Dihydrotestosterone is a determinant of calcaneal bone mineral density in men.

Full study link->DHT and IGF2

“Hundred osteoporotic men with age matched normal were studied for serum levels of sex steroids, PTH, IGF system components, cytokines and bone turnover markers. Our findings show that serum DHT, IGF-I, IGF-II and IGFBP-3 levels were significantly decreased while IL-1beta and bone turnover markers were significantly increased in osteoporotic men compared to normal. Pearson correlation analysis revealed that serum DHT, IGF-I, IGF-II and IGFBP-3 levels were positively and strongly correlated with BMD, while serum IL-1beta levels were negatively correlated with BMD. Serum PTH, testosterone, estradiol, IGFBP-4, TNF-alpha, IL-4 and IFN-gamma levels were similar between the two groups. We observed that DHT levels significantly declined with age. However, the significant difference in DHT between the osteoporotic and normal groups is the same regardless of age. A multiple regression model adjusted for age demonstrated that DHT/BMD association is fairly stronger among those with osteoporosis than the normal. Our findings for the first time point out that DHT is an important determinant of BMD in men. Most importantly, the strong positive correlation of serum DHT with BMD offers new perspectives in understanding the role of non-aromatizable androgen in regulating bone metabolism in men, and might serve as a potential clinical marker in the diagnosis of male osteoporosis.”

Serum levels of estrogen and testosterone are slightly lower in osteoperotic men than normal.

“DHT increased the levels of IGF-I and IGFBP-3 in human osteoblastic cell line (hFOB/AR-6). DHT enhances the mitogenic effect of IGF-II in bone cells.”

This is the study that mentions the link between IGF-II and DHT:
Studies of the Mechanism by which Androgens Enhance Mitogenesis and Differentiation in Bone Cells

DHT did not increase the quantity of IGF-2.

“Because FGF and IGF-II are known to synergize with TGFB, the enhanced response to FGF and IGF-II due to DHT treatment may be dependent upon the increased production of TGFB.”

DHT pre-treatment approximately doubled the effect of IGF2.

Previously, I stated that my wingspan has increased from 72.5″ to 74.5″ but I didn’t have any proof because I didn’t take any before pictures.  I’ve been trying to get my wingspan increase but haven’t had significant enough measurements for undeniable proof.  I’m keep trying to increase height and wingspan but what I can do is try to create new photos to compare to the old ones

.Here’s an image from about 2012.  I tried to recreate something like this picture as best as I could.

This was from today.  The dumbell acts as sort of a constant.

The problem is the image is not 3D so it can’t account things like the dumbell tilt.  Right now my forearm measures 11 inches elbow to wrist “bump”.  Using the dumbell handle as a constant, I compared the forearm length elbow to wrist(although it was harder to identify wrist in the before picture.  I was pretty generous to the before picture.

Before forearm length as dumbell handle lengths: 2.4 dumbell handles

After: 2.48 dumbell handles

Which is about 3%.  My wingspan increased by 2 inches.  Assume a 0.5″ of that is in my left forearm.  .5″ is about 4.76% of 10.5″.

So given the inaccuracies of the photo I don’t think it’ll be easy to have definitive proof using the two unless someone has ideas of creating a new photo standardized against the first.

Due to the significant response to my earlier post on CNP, I wanna go over all the significant studies on CNP so far.  CNP and IGF-2 seem to be the two supplement targets with the greatest potential with IGF-2 having the most potential to those without open growth plates.

BMN111 is a potential CNP analogue undergoing testing.

The bone length overgrowth effects are likely mostly due to the inhibition of FGFR3 and ERK1/2.  However, those tend to be anabolic in other tissues so CNP will most likely make you taller and lankier.

Meclizine is a supplement that is similar to some effects of CNP, inhibition of ERK1/2 but is available for sale.  This post has some other information about meclizine as well as why FGFR3 inhibition is effective for height growth.

Meclizine Chewable Tablets – 25mg – Model 85207 – (3 Bottles of 100)

Note: Disobey any directions on the bottle at your own risk. I don’t know the optimal dosage. Also, this should only be offective on open plates.

Inflammation in children reduced CNP production so inhibiting inflammation should increase CNP levels.

As for possible ways CNP could increase height in those with closed growth plates:

Increased bone turnover and possible accelerated fracture healing in a murine model with an increased circulating C-type natriuretic peptide.

” we investigated the bone phenotype of a mouse model with elevated plasma CNP concentrations (SAP-CNP-Tg mice) in the present study. Micro-CT analysis revealed less bone in femurs, but not in lumber vertebrae, of young adult SAP-CNP-Tg mice than that of wild-type mice{CNP could weaken bone allowing for neo-growth plate formation}. Bone histomorphometry of the tibiae from 8-week-old SAP-CNP-Tg mice showed enhanced osteoblastic and osteoclastic activities, in accordance with elevated serum levels of osteocalcin and TRAP5b, respectively. Next we performed an open and stabilized femoral fracture using 8-week-old SAP-CNP-Tg mice and compared the healing process with age-matched wild-type mice. Immunohistochemical study revealed that CNP and its receptors, natriuretic peptide receptor-B (NPR-B) and natriuretic peptide clearance receptor are expressed in hard calluses of wild-type mice, suggesting possible role of CNP/NPR-B signaling in fracture repair, especially in bone remodeling stage. On micro-CT analysis, rapid decrease in callus volume was observed in SAP-CNP-Tg mice, followed by generation of significantly higher new bone volume with a tendency of increased bone strength. In addition, micro-CT analysis also showed that bone remodeling was accelerated in SAP-CNP-Tg mice, which was also evident from increased serum osteocalcin and TRAP5b levels in SAP-CNP-Tg mice at remodeling stage of fracture repair. These results indicate that CNP activates bone turnover and remodeling in vivo and possibly accelerates fracture healing in our mouse model.”

CNP overexpression also decreased bone stiffness.

We know that CNP is important for height growth but we don’t know why it affects height so strongly.  This study provides us with the information that elevated systemic levels of CNP increase longitudinal bone growth meaning that a CNP supplement to increase height in the growing has great promise.  If only cartilage specific CNP increases height, than a CNP supplement would not help.

The Local CNP/GC-B system in growth plate is responsible for physiological endochondral bone growth.

“C-type natriuretic peptide (CNP) and its receptor, guanylyl cyclase-B (GC-B) are potent stimulators of endochondral bone growth. As they exist ubiquitously in body, we investigated the physiological role of the local CNP/GC-B in the growth plate on bone growth using cartilage-specific knockout mice. Bones were severely shorter in cartilage-specific CNP or GC-B knockout mice and the extent was almost the same as that in respective systemic knockout mice. Cartilage-specific GC-B knockout mice were shorter than cartilage-specific CNP knockout mice. Hypertrophic chondrocyte layer of the growth plate was drastically reduced and proliferative chondrocyte layer, along with the proliferation of chondrocytes there, was moderately reduced in either cartilage-specific knockout mice. The survival rate of cartilage-specific CNP knockout mice was comparable to that of systemic CNP knockout mice. The local CNP/GC-B system in growth plate is responsible for physiological endochondral bone growth and might further affect mortality via unknown mechanisms.”

“we developed transgenic mice with an elevated plasma concentration of CNP under the control of human serum amyloid P component promoter and exhibited that these mice showed prominent skeletal overgrowth phenotype, indicating that CNP can humorally[relating from a hormone] affect endochondral bone growth”

“CNP and GC-B exist in nonhypertrophic and prehypertrophic chondrocyte layers of the growth plate, respectively. Together with the fact that mice with systemic depletion of CNP or GC-B exhibit severely impaired growth of bones formed through endochondral ossification, we could suppose that the local CNP/GC-B system in the growth plate is a physiological stimulator of endochondral bone growth. Nevertheless, it remains possible that the CNP/GC-B physiologically regulates endochondral bone growth via mechanisms other than the local effect on the growth plate; CNP secreted from a tissue other than growth plate cartilage might influence or stimulate endochondral bone growth. In fact, CNP is capable of humorally stimulating endochondral bone growth, as demonstrated by the observation that transgenic mice with elevated plasma concentrations of CNP exhibit skeletal overgrowth phenotype”

“the extent of impairment of endochondral bone growth observed in cartilage-specific CNP or GC-B knockout mice is almost the same as in systemic CNP or GC-B knockout mice, respectively. Thus, the autocrine/paracrine effect of the CNP/GC-B system in the growth plate is the primary physiological stimulator of endochondral bone growth in body.”<-It doesn’t matter if you stimulate CNP or GC-B directly in the growth plate.  As long as you do it systemically you will grow taller while you’re actively growing.

I haven’t gotten all the required information on this post but it’ll be in this post(I’ll bump it when I get more).

A Review of the Epiphyseal Plate in Long Bones

“The human skeleton is a complex organ involved in movement, support, and protection. The epiphyseal plate is the mediator of longitudinal bone growth in long bones. The various layers of the plate function to facilitate growth, and a disturbance to any layer has the potential to cause growth cessation. The Salter-Harris classification system is used frequently to diagnose epiphyseal fractures according to the location of various separations. Youth sports, especially American football, are the leading cause of epiphyseal injuries. Future research is focused on developing a gene therapy to restore bone growth after cessation.”<-Interesting that they feel a gene therapy is sufficient to restore bone growth after cessation without any implants or fracture to make room for the growth plate.  Even if we don’t have access to gene therapy methods, finding a way to stimulate longitudinal bone growth without mechanical intervention would be a boon to supplement only methods of increasing height.

It was written by Cameron Shegos at Kalamazoo College.  So if you have any info please share.

He has a more detailed version

Here

“The human skeleton is a complex organ involved in movement, support, and protection. During a child’s adolescent years, this skeleton is rapidly growing. The epiphyseal plate, better known as the growth plate, is the mediator of longitudinal bone growth in long bones. The various layers of the epiphyseal plate function uniformly to facilitate growth, and a disturbance to any layer has the potential to cause growth cessation. The Salter-Harris classification system is used frequently to diagnose epiphyseal fractures according to the location of various separations. Modern technology has further improved this system by developing a comprehensive classification of pediatric long bong fractures as well as additional classifications to the Salter-Harris scheme. Youth sports, especially American football, are the leading cause of epiphyseal injuries, along with many other sports and recreational actives such as skate boarding and bicycling. Reasons for concern and possible countermeasures to prevent an epiphyseal injury are provided and suggested. The idea of developing a gene therapy to restore bone growth after cessation as well as surrounding damaged tissues due to injuries is the future of medical research with regards to the epiphyseal plate.”

Here’s the things that I’ve been keeping in mind while performing LSJL loading.  First, is that bone adapation itself can not make you taller.  Bone adapts to the stimulus provided to it but not always in the way you want.  If you stretch the bone it won’t get longer but rather stronger and more resistant to stretching(unless you stretch it with enough force as to get into the plastic deformation range).

Since the loads to cause plastic deformation would be extreme and difficult to apply properly the goal is to affect other types of stimulus within the bone to encourage longitudinal bone growth like the stem cells, attached ligament enthesis’, the periosteum, and other surrounding soft tissue.

The previous method of LSJL involved clamping the synovial joint region whereas enthesis LSJL involves clamping two bones against each other.  The enthesis attaches into the bone so it would be a potential region where a new growth plate could form.  The enthesis structurally resembles the zone of ranvier where stem cells reside to provide for the growth plate.

This was the regime I was using.

I noticed that I was getting better results with my arms than my legs as my wingspan had increased from 72.5″ to 74.5″.  The arm method I use with the enthesis method is the same as the standard LSJL method but the leg method is different.  The structure of all the joints is different so the loads are applied differently.  In the LSJL studies, the scientists found that the amount of bone deformation induced by LSJL was actually very small and they theorized that the results(including partially longitudinal bone growth) due to lateral knee loading could be due to the creation of a pressure gradient.  As fluid flows more easily from a lateral direction than an axial one.  However, it’s also possible that the LSJL results were due to the loading of bone against each other(which are attached by ligaments).  The screw that was used to load the rats knee and ankle was huge relative to the size of the knee and ankle so the screw would’ve easily been loading the bones against each other.  This is in contrast to our method where the clamps are small relative to the knee and ankle.

With this new enthesis LSJL method I have not been getting definitive results on my arms and legs.  However, it was a significant amount of time before I noticed that my arms grew longer by about 1 inch each.  With the old method I loaded my arms by about a count of 500(with instances of stopping) with a clamp every other day.  Now I do it for about 30-40 counts several times a day.

It’s possible that the sustained session was more effective than the intermittent sessions.  I don’t think mechanosensitivity is a big issue.  Mechanosensitivity is the decreased response of a tissue to load. We know that increased longitudinal bone growth is not going to come from bone directly.  All cells have mechanosensitivity but not to the degree that osteocytes seem to have in bone.  Osteocytes are more mature cells than stem cells and chondrocytic like cells so they would likely be less prone to adaptation.

So, I don’t think that cycling off of loading would be an issue for enthesis loading.  And you probably need a minimum amount of time for it to be effective.

So I’m going to try to sustain the load on the sites for longer.  I know for sure that I gained about an inch of arm length it’s just a matter of reproducing it.