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how to combat aggresion from tren
- Thread starter hansen215
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If you can't keep a handle on the temper, then you may want to find a substitute.
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I agree.............
deadandgone
Banned
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Mind over matter...If you dont mind, it dont matter...
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Understand also that this is an individual thing. I am a very non-aggressive type and tren has no affect on me in that way.
If however you have a tempter to begin with, then as others have said, find another compound.
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I think they call it vitamine self-control......
BINGO
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I have a pretty short temper mostly when it comes to people being stupid and tren certainly compounds this , its not like I fly into fits of rage but I see my self getting more irritated with the public in general when I'm on it. I can run it to 300mg/wk with little to no trouble but any higher does and it gets noticable.
I run low dose test with it just to keep the libido up or it'll kill the wood in a week.
Honestly hard dieting and lack of sleep make me much more of a dick than any drugs
I run low dose test with it just to keep the libido up or it'll kill the wood in a week.
Honestly hard dieting and lack of sleep make me much more of a dick than any drugs
0o0o0o
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i ve heard about a the mary jane, but thats illegal
but here are somethings you could look into
THE NEUROANATOMY OF AGGRESSION
The neuroanatomic correlates of aggression are becoming increasingly understood. A review last year in Science by Richard J. Davidson, PhD, and colleagues argued that aggression is controlled by an emotion regulation circuit encompassing the prefrontal cortex, amygdala, hippocampus, hypothalamus, insula cortex, anterior cingulate cortex, ventral striatum, and connected areas. “The cynical neuropsychiatric clinician might say, ‘Okay, so what’s not involved in modulation of aggression?’” Dr. Ryan quipped. Nonetheless, he said, “I think this is a useful way to think about it. Davidson and colleagues have really conceptualized this circuit as helping to amplify, attenuate, or maintain an emotional state, and that’s probably a good way of broadly thinking about affective instability, irritability, and aggression.”
The amygdala and prefrontal cortex in particular have received a good deal of attention for their apparent role in aggressive behavior. Dr. Ryan noted that the amygdala receives a vast array of information from sensory areas and projects to other relevant structures, such as the hypothalamus and brain stem. “In a broad sense, you can think of this area as linking cortical sensory information to modulation of basic drives and behaviors.” For example, recent functional imaging studies have found increased amygdala activity associated with emotions elicited by unpleasant visual stimuli and with exposure to threatening words (but not to neutral ones). “I think the bottom line,” said Dr. Ryan, “is that the amygdala probably participates in perception and regulation of unpleasant emotional stimuli, and it may be especially sensitive to perception and modulation of fear.”
Numerous studies of the prefrontal cortex point to the importance of this region in aggression—not as an initiator but as an inhibitor. For example, a recent case report described two adults who had suffered orbitofrontal damage before their second birthday; despite a normal family environment during childhood, as adults the patients exhibited antisocial behavior and a complete lack of empathy. “The authors speculate that the orbitofrontal cortex participates in regulation of moral rules and social behavior in some important way,” Dr. Ryan said. Prefrontal lesions do not have to be large to have an impact; an imaging study comparing aggressive patients and their spouses found that frontal ventral medial lesions were associated with aggression (primarily verbal) and that lesion size was irrelevant. The dorsolateral frontal cortex, lateral orbitofrontal cortex, and anterior cingulate appear to be especially important.
Functional imaging studies have shown that the orbitofrontal cortex and the anterior cingulate are activated when patients see angry facial expressions or are induced to anger themselves. In addition, several studies have shown reciprocal patterns of activity between the orbitofrontal cortex and the amygdala, again suggesting that the frontal regions “may put the brakes on” angry or aggressive emotions induced in the amygdala, Dr. Ryan said.
Not surprisingly, a number of neurotransmitter and hormonal systems appear to play a role in aggression. A good deal of research has focused on serotonergic involvement, but there is also evidence supporting the role of the noradrenergic and perhaps dopaminergic and cholinergic systems; androgens may also be relevant, as there is a strong correlation between testosterone levels and lifetime history of aggression. This variety of neurochemical factors may explain why so many pharmacological agents have been shown to reduce aggressive behavior.
ß-BLOCKERS
The ß-blockers have become a mainstay in the treatment of aggression. However, there have been only a few relevant controlled trials of these agents. (Some of the studies described here and below lump aggression with irritability, anger, and/or impulsivity, an approach that dilutes their applicability to aggression; however, Dr. Ryan noted that all of these behaviors are related.) In one study, sustained-release propranolol (maximum dosage, 520 mg/d) reduced the rate of assaultive behavior in 10 patients with organic brain disease. In a sample of 11 patients with various neuropsychiatric disorders, pindolol (up to 100 mg/d) reduced hostility and impulsivity. And a study published earlier this year found that pindolol augmentation reduced scores on the Overt Aggression Scale in a group of 30 schizophrenic patients. “These are minute numbers [of patients], so this is not a ringing endorsement for use of ß-blockers in neuropsychiatric disorders,” Dr. Ryan commented. Moreover, a second propranolol trial, involving 21 patients with TBI, failed to show a reduction in the number of aggressive incidents, although the intensity of aggressive acts did decrease.
The uncontrolled trials of these agents have also been rather small. One found that 12 of 19 mentally retarded patients tested showed decreases in aggression and self-injurious behavior with pindolol (mean dosage, 120 mg/d). Another study, involving patients with dementia, reported success using very small doses (10 to 80 mg) of propranolol, eight of 12 participants improved, generally within two weeks. In other uncontrolled trials, nadolol (mean dosage, 109 mg/d) has shown benefits in patients with developmental delay, and propranolol (600 mg/d) reduced rage and violent behavior in a patient with Korsakoff’s psychosis.
ATYPICAL ANTIPSYCHOTICS
The advantages of atypical antipsychotics over their conventional counterparts—notably a reduced risk of tardive dyskinesia and extrapyramidal symptoms—are familiar. Several placebo-controlled studies have examined the effects of these medications on aggression. In one multicenter trial, published in 1999, nursing home patients with dementia showed decreases in physical and verbal aggression, psychosis, and overall behavioral problems following a 12-week course of risperidone. Improvements in aggression were not necessarily related to changes in psychosis. Lower doses (0.5 or 1 mg) were well tolerated, but the 2-mg dose resulted in an increased rate of extrapyramidal symptoms.
A second multicenter dementia study, published shortly thereafter, used flexible dosages of risperidone (0.5 to 4 mg/d; mean, 1.1 mg/d), haloperidol (mean dose, 1.2 mg), or placebo. Risperidone again showed efficacy in reducing aggressive behavior; a post hoc analysis indicated that risperidone was more effective than haloperidol for reducing aggression, though the study has been criticized for using relatively low doses of haloperidol, Dr. Ryan said.
There have also been several notable uncontrolled studies involving atypicals. In a small study of patients with TBI, five of nine participants showed reductions in rage, aggression, or agitation following clozapine treatment; two patients, however, had drug-related seizures. In a case series of mentally retarded persons, clozapine reduced aggression, self-injurious behavior, and psychosis in 86% of the 74 patients.
Given the limited data and lack of direct comparisons, “there is no rational algorithm for picking an atypical antipsychotic” for clinical use, Dr. Ryan said. “The bottom line is that they’ve all been proven effective in a number of disorders, and you should probably pick them based on side-effect profile in any specific patient.”
ANTIDEPRESSANTS
The antidepressants are another useful option for reducing aggressive behavior. For example, a placebo-controlled study that included 38 patients with Alzheimer’s disease showed that citalopram (10 to 30 mg/d) reduced patients’ fear, irritability, and anxiety, “[symptoms] which, again, we need to consider in the same spectrum as aggression,” Dr. Ryan noted. Interestingly, 13 additional patients with vascular dementia who took part in the study did not improve. In a second controlled trial, involving mixed types of dementia, there was a nonsignificant trend toward reductions in irritability and fear when patients were given fluvoxamine (150 mg/d).
A number of antidepressant studies have been conducted in subjects with mental retardation or developmental problems. Controlled trials include a 10-week crossover study of pediatric patients with autism and repetitive behaviors; clomipramine proved superior to both desipramine and placebo for decreasing anger and ritualistic behavior. Another study found that fluvoxamine was more effective than placebo for reducing aggression in 30 autistic adults; eight of the 15 fluvoxamine recipients but none of the placebo recipients met the criteria for clinical response.
Relevant uncontrolled trials include a 1992 study in which 17 of 21 patients with severe mental retardation showed moderate or marked reductions in aggression and self-injurious behavior with fluoxetine (20 to 40 mg/d) and two studies in which sertraline reduced aggression in patients with TBI or pervasive developmental disorder. However, a four-month open paroxetine trial involving 15 mentally retarded adults found that initial reductions in the frequency of aggressive acts were no longer apparent after the first month, though aggression severity did remain statistically lower throughout the study.
MOOD STABILIZERS
The mood stabilizers—notably divalproex and carbamazepine—are widely used in the treatment of impulsivity and aggression. Carbamazepine has been used for some time to treat aggressive symptoms in dementia, although the first two controlled trials in this population yielded mixed results, with one reporting benefits and the other not.
However, the third and largest randomized carbamazepine trial, published in 1998, suggests that the drug does have beneficial effects. The study, involving 51 agitated dementia patients living in nursing homes, used flexible doses of carbamazepine; scores on the Brief Psychiatric Rating Scale were lower with the drug than with placebo, and the difference was primarily attributable to reductions in aggression and agitation. A dosage of 300 mg/d appeared to be the most effective.
Unfortunately, carbamazepine’s utility is limited by its side effects, which range from dizziness, ataxia, and drowsiness to rarer but potentially severe events such as agranulocytosis and hepatotoxicity. There is also a relatively high risk of drug interactions.
As a result, divalproex, which is much less likely to cause drug interactions and produces fewer side effects, is usually the more favored mood stabilizer in this setting. Fortunately, it appears to be effective as well. A recent review of 17 case reports, open-label trials, and chart reviews found that 77% of the 164 patients included showed a meaningful decrease in aggressive symptoms (though most of the patients were also using other psychotropics). Another study found that 78% of demented patients had a 50% or greater reduction in physical aggression and almost half had a similar decline in verbal aggression.
Until recently, there had been no controlled trials of divalproex. However, Dr. Ryan’s colleagues at Monroe Community Hospital recently conducted a randomized trial of 56 dementia patients who received a mean dose of 826 mg. Although divalproex recipients showed clinically meaningful improvement—perhaps surpassing the degree of symptom reduction seen in the most recent carbamazepine trial—the placebo group also showed substantial improvement. As a result, carbamazepine was not quite statistically superior to placebo (P = .08). Nonetheless, Dr. Ryan believes that divalproex does have real anti-agitation effects; he suggests that clinicians start patients on 125 to 250 mg bid and increase the dose by 125 mg every five days as needed, up to 2 g/d.
LITHIUM AND OTHER AGENTS
Although tolerability problems can limit its use, lithium has shown benefits in several small controlled and uncontrolled studies. For example, a chart review of 38 patients with mental retardation found that nearly two thirds had a 30% or greater reduction in aggression frequency. Even more impressive, a four-month controlled trial of 42 mentally retarded individuals, published in 1987, found that 73% of lithium patients but only 30% of the control group showed a reduction in aggression; Dr. Ryan noted that in neuropsychiatry a 43% drug-placebo difference is “a whopping response.” More recently, a controlled four-week trial of 40 pediatric inpatients with conduct disorder showed that 80% responded to lithium, compared to only 30% of the placebo group. These findings, Dr. Ryan said, suggest that lithium “is pretty effective in a short period of time for reducing aggression,” at least in certain patient populations.
The consistent reports of a relationship between aggression and testosterone levels in dementia patients points to the need for anti-androgen trials, Dr. Ryan said. Clinical data remain scarce, though a double-blind trial found reduced aggression when 15 dementia patients were given estrogen.
Nor have stimulants been tested extensively in this setting, though a small trial involving TBI patients yielded positive results. However, patients with irritability may not respond favorably to stimulants.
Another promising development is the introduction of cholinesterase inhibitors. “There are some early hints that these agents may be useful for reducing behavioral symptoms in dementia,” Dr. Ryan noted. An open tacrine trial found reduced disinhibition and a nonsignificant trend toward decreased aggression; retrospective analysis of another tacrine study revealed benefits for agitation. Data from a third trial suggest that galantamine may delay emergence of behavioral problems in dementia patients. Dr. Ryan suspects that cholinesterase inhibitors will prove to have modest effects on behavioral symptoms for most patients but will be very important for certain individuals, particularly for reducing psychotic symptoms. Although agitation may also improve, some patients do become more agitated on these medications.
here is the link http://www.neuropsychiatryreviews.com/oct01/npr_oct01_aggression.html
but here are somethings you could look into
THE NEUROANATOMY OF AGGRESSION
The neuroanatomic correlates of aggression are becoming increasingly understood. A review last year in Science by Richard J. Davidson, PhD, and colleagues argued that aggression is controlled by an emotion regulation circuit encompassing the prefrontal cortex, amygdala, hippocampus, hypothalamus, insula cortex, anterior cingulate cortex, ventral striatum, and connected areas. “The cynical neuropsychiatric clinician might say, ‘Okay, so what’s not involved in modulation of aggression?’” Dr. Ryan quipped. Nonetheless, he said, “I think this is a useful way to think about it. Davidson and colleagues have really conceptualized this circuit as helping to amplify, attenuate, or maintain an emotional state, and that’s probably a good way of broadly thinking about affective instability, irritability, and aggression.”
The amygdala and prefrontal cortex in particular have received a good deal of attention for their apparent role in aggressive behavior. Dr. Ryan noted that the amygdala receives a vast array of information from sensory areas and projects to other relevant structures, such as the hypothalamus and brain stem. “In a broad sense, you can think of this area as linking cortical sensory information to modulation of basic drives and behaviors.” For example, recent functional imaging studies have found increased amygdala activity associated with emotions elicited by unpleasant visual stimuli and with exposure to threatening words (but not to neutral ones). “I think the bottom line,” said Dr. Ryan, “is that the amygdala probably participates in perception and regulation of unpleasant emotional stimuli, and it may be especially sensitive to perception and modulation of fear.”
Numerous studies of the prefrontal cortex point to the importance of this region in aggression—not as an initiator but as an inhibitor. For example, a recent case report described two adults who had suffered orbitofrontal damage before their second birthday; despite a normal family environment during childhood, as adults the patients exhibited antisocial behavior and a complete lack of empathy. “The authors speculate that the orbitofrontal cortex participates in regulation of moral rules and social behavior in some important way,” Dr. Ryan said. Prefrontal lesions do not have to be large to have an impact; an imaging study comparing aggressive patients and their spouses found that frontal ventral medial lesions were associated with aggression (primarily verbal) and that lesion size was irrelevant. The dorsolateral frontal cortex, lateral orbitofrontal cortex, and anterior cingulate appear to be especially important.
Functional imaging studies have shown that the orbitofrontal cortex and the anterior cingulate are activated when patients see angry facial expressions or are induced to anger themselves. In addition, several studies have shown reciprocal patterns of activity between the orbitofrontal cortex and the amygdala, again suggesting that the frontal regions “may put the brakes on” angry or aggressive emotions induced in the amygdala, Dr. Ryan said.
Not surprisingly, a number of neurotransmitter and hormonal systems appear to play a role in aggression. A good deal of research has focused on serotonergic involvement, but there is also evidence supporting the role of the noradrenergic and perhaps dopaminergic and cholinergic systems; androgens may also be relevant, as there is a strong correlation between testosterone levels and lifetime history of aggression. This variety of neurochemical factors may explain why so many pharmacological agents have been shown to reduce aggressive behavior.
ß-BLOCKERS
The ß-blockers have become a mainstay in the treatment of aggression. However, there have been only a few relevant controlled trials of these agents. (Some of the studies described here and below lump aggression with irritability, anger, and/or impulsivity, an approach that dilutes their applicability to aggression; however, Dr. Ryan noted that all of these behaviors are related.) In one study, sustained-release propranolol (maximum dosage, 520 mg/d) reduced the rate of assaultive behavior in 10 patients with organic brain disease. In a sample of 11 patients with various neuropsychiatric disorders, pindolol (up to 100 mg/d) reduced hostility and impulsivity. And a study published earlier this year found that pindolol augmentation reduced scores on the Overt Aggression Scale in a group of 30 schizophrenic patients. “These are minute numbers [of patients], so this is not a ringing endorsement for use of ß-blockers in neuropsychiatric disorders,” Dr. Ryan commented. Moreover, a second propranolol trial, involving 21 patients with TBI, failed to show a reduction in the number of aggressive incidents, although the intensity of aggressive acts did decrease.
The uncontrolled trials of these agents have also been rather small. One found that 12 of 19 mentally retarded patients tested showed decreases in aggression and self-injurious behavior with pindolol (mean dosage, 120 mg/d). Another study, involving patients with dementia, reported success using very small doses (10 to 80 mg) of propranolol, eight of 12 participants improved, generally within two weeks. In other uncontrolled trials, nadolol (mean dosage, 109 mg/d) has shown benefits in patients with developmental delay, and propranolol (600 mg/d) reduced rage and violent behavior in a patient with Korsakoff’s psychosis.
ATYPICAL ANTIPSYCHOTICS
The advantages of atypical antipsychotics over their conventional counterparts—notably a reduced risk of tardive dyskinesia and extrapyramidal symptoms—are familiar. Several placebo-controlled studies have examined the effects of these medications on aggression. In one multicenter trial, published in 1999, nursing home patients with dementia showed decreases in physical and verbal aggression, psychosis, and overall behavioral problems following a 12-week course of risperidone. Improvements in aggression were not necessarily related to changes in psychosis. Lower doses (0.5 or 1 mg) were well tolerated, but the 2-mg dose resulted in an increased rate of extrapyramidal symptoms.
A second multicenter dementia study, published shortly thereafter, used flexible dosages of risperidone (0.5 to 4 mg/d; mean, 1.1 mg/d), haloperidol (mean dose, 1.2 mg), or placebo. Risperidone again showed efficacy in reducing aggressive behavior; a post hoc analysis indicated that risperidone was more effective than haloperidol for reducing aggression, though the study has been criticized for using relatively low doses of haloperidol, Dr. Ryan said.
There have also been several notable uncontrolled studies involving atypicals. In a small study of patients with TBI, five of nine participants showed reductions in rage, aggression, or agitation following clozapine treatment; two patients, however, had drug-related seizures. In a case series of mentally retarded persons, clozapine reduced aggression, self-injurious behavior, and psychosis in 86% of the 74 patients.
Given the limited data and lack of direct comparisons, “there is no rational algorithm for picking an atypical antipsychotic” for clinical use, Dr. Ryan said. “The bottom line is that they’ve all been proven effective in a number of disorders, and you should probably pick them based on side-effect profile in any specific patient.”
ANTIDEPRESSANTS
The antidepressants are another useful option for reducing aggressive behavior. For example, a placebo-controlled study that included 38 patients with Alzheimer’s disease showed that citalopram (10 to 30 mg/d) reduced patients’ fear, irritability, and anxiety, “[symptoms] which, again, we need to consider in the same spectrum as aggression,” Dr. Ryan noted. Interestingly, 13 additional patients with vascular dementia who took part in the study did not improve. In a second controlled trial, involving mixed types of dementia, there was a nonsignificant trend toward reductions in irritability and fear when patients were given fluvoxamine (150 mg/d).
A number of antidepressant studies have been conducted in subjects with mental retardation or developmental problems. Controlled trials include a 10-week crossover study of pediatric patients with autism and repetitive behaviors; clomipramine proved superior to both desipramine and placebo for decreasing anger and ritualistic behavior. Another study found that fluvoxamine was more effective than placebo for reducing aggression in 30 autistic adults; eight of the 15 fluvoxamine recipients but none of the placebo recipients met the criteria for clinical response.
Relevant uncontrolled trials include a 1992 study in which 17 of 21 patients with severe mental retardation showed moderate or marked reductions in aggression and self-injurious behavior with fluoxetine (20 to 40 mg/d) and two studies in which sertraline reduced aggression in patients with TBI or pervasive developmental disorder. However, a four-month open paroxetine trial involving 15 mentally retarded adults found that initial reductions in the frequency of aggressive acts were no longer apparent after the first month, though aggression severity did remain statistically lower throughout the study.
MOOD STABILIZERS
The mood stabilizers—notably divalproex and carbamazepine—are widely used in the treatment of impulsivity and aggression. Carbamazepine has been used for some time to treat aggressive symptoms in dementia, although the first two controlled trials in this population yielded mixed results, with one reporting benefits and the other not.
However, the third and largest randomized carbamazepine trial, published in 1998, suggests that the drug does have beneficial effects. The study, involving 51 agitated dementia patients living in nursing homes, used flexible doses of carbamazepine; scores on the Brief Psychiatric Rating Scale were lower with the drug than with placebo, and the difference was primarily attributable to reductions in aggression and agitation. A dosage of 300 mg/d appeared to be the most effective.
Unfortunately, carbamazepine’s utility is limited by its side effects, which range from dizziness, ataxia, and drowsiness to rarer but potentially severe events such as agranulocytosis and hepatotoxicity. There is also a relatively high risk of drug interactions.
As a result, divalproex, which is much less likely to cause drug interactions and produces fewer side effects, is usually the more favored mood stabilizer in this setting. Fortunately, it appears to be effective as well. A recent review of 17 case reports, open-label trials, and chart reviews found that 77% of the 164 patients included showed a meaningful decrease in aggressive symptoms (though most of the patients were also using other psychotropics). Another study found that 78% of demented patients had a 50% or greater reduction in physical aggression and almost half had a similar decline in verbal aggression.
Until recently, there had been no controlled trials of divalproex. However, Dr. Ryan’s colleagues at Monroe Community Hospital recently conducted a randomized trial of 56 dementia patients who received a mean dose of 826 mg. Although divalproex recipients showed clinically meaningful improvement—perhaps surpassing the degree of symptom reduction seen in the most recent carbamazepine trial—the placebo group also showed substantial improvement. As a result, carbamazepine was not quite statistically superior to placebo (P = .08). Nonetheless, Dr. Ryan believes that divalproex does have real anti-agitation effects; he suggests that clinicians start patients on 125 to 250 mg bid and increase the dose by 125 mg every five days as needed, up to 2 g/d.
LITHIUM AND OTHER AGENTS
Although tolerability problems can limit its use, lithium has shown benefits in several small controlled and uncontrolled studies. For example, a chart review of 38 patients with mental retardation found that nearly two thirds had a 30% or greater reduction in aggression frequency. Even more impressive, a four-month controlled trial of 42 mentally retarded individuals, published in 1987, found that 73% of lithium patients but only 30% of the control group showed a reduction in aggression; Dr. Ryan noted that in neuropsychiatry a 43% drug-placebo difference is “a whopping response.” More recently, a controlled four-week trial of 40 pediatric inpatients with conduct disorder showed that 80% responded to lithium, compared to only 30% of the placebo group. These findings, Dr. Ryan said, suggest that lithium “is pretty effective in a short period of time for reducing aggression,” at least in certain patient populations.
The consistent reports of a relationship between aggression and testosterone levels in dementia patients points to the need for anti-androgen trials, Dr. Ryan said. Clinical data remain scarce, though a double-blind trial found reduced aggression when 15 dementia patients were given estrogen.
Nor have stimulants been tested extensively in this setting, though a small trial involving TBI patients yielded positive results. However, patients with irritability may not respond favorably to stimulants.
Another promising development is the introduction of cholinesterase inhibitors. “There are some early hints that these agents may be useful for reducing behavioral symptoms in dementia,” Dr. Ryan noted. An open tacrine trial found reduced disinhibition and a nonsignificant trend toward decreased aggression; retrospective analysis of another tacrine study revealed benefits for agitation. Data from a third trial suggest that galantamine may delay emergence of behavioral problems in dementia patients. Dr. Ryan suspects that cholinesterase inhibitors will prove to have modest effects on behavioral symptoms for most patients but will be very important for certain individuals, particularly for reducing psychotic symptoms. Although agitation may also improve, some patients do become more agitated on these medications.
here is the link http://www.neuropsychiatryreviews.com/oct01/npr_oct01_aggression.html
Last edited:
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Not to highjack, but I'm kind of curious how I can be so blaze and non-aggresive on 1g of T and 400mg of tren a week.
It just never seems to affect me. Also possibly related - I never have high libido, ever, on anything, or clean. I wonder what this means in regards to androgen receptors in the brain of different individuals.
It just never seems to affect me. Also possibly related - I never have high libido, ever, on anything, or clean. I wonder what this means in regards to androgen receptors in the brain of different individuals.
In my late 20s I started using Tren and had a very short temper. I wouldn't actually do any outburst, mostly just fantasized about hurting people. LOL But in my 30s, for some reason it seems I no longer have any temperament problems at all when using Tren. Something with the nerves maybe?
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