This episode & post will be a very long one since a 16 year old male named Matheus from Brazil recently came to me to report about all the research he has been doing on how to possibly increase his own height.

Episode #11: I Review And Outline All The Research And Studies Matheus Has Shown To Me

This podcast episode will focus on where I will be looking at all the research and studies a guy named Matheus from Brazil has shown me since getting in contact with me since last month. I have sent an email to him asking that he come on to the podcast to discuss in his own words what he has been up to but his claim that he has weak English speaking skills means I will again be speaking alone.

Some of the stuff he has found has definitely helped in clearing up a few blind spots me and Tyler have had in our own research.

The thing is that he has been linking to so many articles, studies, and papers that it has been very hard for me to organize and arrange all the information he has thrown out at me so I will try to just break down each individual compound down to whether there are inhibiting or helping increased growth.

Chemical compounds which stimulate increased bone longitudinal growth

Vitamin K2 (aka Menaquinone) – is animal based which increases Testosterone (source)

MGP(Matrix Gla Protein-derived K2) which is produced by Vitamin K2 – inhibits the calcification of tissues and cartilages – is the major inhibitor of human body tissue calcification and seems to have much influence on chondrocytes. (Coordinated expression of matrix Gla protein is required during endochondral ossification for chondrocyte survival)

Ursolic acid – it interacts with the receptors for IGF-1, and increases sensitivity to IGF-1. (Ergo-log.com)

Asthaxanthin – good antioxidant

Cissus quadrangularis – it increases the production of IGF-1 by osteoblasts.

Glutathione – (source: Nitric oxide decreases IGF-1 receptor function in vitro; glutathione depletion enhances this effect in vivo.)

N-Acetylecysteine (NAC) – (source: N-acetylcysteine prevents nitric oxide-induced chondrocyte apoptosis and cartilage degeneration in an experimental model of osteoarthritis.)

Alfalfa (aka Ipriflavone) – (Source: Ipriflavone modulates IGF-I but is unable to restore bone in rats.)

Amomum villosum – (Source: Amomum villosum induces longitudinal bone growth in adolescent female rats.)

Herbal formula HT042 (made of three elements, 1. Astragalus (most important), 2. Eleutherococcus senticosus, 3. Phlomis umbrosa) – (Source: http://www.ncbi.nlm.nih.gov/pubmed/21091251)

Commelina communis – (Source: http://www.naturalheightgrowth.com/2012/12/29/korean-medicine-extracts-hansogdan-phlomis-umbrosa-and-dalgaebi-commelina-communis-in-milk-enhances-height/)

Artemisia Capillaris – (Source: http://www.naturalheightgrowth.com/2012/12/29/kiwoomi-rice-with-eleutherococcus-senticosus-and-artemisia-capillaris-extract-shows-proof-that-it-can-increase-childrens-height-breakthrough/)

Jaoga-Yukmiwon (R) – Effects of Jaoga-Yukmiwon(R), a Korean herbal medicine, on chondrocyte proliferation and longitudinal bone growth in adolescent male rats.

Carnitine – (Supplementation of carnitine leads to an activation of the IGF-1/PI3K/Akt signalling pathway and down regulates the E3 ligase MuRF1 in skeletal muscle of rats.)

Sesamin (a lignan) – (Source: http://www.heightquest.com/search?q=sesamin)

Genistein – (Source: Mechanism involved in genistein activation of insulin-like growth factor 1 receptor expression in human breast cancer cells.)

Daidzein – (Source: Feeding daidzein to late pregnant sows influences the estrogen receptor beta and type 1 insulin-like growth factor receptor mRNA expression in newborn piglets.)

Isoflavone – bind to estrogen receptors shielded them and preventing the binding of the true hormones. Can only bind to the beta receptors. Genistein binds to the alpha receptors. Increases the synthesis of IGF-1 and VEGF, and is 100X less estrogenic than estrodial.

Letrozole -Can decrease the level of estradiol

Niacin – is the precursor to NADPH

Vitamin D3 – increases the expression of VEGF only in bone – Higher serum vitamin D concentrations are associated with longer leukocyte telomere length in women.

Tuarine – (source: http://www.heightquest.com/search?q=taurine)

• IGF-1
• Zinc
• Lactoferrin
• GH
• Androgens 
• Hyaluronic

Chemical compounds which inhibit bone longitudinal growth

Estradiol – Matheus would cite many sources showing that this is very bad for height increase and growth… the effect of estradiol on the growth spurt at puberty is increasing GH and overexpression of VEGF… the effects of estradiol on chondrocyte senescence… reduces the proliferation of chondrocytes and enhances endochondral ossification

Retinoic acid – inhibits the proliferation of chondrocytes.

Accutane / Roaccutane (derived from retinol / vitamin A) – closes the growth plates (used by people w/ acne) Instead, choose the acne treatment with vitamin B5 and Zinc

Nitric Oxide – seems to do many things to decrease chondrocyte proliferation including decrease TGF-Beta production, induce chondrocyte apoptosis, decreases sensitivity of the IGF-1 receptors, decrease IGF-1 receptor function, etc. (Source: Nitric oxide inhibits chondrocyte response to IGF-I: inhibition of IGF-IRbeta tyrosine phosphorylation)

Corticosteroids – examples are Cortisone and Cortisol – decreasing the expression of receptors of IGF-1 and GH, and acting directly on the resting area and decrease the proliferation of chondrocytes

Homocysteine – is responsible for the shortening of telomeres during methylation, and and can also increase the effects of oxidative stress (source: Homocysteine levels and leukocyte telomere length.)

Oxidative stress – leading to senescence not just of the growth plate but of the entire organism… almost always responsible for the shortening of telomeres – a result of accumulation of excess free radicals that are generated during the cell cycle or by high levels of homocysteine – (Source: Potential involvement of oxidative stress in cartilage senescence and development of osteoarthritis: oxidative stress induces chondrocyte telomere instability and downregulation of chondrocyte function.)

Vitamin A – Converted into retinoic acid

About Growth Plate Senescence

The senescence of the growth plate is not genetically programmed…it occurs after the biochemical factors that occur during the growth spurt at puberty

Chondrocytes have an infinite proliferation and they have longer than average telomeres than all the other cells of the body. The that the cells divide, the more free radicals they produce as well as oxidative stress. The chondrocytes in the growth plate seem to proliferate and divide at a much faster rate than any other types of cells in the body. That is why they are one of the first types of cells that go extinct. the other cells don’t go completely out until old age. it seems that oxidative stress is really bad and causes cartilage senescence and chondrocyte telomere instability.

I personally did not want to look through the list of PubMed studies but for anyone who is interested, go right ahead. The truth is that I looked at the titles of this studies and some of them I have already read and am aware of.

• http://www.ncbi.nlm.nih.gov/pubmed/10912528
• http://www.ncbi.nlm.nih.gov/pubmed/7925098
• http://www.ncbi.nlm.nih.gov/pubmed/16614378
• http://www.ncbi.nlm.nih.gov/pubmed/11641457
• http://www.ncbi.nlm.nih.gov/pubmed/18174286
• http://www.ncbi.nlm.nih.gov/pubmed/10912529
• http://www.ncbi.nlm.nih.gov/pubmed/1415528
• http://www.ncbi.nlm.nih.gov/pubmed/21164272
• http://www.ncbi.nlm.nih.gov/pubmed/21865751
• http://www.ncbi.nlm.nih.gov/pubmed/21441345

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• Length of time: 26 mins
• Beginning of actual interview: 1:15 

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