Me: I wanted to go deeper in the research for this method because it looks very promising as another tool. In my opinion, it might be better than LIPUS in helping achieve height increase.

From study 1…

The researchers tried the application of radial extracorporeal shock wave therapy (rESWT) to get bones to growth and form. There was 4000 impulses of the shock waves used on one of the hind legs of 13 rabbits. The other is not treated with rESWT as the control. after a week the shockwaves were doen again. What they found was that the rESWT significantly increase new bone formation at all time points throughout the study’s time period. It is interesting that the rate of bone formation was at the maximum at 4 weeks. The most amazing thing was the the location of the long bone which was closest to the shock wave application was where the most bone formation was found. It seems that the ESWT induced osteogenesis is dosage dependent. The best thing is that so trauma like hemmorhage or microfractures were found. The researchers conclude with “This is the first study demonstrating low-energy radial shock waves to induce new bone formation in vivo. Based on our results, repetition of ESWT in 6-week intervals can be recommended.”

From study 2…

The researchers found that using ESWT was safe and a great alternative for fracture/ non union healing. It seemed to work better for tropic nonunions (with calluses) than atropic nonunions (without calluses). The study dosage is …”The shock waves were applied in 3-5 sessions of 2500 to 3000 impulses each given at 0.25-0.84 mJ/mm2, at intervals of 48-72 hours between sessions. A maximum of 3 cycles of treatment was given, at 3-month intervals.” The healing reduced the time needed for a large percentage but a smaller percentage did not see any healing.

From study 3...

This is another study which comfirms that ESWT is amazing. It has been used to heal achilles tendinitis and the researchers in this study wanted to shows that it heals the tendinitis by increasing the expression of TGF-Beta1 and IGF-1. The study varied the impulse dosage from 0, 200, 500, and 1000 impulses. The optimal dosage for the mice in the study was around 200 impulse at around 0.2 mJ/mm^2. Through out the entire study the expression of IGF-1 was elevated dramatically. It seems to show that cell proliferation, cell hypertrophy, and tissue regeneration were all effects. There was also a proliferation of tenocytes and neovascularization (new blood vessels).

From ScienceDirect.com study link HERE…

Radial Extracorporeal Shock Wave Therapy (rESWT) Induces New Bone Formation in vivo: Results of an Animal Study in Rabbits

Abstract

The aim of this study was to investigate if radial extracorporeal shock wave therapy (rESWT) induces new bone formation and to study the time course of ESWT-induced osteogenesis. A total of 4000 impulses of radial shock waves (0.16 mJ/mm²) were applied to one hind leg of 13 New Zealand white rabbits with the contralateral side used for control. Treatment was repeated after 7 days. Fluorochrome sequence labeling of new bone formation was performed by subcutaneous injection of tetracycline, calcein green, alizarin red and calcein blue. Animals were sacrificed 2 weeks (n = 4), 4 weeks (n = 4) and 6 weeks (n = 5) after the first rESWT and bone sections were analyzed by fluorescence microscopy. Deposits of fluorochromes were classified and analyzed for significance with the Fisher exact test. rESWT significantly increased new bone formation at all time points over the 6-week study period. Intensity of ossification reached a peak after 4 weeks and declined at the end of the study. New bone formation was significantly higher and persisted longer at the ventral cortex, which was located in the direction to the shock wave device, compared with the dorsal cortex, emphasizing the dose-dependent process of ESWT-induced osteogenesis. No traumata, such as hemorrhage, periosteal detachment or microfractures, were observed by histologic and radiologic assessment. This is the first study demonstrating low-energy radial shock waves to induce new bone formation in vivo. Based on our results, repetition of ESWT in 6-week intervals can be recommended. Application to bone regions at increased fracture risk (e.g., in osteoporosis) are possible clinical indications.

Me: For me this is quite possibly the biggest find I have encountered in a long time and a major breakthrough. I know that the LIPUS technology used low intensity pulsed sound waves but this approach is the exact opposite, which uses high intensity shockwaves to get bones to heal. The amount of research and information out there is very high and it’s application for bone remodeling is high as well.

From study 1…

What we are seeing is that the ESWT technology has been around and acknowledged by medical professionals for at least 2 decades. This study shows that just like the PEMF and LIPUS technology, it can cause bone fractures or non-unions to heal together. The amount of high intensity pulsed wave is 6000 at 28kV in one session. A amall sample of blood was taken to test for NO level, TGF-Beta 1, VEGF, and BMP2, as well as calcium, alkaline phosphatase, calcitonin, and parathyroid hormone during 5 time zones, before the treatment, 1 day afterwards, and 1,3,and 6 months afterwards. In over 3/4th of the patients, there was union of the fracture. It seems that shockwaves caused an increase in the NO level and other osteogenic growth factors.

From study 2...

It seems that the ESWT technology has been used quite extensively in recent years as an alternative treatment from surgery. There are success in clinical and in vitro studies. The final conclusion…”FGF-2, an important growth factor in new bone formation, was shown to be produced by human fibroblasts and osteoblasts after treatment with ESWT. These findings demonstrate that ESWT is able to cause bone healing through a molecular way by inducing growth factor synthesis.”

From study 3…

Apparently the researchers have already looked into how to increase the long bong longitudinal growth rate by “We have studied several possibilities in order to stimulate longitudinal growth by means of enhancement of the vascular supply to the growth plate through perforations, implants or electromagnetic pulses.” So they looked into make a distraction, adding implants, and trying out E&M pulses like the PEMF technology. In this specific study it is stated…”we explored the effects of Extracorporeal Shockwave Therapy (ESWT) in the same animal model, to determine a possible longitudinal bone growth stimulation“. This is huge!! It is almost very much like the noninvasive electrical device patent we looked at a month back. The performed it on 24 rabbits putting the ESW stimulation on the tibia and femur using both a mid level pulse and a high level pulse. The left limbs were treated with 2000 pulses. There doesn’t seem to be any differences in cell count, fracture formation, periosteal reaction. However the longitudinal increase was 4.1% on average for all the limbs.

From PubMed study 1 link HERE…

Nitric Oxide. 2009 Jun;20(4):298-303. Epub 2009 Mar 10.

The effects of shockwave on bone healing and systemic concentrations of nitric oxide (NO), TGF-beta1, VEGF and BMP-2 in long bone non-unions.

Me: When I was doing research on the effects of  combining Gonadotropin releasing hormone analogues (GnRH-A) with human growth hormones (hGH) as a way to treat the many diverse forms of short stature, this very interesting disorder really caught my attention and I wanted to devote some time to learn more about this disorder since it might help us remove some confusion over certain issues. We know that the control and flow of the sex hormones is what can ultimately determine out final height since we have already seen how certain people without the right types of hormones or hormone receptors never even reach puberty or don’t have closed growth plates resulting in continued growth even into their 30s.

Analysis & Interpretation:

There is two main conditions we are finding with very similar names, except that one process is the opposite of the other. One is called Hypogonadotropic Hypogonadism and the other is called Hypergonadotropic Hypogonadism. The prefix “hyper” has always meant “excessive” in common english terms while the prefix “hypo” means “not enough” in common english terms. From the two Wikipedia articles I have posted below, the summarize idea is that HH and HH, the hyper and the hypo, both results in hypogonadism, which is where the body doesn’t get enough hormones from the gonads, the reproductive organs. The hypogonadotropic hypogonadism sees an impaired secretion of the gonadotropins like the FSH and LH by the pituitary gland and the hypothalamus of the brain. Since the endocrine system works from a top–>down approach, this will eventually lead to less sex hormones produced in the gonads of the person. The is why the 2nd term is hypogonadism.

The hypergonadotropic hypogonadism in comparison has the pituitary gland and the hypothalamus being just fine in function and releasing the neccessary amount of gonadotropins like the FSH and the LH but the problem is that the gonads can’t seem to be able to receive the gonadotropins or can’t process them correctly to release the high enough levels of gonad hormones, like the androgen and estrogen. The symptoms of hypogonadism in general is low sex drive, infertility, and not puberty signs like hair growth, etc. To treat the first type, where the brain areas don’t release enough, physicians can directly add the needed hormones using a GnRH agonist or a gonadotropin formulation. To treat the 2nd type, the physician can just add synthetic androgens as a hormone therapy to get the level of sex hormones in the body correct.

The connection with height increase with the two conditions is that from many genetic disorders and cases, we find that people who have no sensitivity to the sex hormones like the androgens or estrogen have often led to delayed puberty, and thus resulted in a later age for growth plate cartilage closure. There are at least 3 cases of males who had no receptors for the estrogen in their growth plates and they resulted in being very tall with the cartilage still existing in late adulthood.

From my personal analysis, it would seem that the case for tall stature can only be found with people who suffer from hypergonadotropic hypogonadism, NOT hypogonadotropic hypogonadism.  I would guess that the lack of ability to release the FSH and the LP by the hypothalamic-pituitary connection would also cause insufficient release of the growth hormones too. So it would make logical sense then that the human body which can release growth hormones but stop the process of reeleasing the testosterone and estrogens which will lead to both puberty/increased growth rate but also growth plate closure means that the person who suffers only from hypergonadotropic hypogonadism will note that they never went through the great growth spurt that their peers did in adolescent, noticed that they were more likely on the short side while young, but as they grew older, they did not stop growing completely like their peers but eventually surpasses in height of their peers in their late 20s due to their open growth plate cartilage.

From the Wikipedia article on it HERE…

Hypogonadotropic hypogonadism (HH), also known as secondary or central hypogonadism, as well as gonadotropin-releasing hormone deficiency or gonadotropin deficiency (GD), is a condition which is characterized by hypogonadism due to an impaired secretion of gonadotropins, including follicle-stimulating hormone (FSH) and luteinizing hormone (LH), by the pituitary gland in the brain, and in turn decreased gonadotropin levels and a resultant lack of sex steroid production.

Causes

The type of HH, based on its cause, may be classified as either primary or secondary. Primary HH, also called isolated HH, is responsible for only a small subset of cases of HH, and is characterized by an otherwise normal function and anatomy of the hypothalamus and anterior pituitary. It is caused by congenital syndromes such as Kallmann syndrome and gonadotropin-releasing hormone (GnRH) insensitivity. Secondary HH, also known as acquired or syndromic HH, is far more common than primary HH, and is responsible for most cases of the condition. It has a multitude of different causes, including brain orpituitary tumors, pituitary apoplexy, head trauma, ingestion of certain drugs, and certain systemic diseases and syndromes.

Symptoms

Examples of symptoms of hypogonadism include delayed, reduced, or absent puberty, low libido, and infertility.

Treatment

Treatment of HH may consist of administration of either a GnRH agonist or a gonadotropin formulation in the case of primary HH and treatment of the root cause (e.g., a tumor) of the symptoms in the case of secondary HH. Alternatively, hormone replacement therapy with androgens and estrogens in males and females, respectively, may be employed.

Now let’s look at the opposite of it which is termed Hypergonadotropic Hypogonadism

From the Wikipedia article on it HERE…

Hypergonadotropic hypogonadism (HH), also known as primary or peripheral/gonadal hypogonadism, is a condition which is characterized by hypogonadism due to an impaired response of the gonads to the gonadotropins, follicle-stimulating hormone (FSH) and luteinizing hormone (LH), and in turn a lack of sex steroid production and elevated gonadotropin levels (as an attempt of compensation by the body). HH may present as either congenital or acquired, but the majority of cases are of the former nature.

Causes

• Chromosomal abnormalities (resulting in gonadal dysgenesis) – Turner’s syndrome, Klinefelter’s syndrome, Swyer’s syndrome, XX gonadal dysgenesis, and mosaicism.
• Defects in the enzymes involved in the gonadal biosynthesis of the sex hormones – 17α-hydroxylase deficiency, 17,20-lyase deficiency, 17β-hydroxysteroid dehydrogenase III deficiency, and lipoid congenital adrenal hyperplasia.
• Gonadotropin resistance (e.g., due to inactivating mutations in the gonadotropin receptors) – Leydig cell hypoplasia (or insensitivity to LH) in males, FSH insensitivity in females, and LH and FSH resistance due to mutations in the GNAS gene (termed pseudohypoparathyroidism type 1A).

Acquired causes (due to damage to or dysfunction of the gonads) include gonadal torsion, vanishing/anorchia, orchitis, premature ovarian failure, ovarian resistance syndrome, trauma, surgery, autoimmunity,chemotherapy, radiation, infections (e.g., sexually-transmitted diseases), toxins (e.g., endocrine disruptors), and drugs (e.g., antiandrogens, opioids, alcohol).

Symptoms

Examples of symptoms of hypogonadism include delayed, reduced, or absent puberty, low libido, and infertility.

Treatment

Treatment of HH is usually with hormone replacement therapy, consisting of androgen and estrogen administration in males and females, respectively.

Me: This study is one of those studies which make me believe that the LSJL method may actually indeed work in causing some form of long bone lengthening. Sure, there are some obvious clear differences between the two ideas. The biggest one is that while this study involved axial compression on the long bone, the LSJL loading method involved loading and compression in a lateral direction. Right off the bat the researchers admit that with again, the skeleton lose its ability to respond to mechanical stimuli, so at least they get that quick rebuttal in theory arguement taken care of. They are hypothesizing that the loading would be less responsive but we already know that (so why are they doing this experiment??). From both the aged and young mice, if we load on the mid diaphysis area of the long bones, there is an analbolic response from the periosteal side (outside layer) and the endocortical side (inside layer). They say that with increase peak force, the bone formation was higher. Apparently aged mice had a far bigger response to the loading than young mice at least for the endocortical (inside) layer which surprised the researchers. The results…”Responses at the periosteal surface did not differ between age groups (p > .05). The loading-induced increase in bone formation resulted in increased cortical area in both age groups (loaded versus control, p < .05).”  They conclude with..”In summary, 1 week of daily tibial compression stimulated a robust endocortical and periosteal bone-formation response at the mid-diaphysis in both young-adult and aged male BALB/c mice. We conclude that aging does not limit the short-term anabolic response of cortical bone to mechanical stimulation in our animal model.

Implications: This does make me wonder whether LSJL might really do work since we can use a thought experiment (like how einstein used to do). Let’s imagine that the long bone is surrounding by some thicker layer of cortical bone even in the epiphysis. If the compression at a axial direction on the middle diaphysis area results in the same rate of periosteal growth in both aged and young mice, then the compression of the epiphysis may actually in crease bone lengthening because the periosteum wraps around the entire long bone and even underneath the articular cartilage of the. The loading of the epiphysis would lead the bones to react by causing the peristeal layer to grow appositionally on the epiphysis which means that the axial ends do indeed get thicker and thicker which means the bones really do get longer so height is increased. Age seems to have no effect in decreased bone sensitivity, at least for the initial beginning loading. It might be that what you do from the beginning of LSJL program is what can result in the most bone/ periosteal growth lengthening, or at least until you might stop doing it for a while and go back to it a few weeks later allowing for the bone sensitivity to come back, if it ever truly do. 

From PubMed study link HERE…

J Bone Miner Res. 2010 Sep;25(9):2006-15.

Aged mice have enhanced endocortical response and normal periosteal response compared with young-adult mice following 1 week of axial tibial compression.

This is something which I found today while I was going around the internet checking links. It is from a site HerbalCureIndia.Com. What is really interesting is that this webpage actually provides a height increase compound mixture which is really surprising. What I wanted to do is maybe go through this list and see what are the English, or scientific, or chemical names for these compounds. This is a list of minerals and plants you combine their extracts together to form a height increasing aryuveda homeopathic medicine capsule.

Ingredients

• Withinia somniferra 75 mg
• Puraria tuberose 75 mg
• Lepidium sativum 150 mg
• Gentiana sativum 150 mg
• Acacia Arabica 50 mg
• Ephedra gerardiana 5 mg
• Cassia tora 30 mg
• Oroxylum indicum 30 mg
• Mucana pruries 50 mg
• Cassytha filiformis 10 mg
• Lauh bhasam 10 mg

One thing that has already caught my eye is the mucana pruries which I have looked into before (velvet beans) which does have a link to extra HGH release and L-Dopa. It should be spelled actually Mucuna pruriens. From the wikipedia article on the pruriens HERE…

Pharmacology

M.pruriens seeds contain high concentrations of levodopa, a direct precursor of the neurotransmitter dopamine. It has long been used in traditional Ayurvedic Indian medicine for diseases includingParkinson’s disease. In large amounts (e.g. 30 g dose), it has been shown to be as effective as pure levodopa/carbidopa in the treatment of Parkinson’s disease, but no data on long-term efficacy and tolerability are available.

In addition to levodopa, it contains serotonin (5-HT), 5-HTP, nicotine, N,N-DMT (DMT), bufotenine, and 5-MeO-DMT. As such, it could potentially have psychedelic effects, and it has purportedly been used in ayahuasca preparations.

The mature seeds of the plant contain about 3.1-6.1% L-DOPA, with trace amounts of 5-hydroxytryptamine (serotonin), nicotine, DMT-n-oxide, bufotenine, 5-MeO-DMT-n-oxide, and beta-carboline. One study using 36 samples of the seeds found no tryptamines present in them.

The leaves contain about 0.5% L-DOPA, 0.006% dimethyltryptamine (DMT), 0.0025% 5-MeO-DMT and 0.003% DMT n-oxide. The ethanolic extract of leaves of Mucuna pruriens possesses anticataleptic and antiepileptic effect in albino rats. Dopamine and serotonin may have a role in such activity.

Me: This is the actual ingredients of the capsule which is very interesting! If I even do a quick search on the first plant/mineral on the list Withinia somniferra, it turns up a PubMed study (link HERE). Another name for it is ashwagandha. From another study (source HERE) it seems that ashwagandha can reverse Alzheimer’s Disease Pathology suggesting it does it by enhancing low-density lipoprotein receptor-related protein in liver

Altern Med Rev. 2000 Aug;5(4):334-46.

Scientific basis for the therapeutic use of Withania somnifera (ashwagandha): a review.

Me: What is below is from the webpage which is linked above.

Increase your Height Growth Naturally

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This is because in addition to the length of the femur bone (thighbone), shinbone, and other bones in the lower body, the length of the spinal column in the upper body also significantly addto human height (about 35% of the total height). Anatomically human spinal cord consists of 33 bone segments known as vertebrae detained together by ligaments (tough and fibrous tissue). Out of these 33 vertebrae, only the lowest 9 vertebrae are merged into two immovable bones, the sacrum and the coccyx, forming the back of the pelvis. All the other 24 vertebrae are enduringly movable and thus will never get fused (until some deformity). These 24 vertebrae are the 7 cervical (neck), 12 thoracic (back of chest), and 5 lumbar (loin). Situated between each of these twenty four vertebrae bones are cartilage pads known as disks . The thickness of the disks establishes the length of the spinal cord and unswervingly influencing the height. There are totally twenty five such disks, their mutual length accounts twenty five percent of the total height. As these disks never fuse, they continuously grow thicker under the spur of growth hormone all our life.  The thicker these disks are, the longer the spinal cord is and the taller you grow. Even each disk grows only 0.25 cm thicker, that means you will grow 0.25 * 25 = 6.25 cm i.e. 2.5 inches taller! Wow….. that’s amazing. In addition providing you the extra centimeters you always desired, you has been proven to boost blood circulation, improve digestion, augment metabolism, decrease tiredness, retard aging, regularizes breathing and promote general good health. Truly Height Increasing Capsulesis the fantastic way to grow taller and remain healthy at the same time! Increase your height the best way without any side effects and at the lowest prise ever. Recent Questions Is there any herbal Supplement To Increase Height? I am a 15 years old female. 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Me: These types of studies are really the best type for us to see how they would effect the bones. From the 1st study, we see that from just adding 1 microgram of aFGF either every other day or every day we can get larger callus size, greater collagen content, more DNAm and also soft cartilagous callus. The calluses for the aFGF injected are bigger for at least 4 weeks until it was taken over by trabecular bone. However there was evidence from the histological testing that the mRNA expression for certain types of procollagen was lower.

From study three, we have just one injection of 100 microgram of basic FGF (bFGF) which increases the Collagen Type X and Type II mRNA expression (in hypertrophic and proliferative chondroctyes respectively) and increase the proliferation of chondroprogenitor cells in fracture callus, and thus contributes to the formation of a larger cartilage. This does not cause the ossification and maturation of the chondrocytes though. The healing process has not been decreased. In terms of height increase, this is a fascinating growth factor because it does not cause the ossification to overcome the new chondrocytes too quickly. Since maturation and ossification is the irriversible proess hypertrophic chondrocytes turn into the eventual bone, what we should be doing is maximizing the number of chondrocytes but also delaying the time of maturation. 

From study two, we have the experiment repeated with one injection of 100 microgram of bFGF encapsulated in 200 microliter of fibrin gel. The results and evaluated parameters of the bone union rate, bone mineral density (BMD), and mechanical properties (strength and stiffness) of the callus was no different between the control group and the FGF injected group. the mRNA expression was also not changed much between the two groups. Again, the author states that the FGF makes the callus from the distraction larger but the healing process is not accelerated. 

From PubMed study link HERE

Acidic fibroblast growth factor (aFGF) injection stimulates cartilage enlargement and inhibits cartilage gene expression in rat fracture healing.

From PubMed study link HERE 

Effects of a single percutaneous injection of basic fibroblast growth factor on the healing of a closed femoral shaft fracture in the rat.

From PubMed study link HERE

Spatial and temporal gene expression in chondrogenesis during fracture healing and the effects of basic fibroblast growth factor.