Growing familiarity with marijuana has been accompanied by growing support for legalization because people discovered through personal experience that the government was lying to them about the drug’s hazards. But it is easier to demonize less popular drugs such as crack cocaine and methamphetamine, which in the public mind are still linked, as marijuana once was, with addiction, madness, and violence. Any attempt to question the use of force in dealing with these drugs therefore must begin by separating reality from horror stories.That is where Carl Hart comes in. Hart, a neuropsychopharmacologist at Columbia who grew up in one of Miami’s rougher neighborhoods, has done bold, path-breaking research that challenges widely accepted beliefs about crack and meth. In his inspiring and fascinating new memoir High Price, he describes both how he overcame his early disadvantages to secure a tenured position at an Ivy League university and how he came to question everything he thought he knew about drugs as he learned to think critically about the issue.Before he became a scientist, Hart believed that people who use crack generally get hooked on it and thereby lose control of their behavior. But when he looked at the data on patterns of drug use as an academic, he could plainly see that only a small minority of people who try crack become heavy users. “Even at the peak [of] widespread use,†he writes, “only 10–20 percent of crack cocaine users became addicted.†According to the National Survey on Drug Use and Health, just 3 percent of Americans who have tried this reputedly irresistible and inescapable drug have smoked it in the last month.Contrary to what anti-drug ads claim, Hart observes, addiction “is not an equal-opportunity disorder.†He notes that even rats, whose voracious consumption of cocaine in certain contrived conditions supposedly shows how powerfully addictive that drug is, tend to use it in moderation when they have other options, such as food, sex, or an interesting environment to explore.Crack “gained the popularity that it did in the hood…because there weren’t that many other affordable sources of pleasure and purpose,†Hart writes. “And that was why, despite years of media-hyped predictions that crack’s expansion across classes was imminent, it never ‘ravaged’ the suburbs.â€. . .Hart is well aware of the hostility he is apt to provoke by challenging the myths underlying the war on drugs. He describes a 2005 meeting with journalists, arranged by the Office of National Drug Control Policy, where he tried to put the dangers of methamphetamine in perspective, noting that the drug is a government-approved treatment for narcolepsy and attention deficit hyperactivity disorder (ADHD). He cited his own research finding that methamphetamine has “the same effects†as a more familiar ADHD drug, Adderall, which has a “nearly identical†chemical structure. He added that pilots and soldiers commonly use amphetamines to stay alert.
Cocaine addiction is a life-threatening disease for which there is currently noeffective pharmacotheraphy (1). Both clinical and preclinical findings indicatethat the behavioral response to cocaine, including discriminative stimulus andrewarding effects as well as reinstatement of cocaine seeking behavior, depend onthe drug ability to block the dopamine transporter, thereby increasing dopamineextracellular concentration within the mesocorticolimbic system and indirectactivation of dopamine D1 and D2 receptors (for review see: 2 - 5).Confirming further the role of dopamine neurotransmission in cocainebehaviors we have recently demonstrated that 1-methyl-1,2,3,4-tetrahydroisoquinoline (1MeTIQ) prevents the expression of the behavioral andneurochemical consequences of cocaine-primed induced reinstatement (6).1MeTIQ is a member of endogenous tetrahydroisoquinolines (7, 8) and showsneuroprotective properties depending on alterations in both the dopaminergic (9,10) and glutamatergic neurotransmitter systems (11). In fact, 1MeTIQ inhibits theMAO-dependent oxidative deamination of dopamine and shifts catabolism ofdopamine towards COMT-dependent O-methylation (12). In the in vitro bindingassays, 1MeTIQ displaced the non-selective dopamine agonist [3H]apomorphinewith a potency comparable to that of the endogenous dopamine, but not thedopamine antagonist [3H]spiperone what indicates its direct interaction with theagonistic (active) conformation of dopamine receptors (6). On the other hand, inthe in vivo studies it shows antidopaminergic activity (12). 1MeTIQ was alsoshown to prevent the glutamate-induced cell death in granular cell cultures and inthe in vivo microdialysis it decreased the release of excitatory amino acids evokedby intra-prefrontal cortex kainate injection in the rat (13). Additionally, 1MeTIQdisplays an affinity for the NMDA glutamatergic receptors as confirmed by theinhibition of [3H]MK-801 binding (13)
Summary.Drug abuse disorder is induced by a variety of substances and results from their interaction with the brain reward system. It is characterized by a high frequency of relapse, usually associated with to craving. In this study we investigated the effects of 1-methyl-1,2,3,4-tetrahydroisoquinoline, an endogenous compound with antidopaminergic and neuroprotective activity, on cocaine-induced reinstatement in cocaine-dependent, self-administering rats. 1-methyl-1,2,3,4-tetrahydroisoquinoline (50 mg/kg i.p.) completely inhibited the expression of reinstatement of cocaine self-administration and accompanying neurochemical changes induced by a single priming cocaine dose (10 mg/kg i.p.). The priming cocaine dose inhibited dopamine metabolism in the structures containing nerve endings (frontal cortex, nucleus accumbens, and striatum) but not in the substantia nigra and ventral tegmental area. A behaviorally active dose of 1-methyl-1,2,3,4-tetrahydroisoquinoline administered 30 min before a priming dose of cocaine significantly increased the dopamine concentration in the limbic structures, and strongly inhibited dopamine metabolism in the substantia nigra and ventral tegmental area. Cocaine also inhibited noradrenaline and serotonin metabolism, and 1-methyl-1,2,3,4-tetrahydroisoquinoline abolished the inhibition in noradrenaline metabolism, while it intensified the inhibition of serotonin metabolism. Our results strongly support the view that 1-methyl-1,2,3,4-tetrahydroisoquinoline, an endogenous compound, has considerable potential as a drug for combating substance abuse disease through the attenuation of craving.
Legalizing pot is one thing. Legalizing stuff that is possible to OD on the first time you use it is something else (meth, heroin, coke, etc). Except for alcohol of course, that stuff's delicious.
I hate cocaine...I just like the way it smells.
Seriously! Legalize EVERYTHING as long as we also take away the safety nets and other gubm'et giveaway programs. Give Darwin's theory a chance. In 6-12 months, the Democrats would have lost half their constituents, and much of the remaining deadbeat culture demanding all of the freebies would be too stoned to give a shit.
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