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dbol (dball) + prozac = ?

HugeWannabe

New member
Hey guys I went to my doc today and got a script for prozac, its what he suggest for my anxiety that is always there whether I am on or off a cycle. I was currently on dbol, can I continue on 20 mg of prozac ED? I did have the crazy unstoppable feeling of dbol when i first started last week but then it faded
 
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come on someone reply to this one..its important..can someone continue dbol with an SSRI ?? dbol makes my anxiety worse..it elevates the heart rate..i feel whacky on it..always thinking of having a heart attack/anxiety attack..

shawn
 
Numerous studies in animals and humans have implicated low serotonin levels in agressiveness, violence, and antisocial behavior. Moreover, treatment with SSRI's reduces impulsiveness and aggression in these subjects.

Studies (for example, see abstract below) have shown that anabolic steroids increase the metabolic turnover of serotonin. The resulting low serotonin levels have been suggested as the cause of "roid rage". (I personally think agressive people will remain aggressive, and mellow people will stay mellow on AAS.)

The study cited is interesting in that anadrol is particularly effective in increasing monomine oxidase levels. This is a key enzyme in the metabolic breakdown of serotonin, and anadrol is famous for increasing aggression.

So, taking SSRI's while cycling could be a double edged sword:
You may suffer from less anxiety, but might lose some of the aggressiveness to get through tough workouts.

1: Br J Pharmacol 1999 Mar;126(6):1301-6


Increased dopaminergic and 5-hydroxytryptaminergic activities in male rat brain following long-term treatment with anabolic androgenic steroids.

Thiblin I, Finn A, Ross SB, Stenfors C.

Department of Forensic Medicine, Karolinska Institute, Stockholm, Sweden.

1. The effects of treating groups of rats with four different anabolic androgenic steroids (AAS) (testosterone, nandrolone methandrostenolone, and oxymetholone) on 5-hydroxytryptamine (5-HT) and dopamine (DA) neurones in different brain regions were examined. The AAS was injected six times with 1 week's interval and the rats were sacrificed 2 days after the final injection. 5-HT and its metabolite 5-hydroxyindoleacetic acid (5-HIAA), DA and its metabolites 3,4-dihydroxyphenylacetic acid (DOPAC) and homovanillic acid (HVA) were measured. The effect on DA and 5-HT synthesis rate was analysed as the accumulation of 3,4-dihydroxyphenyl-alanine (DOPA) and 5-hydroxytryptophan (5-HTP), respectively, after inhibition of the amino acid decarboxylase with NSD-1015 (3-hydroxy-benzylhydrazine dihydrochloride). Additionally, the monoamine oxidase (MAO) activity was analysed in the hypothalamus. 2. The DOPAC + HVA/DA ratio was increased in the striatum in all treatment groups. However,the synthesis rate of DA was significantly increased only in the methandrostenolone treated group. 3. The 5-HIAA/5-HT ratio was increased in all treatment groups in the hippocampus, in the frontal cortex in the methandrostenolone-treated animals and in the hypothalamus in the testosterone- and oxymetholone-treated rats, while the 5-HT synthesis rate was not affected by the AAS-treatments. 4. The MAO-A activity was increased in the oxymetholone-treated rats while the other treatment groups were unaffected. The MAO-B activity was not changed. 5. The results indicate that relatively high doses of AAS increase dopaminergic and 5 -hydroxytryptaminergic metabolism in male rat brain, probably due to enhanced turnover in these monaminergic systems.
 
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