Is anyone on anxiety/depression medicine?

Ouch! Tired like a moron... Ouch!

Actually, I take Celexa and Wellbutrin. The Celexa did make me a bit tired at first, but you get over it. The Wellbutrin is good. The combo has worked really well for me. I used to get seriously depressed, to the point of contemplating suicide. Definitely couldn't get "up" to lift. Always really embarassed about it. Until the doc told me that it's a chemical imbalance in the brain (serotonin) and more than 10% of the population has it (even a higher proportion of those of Irish descent, like myself). Cool, it's not psycho, it's out of balance. Take a pill.

Flying high since. The only down that I've noticed is that it evens out the highs as well as the lows. Don't get really sad, but don't get really amped either. No temper tantrums. If that's what you're juicing off to lift, it might impact. I've noticed a lot more upside, though.

Any specific questions, you can PM me.

i found that 5htp and vitamin C seem to take the edge off for me.

ah then might i suggest Zoloft, works, doesnt make you a veggie like xanax, and doesn't hinder your motivation .

Effexor works well but you can get dizzy from using it which isn't good lol especially when lifting.

i have been on just about every prescribed medication for the treatment of severe manic depression since the age of 7

its really trial and error bro, some work better then others with certain people, and depending on your symptoms they can also be prescribed that way as well.

zoloft is excellant for use with general depression and anxiety, and its way better then say prozac which takes 6weeks-4 months to build in your system and then you feel as if you can't be anything but happy, like a circus clown

Buspirone(Buspar) is an alternative anxiolytic to benzodiazpams(like Xanax) that won't make you tired or dumb the next day. It's not for depression like the SSRI drugs(Paxil/Zoloft/Prozac/Celexa)but is similar in that you take it every day,not just when your feeling an attack,but it predominantly affects dopamine instead of seratonin.

Made by Bristol-Myers-Squibb. No generic around that I know of. Is expensive so helps to have a drug card. It's not considered habituating,so it's not scheduled.

there is a generic available for buspar im about 85% sure.

Anxiety Disorders
Buspirone is used for the management of anxiety disorders (anxiety and phobic neuroses)and for short-term relief of symptoms of anxiety. Anxiety or tension associated with the stress of everyday life usually does not require treatment with an anxiolytic.The efficacy of buspirone for long-term use (i.e., longer than 3—4 weeks) as an anxiolytic has not been established by controlled studies,but the drug has been used in some patients for substantially longer periods (e.g., 6—12 months) without apparent loss of clinical effect.If the drug is used for extended periods, the need for continued therapy should be reassessed periodically.Efficacy of buspirone has been established principally in outpatient settings for the management of generalized anxiety disorderin which anxiety was present for periods of 1 month up to 1 year (average symptom duration: 6 months) of continual duration.Generalized anxiety disorder is characterized principally by unrealistic or excessive anxiety and worry (apprehensive expectation) about 2 or more life circumstances (e.g., worry about possible misfortune to a child who is in no danger, worry about personal finances for no good reason, anxiety and worry about academic, athletic, and/or social performance).The disorder is manifested as symptoms of motor tension (e.g., trembling, twitching, shakiness, muscle tension, restlessness), autonomic hyperactivity (e.g., sweating, palpitation and/or tachycardia, dyspnea, dry mouth, dizziness, clammy hands, hot flushes [flashes]), and vigilance and scanning (e.g., hyperattentativeness, feeling keyed up or on edge, difficulty concentrating, insomnia, irritability).Although patients with generalized anxiety disorder may have another underlying mental disorder (axis I disorder), the focus of the anxiety and worry is unrelated to the latter disorder.In addition, symptoms of generalized anxiety disorder should not occur only during the course of a mood or psychotic disorder,nor should the anxiety be initiated and maintained by an underlying organic factor (e.g., hyperthyroidism, caffeine intoxication).Controlled studies in patients with generalized anxiety disorder have shown that buspirone at usual dosages is as effective as usual dosages of benzodiazepines (e.g., alprazolam,clorazepate,diazepam,lorazepam)and more effective than placeboin reducing symptoms associated with anxiety. Limited evidence suggests that buspirone may be more effective for cognitive and interpersonal problems, including anger and hostility, associated with anxiety,while benzodiazepines may be more effective for somatic symptoms of anxiety.The drug also has been shown to reduce symptoms of anxiety in patients with coexisting depressive symptoms. Buspirone therapy generally is associated with fewer and less severe adverse CNS effects (e.g., sedation, psychomotor impairment) compared with benzodiazepinesand appears to have little, if any, dependence liability.Because of these differences, buspirone may be preferred as initial therapy in some patients with generalized anxiety disorder. The drug may be particularly useful in patients in whom potential adverse effects of benzodiazepines would be of concern (e.g., patients whose work or life-style requires mental acuity, geriatric patients who may be particularly sensitive to the adverse CNS effects of benzodiazepines)and/or those in whom the abuse potential, dependence liability, and/or potential withdrawal associated with benzodiazepines are of concern. In addition, buspirone may be safer than benzodiazepines in those patients with anxiety disorders who, despite all warnings, are considered likely to combine anxiolytic therapy with CNS depressants and/or alcohol.(See Drug Interactions: Alcohol and also Other CNS Depressants.)Because buspirone may diminish anger and hostilityand appears to be less likely than benzodiazepines to cause disinhibition,some clinicians suggest that buspirone may be preferred in patients with a history of aggression or in whom disinhibition has occurred during benzodiazepine therapy.Benzodiazepines may be preferred as initial therapy in patients with anxiety symptoms (e.g., insomnia, muscle tension) that might benefit from the sedative and/or muscle relaxant effects of these drugs. If buspirone is used in patients whose anxiety includes insomnia as a component, concomitant use of a sedative/hypnotic at bedtime may be necessary. Because buspirone may have a slower onset of action than some anxiolytics (e.g., diazepam) (see Dosage and Administration: Dosage),patients may become discouraged during initial therapy with the drug,particularly when buspirone is used for the short-term management of anxiety associated with severe stress.The influence of previous, long-term benzodiazepine therapy on the anxiolytic response to buspirone remains to be fully elucidated,but response may be discouraging in some patients,possibly because buspirone has a slower onset of actionand does not attenuate manifestations of benzodiazepine withdrawal.In addition, the anxiolytic expectations of some patients who previously have received long-term benzodiazepine therapy may differ considerably from the actual effects of buspirone therapy, which also could contribute to a discouraging response to buspirone in such patients.Because of the sometimes discouraging response to buspirone in such patients, some clinicians suggest that newly diagnosed patients and those with no previous benzodiazepine use may be optimal candidates for buspirone therapy.In addition to symptoms of anxiety, buspirone has reduced depressive symptoms in patients with generalized anxiety disorder, as determined using the Hamilton (HAM-D) or Raskin depression rating scale.Buspirone generally has been as effective as benzodiazepines in relieving symptoms of depression in these patients,although the drug may be less effective than benzodiazepines in relieving sleep disturbances.It has been suggested that improvement in depressive symptoms observed in these patients actually may reflect improvement in anxiety symptoms that are included in the depression rating scales rather than an antidepressant effect per se,and additional study is needed to determine whether the drug has clinically important antidepressant activity. Buspirone also has been used in combination with antidepressants in a limited number of patients with symptoms of both anxiety and depression.The efficacy of buspirone for the management of sexual dysfunction in patients with generalized anxiety disorder has not been established, but limited data suggest that the drug may improve sexual function in these patients.Although the improvement in sexual function paralleled improvement in anxiety in one study, other mechanisms may have been involved.Further study is needed to more fully elucidate the value of buspirone in these patients

excellant post decadent i read the same thing in my Pharmacists reference guide 2002

Here's the chemical backround on Buspar:
The principal pharmacologic effect of buspirone is anxiolysis.Buspirone has been described as an anxioselective drugsince, unlike benzodiazepines, it has no anticonvulsantor muscle relaxantctivity, does not substantially impair psychomotor function,and has little sedative effect. Buspirone’s anxiolytic potency is approximately equivalent to that of diazepam on a weight basis following oral administration.The precise mechanism of buspirone’s anxiolytic action is not known but appears to be complex and distinct from benzodiazepines,and probably involves several central neurotransmitter systems.Likewise, a variety of sites in the CNS have been postulated as contributing to the anxiolytic action of the drug.Because of the variety and location of the drug’s effects on central neurotransmitter systems, including serotonergic,dopaminergic,cholinergic,and noradrenergic (alpha-adrenergic) systems,buspirone has been described as a midbrain modulator.Buspirone has no appreciable affinity for the benzodiazepine receptor complex,nor does it inhibit or stimulate benzodiazepine binding at the receptor complex in vitro,although binding may be stimulated in vivo.Buspirone also does not appear to directly affect Gamma-aminobutyric acid (GABA) binding in vitroor in vivo.In vitro radioligand studies indicate that buspirone does not directly affect cholinergic (muscarinic),alpha-adrenergic,type 2 serotonergic (5-HT2),beta-adrenergic,histamine (H1 or H2),opiate,adenosine (A1 or A2),glutamate,or glycinereceptors or uptake of dopamine,GABA,norepinephrine,or serotonin.The drug does exhibit high affinity for type 1 serotonergic (5-HT1) receptorsand moderate affinity for dopamine D2receptors in vitro.
Serotonergic Effects
The contribution of the serotonergic system to anxiety has not been fully characterized,and the extent to which the anxiolytic action of buspirone might depend on this neurotransmitter system has not been fully elucidated.It has been suggested that serotonergic mechanisms may play a predominant role in the drug’s anxiolytic activity;however, because of conflicting evidence,additional study is needed to establish the role of serotonergic receptors in mediating anxiolysis.The anticonflict effect of the drug has been shown to be reduced in serotonin-depleted animals.In addition, buspirone has been shown to inhibit spontaneous firing of serotonergic neurons in the dorsal raphe nucleus,an effect that also is exhibited by benzodiazepinesand may be related to anxiolytic activity,and to inhibit stress-induced renin secretion that is mediated by serotonin.Buspirone has a high affinity for 5-HT1 receptors in the CNS,and appears to have a higher relative affinity for the 5-HT1A site on this receptor than for the 5-HT1B site.Buspirone appears to act as a partial agonistor mixed agonist/antagonist at this receptor,and there is some evidence to suggest that such activity may be associated with anxiolysis. Although buspirone has failed to induce the serotonin behavioral syndrome in some animal studies,the drug has exhibited agonist properties by inducing the syndrome in other studies that focused on 5-HT1- rather than 5-HT2-mediated behaviors;differences in methodology and interpretation and lack of insight regarding characterization of serotonin receptor subtypes and associated behaviors likely contributed to these discrepancies.It also has been suggested that agonist activity at the 5-HT1A receptor may be associated with antidepressant activity.Reports of buspirone’s effects on serotonin metabolism have been conflicting.The drug has been reported to decreaseor have no effecton striatal concentrations of serotonin and its principal metabolite, 5-hydroxyindoleacetic acid (5-HIAA), to decrease or have no effecton hippocampal serotonin and 5-HIAA concentrations, and to decrease serotoninbut not 5-HIAAconcentrations in the frontal cortex.
Dopaminergic Effects
The effects of buspirone on the dopaminergic neurotransmitter system are complex and have not been clearly elucidated.The drug appears to possess mixed dopamine agonist and antagonist activities.Buspirone may act as an agonist at postsynaptic dopamine receptor sitesand as an antagonist at both presynaptic autoreceptorand postsynaptic sites.The relative contribution of these effects to the anxiolytic activity and toxic potential of the drug has not been clearly established and requires additional study.Buspirone has moderate affinity for dopamine D2 receptors in the CNS.Unlike most antipsychotic agents,buspirone appears to preferentially block presynaptic dopamine autoreceptors rather than postsynaptic D2 receptors in the striatum.The resultant buspirone-induced increases in dopamine metabolismand impulse formation,however, appear to resemble those of antipsychotic agents. The drug reportedly stimulates dopamine metabolism in a dose-related manner,and has increased striatal concentrations of the dopamine metabolites, 3-methoxy-4-hydroxyphenylacetic acid (homovanillic acid, HVA) and 3,4-dihydroxyphenylacetic acid (DOPAC). Buspirone also has been reported to increase tyrosine 3-monooxygenase (tyrosine hydroxylase) activity in the striatum but not in the frontal cortex, which appears to lack autoreceptors,and has blocked apomorphine-induced inhibition of this enzyme.Unlike benzodiazepines but like butyrophenones (e.g., haloperidol), buspirone enhances spontaneous firing of dopaminergic neurons.Such effects on dopamine metabolism and impulse flow are consistent with presynaptic autoreceptor blockade.

There is some evidence from animal studies that buspirone may act as an antagonist at postsynaptic D2 receptors and potentially may possess antipsychotic activity;the drug has inhibited conditioned avoidance behavior,blocked apomorphine-induced stereotypyand emesis,and blocked amphetamine-induced stereotypy.However, unlike most antipsychotic agents, buspirone does not induce catalepsy in animals,indicating that the drug may not produce substantial postsynaptic D2 blockade usually associated with antipsychotic activity. Although buspirone reportedly has produced transient antipsychotic effects when administered in large dosages (e.g., 600—2400 mg daily) to humans,the drug has no established clinical antipsychotic efficacy at usual anxiolytic dosages. The failure of buspirone to induce catalepsy in animal studiesalso suggests that the risk of drug-induced extrapyramidal reactions is minimal. No definitive extrapyramidal reactions have been attributed directly to buspirone therapy at usual anxiolytic dosages to date,although such reactions (e.g., akathisia,hypertonia,dystonia,tremor)reportedly have been associated with anxiolytic therapy with the drug in a few patients and also have occurred in at least one patient receiving a large dosage for potential antipsychotic effects.Unlike most antipsychotic agents, buspirone does not produce postsynaptic receptor supersensitivity following long-term therapy and has reversed such supersensitivity induced by antipsychotic agents; therefore, the drug appears unlikely to produce tardive dyskinesia.However, additional clinical experience is needed to determine buspirone’s potential for inducing dopamine-mediated neurologic sequelae with long-term use.(See Cautions: Nervous System Effects and also Precautions and Contraindications.) Buspirone has been shown to produce a dose-dependent elevation in plasma prolactin concentrations (see Neuroendocrine Effects),possibly mediated by postsynaptic dopamine receptor blockade in the pituitary gland.Buspirone appears to possess some dopamine agonist activity.Like apomorphine, buspirone produces weak turning behavior in lesioned animalsand, like amantadine, potently reverses catalepsy induced by antipsychotic agents,suggesting that the drug has some dopamine agonist activity.Buspirone reportedly elevates plasma somatotropin (growth hormone) concentrations (see Neuroendocrine Effects),an effect possibly mediated by postsynaptic dopamine agonist activity in the hypothalamus.
Effects on GABA and the Benzodiazepine Receptor Complex
Buspirone has no appreciable affinity for the GABA-benzodiazepine-chloride ionophore receptor complex,and does not appear to inhibit or stimulate binding of benzodiazepines at the receptor complex in vitro,although binding may be stimulated in vivo.It is not known whether the increase in in vivo benzodiazepine binding observed in some studies reflects a change in the number of binding sites or an increase in receptor affinity.Buspirone does not appear to directly affect GABA binding in vitro or in vivo,and does not influence uptake of GABA.Benzodiazepine antagonists do not appear to block the anticonflict action of buspirone, suggesting that the drug does not exert its anxiolytic effect by directly affecting benzodiazepine receptors.Buspirone or an active metabolite may indirectly affect some component of the GABA-benzodiazepine-chloride ionophore receptor complex other than the benzodiazepine or GABA binding site, such as picrotoxin-sensitive chloride ionophore segments. It has been suggested that the drug may have a picrotoxin-like antagonistic effect on presynaptic GABA receptors, thereby enhancing GABA transmission;however, inhibitory effects of GABA on impulse flow do not appear to be altered by the drug.Further study is required to determine whether there is an association between buspirone’s effects on the benzodiazepine receptor complex and the anticonflict and anxiolytic actions of the drug.
Adrenergic Effects
Buspirone does not appear to have a direct effect on alpha1-, alpha2-, or beta-adrenergic receptors in vitro,and has no apparent effect on biogenic amine uptake, including norepinephrine.The drug does, however, appear to exhibit weak central alpha-adrenergic blocking activity in vivo. Limited evidence suggests that 1-pyrimidinylpiperazine (1-PP), a metabolite of buspirone, possesses central and peripheral alpha2-adrenergic blocking activity, which may contribute to the drug’s anxiolytic and/or antidepressant effects. Unlike benzodiazepines, which inhibit spontaneous firing of noradrenergic neurons in the locus ceruleus and decrease norepinephrine metabolism in the brain,buspirone and its metabolite 1-PP enhance neuronal activity in the locus ceruleus and increase norepinephrine metabolism,suggesting that a reduction in locus ceruleus output is not a prerequisite for anxiolytic activity.It has been suggested that buspirone-induced facilitation of noradrenergic neuronal firing may contribute to alertness and alleviate any benzodiazepine-like impairment of psychomotor performance, thereby preserving arousal and attentional processes.The drug has been shown to decrease striatal concentrations of norepinephrine and to increase striatal concentrations of 3-methoxy-4-hydroxyethylenephenylglycol (MOPEG, MHPG), a major metabolite of norepinephrine.The drug does not appear to alter monoamine oxidase (MAOA or MAOB) activity.
Cholinergic Effects

I WAS ON SOME BEFORE BUT NOT FOR DEPRESSION IT WAS AS A FINAL TRY BY MY DOCTOR TO HELP ME S;EEP MORE THAN 15 TO 30 MIN AT A TIME ALL OTHER SLEEPING MEDS THAT I TRIED DIDNT WORK EVEN ;UDES THEY JUST MADE ACT LIKE I WAS DRUNL THE ANTI DEPRESSION MEDS DIDNT WORK BUT WHEN ON THEM ND I SLEPT FOR MY USUAL 15 TO 30 MIN. ID HAVE SOME WEIRD DREAMS. I HAVE A FEW FRIENDS ON ANTI DEPRESENTS AND THEY WORK FOR THEM BUT TO ME IT SEEMS TO MAKE THEM KINDA SPACEY OR ZOMBIE LIKE. BUT THERE NOT ANCIOUS OR DSPRESSED.

I know this is sort of Taboo to the bodybuilding world, but IF you do not have an addictive personality and are mature enough to handle it... I suggest GHB, it is very accessible, cheap and prezcribed as an antidepressant in a few countries... Also improves Libido and PROMOTES FAT LOSS! But, it is ADDICTIVE if you are not strong... Like me!

CJ

Presser I lived with anxiety for a long time. I had anxiety so bad it felt like I was going to passout in public. I didn't like to go anywhere or drive. I worried about stupid shit. Could never fall asleep cause my mind would never slow down enough to. I tried buspar first and it didn't work for me. Then I tried prozac and that made it worse! 3rd time was a charm. Doc put me on paxil and it took over 3 months but it started working. I just go off of it about 3 weeks ago. Paxil gets a bad rap for side effects and coming off of it can be hard. The side effects I got happened mostly it the sex department. Talk about taking hours to reach an orgasm. It really didn't make me lazy. In my opinion the side effects out wieghed the benifits of getting rid of anxiety. Coming off the paxil was hell though. For two weeks I had headaches all day and was pretty grumpy. It passed though. I also had xanax and ativan for times when I needed it. I rarely took it though because they did make me very tired and lazy. So in the end if it wasn't for me going on paxil I would be in bad shape. I feel better now then I have in a over a year.

Presser said:

how the hell does the dr determine wich is right for me, a crazy test?lol

Click to expand...

They get kick backs for prescribing certain drugs, that is why they always prescibe paxil first, because they get the most kick backs from paxil. Clexa is far better than paxil, much less sides. Good luck trying to bust a nut on paxil or even getting hard. I could not stand paxil. Wellbutrin effected my concentrarion. Paxil also has withdrawls. I suggest you do your own research and present your case to the doctors. Rxlist.com is a good place to look one you get names. xanax works good, just take .25mg and you won't get as tired as .5mg, quite a difference actually. If you have any questions PM me. I have gone through all that you are now with my doc, and a phsyciatrist and have done tons of my own research. Good Luck, Dragon

have you combined the St-John Wort with Valerian? I think it wrks great. Really puts the pressure off in my case.

I dont have health insurance, but I could use some meds ive been down lately, is this shit costly?

I use 20 mg valium to get me to sleep at night for last month,and I have never been sleeping better in years....Boooooooyaaaahw!!!The side effects are since I sleep better I'm feel better.But I also relate to your anxiety,and I can tell a huge difference from the valium......and there cheap....if you don't already know where to get them,email me.......good luck bro.