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Vecchio 16-07-2018, 15:55   #481
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Originariamente inviata da Drugs.com
The recommended starting dose for ABILIFY as adjunctive treatment for patients already taking an antidepressant is 2 to 5 mg/day. The recommended dosage range is 2 to 15 mg/day. Dosage adjustments of up to 5 mg/day should occur gradually, at intervals of no less than 1 week [see CLINICAL STUDIES (14.3)]. Patients should be periodically reassessed to determine the continued need for maintenance treatment.
Addirittura fino a 15 mg si può usare l'Abilify nella terapia antidepressiva.
Vecchio 19-07-2018, 20:06   #482
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Mephedrone is one of hundreds of designer drugs or legal highs that have been reported in recent years, including artificial chemicals such as synthetic cannabis and semisynthetic substances such as methylhexanamine. These drugs are primarily developed to avoid being controlled by laws against illegal drugs, thus giving them the label of designer drugs.[11] According to the European Monitoring Centre for Drugs and Drug Addiction, the synthesis of mephedrone was first reported in 1929 by Saem de Burnaga Sanchez in the Bulletin de la Société Chimique de France, under the name "toluyl-alpha-monomethylaminoethylcetone",[4]:17[50] but the compound remained an obscure product of academia until 2003, when it was "re-discovered" and publicised by an underground chemist on The Hive website, working under the pseudonym "Kinetic".[51] Kinetic posted on the site, "I’ve been bored over the last couple of days and had a few fun reagents lying around, so I thought I’d try and make some 1-(4-methylphenyl)-2-methylaminopropanone hydrochloride, or 4-methylmethcathinone." before going on to describe that after taking it, the user had a "fantastic sense of well-being that I haven’t got from any drug before except my beloved Ecstasy."[52] In interviews Kinetic was described as "a mathematician who used to design sleeping pills for a major pharmaceutical company" and he stated that he was based in Israel when he rediscovered mephedrone.[53][54]

A drug similar to mephedrone, containing cathinone, was sold legally in Israel from around 2004, under the name hagigat. When this was made illegal, the cathinone was modified and the new products were sold by the Israeli company, Neorganics.[55][56][57] The products had names such as Neodoves pills, but the range was discontinued in January 2008 after the Israeli government made mephedrone illegal.[5][48][58] The Psychonaut Research Project, an EU organisation that searches the internet for information regarding new drugs, first identified mephedrone in 2008. Their research suggested the drug first became available to purchase on the internet in 2007, when it was also discussed on internet forums.[11][59] Mephedrone was first seized in France in May 2007, after police sent a tablet they assumed to be ecstasy to be analysed, with the discovery published in a paper titled "Is 4-methylephedrone, an "Ecstasy" of the twenty-first century?"[46] Mephedrone was reported as having been sold as ecstasy in the Australian city of Cairns, along with ethylcathinone, in 2008.[60][61] An annual survey of regular ecstasy users in Australia in 2010 found 21% of those surveyed had used mephedrone, with 17% having done so in the previous six months. The price they paid per gram varied from A$16 to $320.[2]

Europol noted they became aware of it in 2008, after it was found in Denmark, Finland and the UK.[62] The Drug Enforcement Administration noted it was present in the United States in July 2009.[63] By May 2010, mephedrone had been detected in all 22 EU member states that reported to Europol, as well as in Croatia and Norway.[4]:21 The Daily Telegraph reported in April 2009 that it was manufactured in China, but it has since been made illegal there.[64][65] In March 2009, Druglink magazine reported it only cost a "couple of hundred pounds" to synthesise a kilogram of mephedrone,[55] the same month, The Daily Telegraph reported manufacturers were making "huge amounts of money" from selling it.[66] In January 2010, Druglink magazine reported dealers in Britain spent £2,500 to ship one kilogram from China, but could sell it for £10 a gram, making a profit of £7,500.[52][67] A later report, in March 2010, stated the wholesale price of mephedrone was £4000 per kilogram.[68]

In March 2011, the International Narcotics Control Board published a report about designer drugs, noting mephedrone was by then being used recreationally in Europe, North America, Southeast Asia, New Zealand and Australia.[69][70]
Che storia!
Vecchio 19-07-2018, 20:40   #483
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Originariamente inviata da Svers0 Visualizza il messaggio
Ho appena scoperto che esistono anche sostanze che non agiscono sulla ricaptazione ma proprio fanno rilasciare dopamina, sinceramente pensavo fosse un mito.
c'è anche l'amisulpride che agisce da agonista dei recettori dopaminergici
Vecchio 21-07-2018, 21:56   #484
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Originariamente inviata da Sostanze.info
La produzione di sempre nuove sostanze psicoattive è molto attiva. Tali sostanze vengono chiamate “designer drugs” e non sono illegali (almeno in Italia) finchè non vengono inserite nelle tabelle ministeriali. Si tratta di sostanze di cui viene cercato l’effetto psicoattivo che hanno un mercato specialmente tramite internet. Molte di esse sono sostanze poco conosciute dal punto di vista farmacologico ed, in particolare tossicologico. Il mephedrone (2-methylamino-1-p-tolylpropane-1-one), conosciuto anche con il nome dimethylmethcathinone (4-MMC) o methylephedrone.(4-mmc) è una di esse.
Il Progetto di Ricerca della Comunità Europea “Psycoanauta”, una organizzazione che individua sulla rete le nuove droghe che vi vengono vendute, ha individuato per la prima volta il mephedrone nel 2008. Una sua prima produzione fu resa illegale e quindi tolta dal commercio dopo che il governo israeliano ne dichiarò l'illegalità e costrinse l'azienda che lo produceva a ritirarlo dal commercio.
Questa sostanza sembra che abbia principalmente un affetto entactogeno. La sua farmacologia e la sua tossicità sono al momento praticamente sconosciute. Ovviamente non possiamo, proprio alla luce delle poche conoscenze che si hanno su di essa, che sconsigliarne l’assunzione. I suoi effetti tossici infatti non possono essere previsti.
Vecchio 21-07-2018, 23:54   #485
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In the United States about 1.6 percent of people have used heroin at some point in time.
Vecchio 22-07-2018, 00:17   #486
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Little research has been focused on the suppository (anal insertion) or pessary (vaginal insertion) methods of administration, also known as "plugging". These methods of administration are commonly carried out using an oral syringe. Heroin can be dissolved and withdrawn into an oral syringe which may then be lubricated and inserted into the anus or vagina before the plunger is pushed. The rectum or the vaginal canal is where the majority of the drug would likely be taken up, through the membranes lining their walls.
Vecchio 22-07-2018, 01:03   #487
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Confondere euforia con felicità è un grosso sbaglio
Vecchio 22-07-2018, 01:09   #488
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L'Abilify non mi convince mica.
Vecchio 22-07-2018, 01:11   #489
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Latte, caffè, succo di frutta alla pera, e sertralina, sapore disgustoso, ma è una bevanda molto "frizzante".
Vecchio 22-07-2018, 01:15   #490
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Latte, caffè, succo di frutta alla pera, e sertralina, sapore disgustoso, ma è una bevanda molto "frizzante".
La sertralina presa a parte o proprio sciolta nel miscuglio?
Vecchio 22-07-2018, 01:26   #491
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La sertralina presa a parte o proprio sciolta nel miscuglio?
Disciolta
Vecchio 22-07-2018, 01:34   #492
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Disciolta
Prossima volta mettici pure della cioccolata e mi sa che sarà una bomba.
Vecchio 22-07-2018, 15:23   #493
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In Italia come siamo messi a reperibilita di questi farmaci? Negli Stati Uniti anche parecchie star ci sono rimaste secche com questa roba
Opioids: Why 'dangerous' drugs are still being used to treat pain http://www.bbc.co.uk/news/health-44797545
Vecchio 24-07-2018, 14:24   #494
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The atypical antipsychotics integrate with the serotonin (5-HT), norepinephrine (α, β), and dopamine (D) receptors in order to effectively treat schizophrenia.

D2 Receptor: Hyperactive dopaminergic activity on D2 receptors in the mesolimbic pathway is responsible for the positive symptoms of schizophrenia (hallucinations, delusions, paranoia). After taking an antipsychotic, antagonism of D2 receptors occurs throughout the entire brain, leading to a number of deleterious side effects from D2 receptor antagonism throughout the entire dopamine pathway system. Unfortunately, it’s not possible to affect D2 receptors only in the mesolimbic pathway.[58][Stahl AP Explained 1 - 1] Fortunately, 5-HT2A receptor antagonism reverses these side effects to some extent.[Stahl AP Explained 1 - 2] Reducing D2 dopaminergic activity in the mesolimbic pathway also results in an anhedonic effect, reducing pleasure, motivation, and the salience of one’s life experience. In the mesocortical pathway to the DLPFC and VMPFC, endogenous D2 receptor dopamine activity is sometimes low in schizophrenia, resulting in cognitive, affective, and, broadly, the negative symptoms of schizophrenia. D2 receptor antagonism here further compounds these problems. In the nigrostratial pathway, D2 receptor antagonism results in extrapyramidal symptoms. If this antagonism occurs long enough, symptoms of EPS may become permanent, even if antipsychotic use is discontinued. In the tuberoinfundibular pathway, D2 receptor antagonism results in elevated prolactin. If prolactin levels become high enough, hyperprolactinaemia may occur, resulting in sexual dysfunction, weight gain, more rapid demineralization of bones, and possibly galactorrhea and amenorrhea.[Stahl AP Explained 1 - 1]

5-HT2A Receptor: When serotonin is released on to postsynaptic 5-HT2A receptors, the dopamine neuron is inhibited, thus acting as a brake on dopamine release.[Stahl AP Explained 1 - 2] This brake is disrupted through action of a 5-HT2A antagonist, which cuts the brake cable, disinhibiting the dopamine neuron, and stimulating dopamine release. The result of this is that dopamine competes with antipsychotic D2 antagonistic action at D2 receptors, thereby reducing antagonistic binding there and eliminating or lowering D2 antagonistic effects in several pathways of the dopamine system.[Stahl AP Explained 1 - 2] In the nigrostratial pathway, it reduces EPS. In the tuberoinfundibular pathway, it reduces or eliminates prolactin elevation.[Stahl AP Explained 1 - 3] Dopamine release in the mesolimbic pathway from 5-HT2A antagonism does not appear to be as robust as in the other pathways of the dopamine system, thereby accounting for why atypical antipsychotics still retain part of their efficacy against the positive symptoms of schizophrenia through their D2 antagonism.[Stahl AP Explained 1 - 3] When 5-HT2A antagonistic agent particles occupy 5-HT2A receptors in the mesocortical pathway and in the prefrontal cortex, the negative symptoms of schizophrenia, affective symptoms, and cognitive deficits and abnormalities are treated and reduced.[Stahl AP Explained 1 - 3] Furthermore, 5-HT2A receptor antagonism blocks the serotonergic excitation of cortical pyramidal cells, reducing glutamate release, which in turn lowers hyperactive dopaminergic D2 receptor activity in the mesolimbic pathway, reducing or eliminating the positive symptoms of schizophrenia.[Stahl AP Explained 1 - 3][59][60]

Some effects of 5-HT1A receptor activation include decreased aggressive behavior/ideation,[61] increased sociability, and decreased anxiety and depression.[non-primary source needed] 5-HT2C activation blocks dopamine and inhibits norepinephrine release. Blockade of the 5-HT2C receptor increases serotonin, releasing norepinephrine and dopamine within the brain.[58] But neuronal reuptake of norepinephrine is limited sharply by some antipsychotics, for example ziprasidone. Increased norepinephrine can cause increased glucose levels, which is to say blood sugar levels.[62][63][64] Increased blood sugar levels by increased norepinephrine causes hunger in many humans, which is why weight gain occurs with some antipsychotics if the norepinephrine is not inhibited.[65][66][67][68][69] Inhibition of norepinephrine stabilizes mood in humans.[70] 5-HT6 receptor antagonists improve cognition, learning, and memory.[71] The 5-HT7 receptor is very potent for the mitigation of bipolar conditions and also yields an antidepressant effect. The antipsychotics asenapine,[72] lurasidone,[73][74] risperidone,[75] and aripiprazole[76] are very potent at the 5-HT7 receptor. Antagonistic affinity for the H1 receptor also has an antidepressant effect. H1 antagonism blocks serotonin and norepinephrine reuptake. Patients with increased histamine levels have been observed to have lower serotonin levels.[77] However, the H1 receptor is linked to weight gain. To have partial agonism at the 5-HT1A receptor can yield absence of weight gain in an antipsychotic. This is very relevant for ziprasidone,[78][79] but it creates a risk for a prolonged QTc interval.[80][81] On the other hand, blockade of the 5-HT3 receptor removes the risk for a prolonged QTc interval,[73] but then creates a larger risk for weight gain. Relation to the 5-HT3 receptor increases caloric uptake and glucose,[82] which is seen in clozapine and olanzapine.[83][84] Other ways for dopamine to resolve is to have agonism at both the D2 receptor and 5-HT1A receptor, which normalizes the dopamine level in the brain. This occurs with haloperidol and aripiprazole.

Whether the anhedonic, loss of pleasure and motivation effect resulting from dopamine insufficiency or blockade at D2 receptors in the mesolimbic pathway, which is mediated in some part by antipsychotics (and despite dopamine release in the mesocortical pathway from 5-HT2A antagonism, which is seen in atypical antipsychotics), or the positive mood, mood stabilization, and cognitive improvement effect resulting from atypical antipsychotic serotonergic activity is greater for the overall quality of life effect of an atypical antipsychotic is a question that is variable between individual experience and the atypical antipsychotic(s) being used.[58]
Come funzionano gli antipsicotici atipici.
Vecchio 24-07-2018, 17:29   #495
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Mannaggia ho chiesto di aumentarmi il depakin preso da un attacco d'ansia e ora ho l'ansia che mi faccia ingrassare ancora di più,l'anno scorso ero 75kg,ora 80kg,2 anni fa invece ero 70/68 kg
Vecchio 24-07-2018, 23:01   #496
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Chissà che effetto fa la metanfetamina ai fobici.
Vecchio 24-07-2018, 23:43   #497
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Mi chiedo come mai la psichiatria non si riservi come trattamento estremo di casi di depressione resistenti a tutto l'utilizzo di metanfetamina, credo sia impossibile essere depressi con quella roba in corpo e i danni che fa in teoria son comunque minori del suicidio che è la distruzione totale del corpo.

Mi pare che l'anfetamina è usata in casi disperati di depressione ma la metanfetamina è davvero troppo potente e non la si usa anche perché poi è dipendenza garantita specie nella forma di cristalli che viene fumata.


La metanfetamina strabatte la cocaina come stimolante, credo sia lo stimolante più potente in natura, non fa dormire per giorni quindi pure la durata dell'effetto è superiore alla cocaina.
Vecchio 04-08-2018, 13:46   #498
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Ma qui si può postare oppure no?
Vecchio 04-08-2018, 14:41   #499
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Ma qui si può postare oppure no?
Ti daremo una risposta in tempi brevi.
Vecchio 04-08-2018, 21:06   #500
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Se in questa discussione ti limiterai a parlare degli effetti basati su ciò che risulta scientificamente evidente in connubio alla tua esperienza personale nessun problema ma è finito il tempo delle "droghe miracolose" o dei rimedi da te improvvisati.
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