Product Review XII: Increase Height And Grow Taller Using GHenerate And I-GH-1

From looking through the old forums, another product or substance was talked about a lot, a type of Growth Hormone spray named GHenerate. It is a clever marketing name of putting GH and generate together.

In terms of real use, the product from the LG Sciences website HERE was created to have these types of benefits…

  • Massive pumps
  • Increased Recovery
  • Increased Sleep Quality
  • Body Recomposition
  • Increased Erection “hardness”
Nothing states anything about potential height increase. It is important to note that when you decide to take this compound Ghenerate, you also seem to get another supplement along with it, (or at least you are supposed to), the I-GH-1.

Supplement Facts

Serving Size: 6 Sprays (Approx 1ml)
Servings Per Container: 120
% Daily
Value *
Amount Per Serving
Proprietary Blend†mg83
Hydroxy Propyl Beta Cyclodextrin
Puerarin 98%
GHRP – Marus Alba Extract
*Percent Daily Values are based upon a 2,000 calorie diet.
† Daily Value not Established
OTHER INGREDIENTS: Citric Acid, Soy Lecithin, Potassium Sorbate Calcium EDTA(freshness), Sodium Benzoate, Sucralose, Natural and Artificial Flavor, Purified Water, Chitosan.
DIRECTIONS: Spray 6 pumps under your tongue. Enjoy the flavor under your tongue for 60 seconds, then swish around the mouth and finally swallow completely. On workout days: take 6 sprays before training and 6 sprays prior to sleep. On off days: take 6 sprays before noon and 6 sprays prior to sleep.

From the supplements  page HERE, this is what is inside the product.

For the I-GH-1 product, these compounds are inside.

I-GH-1

Supplement Facts

Serving Size: 1 Capsule
Servings Per Container: 100
% Daily
Value *
Amount Per Serving
GH Secretagogue Complex†mg760
Arginine Pyroglutamate
Ornithine AKG
Murcuna Puriens (standardized for L-Dopa)
Astragalus Membranaceus (Root)
L-Lysine
*Percent Daily Values are based upon a 2,000 calorie diet. † Daily Value not Established
OTHER INGREDIENTS: DiCalcuim Phosphate Dihidrate, Magnesium Stearate, Gelatin FD&C Red Dye #40, FD&C Blue Dye #1, Titanium Dioxide.
RECOMMENDATION: Take 4-7 capsules per day on an empty stomach. On workout days take 20 minutes prior to workout. On non-workout days, take before bedtime. Stack with Methyl 1-D to increase strength and mass or Speed V2 to increase fat burning.

—————————-
“LG Sciences GHenerate Puerariae Radix is a plant that has one particular constituent that is set to be the next superstar. It is called puerarin. Puerarin is an amazing nutrient that shows a 520% increase in growth hormone release by stimulating the GHRH receptor. This ingredient was an amazing find but the key is the liquid “under the tongue” bioavailability which makes it biologically active. 520% increase in circulating GH is a huge increase and shows that this second pathway is very potent at releasing GH.”

Me: From the website Supplement Reviews, most people who bought it gave it a very low rating (2 out of 10) and it sells for from $9-$26. From the LG Science website, this is the claims…

So the key ingredient that is in the GHenerate is something called puerarin which is supposed to be able to show a increase of GH release by stimulating the GHRH receptors. Of course, we all remember that there are many other compounds out in the market that claims to do the same thing. The majority of claims state that the Ghenerate product seems to allow them to sleep better, and nothing about the possibility of growing taller.

So let’s see if there is a real link between height increase and the use of GHenerate. From a discussion on the Bodybuilding website HERE…Most of the responses on the bodybuilding forum states that the product will not work if you are physically mature and your growth plates are gone.

It appears that HeightQuest also did a post about the possibility of using GHenerate to increase height HERE. Tyler’s states,

“”GHenerate, which is produced by LGSciences, contains puerarin which is a strong bone growth and PI3K pathway stimulator.  PI3K is a potent anabolic stimulus.  Puerarin stimulates osteoblasts and may increase height if the osteoblasts decide to deposit new bone on the surface of the long bones.  PI3K is also anabolic to chondrocytes but I don’t see how a PI3K stimulator alone is making people 1 to 2 inches taller in such a short time frame””

He does show from the post that the compound ingredients do have studies done that show that they have some effect on chondrocyte proliferation and differentiation, for the puerarin and Marus Alba. His advice at the end was to skip the GHenerate product and just buy plain puerarin.

From the Anabolc Minds website HERE , one of the posters names PhenomHCL wrote two REALLY interesting posts which you definitely need to read about what can be done, which my research have already sort of concluded.

  1. PhenomHCL

    Registered User

    Hexarelin only increases cortisol and prolactin, during a PRE-BED dose from one of the studies ive read, before sleep, its fine to dose it in the morning and noon.

    You want to take Hexarelin because its a potent activator of the pi3k pathway, it activates the “pi3k pathway” which is responsible for quite a bit of longitude bone growth.

    Yes you use the blockers to keep the counteractive effects of Hexarelin and the daily grind at bay.

    The Fluoride blockers are (Note** they dont totally remove fluoride from your body, but they will remove a good amount of it away from your bones, teeth, and pineal gland and w/e else fluoride is stored in your body, you will DEFINITELY need this to achieve bone growth and neurogenesis) –

    Melatonin
    Niacin
    Potassium
    Iodine
    Tumeric Powder (this is in indian foods, especially currys, it helps kill fluoride, if you can get this by itself use THIS to brush your teeth instead)
    Multi-Vitamin
    COD Fish Oil
    Omega-3
    Calcium Tablets

    Dont worry about buying a “Water filter” they may claim to remove fluoride from the water supply in your house, but no water purifier/filter actually does remove fluoride.

    Prolactin Blockers –
    L-Dopa
    DOPA Mucuna by NOW Foods- You can get this from Nutraplanet

    Cortisol Blockers –
    Staying Positive
    EndoAmp Max – Primordial Performance – You can get this from Nutraplanet
    Erase – Performance Enhancing Supplements – Nutraplanet

    Foods Best to stay away from –
    Milk/Dairy in general
    Soda
    Junk food in general
    If you could stay away from red meat, and eat fish, and to a lesser extent chicken, then that will be very good.
    Breads
    Processed foods
    Candy

    Goods foods –
    Rice
    Herbs/Veggies (is where your calcium should come from, herbs are packed with calcium that your bone can actually use)
    Fish
    Beans
    Lentins
    Anything vegetarin with fish and to a lesser extent chicken is good.
    Eggs
    Fruit
    Nuts

    Also add in –
    MSM and Chondroitin – NOW FOODS- Nutraplanet
    SAM-e – – NOW FOODS – Nutraplanet
    Creatine Mono -A Standard one will be fine – Nutraplanet
    BCAA’s – A Standard one will be fine – Nutraplanet
    It will also help a lot if you had an N.O product, for better blood flow, which will help greatly, not a lot of N.O products are really legit tho, but Amplify 02 is pretty good, i recommend that – Need2BuildMuscle

    Now thats just the info im gathering from the studies i’ve read, i’ve also read studies where, HEX doesnt cause de-sensitization, doesn’t increase PRL, and actually decreases cortisol.

    But it’s best to take these pre-cautions since its not guaranteed and its best to be prepared just incase HEX does cause a slight rise in cortisol and PRL.

  2. PhenomHCL

    Registered User

    And if your really desperate for height, the steroids, Anavar, Oxandrolone, Letrozole (this will slow down estrogen sealing your growth plates) and Sustanoon 250, will give you height, a max of about 3-4 inches, but one the cycle is over, thats pretty much GAME OVER, for continuing to grow after that, im not against steroids, but from the studies ive read, they help “kids with short stature” in growing taller but “long term growth is stunted” as in overall long term “growth”

    IMO i think the peptides are a far better choice, since they stimulate your own GH production, cheaper, easier to get a hold of, and you can use them for a very very very long time AND they also increase your I.Q and brain power through neurogenesis!!!! 

    Also the C-type natriuretic peptide (CNP) regulates endochondral bone growth, and from the studies ive read, im pretty sure Niacin and Melatonin is a CNP stimulator, so is GH -> IGF-1 and the Pi3k pathway.

    I ALSO FORGOT, add HUPERZINE A to the stack aswell, you will definitely need it 

    You will definitely grow taller with these compounds even if its over the course of 2 years what height do you want exactly tho ? 6’1?

    P.S
    Dont worry about Acromegaly, you have to be born with the genes to pick it up.
    We’re really small for our ages, so we won’t get it, also don’t worry about horizontal bone growth, since the blockers and extra supplements, will open up the metaphorically “locked doors” in your body for longitude bone growth instead of horizontal bone growth as long as you take the blockers and extra supps it will be fine , from the studies ive read.

    Oh and here are the sports/physical activities you will need to do (Anti-Gravity training) –
    Stretching
    Sleeping (WITHOUT A PILLOW, so the spine can stretch out, since during the day you head/spine is fully straightened out its only when you go to sleep, and sleep with your head on the pillow that the spine has slight tilt up, thats not natural, you NEED to sleep without a pillow for max growth)
    Doing the monkey bars for at least 20-30 minutes, wear gloves when you do it, since it causes blisters on your hands, and it stings your hands , it stung mine :P.
    Doing sprints
    Doing Squats
    Doing Pull-ups
    Doing Push Ups
    Vertical Jumps
    If you play basketball that helps, but its not “basketball” that helps, its all the sprinting, quick turning and jumping that helps, you can do all those activities outside of basketball, but if you play b-ball it saves time, i dont play b-ball.
    And cycling for 30-60 minutes a day, real cycling outside, not stationery.

    Keep “ejaculation” down to a max of 2 times a week since the IGF-1 will go into repairing your semen instead of the bones, but i guess you could theoretically supplement with Zinc/Multi after ejaculation, just depends how important growing taller is to you :P.
    Dont, not-ejaculate, since you need to keep your feedback loop positive, just minimise it to 2 times a week.

This compound was also talked about on the GrowTallerForum.com website and well as giant scientific. On GS, one of the posters named Monaug5 used the Ghenerate product with I-GH-1 in a routine to increase his height from 5’8″-5’10”. He was also using the sleeping with ankle weights method which is sort of controversial and has been known to cause a lot of pain. The forum discussion can be found HERE.

Conclusion: This product is one of those compounds that I can not make a full claim on. It seems to increase height for a few select height increase enthusiasts, which they had implemented in a long term height increase routine and program. The active ingredients seem to have some study backing them up. If I was to bet though, I would rather buy the peurarin instead of the GHenerate product to try it out.

The Wolff’s Law On Bone Transformation And Remodeling, Part I

From Sky’s EasyHeight website I was introduced to this old theory created by a german bone surgeon, Julius Wolff. Wolff created the law called the Wolff Law For Bone Remodeling or Bone Transformation.

One of Sky’s main reasons and driving forces on why he believed human height increase was possible from using ordinary exercises and stretching methods was from the Wolff Law h was introduced to in his studying and research. From using the WayBack Machine on his website HERE…, he writes

Proof – how bone remodeling works

By: Ryan Nguyen

In 1892, Dr. Wolff’s theory about bone transformation was published. One hundred years later, bone remodeling is now a medical fact!

Bone is anisotropic (it has different strength and stiffness depending on the direction of the load). Bone will grow, build, adapt, transform, and remodel due to enormous stress or force. The larger the forces the shin bone sustains, the greater the osteoblast response.

For example, by sitting with 30 lb ankle weight on each leg, the ankle weight and the earth’s gravitational pull will cause your shin bone to remodel. Thus, by eating nutritional foods and taking supplements daily, your shin bone mass density begins to thicken and lengthen due to the downward force exerted by the weights & gravity.

It’s not only about “bone remodeling”, it’s about “bone transformation,” “bone adaptation”.. just type those terms on Google search engine and i’m sure u’ll find a zillion pages to support it.. As matter of fact, these beautiful pictures below already do most of my talking.. be sure to carefully read the caption.


Facts that bones remodel throughout your entire life
FACT #1: Limb lengthening surgery is an excellent example to prove that bones remodel, re-build, grow, thicken, and lengthen due to a stretching force (either by bone growth electric stimulator, or by heavy ankle weights).FACT #2: The Padung or “long-necked” Karen is one of the Karen groups residing in Thailand’s Mae Hong Son province. The Term “long-necked” signifies the practice of adorning their women with brass rings around the neck. Bones in the neck are forced to grow longer because additional rings are added every few months which provide a repetitive and powerful force. One woman in Plam Piang Din Village wears 37 brass rings around her neck and she’s an old lady. Click here for pictures!FACT #3: In USA sports, professional baseball pitchers throwing arm is usually 1 to 2 inches longer than his other arm. (it is due to the vigorous exercise that the “throwing” arm exerts a more powerful force on the bone thus results in the remodeling of the arm). Click here for pictures!FACT #4: In professional Jai Alai almost every player’s right arm is about 1 to 2 inches longer than his left arm (this is considered as of a direct result of repetitive exercise motions). Click here for pic 1, pic 2, pic 3

FACT #5: Bone is a LIVING TISSUE (ask any medical student) and adapt in response to exercise and constantly adjust to the demands placed upon it.

Bone is constantly being formed and resorbed. Bone growth occurs when calcified matrix is formed faster than it is resorbed. Diameter growth occurs when matrix deposition occurs on the outer surface of the bone. Linear growth in long bones occurs at epiphyseal plates. These plates are between the epiphyses and diaphysis of the bone. Columns of chondrocytes on the epiphyseal side divide continuously causing this growth (Silverthorn, 2001).

As the collagen layer thickens, older collagen calcifies and older chondrocytes deteriorate. Osteoblasts lay down a bone matrix on top of a cartilage base. The shaft lengthens as new bone is added at the ends. As long as the epiphyseal plate is active, long bone growth continues (Silverthorn, 2001). Eventually, when the level of sex steroid hormones ceases to increase, the epiphyseal plate is inactivated. This causes long bone growth to stop (Silverthorn, 2001). And this may be the case that many people believe that growing taller after puberty is impossible. Source:www.bae.nesu.edu

FACT #6: Bone will constantly remodel throughout life (ask any doctor). It is necessary to tell the bone where the areas of stress are going to be so that it can remodel and strengthen in preparation for the event. Bone cells, in particular osteocytes, are extremely sensitive to mechanical stress, a quality that is probably linked to the process of mechanical adaptation.

“Throughout life, bone is constantly renewed through a process called remodeling. This process consists of two stages: resorption and formation. During resorption, old bone tissue is broken down and removed by special cells called osteoclasts. Once this has been done, bone formation begins and new bone tissue is laid down to replace the old. This task is performed by special cells called osteoblasts. Osteoblasts produce collagen, enzymes, and other proteins that make up the organic portion of the bone matrix.”

FACT #7: Vigorous exercise and healthful diet with adequate calcium, protein, and vitamin D are essential in achieving sufficient bone mass during the bone adaptation process.

FACT #8: Just like muscle, bones respond to certain kinds of training by hypertrophying. Source: http://www.apsu.edu/glassr/10

FACT #9: Bones are richly supplied with blood from periosteal vessels. Bone growth requires adequate amounts of nutrients, protein, calcium, vitamin D, etc.

FACT #10: By putting enormous stress on bones, cartilage inside bones may become bones.

FACT #11: The actual amount of growth in a bone depends upon the NEED for it (ask any researcher or doctor. As force is applied, the bone will remodel itself to better handle the force. In a basketball player, for example, the bones of the lower legs and feet strengthen to handle the impact of jumping.

Although this will alter throughout life, the main effects will be seen during the period of growth, when remodeling is most evident. It is in this period that the actual length of a limb bone is being determined. The actual amount of growth in a bone depends upon the need for it.

If u sit with weights on a high platform, the shin bone will need to reach deeper & deeper to the ground b/c the weights are pulling it down & that’s where the NEED is..for another instance, if u bike with raised saddle seat, the shin bone will NEED to reach more & more to reach the pedals..

FACT #12: Loading (stressing) a bone produces in it a small electrical field called piezo electric force, that needed to stimulate new bone formation (for anyone at any age who has sufficient calcium & vit. D).

The vibrating platform appears to work by triggering bones to generate tiny electric fields. These tiny currents may turn on genes that affect bone remodeling and growth.That’s when a series of experiments showed that bone is piezoelectric, meaning that bending or deforming its crystal structure creates local electric currents. Physiologists quickly linked these currents to bone growth in studies that seemed to explain why exercise strengthens bones and immobilization weakens them.”
Source: http://www.rense.com/politics5/mag.htm

Bone remodeling appears to be governed by a feedback system in which the bone cells sense the state of strain in the bone matrix around them and either add or remove bone as needed to maintain the strain within normal limits. The process or processes by which the cells are able to sense the strain and the important aspects of the strain field are presently unknown. Bassett and Becker (4.2.1) reported that bone is piezoelectric, i.e. that it generates electric fields in response to mechanical stress; they advanced the hypothesis that the piezoelectric effect is the part of the feedback loop by which the cells sense the strain field.

Source: http://silver.neep.wisc.edu/~lakes/BoneRemod.html

Lastly, the discovery about piezo electric force inspired scientists to create different devices to encourage the body to make its own electric fields for building bones.” (Source: http://www.rense.com/politics5/mag.htm

FACT #13: Bone adaptation was entirely defined by three constitutive laws:

– The stress-strain law
– The bone density evolution law
– The bone anisotropy evolution law, etc.

More facts and proof coming this Fall & Winter 2004


Ryan’s explanation
For anyone who is 21 years old or younger, the epiphyseal plate remains active and plays a major part in bone growth. Thus, many doctors and researchers believe that growing taller after puberty is not possible because the epiphyseal plate is closed.In contrast to the theory above, I believe that for those who are 21 years old or older, vigorous exercise and healthful diet with adequate calcium, protein, vitamin D, and supplements may replace the role of epiphyseal plate. Thus, bone adaptation is forced to occur because stress is exerted and supplements & vitamins continuously supply nutrients and food for bones.In other words, anyone who is 21 years old or younger, the epiphyseal plate remains active to give you that natural growth and your height is determined mostly by heredity or genetic factors. Whereas, those who are 21 years old or older do NOT depend on genetic factors but on stress factors & vitamins & supplements.

Fact: The shape, strength, growth and form of a bone is determined not only by heredity but by the work it has to perform.

Proof – how bone remodeling works


Factors part of bone growth remodeling stage:

Piezo weak electrical currents (from kicking/biking with ankle weights)

Osteocytes

Osteoblasts

Stress factors (from sitting with ankle weights)

Calcium

Vitamin D

Centrum multi-vitamin (proteins)

Glucosamine

Chondroitin

Collagen fibers

Fibroblasts

Spongy bone

Bony callus

Compact bone

Shin bone (tibia)

Fibula

Enzymes

Bone matrix

Blood

Etc.

Below are some breathtaking pictures about bone remodeling.. be sure to read the caption carefully.

Did you know that your body gets taller in space? Because the spine is no longer compressed by the force of gravity, the vertebrae separate slightly from one another and the person’s body lengthens. This is NOT an example of bone remodeling because there is no force exerted on your body. However, it’s a great comparison between force and gravity. Lastly, your spine lengthens in space because gravity does not on act on it.
Gravity does an amazing job in remodeling your bone. That explains why and how astronauts lose bone mass after being exposed to the weightlessness of space.

More pictures & proof coming this fall & winter 2004!

Me: This is what Wikipedia states about the Wolff’s Law (source HERE)

Wolff’s law is a theory developed by the German anatomist and surgeon Julius Wolff (1836–1902) in the 19th century that states that bone in a healthy person or animal will adapt to the loads it is placed under.[1] If loading on a particular bone increases, the bone will remodel itself over time to become stronger to resist that sort of loading. The internal architecture of the trabeculae undergoes adaptive changes, followed by secondary changes to the external cortical portion of the bone,[2] perhaps becoming thicker as a result. The converse is true as well: if the loading on a bone decreases, the bone will become weaker due to turnover, it is less metabolically costly to maintain and there is no stimulus for continued remodeling that is required to maintain bone mass.[3]

In relation to soft tissue, Davis’s Law explains how soft tissue remolds itself according to imposed demands.[edit]Associated laws

  • Refinement of Wolff’s Law: Utah-Paradigm of Bone physiology (Mechanostat Theorem) by Harold Frost.

Examples

Tennis players often use one arm more than the other
  • The racquet-holding arm bones of tennis players become much stronger than those of the other arm. Their bodies have strengthened the bones in their racquet-holding arm since it is routinely placed under higher than normal stresses.
  • Surfers who knee-paddle frequently will develop bone bumps, aka exostoses, on the tibial eminence and the dorsal part of the navicular tarsal bone from the pressure of the surfboard’s surface. These are often called “surf knots.”
  • Astronauts who spend a long time in space will often return to Earth with weaker bones, since gravity has been absent and therefore has not exerted a force on their bodies.
  • Weightlifters often display increases in bone density in response to their training.
  • Martial artists who strike objects with increasing intensity (e.g. repeated elbow strikes), display increases in bone density in the striking area. This process is termedcortical remodeling.

From the website Teambone.Com….

After nearly 25 years of work in skeletal anatomy, adaptation, and orthopaedics, Julius Wolff published his seminal 1892 work on bone ‘transformation’ (known today as bone remodeling and modeling). Wolff’s work and his general view of how a limb bone’s morphology develops has evolved into a nebulous concept known as “Wolff’s law”, which is essentially the observation that bone changes its external shape and internal (cancellous) architecture in response to stresses acting on it. Although the rationale for the existence of Wolff’s law has been challenged on many fronts (e.g., Bertram and Swartz, 1991; Cowin, 1997; Currey, 1997; Cowin, 2001), many contemporary investigators still ascribe to the idea that there is a “Wolff’s law” that states that bone models and remodels in response to the mechanical stresses it experiences so as to produce a minimal-weight structure that is ‘adapted’ to its applied stresses.

For example, should a fracture of a weight-bearing long bone heal with an angulation, each step that the patient subsequently took would result in a bending stress with compression on the concave side at the angulation and tension on the convex side. Rather than progressively weaken the bone structure at this site, such repeated mechanical stress results in a modeling and remodeling, with new bone growth on the concave side and bone resorption on the convex side. If the patient is young enough, the bone will ultimately grow straight. In control-system terms, the applied mechanical stress causes a growth response that negates the applied stress — a closed-loop negative-feedback control system.

Many authors have made relevant observations regarding the phenomena of bone modeling and remodeling. An orthopaedic surgeon named Harold Frost made the following salient points:

  1. Remodelling is triggered not by principal stress but by “flexure”.
  2. Repetitive dynamic loads on bone trigger remodelling; static loads do not.
  3. Dynamic flexure causes all affected bone surfaces to drift towards the concavity which arises during the act of dynamic flexure.

To define some basic terms of bone growth, we have compiled the following list of characteristics in the formation (osteogenesis), modeling and remodeling of bone.

Osteogenesis

  • Bone formed on soft tissue
  • Occurs during embryonic development, early stages of growth, and during healing
  • Two major subclassifications: intramembranous ossification and endochondral ossification
  • Intramembranous: bone formed on soft fibrous tissue
  • Endochondral: bone formed on cartilage
  • Osteoblasts derived from mesenchymal cells act indepdendent of osteoclasts
  • Potential to create large amounts of bone

Modeling

  • Bone formed on existing bone tissue
  • Occurs during growth, and during healing
  • Osteoblasts and osteoclasts act independently at different sites
  • Potential to create or resorb large amounts of bone

Remodeling

  • Bone both resorbed and formed at the same site
  • Occurs from growth through death.
  • The only normal physiologic mechanism for altering bone structure in adult skeleton
  • At best leads to maintenance of bone; however as we age leads to net loss of bone (osteoporosis)

Me: The topic and controversy of Wolff’s Law is actually something I believe is critical to understand for any one who truly believes that height increase is possible using any form of non-surgical method of exercise or loading. This subject will be continure further in another article for another day.

Here’s a paper with a more detailed explanation of Wolff’s Law:

The Aging of Wolff’s “Law”:Ontogeny and Responses to Mechanical Loading in Cortical Bone

“The premise that bones grow and re-model throughout life to adapt to their mechanical enironment is often called Wolff’s law. Wolff’s law, however, is not always true, and in fact comprises a variety of differ-ent processes that are best considered separately. Here we review the molecular and physiological mechanisms by which bone senses, transduces, and responds to mechaical loads, and the effects of aging processes on the relationship (if any) between cortical bone form and mechanical function. Experimental and comparative evidence suggests that cortical bone is primarily responsive tos train prior to sexual maturity, both in terms of the rate of new bone growth (modeling) as well as rates of turnover(Haversian remodeling). Rates of modeling and Haversian remodeling, however, vary greatly at different skeletal sites. In addition, there is no simple relationship between the orientation of loads in long bone diaphyses and their cross-sectional geometry. In combination, these data caution against assuming without testing adaptationist views about form-function relationships in order to infer adult activity patterns from skeletal features such as cross-sectional geometry, cortical bones density, and musculoskeletal stress markers. Efforts to infer function from shape in the human skeleton should be based on biomechanical and developmental models that are experimentally tested and validated. ”

“ratios of articular width relative to bone length were closely correlated among long bones throughout the skeleton (with the exception of the clavicle) and that these”

““Wolff’s law” today (see be-low), actually incorporates three concepts : bone is deposited and resorbed to achieve an optimum balance between strength and weight, trabeculae in cancellous bone tend to line up with the directions of principal stresses that they experience, and both phenomena occur through self-regulating mechanisms that respond to mechanical forces acting upon bone tissues”<-it would be interesting to see how much atypical loading could change bone.  For example, bone is highly subject to axial loading rather than lateral loading.

“Bone is essentially a two-phase substance (like fiberglass or reinforced concrete):about 35% of a bone’s weight is organic, comprised mostly of collagen fibers, along with a small percentage of noncollagenous proteins; the other 65% of bone is largely a calcium-phosphate mineral known as hydroxyapatite, Ca10(PO4)6(OH)2, that contains traces of various impurities such as citrate, fluoride, and magnesium. Osteoblasts synthesize bone in a two-step process. First, they secrete an initial collagen matrix (osteoid), typically in an organized lattice that forms the basic histological framework of the tissue. Osteoblasts then mineralize the collagen by precipitating crystallites in the form of needles, rods, and plates within and between the collagen fibers”

“Young’s modulus is a critical parameter that in-fluences bone function because of the deleterious effects of strain on bone structure via creep and fatigue, both of which contribute to fracture damage.  Cyclic stresses produce fatigue and promote creep, but creep can also happen in response to continuously applied loads, and tensile and compressive loads produce somewhat different effects”

” strains initiate microcracks, whose size and rate of accumulation are primarily determined by the tis-sue’s structure as well as by variations in applied stress magnitudes, strain rate, and number of cycles. Second, these cracks grow and propagate largely as a result of the structural characteristics of the tissue. The greatest potential danger of micro-damage accumulation is that cracks can begin to coalesce at some threshold, rapidly weakening the tissue and leading to mechanical failure.”

“mechanotransduction, the process by which cells sense mechanical stimuli in their external environment and then translate the informationinto a signal that can potentially elicit some response either within the cell or in another cell.  [possible hyptothesis]  is that specialized osteoblast cells called osteocytes act as strain receptors and transducers ”

“Osteocyte canaliculi are filled with fluid that is displaced every time a bone deforms, and the cells appear to be quite sensitive to pressure changes from these flows, inducing prostaglandin and nitric oxide (NO) production, and triggering communication at gap junctions”

“strain-induced fluid flow within bone matrix generates small changes inelectrical charge”

The Thigh Bone Routine Of EasyHeight.Com

When I was going through the old EasyHeight website, I remember I found a link where Sky talked about a routine he developed to increase the length of the thigh bone called the “Thighbone Routine“. I want to make a post about the routine by copying and pasting his instructions.

Unfortunately, at this time I have not been able to find the link which is very strange. Now, I do note here that Sky and his team did try out the thigh bone routine years ago and if I remember correctly, the results were that there was little to no increase in height.

When I do find the actually routine again, this post will be edited and added upon to include what is suggested to be done.

Depressed Mothers Have Shorter Children

This article written for MSNBC was published very recently and I found it rather appropriate for this site. I have talked before about the link between an individual’s  mental state and the growth development and height they reach. negative life situations leads to a higher level of stress and anxiety, and that does cause kids who are still growing to stunt their growth path. The condition for that is called Psychosocial Short Stature or Psychosocial Dwarfism. The Medscape Reference for this term is found HERE.

What is fascinating about this article was that the link was not to the person’s psychological state and height, but to the person’s psychological state and their children’s height.

The link is from MSNBC HERE. Again, the most important parts are highlighted.

Depressed moms might have shorter kids, new study suggests

NBC News
updated 9/10/2012 8:57:02 AM ET

Moms suffering the blues in the months after giving birth may be more likely to end up with kids who are shorter than their peers, a new study shows

Researchers who followed more than 6,000 mothers and babies found that when moms reported moderate to severe symptoms of depression in the nine months following delivery, their children were more likely to be shorter than others as kindergarteners, according to the report published in the journal Pediatrics.

In fact, 5-year-olds with moms who’d suffered symptoms of postpartum depression were almost 50 percent more likely than their peers to be in the shortest 10 percent of kids that age.

The new research doesn’t explain how kids with depressed moms end up shorter. That’s something the researchers are looking into right now, said the study’s lead author Pamela J. Surkan, an assistant professor at the Johns Hopkins Bloomberg School of Public Health.

Surkan suspects, however, that depression might get in the way of nurturing.

“We think that mothers who are depressed or blue might have a hard time following through with caregiving tasks,” Surkan said.

“We know that children of depressed mothers often suffer from poor attachment and the depression seems to have effects on other developmental outcomes. It makes sense that mothers who have depressive symptoms might have reduced ability to take care of infants, that they might not always pick up cues from their kids.”

That makes a lot of sense to Dr. Andrew Leuchter, a professor of psychiatry at the University of California, Los Angeles.

“We’ve known for some time that maternal depression is bad for kids,” Leuchter said.

Depressed moms don’t interact as often with their kids and they may neglect basic needs ranging from food and clothing to emotional availability, Leuchter said.

The study’s findings may give doctors a new tool that could help spot problems in the making, Leuchter said.

“I think what the study does is it quantifies this in a new and potentially important way, “Leuchter said.  “These children have growth patterns that are different from children whose mothers are not depressed.”

And that means that doctors might want to use being short for age as a potential warning sign.

“It raises a red flag for us,” Leuchter said. “And it’s more evidence that depression in the mom can have negative health effects on the kids. So it really underlines the urgency of treating depression in these mothers so the kids don’t suffer.”

For the new study, Surkan and her colleagues scrutinized data from 6,550 moms and kids collected as part of the nationally representative Early Childhood Longitudinal Study Birth Cohort conducted by the National Center for Education Statistics.

When the children were 9 months old, the moms were surveyed about their moods. A full 24 percent of mothers reported mild depressive symptoms, while 17 percent said they were suffering moderate to severe symptoms.

By the time they were 4, kids with mildly depressed mothers seemed to be suffering some loss of stature, which disappeared by the time these children reached age 5.

But among children whose mothers reported moderate or severe symptoms of depression, the odds of being short for age had grown larger, from 40 percent at age 4 to almost 50 percent at age 5.

Surkan and her colleagues have data on depression only from nine months after moms gave birth, so they don’t know whether the women continued to suffer from the problem. It will take more research to see if the blues linger — and whether they have lasting impact on children’s growth.

“Having symptoms of depression for a lot of people is a fairly chronic state,” Surkan said.

Conclusion: This really is a critical article for parents who are expecting a baby that will be coming along. While the story and article is not showing the link to pregnant mother and their newborn babies and toddler’s eventual height, they are showing the link to the newborn’s heigth to the mother’t psychiatric state after the birth, especially around the 0-1 year mark. This shows just how critical and important the element of having a good, loving, and nurturing is to a person’s well being. A depressed mother leads to less well raised and taken care of kids, which reduce and stunt the child’s growth process and ultimate height.

Product Review XI: Height Enhancement Bible

I came across this Internet book entitled “Height Enhancement Bible” in the beginning of my searching and I always wanted to do a product review on the book. What is the problem is that I don’t know how to get a copy of the book without actually buying it. I don’t know what is inside the book. I don’t want to state that this E-product ‘Height Enhancement Bible” is like all the other height increase E-products on the internet. I do want to try to make a fairly objective analysis on the book thought.

The link to the actual product’s website is HERE. On the website, you can get to read through the first 11 pages of material. The website is interactive and dynamics and it is kind of cool how you can move your cursor and move the virtual pages around. [Note: The book is only 42 pages of material] It seems like some of the material is intended to promote a physics/ quantum mechanical viewpoint to make the reader believe that anything is possible if one uses mental jedi tricks.

The book is written by a guy named Michael T. and this is what is written on the Lulu product page….

HEIGHT ENHANCEMENT BIBLE is a complete guide on how to grow taller, based on real experience and research by people who are intimately familiar with the physiology of the human body.

INSIDE THE BOOK YOU WILL FIND… 1) what Wolff’s law is and what relation it has to body development 2) why the human body evolves based on the requirements found in it’s environment 3) why vigorous physical exercise and stretching force the body to grow taller 4) what happens in the brain during vigorous physical exercise 5) how to naturally increase growth hormone levels 6) why a balanced diet and quality sleep contribute to the development of the body 7) one month program. What exercises you should do, what is the correct way to do them and what diet to follow 8) why is attitude the most fundamental factor in increasing height 9) how does Quantum physics look at the human body and how science deals with the structure of matter and energy 10) who is Masaru Emoto and what his experiments showed.

I just wrote two posts about the Wolff’s Law and showed what is actually possible from applying that “law” in the lab. We already know that vigorous exercise does cause the body, specifically the bone and endocrine system to react. The book has a 1 month program with exercises for you to do, but so far I have not found any programs out there that can show noticeable results in one’s height after just one month. It turns out that the wikipedia article on Masaru Emoto talks about his claims that one can use one’s consciousness to communicate with water. That is clearly some pseudoscience. I personally have never heard of anyone try to connect the subject of height increase with quantum physics. If the author is trying to state that the quantum mechanics interpretation of reality states that the subjective viewpoint and experience of reality shapes everything around it, then he could then stretch that argument to state that one can use one’s mind to alter one’s body and environment, thus increase one’s height.

I have written in the past that for height increase, just like weight loss, there is not magic bullet to have a solution so easily and quickly. I strongly doubt that the E-Product “Height Enhancmeent Bible” will have some form of solution or idea that has not already been thought of in either one of the other E-books out there or on this website. I would not suggest buying the book because I don’t believe the book has any more or new information that has not already been covered somewhere in this website already.

I don’t want to claim it is a scam but I don’t think it is useful though.

Apparently you can get the book for $25.11 at Lulus from this link HERE or $30 from the product’s website. I am NOT saying that you should buy it, just know that it is there and that if you wanted to get it, it is around.

Increase Height And Grow Taller Using Bone Morphogenetic Proteins, BMPs (Guest Post)

[Note: This is the 2nd post written by my collaborator on this project. She is a very welcome addition and it shows in her research and writing that she is very dedicated to the cause. Thanks Nicki.]

BMPS  and Growth

BMPS are most associated with BMPRs (Bone morphogenetic protein receptors). Defects in BMPS can lead to many skeletal disorders.  Other names for BMPS are CDMPS (cartilage derived morphogenetic proteins) and GDFS (growth differentiation factors). The family of BMPs is comprised of at least 15 members, which are all part of the TGFβ superfamily. BMPs were originally identified as stimulators of bone formation but are now recognized as important regulators of growth, differentiation, and morphogenesis during embryology.

Within the developing limb cartilage elements, BMP2, -4, and -7 have been detected in the perichondrium, whereas BMP6 was found in  prehypertrophic and hypertrophic chondrocytes.In addition, BMP7 was detected in chick sternal prehypertrophic and mice metatarsal proliferating chondrocytes.

The effects of BMPs are mediated by two type I receptors, BMPRIA and -IB, which heterodimerize with the type II receptor, BMPRII. The type I receptors are differentially localized in embryonic limbs; BMPRIB is detected in early mesenchymal condensations and is involved in early cartilage formation, whereas BMPRIA expression is confined to prehypertrophic chondrocytes.Constitutive active and/or dominant negative forms of BMPRIA and -IB revealed that the type IA receptor controls the pace of chondrocyte differentiation, whereas the type IB receptor is involved in cartilage formation and cell death (apoptosis).

Because various BMPs are expressed in chondrocytes, cartilage defects may be anticipated in BMP-related disorders in mice. Mice bred with homozygous null mutations in BMP2 and -4 are not compatible with life whereas other family members such as growth and differentiation factor 5 (GDF5) and BMP5 are important mediators of chondrocyte differentiation in mesenchymal condensations at various sites. In addition, mice carrying a targeted disruption of BMPRIB show defects in proliferation of prechondrogenic cells and chondrocyte differentiation in the phalangeal region.Additional BMPRIB/GDF5 and BMPRIB/BMP7 double knockout studies revealed that GDF5 is a ligand for BMPRIB and that in the absence of BMPRIB, BMP7 plays an essential role in appendicular skeletal development . In humans, only a few mutations in members of the TGFβ superfamily cause cartilage disorders. Genomic mutations in the human GDF5 gene have been shown to cause chondrodysplasia Grebe type, acromesomelic chondrodysplasia Hunter Thompson type, and brachydactyly type C, all of which are mainly characterized by defects of the limbs, with increasing severity toward the distal regions. Several mutations in the BMP antagonist noggin result in proximal symphalangism and multiple synostoses syndrome.

Recently, BMP6 was introduced as a possible mediator in the growth-restraining feedback loop involving Ihh and PTHrP. The fact that BMPRIA is expressed in the same region and that it has been shown to be critical for chondrocyte hypertrophy further strengthens an autocrine/paracrine role for BMP6 in prehypertrophic chondrocytes. Still, the BMP6 knockout mouse hardly has any phenotype, leaving little evidence for an important physiological role for BMP6 in chondrocyte differentiation. This was underscored by Minina et al. who elegantly showed that BMPs do not act as a secondary signal of Ihh to induce PTHrP expression or to delay the onset of hypertrophic differentiation. Despite this, they showed that normal chondrocyte proliferation requires parallel signaling of both Ihh and BMPs and that BMPs are capable of inhibiting chondrocyte differentiation independently of the Ihh/PTHrP pathway.

In another study, inhibition of chondrocyte differentiation by TGFβ was shown to be at least partly mediated by induction of PTHrP expression. In a second study by the same group, it was established that Shh, a functional substitute for Ihh, stimulates expression of TGFβ2 and -3 in mouse metatarsals and that TGFβ2 signaling is required for inhibition of differentiation and regulation of PTHrP expression by Shh. They concluded that TGFβ2 acts as a signal relay between Ihh and PTHrP in the regulation of chondrocyte differentiation . These data imply that the BMPs/TGFβ and their receptors act as a signaling system, both dependently and independently of the Ihh/PTHrP feedback loop, at different levels during embryonic bone formation.

Understanding BMPS

The roles of BMPs in embryonic development and cellular functions in postnatal and adult animals have been extensively studied in recent years. Signal transduction studies have revealed that Smad1, 5 and 8 are the immediate downstream molecules of BMP receptors and play a central role in BMP signal transduction. Studies from transgenic and knockout mice and from animals and humans with naturally occurring mutations in BMPs and related genes have shown that BMP signaling plays critical roles in heart, neural and cartilage development. BMPs also play an important role in postnatal bone formation. BMP activities are regulated at different molecular levels. Preclinical and clinical studies have shown that BMP-2 can be utilized in various therapeutic interventions such as bone defects, non-union fractures, spinal fusion, osteoporosis and root canal surgery. Tissue-specific knockout of a specific BMP ligand, a subtype of BMP receptors or a specific signaling molecule is required to further determine the specific role of a BMP ligand, receptor or signaling molecule in a particular tissue. BMPs are members of the TGFbeta superfamily. The activity of BMPs was first identified in the 1960s. “Bone formation by autoinduction”. but the proteins responsible for bone induction remained unknown until the purification and sequence of bovine BMP-3 (osteogenin) and cloning of human BMP-2 and 4 in the late  “Novel regulators of bone formation: molecular clones and activities”. “Purification and partial amino acid sequence of osteogenin, a protein initiating bone differentiation”. “The bone morphogenetic protein family and osteogenesis”.To date, around 20 BMP family members have been identified and characterized. BMPs signal through serine/threonine kinase receptors, composed of type I and II subtypes. Three type I receptors have been shown to bind BMP ligands, type IA and IB BMP receptors (BMPR-IA or ALK-3 and BMPR-IB or ALK-6) and type IA activin receptor.”Characterization and cloning of a receptor for BMP-2 and BMP-4 from NIH 3T3 cells”.”Identification of type I receptors for osteogenic protein-1 and bone morphogenetic protein-4″.”Specific activation of Smad1 signaling pathways by the BMP7 type I receptor, ALK2″. Three type II receptors for BMPs have also been identified and they are type II BMP receptor (BMPR-II) and type II and IIB activin receptors. “Osteogenic protein-1 binds to activin type II receptors and induces certain activin-like effects”. “Cloning and characterization of a human type II receptor for bone morphogenetic proteins”. “Cloning of a novel type II serine/threonine kinase receptor through interaction with the type I transforming growth factor-beta receptor”. Whereas BMPR-IA, IB and II are specific to BMPs, ActR-IA, II and IIB are also signaling receptors for activins. These receptors are expressed differentially in various tissues. Type I and II BMP receptors are both indispensable for signal transduction. After ligand binding they form a heterotetrameric-activated receptor complex consisting of two pairs of a type I and II receptor complex.”From mono- to oligo-Smads: the heart of the matter in TGFbeta signal transduction”.The type I BMP receptor substrates include a protein family, the Smad proteins, that play a central role in relaying the BMP signal from the receptor to target genes in the nucleus. Smad1, 5 and 8 are phosphorylated by BMP receptors in a ligand-dependent manner. “MADR1, a MAD-related protein that functions in BMP2 signaling pathways”,  “Smad5 and DPC4 are key molecules in mediating BMP-2-induced osteoblastic differentiation of the pluripotent mesenchymal precursor cell line. After release from the receptor, the phosphorylated Smad proteins associate with the related protein Smad4, which acts as a shared partner. This complex translocates into the nucleus and participates in gene transcription with other transcription factors. A significant advancement about the understanding of in vivo functions of BMP ligands, receptors and signaling molecules has been achieved in recent years. BMP signals are mediated by type I and II BMP receptors and their downstream molecules Smad1, 5 and 8. Phosphorylated Smad1, 5 and 8 proteins form a complex with Smad4 and then are translocated into the nucleus where they interact with other transcription factors, such as Runx2 in osteoblasts. BMP signaling is regulated at different molecular levels: Noggin and other cystine knot-containing BMP antagonists bind with BMP-2, 4 and 7 and block BMP signaling. Over-expression of noggin in mature osteoblasts causes osteoporosis in mice. Smad6 binds type I BMP receptor and prevents Smad1, 5 and 8 to be activated. Over-expression of Smad6 in chondrocytes causes delays in chondrocyte differentiation and maturation. Tob interacts specifically with BMP activated Smad proteins and inhibits BMP signaling. In Tob null mutant mice, BMP signaling is enhanced and bone formation is increased. Smurf1 is a Hect domain E3 ubiquitin ligase. It interacts with Smad1 and 5 and mediates the degradation of these Smad proteins. Smurf1 also recognizes bone-specific transcription factor Runx2 and mediates Runx2 degradation. Smurf1 also forms a complex with Smad6, is exported from the nucleus and targeted to the type I BMP receptors for their degradation. Over-expression of Smurf1 in osteoblasts inhibits postnatal bone formation in mice .

BMP-2 And Longitudinal Growth

Abstract

Bone morphogenetic proteins (BMPs) regulate embryonic skeletal development. We hypothesized that BMP-2, which is expressed in the growth plate, also regulates growth plate chondrogenesis and longitudinal bone growth. To test this hypothesis, fetal rat metatarsal bones were cultured for 3 days in the presence of recombinant human BMP-2. The addition of BMP-2 caused a concentration-dependent acceleration of metatarsal longitudinal growth. As the rate of longitudinal bone growth depends primarily on the rate of growth plate chondrogenesis, we studied each of its three major components. BMP-2 stimulated chondrocyte proliferation in the epiphyseal zone of the growth plate, as assessed by [3H]thymidine incorporation. BMP-2 also caused an increase in chondrocyte hypertrophy, as assessed by quantitative histology and enzyme histochemistry. A stimulatory effect on cartilage matrix synthesis, assessed by 35SO4 incorporation into glycosaminoglycans, was produced only by the highest concentration of BMP-2. These BMP-2-mediated stimulatory effects were reversed by recombinant human Noggin, a glycoprotein that blocks BMP-2 action. In the absence of exogenous BMP-2, Noggin inhibited metatarsal longitudinal growth, chondrocyte proliferation, and chondrocyte hypertrophy, which suggests that endogenous BMPs stimulate longitudinal bone growth and chondrogenesis. We conclude that BMP-2 accelerates longitudinal bone growth by stimulating growth plate chondrocyte proliferation and chondrocyte hypertrophy.

BMPS AND IHH /PHTrP INTERACTION

During endochondral ossification, two secreted signals, Indian hedgehog (Ihh) and parathyroid hormone-related protein (PTHrP), have been shown to form a negative feedback loop regulating the onset of hypertrophic differentiation of chondrocytes. Bone morphogenetic proteins (BMPs), another family of secreted factors regulating bone formation, have been implicated aspotential interactors of the Ihh/PTHrP feedback loop.To analyze the relationship between the two signaling pathways, we used an organ culture system for limb explants of mouse and chick embryos. We manipulatedchondrocyte differentiation by supplementing these cultures either with BMP2, PTHrP and Sonic hedgehog as activators or with Noggin and cyclopamine as inhibitors of the BMP and Ihh/PTHrP signaling systems. Overexpression of  Ihh in the cartilage elements of transgenic mice results in an upregulation of  PTHrP expression and a delayed onset of hypertrophic differentiation. Noggin treatment of limbs from these mice did not antagonize the effects of  Ihh overexpression. Conversely, the promotion of chondrocyte maturation induced by cyclopamine, which blocks Ihh signaling, could not be rescued with BMP2. Thus BMP signaling does not act as a secondary signal of Ihh to induce PTHrP expressionor to delay the onset of hypertrophic differentiation. Similar results were obtained using cultures of chick limbs.  We further investigated the role of BMP signaling in regulating proliferation and hypertrophic differentiation of chondrocytes and identified three functions of BMP signaling in this process. First we found that maintaining a normal proliferation rate requires BMP and Ihh signaling acting in parallel. We further identified a role for BMP  signaling in modulating the expression of Ihh. Finally, the application of Noggin to mouse limb explants resulted in advanced differentiation of terminally hypertrophic cells, implicating BMP signaling in delaying the process of hypertrophic differentiation itself. This role of BMP signaling is independent of the Ihh/PTHrP pathway.

We have identified several Ihh-independent functions of BMP signaling. One of these is to regulate the process of terminal hypertrophic differentiation. Blocking of BMP signaling by Noggin results in an increased number of  Osp-expressing, terminal hypertrophic cells. By contrast, cyclopamine treatment, which leads to an advanced onset of hypertrophicdifferentiation, does not increase  Osp expression. Double treatment experiments support the idea that BMP and

Analysis of mutations in single Bmp genes has not given significant insight into their role during skeletal differentiation. Targeted disruption of either Bmp2 or Bmp4 leads to early embryonic lethality (Winnier et al., 1995; Zhang and Bradley, 1996), whereas mutations in Bmp5, Bmp6 or Bmp7 only display mild skeletal phenotypes (Dudley et al., 1995; King et al., 1994; Kingsley et al., 1992; Luo et al., 1995; Solloway et al., 1998), indicating a highly redundantrole of Bmp genes in regulating bone development. In this study we have attempted to analyze the role of BMP signaling during chondrocyte maturation without differentiating between individual Bmp genes. As BMP proteins can substitute for each other in experimental systems, we have used BMP2 protein to mimic the role of several BMPs. Similarly, Noggin has been shown to inhibit signaling of various members of the BMP family (Zimmerman et al., 1996; Kawabata et al., 1998).  Several Bmp genes are expressed in specific regions of the developing cartilage elements and might thus be important for different aspects of chondrocyte differentiation during normal development.  Bmp7 is expressed in the proliferating chondrocytes distal to Ihh (Haaijman et al., 2000; Solloway et al., 1998) and may be responsible for regulating chondrocyte proliferation and Ihh expression. Other Bmps, including Bmp2, Bmp3, Bmp4 and Bmp7, are expressed in the perichondrium/ periosteum (Pathi et al., 1999; Zou et al., 1997; Daluiski et al.2001; Haaijman et al., 2000) .

Conclusion 

BMPs are the only molecules so far discovered capable of independently inducing endochondral ossification in vivo. TGF-b1 and TGF-b2 enhance the osteoinductive properties of BMPs; however, injection of TGF-bs on their own leads to extensive fibrous tissue formation only (Bentz, Armstrong & Seyedin, 1987). The mechanism of action of the BMPs has yet to be defined. However, the availability of recombinant forms has led to much work on their biological activity in vivo and in vitro. Recombinant forms of BMP2 and BMP4 induce ectopic bone formation, and BMP2 will heal cortical bone defects by an endochondral process (Hammonds et al., 1991; Wang, Rosen & Cordes, 1990; Yasko et al., 1992). BMP2 stimulates the growth and differentiation of growth plate chondrocytes in vitro, and results in the development of the osteoblast phenotype in a rat pluripotential cell line (Hiraki et al., 1991). Osteoblasts have been shown to have high affinity binding  proteins for BMP on the cell surface (Paralkar, Hammonds & Reddi, 1991).

Indirect lines of evidence demonstrate that BMPs have a critical role in bone development. Firstly, the protein encoded by the decapentaplegic locus (dpp) in Drosophila is a member of the TGF-b family member with 75% sequence homology to BMP2, suggesting a common ancestral gene. Developmental anomalies produced by mutations of the dpp gene are similar to patterns of disease expression in fibrodysplasia ossificans progressive, a developmental disorder characterised by deformations of the hands and feet and heterotopic chondrogenesis (Kaplan, Tabas & Zasloff, 1990). In addition, the chromosomal locations of the BMP genes overlap with the loci for several disorders of cartilage and bone formation (Tabas et al., 1991). More direct evidence is provided by a recent study which demonstrated that BMP2, together with fibroblast growth factor-4, is important in regulating limb growth in the mouse embryo (Niswander & Martin, 1993).

Me:: As you can see the group for Bone Morphogenetic Proteins (BMPs) is one of the most critical elements involved in the endochondral growth process. If I was to guess with the knowledge I have right now, I would move away from looking for way to increase GH release in the body but focus more on finding ways to get specifically the 20 discovered BMPs analyzed. The best way to start on that is to start on looking into BMP2, BMP5 and BMP7. My hypothesis is that the BMPs are the proteins that allow for the growth plates to run so efficiently for the chondrocytes to move form the proliferative layer to the ossification layer since there are two different processes going on right next to each other.

The parathyroid hormone-related protein (PTHrP) group is another possibility we need to study on because I have at least 3 papers so far showing that the Thyroid hormone proteins have been used as a template to create similar synthetic compounds used for bone growth. The other area to look into as well is the BMP2 inhibiting Noggin glycoprotein.