I have been recently looking more towards the old Grow Tall Forum website for clues on what types of research and methods height increase seekers before me were up to. One website or company which were claiming that they had a working product was called Height FX which had the website HeightEffects.com. I typed in the url but nothing showed up. A look through the forums back in 2008-2009 shows that this website was definitely something that was talked about. From checking the WayBack Machine it seems that the website was around from 2008 to 2011. The board members seemed to show some serious interest in it and whoever was the person doing the scientific research on trying to figure out a proposed method was doing real research.  

It seems that through using the WayBack Machine and clicking on a save copy of the website from back in Feb of 2011 I managed to get a copy of the pills/product that was being sold on the website. I managed to do a clipping of the website and pasted the pics below.

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I looked for a copy of the ingredients and science section of this product and did find an old copy of the information on the page. There seems to be nothing on the Research page but when I clicked on the “view the science behind this” link I am taken to a section is quite scientifically intensive.

I took the liberty to copy and paste all of the information from the old website to this post which is below….
Note: My review of the website and the science of this proposed pill is at the very bottom of this post, which you will have to scroll all the way down to read. This proposed height increase idea is quite advanced.

 

 

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HeightFX Biotechnology

Introduction to the HeightFX Technology

The HeightFX longitudinal growth complex is unlike any other height growth product ever developed. Based upon real science to provide real results, HeightFX incorporates some of the most cutting edge science available today. The HeightFX formulation can be broken down into 4 major components detailed below. Each component shown below includes decades of clinical research conducted by a wide variety of institutions from around the world in support of the technologies used. Many of the components used in HeightFX mimic the very same mechanisms used in clinical hormonal treatments for short stature by the medical community. .These mechanisms represent the leading and most effective treatments for short stature currently available.

Proprietary Extraction Techniques

Not all plant extracts are created equal. Many plants contain dozens, if not hundreds, of naturally occuring active compounds called phytonutrients. The extraction technique used determines what fraction of these phytonutrients is captured in the finished extract, and it is these phytonutrients that elicit the potent effects behind HeightFX. We at the Herbal Height company, alongside our manufacturing partners, are continuously developing and refining our own proprietary extraction techniques to capture the optimal phytonutrient fractions of the plants used in the HeightFX formulation. The plant extracts used in HeightFX contain highly specialized, custom tailored, phytonutrient compositions not found replicated in other extracts of the same plants. It is these fine details that define the effects of HeightFX, and set it apart from other extracts currently available on the market today.

Anti-Fusion Inhibiting Complex

One of the primary mechanisms behind the revolutionary HeightFX formulation is its ability to suppress estrogen production within the body by inhibiting activity of the P450 cytochrome families aromatase enzyme in a reversible manner. The aromatase enzyme is responsible for converting a portion of testosterone into estrogen within the male body. This same mechanism has had a major impact in shaping the clinical therapies used in the new millenium for treatment of short stature. Ample clinical studies conducted in recent years, as well as novel cases of aromatase enzyme gene mutation in certain individuals, have shown that the suppression of estrogen in the male body by use of aromatase enzyme inhibitors delays growth plate fusion, thereby extending the length of time the patient can continue to grow taller and significantly increasing their final adult height [1, 2, 3, 4, 5, 6], an outcome in direct defiance of their genetics. Recorded medical cases [7, 8], as well as clinical studies, have shown that estrogen is the major mediator of epiphyseal growth plate fusion, likely through agonist activity at the estrogen receptor alpha [9, 10, 11]

The HeightFX longitudinal growth complex utilizes dual inhibitors [12, 13, 14] of the aromatase enzyme to accomplish significant suppression of endogenous estrogens thereby extending the period of time that the users epiphyseal growth plates can continue to develop new skeletal tissue . However, unlike clinically used aromatase inhibitors (AI) such as the triazole family of reversible inhibitors; Letrozole and Anastrozole, the primary AI used in HeightFX, a proprietary extract of grape seeds, has been shown not only to inhibit existing aromatase enzymes, but also to suppress the expression of the aromatase enzyme gene [5]. Suppression of aromatase enzyme gene expression can result in an overall decrease in the amount of newly forming aromatase enzymes, thereby furthering the effectiveness over time of HeightFX’s anti-fusion inhibiting complex.

HeightFX’s anti-fusion inhibiting complex leads to a delay in growth plate fusion thereby allowing the user to continue to grow taller for a longer period of time than they otherwise could naturally.

Androgen Optimizing Complex

Considered to be the most potent class of clinical hormonal therapy utilized for the acceleration of height growth in growing adolescents, androgen therapy is a cornerstone of the HeightFX longitudinal growth complex. The most well known androgen is the male sex hormone Testosterone. Other androgens used in the clinical treatment of short stature include the synthetic anabolic androgenic steroids Oxandrolone and Fluoxymesterone. The administration of androgens, wether naturally occuring or synthetic, leads to a significant acceleration in the rate of longitudinal height growth with minimal side effects, are well tolerated in the majority of patients, and result in the most significant increases in height growth of any treatments used clinically [15, 16, 17, 18, 19, 20, 21, 22]

HeightFX elicits functional androgenic effects by increasing androgen receptor agonist activity in the epiphyseal growth plates. The first major androgenic mechanism utilized involves the use of sex hormone binding globulin inhibitors to prevent its binding to its receptors and circulating androgens [23, 24, 25, 26]. Sex hormone binding globulin (SHBG) is a glycoprotein found in both sexes that binds with androgens and estrogens circulating through the blood stream and deactivates them. A portion of the testosterone and other androgens in circulation are bound to SHBG and therefore inhibited from eliciting an androgenic effect on tissue [27, 28]. Certain phytonutrients utilized in HeightFX function by binding to existing SHBG and rendering it incapable of deactivating endogenous androgens. The result is an increase in the serum blood levels of active-unbound androgenic hormones able to promote longitudinal growth.

Another major mechanism by which the phytonutrients utilized in HeightFX increase androgen receptor binding activity is by directly increasing production of androgenic hormones, primarily testosterone and its 5-alpha-reductase catalyzed derivative dihydrotestosterone. One way in which HeightFX accomplishes this is by increasing steroidogenesis, the production of testosterone, within the leydig cells of the testicles [29, 30, 31, 32, 33, 34, 35]. The aromatase inhibitors used in the HeightFX formulation also work to increase testosterone levels through endocrine feedback mechanisms and by preventing a portion of produced testosterone from being aromatised into estrogen. Additionally, HeightFX employs the novel phytonutrient Icariin which elicits a testosterone-mimetic effect by directly binding to androgen receptors thereby functioning as a selective androgen receptor modulator (SARM) [36]

The androgen optimizing complex utilized in HeightFX leads to a significant acceleration in the rate of longitudinal height growth.

Somatotropic Signaling Complex

Human Growth Hormone (HGH) and Insulin-like Growth Factor-one (IGF-1) have long been used alone or in combination with androgens clinically to treat growth disorders such as short stature by accelerating longitudinal growth velocity [37, 38, 39, 40, 41, 42, 43, 44, 45, 46, 47, 48, 49, 50, 51]. Growth hormone and IGF-1 elicit the majority of their height growth promoting benefits through the modulation of chondrocyte activity, cartilage cells, within epiphyseal growth plate tissue [52, 53, 54, 55, 56, 57, 58]. Additionally, studies suggest that HGH and IGF-1 have direct effects on osteoblasts and osteoclasts and therefore play a major role in not just the growth of growth plate cartilage, but also the ossification of that cartilage to bone as well as the remodeling of existing skeletal structures [59, 60, 61]

HeightFX has a vast spectrum of somatotropic effects within the growth plate, effects that promote a far broader array of synergistic benefits than that experienced from increasing HGH and IGF-1 levels alone. The cornerstone of HeightFX’s somatotropic signaling complex is its direct effects regulating the release of HGH and IGF-1 through a cutting edge complex of secretagogues and sensitizing agents. HeightFX’s androgen optimizing effects are able to blunt the negative feedback mechanisms controlling the pulsatile release of growth hormone [62], thereby allowing greater release of growth hormone from the pituitary gland in response to HGH secretagogues utilized in the HeightFX formulation. Research studies also show that androgens increase IGF-1 receptor abundance and gene expression in skeletal chondrocyte tissue [63, 64], an effect that allows a stronger IGF-1 growth response to occur. Further evidence suggests that increased androgen activity, such as that promoted by HeightFX, modulates HGH and IGF-1 release responsiveness at different points in the somatotropic endocrine cascade [65, 66, 67, 68, 69]

The primary mechanism making up the somatotropic signaling complex utilized in HeightFX involves the combination of an acetylcholinesterase inhibitor [70, 71, 72] alongside a potent growth hormone secretagogue [73, 74, 75, 76, 77, 78, 79, 80]. Inhibition of acetylcholinesterase potentiates growth hormone release response to the primary secretagogue used in HeightFX [81], a result of increased acetylcholine levels resulting in the inhibition of somatostatin [82, 83, 84, 85, 86, 87]. Furthermore, the inhibition of somatostatin also prolongs the duration of growth hormone secretion pulses [88]

The end result of HeightFX’s somatotropic signaling complex is a rapid acceleration in the rate of chondrogenesis by stimulating increased chondrocyte proliferation and hypertrophy.

Intracrine Augmenting Complex

The intracrine systems of the epiphyseal growth plates are extremely complex systems of autocrine origin hormones, cytokines, growth factors, binding proteins, morphogens, and other highly specialized cellular signaling ligands, many of which are specific to skeletal tissue only. The majority of HeightFX’s growth promoting effects focus on accelerating chondrogenesis, the creation of new cartilage within the epiphyseal growth plate. One major element of HeightFX’s intracrine augmenting complex however, focuses on enhancing osteogenesis, the calcification of newly formed growth plate cartilage into bone tissue. Osteogenesis is the result of osteoblast cell activity depositing calcium into the cartilage matrix formed by chondrocytes, and the HeightFX formula aims to accelerate osteogenesis in harmony with chondrogenesis.

HeightFX promotes increased osteogenesis by stimulating the differentiation and proliferation of osteoblasts via the increased production and mRNA synthesis of bone morphogenetic protein-2 levels (BMP-2) in osteoblasts, as well as by increasing osteoblast alkaline phosphatase (ALP) activity [89, 90, 91]. HeightFX can also accelerate the proliferation and ALP excretion capabilities of bone marrow stromal cells (BMSCs), resulting in greatly improved osteogenesis activity of BMSCs [92].

The overall result of the intracrine augmenting complex used in HeightFX is a significant increase in osteoblast activity leading to an acceleration in the formation of new skeletal tissue via endochondral ossification.

Biotechnology Summary

HeightFX accomplishes its incredible height growth promoting effects through mechanisms that mimic those employed in the most effective and widely used clinical therapies for short stature. It is through this wide spectrum of synergistic pharmacologic effects that makes HeightFX unlike anyother height growth product to ever exist on the market. The inhibition of the aromatase enzyme and its gene expression allows a dramatic prolonging of the longitudinal growth phase in growing adolescents, while the increased androgenic, somatotropic, and intracrine effects simultaneously accelerate the rate of longitudinal skeletal growth to supraphysiological levels otherwise unachievable. This unique complex of growth promoting mechanisms makes HeightFX the first and only product ever made available to the height growth community that uses real science supported by real research to promote real height growth. You no longer have to accept the height your genetics have dictated for you, biotechnologies as effective if not more effective than those used in clinical treatments are now available at your fingertips thanks to the HeightFX longitudinal growth complex brought to you by the Herbal Height company.

The Future of HeightFX

The Herbal Height company will continue to develop, refine, and improve the HeightFX longitudinal growth complex for years to come. Not only do we have many plans for future generations of the HeightFX formula, some of which are currently in development stages, but we are also developing additional products and informational resources to be used in conjunction with the HeightFX longitudinal growth complex, or on their own.

Clinical Study References

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[41] Wacharasindhu S, Supornsilchai V, Aroonparkmongkol S, Srivuthana S. (2007) Diagnosis and growth hormone (GH) therapy in children with GH deficiency: experience in King Chulalongkorn Memorial Hospital, Thailand.

[42] Angulo MA, Castro-Magana M, Lamerson M, Arguello R, Accacha S, Khan A. (2007) Final adult height in children with Prader-Willi syndrome with and without human growth hormone treatment.

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[46] Davenport ML, Crowe BJ, Travers SH, Rubin K, Ross JL, Fechner PY, Gunther DF, Liu C, Geffner ME, Thrailkill K, Huseman C, Zagar AJ, Quigley CA. (2007) Growth hormone treatment of early growth failure in toddlers with Turner syndrome: a randomized, controlled, multicenter trial.

[47] Rosilio M, Carel JC, Ecosse E, Chaussainon JL. (2005) Adult height of prepubertal short children born small for gestational age treated with GH.

[48] Chernausek SD, Backeljauw PF, Frane J, Kuntze J, Underwood LE. (2007) Long-term treatment with recombinant insulin-like growth factor (IGF)-I in children with severe IGF-I deficiency due to growth hormone insensitivity.

[49] Backeljauw PF, Underwood LE. (2001) Therapy for 6.5-7.5 years with recombinant insulin-like growth factor I in children with growth hormone insensitivity syndrome: a clinical research center study.

[50] Azcona C, Preece MA, Rose SJ, Fraser N, Rappaport R, Ranke MB, Savage MO. (1999) Growth response to rhIGF-I 80 microg/kg twice daily in children with growth hormone insensitivity syndrome: relationship to severity of clinical phenotype.

[51] Ranke MB, Savage MO, Chatelain PG, Preece MA, Rosenfeld RG, Blum WF, Wilton P. (1995)Insulin-like growth factor I improves height in growth hormone insensitivity: two years’ results.

[52] Hutchison MR, Bassett MH, White PC. (2007) Insulin-like growth factor-I and fibroblast growth factor, but not growth hormone, affect growth plate chondrocyte proliferation.

[53] Oberbauer AM, Peng R. (1995) Growth hormone and IGF-I stimulate cell function in distinct zones of the rat epiphyseal growth plate.

[54] Olney RC, Mougey EB. (1999) Expression of the components of the insulin-like growth factor axis across the growth-plate.

[55] Oberbauer AM, Peng R. (1995) Fractionation of growth plate chondrocytes: differential expression of IGF-I and growth hormone and IGF-I receptor mRNA in purified populations.

[56] Cruickshank J, Grossman DI, Peng RK, Famula TR, Oberbauer AM. [2005] Spatial distribution of growth hormone receptor, insulin-like growth factor-I receptor and apoptotic chondrocytes during growth plate development.

[57] Ohlsson C, Nilsson A, Isaksson O, Bentham J, Lindahl A. (1992) Effects of tri-iodothyronine and insulin-like growth factor-I (IGF-I) on alkaline phosphatase activity, [3H]thymidine incorporation and IGF-I receptor mRNA in cultured rat epiphyseal chondrocytes.

[58] Kiepe D, Ciarmatori S, Hoeflich A, Wolf E, Tönshoff B. (2005) Insulin-like growth factor (IGF)-I stimulates cell proliferation and induces IGF binding protein (IGFBP)-3 and IGFBP-5 gene expression in cultured growth plate chondrocytes via distinct signaling pathways.

[59] Chihara K, Sugimoto T. (1997) The action of GH/IGF-I/IGFBP in osteoblasts and osteoclasts.

[60] Wang Y, Nishida S, Elalieh HZ, Long RK, Halloran BP, Bikle DD. (2006) Role of IGF-I signaling in regulating osteoclastogenesis.

[61] Ueland T. (2005) GH/IGF-I and bone resorption in vivo and in vitro.

[62] Veldhuis JD, Anderson SM, Iranmanesh A, Bowers CY. (2005) Testosterone blunts feedback inhibition of growth hormone secretion by experimentally elevated insulin-like growth factor-I concentrations.

[63] Phillip M, Maor G, Assa S, Silbergeld A, Segev Y. (2001) Testosterone stimulates growth of tibial epiphyseal growth plate and insulin-like growth factor-1 receptor abundance in hypophysectomized and castrated rats.

[64] Maor G, Segev Y, Phillip M. (1999) Testosterone stimulates insulin-like growth factor-I and insulin-like growth factor-I-receptor gene expression in the mandibular condyle–a model of endochondral ossification.

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A Personal Assessment of the Science

It is quite clear that the website, which is only 5 pages big from what I can tell is quite accurate on many of the big points. The main ways that these groups of people/researchers are trying to help kids who are still growing is to promote 4 process that are all controlling somatic growth, which they have called

1. Anti-Fusion Complex
2. Androgen Optimizing
3. Somatotropic Signaling
4. Intracrine Augmenting

Aftre spending a good 30 minutes reading over the notes, I am going to write a very simple summary of what each process is supposed to do.

For the anti-fusion complex, it seems that there is a part of this pill formulation that inhibits the formation and function of estrogens to delay the closure of the plates. The exact inhibition is on something known as the P450 cytochrome family of aromatase enzyme. The exact compound that is supposed to do the inhibiting is “a proprietary extract of grape seeds” which is said to also be able “to suppress the expression of the aromatase enzyme gene”.

For the androgen optimizing, here is another part that causes more testosterone to go through the body as well as increase the amount of testosterone receptors and testosterone receptor sensitivity. There is many studies that support the theory that man who have more testosterone going through their body are on average slightly taller and bigger than males with less testosterone going through their body. Some synthetic anabolic androgenic steroids like Oxandrolone and Fluoxymesterone have been used multiple times to increase longitudinal growth. The phytonutrient Icariin is used and there is another part of the formulation that is supposed to inhibit globulin.

For the somatotropic signaling, supposedly the formula has another part (a combination) that can cause more IGF-1 and GH to go through the system and make them more effective, without the usual negative feedback loop which would limit the rate of the amount of GH that can be release by the pituitary. This is done from a combination of an acetylcholinesterase inhibitor with growth hormone secretagogues in the pill. It turns out that if you increase the level of acetylcholine in the brain, the level of somatostatin is decreased. By removing the negative feedback loop, the GH secretagogues would be more effective on the pituitary since the somatostatin was inhibited.

For the intracrine augmenting, the idea is that bone deposition below the growth plate will be increased through increasing osteoblast formation and increased alkaline phosphatase. Apparently there is some element in this pill that can cause the mRNA of BMP-2 to be increased.

Overall Assessment

The science is right, and the information is better presented and written than anything that I can do at this time. Whoever wrote the page has a better grasp on how to make children with open growth plates grow then probably even me or Tyler, however the same problem occurs again. This formulation has a good chance on working on children if it does have the many compounds that it claims it does.

Tyler wrote a post reviewing this website entitled “Height FX Review“ from back in April of 2010.

It seems that in the post, he notes that the website is quite impressive in the depth of their knowledge on the subject. The thing Tyler wanted back then was that this company who is selling a product should go through with a clinical trial to make sure that any results that they did see was not due only to the placebo effect.

However the critical part is from HeightQuest.com which found the list of ingredients inside, which are…

This link I found seems to validate some ideas previous height increase researchers had about possible supplements that can be orally taken to lead to increased growth.

The website or source I found this list from is Healing Pastures back in 2009. The entire list and details is taken from that website posting. However I would like to give an analysis of the list at the end of this post to see whether we can find any useful information that can help us in our own research.

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Quercetin – Cabbage, kale, brussel sprouts, onions and garlic, citrus fruits, apples, parsley, tea, and red wine are the primary dietary sources of quercetin. Olives and olive oil, grapes, black currants, cranberries, dark cherries, and dark berries such as blueberries, blackberries, bilberries, lingonberries and red raspberries are also high in flavonoids, including quercetin. Quercetin seems to work better when used in conjunction with bromelain, a digestive enzyme found in pineapples.

Chrysin  – This is a flavonoid from the passion flower plant, bee propolis, bee pollen and raw honey. Chrysin has poor bioavailability so it is normally taken as a supplement along with piperine (from black pepper) which greatly enhances its bioavailability.

Naringenin  – This is found in all citrus fruits, like orange, tangerine, lemon and lime. Avoid obtaining it from grapefruit or grapefruit juice, which has an inhibitory effect on the human cytochrome P450 isofrom, another enzyme in the same complex as the aromatase enzyme. This enzyme is involved in breaking down and metabolizing sex hormones and preventing their excess accumulation in the body, so inhibiting it will allow estrogen levels to rise.

Apigenin – Dietary sources include celery, parsley, artichokes, basil, chamomile, thyme, peppermint, gingo biloba, and other herbs like horsetail herb, lemon balm herb, perilla herb, vervain herb, and yarrow. The highest concentrations of apigenin seem to be in chamomile and thyme.

Genistein  – This is an isoflavone found in herbs like red clover (the herb of Hippocrates), parsley, sage, green vegetables, fruits and particularly pulses and legumes like chick peas and beans, and soy. Soy and soy foods contain high amounts of plant estrogens or phytoestrogens. These estrogens are very weak and have almost no harmful effects. They compete with the estrogen receptor sites in the body, and prohibit the more potent and harmful estrogen. Phytoestrogens are only 1/500th as potent as estradiol, the most dangerous form of estrogen. The body senses the estrogen level to be high and stimulates the P450 system in the liver to metabolize the estrogen. This helps keep estrogen levels where they should be. There is some controversy about whether soy is protective against breast cancer or promotes it. Much depends on variables like genes. Asians have a long history of soy consumption and their bodies process it far more efficiently than Westerners.

Diadzein – Another isoflavone found in soy products. Genistein accounts for approximately 50% of total soy isoflavones, whereas daidzein accounts for about 40%.

Oleuropein  – Oleuropein gives olive oil its distinctive flavor, It is found in abundance in the leaves of the olive tree.

Resveratrol  – Good sources are the skin and seeds of red grapes, grape seed extract, and black and red berries. Muscadine grapes, often used to make red wine, have the highest content. Although supplements of resveratrol are popular and widely available, getting resveratrol from red wine allows you to get the entire grape polyphenol group of nutrients, a group that has been shown to work much better synergistically. Breast tumor growth and metastasis to bone and liver have been shown to be better inhibited by the complete grape polyphenol complex.

Linoleic Acid  – An essential fatty acid from the Omega-6 family, linoleic acid can be found in common mushrooms like button mushrooms, shitake, portabello and crimin, as well as vegetables, fruits, nuts, grains and seeds. Good sources are oils made from safflower, sunflower, corn, soya, evening primrose, pumpkin, olives and wheat germ. In a study conducted by Dr. Shiuan Chen of the Beckman Research Institute of the City of Hope in Duarte, California, it was found that in laboratory and animal experiments, mushroom extracts reduced the proliferation of breast cancer cells. This study also surmised that it is the linoleic acid that may be responsible for the anti-cancer effects.

Interestingly, the study also found that white button mushrooms suppressed production of the enzyme 5-alpha reductase. This enzyme plays a big role in development of prostate cancer.

Progesterone  – A popular source is wild yam extract cream for topical application, such as Neways’ “Endau” progesterone cream. A study (Formby and Wiley, Journal Nat. Cancer Inst. June 7997) shows that natural progesterone actually inhibits growth and induces cell death in breast cancer cells by affecting p53 and Bcl-2 gene expression.

This followed work by Chang, Lee et al (Fertility and Sterility vol 63 7995) that showed that whilst oestradiol (the most potent oestrogen hormone) increases the number of cycling epitbelial cells, natural progesterone actually decreases them. The study further states that natural progesterone secretion suppresses oestradiol receptors in both the endometrium and breast tissue, and has an anti-oestrogen effect (just as, for example, the latest aromatase inhibitors aim to do), but that very high concentrations of synthetic progestins can stimulate human breast cancer cells.

Zinc – The best sources are wheat germ, oysters and liver, Less zinc-rich sources include meat, sesame, sunflower and pumpkin seeds, nuts like pecans and brazils, spinach, mushrooms etc.

Those searching for an aromatase-inhibiting diet may wish to take a closer look at the Mediterranean diet, Fresh fruits, vegetables, olive oil and red wine are components of this diet, the one diet that has consistently correlated with lower death rates from all causes. Flavonoids from each of these foods inhibit aromatase activity to reduce incidence of breast cancer.

A final thought: the aromatase enzyme resides in fat cells. It is no surprise that being overweight and obese is linked with breast and other hormone-sensitive cancers. Fewer fat cells in the body means that less unbalanced estrogen is produced. High levels of insulin, a big factor in weight gain and fat mass accumulation, promote production of the aromatase enzyme. Avoiding processed foods and foods with chemicals helps keep insulin levels under control, in turn resulting in lower levels of aromatase and as a consequence, lower levels of unbalanced estrogen in the body

Analysis

This list is interesting because of the first two types of compounds listed, Quercetin and Chrysin. At one point in the research, I had listed both of these compounds as possible things a person can ingest to grow taller in the Supplements Section of the website. I even at one point said that Quercetin might help people with closed plates grow taller.

Two posts were written about the height increase potential of the two compounds…

1. Can Quercetin Really Help People Grow Taller And Increase Their Height After Reaching Adulthood?
2. Increase Height And Grow Taller Using Chrysin

After doing more research, I had to state that it seems that I was previously wrong about the efficacy of these compounds. The whole idea with chrysin was that it was an aromatase inhibitor. With Quercetin, I forgot why it was a viable idea.

Two of the compounds were isoflavones which can be found in soy products. The section that I will talk about is on the phytoestrogens, which is something which I have been looking into recently…

“Phytoestrogens are only 1/500th as potent as estradiol, the most dangerous form of estrogen. The body senses the estrogen level to be high and stimulates the P450 system in the liver to metabolize the estrogen. This helps keep estrogen levels where they should be.”

There is enough evidence that estradiol is harmful towards growth in the literature but this section seems to imply that phytoestrogens may be actually good for growth, since they prevent the much stronger estrogens from binding to estrogen receptors. There is even ways for the human body to regulate estrogen levels using the liver to metabolize estrogen.

The last compound which is something which I am remotely curious about is the compound progesterone. I wrote about the connection between progesterone and growth in the old post “Analysis On The Possible Cause For Height Increase During Pregnancy”

I was doing research for adipose derived stem cells when I read something from the Wikipedia article on Adipose Tissue which made me see that there might indeed be a connection between the issue of childhood obesity, an earlier onset of puberty, and possible effects of stunted growth leading to shorter final height.

It seems that adipose tissue, which is what our fat is greatest peripheral source of aromatase in both males and females.

Since we know that having a lot of aromatase means more conversion into estrogen, it would means that there are going to be higher levels of estrogen, which is something which we have always said for the developing child with open growth plates is a bad thing.

I remember reading years ago about the fact that “fatter” than average children would start puberty earlier in age than children who are not as overweight. The journalist who wrote the article would talk about how the over excess of food and eating behavior caused an increase in the amount fo hormones going through the body.

This idea seems to have some validation when we realize that adipose tissue is supposed to be the biggest source of aromatase in the bodies of females and males.

Aromatase would convert any type of hormones that can be converted into estrogen or estrogen like compounds which would cause the initial spark in physical development starting puberty. As we know from our research, an earlier onset of puberty usually means an earliest onset of complete endochondral ossification closure. It doesn’t always have to mean that earlier puberty means earlier growth plate closure, but there is a positive correlation.

This would then imply then that people who have more adipose tissue probably have a higher level of aromatase in their blood stream than a person of similar age with different tissue composition.

We know that females are supposed to have higher fat composition levels than males on average. This is supposed to be because the female reproductive organs and hormones require more fat than the male reproductive organs and hormones. If the fat percentage in the female body falls below a certain amount, their fertility rate would actually drop. This is often seen when female bodybuilders start to take supplements to make their body fat percentage to drop. They develop masculine and male physiques and traits, increased muscularity, muscle leanness, etc. In addition, their fertility also sees strange changes.

It could be that from the higher body percentage fat in females, that is one of the main reasons why they go through puberty as a an earlier age than men. This also leads to females being on average shorter than men.

So the correlation goes…

Overweight child or Obese Child —> Increased levels of fat to overall body composition —> The fat is composed of adipose tissue —> The adipose tissue is the main peripheral source of aromatase —> The increased aromatase causes more estrogen to be made from aromatization —-> The extra estrogen causes puberty to start earlier —> There is less years for natural growth —-> Earlier onset of bone maturity leading to a shorter final adult height

The correlation may be weak, but I would guess that the correlation is still positive.

From another source, the USMLE Forum, a post did ask about which places aromatase seem to come from, besides just the adipose tissue. 

Other locations where the aromatase seems to originate are….

1. Granulosa Cell –
2. Sertoli Cells –
3. Leydig Cell – 

For the sertoli cell someone writes…

“…aromatase is present in sertoli cells ….here it converts testosterone to estradiol…one third of estradiol in men comes through this, remainder comes by aromatase in adipose tissue..
leydig cells make testosterone that is made from cholesterol. this testosterone is secreted and taken up by sertoli cells.”

For the leydig cell something states…

“…i just wanted to say that leydig cells are also capable of producing aromatase in klienfelters synd….but goljan book says hyperplasia of leydig cells and incresed aromatase there caused by increased FSH….so increase conversion of testosterone to estrogen…reason for increased estrogen in kleinfelters”

The discussion seems to reach a really interesting ending by the post by someone named JonBC

“Testicular production of estrogen is poorly understood. The Sertoli cells manufacture estrogens during fetal and neonatal life. However, beginning at puberty and continuing through adulthood the site of estrogen synthesis shifts to the Leydig cell. The Leydig cells express high mRNA and protein levels of the CYP19 (aromatase) enzyme. The mechanisms regulating the site of estrogen synthesis, and the shift of estrogen production between Sertoli and Leydig cells, are completely unknown.”

Analysis:

This may be a good breakthrough for the research because this is the first place where I finally realize that apparently the location of where estrogen is produced actually changes from when the human is in develop in the uterus and when the person is going through the stages of puberty.

This might explain why estrogen levels cause the onset of puberty. Let’s look at what the person says…

• Sertoli Cells – manufacture estrogen during fetal and neonatal life.
• Leydig Cell – site of estrogen synthesis during puberty and throughout adulthood.

It seems that the leydig cells express high mRNA and protein levels of the aromatase enzyme, which goes by the name CYP19.

So for the height increase seeker, does that mean that the spark in every person’s development, which causes them to go from Sertoli Cell to Leydig Cell production of estrogen is what causes this entire thing???

The person does state that the mechanism of how estrogen production is shifted from Sertoli Cell to Leydig Cell is not known at this time. This may be the very key that we should be looking for. This may be the key to everything. If we can somehow break the process of the shift, by preventing the Leydig Cells from ever given the chance to produce estrogens, since they are the cells that really have the high mRNA and protein production of the aromatase, then maybe we can completely hold off puberty until we want to.

This would be the one step in the entire growth process where we can manipulate and modulate slightly to control our growth rate and how long we would wish to grow. Remember, if we can control at which age we wish to start puberty, we can control the amount of time we have left to grow, which means that we can continue to grow as much as we want, at least theoretically.

 

This post is one of the most controversial ideas I have been thinking about since it would require that the human body change in shape and physiology in a dramatic way. One of the basic ideas of innovation by business analysts is that the person who is trying to figure out how to think outside-of-the-box needs to question and challenge all assumptions to test to see if they are all valid. Well this post is going to challenge some of our most basic ideas on how endochondral ossification and how the structure and alignment of the growth plates to the bones might work.

When I was reading over on how the long bones are even formed in the beginning from chondrogenic condensation & aggregation, I started to wonder whether it might be possible to create more than just the primary and secondary ossification center as expected from the neonatal development of humans. I am proposing that if we had more than the usual 1 primary and 2 secondary ossification centers , but had an additional primary ossification center then we would have more than just the two growth plates on each side, proximal and distal, of each long bone in our limbs. We might be able to create 4 growth plates on each limb. So, an we create the long bone development to have two secondary ossification centers and two or even three primary ossification centers?

We know that humans naturally develop ‘growth plates’ because the specific areas when the cartilage tissue starts to ossify/turn into bone are pushing against each other, turning what used to be entirely made from cartilage tissue into a band of cartilage that is left. Cartilage can expand due to the elastic, deformable nature of the extracellular matrix composition. the cells in the matrix can expand and push against each other, which would cause the entire tissue to expand with the expansion of the cells.

First, from basic anatomy, we have to realize that there is really no such thing as ‘growth plates’. The actual term for growth plates is just a name given to the band of cartilage that has not been encroached upon and turned into bone. I refer to picture to the right is taken from a class at Midlands Tech. The picture is small so it might be smart to click on the picture to make it bigger.

We see that in the actual development of the bones which grow not just longer but also wider, that the bones start out as completely cartilage, when the human is still in the womb and growing as an embryo. I don’t know enough about obstetrics but I would guess that the fetus starts to have some of the earliest cartilage tissue ossify before it is even born. If that was not the case and the long bones were still cartilage, from the process of birth where the fetus’s head has to pass through the birth canal, it’s cartilage head would be completely deformed or even crushed by the PC muscles of the female vulva region. Its body and limbs should also be partly bone or the mother and father in the hospital room would not be ale to hold the baby that was just born without hurting it through deformation of the cartilage.

Without reading anything on pediatrics or pediatrics growth, I am assuming right now that when the baby is just born, it already has the ends of the cartilage structure start to ossify and the diaphysis also ossify too. This is the beginning of where the ossification centers are.

So the growth plates are just where the ossification centers meet and where they haven’t encroached completely on through vascularization and mineralization.

I am proposing that it might be possible to have a limb bone growth with almost unlimited length if we can get a second band of cartilage alongside the original band of cartilage in the long bone’s bone tissue.

Depending on how the double growth plate would go together, and in which arrangement might be slightly tricky, at least at this stage. We know that the growth plates have around 4 basic zones which must all function in continuous, sequential path.

1. Resting Zone – where the progenitor mesenchymal stem cells differentiate into the chondrocytes
2. Proliferation Zone – the area where the cartilage cells multiply through the process of mitosis
3. Hypertrophic Zone – the area where the actual bone lengthening (or actually cartilage matrix expansion) is being done.
4. Calcification Zone – the area that is being infiltrated, vascularized, and mineralized to turn the cartilage tissue matrix into bone tissue matrix

The smooth sequential series of cell differentiation steps must also work for the 2nd growth plate, which would be implanted into the limb’s long bone, around the metaphyseal area, in parallel with the natural one.

The Actual Arrangment 

I remember reading that the way that the cartilage/growth plate actually manage to make the overall bone structure longer is that while the middle part of the long bone stays where it is, there is a part of the bone that is slowly being PUSHED away from the other area/ distance of the overall bone structure. Technically, the epiphyseal ossification center, which is the secondary center is being pushed outward by the continuous cartilage into bone tissue process of calcification aka ossification.

So remember this part – The natural process of how long bones get longer is that the resting zone is actually pushing the long bone’s ends, the epiphysis away from the center of the long bone structure. From physics, we have to remember that there really is no such thing as a PULLING FORCE. Anything that is moving is the result of a force that is doing PUSHING, NOT PULLING.

So what surface of tissue is pushing which surface of tissue to make the long bone longer?

The general current medical conclusion is that the edge of the growth plate that is on the epiphysis side (aka the resting zone side) is pushing distally the epiphysis away from the spatial center of the bone.

So how does this relate to the principle of height increase through double growth plate implants?

We have to decide in which direction should the growth plate go in, with either the resting zone facing outwards from the center of the bone, or facing inwards towards the center of the bone. Remember that the natural growth plate is facing away from the medium.

The 2nd thing to remember is that there has to be a continuous source of bone marrow derived mesenchyme that can differentiate into the cartilage cells/chondrocytes that we want. If we put the growth plate in the wrong direction, the bone marrows progenitor mesenchymal stem cells might not be enough and get depleted.

I present a picture found elsewhere below.

Notice that the blood vessels are going in only certain parts of the long bone so that the organic tissue in the cavity in the middle is kept alive. This would be the same blood vessel which would continue to make new progenitor mesenchyme. While there is maybe one major vessel going into the epiphysis, there is much more going into the middle of the bone. That is why I propose that the direction which a 2nd growth plate on each side should be put in be facing the direction where the resting zone would be on the side closer to the middle. The result is an overall long bone that actually has 5 sections, instead of the usual 3 sections, which results in 4 growth plates on each limb.

Complications With This Idea

The main issue with this proposal is from the failure of the long bone’s structural integrity because it became too long and the body became too heavy. The loading on the continuous cartilagenous area from above the growth plate would get heavier and heavier as the person got older, and the cartilage may not longer be able to support the body. If the bone, like a femur, became too long, it might become too weak

This study I recently found seems to put the old idea of using PEMF (Pulsed Electromagnetic Field) to grow taller really into question.

The truth is that in the very beginning, we had found studies which showed that PEMF helps towards accelerated bone fracture healing times, meaning that it was potentially good toward bone tissue growth.

1. Pulsed electromagnetic field treatments enhance the healing of fibular osteotomies.
2. Additive effects of prostaglandin E2 and pulsed electromagnetic fields on fracture healing.
3. The effects of pulsed electromagnetism on fresh fracture healing: osteochondral repair in the rat femoral groove.

The article titles are above without the right links.

These studies showed that after say a surgical cut through the bone or a fracture, the non-union of the two part can be increased in healing by applying PEMF in short durations.

For me at this point in the research, I am no longer looking for techniques or compounds that will lead to bone growth since that implies bone tissue increase from bone mineral density increasing. I am almost completely focused on finding growth factors and methods to induce cartilage mainly because cartilage has been the only type of tissue that would work if we wanted to try to stretch human limbs. Bone tissue is just too hard, strong, and brittle to pull and create plastic deformation.

Study #1: AUTORADIOGRAPHIC STUDY OF THE EFFECTS OF PULSED ELECTROMAGNETIC FIELDS ON BONE AND CARTILAGE GROWTH IN JUVENILE RATS

Analysis: 

Right off the bat we see that the point of PEMF is towards repair of non-union bone fractures.

We remember that for new bones to form, something called a callus is first developed. This callus will have a type of cartilage known as fibrocartilage inside.

The fibrocartilage and the cartilage found in the condyle area of the synovial joints are similar. The PEMF was applied to the articular cartilage in the condyle region.

There was 3 groups, the control, the group with only PEMF-M, and the last is PEMF-E. The fields were applied for 8 hours a day on the lab animals. The results show that for the PEMF-M group, the cartilage in the condyle region was most reduced. The researchers do note the fact that with different variations of time for PEMF application, there was varying degrees of articular cartilage thickness. It seems that as the animals grew older, the amount of cartilage growth decreased.

The ending may sum it best – The PEMF_M had a negative effect on the chondrogenic layer of the articular zone, but no chondrogenic or osteogenic effects were noted 

Interestingly, other studies seem to have contradictory conclusions…

Effects of Pulsing Electromagnetic Fields on Bone Growth and Articular Cartilage

Abstract

Observations made during treatment of juvenile pseudarthrosis by pulsing electromagnetic fields (PEMF) suggested that bone growth might be altered. PEMF applied to immature rabbits under conditions of continuous stimulation (24 hours/day for 8 weeks) produced no major changes in bone growth. Continuous stimulation by PEMF induced a statistically significant increase (22%) in femoral articular cartilage glycosaminoglycan. Intermittent PEMF stimulation (12 hours with stimulation/12 hours without stimulation) for 18 weeks produced no significant change in bone growth or time of epiphyseal plate closure. No significant changes in the physical characteristics of growing bone were observed with any treatment.

Analysis

This study seems to show that at least for the type of material inside, the glycoaminoglycan, that was increased if the PEMF was applied continuously 24 hours a day. The application showed no big changes in the growth of the bones or at what time the growth plates would have closed.

So for developing human children who still have their growth plates, PEMF doesn’t seem to increase the endochondral ossification process which would result in increased bone tissue formation rate. The glycoaminoglycan content level did go up but that did not cause the cartilage to thicken.

Implications For Height Increase

For a long time it was proposed that PEMF application would stimulate growth of bone. In the beginning it was looked at as a viable option to increase height. Now it seems that it can’t even make the growth of bone tissue increase in immature lab animals (and thus human as well) or the cartilage of the growth plates. I am willing to conclude at this point that maybe it is only possible to see the PEMF have any effect when there is a real fracture causing a non-union and we need accelerated healing. It still might be possible to use the PEMF technology after limb lengthening surgery to speed up the healing process.