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ANDROSTENTRIOL i inne inhibitory 11 beta HSD

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Jeżeli interesuje kogoś androstentriol i działające podobnie środki, to tutaj znajdzie więcej informacji:

http://slawomirambroziak.pl/termogeniki-i-inne-spalacze/androstentriol-i-inne-inhibitory-11-beta-hsd/#more-237 

S. Ambroziak

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Masz problem z przybraniem na wadze lub zgubieniem zbędnych kilogramów? Indywidualne plany dietetyczne i treningowe
  • 23 383 spalonych kg tłuszczu
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Podbiję. Może ktoś jeszcze przeczyta?...

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Gdzieś wpadłem na badania, że węglowodany aktywizują 11 beta HSD1 i mogą podnosić poziom kortyzolu. Muszę się w to wczytać i przeanalizować...

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Ten artykuł odpowiada tez na pytania zawarte w tym wątku:

http://www.sfd.pl/DHEA_wali_po_ciśnieniu!-t570554-s3.html#post5 

S. Ambroziak

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Daję temu artowi ostatnią szansę...

S. Ambroziak

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ciekawy artykuł !

mówi się że poziom kortyzolu odzwierciedla
po treningu wielkość penisa , jak to przeczytałem
to od razu po treningu sprawdziłem i co się okazało !
był wielkości jak bym moczył się w wodzie z 5 godzin
ciekawe prawda ??

panie Sławku czy pisał pan kiedyś artykuł o tribulusach ??
jeśli tak to proszę o link

a połączenie tribulusa DHEA i żeń szenia sprawdzę na pewno
na PCT

i sporo kwasów DHA jest w makreli wędzonej
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Dobry Art Slawek.

W praktyce jak i w badaniach tak jak napisales na dzien dzisiejszy liczy sie jedynie dhea i androstenetriol. Z tych hmmm lagodniejszych bo jak wiadomo kazdy inny steryd anaboliczno androgeniczny dziala na obnizenie kortyzolu.

Jednak szkoda ze tak malo osob bierze sobie do serca ze imho za spadki po cyklu na SAA odpowiada niski poziom tescia i wysoki kortyzolu - idealna mieszanka kataboliczna dla miesni
Biorac Sermy/AI oraz DHEA/Androstenetriol atakujemy ten stan z 2 strn na raz i PCT idzie z górki.

Ja odkad dodalem Dhea na PCT, to totalnie zmienily sie moje spadki po cyklach. Sa one naprawde minimalne.


Ogolnie jak ktos nie chce bawic sie w powazne sterydy i kox to mam dla niego cos lagodniejszego - zbudowanie bazy anabolicznej na w miare naturalnej puli hormonow(a raczej ich regulacji). Wszystko to bez igerencji (blokady) hpta

20mg nolvadexu przez 2-3 miesiace
100-200mg dhea przez 2-3 miesiace (2 razy dzienie dawka dzielona)
Formestane lub inne AI (ale juz nie ATD heheheh o tym kiedy indziej) tez przez 2-3 miesiace

serm podbija tescia
Dhea obniza kortyzol
AI zapobiega konwersji tescia do estro robiac lepsze ratio testosteron-estradiol a do tego AI jak wiadomo obniza SHBG.

Srodowisko idealne do budowy miesni bez blokady hpta, obciazania watroby, itp. W porownaniu do siegania po SAA jest to lajcik a naprawde mozna osiagnac na nim fajne rezultaty

Troche nie na temat ale co tam heheh


Slawek moze nawiazemy wspolprace - Ty bedziesz pisal teorie a ja sprawdzal ja w praktyce na sobie




Jeszcze jak kogos interesuje

Androstenetriol: An Interesting DHEA Metabolite

By Thomas Incledon, PhD(c), RD, LD/LN, RPT, NSCA-CPT, CSCS, CFT

What is this stuff

In this article, I will dig deep into the research and present all of the current scientific information on androstenetriol. While things may get a little technical, don’t split your Speedos. I’ll spell it out in simple terms and you will understand all that the scientists know.

Which is the real androstenetriol?
Triols are simply steroids with three hydroxyl (OH) groups attached to their carbon structures. After reviewing through every study I could find, it appears that there are at least 3 possible androstenetriols:

1) 5-androstene-3 beta, 16 alpha, 17 beta-triol
2) 5-androstene-3 beta, 7 alpha, 17 beta-triol
3) 5-androstene-3 beta, 7 beta, 17 beta-triol


All of these agents are structurally classified as steroids. The first one has been isolated from human placenta and can be converted into the estrogen estriol [1]. This 16 alpha-androstenetriol version was first isolated from the urine of a patient with cancer of the adrenal glands in 1943 and was later identified in human umbilical plasma [2] and also isolated from the urine of infants [3] and men [4]. There isn’t much known about the function of this triol. It appears to inhibit the enzyme 16-alpha hydoxylase [5] and can be produced from DHEA by human macrophages (specialized white blood cells) [6]. Until more is learned about this agent, it would be best to avoid the 16 alpha-androstenetriol version.

The second and third versions of androstenetriol are basically isomers of each other. They have the same chemical formula, but the difference is in the orientations of the hydroxyl groups attached to the 7th carbon. Most of the research appears to be on the 7-beta androstenetriol, so this will be the focus of this article and from here on referred to as androstenetriol.

Synthesis of androstenetriol (5-androstene-3 beta, 7 beta, 17 beta-triol)
Research using abdominal skin from men and women indicates that androstenetriol can be formed from two separate pathways [7]. First, DHEA can be converted into 5-Androdiol (5AD or 5-androstene-3 beta, 17 beta-diol). 5AD in turn can be converted into androstenetriol (5AT). 5AT can also be formed from the 7-keto version of 5AD. To make this easier to follow here is a chart:

DHEA

5-androstene-3 beta, 17 beta-diol (5AD)
/
5-androstene-3 beta, 7 beta, 17 beta-triol (5AT)
/
and/or
/
5-androstene-3 beta, 17 beta-diol (5AD)
/
5-androstene-3 beta, 7 alpha, 17 beta-triol
/
7-keto-5-androstene-3 beta, 17 beta-diol
/
5-androstene-3 beta, 7 beta, 17 beta-triol (5AT)

The arrows indicate which way the reactions can proceed. The synthesis of 5AT comes primarily from the direct conversion of 5AD to 5AT. Since both 5AD and 5AT can come from DHEA, they are referred to as DHEA metabolites in the literature, hence the title of this article.

A Little 5AT History
It was established that DHEA could counteract the effects of glucocorticosteriods (like cortisol) and boost immunity [8]. Later after realizing that DHEA could be metabolized by skin and brain into 5AD and 5AT [9, 10], researchers started to investigate the DHEA metabolites. In vitro studies with mice lymphocytes (specialized white blood cells) indicated that 5AT strongly counteracted cortisol and boosted lymphocyte activity, whereas DHEA did not counteract cortisol and suppressed lymphocyte activity [11]. Additional in vitro studies demonstrated that 5AT was more effective against a viral infection in mice than its precursor 5AD [12]. 5AT potentiated immune responses and counteracted the immunosuppressive actions of cortisol. The researchers also found that the 7-beta version of 5AT was more potent than the 7-alpha version of 5AT.

Immune Boosting Effects of 5AT
Traditionally when we learn or discuss the immune system, it is treated as a separate physiological system from the endocrine and nervous systems. In 1988 Loria et al reported that DHEA could regulate immune responses against lethal virus and bacterial infections [13]. Over the next two decades, scientists started piecing together a process that involved components of the nervous system, endocrine system, and immune system. 5AT appears to have a dose response effect. Using mouse spleen cells and concentrations ranging from 5 nanomoles per liter to 5 micromoles per liter, 5AT stimulated the production of the cytokines interleukin-2 (IL-2) by 111-122% and interleukin-3 (IL-3) by 30-47% [12]. T-cells and B-cells were also simulated by this DHEA metabolite. In other studies using mouse macrophages, 5AT increased tumor necrosis factor alpha (TNF-alpha) and IL-1 secretion while not influencing IL-6 production [14].

The data I have reviewed thus far is all from rodents (particularly mice). Since 5AT boosts the immune system of rodents, one asks the logical question: can this data also be applied to humans? Since 5AT is present in a variety of mammals, including humans, it seems plausible that 5AT could boost the immune response in humans. This needs to be confirmed by research and questions as to how much is needed in humans to get a decent effect need to be answered.

Antiglucocorticoid Effects of 5AT
DHEA and its metabolites (5AD and 5AT) counteract the stress-induced immunosuppressive action of glucocorticoids [15]. This results in stronger responses to immune system challenges. Hydrocortisone (cortisol) classically is used to suppress immune function in cells treated with an immune challenge. DHEA was unable to counteract the immunosuppressive effects of cortisol, while 5AD counteracted it only at high doses. 5AT significantly counteracted the immunosuppressive effects of the glucocorticoid on lymphocyte growth and cytokine production [15]. Research overall indicates that in the body, DHEA, 5AD, and 5AT may have some similar functions, while in cell culture studies their effects are dramatically different from one another. In another study, 5AT counteracted the down-regulatory effect of hydrocortisone on macrophages and may function to counterbalance glucocorticoid function [14].

An abstract was presented in 1997 at the Conference on Cortisol and Anti-Cortisols in Las Vegas Nevada. In vitro work indicated that 5AT counteracted the immunosuppressive effects of glucocorticoids on immune cells from patients with hypercortisolemia [16]. This data is preliminary and has yet to be published (or is not indexed on any database I searched through).
tissue weights during a sever infection. Could this have potential application for bodybuilders and athletes? The obvious application would be to marathon runners, triathletes, and wrestlers who are traditionally overtrained. I am working on some projects right now and hope to have a definitive answer in the future as to how Androstenetriol can be used by athletes. Keep reading ASMJ and you’ll be the first to know.

References

1. Ryan, K.J., Conversion of delta 5-androstene-3 beta, 16 alpha, 17 beta-triol to estriol by human placenta. Endocrinology, 1958. 63: p. 392-394.
2. Colas, A., W.L. Heinrichs, and H.J. Tatum, Pettenkofer chromogens in the maternal and fetal circulations: Detections of 3 beta, 16 alpha, dihydroxy-androst-5en-17 -one in umbilical cord blood. Steroids, 1964. 3(4): p. 417-434.
3. Reynolds, J.W., The identification and quantification of delta-5-androstenetriol (3-beta, 16-alpha, 17-beta-trihydroxyandrost-5-ene) isolated from the urine of premature infants. Steroids, 1966. 8(5): p. 719-727.
4. Fotherby, K., The isolation of 3 beta-hydroxy-delta 5- steroids from the urine of normal men. Biochemical Journal, 1958. 69: p. 596-600.
5. Sano, Y., et al., Steroid 16 alpha-hydroxylase from human fetal liver; inhibition by steroids. Acta Obstetricia et Gynecologica Scandinavica, 1980. 59(3): p. 245-249.
6. Schmidt, M., et al., Conversion of dehydroepiandrosterone to downstream steroid hormones in macrophages. Journal of Endocrinology, 2000. 164(2): p. 161-169.
7. Faredin, I. and I. Toth, The metabolism of [4-14C]5-androstene-3beta, 17beta-diol by normal human skin in vitro. Acta Medica Academiae Scientarum Hungaricae, 1975. 32(2): p. 139-152.
8. Loria, R.M. and D.A. Padgett, Mobilization of cutaneous immunity for systemic protection against infections. Annals of the New York Academy of Sciences, 1992. 650: p. 363-366.
9. Akwa, Y., et al., Neurosteroid metabolism. 7 alpha-Hydroxylation of dehydroepiandrosterone and pregnenolone by rat brain microsomes [published erratum appears in Biochem J 1993 May 1;291(Pt 3):952]. Biochemical Journal, 1992. 288(Pt 3): p. 959-964.
10. Mathur, C., et al., Steroids and their conjugates in the mammalian brain. Proc Natl Acad Sci U S A, 1993. 90(1): p. 85-88.
11. Padgett, D.A. and R.M. Loria, In vitro potentiation of lymphocyte activation by dehydroepiandrosterone, androstenediol, and androstenetriol. Journal of Immunology, 1994. 153(4): p. 1544-1552.
12. Loria, R.M., D.A. Padgett, and P.N. Huynh, Regulation of the immune response by dehydroepiandrosterone and its metabolites. Journal of Endocrinology, 1996. 150(Suppl): p. S209-S220.
13. Loria, R.M., et al., Protection against acute lethal viral infections with the native steroid dehydroepiandrosterone (DHEA). Journal of Medical Virology, 1988. 26(3): p. 301-314.
14. Padgett, D.A. and R.M. Loria, Endocrine regulation of murine macrophage function: effects of dehydroepiandrosterone, androstenediol, and androstenetriol. Journal of Neuroimmunology, 1998. 84(1): p. 61-68.
15. Loria, R.M., Antiglucocorticoid function of androstenetriol. Psychoneuroendocrinology, 1997. 22(Suppl 1): p. S103-S108.
16. Norbiato, et. al. In Vitro Immunomodulatory Effects of Delta 5-Androstene-3b,7b,17b Triol (AET) in Hypercortisolemic Patients. In: Conference on Cortisol and Anti-Cortisols. 1997. Las Vegas, NV.

Zmieniony przez - Roid_rage w dniu 2010-02-21 20:43:10

".... Then we'll see which are better, his steroids or mine"

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Roid, fajny ten artykuł. Ściągam go na dysk, bo na pewno się przyda.

Ta Twoja propozycja - ciekawa. Nie wiem tylko - czy to by się udało w praktyce.

Ale świetny i przydatny jest ten Twój praktyczny komentarz do arta. Może więc jakiś duet autorski... Jakieś artykuły - gdzie ja piszę cześć teoretyczną, zaś Ty komentujesz to okiem praktyka?...

S. Ambroziak

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Nie ma sprawy Slawek :) Jakos sie dogadamy hehe
Co do komentsow od strony praktycznej to moge oczywiscie takowe wypowiadac na temat czegos co wstrzykiwalem/polykalem/wcieralem w organizm hehehe. Na szczescie albo i nieszczescie (to sie okaze w przyszlosci) z kazdym dniem ilosc substancji przetestowanych przeze mnie wzrasta.......w zastraszajacym tempie
Po prostu taka a nie inna mam pasje. Najpierw teoria obryta od deski do deski (badania,arty, opinie innych ludzi) a potem automatycznie krok nastepny - praktyka na sobie :)
Na szczescie na tyle (takie przynajmniej ja uwazam) rozsadny ze mnie gosc, ze nie balansuje na krawedzi zycia i smierci. Takie experymenty mnie nie interesuja. Wszystko jest dla ludzi ale robmy to z glowa

".... Then we'll see which are better, his steroids or mine"

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Zapomnialem w swoim arcie Slawku piszesz o kwasie glicyretynowym. Widzialem juz i badania i suple transdermalne oparte o ten srodek.

Tu masz Sławek to badanie

Glycyrrhetinic acid, the active principle of licorice, can reduce the thickness of subcutaneous thigh fat through topical application.

Armanini D, Nacamulli D, Francini-Pesenti F, Battagin G, Ragazzi E, Fiore C.

Department of Medical and Surgical Sciences-Endocrinology, University of Padua, Via Ospedale 105, 35100 Padua, Italy. decio.armanini@unipd.it

Cortisol is involved in the distribution and deposition of fat, and its action is regulated by the activity of 11beta-hydroxysteroid dehydrogenase. Glycyrrhetinic acid, the active principle of licorice root, blocks 11beta-hydroxysteroid dehydrogenase type 1, thus reducing the availability of cortisol at the level of adipocytes. We evaluated the effect of topical application of a cream containing glycyrrhetinic acid in the thickness of fat at the level of the thigh. Eighteen healthy women (age range 20-33 years) with normal BMI were randomly allocated to treatment, at the level of the dominant thigh, with a cream containing 2.5% glycyrrhetinic acid (n=9) or with a placebo cream containing the excipients alone (n=9). Before and after 1 month of treatment both the circumference and the thickness of the superficial fat layer of the thighs (by ultrasound analysis) were measured. The circumference and the thickness of the superficial fat layer were significantly reduced in comparison to the controlateral untreated thigh and to control subjects treated with the placebo cream. No changes were observed in blood pressure, plasma renin activity, plasma aldosterone or cortisol. The effect of glycyrrhetinic acid on the thickness of subcutaneous fat was likely related to a block of 11beta-hydroxysteroid dehydrogenase type 1 at the level of fat cells; therefore, glycyrrhetinic acid could be effectively used in the reduction of unwanted local fat accumulation.

A przyklad supli to na przyklad (maslo maslane hehe) to - Liposolv , Eviscerate, Napalm.

Wszystkie te transdermale opieraja sie wlasnie o kwasie glicyretynowym (choc obok podpowiadaja mi ze tlumaczenie powinno byc kwas glicyryzynowy), yohiminie, synefrynie, ketonach malinowyvh itp.
O dziwo wszystkie maja naprawde dobre opinie
I oczywiscie next week idzie to pod testy u mnie (u mojej 2 polowki) wiec dam znac. My kupujemy wsio co dziala i jest nowe hehe taka mania :D

".... Then we'll see which are better, his steroids or mine"

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roid rage a jak wedlug ciebie wygladal by odblok z uzyciem srodkow ktore wymieles to znaczy wiem jak wyglada ta jedna faza[clom hcg nolva]chodzi mi o te srodki obnizajace kortyzol.cykl bedzie po20 tyg pytam tak ciekawosci jestem dopiero po 10 ale jakos nie chce mi sie konczyc moglbys cos rozpisac[cykl byl z uzyciem;deca,test metka gdzies w miedzyczasie bedzie].
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