TREN advice pls

[EXCELLENCE]

ok so waiting to satrt cycle this week just wondering ive never used tren before im reading alot of mixed things about side effects im worried about the acne and over aggression so what im going to do is run @ 50mgED and possibly bump up to 75mg if side effects are manageable oh yes and ill be running with 500mg test cyp a week but with a dosing of 50mg ED i think they should be manageable as far as acne goes what do you guys think?

[10nispro]

Cycle history? and Pct.

[dece870717]

If your worried about over aggression use a lot less test, will make a huge difference, use no more than 250mg a week of Test.

[EXCELLENCE]

is it because the test reacts with tren ? because if thats not the case when im on test i have no agression problems but if it acts differently with tren then i should drop dosage for the cyp

[EXCELLENCE]

26years old 222lbs 6'3 8.3%BF 5th cycle
pct letro & hcg

[millionairemurph]

tren 's sides are somewhat overrated. I dont get alot of acne on it. I do feel more aggressive on it, but im the only one who knows that. The sides that i have gotten are constant sweating and feeling hot all the time. Loss of cardiovascular fitness. Night sweats, vivid dreams, slight sleeplessness.
Over all its not that bad. I use a special antiperspirtant, take sleeping pills a few times a week. Put a box fan on my night stand pointing at my head. So i deal with it.
Yeah id say start out with 50mg ed, do that for a week and a half or two and assess your side effects. Then move up a little from there. Pct needs a little work. Maybe add in a serm

[EXCELLENCE]

hows clomid & arimidex instead??? those are readily available to me

[Merc..]

Tren increases chemicals called serotonergic amines and decrease serotonin( this is why tren causes aggression)




Merc.

[Merc..]

Also HCG is suppressive .. You have to use nolva with HCG to block its suppressive nature ..

I like Anthony Roberts pct ..


http://forums.steroid.com/showthread.php?t=209758




Merc.

[EXCELLENCE]

unfortunatley clomid and arimidex and letro is all i have avail

[taiboxa]

If your worried about over aggression use a lot less test, will make a huge difference, use no more than 250mg a week of Test.

spot on.

[Titleist]

ok so waiting to satrt cycle this week just wondering ive never used tren before im reading alot of mixed things about side effects im worried about the acne and over aggression so what im going to do is run @ 50mgED and possibly bump up to 75mg if side effects are manageable oh yes and ill be running with 500mg test cyp a week but with a dosing of 50mg ED i think they should be manageable as far as acne goes what do you guys think?

Jesus H. Christ and a couple of by-Gods. Use some sort of punctuation man, shit.

It should be a rule, you can't use steroids until you can properly form a sentence. Can't do that though, our ninja friend would be SOL.

[BG]

tren's sides are somewhat overrated. I dont get alot of acne on it. I do feel more aggressive on it, but im the only one who knows that.

One persons point of veiw.

[J-Dogg]

I am prone to acne and it never had a bad effect on me. The thing I would worry most about is the gyno. For me, Letro did not work. Some people are prone to it, some are not, it is different for every person so you really don't know until you do it.

[Sir Lifts-a-lot]

I think the advice about lowering your test is the best way to go. I have only done tren once and I used 50mg a day and I liked the results. The biggest negative has got to be the decrease of cardo performance. I felt like 1 500lb man on it.

[Mike Dura]

Can you sight the source that says this (about the serotonin). If this is the case, it would seem that those prone to depression should stay clear of tren .

Tren increases chemicals called serotonergic amines and decrease serotonin( this is why tren causes aggression)




Merc.

[Merc..]

Can you sight the source that says this (about the serotonin). If this is the case, it would seem that those prone to depression should stay clear of tren.

Highly androgenic steroids do this ....


Here ya go ..


Titre du document / Document title
Nandrolone decanoate enhances hypothalamic biogenic amines in rats
Auteur(s) / Author(s)
TAMAKI Tetsuro (1) ; SHIRAISHI Takemasa (1) ; TAKEDA Hiroshi (2) ; MATSUMIYA Teruhiko (2) ; ROY Roland R. (3) ; EDGERTON V. Reggie (4) ;
Affiliation(s) du ou des auteurs / Author(s) Affiliation(s)
(1) Department of Physiology, Division of Human Structure and Function, Tokyo Medical College, Tokyo, JAPON
(2) Department of Pharmacology, Tokyo Medical College, Tokyo, JAPON
(3) Brain Research Institute, Los Angeles, CA, ETATS-UNIS
(4) Department of Physiological Science, University of California, Los Angeles, CA, ETATS-UNIS

Résumé / Abstract
Purpose: To identify possible mechanisms for an anabolic -androgenic steroid induced increase in aggressive behavior and work capacity, the levels of some biogenic amines considered to be closely related to a systemic hyper-adrenergic state were measured in selected regions of the brain. Methods: Wistar male rats were divided randomly into five groups: nontreated (control), oil-vehicle-treated (vehicle) or one of three (therapeutic dose and 10- or 100-fold higher dose) anabolic-androgenic steroid-treated (steroid-1, -2, -3) groups. Rats in the steroid and vehicle groups were given a single dose of nandrolone decanoate or oil vehicle, respectively, one week before tissue sampling. The levels of norepinephrine (NE) and its metabolites, 4-hydroxy-3-methoxyphenylglycol (MHPG), serotonin (5-HT) and its metabolite, 5-hydroxyindole-3-acetic acid (5-HIAA) were measured in the cerebral cortex, hypothalamus and cerebellum by high-performance liquid chromatography. Immunostaining for c-fos was performed as a confirmation of increased neural activity. Results: The levels of NE and MHPG were increased by ∼2- and -7-fold in the hypothalamus of the steroid-2 compared with the control and vehicle groups. The levels of 5-HT and 5-HIAA were -40 and ∼50% higher in the steroid-2 compared with the control and vehicle groups. A significantly higher number of c-fos expressing neurons were observed in the periventricular region of the steroid-2 than the control and vehicle groups, indicating enhanced neuronal activity after nandrolone decanoate treatment. Conclusions: The present results, combined with previously reported findings of physical performance enhancement after anabolic-androgenic steroid treatment, are consistent with the interpretation that elevated levels of adrenergic and serotonergic amines in the hypothalamus could contribute to aggressive behaviors as well as improved physical performance.
Revue / Journal Title
Medicine and science in sports and exercise (Med. sci. sports exerc.) ISSN 0195-9131

[Mike Dura]

Cool but where does it mention serotonin being decreased?

Highly androgenic steroids do this ....


Here ya go ..


Titre du document / Document title
Nandrolone decanoate enhances hypothalamic biogenic amines in rats
Auteur(s) / Author(s)
TAMAKI Tetsuro (1) ; SHIRAISHI Takemasa (1) ; TAKEDA Hiroshi (2) ; MATSUMIYA Teruhiko (2) ; ROY Roland R. (3) ; EDGERTON V. Reggie (4) ;
Affiliation(s) du ou des auteurs / Author(s) Affiliation(s)
(1) Department of Physiology, Division of Human Structure and Function, Tokyo Medical College, Tokyo, JAPON
(2) Department of Pharmacology, Tokyo Medical College, Tokyo, JAPON
(3) Brain Research Institute, Los Angeles, CA, ETATS-UNIS
(4) Department of Physiological Science, University of California, Los Angeles, CA, ETATS-UNIS

Résumé / Abstract
Purpose: To identify possible mechanisms for an anabolic -androgenic steroid induced increase in aggressive behavior and work capacity, the levels of some biogenic amines considered to be closely related to a systemic hyper-adrenergic state were measured in selected regions of the brain. Methods: Wistar male rats were divided randomly into five groups: nontreated (control), oil-vehicle-treated (vehicle) or one of three (therapeutic dose and 10- or 100-fold higher dose) anabolic-androgenic steroid-treated (steroid-1, -2, -3) groups. Rats in the steroid and vehicle groups were given a single dose of nandrolone decanoate or oil vehicle, respectively, one week before tissue sampling. The levels of norepinephrine (NE) and its metabolites, 4-hydroxy-3-methoxyphenylglycol (MHPG), serotonin (5-HT) and its metabolite, 5-hydroxyindole-3-acetic acid (5-HIAA) were measured in the cerebral cortex, hypothalamus and cerebellum by high-performance liquid chromatography. Immunostaining for c-fos was performed as a confirmation of increased neural activity. Results: The levels of NE and MHPG were increased by ∼2- and -7-fold in the hypothalamus of the steroid-2 compared with the control and vehicle groups. The levels of 5-HT and 5-HIAA were -40 and ∼50% higher in the steroid-2 compared with the control and vehicle groups. A significantly higher number of c-fos expressing neurons were observed in the periventricular region of the steroid-2 than the control and vehicle groups, indicating enhanced neuronal activity after nandrolone decanoate treatment. Conclusions: The present results, combined with previously reported findings of physical performance enhancement after anabolic-androgenic steroid treatment, are consistent with the interpretation that elevated levels of adrenergic and serotonergic amines in the hypothalamus could contribute to aggressive behaviors as well as improved physical performance.
Revue / Journal Title
Medicine and science in sports and exercise (Med. sci. sports exerc.) ISSN 0195-9131

[Merc..]

The nuclear factor kappa B (NFκB) transcription factor was originally identified as a protein complex consisting of a 65-kd DNA-binding subunit and an associated 50-kd protein. NFκB can exist in both cytoplasmic and nuclear compartments.1 Upon cytokine receptor activation, NFκB translocates to the nucleus, binds to NFκB response elements and promotes gene transcription. Cytokines have been strongly implicated in depression. Administration of cytokines to patients can precipitate depression, and depressed subjects have elevated levels of cytokines.2,3 These and similar correlations have led to a cytokine hypothesis of depression. However, the central nervous system targets of cytokines are not well defined.

Serotonin plays an important role in affective regulation, and dysfunction of the serotonin system is found in depressed patients.4,5 Work from this laboratory indicates that the ovarian steroids , estrogen and progesterone, regulate gene and protein expression in serotonin neurons.6 Estrogens bind with high affinity to nuclear transcription factors called ERα and ERβ,7 which in turn bind to estrogen response elements in the promoter region of target genes and/or interact with other transcription factors in a manner so as to either increase or decrease gene expression in a tissue-specific fashion.8

Serotonin neurons express the β form of the estrogen receptor, ERβ,9,10 and estrogen, with or without progesterone supplementation, acts in serotonin neurons to alter gene expression. In brief, estrogen treatment of spayed macaques increased progestin receptor protein11 and increased expression of the gene that controls brain serotonin synthesis, called tryptophan hydroxylase-2 (TPH-2).12 However, estrogen decreased expression of the serotonin reuptake transporter (SERT), serotonin-1A (5-HT1A) and monoamine oxidase-A (MAOA) genes in the dorsal raphe nucleus (DRN).13–15 The SERT, 5-HT1A and MAOA genes lack any known form of an estrogen response element;16–18 however, the SERT and 5-HT1A genes do contain NFκB response elements in their promoter regions.16,19

Ligand-activated steroid receptors sequester NFκB and thereby decrease gene transcription that is dependent upon this factor.20 In transfection studies, ERα markedly repressed NFκB-driven gene expression in an estrogen-dependent manner.21 Moreover, estrogen inhibited cytokine production by decreasing NFκB binding activity.22 Treatment of cells in culture with cytokines leads to I kappa B α (IκBα) serine phosphorylation and degradation and, in turn, NFκB translocation to the nucleus.1 However, the expression of NFκB is thought to be constitutive in immortalized cell lines.

We questioned whether serotonin neurons express NFκB and whether steroid receptors could sequester NFκB in serotonin neurons, thereby decreasing NFκB response element–driven gene expression, and whether NFκB gene or protein expression is regulated or constitutive in the macaque midbrain. We presented preliminary data in a review article,6 which indicated that treatment of monkeys with estrogen or estrogen plus progesterone decreased the number of raphe neurons with NFκB immunostaining in the nucleus. However, only 3 anatomical levels were examined, the antibody was not generated against nuclear location–specific (NLS)-NFκB, and the positive neurons were hand marked with the aid of camera lucida equipment and then counted.

Therefore, in this study we (1) determined whether serotonin neurons in the dorsal raphe of rhesus macaques contain NFκB, (2) extended the preliminary analysis with an antibody to NLS-NFκB and counted NFκB-positive neurons at 9 anatomical levels of the DRN with a computer-assisted stereology workstation, (3) used an antigen-retrieval buffer to unmask all of the intracellular NFκB for comparison with NLS-NFκB and (4) determined whether gene or protein expression of NFκB in the midbrain raphe region was altered by hormone therapy.

[Merc..]

I have another study on this as well but I cant find it on my CPU.. I am searching for it ( i have tons of stuff in my favs)..



Merc.

[J*U*icEd]

letro and HCG ... that is a really really crappy and not well thought out PCT at all... ur gonna mess ur self up something bad using HCG and letro for PCT with no serm to help increase test production, and to help block the suppressive nature of HCG... and letro is suppressive as well, and is not a great choice for PCT either