Lack of adverse interactions between concomitantly
administered selegiline and citalopram
by
Laine K, Anttila M, Heinonen E, Helminen A, Huupponen R,
Maki-Ikola O, Reinikainen K, Scheinin M
Department of Pharmacology and Clinical Pharmacology,
University of Turku, Finland
Clin Neuropharmacol 1997 Oct; 20(5):419-33

ABSTRACT
We have evaluated the risk for pharmacokinetic and/or pharmacodynamic interactions of concomitantly administered selegiline, a selective monoamine oxidase type B inhibitor, and citalopram, a widely used selective serotonin uptake inhibitor antidepressant. Two parallel groups of healthy volunteers received 20 mg of citalopram (n = 12) or placebo (n = 6) once daily for 10 days in a randomized, double-blind fashion, followed by concomitant selegiline 10 mg once daily for 4 days. The safety of this drug combination was assessed by measurements of blood pressure, heart rate, body temperature, and inquiries for adverse events. Blood samples were taken for the analysis of serum concentrations of both study drugs and their metabolites and plasma prolactin, adrenaline, noradrenaline, and 3,4-dihydroxyphenylglycol (DHPG); urinary excretion of serotonin and 5-hydroxyindoleacetic acid (5-HIAA) were assessed. After a 5-week washout, the 12 subjects who took citalopram in the first part of the study received 10 mg of selegiline once daily for 4 days to compare the pharmacokinetics of selegiline with and without concomitant citalopram. The safety analysis showed no significant differences in vital signs or the frequency of adverse events between the study groups. Plasma prolactin concentrations were increased by 40% after 10 days' treatment with citalopram (p = 0.03); this was not potentiated by concomitantly administered selegiline. The comparison of plasma concentrations of noradrenaline, adrenaline, and DHPG and the amount of serotonin and 5-HIAA excreted into urine between the study groups indicated no signs of subclinical pharmacodynamic interaction between selegiline and citalopram. The relative bioavailability of selegiline was slightly reduced (by 29%; p = 0.008) when citalopram was coadministered compared with selegiline alone. However, no indication of a pharmacokinetic interaction was found in the analysis of serum concentrations of the three main metabolites of selegiline. The pharmacokinetics of citalopram remained unaffected by concomitant selegiline. The present results indicate lack of clinically relevant pharmacodynamic or pharmacokinetic interactions between selegiline and citalopram.

Lack of adverse interactions between concomitantly
administered selegiline and citalopram
by
Laine K, Anttila M, Heinonen E, Helminen A, Huupponen R,
Maki-Ikola O, Reinikainen K, Scheinin M
Department of Pharmacology and Clinical Pharmacology,
University of Turku, Finland
Clin Neuropharmacol 1997 Oct; 20(5):419-33

ABSTRACT
We have evaluated the risk for pharmacokinetic and/or pharmacodynamic interactions of concomitantly administered selegiline, a selective monoamine oxidase type B inhibitor, and citalopram, a widely used selective serotonin uptake inhibitor antidepressant. Two parallel groups of healthy volunteers received 20 mg of citalopram (n = 12) or placebo (n = 6) once daily for 10 days in a randomized, double-blind fashion, followed by concomitant selegiline 10 mg once daily for 4 days. The safety of this drug combination was assessed by measurements of blood pressure, heart rate, body temperature, and inquiries for adverse events. Blood samples were taken for the analysis of serum concentrations of both study drugs and their metabolites and plasma prolactin, adrenaline, noradrenaline, and 3,4-dihydroxyphenylglycol (DHPG); urinary excretion of serotonin and 5-hydroxyindoleacetic acid (5-HIAA) were assessed. After a 5-week washout, the 12 subjects who took citalopram in the first part of the study received 10 mg of selegiline once daily for 4 days to compare the pharmacokinetics of selegiline with and without concomitant citalopram. The safety analysis showed no significant differences in vital signs or the frequency of adverse events between the study groups. Plasma prolactin concentrations were increased by 40% after 10 days' treatment with citalopram (p = 0.03); this was not potentiated by concomitantly administered selegiline. The comparison of plasma concentrations of noradrenaline, adrenaline, and DHPG and the amount of serotonin and 5-HIAA excreted into urine between the study groups indicated no signs of subclinical pharmacodynamic interaction between selegiline and citalopram. The relative bioavailability of selegiline was slightly reduced (by 29%; p = 0.008) when citalopram was coadministered compared with selegiline alone. However, no indication of a pharmacokinetic interaction was found in the analysis of serum concentrations of the three main metabolites of selegiline. The pharmacokinetics of citalopram remained unaffected by concomitant selegiline. The present results indicate lack of clinically relevant pharmacodynamic or pharmacokinetic interactions between selegiline and citalopram.

ssri er i ikke godt til MDMA harm reduction fordi man skal tage det i en til to uger før det virker! har jeg da læst...?
Det med at det skulle være farligt kunne jeg forestille mig var hvis man tog det mens man var blæst og havde en masse serotonin i omløb. ssri hæmmer jo genoptaglsen af sorotonin så det ville nok forlænge virkningen af MDMA'en.

Ja men nu var det jo den antidepressive virkning ~oym~ spurgte efter

Nefadar os kendt som nefazodon, Øger mængden af serotonin og noradrenalin.
Ville dette være en oplagt mulighed efter et lækkert mdma trip?.

~oym~ skrev

Jeg forstår det som om det er den antidepressive virkning han er ude efter. Hvorfor skulle han ellers skrive det med at det øger mængden af serotonin og noradrenalin??

Det med at ssri stofferne forlænger virkningen er hvis man tager dem efter MDMA'en er optaget. Det med at folk under behandling ikke får så meget ud af kix har jeg skam hørt før.
Men jeg skrev også bare jeg kunne forestille mig at det var sådan!

Det må han hellere selv svare på. Men en mulighed er at han ønsker at hjælpe kroppen med at genskabe det oprindelige serotonin-niveau.

Ja men nu var det jo den antidepressive virkning ~oym~ spurgte efter