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.