erase pro e t up nutrex

[albertodrol]

cosa ne pensate dell erase pro che contiene anche delle erbe che dovrebbero fungere da serm? è inutile usare un prodotto come l erase pro che funge sia da ai che da serm?

io sto per iniziare erase pro + t up nutrex (basato sul daa)

[fenix91]

Quali sono i tuoi obbiettivi?
Se è la prima volta che utilizzi un AI, l'erase pro potrebbe essere troppo, ma non a causa degli estratti erbacei che fungerebbero da SERM, ma per via del dosaggio elevato (75 mg per capsula) di Androst-3,5-dien-7,17-dione. Utilizzando l'erase normale, hai più versatilità nei dosaggi (ogni cps ha 25 mg di principio attivo) e potresti ridurre la dose di una cps qualora dovessi avvertire sides quali dolori articolari o letargia al risveglio mattutino. Alternativamente potresti assumere l'erase pro a giorni alterni, ma io ti consiglio l'erase normale, anche perchè risparmieresti parecchio

[albertodrol]

i miei obiettici sono : massa pulita.
l'erase pro gia ce l ho.da oggi sto prendendo anabeta e tra 15 giorni volevo iniziare anche erase pro e t up (ho distanziano l assuonzione di erase pro per fare passare 15 giorni dalla mia ultima assunzione di lean extreme che risale a ieri)

[fenix91]

Allora tra una settimana inizia con il T-up, e dopo una settimana/10 giorni di T-up inizia con l'erase pro. Se sperimenti sides tipo calo di libido o dolori articolari, assumi l'erase pro a giorni alterni.

[barney137]

Ma e' cosi' probabile la perdita di libido da estrogeni troppo bassi? Perche' secondo me, nel 90% dei casi (sparo una percentuale a caso), la perdita di libido maschile, specialmente nei soggetti non piu' giovanissimi, e quindi con un aromatasi piu' "aggressivo", dovrebbe essere data da un rapporto sbilanciato verso gli estrogeni. O sbaglio?

[fenix91]

Si, è molto probabile riscontrare cali di libido in soggetti maschi se i livelli di estrogeni sono troppo bassi, fenomeno che se causato dall'assunzione di un AI, è transitorio, non appena viene ristabilita la situazione di partenza dopo l'interruzione dell'AI, tutto torna come prima.
Tra gli svariati e fondamentali ruoli che gli estrogeni rivestono nel maschio, c'è l'influenza della libido e del comportamento sessuale. Attualmente è stato abbandonato il modello che vede gli androgeni come ormoni esclusivamente maschili e gli estrogeni come ormoni esclusivamente femminili. Entrambi sono importanti per ambedue i sessi, anche per quanto riguarda le funzioni sessuali-riproduttive.
Numerosi studi dimostrano l'importanza degli estrogeni nell'influenzare la libido e le funzioni sessuali maschili. Per citarne alcuni:

Estrogen masculinizes neural pathways and sex-specific behaviors.

Wu MV, Manoli DS, Fraser EJ, Coats JK, Tollkuhn J, Honda S, Harada N, Shah NM.

Source

Program in Neuroscience, University of California-San Francisco, San Francisco, CA 94158, USA.

Abstract

Sex hormones are essential for neural circuit development and sex-specific behaviors. Male behaviors require both testosterone and estrogen, but it is unclear how the two hormonal pathways intersect. Circulating testosterone activates the androgen receptor (AR) and is also converted into estrogen in the brain via aromatase. We demonstrate extensive sexual dimorphism in the number and projections of aromatase-expressing neurons. The masculinization of these cells is independent of AR but can be induced in females by either testosterone or estrogen, indicating a role for aromatase in sexual differentiation of these neurons. We provide evidence suggesting that aromatase is also important in activating male-specific aggression and urine marking because these behaviors can be elicited by testosterone in males mutant for AR and in females subjected to neonatal estrogen exposure. Our results suggest that aromatization of testosterone into estrogen is important for the development and activation of neural circuits that control male territorial behaviors.




Sexual incentive motivation in male rats requires both androgens and estrogens.

Attila M, Oksala R, Agmo A.
Source

Orion Pharma, Department of Oncology and Critical Care Research, Turku, Finland.

Abstract

In Experiment 1 castrated male rats were implanted with a Silastic capsule containing either E or cholesterol (CHOL) 35 days after castration. They were then tested for sexual incentive motivation and copulatory behaviors every 5th day for 3 weeks. None of the treatments affected sexual incentive motivation. After the last test, all subjects were implanted with DHT-containing Silastic capsules, and tests continued for another 3 weeks. While E+DHT enhanced sexual incentive motivation and copulatory behavior, DHT alone failed to do so. In Experiment 2 the aromatase inhibitor fadrozole (F) was combined with testosterone (T). T restored all behaviors to the level seen in intact rats, and F significantly reduced these effects. In fact, T+F was not different from DHT. T and DHT restored the weight of the prostate and seminal vesicles to levels close to those of intact rats. In Experiment 3 a lower dose of E was employed. Also this dose of E failed to affect sexual incentive motivation while E+DHT restored it to the level of intact animals. Castration enhanced the serum concentrations of LH and FSH. E alone caused a marked reduction, and E+DHT brought both gonadotropins back to the level of intact animals. It was concluded that the doses of E and DHT employed in these experiments were within or close to the physiological range, and that such doses of E completely fail to enhance sexual incentive motivation in castrated animals. DHT has small or no effects. It appears that sexual incentive motivation and copulation require simultaneous stimulation of androgen and estrogen receptors.

Copyright 2009 Elsevier Inc. All rights reserved.



Ovviamente, anche e soprattutto un rapporto testosterone/estrogeni favorevole ai secondi è causa nel maschio di problemi legati alla sfera sessuale non solo. Recenti studi hanno evidenziato la correlazione tra un elevato livello di estrogeni ed il cancro alla prostata, patologia che si pensava essere causata soltanto da livelli di androgeni elevati, in particolare il diidrotestosterone (DHT). Nello specifico, gli estrogeni nella prostata presentano due tipi di recettori: ER-alfa ed ER-beta. L'attivazione dell'ER-beta sembrerebbe svolgere effetti protettivi sullo sviluppo di neoplasie, mentre l'attivazione degli ER-alfa sembrerebbe favorire l'insorgenza del carcinoma prostatico. Inoltre, livelli sovrafisiologici di estrogeni sono spesso causa dell'ipertrofia prostatica benigna, che può rappresentare l'anticamera del cancro.


Estrogen and prostate cancer: an eclipsed truth in an androgen-dominated scenario.

Carruba G.
Source

Experimental Oncology, Department of Oncology, M. Ascoli Cancer Center, ARNAS-Civico, Palermo, Italy. lucashbl@unipa.it

Abstract

Prostate cancer is the commonest non-skin cancer in men. Incidence and mortality rates of this tumor vary strikingly throughout the world. Although several factors have been implicated to explain this remarkable variation, lifestyle and dietary factors may play a dominant role, with sex hormones behaving as intermediaries between exogenous factors and molecular targets in development and progression of prostate cancer. Human prostate cancer is generally considered a paradigm of androgen-dependent tumor; however, estrogen role in both normal and malignant prostate appears to be equally important. The association between plasma androgens and prostate cancer remains contradictory and mostly not compatible with the androgen hypothesis. Similar evidence apply to estrogens, although the ratio of androgen to estrogen in plasma declines with age. Apart from methodological problems, a major issue is to what extent circulating hormones can be considered representative of their intraprostatic levels. Both nontumoral and malignant human prostate tissues and cells are endowed with key enzymes of steroid metabolism, including 17betahydroxysteroid dehydrogenase (17betaHSD), 5beta-reductase, 3alpha/3betaHSD, and aromatase. A divergent expression and/or activity of these enzymes may eventually lead to a differential prostate accumulation of steroid derivatives having distinct biological activities, as it occurs for hydroxylated estrogens in the human breast. Locally produced or metabolically transformed estrogens may differently affect proliferative activity of prostate cancer cells. Aberrant aromatase expression and activity has been reported in prostate tumor tissues and cells, implying that androgen aromatization to estrogens may play a role in prostate carcinogenesis or tumor progression. Interestingly, many genes encoding for steroid enzymes are polymorphic, although only a few studies have supported their relation with risk of prostate cancer. In animal model systems estrogens, combined with androgens, appear to be required for the malignant transformation of prostate epithelial cells. Although the mechanisms underlying the hormonal induction of prostate cancer in experimental animals remain uncertain, there is however evidence to support the assumption that long term administration of androgens and estrogens results in an estrogenic milieu in rat prostates and in the ensuing development of dysplasia and cancer. Both androgen and estrogen have been reported to stimulate proliferation of cultured prostate cancer cells, primarily through receptor-mediated effects. As for estrogens, the two major receptor types, ERalpha and ERbeta, are expressed in both normal and diseased human prostate, though with a different cellular localization. Since these two receptors are different in terms of ligand binding, heterodimerization, transactivation, and estrogen response element activity, it is likely that an imbalance of their expression may be critical to determine the ultimate estrogen effects on prostate cancer cells. In prostate cancer, ERbeta activation appears to limit cell proliferation directly or through ERalpha inhibition, and loss of ERbeta has been consistently associated with tumor progression. Several splicing variants of both ERalpha and ERbeta exist. Little is known about their expression and function in the human prostate, although reciprocal regulation and interaction with gene promoter both warrant further investigation. In summary, although multiple consistent evidence suggests that estrogens are critical players in human prostate cancer, their role has been only recently reconsidered, being eclipsed for years by an androgen-dominated interest.