I recently posted the abstract below in response to a reader's question regarding combining steroids and SSRI antidepressants. Low levels of serotonin have been implicated in anxiety disorders as well as depression. Moreover, numerous studies have implicated low serotonin levels in violent, antisocial behavior, aggression, and impulsiveness.
Although the study does not deal with EQ specifically, I would be surprised if it did not have the same anxiety inducing effects as the other drugs.
It is also thought that anabolic steroids also act on the body's natural opioid system to somehow induce anxiety and aggressiveness.
The abstract shows that certain anabolic steroids increase the metabolism of serotinin, leading to low levels of serotonin in the body. This could be responsible for the anxiety felt by many steroid users, as well as for "roid rage" ( I personally think that a jerk will remain a jerk, and a mellow person will remain mellow on steroids.) It is particularly interesting that anadrol was the only agent to raise monamine oxidase levels. This is a key enzyme responsible for metabolizing serotonin. Anandrol is notorious for increasing aggression.
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 5hydroxytryptamine (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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