- Details
- Hits: 2271
PREVENTION ALLIANCE
Electronic cigarettes, or e-cigarettes, were invented in 2003 by Chinese inventor and pharmacist Hon Lik. Although many companies and advocates continue to bill them as a safer, smokeless alternative to traditional cigarettes, a U.S. Surgeon General report alarmingly found that 16% of high school students regularly use e-cigarettes. What’s worse, many young people who begin using nicotine through e-cigarettes will start to use traditional cigarettes later, according to the National Institute on Drug Abuse.
Smokers need help to quit, and those who can’t quit deserve a safer alternative. However, there’s a growing body of research indicating that e-cigarettes do more harm than good, and the companies selling them shamelessly advertise these products to youth in order to attract lifelong, valuable customers in ways that tobacco companies are prohibited from doing:
- E-cigarette companies use candy and fruit flavors that are known to attract youth.
- They spend millions of dollars on aggressive marketing tactics.
- They spend millions more lobbying to stop life-saving regulations.
- They produce their own research, claiming that e-cigarettes pose only a minimal risk to users despite having no long-term evidence to make that claim.
- And, their products only minimally increase the number of smokers who are able to quit.
We support the Food and Drug Administration’s crackdown on e-cigarettes because with millions of teens using e-cigarettes every year, this is the beginning of an epidemic of nicotine addiction, and we invite you to learn more about these new nicotine delivery systems from the resources below.
- Details
- Hits: 2052
Teens who drink more than one energy drink per day are less likely to believe drugs like cocaine and heroin are dangerous, according to new research.
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.
- Details
- Hits: 2301
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:
- Nutt stated that ‘for drugs which have only recently become popular such as Ecstasy or MDMA, the longer term health consequences can only be estimated from animal toxicology at present’. This statement was grossly incorrect. Numerous articles (indeed several hundred) had been published before 2006 by various research groups worldwide, including many papers from my own group. These papers revealed a wide range of adverse health and related problems.
- One of the Nutt harm scales was ‘intensity of pleasure’, since it is well documented that the most powerful mood enhancers also cause the most problems. Nutt’s article gave heroin and cocaine the maximum scores of 3.0, while nicotine was rated at 2.3, whereas MDMA was given the surprisingly low rating of 1.6. This made MDMA one of the least pleasurable of all their drugs (16th lowest out of their 20 drugs). This low pleasure score for MDMA is simply incomprehensible. How can anyone with even a rudimentary knowledge of human psychopharmacology state that Ecstasy/MDMA is less pleasurable than a cigarette? Yet this low rating was apparently given by Nutt’s group of experts! Recreational Ecstasy/MDMA users would certainly be very surprised at this low rating. It should be noted that this very low ‘pleasure’ score contributed directly to MDMA’s low ‘harm’ score.
- Drug ‘injection potential’ was another scale, with heroin and cocaine again being given maximum scores of 3.0. In contrast MDMA was given a score of 0.0. This zero score was again bizarre, since MDMA is injected by some heavy users, and they suffer from the problems typically associated with drug injecting. This practice has been noted in various academic papers. Hence the injection score for MDMA should have been similar to that given for cocaine – namely 3.0. The zero score in Nutt et al may be difficult to comprehend, but again it was crucial for generating MDMA’s low overall harm score.
- In my commentary paper (Parrott, 2009, see above), I provided harm estimates based on the empirical literature, and MDMA rose from 18th to 5th in the list of most damaging drugs. Hence the position of 18th given by Nutt et al in their Lancet paper is extremely misleading – and has no basis in science.
- So what exactly are the problems caused by MDMA?
- In 2011 I was asked by the USA Deputy Attorney General to be an expert witness in a court case, which debated the issue of the most appropriate sentences for Ecstasy/MDMA drug traffickers. I was asked to write a comprehensive report, based on all the available scientific research. This was later expanded into a comprehensive review (Parrott, 2013, Neuroscience and Biobehavioral Reviews 37: 1466-1484). The following brief summaries are based on that review, and many of my more recent papers.
- MDMA is damaging when taken acutely, since it heats up the brain, impairs thermal control, increases neurotransmitter release, and generates extreme mood changes. It also leads to cognitive confusion, and a marked increase in neurohormonal activity. Death rates from acute abreactions are comparatively rare (around 60 per year in the UK), but have been increasing due probably to the increasing levels of MDMA in Ecstasy tablets (see reports by Professor Fabrizio Schifano for the UK, with similar increases reported within mainland Europe).
- MDMA is also damaging when taken repeatedly. It leads to alterations and/or deficits in brain activity which may be permanent, with reductions in memory ability, reductions in problem-solving skills, deficits in complex visual abilities, impairments in some psychomotor skills, various health impairments, increased levels of depression, increased levels of aggression, and other deficits. Young women should certainly avoid MDMA if there is any possibility of pregnancy – since it can lead to impairments in subsequent child development (Professor Lynn Singer, et al, Neurotoxicology and Teratology, vol 54, pages 22-28).
- I could go on describing more of the problems caused by MDMA – but will limit myself to one final point. MDMA has been medically tested for cancer therapy, since it can damage/kill human cells. The medical term for this is apoptosis, and it was first demonstrated in laboratory animals, but has subsequently been confirmed in human cells (the relevant medical papers were cited in Parrott, 2013, Human Psychopharmacology, vol 28, pages 289-307).
- In summary, alcohol is certainly a damaging drug, and when misused it causes massive problems to individual drinkers, their families, and wider society. However the majority of alcohol drinkers are able to use it safely over their lifetimes. In contrast, MDMA is a far more powerful and damaging drug. Current evidence suggest that its regular usage is not only damaging to many young users, but that this damage may endure for several years following drug cessation (Taurah et al, 2013, Psychopharmacology vol 231, pages 737-751).
MDMA Madness
- Details
- Hits: 2206
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.