The real cost of cocaine: Following the drug from Colombian rainforests to suburbia
‘There are some Londoners who think it is a victimless crime, taking cocaine at “middle-class parties”,’ Khan said. Dick criticised otherwise ethically minded users ‘who will sit round happily talking about global warming, fair trade, environmental protection and organic farming, but think there’s no harm in taking a bit of cocaine. Well, there is. There is misery throughout the supply chain.’
It’s a reasonable point. In an age when we put so much stock in consumer ethics, considering our footprint on the planet with every stride, why not investigate where your drugs come from, too?
If it ends with a snort, it begins with a seed…. In the first of a litany of environmental crimes occurring throughout the supply chain, the creation of clandestine farms means tearing down swathes of forest.
Rosie had no idea about its origins and doesn’t think about her complicity. She has two degrees, but thought cocaine came ‘from Cuba’ and was always ‘a powder… coming on a boat in the middle of the night’. She likes how coke makes her feel, but didn’t know about the environmental destruction, or cartel violence, or the risks taken by smugglers, or the bribes, or levamisole, or necrosis syndrome, or the young lives being ruined by county lines or lost in gang violence. (She did know about the Kinder eggs, but doesn’t seem very bothered.)
‘I had never really put too much thought into how it got here, just how I can get it,’ she says. And so the cocaine will keep on coming.
University of Texas at San Antonio researcher Dr. Dylan Jackson and his team studied data from 8th and 10th graders between 2010 and 2016. Teens that drank an energy everyday are “125 percent more likely to fail to perceive any risk in trying to consume cocaine,” compared to their peers. And when it came to heroin, they were 143 percent more likely to not see the risk of trying that drug when compared to other teens.
By Professor Andy Parrott one of the world’s leading experts on MDMA, Andy Parrott, Professor of Human Psychopharmacology, School of Health Sciences, Swansea University.
Comparing alcohol with MDMA.Alcohol is certainly a damaging drug, but to suggest that MDMA is less damaging than alcohol does not agree with the scientific evidence (Professor Nutt, 21st May). Comparing these two drugs is like comparing an F1 sports car to a basic family saloon. MDMA is an extremely powerful drug, which heats up the brain, causing a massive increase in neurochemical activity, dramatic changes in mood state, and it takes the brain several days to recover. Regular MDMA usage impairs memory, reduces problem-solving ability, reduces white cell blood count, increases susceptibility to infections, causes sleep problems, and enduring depression. In pregnant women MDMA impairs foetal development. We and other research groups worldwide have compared the psychobiological functioning of recreational Ecstasy/MDMA users with alcohol drinkers, and in numerous studies it is always the Ecstasy/MDMA users who are comparatively worse. The ‘family car’ may kill more people each year than the F1 speed machine, but to suggest that the latter would be safer for everyday driving is completely erroneous. MDMA kills many young people each year, and the death toll is currently rising. Yours etc . . .
In the next few paragraphs, I have provided more information on this topic. What is the basis for Professor Nutt claiming that MDMA is a safer drug than alcohol? This statement was based primarily on a survey he published in the Lancet (Nutt et al, 2007, vol 369; 1047). However this article contains some astounding errors. Indeed when I was first shown it, I contacted the Lancet stating that they needed to publish a detailed reply from me, since it was important to point out these errors. After some email exchanges with one of the Lancet editors, the journal decided not to publish my letter. However I presented some of my criticisms as a conference paper (Parrott, 2009. ‘How harmful is Ecstasy/MDMA: an empirical comparison using the Lancet scale for drug-related harm’. Journal of Psychopharmacology, vol 23, page 41).
I have listed below my main criticisms:
Cardiac sequelae are the second most common cause of death (behind overdose) in patients who use methamphetamines (“meth”). Like cocaine use, use of methamphetamines can produce both acute and chronic cardiovascular disease. Acute intoxication with methamphetamines produces a hyperadrenergic state, not unlike having a pheochromocytoma. The hypertension and tachycardia that result can lead to myocardial ischemia and infarction, aortic dissection, malignant arrhythmias, Takotsubo’s (stressinduced) cardiomyopathy, and cardiac arrest. Chronic methamphetamine use can lead to hypertrophic cardiomyopathy (due to persistent severe hypertension) or dilated cardiomyopathy (due to the drug’s toxic effects on myocardium), and the clinical syndrome of heart failure. In addition, chronic meth use can also cause pulmonary arterial hypertension (PAH). Meth-associated PAH is a devastating disease, with five-year mortality rates above 50%.
Diagnosing and managing acute methamphetamine intoxication:
Patients who present with suspected acute methamphetamine intoxication should undergo a full physical exam, electrocardiogram, and basic lab work (including basic metabolic panel, blood counts, clotting times (prothrombin time and international normalized ratio), liver function tests, creatine phosphokinase (CPK), urinalysis, and urine and serum toxicology screens). Amphetamine intoxication or toxicity is ultimatelydiagnosed by confirming the presence of amphetamines in urine or serum. However, if patients present with signs and symptoms which raise concern for amphetamine intoxication—including hyperthermia, agitation, hypertension, and tachycardia—treatment should not be delayed while waiting for these test results to return.
If there is concern for myocardial ischemia or infarction (for example, if the patient complains of chest discomfort or shortness of breath or the ECG shows ischemic changes), then cardiac biomarkers should be checked as well (i.e. troponin I or T). Acute methamphetamine intoxication with secondary sequelae (i.e. agitation, hypertension, tachycardia) should be managed initially with sedatives (benzodiazepines and 2nd generation atypical antipsychotics).
Hyperthermia should be managed aggressively by controlling core body temperature with sedatives and, if necessary, with paralysis and intubation (but antipyretics should not be used).
Rhabdomyolysis is common, and a CPK level should always be checked in patients who are acutely intoxicated with meth. If the hypertension is refractory to treatment with an adequate trial of sedation, then nitrates and/or phentolamine should be used. Calcium channel blockers can also be used, and are effective agents for managing tachycardia that persists despite sedation. Beta-blockers should be avoided in the acute setting to avoid precipitating unopposed alpha-mediated vasoconstriction (via identical mechanisms to those described above). If beta blockers are necessary for chronic management of a different disease process (e.g. cardiomyopathy or coronary artery disease), then labetalol or carvedilol are the preferred agents due to their partial alphaantagonism. Myocardial infarction in the setting of methamphetamine intoxication should be managed per evidence-based guidelines for the management of heart attacks, and as described above (for cocaine). The one exception is that, if heart rate control is needed, calcium channel blockers, not beta blockers, should be used. Interestingly, monoclonal antibodies against methamphetamine have been developed and are currently in clinical trials.
Chest pain in the setting of acute methamphetamine intoxication should raise concern not only for myocardial infarction, but also for acute aortic dissection. Methamphetamine abuse is the second most common cause of acute fatal aortic dissection in the US, after hypertension. Unlike chest discomfort due to myocardial ischemia, which often starts as mild or moderate discomfort and worsens progressively over minutes-hours, chest discomfort due to aortic dissection is typically extreme from the outset.
However, while many adult users opt for e-cigarettes to ease themselves out of their smoking habit, some researchers have raised concerns that teenagers may be using them as a gateway into this very habit. E-cigarette usage seems to be popular among many teenagers, despite the fact that the Food and Drug Administration (FDA) have banned the sale of such devices to people under 18.
Carcinogens threaten teenagers' health
In order to reach their conclusions, Dr. Rubinstein and team collected and analyzed urine samples from 104 adolescents, aged 16.4 years, on average. Of these, 67 were e-cigarette users, 17 used e-cigarettes as well as traditional ones, and 20 did not smoke or vape (the controls).
Their analysis revealed that the teenagers who vaped had a three times higher concentration of toxic compounds in their bodies than their non-vaping peers. In the case of teenagers who used both tobacco cigarettes and e-cigarettes, the concentration of toxic chemicals in the body was three times higher than in the case of adolescents who only vaped. "E-cigarettes," Dr. Rubinstein says, "are marketed to adults who are trying to reduce or quit smoking as a safer alternative to cigarettes. While they may be beneficial to adults as a form of harm reduction, kids should not be using them at all."