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Isoflavones Seem to Delay Puberty Onset In Girls Thus Increasing Adult Height

Isoflavones Seem to Delay Puberty Onset In Girls Thus Increasing Adult Height

IsoflavonesFor the longest time I always suspected that the superficial level of research and understanding that a person with no scientific training would know about some specific area of the hard sciences from just a few hours of study was not enough. I am ashamed to say that I myself suffer greatly from that aspect, since I mostly try to skim through the abstracts of studies, which is not enough to really understand the material. This post is a clear example of that, which seems to refute a previous claim I had made from making the wrong assumption of the effects of a chemical compound, based on not understand the biochemistry well enough.

Many months ago I wrote the post “Phytoestrogens Found In Soy Based Foods May Explain Why Vegetarians and Asian Ethnicities Have Been Historically Shorter (Very Important!)” which proposed an idea that since people of East Asia eat so much soy based products like tofu, the phytoestrogen in their food was probably what was causing them to end up shorter than other ethnicities on average. The idea was that the phytoestrogen found in tofu is very similar to estrogen, which has been responsible for the onset of growth plate fusion. Of course, the problem there was that there were studies which seemed to contradict themselves on the final result.

My argument was something which was raise before on other height increase forums, when the idea of taking Alfalfa to increase height was contested. (Take a look at the thread “worried about isoflavone content in alfalfa and soybeans“)

Isoflavones prefer to bind to ER-Beta. Estrogen goes for ER-Alpha. (The ER stands for Estrogen Receptor). At the time, I was confused as to which type of estrogen receptor (alpha or beta) the phytoestrogen & the isoflavone were more susceptible to attach to.

Matheus, another height increase researcher called me out on my mistake in assuming that ER-Alpha and ER-Beta binding would have similar effects. Clearly they might not after this recent study I have found.

Read his comment/message made to me below

Increasing Adult Height

Matheus might have been right along. The argument made that eating tofu, soy-based products, phytoestrogens, and isoflavones would cause earlier than usual growth plate ossification was not validated.

I refer to the study…

Relation of isoflavones and fiber intake in childhood to the timing of puberty.

From the abstract, we find that for girls who are in the pre-puberty stages, having a higher than average isoflavone diet meant that they actually started puberty much later than their counterparts.

Based on what we understand on the growth progression of adolescents, the girls who started puberty later would on average end up taller when they are adults and have reached full adult bone maturity. This fact is that the main reason why males are on average taller than females later in life is because they started puberty around 1-2 later than females.

There was a 2nd study “Low Phytoestrogen Levels in Feed Increase Fetal Serum Estradiol Resulting in the “Fetal Estrogenization Syndrome” and Obesity in CD-1 Mice” seems to validate this idea. If you take away the phytoestrogen from the diet of pregnant female lab rats, they ended up having earlier than average puberty. In the experiment, the researchers had two groups of pregnant lab rats, which were feed non-soy low-phytoestrogen feed or soy-based high-phytoestrogen feed, and then had the the offspring compared of the two groups.

In addition the baby that they gave birth to started to develop obesity, which is correlated by an increase in the level of estrodial.

At this point, I think we can agree that out of almost every compound we found, estrodial has been one of the worst offenders of growth and would almost always lead to stunted growth.

Increased Height with Iron

Increased Height in HFE Hemochromatosis

” the growth rate affects iron status, and iron demand tends to exceed supply in periods of rapid growth”

“We assessed height in a cohort of 176 patients with HFE hemochromatosis at the University Hospital Zurich”

“All patients had verified iron overload, defined as a serum ferritin level of more than 300 μg per liter or a transferrin saturation of more than 45%. Height in patients with hemochromatosis was compared with that in an age- and sex-matched Swiss reference population”

“Men with hemochromatosis (120 patients) were 4.3 cm taller, on average, than those in the reference population (458,322 persons)”

“The height was 178.2 cm in men with hemochromatosis, versus 173.9 cm in controls. The difference in height between women with hemochromatosis (56 patients) and those in the reference population (10,260 persons) was 3.3 cm. The height was 167.1 cm in women with hemochromatosis versus 163.8 cm in controls.”

“we did not find evidence for an association between the HFE C282Y mutation and so far identified genetic determinants of height.”<-So it was likely the iron that was the factor causing the increased height.

Iron was associated with FGF-23 which may have caused “pseudo-reactivation of the growth plates”.  Iron is inversely correlated with FGF23 and high FGF23 levels were associated with shorter stature.  However, FGF23 was also associated with pseudo-reactivation of growth plates.  Iron reduces LCN2 levels which may also reduce height.

The height difference due to iron is pretty big.  After aging lower iron concentrations may be beneficial to allow for higher FGF23.

Can twisting increase vertebral disc length?

This study seems to indicate that stretching may very well increase vertebral disc height.

Mechanics and Validation of an In-Vivo Device to Apply Torsional Loading to Caudal Vertebrae. 

Torque is the force that rotates around an object.  Torsion is the twisting of an object.

“Axial loading of vertebral bodies has been shown to modulate growth. Longitudinal growth of the vertebral body is impaired by compressive forces while growth is stimulated by distraction. The purposes of this study were two-fold: (1) to develop a torque device to apply torsional loads on caudal vertebrae and (2) investigate numerically and in vivo the feasibility of the application of the torque on the growth plate. A controllable torque device was developed and validated in the laboratory. A finite element study was implemented to examine mechanically the deformation of the growth plate and disk. A rat tail model was used with six 5-week-old male Sprague-Dawley rats. Three rats received a static torsional load, and three rats received no torque and served as sham control rats. A histological study was undertaken to investigate possible morphological changes in the growth plate, disk, and caudal bone. The device successfully applied a controlled torsional load to the caudal vertebrae. The limited study using finite element analysis (FEA) and histology demonstrated that applied torque increased lateral disk height and increased disk width. The study also found that the growth plate height increased, and the width decreased as well as a curved displacement of the growth plate. No significant changes were observed from the in vivo study in the bone. The torsional device does apply controlled torque and is well tolerated by the animal. This study with limited samples appears to result in morphological changes in the growth plate and disk. The use of this device to further investigate changes in the disk and growth plate is feasible.”

vertebraetorquevtorsionFigures of the spine and of the torsion device.

growthplateLeft growth plate is under torsion whereas right is the control group.  You can’t tell if there is any ectopic differentiation of MSCs to chondrocytes as the magnification isn’t high enough.

“Torsional loads are involved [in scoliosis]. While treatment of the spine to generate rotation by application of posterior flexure has been applied, it has been shown that the derotation maneuver using a posterior spine instrument does not consistently correct transverse rotation”

As torque increases, compressive loading becomes more tensile.

“[Torsional loading caused] remodeling at the epiphysial plate with bending of the cartilaginous columns of the growth plate”

5 week old sprague dawley rats were used.

“The morphology of the growth plate was seen to be more curved in the torque-loaded rat, while more flat in the sham rat”

“Overall, the growth plate area in the TG[Torque Group] (0.47 mm2) was greater than the area in the SG[Sham Group] (0.24 mm2)”

“lateral disk space was increased (55–65%), and the middle disk space was reduced by 15%”

“growth plate height is increased and its width is decreased [under torque]. The shear forces derived from the torque may stimulate greater number of endochondral cells in the proliferative zone compared to those in the control group with no shear forces.”

Note that under LSJL the growth plate curves in shape too.  In contrast to the growth plates here, in LSJL the growth plates curve so that the center is the highest part of the growth plate.  Although since only a small portion of the growth plate is shown in LSJL, it’s possible that in LSJL that the extremities curve upwards as well and it’s displaying the same center curvature as shown in these torsion growth plates.

“this curvature may be the result of the shear stress distribution in the growth plate. The sides of the growth plate are pushed toward the center by the shear stress, where the effect is most pronounced, leading to a curved appearance in the growth plate. This curved growth pattern forces the height of the center of the disk to decrease. Furthermore, the disk flows outward because of lower pressure at the outer boundary of the disk leading to increased disk width.”<-LSJL involves shear strain forces too which could also cause the curved shape.

curvedgrowthplateLeft is growth plate under torque whereas right is control.  You can definitely see the enhancement in growth plate quality.

“0.07 mm increase in the disk height at the lateral side of the disk and no change in the disk height at the center of the disk.”

We’re looking mainly at disc height as there’s likely no growth plates in adult vertebrae.

There are 23 intervertebral discs which is 1.61mm total(or .161cm) if every disk gains 0.07mm.  So assuming this a human being could gain 0.06 inches of height.  Of course a human being is bigger than a rat so they would likely gain more mm’s than a rat.  However, only the lateral side increases and not the center of the disc so you may not gain all the height.

Also, it’s not clear if there’s a limit on the height that can be gained this way.

Golfing, pitching, batting, throwing, twisting could all cause torque on the spine to various degrees.

Some stretches would also cause torque on the spine.

Too much torsion can cause hernias.  So it seems as though for now twisting would have only a minor effect on height.

Regenerate Articular Cartilage Using Silver Electrode and Direct Current Electrical Stimuli

Regenerate Articular Cartilage Using Silver Electrode and Direct Current Electrical Stimuli

This post will be a followup post to one of the most important posts I have ever written for this website “Electromagnetic Stimuli Will Increase Ossification and Make Bones Longer, Big Breakthrough!“. This is an idea which will definitely lead to at least 1-2 mm of extra increases in height, but it would probably be most applicable for people who are already suffering from some type of cartilage tissue degeneration.

As some of us might know, certain types of arthritis that older people suffer from is from the loss of thickness in the articular cartilage at the end of their long bones, at the joint area. The decrease in thickness means that bones will be rubbing against bone. There is no lubricant. That means that it is extremely painful to walk if your knees have all the cartilage gone.

Apparently if you take an electrode of at least a silver–platinum combination soldered with a resistor in the middle (to lower the current) and then apply a DC current, you can stimulate an area of articular defect to regenerate the hyaline cartilage back.

Regenerate Articular Cartilage

Dr. Becker with Bruce Baker showed in a standard experimental study using lab rabbits which they performed and then sacrificed, that you can regenerate hyaline cartilage back in using this method. Of course their approach was again similar to what they have been promoting for decades.

Here are the key points that they stated which we should remember

1. Use Silver

It turns out that silver is extremely effective in killing bacteria. The way that the silver ions diffuse, somehow they can disrupt the protein layers that form the outer membrane of bacterias (and even some viruses). Somehow Silver is also not poisonous to the human body and its cells.

2. Using a low level Current

You don’t need a very high current to stimulate the cells to do much. It is more likely that high currents would do more damage than good, since the current could cause the cells to go into rapid mitosis and turn malignant. Brighton and Friedenberg used high levels of current (10,000-20,000 nanoamps) but that might not be needed. Becker’s group found that you can use just around 100-200 nanoamps per centimeter of electrode and it would have some effect.

That is also the reason you see in the schematic above (taken from page 189 of his book) there is a resistor. The resistor is used to lower the current to a very, VERY low rate. The rating on the resister is at 10 MEG!!. We are talking about 10 MegaOhms. The voltage you need is less than 1 Volt. Using V=IR, and find for the current, we should understand why just a high level resistor is used. You want just a tiny bit of current, and that is enough apparently.

3. Stimulate close to either the periosteum and/or the marrow, but not the actual bone

Notice how there is a defect made on the joint area purposely on the lab rabbit. One of the electrode tips gets embedded into the bone layer underneath, which has the bone marrow in the epiphysis/ joint head.

Previously I had talked about the virtues of micro-fracture surgery “A Proposed Height Increase Method Using Microfracture Surgery Techniques With Fibrocartilage Formation“. However at the end of that post, I had lamented that it would be fibrocartilage we have to work with, instead of the hyaline cartilage. If you drill holes around the entire perimeter of the bone, you would theoretically for maybe a few days turn the defect into cartilage, which we can actually manipulate. If instead, we can use silver electrodes and small DC electrical stimuli to create our preferred hyaline cartilage, then we would be much, much closer in created a full plan of cartilage which we have work with.

We want the cells in the adult bone marrow (adipocyte derived stem cells) to turn into the type which we want to work with, which is either chondrocytes or cartilage which is stable.

The experiment that they did back in the 1970s-1980s showed that with such a small battery and simple device, you can regenerate hyaline articular cartilage almost completely back.

Something to remember: Bone tissue don’t actually grow.

It is the periosteum and the bone marrow which has the cells that can actually make the bone tissue expand in any way.

Low-Intensity Pulsed Ultrasound LIPUS Does Not Increase Longitudinal Growth Of Bone

Low-Intensity Pulsed Ultrasound LIPUS Does Not Increase Longitudinal Growth Of Bone

Update March 6th 2014: Tyler did leave a response to this post originally but there is now even more evidence found which tips the question of the effect of Low-Intensity Pulsed Ultrasound on bone longitudinal growth to the side of having no affect at all.

Study #1: Effects of therapeutic ultrasound on longitudinal growth of the femur and tibia in rats

The conclusion for this particular study was that using the three different intensities of LIPUS at 0.5, 1.0 W/cm2, and 1.5 W/cm^2 it was found that the emissions had no effect. There was no inhibitory effect and there was no stimulatory effect. If we were to be extremely accurate, there was a very slight stimulatory effect in the first two groups and an inhibitory effect in the third group, but the slight deviations were too small to be considered significant.

There have been some studies like the Chapter 5 “Low-intensity ultrasound stimulates endochondral ossification in vitro” which shows that using LIPUS is critical when going through the beginning stages of endochondral ossification though.

This recent news is slightly sad to hear but this is one study I did find by Joseph Spadaro, who collaborated with Dr. Robert Becker about 30 years ago, which shows that the LIPUS technology which we had previously believed to work in increasing bone growth (at least density wise) seems to do very little towards the longitudinal growth of bones “Application of low-intensity ultrasound to growing bone in rats.”

Abstract Below

Low-intensity pulsed ultrasound recently has been shown to accelerate long bone fracture healing, but its effect on bone growth and development is unknown. The longitudinal growth and bone density of the femur and tibia in young rats was measured after application of an ultrasound transducer emitting 1.5-MHz pulsed ultrasound (30 mW/cm2, SATA) for 20 min/day. After 28 days, no length difference was detected (< or = 2%) compared to the sham-treated leg or to unexposed controls. Also, no significant difference in bone mineral density (BMD) of the femur or tibia was found (< or = 6%). In a repeated experiment in which a periosteal trauma stimulus was created in the femoral diaphysis, the ultrasound also had no effect on growth or BMD. This results suggests that physeal bone growth is far less sensitive to this level of ultrasound application than is fracture repair. This may be related to the cascade of cellular events and regulatory factors that are present after a fracture.

So what does this mean for us?

Recently I have been looking into the piezoelectric properties of the bone, as described by the book The Body Electric. Dr. Becker wrote that back in the 1975-1980 year range, he had found that from the arrangement of how the collagen fibers and apatite crystals are aligned next to each other, they created a PN Junction as well as being piezoelectric. The bones in our body are actually semi-conductors.

While the research group originally thought that the apatite, being a crystal, would be piezoelectric, it turned out that the large collagen fibers seemed to be the real compound.

The author of this paper was one of his colleagues, whom he collaborated extensively with. I’ve searched through the PubMed database to see what he has written in the decades that followed. This particular study done by the current professor emeritus of at SUNY suggest that even using young lab rats (which means that they have healthy growth plates available), the LIPUS technology of placing a transducer emitting Ultrasound at levels of 1.5-MHz pulsed ultrasound (30 mW/cm2, SATA) for 20 minutes every day.

If the transducer has no effect on young rats with clearly available cartilage to possibly stimulate, then it would most likely not have any effect on humans with no cartilage at all.

Note the following points made

  • There was no effect on longitudinal growth of the leg bones (femur and tibia) after 30 days
  • There was no effect on the bone mineral density of the same bones after 30 days.
  • When a load was tried on the diaphysis of the femur, there was no effect on the factors again

It seems that while LIPUS might work in somehow increasing the rate of bone non-union healing, it has almost no effect on bone physeal growth. It doesn’t even work on young lab rats.

At this point, I propose that we STOP going down this line of research, on the possibility of using the Low-Intensity Pulsed Ultrasound as a possible way to increase height, especially for adults with no cartilage to work with.

Tyler-I looked over this full study

“Four-week-old Sprague–Dawley male rats (approximately 90 g) were treated for 20 min/day with ultrasound applied to the left leg during four weeks, while the right leg served as internal control”

leg differenceExperiment 2 is with periosteal abrasion.

Exposure time (days) Treatment group Experiment 1 (ultrasound only)

 Experiment 2 (ultrasound + periosteal trauma)
n Left femur (treated) Right femur (control) Left tibia (treated) Right tibia (control) n Left femur (treated) Right femur (control) Left tibia (treated) Right tibia (control)
0 Active 6 22.00 ± 0.50 21.82 ± 0.39 25.80 ± 0.87 25.90 ± 0.79 6 19.24 ± 0.80 19.11 ± 0.81 26.75 ± 0.70 26.89 ± 0.79
Sham 6 21.47 ± 0.45 21.93 ± 0.60 25.65 ± 0.47 26.13 ± 0.90 6 19.64 ± 0.23 19.89 ± 0.75 27.25 ± 0.79 27.20 ± 0.93
Normal 4 22.32 ± 0.25 21.55 ± 0.89 24.29 ± 0.78 26.07 ± 0.92
14 Active 6 28.39 ± 0.71 28.55 ± 0.65 32.17 ± 0.47 32.35 ± 0.87 6 25.89 ± 0.70 26.36 ± 0.62 33.32 ± 0.62 33.49 ± 0.71
Sham 6 27.91 ± 0.97 28.00 ± 0.60 31.64 ± 0.45 31.53 ± 0.62 6 26.77 ± 0.80 26.93 ± 1.09 34.14 ± 0.80 34.20 ± 0.17
Normal 4 28.69 ± 0.47 28.52 ± 0.77 33.42 ± 1.53 32.84 ± 0.28
28 Active 6 31.25 ± 0.64 31.07 ± 0.64 35.36 ± 0.41 35.34 ± 0.69 6 27.58 ± 1.43 28.72 ± 1.33 36.82 ± 0.59 36.83 ± 0.58
Sham 6 31.02 ± 0.67 31.18 ± 0.97 34.49 ± 0.72 34.45 ± 0.81 6 28.13 ± 1.68 27.87 ± 1.35 37.20 ± 1.11 37.17 ± 1.01
Normal 4 32.16 ± 0.73 32.03 ± 0.41 36.03 ± 0.62 35.89 ± 0.40

In one study I mentioned on this post on ultrasound, Pulsed Wave Ultrasound on the metatarsal was able to increase longiudinal bone growth rate.

Looking at this study:

Effects of growth hormone and ultrasound on mandibular growth in rats: MicroCT and toxicity analyses.

“Mandibular growth can be enhanced by the systemic administration of recombinant growth hormone (rGH) and/or local application of therapeutic low intensity pulsed ultrasound (LIPUS). The purpose of this study was to determine if local injection of rGH and application of LIPUS to the temporomandibular joint (TMJ) would synergistically enhance mandibular growth. In an animal study, the effect of rGH, LIPUS, and combination of rGH and LIPUS on male Sprague-Dawley rats was observed. Mandibular growth was evaluated by measuring total hemimandibular and condylar bone volume and bone surface area as well as condylar bone mineral density (BMD) after 21 days on dissected rats’ mandibles using micro-computed tomography (MicroCT). The expression of c-jun mRNA extracted from the liver of each of these rats was also quantified by real-time polymerase chain reaction to evaluate possible systemic effect of local rGH administration. Significant growth stimulation was observed in the mandibular and condylar bone of the animals treated with rGH, LIPUS, and rGH/LIPUS combined when compared with the control group. Bone volume, surface area, condylar bone mineral density, and c-jun expression were also compared between the treatment groups and the control in the liver. The results suggest that mandibular growth may be enhanced by injection of rGH or LIPUS application. The current study although showed synergetic effect of rGH and LIPUS application in increasing mandibular condylar head length, there was no significant changes in mandibular bone volume using both treatments together when compared to the two individual treatments. Moreover, combined rGH and LIPUS decreased condylar bone mineral density than each treatment separately. Future research could be directed to investigate the effects of different rGH doses and/or different LIPUS exposures parameters on lower jaw growth. ”

Both LIPUS and HGH increased c-Jun expression but HGH did it to a far greater degree.

” 8-week-old male Sprague–Dawley rats weighing 200 g”

Mandibular Condyle seems to respond to different things than other bone types(like femur and tibia) respond to stimuli though.  It’s been shown that LIPUS can affect stimuli involved in height growth like the growth plate directly and mesenchymal stem cells.  Maybe just specific application of LIPUS is needed.  Different frequencies for example could be required to induce longitudinal bone growth.

Update #11 – Decalcification of Bone Layer – February 1, 2014

Update #11 – Decalcification of Bone Layer – February 1, 2014

Decalcification of Bone LayerIn a seminal post I wrote about half a year ago (Why Growing Taller With Closed Growth Plates Is So Difficult To Figure Out And Impossible To Almost All People), I was talking about why it is close to impossible to stretch out bones to make them longer. Bones are not designed to be easily stretched out. From billions and billions of years of natural evolution, the way that the individual units inside the bones are aligned next to each other means that it would be rather difficult to mold the bones into a certain size or shape. (and yes, we are perfectly aware of Wolff’s Law). The problem is not just one problem, but multiple problems. For a long time, I was not sure how to tackle this problem, since it was a nested layer of problems we have to resolve. The way that the bones are actually structured, with the osteons, lamellar layers, and lacunae of osteoblasts, suggest that it would be very hard with today’s technology to say lengthen the bones or regrow growth plates in any way.

In recent months, we have been inundated with quite a few people who commented and said that we need to search for real solutions to the problem. Move away from talking about the problem and actually search for a real solution. Well, I can only say that we are trying our best with the resources that we have at our disposal at this time.

If you add in the fact that we all have our own lives to live, with other responsibilities, it means that the research is going at a snail’s pace. However, that doesn’t mean that we can’t get and find breakthroughs. So far, I would say that we have found at least half a dozen discoveries which can open more doors and paths for us to look into.

How to reopen growth platesA lot of people have been finding this website through searching for terms like “How to reopen growth plates” on Google. Well, we are not sure that you can using some type of normal pill or chemical reopen those growth plates. A common argument we hear is that there is still a thin line called the epiphyseal growth plate line which stays around and never goes away. Maybe we can do something to turn that line back. Well, from the research Ive done, I suspect that even that epiphyseal line would eventually go away after maybe 10 years after full one maturity. After I had to get an X-Ray on my knee about 4 years ago to check for bone spurs from knee pain, I looked very closed at the X-Ray of my tibia/fibula bone couplet and did not see any trace of even the epiphyseal line.

What I would be willing to propose at this point is a two pronged approach, if not a 3 pronged approach.

1. We first have to use something to change the adult adipocyte stem cells in the yellow bone marrow to start to differentiate into the chondrogenic lineage.

Two PubMed studies I haven’t read over yet suggest that it might be possible, if we keep up with the research for another 3-5 years and then create our own lab to test on ourselves.

2. We than have to figure out how to remove the crystals in the cortical layer of the bone which is the main reason we can’t stretch out the bone. Yes, we realize perfectly that the hydroxyapatite is the main component that gives the long bone the ultra-high compressive strength and the collagen is the main component that gives the long bone the nearly as high tensile strength. I however believe that if we can remove enough calcium crystals, but still keep the collagen, the range of a externally loaded Pressure (force/area) at which the bones can stretch, without causing a major fracture would be lowered. Not only that, the range at which you can use the pressure  (as drawn on a stress-strain curve) would be widened. You would be less likely to get a major fracture.

3. The third option I propose is to use a type of high intensity vibration amplifier to get the resonance frequency of the bone, place a sharp edge to the bone, and make micro-fracture cracks on it. The marrow seeps through the cortical bone layer, and turns into cartilage tissue. Of course we have not considered the trabecular bone area at all though, and that could be a big issue.

It might be worth looking over the University of California, Berkeley’s paper “The effect of matrix stiffness on the differentiation of mesenchymal stem cells in response to TGF-Beta“

The Main Issue

Thee main problem (in my opinion) have always been the fact that the bones are just too strong in material strength. They are as strong as stainless steel. I personally think that while the first strategy can be figured out in say 3-5 years, using the right type of electrical stimuli or chemical compound, the 2nd strategy is something that will perplex even the highly trained orthopedic surgeon.

There is the idea of using a series of needles with some type of weak acid (like Apple Cider Vinegar) to slowly diffuse through the skin and react with the calcium crystals of the bone. In theory the calcium crystals are bases and the acid mixed with the bases, mixed with whatever enzyme and catalyst is in the human body, might be able to dissolve the crystals into the blood stream, making a band on the lone bone just weak enough to allow for pulling of the bone.

The last month has been focused on me trying to look up on Google Scholar and Google Patents ideas that people have proposed on how to decalcify or reverse the calcification of bone. I’ve only found mostly quack ideas by people on how to decalcify the pineal gland related to ancient indian medicine, so the search has been elusive.

What I would love to figure out now is what compound is safe enough for us to diffuse into the bone to remove the crystals (aka decalcification of bone layer) and make the bones weaker. Of course, based on how high the material strength is, this idea would not be practical. If a small band on your long bones are weak enough to be stretched out, your body weight pushing down on it due to gravity would shorten it as well. That would be the other problem.

As for My Own Height Increase Progression

I recently spent the half of January in Osaka, Japan for a business trip so there was no way for me to check my height and see whether it has increased. I have been taking the glucosamine sulfate 1000 mg, Vitamin K3, and started to do about 10 minutes of daily stretching so that is fine for now.

I realize now that instead of keeping people on track on the progress of my height increase and whether anything really works, these monthly posts are a good way to tell people thoughts, ideas, and research that I have been getting into. This is good enough for me.