The answer to your question on why you are feeling so aggressive lies in the binding of these steroid analogs to receptors within the brain.
First off, stress and agression have been shown to reinforce one another:
Stress And Aggression Reinforce
Each Other At The Biological Level
WASHINGTON -- Scientists may be learning why it's so hard to stop the cycle of violence. The answer may lie in the nervous system. There appears to be a fast, mutual, positive feedback loop between stress hormones and a brain-based aggression-control center in rats, whose neurophysiology is similar to ours. It may explain why, under stress, humans are so quick to lash out and find it hard to cool down. The findings, which could point to better ways to
prevent pathological violence, appear in the October issue of Behavioral Neuroscience, which is published by the American Psychological Association (APA).
In five experiments using 53 male rats, behavioral neuroscientists from the Netherlands and Hungary studied whether stimulating the brain's aggression mechanism raised blood levels of a stress hormone and whether higher levels of the same hormone led to the kind of aggression elicited by that mechanism. The results showed a fast-acting feedback loop; the mechanism works in both directions and raising one variable raises the other. Thus, stress and aggression may be mutually reinforcing, which could explain not only why something like the stress of traffic jams leads to road rage, but also why raging triggers an ongoing stress reaction that makes it hard to stop.
In the study, the scientists electrically stimulated an aggression-related part of the rat hypothalamus, a mid-brain area associated with emotion. The rats suddenly released the stress hormone corticosterone (very like cortisol, which humans release under stress) -- even without another rat present. Normally, rats don't respond like that unless they face an opponent or another severe stressor.
Says lead author Menno Kruk, PhD, "It is well known that these stress hormones, in part by mobilizing
energy reserves, prepare the physiology of the body to fight or flee during stress. Now it appears that the very same hormones 'talk back' to the brain in order to facilitate fighting."
To study the hypothesized feedback loop from the other direction, the scientists removed the rats' adrenal glands to
prevent any natural release of corticosterone. Then researchers injected the rats with corticosterone. Within minutes of injection, the hormone facilitated stimulation-evoked attack behavior.
Thus, in rapid order, stimulating the hypothalamic attack area led to higher stress hormones and higher stress hormones led to aggression – evidence of the feedback loop within a single conflict. Write the authors, "Such a mutual facilitation may contribute to the precipitation and escalation of violent behavior under stressful conditions."
They add that the resulting vicious cycle "would explain why aggressive behavior escalates so easily and is so difficult to stop once it has started, especially because corticosteroids rapidly pass through the blood-brain barrier." The findings suggest that even when stress hormones spike for reasons not related to fighting, they may lower attack thresholds enough to precipitate violent behavior. That argument, if extended in research to humans, could ultimately explain on the biological level why a bad day at the office could prime someone for nighttime violence toward family members.
It is speculated that the findings may help also to explain why people who are not typically violent become violent in settings previously associated with aggression: Their stress hormones rise, facilitating the onset of aggression and making them more likely to become violent in seemingly benign settings. The adrenocortical (hormonal) and hypothalamic (aggressive) responses are ancient, inbred and found across many mammalian species including rats, cats and monkeys. As a result, scientists cannot help but wonder whether the stress-aggression feedback loop could well operate in the real world, not just the lab, and – most importantly -- in humans. Further study is clearly required.
The authors comment that their findings, if extended, could explain why "the adrenocortical stress response that accompanies conflict may effectively cancel out the effect of therapies intended to reduce violent behavior. Regulation of the stress response may offer a novel approach to the understanding and control of violent behavior." They speculate that medications, perhaps as-yet undeveloped anxiety-reducers that regulate the stress response, might conceivably help to lower acute stress-precipitated violence.
Article: "Fast Positive Feedback Between the Adrenocortical Stress Response and a Brain Mechanism Involved in Aggressive Behavior;" Menno R. Kruk, W. Meelis, J. Halász,and J. Haller. Behavioral Neuroscience, Vol. 118, No. 5.
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You may remember that I wrote a discussion on the neurochemistry of exogenous steroids. Here are a few of many recently published articles that point to the neurochemical shift when exogenous steroids are used that alter neurotransmitter activity in brain.
Neurosteroids, GABAA receptors, and escalated aggressive behavior. Miczek KA, Fish EW, De Bold JF. Horm Behav. 44(3):242-57 (2003).
Aggressive behavior can serve important adaptive functions in social species. However, if it exceeds the species-typical pattern, it may become maladaptive. Very high or escalated levels of aggressive behavior can be induced in laboratory rodents by pharmacological (alcohol-heightened aggression), environmental (social instigation), or behavioral (frustration-induced aggression) means. These various forms of escalated aggressive behavior may be useful in further elucidating the neurochemical control over aggression and violence.
One neurochemical system most consistently linked with escalated aggression is the GABAergic system, in conjunction with other amines and peptides. Although direct stimulation of
GABA receptors generally suppresses aggression, a number of studies have found that positive allosteric modulators of GABAA receptors can cause increases in aggressive behavior. For example, alcohol, benzodiazepines, and many neurosteroids are all positive modulators of the GABAA receptor and all can cause increased levels of aggressive behavior. These effects are dose-dependent and higher doses of these compounds generally shift from heightening aggressive behavior to being sedative and anti-aggressive. In addition, these modulators interact with each other and can have additive effects on the GABAA receptor and on behavior, including aggression. The GABAA receptor is a heteropentameric
protein that can be constituted from various subunits. It has been shown that subunit composition can affect sensitivity of the receptor to some modulators and that subunit composition differentially affects the sedative vs anxiolytic actions of benzodiazepines. Initial studies targeting alpha subunits of the GABAA receptor point to their significant role in the aggression-heightening effects of alcohol, benzodiazepines, and neurosteroids.
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Aggression in male rats receiving anabolic androgenic steroids: effects of social and environmental provocation. Breuer ME, McGinnis MY, Lumia AR, Possidente BP. Horm Behav 40(3):409-18 (2001).
ABSTRACT
This study examined the effects of anabolic androgenic steroids (AAS) on aggression under different social and environmental conditions. Three AAS were tested in gonadally intact male rats: testosterone propionate (TP), nandrolone (ND), and stanozolol (ST). Doses of 5 mg/kg were given 5 times/week, with gonadally intact controls receiving vehicle only (propylene glycol). Animals received six weekly tests under each condition in a counterbalanced order. Results show that the three AAS differed in their ability to elicit aggression. Males receiving TP were more aggressive than controls, ND males were similar to controls, and ST males were less aggressive than controls.
In the social and environmental provocation tests TP-treated males were more aggressive than other groups, but were able to discriminate between intact and castrated opponents and between their home cage and a neutral cage. In the environmental provocation test, TP males were also more aggressive against opponents when tested in the opponent's home cage. It is suggested that chronic exposure to high levels of TP does not eliminate the ability to discriminate between social or environmental cues, as might be expected if it induces a " 'roid rage." However, TP does increase the likelihood that the animal will respond with aggression/dominance in a provoking situation. All three AAS variably affected serum testosterone and LH levels, as well as testes, seminal vesicle, and prostate weights. No effect on body weight was observed.
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J1Q's -- S1+/Superdrol Log
