the femoral head in a rat model. This effect might be attributed to promoting vessel remodeling, suppressing osteoclast development, and increasing osteoblast and fibroblast differentiation. In summary, the current study suggests that knee loading might potentially be employed as a non-invasive therapy for osteonecrosis of the femoral head.”

“The mechanism of knee loading is considered to change intramedullary pressure of femoral and tibial bone cavities. The load driven pressure may generate fluid flow in a lacuna canalicular network in bone cortex. The pressure also activates bone metabolism-related genes in femur and tibia”<-what we are interested in an increase in fluid flow and hydrostatic pressure to induce chondrogenic differentiation.  Hydrostatic pressure by itself isn’t likely to induce chondrogenic differentiation by itself as it is typically three orders of magnitude below the pressure needed to induce chondrogenic differentiation.  But the addition of bone deformation and fluid flow may bridge the gap and induce chondroinduction.

“Male Sprague–Dawley rats (~12weeks of age)”

“knee loading was achieved through dynamic loads applied to the left and right knee joints of rats in the lateral–medial direction, respectively. To position the knee properly, the lower end of
the loading rod and the upper end of the stator were designed to form a pair of semispherical cups. The lateral and medial epicondyles of the femur together with the lateral and medial condyles of the tibia were confined in the cups.  The tip of the loader had a contact
area of 15 mm in diameter.”

See Figure 1 of the paper(first link on the page) for an image of the knee loader.

Loading increased vascular remodeling in the osteonecrosis + LSJL group but not versus control.  But there was no normal bone plus loading group.

Joint Loading actually seemed to reduce the number of mesenchymal stem cells but that could be due an increase in differentiation.  Mesenchymal condensation was more visible in the osteonecrosis group and mesenchymal condensation is a prerequisite for neo-growth plate formation.  See figure 4.

Knee Loading seemed to restore osteoclast adhesion and migration to slightly above control levels (Fig 5) but that slightly above could indicate activity that would remodel the bone enough to allow for mesenchymal condensation.

Knee loading greatly increased CFU-F and Osteoblast differentiation versus both osteonecrosis and control group(Fig 6).  Fibroblastic tissue(marked by CFU-F) could potentially become chondrogenic tissue.  Fibrocartilage is a thing.  But to be a true growth plate, additional mechanical stimulation would be needed to turn that fibrocartilage into pure cartilage.

The perichondrial ring of the growth plate is fibrocartilagenous in nature and may be the source to provide cells to the growth plate.

Vosoritide, A Drug To Help Make People Taller Already Developed and Currently Being Tested!

VosoritideI was reading some random study in the field of orthopedics today and someone mentioned the condition SED, or Spondyloepiphyseal dysplasia congenita based Dwarfism, and that made me remember a few things that I had not looked at for a long time.

I remember people telling me about quack-pseudo-scientific ideas on how to treat SED before on other websites, but I wondered whether the Patent databases had anything written about treating it, in a more scientifically legitimate way. So I googled “Spondyloepiphyseal Dysplasia Congenita” into the Google Patent database to see what would come up.

Some of the first few results were obviously crazy, like the following Drug composition for treating spondyloepiphyseal dysplasia – CN 103142900 A”. This patent apparently was only filed in the China based database, and it is based on a combination of strange vegetables, minerals, and plants. The idea from this ancient formulation I would guess is to reduce the curvature of the spinal or straighten it out, which would obviously give the person a little bit of height increase. However, I would not be willing to put money on an idea based on Traditional Chinese Medicine practices.

It would be the next search result, which really caught my eye. Refer to the patent Variants of C-Type Natriuretic Peptide – US 20100297021 A1″. This was a patent which I don’t believe I have talked about before, and the name of it would not be an indication to most people searching the Patent Database that it is anything of importance, but this patent is basically a patent for a way to help people become taller.

Tyler and I have in our research throughout the years have seen multiple similar patents working on the similar idea which was also for increasing stature. 

Refer to the Abstract below….

The present disclosure provides variants of C-type natriuretic peptide (CNP), pharmaceutical compositions comprising CNP variants, and methods of making CNP variants. The CNP variants are useful as therapeutic agents for the treatment of diseases responsive to CNP, including but not limited to bone-related disorders, such as skeletal dysplasias (e.g., achondroplasia), and vascular smooth muscle disorders (e.g., restenosis and arteriosclerosis).

The Inventor is a Daniel Wendt from Biomarin Pharmaceutical. If we need to remember, Biomarin was the company which made the BMN 111 compound, which is used to treat childhood achondroplasia. I remember reading about this drug maybe a year ago on a website that focused specifically on how to help cope with a child who has the condition.

As one can see, this patent was filed back in 2010 and it has been filed in the USA, Canada, Europe, China, and the World Patent Database System. If I was to guess, I probably had linked to this patent multiple times before, but never really read the patent thoroughly..

Refer to the sections in the patent which I will highlight below…

“….In contrast, mice engineered to produce elevated levels of CNP display elongated long bones and vertebrae.”

I would learn further that in the growth plate, the proliferative zone expresses a compound called NPR-B while the hypertrophy zone expresses NPR-C. CNP (which stands for C-Type Natriuretic Peptide) is an agonist for the NPR-B. Agonist just means some type of chemical or protein that assists or increases a biochemical process. Further down the chain of chemical processes (which in the chemical/medical industry call downstream), the CNP and NPR-B pathway causes the FGFR3 pathway to be blocked. Remember that Achondroplasia is most often caused by a mutation of the FGFR3 causing it to be overstimulated or extra-sensitive. In the FGFR3 pathway, there is a step in the MAPK section. It seems that the CNP/NPR-B disrupts the pathway at MAPK, causing the FGFR3 to become inhibited, thus removing the stunted height morphology.

Refer to the section below from the patent….

“In humans activating mutations of FGFR-3 are the primary cause of genetic dwarfism. Mice having activated FGFR-3 serve as a model of achondroplasia, the most common form of the skeletal dysplasias, and overexpression of CNP rescues these animals from dwarfism. Accordingly, CNP and functional variants of CNP are potential therapeutics for treatment of the various skeletal dysplasias.”

Something that I would further learn is that the plasma-half life of CNP in the human blood stream is very short, only 2.6 minutes (in-vivo). This means to get this biomedical technique to work out, the CNP would need to be continuously pumped into the subject’s body. Apparently the basic level of CNP in the human body is around 5 picoMolar (5*10^(-9) Molar). The level of CNP must be higher than this concentration.

Refer also to more sections from the patent…

“…In a further embodiment, the CNP variants are useful for increasing the size of the growth plate of a bone (e.g., a limb bone). In another embodiment, the CNP variants are useful for elongating a bone or increasing long bone growth. In still another embodiment, the CNP variants are useful for enhancing matrix production, proliferation and differentiation of chondrocytes.”

Apparently to make the femur longer at the highest rate, you want to use a variant of CNP known as N-terminal PEGylated CNP variant.

“…Ex vivo studies of cultures of mouse bones indicated that CNP37 was delivered to the growth plate and was able to increase chondrocyte cellularity and hypertrophy, which are associated with growth plate expansion and longitudinal bone growth.”

“…These results demonstrate that CNP variants of the disclosure penetrate into the growth plate of wild-type and achondroplastic animals, increase the number and size of chondrocytes, increase the thickness of the proliferating zone and the hypertrophic zone of the growth plate, and increase longitudinal bone growth in treated wild-type and achondroplasic animals. Therefore, the CNP variants are useful for stimulating bone growth in achondroplastic subjects.”

There apparently was even news stories published in the Major Online News Websites talking about this drug/invention. (Note: Yes, I am fully aware that I am assuming that the patent I found is referring to the Vosoritide/BMN 111 chemical compound)

Drug Accelerated Growth in Children With Dwarfism, Pharmaceutical Firm Says – 6/17/2015 – The news reported that children would be growing around 6 cm/year than 4/cm by taking the drug. The other name for BMN 111 is vosoritide. There has been questions about the efficacy of this chemical after the first year of use, and whether after the first year the drug would still be as effective as the first year. In addition, it seems that people who did not suffer from Achondroplasia did not get any type of increased bone longitudinal growth benefit from using it. Since the article was written back in June of just this year, the drug is now in Phase 3 Trials, where around 50-150 children will be subjects for this new treatment.

BioMarin drug boosts growth in children with dwarfism – the source here seems to make a correction on something the previous source said, which is that the 6 cm of increased height is actually from just 6 months of tabulated data, not a full year.

BMN 111 (vosoritide) Improves Growth Velocity in Children With Achondroplasia in Phase 2 Study – This source suggest that the efficacy of BMN 111 will continue past the 6 month range in Phase 2 –

  • There was a dose-related increase in urinary excretion of cGMP measured over the 6 month duration of the study. cGMP is a biochemical marker that may indicate that BMN 111’s  biological effect will continue beyond 6 months.

Refer to the chart from the source below….

BMN 111

It would seem that National Health Industries and Organizations will not fund for a condition unless it has been diagnosed as a real medical condition or a disability. Short stature is not technically a disability, but having achondroplasia or dwarfism does qualify as a medical condition. This is where biomedical research will go and the funding will flow towards.

If you guys are interested in learning more about this compound, just type in the common name for it, Vosoritide or BMN 111. Biomarin even has itself listed on the Nasdaq under the acronym BMRN.

Video Of A 7 Feet Tall Chinese Yeren, A Human Bigfoot Hybrid?

Note: If you really want to see the video of this unique creature, just scroll down this post to the very bottom. I found quite a few videos of this creature off of the Chinese website and, and the Chinese documentaries and expeditions to find more information about it.

I was made aware today of a very interesting viral video that has been on the Youtube universe for a few years now. So far, it has already gained over 10 Mil views. Apparently there is even more old videos of what appears to be a very tall chinese/asian looking ape-like creature from the Chinese internet sources, which I found.

Just like the North American Bigfoot, the Chinese media also like to bring up this case on occasion to have “experts” discuss this person. Apparently very little information is known about him except maybe 1-2 minutes of reel on him, walking around and squatting in a very primitive fashion.

What I do know for a fact, from a lifetime of being fascinated with the paranormal and supernatural is that maybe half of the cultures in the world have some story about giant primate type animals that lived close to humans.

Bigfoot, Sasquatch, Alma, Yeren, Yeti, Abominable Snowman, etc. these are all labels we have given these animals.

In the video below, we see a human that is clearly very tall. His head size compared to his torso and his arms, legs, limbs is just incredible. The average length ratio of most human’s heads to overall body length is supposed to be 1/8.5, but the head/body ratio seems to be much greater here. Personally, I estimate the size of him to be around 7 feet tall, which is tremendously unusual, similar to the case of Siah Khan, the 8 feet tall Iranian farmer. However, if you look at the way this Chinese giant is walking, he seems to be just fine with no ailments. His ability to cognitively function is obviously not at the level of most humans.

If this person only had that shaped head without his great size, then most people would have written his mother’s story about being raped by a Yeren as fake. However, it is his great height and size that is most striking. We realize that the most likely medical explanation is that this human just suffers from microcephaly similar to the Pinhead from the old Freaks movie. Wikipedia says the name was Schlitzie. However, Schlitzie only stood 4 feet tall. This chinese version of a microcephaly seems to be 7 feet tall, if not more.

Of course, we have to realize that this creature/human’s body would look big compared to most Chinese women in the rural area. When we look up the Wikipedia article on Microcephaly, it states that most babies that have shrunken brains develop dwarfed bodies, not giant sized bodies.

This is not the only thing. Pictures from the videos of this Chinese Yeren shows underneath the hair on his head that he had grooves on his skull, similar to the skull of gorillas. I personally don’t understand the Chinese being spoken in the video but I can guess from the pictures that the researchers are analyzing that they are focusing on the head, to see whether this yeren was really human or some type of bigfoot hybrid.

I am not willing to say that this Chinese giant is the missing link, or a human-bigfoot hybrid. His mothers claims of being raped by a Chinese Yeren is also very suspicious. When you look at the video, obviously you know it is not a man in a suit, like people who do hoax for bigfoot sighting. The creature is nearly completely naked. This is video which seems to have been shot decades ago, so there is probably no video editing or graphics design done. The story is probably real, this human did exist, but most likely dead now.

Brent Collins, A Dwarf Suffering From Marfan Syndrome Who Had A Growth Spurt As An Adult

I was informed today of a most interesting case. There was a well known actor who was on the show The Golden Girls back in the 1980s, named Brent Collins, who apparently had the medical conditions of dwarfism and marfan’s syndrome.

The general claim made by the sources I find on google is that this guy had a growth spurt as an adult, maybe around the age of 30 or higher. This is most unusual. The only case which most people had found similar is Adam Rainer. He died in 1988 from a heart attack, which is believed to have been induced by the growth spurt.

Some people on the forums say that he started growing at the age of 46, which was just a year before he died.

There are maybe just a few videos on Youtube of him acting, and if you look at his body, his arm limbs are abnormally long. Since we can’t really get a good look at his legs, I will just assume his legs are also disproportionately long compared to his body.

Here are some things that have been guessed by others who tried to analyze his unique case.

Roger – I guess his dwarfism might be caused by an osteodysplasia, due to a genetic mutation, (not sure what kind of dwarfism, maybe SED dwarfism) rather than an endocrine origin, and although radiographic evidences show that development in epiphyseal regions in subjects with SED dwarfism is markedly delayed, when reached the early adulthood the plates shoud be closed, so I do find extraordinary that the epiphyseal plates of Mr.Collins were potentially functional at age 46, unless the ossification centers remained open due to some circumstance. Looks like, as long as he was working, he didn’t show any sign of MFS, as we can see on the 1987 Another World video, so I am surprised that marfan developed so spontaneously, and killed him so fast. (source)

GodsGadfly – I just saw his appearance on _The Golden Girls_–and apparently garnered a few search hits from it. If you know what you’re looking at, you can tell that his arms and fingers were very Marfanoid in proportion to his body, and relative to the normal proportions of a dwarf. I had gotten to wonder if he had Weill-Marchesani Syndrome, but that is not associated with aortic dilation. (source)

It seems that we might be incorrect in assuming that he died at the age of 48, but instead 46.

Can we extrapolate this very unique medical case of this rather good actor to something we can take away?

Brent Collins was said to have started growing around late 1987 and that triggered the heart problem, which is a Marfan’s symptom, to have a problem, causing his death.

It doesn’t make any sense at this point how this man, who would have been in his mid 40s could have still had functional growth plates. I once theorized in an old post that maybe it is possible that a very small minority of females still have functional growth plates even into their 30s, but this case is much more extreme.

Human bones are very hard material that is not malleable using normal magnitudes of force. Maybe, just maybe, because Collins was a dwarf, probably weighing just around 60-80 lbs, the cartilage in his body did not ever experience the amount of gravitational loading needed to ossify the epiphyseal cartilage.

Of course, now I am just completely guessing.

“I Wish I Was Taller”

These are the exact words someone told me today. How often do these words come out of someone’s lips?

Enough times in my life to realize that height is very important for some people.

I decided to try a new gym today and could not get any type of Guest Trial Pass in the local LA Fitness close to my house. Did some searching and found out that while I can’t get a guest pass when I an physically at the facility, I can apply for the pass online, fill out my info, and then take some barcode to be scanned in. So I did that. Went to the gym, and showed it to the trainer/worker at the front desk/guest location, where they check people in. Apparently they don’t get enough people like me so they didn’t really know what to do so I was escorted to be sat down with another worker to put my personal info into the gym database. I mentioned that my name was already in, I didn’t want to take any gym tour, and just wanted to play around the gym to see if I wanted to switch from the YMCA, which had a higher monthly gym fee. The worker asked me what I wanted to do and I replied that I just wanted to play basketball.

So he mentions that he loves basketball and used to play a lot. Then he had to take the job at LA Fitness and couldn’t play much anymore. So I make the off-handed remark (which was also a joke) that all all he needed was to “be a little taller and have a little more skill to become a professional basketball player”. Then he says “I wish I was taller”.

A 2nd look at him tells me that he is already 5′ 11″, maybe even 6′ 0″. White, in his 20s, bearded, seems to be bored of his job, but goes through the motions and decently polite.

Apparently being even 5′ 11″ (or even 6′ 0″) is not enough anymore. He is still wishing he is taller. At what point does a normal guy stop wishing that he is taller? 

I think back in my life to the number of people who I have met who desperately wished that they could just grow taller.

The most extreme case was a Southeast Asian girl I dated for a short time. She would mention her short stature and tell me in confidence that becoming taller was her main wish in life. Not making more money, not getting married, not becoming successful. I would ask her whether she would choose ten million dollars or 9 inches in height. She choose to be taller. That relationship did not last.

Do these people, become bitter and resentful at some point at people who are taller than them after they reach a certain age and realize that there is almost nothing that they can do to change something about themselves which they don’t like?

Readers: I plan to do a short series of posts on topics related to medicine and biohacking in the next few weeks, sort of as a short guide on how to improve other areas of one’s body.