5-alpha DiHydroTestosterone (DHT) grows everything in the male body for the good, the bad, and the ugly

5-alpha DiHydroTestosterone (DHT) grows everything in the male body for the good, the bad, and the ugly. ( http://www.ajandrology.com/preprintarticle.asp?id=123664 )

( Source: http://en.wikipedia.org/wiki/File:Dihydrotestosterone-3D-balls.png )

(Source: http://upload.wikimedia.org/wikipedia/commons/1/13/Steroidogenesis.svg )

Man, DHT (Dihydrotestosterone) grows your penis during your puberty and maximizes your erectile size during age 20-30 when it reaches the peak level, but causes no problems for your prostate. When you get older and your DHT level starts to drop, you start to experience prostate enlargement, even cancer!
What is wrong? DHT grows everything, but why does your prostate cell become inflammatory and change itself to cancerous cell? Biological clock onset of cancerous genes? The clock is ticking if you carry the gene. Can you silence the gene (clock)?
Yes, reduce cellular prostaglandin E2 (PG-E2) release. PG-E2 activates stem cells (good or bad/cancerous) to multiplicate the cells and to grow the bone/brain. This is why you have growing pains.

Although Prostaglandin E2 starts your life by allowing a sperm to fertilize an egg (disabling the egg immunity), lets you get out of the uterus (uterine ripping for childbirth) and grows your body (stimulating your cell, brain, memory, and bone growth), it can end your life with infection, inflammation, fever, immune disorders and cancers. During your puberty, it lets you experience growing pains. After you pass puberty, you should reduce/adjust your cellular prostaglandin E2 release, so that it won’t activate cancerous DNA for you.

Prostaglandin E2 can be induced by mechanical stretching of muscles, tissues or bones. For example, stretching boned promotes bone growth via prostaglandin E2. This principle has been used for manhood enlargement exercises or stretching. Over-stretching tissues (including erectile tissues and smooth muscles) generally stimulate the collagen protein release for tissues scaring. The tissue scarring can extended to compress the nerves and blood vessels in addition to stretching induced nerve and blood vessel damage or scarring. You should avoid mechanically stretching damage of the nerves, tissues and blood vessels, upregulate your DHT and 5-alpha reductase receptors in your erectile tissues, increase your hGH production to activate the penile somatic stem cells, boost the release of beta endorphin, and activate the genes cytokeratin 16 and transformation growth factor beta-3 for enbryonic scar-free healing and cellular growth (http://www.actionlove.com/cases/case11311.htm )!
http://jn.physiology.org/content/early/2010/10/27/jn.00730.2010.full.pdf+html ,
http://www.ncbi.nlm.nih.gov/pubmed/11311513 ,
http://www.ncbi.nlm.nih.gov/pubmed/9626402 ,
http://www.ncbi.nlm.nih.gov/pubmed/8666581 , and

http://www.researchgate.net/publication/14249866_In_situ_microdialysis_in_bone_tissue._Stimulation_of_prostaglandin_E2_release_by_weight-bearing_mechanical_loading )

Stress neurohormones norepinephrine and epinephrine can induce prostaglandin E2 release via stimulation of α1- and α2-noradrenergic receptors.
“Preoptic α1- and α2-noradrenergic agonists induce, respectively, PGE2-independent and PGE2-dependent hyperthermic responses in guinea pigs. ”
Carlos Feleder , Vit Perlik , Clark M. Blatteis, American Journal of Physiology – Regulatory, Integrative and Comparative PhysiologyPublished 1 June 2004Vol. 286no. R1156-R1166DOI: 10.1152/ajpregu.00486.2003
“Effect of norepinephrine and renal denervation on renal PGE2 and kallikrein in rats.”
Diz DI, Baer PG, Nasjletti A. Am J Physiol. 1981 Nov;241(5):F477-81.
“Increased renal secretion of norepinephrine and prostaglandin E2 during sodium depletion in the dog.” J A Oliver, J Pinto, R R Sciacca and P J Cannon, J Clin Invest. 1980;66(4):748–756. doi:10.1172/JCI109912.
“Physiological concentrations of melatonin inhibit the norepinephrine-induced activation of prostaglandin E2 and cyclic AMP production in rat hypothalamus: A mechanism involving inhibition of nitric oxide synthase”, Ilham Bettahi1, Juan M. Guerrero1, Russel J. Reiter2, Carmen Osuna1,* Journal of Pineal Research, Volume 25, Issue 1, pages 34–40, August 1998
“Role of the Prostaglandins in Norepinephrine Release during Augmented
Renal Sympathetic Nerve Activity in the Dog” JUAN A. OLIVER, ROBERT R. SCIACCA, JOHN PINTO, AND PAUL J. CANNON, Circ Res 48: 835-843, 1981
“Modulation of Norepinephrine Release from Sympathetic Neurons of the Rabbit Aorta by Prejunctional Prostanoid Receptors”, TENNA JUUL JENSEN and OVE A. NEDERGAARD, JPET 291:7–11, 1999
“Norepinephrine enhances the LPS-induced expression of COX-2 and secretion of PGE2 in primary rat microglia “, Johannes CM Schlachetzki1,2†, Bernd L Fiebich1*†, Elisabeth Haake1, Antonio CP de Oliveira1, Eduardo Candelario-Jalil3, Michael T Heneka4, Michael Hüll1*, BioMed Central Ltd. 2010
Effects of norepinephrine and other pharmacological agents on prostaglandin E2 release by rabbit and bovine irides.” Sardar Y.K. Yousufzai, Ata A. Abdel-Latif,
Experimental Eye Research, Volume 37, Issue 3, September 1983, Pages 279–292
“Changes in the Hypothalamic Interaction between Norepinephrine and Prostaglandin E2 during Sexual Maturation in Female Rats” Franchi A. · Gimeno M. · Szwarcfarb B. · Carbone S. · Rondina D. · Moguilevsky J.A
“Diminished Prostaglandin-Mediated Inhibition of Norepinephrine Release from the Sympathetic Nerve Endings in Spontaneously Hypertensive Rats”, Kazushi Tsuda1, Ichiro Nishio1 and Yoshiaki Masuyama1 , Clinical and Experimental Hypertension, 1987, Vol. a9, No. 10 , Pages 1601-1614
“The Effect of Prostaglandin E2 and Indomethacin on the Placental Vascular Response to Norepinephrine” Anne Berssenbrugg, Debra Anderson, Terrance Phernetton, John H. G. Rankin, Exp Biol Med (Maywood) November 1978 vol. 159 no. 2 281-285http://ebm.sagepub.com/content/159/2/281.abstract
Prostagladnin E2 (PGE2) and cancer examples:

1. “Cancer-stimulated mesenchymal stem cells create a carcinoma stem cell niche via prostaglandin E2 signaling.” – http://www.ncbi.nlm.nih.gov/pubmed/22763855 ;
2. “Interleukin-17 and prostaglandin E2 are involved in formation of an M2 macrophage-dominant microenvironment in lung cancer.” –http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3378786/pdf/nihms369069.pdf ;
3. “The role of the EP receptors for prostaglandin E2 in skin and skin cancer.” –http://www.ncbi.nlm.nih.gov/pubmed/22012553 ;
4. “Prostaglandin E2 EP receptors as therapeutic targets in breast cancer.” –http://www.ncbi.nlm.nih.gov/pubmed/22002714
Here is a simple, natural anti-PGE2 drug “Resolvin” : Omega-3 + Aspirin or water willow’s salicin –http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3186038/pdf/medrep-03-19.pdf;http://en.wikipedia.org/wiki/Resolvin

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