Nella mia (non ampissima) esperienza di utilizzo non ho mai avuto un down post-utilizzo. So che si può verificare, ed è variamente documentato, ma non escludo che possa essere dovuto, oltre al notorio calo del livello di serotonina nel cervello (o allo sviluppo di una maggiore tolleranza nei recettori, non lo so) a fattori ambientali o stanchezza, disidratazione ecc.
Per quanto riguarda la neurotossicità ammetto di non essere del campo, ma mi sembra che, mentre per le metanfetamine (ie meth) la neurotossicità nel breve e lungo periodo sia unanimemente riconosciuta, il discorso sia diverso e più controverso per la 3,4-Methylenedioxymethamphetamine (mdma e ecstasy che dir si voglia) (che penso sia anch'essa un'anfetamina: qualche chimico mi illumini perché non l'ho ancora capito).
Guarda qua per la dannosità minore a p. 1050:
https://sci-hub.se/10.1016/S0140-6736(07)60464-4 (è lo stesso grafico che si trova in svariate pagine di wikipedia, che comunque non è la scienza infusa)
Ho trovato questo paper edito dalla Springer che confronta le due sostanza, ne cito una parte: (miei i grassetti)
A direct comparison of the behavioral and physiological effects of methamphetamine and 3, 4-methylenedioxymethamphetamine (MDMA) in humans - Springer, 2012 [
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4430833/]
Despite many overlapping effects, methamphetamine and MDMA are commonly regarded as distinct. For example, an impressively large human literature suggests that methamphetamine produces particularly pernicious long-term effects, including cognitive impairments (e.g., Baicy and London 2007), tooth decay (i.e., “meth mouth”: e.g., Hamamoto and Rhodus 2009), and psychological disturbances (e.g., Grelotti et al. 2010). A comparable literature for MDMA does not exist. The MDMA literature concerning long-term cognitive deficits is characterized by conflicting results (see Lyvers 2006 for review). Some researchers have found persistent cognitive impairments in MDMA users (e.g., Bolla et al. 1998), while others have observed few differences between MDMA users and controls (e.g., Hoshi et al. 2007). On the other hand, some reports indicate that MDMA use produces unique effects that are unlike other amphetamines, such as a temporary depressive state colloquially referred to as “Suicide Tuesday” in the days following use (e.g., Parrott and Lasky 1998). It is possible that the route by which these drugs are most often used recreationally might account for some differences. Methamphetamine, for instance, is used via routes other than oral (e.g., smoked and intravenous), which increases the likelihood of abuse and other deleterious effects.
Another possible explanation is that the chemical structural variations between methamphetamine and its ring-substituted analog MDMA contribute to the purported divergent profiles. Indeed, there is empirical evidence indicating that these structural differences result in differing neurochemical responses. For instance, although both amphetamines release brain monoamines, the degrees to which they release these neurotransmitters vary depending upon the drug. That is, methamphetamine is a more potent releaser of dopamine (DA) and norepinephrine (NE), whereas MDMA is a more potent releaser of serotonin (5-HT; Rothman et al. 2001). It has been suggested that these neurochemical differences underlie some of the differing behavioral responses observed in laboratory animals. For example, in a study comparing the relative reinforcing effects of amphetamines in rhesus monkeys, Wang and Woolverton (2007) found that methamphetamine was a more potent reinforcer than MDMA and attributed this difference to the relatively greater dopamine to serotonin releasing potency of methamphetamine. Furthermore, Crean et al. (2006) reported that methamphetamine and MDMA produced differential effects on measures of locomotor activity and temperature regulation in rhesus monkeys. These researchers speculated the observed behavioral differences were due to the fact that the amphetamines differentially alter monoamine activity.
Forse la risposta al mio quesito giace nella conclusione:
Only methamphetamine improved cognitive performance and increased self-reported desire to take the drug again, whereas only MDMA acutely increased “negative” subjective-effect ratings
Alla fine l'autore afferma come ritenga che la differenza nell'abuso risieda nella diversa via di somministrazione dell'una rispetto all'altra, ma comunque fa intendere che siano necessari altri studi (materia controversa?)
Inoltre, prova a fare una piccola ricerca su Scholar: molta letteratura sull'mdma negli ultimi 4-5 anni riguarda i suoi utilizzi psicoterapeutici, mentre per le anfetamine non vedo altro oltre a studi sui danni o sull'utilizzo o sulle morti correlate
Ora, non voglio pormi a strenuo difensore della MDMA che droga è e droga rimane, ma penso sia necessario fare le giuste distinzioni.
Forse sì: il mio post è un po' goliardico... ma forse no.
