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Offlineshroominsmurf
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Paxil - anti depressants, with mushrooms
    #816280 - 08/13/02 11:00 PM (14 years, 3 months ago)

i have a buddy that takes paxil, which is an anti depressant, anxiety and i was wondering since it kinda fucks with your brain n shit to make u less depressed obviously if it would be ok for him to do mushrooms or should he stop his meds before he shrooms?


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Invisiblemickey_rourke
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Re: Paxil - anti depressants, with mushrooms [Re: shroominsmurf]
    #816316 - 08/13/02 11:18 PM (14 years, 3 months ago)

If I'm not mistaken, Paxil is an MAOI and would potentiate the effects of the mushrooms.


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"I tried to put it all behind me, but my redneck past is nipping at my heels.." -- Ben Folds Five


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Anonymous

Re: Paxil - anti depressants, with mushrooms [Re: shroominsmurf]
    #816513 - 08/14/02 02:38 AM (14 years, 3 months ago)

Paxil is an ssri.You can take mushrooms with it.


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Offlinehappycamper
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Re: Paxil - anti depressants, with mushrooms [Re: ]
    #816715 - 08/14/02 06:13 AM (14 years, 3 months ago)

Personally I take wellbutrin which is an antidepressant and I have eaten shrooms since i started taking it and I'm still alive. From what I had read I thought you weren't supposed to mix MAOI's and SSRI's together. Paxil and wellbutrin being the SSRI's. Hope this helps.


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OfflineAndroidz17
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Re: Paxil - anti depressants, with mushrooms [Re: happycamper]
    #817304 - 08/14/02 11:20 AM (14 years, 3 months ago)

i've been on zoloft for a year and triped and now i'm on celexa, and i still trip, i feel just fine, if anyting i think i trip harder on my meds than off it.. i've never had any problems...


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OfflineHBS
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Re: Paxil - anti depressants, with mushrooms [Re: Androidz17]
    #817631 - 08/15/02 11:46 AM (14 years, 3 months ago)

I was on Zoloft for a while and tripped during it ... if anything it made the effects less, but nothing truly noticable.


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OfflineFlusH
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Re: Paxil - anti depressants, with mushrooms [Re: shroominsmurf]
    #817742 - 08/15/02 12:21 PM (14 years, 3 months ago)

Here is a write-up on Paxil and the effects on your body from www.medscape.com:

The pharmacology of paroxetine is complex and in many ways resembles that of other antidepressant agents, particularly those agents (e.g., fluoxetine, fluvoxamine, sertraline, clomipramine, trazodone) that predominantly potentiate the pharmacologic effects of serotonin (5-HT).Like other selective serotonin-reuptake inhibitors (SSRIs), paroxetine is a potent and highly selective reuptake inhibitor of serotonin and has little or no effect on other neurotransmitters.
Nervous System Effects
The precise mechanism of antidepressant action of paroxetine is unclear, but the drug has been shown to selectively inhibit the reuptake of serotonin at the presynaptic neuronal membrane.Paroxetine-induced inhibition of serotonin reuptake causes increased synaptic concentrations of serotonin in the CNS, resulting in numerous functional changes associated with enhanced serotonergic neurotransmission. Like other selective serotonin-reuptake inhibitors (e.g., fluoxetine, fluvoxamine, sertraline), paroxetine appears to have only very weak effects on the reuptake of norepinephrine or dopamineand does not exhibit clinically important anticholinergic, antihistaminic, or adrenergic (alpha1, alpha2, beta) blocking activity at usual therapeutic dosages.Although the mechanism of antidepressant action of antidepressant agents may involve inhibition of the reuptake of various neurotransmitters (i.e., serotonin, norepinephrine) at the presynaptic neuronal membrane,it has been suggested that postsynaptic receptor modification is mainly responsible for the antidepressant action observed during long-term administration of antidepressant agents.During long-term therapy with most antidepressants (e.g., tricyclic antidepressants, monoamine oxidase [MAO] inhibitors), these adaptive changes mainly consist of subsensitivity of the noradrenergic adenylate cyclase system in association with a decrease in the number of beta-adrenergic receptors; such effects on noradrenergic receptor function are commonly referred to as ?down regulation.?However, in an animal study, long-term administration of paroxetine was not shown to downregulate noradrenergic receptors in the CNS as has been observed with many other clinically effective antidepressants.In addition, some antidepressants (e.g., amitriptyline) reportedly decrease the number of serotonergic (5-HT) binding sites following chronic administration.The precise mechanism of action that is responsible for the efficacy of paroxetine in the treatment of obsessive-compulsive disorder is unclear.However, because of the potency of clomipramine and other selective serotonin-reuptake inhibitors (e.g., fluoxetine, fluvoxamine, sertraline) in inhibiting serotonin reuptake and their efficacy in the treatment of obsessive-compulsive disorder, a serotonin hypothesis has been developed to explain the pathogenesis of the condition.The hypothesis postulates that a dysregulation of serotonin is responsible for obsessive-compulsive disorder and that paroxetine and these other agents are effective because they correct this imbalance.Although the available evidence supports the serotonergic hypothesis of obsessive-compulsive disorder, additional studies are necessary to confirm this hypothesis.The exact mechanism of action of paroxetine in panic disorder, social phobia, or generalized anxiety disorder has not been fully elucidated but appears to involve inhibition of reuptake of serotonin at the presynaptic membrane.Animal data indicate that serotonergic mechanisms also appear to be involved at least in part in a number of other pharmacologic effects associated with selective serotonin-reuptake inhibitors, such as decreased food intake and altered food selection as well as decreased alcohol intake.
Serotonergic Effects
Paroxetine is a highly selective inhibitor of serotonin reuptake at the presynaptic neuronal membrane.Paroxetine-induced inhibition of serotonin reuptake causes increased synaptic concentrations of the neurotransmitter, resulting in numerous functional changes associated with enhanced serotonergic neurotransmission.Data from in vitro studies suggest that paroxetine is more potent than citalopram, clomipramine, fluoxetine, fluvoxamine, and sertraline as a serotonin-reuptake inhibitor. Unlike some other serotonin-reuptake inhibitors, the metabolites of paroxetine have been shown to possess no more than 2% of the potency of the parent compound as inhibitors of serotonin reuptake;therefore, they are unlikely to contribute to the clinical activity of the drug.At therapeutic dosages in humans, paroxetine has been shown to inhibit the reuptake of serotonin into platelets.
Effects on Other Neurotransmitters
Like other serotonin-reuptake inhibitors, paroxetine has been shown to have little or no activity in inhibiting the reuptake of norepinephrine.Paroxetine appears to have only very weak activity on neuronal reuptake of dopamine.In addition, paroxetine does not inhibit monoamine oxidase (MAO).Unlike tricyclic and some other antidepressants, paroxetine does not exhibit clinically important anticholinergic, alpha- or beta-adrenergic blocking, or antihistaminic activity at usual therapeutic dosages. As a result, the incidence of adverse effects commonly associated with blockade of muscarinic cholinergic receptors (e.g., dry mouth, blurred vision, urinary retention, constipation, confusion), alpha-adrenergic receptors (e.g., orthostatic hypotension), and histamine H1- and H2-receptors (e.g., sedation) is lower in paroxetine-treated patients than tricyclic-treated patients. In vitro studies have demonstrated that paroxetine does not possess clinically important affinity for alpha1- or alpha2-adrenergic,beta- adrenergic,histaminergic (H1-,GABA,benzodiazepine,or dopamine D2-receptors.Although paroxetine has demonstrated weak affinity for muscarinic cholinergic receptors in vitro and has caused mydriasis in vivo, these effects generally occurred only at dosages greatly exceeding those required for increasing serotonergic activity in the CNS.Limited data indicate that mydriasis may also be serotonergically mediated. In addition, serum anticholinergicity of paroxetine was found to be substantially lower than that of nortriptyline in depressed geriatric patients in one study; complaints of dry mouth and tachycardia also occurred more frequently in the nortriptyline-treated patients than in those treated with paroxetine.These findings indicate that, at therapeutic plasma concentrations, paroxetine has approximately 20% the anticholinergic potential of nortriptyline in older patients. Therefore, it appears unlikely that paroxetine will produce adverse anticholinergic events when given in the usual recommended dosage.
Effects on Sleep
Like tricyclic and most other antidepressants, paroxetine suppresses rapid eye movement (REM) sleep. Some evidence suggests that the drug may suppress REM sleep in a dose-dependent manner. Although not clearly established, there is some evidence that the REM-suppressing effects of antidepressant agents may contribute to the antidepressant activity of these drugs.While the precise mechanism has not been fully elucidated, results of animal studies indicate that paroxetine?s effects on REM sleep may be serotonergically mediated.In some studies, paroxetine prolonged REM latency,increased awakenings,increased stage 1 sleep,and/or reduced actual sleep time and sleep efficiency.In one study, administration of single, 40-mg doses of paroxetine in the morning increased sleep latency; however, the drug did not affect sleep latency when given at bedtime.In addition, sleep maintenance parameters (such as nocturnal wake time, total sleep time, and sleep efficiency) deteriorated in a dose-dependent manner both when a single dose of the drug was given in the morning and when given as a single 30-mg dose at bedtime.Overall, the changes in sleep observed with paroxetine are relatively small and are unlikely to be of clinical importance during prolonged administration.In addition, the changes noted with paroxetine are similar to those reported with other selective serotonin-reuptake inhibitors and suggest an alerting effect on sleep that has not been shown to adversely affect sleep quality.
Effects on EEG
Limited data currently are available regarding the effects of paroxetine on the EEG.In animals, EEG studies have revealed an activating effect associated with slight behavioral arousal and weak locomotor stimulation at dosages higher than those required to inhibit serotonin reuptake in the CNS.EEG changes in healthy individuals receiving single, 70-mg oral doses of paroxetine revealed a decrease in delta and theta activity and an increase in beta activity; these changes were still evident after 72 hours.Overall, available data in humans suggest that paroxetine generally does not produce clinically relevant changes on the EEG.
Effects on Psychomotor Function
Paroxetine generally does not appear to cause clinically important sedation and generally does not interfere with psychomotor performance.Controlled studies in healthy young individuals and in patients with major depression did not demonstrate any adverse effects on psychomotor performance in those receiving 20-mg doses of the drug. No adverse effects on psychomotor performance or cognitive function were observed in healthy men older than 60 years of age who received single and repeated doses of paroxetine 20 mg in a controlled study; in some tests (e.g., critical flicker fusion thresholds), paroxetine improved information processing ability.In a controlled study evaluating the effects of paroxetine (20 or 40 mg administered daily for 8 days) on psychomotor performance and car driving in healthy males, the 20-mg dosage was found to have no effect while the 40-mg dosage was not found to affect road tracking but slightly impaired performance in some psychomotor tests in a persistent manner.Further study is needed to clarify whether paroxetine may adversely affect psychomotor performance at dosages of 40 mg daily or more.
Cardiovascular Effects
No clinically important changes in vital signs (systolic and diastolic blood pressure, heart rate, temperature) were observed in patients receiving paroxetine in controlled trials.Paroxetine also appears to have little effect on the ECG.In controlled studies, paroxetine did not produce clinically important changes in heart rate, cardiac conduction, or other ECG parameters in patients receiving the drug.In depressed patients with stable ischemic heart disease, paroxetine did not substantially affect blood pressure or conduction intervals and did not produce sustained effects on heart rate, heart rhythm, or indexes of heart rate variability. However, a small but statistically significant QRS widening relative to placebo was reported in one study,and ECG changes occasionally have been reported in healthy individuals and patients receiving the drug.In addition, the relative safety of paroxetine in patients with underlying cardiac disease, particularly those with severe cardiovascular disease and immediately following a myocardial infarction, remains to be more fully elucidated.Paroxetine did not demonstrate any substantial change in cardiovascular autonomic function tests (such as heart rate variability) in a limited number of depressed patients receiving the drug for 14 days.On the other hand, paroxetine has been shown to increase heart rate variability in a limited number of patients with panic disorder, a condition associated with decreased heart rate variability and consequently an increased risk of serious cardiovascular problems including sudden cardiac death.
Effects on Appetite and Body Weight
Paroxetine appears to possess some anorexigenic activity, although to a lesser degree than certain other serotonergic agents (e.g., fenfluramine [no longer commercially available in the US], fluoxetine, sertraline, zimelidine).Limited data from animal studies suggest that fenfluramine is the most effective inhibitor of food intake followed by fluoxetine, then sertraline, and then paroxetine. Although the precise mechanism has not been clearly established, results from animal studies indicate that the appetite-inhibiting action of these antidepressants may result at least in part from serotonin-reuptake blockade and enhancement of serotonin release thereby increasing serotonin availability at the neuronal synapse.While clinically important weight loss may occur in some patients receiving paroxetine, only minimal weight loss (averaging 0.45 kg) generally occurred in patients receiving the drug in controlled clinical trials.In addition, while decreased appetite was reported in about 6% of patients receiving paroxetine in short-term clinical trials,the drug, unlike fluoxetine, does not appear to exhibit clinically important anorectic effects.(See Cautions: Metabolic and Endocrine Effects.)
Neuroendocrine Effects
Limited data currently are available regarding the effects of paroxetine on the endocrine system.Elevated serum prolactin concentrations have been reported in some women receiving chronic paroxetine therapy.Pharmacokinetics from AHFS DI?
In all human studies described in the Pharmacokinetics section, paroxetine was administered as the hydrochloride salt; dosages and concentrations are expressed in terms of paroxetine.
Absorption
Paroxetine appears to be slowly but well absorbed from the GI tract following oral administration.Although the oral bioavailability of paroxetine in humans has not been fully elucidated to date, the manufacturer states that paroxetine is completely absorbed after oral dosing of a solution of the hydrochloride salt.However, the relative proportion of an oral dose that reaches systemic circulation unchanged appears to be relatively small because paroxetine undergoes extensive first-pass metabolism.The oral tablets and suspension of paroxetine reportedly are bioequivalent.Food does not substantially affect the absorption of paroxetine. In one study, no substantial differences in pharmacokinetic parameters were noted when paroxetine was administered under fasting and nonfasting conditions or with a low- or high-fat diet, milk, water, or antacids.In another study, administration of a single dose of paroxetine with food resulted in a 6% increase in the area under the concentration-time curve (AUC), a 29% increase in peak plasma concentrations of the drug, and a decrease in the time to peak plasma concentrations from 6.4 to 4.9 hours.In healthy males receiving one 30-mg tablet once daily for 30 days, steady-state plasma paroxetine concentrations were achieved after approximately 10 days in most patients, although achievement of steady-state concentrations may take substantially longer in some patients.At steady-state, mean peak plasma paroxetine concentrations of 61.7 ng/mL occurred after an average of 5.2 hours following oral administration; corresponding mean trough concentrations of 30.7 ng/mL were reported.However, wide interindividual variation in peak plasma concentrations of paroxetine has been observed in both single- and multiple-dose studies. In geriatric individuals receiving multiple daily doses of 20?40 mg daily of paroxetine, trough plasma concentrations were 70?80% higher than trough concentrations in nongeriatric individuals.In another multiple-dose study, mean steady-state trough concentrations were approximately 3 times higher in geriatric individuals than in younger adults receiving paroxetine 20 mg daily, although there was considerable overlap between the 2 groups.Therefore, the manufacturer and some clinicians recommend that paroxetine be administered in a reduced dosage (i.e., 10 mg daily) initially in geriatric patients.(See Cautions: Geriatric Precautions and see Dosage and Administration: Dosage in Geriatric and Debilitated Patients.)When compared with a single dose, steady-state peak and trough paroxetine concentrations following multiple dosing were approximately 6 and 14 times higher than what would be expected from single-dose values.In addition, steady-state drug exposure based on AUC (0?24 hour) was about 8 times greater than would have been predicted based on the single-dose data in these individuals. The manufacturer attributed this excess accumulation to the fact that one of the enzymes that metabolizes paroxetine, the cytochrome P-450 isoenzyme CYP2D6, is saturable.In steady-state, dose-proportionality studies involving geriatric and nongeriatric patients receiving 20?40 and 20?50 mg daily of paroxetine, respectively, some nonlinearity was observed in both groups, which also suggests a saturable metabolic pathway.When compared with trough paroxetine concentrations after 20 mg of the drug daily, trough concentrations after 40 mg daily were approximately 2?3 times higher than doubled.As with other serotonin-reuptake inhibitors, the relationship between plasma paroxetine concentrations and the therapeutic and/or toxic effects of the drug has not been clearly established.
Distribution
Distribution of paroxetine and its metabolites into human body tissues and fluids has not been fully characterized.However, limited pharmacokinetic data suggest that the parent drug, which is highly lipophilic, and some of its metabolites are widely distributed throughout body tissues, including the CNS.Only 1% of paroxetine remains in plasma.Although the apparent volume of distribution of paroxetine has not been determined in humans, values ranging from 3.1?28 L/kg have been reported in animal studies.The drug crosses the blood-brain barrier in humans and animals.In vitro, approximately 95 and 93% of paroxetine is bound to plasma proteins at plasma concentrations of 100 and 400 ng/mL, respectively. Under usual clinical conditions, plasma paroxetine concentrations would be less than 400 ng/mL. In vitro, paroxetine does not alter the plasma protein binding of 2 other highly protein-bound drugs, phenytoin and warfarin.Paroxetine is distributed into human milk. In one lactating woman receiving paroxetine 20 mg daily for 1 week, the concentration of paroxetine in breast milk was 7.6 ng/mL 4 hours after the daily dose; no adverse effects were observed in the infant during lactation.Based on an estimated weight-adjusted dose to the infant of 0.34% of the maternal dose, the exposure of infants during breastfeeding appears to be lower for paroxetine and fluvoxamine than for fluoxetine; however, further study is needed to clarify the clinical importance of these findings.
Elimination
The elimination half-life of paroxetine averages approximately 21?24 hours,although there is wide interpatient variation with half-lives (ranging from 7?65 hours in one study). In geriatric individuals, elimination half-life may be increased (e.g., to about 36 hours).The exact metabolic fate of paroxetine has not been fully elucidated; however, paroxetine is extensively metabolized, probably in the liver. The principal metabolites are polar and conjugated products of oxidation and methylation, which are readily cleared by the body.Conjugates with glucuronic acid and sulfate predominate, and the principal metabolites have been isolated and identified. The metabolites of paroxetine have been shown to possess no more than 2% of the potency of the parent compound as inhibitors of serotonin reuptake;therefore, they are essentially inactive.Like some other serotonin-reuptake inhibitors, paroxetine is partially metabolized by the drug metabolizing isoenzyme CYP2D6 (a cytochrome P-450 isoenzyme implicated in sparteine/debrisoquine polymorphism). Saturation of this enzyme at dosages used clinically appears to account for the nonlinearity of paroxetine kinetics observed with increasing dosage and duration of treatment. The role of the CYP2D6 enzyme in paroxetine metabolism also suggests potential drug-drug interactions.(See Drug Interactions: Drugs Undergoing Hepatic Metabolism or Affecting Hepatic Microsomal Enzymes.)Following oral administration, paroxetine and its metabolites are excreted in both urine and feces.Following oral administration of a single, 30-mg dose of paroxetine as an oral solution (not commercially available), approximately 64% of the dose was excreted in the urine within 10 days; unchanged paroxetine accounted for 2% of the dose and metabolites accounted for the remaining 62% of the dose.During the same period, approximately 36% of the dose was eliminated in feces (probably via the bile), mostly as metabolites and less than 1% as the parent drug.The effect of age on the elimination of paroxetine has not been fully elucidated. In healthy geriatric adults, hepatic clearance of paroxetine was mildly impaired leading to slower elimination and increased plasma concentrations of the drug.(See Pharmacokinetics: Absorption.) Studies in depressed, geriatric patients confirm these findings with higher steady-state concentrations and longer elimination half-lives reported compared with younger individuals. These results suggest that older patients may be more susceptible to saturation of hepatic metabolic activity resulting in nonlinear kinetics and higher plasma concentrations occurring at lower dosages of paroxetine.Therefore, the manufacturer and some clinicians recommend that paroxetine be administered in a reduced dosage initially in geriatric patients.(See Cautions: Geriatric Precautions and see Dosage and Administration: Dosage in Geriatric and Debilitated Patients.)Because paroxetine is extensively metabolized by the liver, hepatic impairment can affect the elimination of the drug.In cirrhotic patients with moderate hepatic impairment who received a single 20-mg dose of paroxetine, no significant difference in plasma paroxetine concentrations and pharmacokinetic parameters was observed when compared with corresponding data in healthy individuals.However, accumulation potentially may occur in patients receiving multiple daily doses of paroxetine.The manufacturer states that patients with impaired hepatic function have approximately twofold higher peak plasma concentrations and AUC values. Therefore, the manufacturer recommends that paroxetine be administered in a reduced dosage initially in patients with severe hepatic impairment;caution also should be exercised when increasing the dosage of paroxetine in such patients.(See Cautions: Precautions and Contraindications and see Dosage and Administration: Dosage in Renal and Hepatic Impairment.)The effect of renal impairment on the pharmacokinetics of paroxetine has not been fully evaluated to date.Following oral administration of multiple daily doses of paroxetine in patients with creatinine clearances less than 30 mL/minute, mean plasma concentrations of paroxetine were approximately 4 times greater than those seen in healthy individuals.In patients with creatinine clearances of 30?60 mL/minute, peak plasma concentrations and AUC values were approximately twofold higher when compared with healthy individuals.The influence of renal impairment in patients receiving multiple daily doses of paroxetine has not been evaluated to date. Pending further accumulation of data, the manufacturer and some clinicians recommend that paroxetine be administered in a reduced dosage initially in patients with severe renal impairment.(See Cautions: Precautions and Contraindications and see Dosage and Administration: Dosage in Renal and Hepatic Impairment.)Because of the large volume of distribution of paroxetine and its principal metabolite, peritoneal dialysis, forced diuresis, hemoperfusion, and/or exchange transfusion are unlikely to be effective in removing substantial amounts of paroxetine from the body.Chemistry and Stability from AHFS DI?

Chemistry
Paroxetine hydrochloride, a selective serotonin-reuptake inhibitor antidepressant agent, is a phenylpiperidine-derivative.Paroxetine differs structurally from other selective serotonin-reuptake inhibitor antidepressants (e.g., citalopram, fluoxetine, sertraline)and also differs structurally and pharmacologically from other currently available antidepressants (e.g., tricyclic antidepressants, monoamine oxidase inhibitors).Paroxetine is commercially available as the hydrochloride salt, which occurs as an odorless, off-white powder and has a solubility of 5.4 mg/mL in water.The drug has a pKa of approximately 9.9
Stability
Paroxetine hydrochloride tablets should be stored at 15?30?Cand the oral suspension should be stored at or below 25?C.When stored as directed, the tablets and oral suspension have an expiration date of 3 and 2 years following the date of manufacture, respectively.

I hope this has givin' you more insight on the drug. I personally disagree with using antidepressants especially paxil. I have not taken paxil myself but I have been diagnosed with general anxiety disorder and I have a bottle that I have not even cracked yet after doing a bit of research on this shit. Everybody deals with depression differently, fortunately I was able to use psychedelic's to assist me with great help and was able to stay away from any prescription pills. I really recommend doing research on anything before you take it, ESPECIALLY from your doctor! ( After all they are just drug dealers wanting your cash not really caring about your mental health... but that is from my experiences.)

ps. the exact link: http://www.medscape.com/druginfo/Pharm?id=1-7344&name=PAXIL+ORAL&DrugType=null&MenuID=PHM&ClassID=N&GeneralStatement=N


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Edited by FlusH (08/15/02 12:25 PM)


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OfflineLSD_SNORTER6
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Re: Paxil - anti depressants, with mushrooms [Re: shroominsmurf]
    #822488 - 08/17/02 01:00 AM (14 years, 3 months ago)

I take paxil and shrooms you wont trip hard at all! Its no fair I have to eat 3 times as much i wouldnt do it if i was your friend i know my body pretty well and now what i can take.


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"But the only thing that worried me was the ether. There is nothing more irresponsible and depraved than a man in the depths of an ether binge, and I knew we would be getting into that rotten stuff sooner or later."-RAOUL DUKE


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InvisibleRipple
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Re: Paxil - anti depressants, with mushrooms [Re: FlusH]
    #824879 - 08/18/02 05:40 AM (14 years, 3 months ago)

Coulden't you have posted a bit more info!


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OfflineNeonBlack
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Re: Paxil - anti depressants, with mushrooms [Re: LSD_SNORTER6]
    #824891 - 08/18/02 06:08 AM (14 years, 3 months ago)

I've been taking paxil for a long time now.. I trip very hard pretty easily. It does not take three times as much for me to trip. You may need a little bit more to trip as hard as someone not taking it but certainly not that much more. If I were the person in question I wouldn't worry about it. Shrooms and paxil are fine together. I suppose everyone is different though..


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