Monday, July 21, 2014

Hunting For the Marijuana-Dopamine Connection


Why do heavy pot smokers show a blunted reaction to stimulants?

Most drugs of abuse increase dopamine transmission in the brain, and indeed, this is thought to be the basic neural mechanism underlying the rewarding effects of addictive drugs. But in the case of marijuana, the dopamine connection is not so clear-cut. Evidence has been found both for and against the notion of increases in dopamine signaling during marijuana intoxication.

Marijuana has always been the odd duck in the pond, research-wise. Partly this is due to longstanding federal intransigence toward cannabis research, and partly it is because cannabis, chemically speaking, is damnably complicated. The question of marijuana’s effect on dopamine transmission came under strong scrutiny a few years ago, when UK researchers began beating the drums for a theory that chronic consumption of strong cannabis can not only trigger episodes of psychosis, but can be viewed as the actual cause of schizophrenia in some cases.

It sounded like a new version of the old reefer madness, but this time around, the researchers raising their eyebrows had a new fact at hand: Modern marijuana is several times stronger than marijuana in use decades ago. Selective breeding for high THC content has produced some truly formidable strains of pot, even if cooler heads have slowly prevailed on the schizophrenia issue.

One of the reports helping to bank the fires on this notion appeared recently in the Proceedings of the National Academy of Sciences (PNAS). Joanna S. Fowler of the Biosciences Department at Brookhaven National Laboratory, Director Nora Volkow of the National Institute on Drug Abuse (NIDA), and other researchers compared brain dopamine reactivity in healthy controls and heavy marijuana users, using PET scans. For measuring dopamine reactivity, the researchers chose methylphenidate, better known as Ritalin, the psychostimulant frequently prescribed for attention-deficit hyperactivity disorder (ADHD). Ritalin basically functions as a dopamine reuptake inhibitor, meaning that the use of Ritalin leads to increased concentrations of synaptic dopamine.

In the study, heavy marijuana users showed a blunted reaction to the stimulant Ritalin due to reductions in brain dopamine release, according to the research. “The potency of methylphenidate (MP) was also reported to be stronger by the controls than by the marijuana abusers." And in marijuana abusers, Ritalin caused an increase in craving for marijuana and cigarettes.

 “We found that marijuana abusers display attenuated dopamine responses to MP including reduced decreases in striatal distribution volumes,” according to the study’s conclusion. “The significantly attenuated behavioral and striatal distribution volumes response to MP in marijuana abusers compared to controls, indicates reduced brain reactivity to dopamine stimulation that in the ventral striatum might contribute to negative emotionality and drug craving.”

Down-regulation from extended abuse is another complicated aspect of this: “Although, to our knowledge, this is the first clinical report of an attenuation of the effects of MP in marijuana abusers, a preclinical study had reported that rats treated chronically with THC exhibited attenuated locomotor responses to amphetamine. Such blunted responses to MP could reflect neuroadaptations from repeated marijuana abuse, such as downregulation of DA transporters.”

 Animal studies have suggested that these dopamine alterations are reversible over time.

Another recent study came to essentially the same conclusions. Writing in Biological Psychiatry, a group of British researchers led by Michael A.P. Bloomfield and Oliver D. Howes analyzed dope smokers who experienced psychotic symptoms when they were intoxicated. They looked for evidence of a link between cannabis use and psychosis and concluded: “These findings indicate that chronic cannabis use is associated with reduced dopamine synthesis capacity and question the hypothesis that cannabis increases the risk of psychotic disorders by inducing the same dopaminergic alterations seen in schizophrenia.” And again, the higher the level of current cannabis use, the lower the level of striatal dopamine synthesis capacity.  As for mechanisms, the investigators ran up against similar causation problems: “One explanation for our findings is that chronic cannabis use is associated with dopaminergic down-regulation. This might underlie amotivation and reduced reward sensitivity in chronic cannabis users. Alternatively, preclinical evidence suggests that low dopamine neurotransmission may predispose an individual to substance use.”

The findings of diminished responses to Ritalin in heavy marijuana users may have clinical implications, suggesting that marijuana abusers with ADHD may experience reduced benefits from stimulant medications.

Photo Credit: http://www.biologicalpsychiatryjournal.com/

Sunday, July 20, 2014

Drugs and Disease: A Look Forward


First published 2/18/2014.

Former National Institute on Drug Abuse (NIDA) director Alan Leshner has been vilified by many for referring to addiction as a chronic, relapsing “brain disease.” What often goes unmentioned is Leshner’s far more interesting characterization of addiction as the “quintessential biobehavioral disorder.”

Multifactorial illnesses present special challenges to our way of thinking about disease. Addiction and other biopsychosocial disorders often show symptoms at odds with disease, as people generally understand it. For patients and medical professionals alike, questions about the disease aspect of addiction tie into larger fears about the medicalization of human behavior.

These confusions are mostly understandable. Everybody knows what cancer is—a disease of the cells. Schizophrenia? Some kind of brain illness. But addiction? Addiction strikes many people as too much a part of the world, impacted too strongly by environment, culture, behavior, psychology, to qualify. But many diseases have these additional components. In the end, the meaning of addiction matters less than the physiological facts of addiction.

One of the attractions of medical models of addiction is that there is such an extensive set of data supporting that alignment. Specifically, as set down in a famous paper by National Institute of Drug Abuse director Nora Volkow and co-author Joanna Fowler: “Understanding the changes in the brain which occur in the transition from normal to addictive behavior has major implications in public health…. We postulate that intermittent dopaminergic activation of reward circuits secondary to drug self-administration leads to dysfunction of the orbitofrontal cortex via the striato-thalamo-orbitofrontal circuit.” This cascade of events is often referred to as the “hijacking” of the brain by addictive drugs, but nothing is really being hijacked. Rather, the abusive use of drugs changes the brain, and that should come as no surprise, since almost everything we do in the world has the potential of changing the brain in some way. “Why are we so surprised that when you take a poison a thousand times, it makes some changes in your head?” said the former director of a chemical dependency treatment program at the University of Minnesota. “It makes sense that [addictive drugs] change things.”

Critics like Fernando Vidal object to a perceived shift from “having a brain” to “being a brain.” He is saying that he cannot see the point of “privileging” the brain as a locus for the study of human behavior. In “Addiction and the Brain-Disease Fallacy,” which appeared in Frontiers in Psychiatry, Sally Satel and Scott Lillienfeld write that “the brain disease model obscures the dimension of choice in addiction, the capacity to respond to incentives, and also the essential fact people use drugs for reasons (as consistent with a self-medication hypothesis).”

An excellent example of the excesses of the anti-brain discussions is an article by Rachel Hammer of Mayo Clinic and colleagues, in the American Journal of Bioethics-Neuroscience. “Many believed that a disease diagnosis diminishes moral judgment while reinforcing the imperative that the sick persons take responsibility for their condition and seek treatment.” But only a few paragraphs later, the authors admit: “Scholars have theorized that addiction-as-disease finds favor among recovering addicts because it provides a narrative that allows the person simultaneously to own and yet disown deviant acts while addicted.” Furthermore: “Addiction reframed as a pathology of the weak-brained (or weak-gened) bears just as must potential for wielding stigma and creating marginalized populations." But again, the risk of this potentially damaging new form of stigma “was not a view held by the majority of our addicted participants…”

And so on. The anti-disease model authors seem not to care that addicted individuals are often immensely helped by, and hugely grateful for, disease conceptions of their disorder, even though Hammer is willing to admit that the disease conception has “benefits for addicts’ internal climates.” In fact, it often helps addicts establish a healthier internal mental climate, in which they can more reasonably contemplate treatment. Historian David Courtwright, writing in BioSocieties, says that the most obvious reason for this conundrum is that “the brain disease model has so far failed to yield much practical therapeutic value.” The disease paradigm has not greatly increased the amount of “actionable etiology” available to medical and public health practitioners. “Clinicians have acquired some drugs, such as Wellbutrin and Chantix for smokers, Campral for alcoholics or buprenorphine for heroin addicts, but no magic bullets.” Physicians and health workers are “stuck in therapeutic limbo,” Courtwright believes.

“If the brain disease model ever yields a pharmacotherapy that curbs craving, or a vaccine that blocks drug euphoria, as some researchers hope,” Courtwright says, “we should expect the rapid medicalization of the field. Under those dramatically cost-effective circumstances, politicians and police would be more willing to surrender authority to physicians.” The drug-abuse field is characterized by, “at best, incomplete and contested medicalization.” That certainly seems to be true. If we are still contesting whether the brain has anything essential to do with addiction, then yes, almost everything about the field remains “incomplete and contested.”

Sociologists Nikolas Rose and Joelle M. Abi-Rached, in their book Neuro, take the field of sociology to task for its “often unarticulated conception of human beings as sense making creatures, shaped by webs of signification that are culturally and historically variable and embedded in social institutions that owe nothing substantial to biology.”

And for those worried about problems with addicts in the legal system, specifically, over issues of free will, genetic determinism, criminal culpability, and the “diseasing” of everything, Rose and Abi-Rached bring good news: “Probabilistic arguments, to the effect that persons of type A, or with condition B, are in general more likely to commit act X, or fail to commit act Y, hold little or no sway in the process of determining guilt.” And this seems unlikely to change in the likely future, despite the growing numbers of books and magazine articles saying that it will.

Opponents of the disease model of addiction and other mental disorders are shocked, absolutely shocked, at the proliferation of “neuro” this and “neuro” that, particularly in the fields of advertising and self-improvement, where neurotrainers and neuroenhancing potions are the talk of the moment. Sociologists claim to see some new and sinister configuration of personhood, where a journalist might just see a pile of cheesy advertising and a bunch of fast-talking science hucksters maneuvering for another shot at the main chance. When has selling snake oil ever been out of fashion?

For harm reductionists, addiction is sometimes viewed as a learning disorder. This semantic construction seems to hold out the possibility of learning to drink or use drugs moderately after using them addictively. The fact that some non-alcoholics drink too much and ought to cut back, just as some recreational drug users need to ease up, is certainly a public health issue—but one that is distinct in almost every way from the issue of biochemical addiction. By concentrating on the fuzziest part of the spectrum, where problem drinking merges into alcoholism, we’ve introduced fuzzy thinking with regard to at least some of the existing addiction research base. And that doesn’t help anybody find common ground.

Graphics Credit: http://www.docslide.com/disease-model/

Saturday, June 28, 2014

Vitamin C and Pregnant Women Who Smoke


Improving pulmonary function in newborns.

500 mg of daily vitamin C given to pregnant smoking women “decreased the effects of in-utero nicotine” and “improved measures of pulmonary function” in their newborns, according to a study  by Cindy T. McEvoy and others at the Oregon Health and Science University in Portland, published in a recent issue of the Journal of the American Medical Association (JAMA).

Researchers have long known that smoking during pregnancy can harm the respiratory health of newborns. Maternal smoking during pregnancy can interfere with normal lung development, resulting in lifelong increases in asthma risk and other pulmonary complications. The researchers note that “more than 50% of smokers who become pregnant continue to smoke, corresponding to 12% of all pregnancies.” That adds up to a lot of newborns each year who will start off with more wheezing, respiratory infections, and childhood asthma than their counterparts born to non-smoking mothers.

McEvoy and her colleagues wanted to find out whether a daily dose of vitamin C would improve the results of pulmonary function tests in newborns exposed to tobacco in utero.

It did. In an accompanying editorial, Graham L. Hall calls the randomized, double-blind, placebo-controlled clinical trial “well-conceived and executed…. Lung function during the first week of life was statistically significantly better (by approximately 10%) among infants born to mothers randomized to receive Vitamin C compared with infants born to mothers randomized to received placebo.” Moreover, the prevalence of wheezing in the first year was reduced from 40% in the placebo group to 21% in the Vitamin C group.

The decreases in asthma and wheezing in the Vitamin C newborns were documented through the first year of life. 

A 10% reduction does not sound like a lot, but, as Hall writes, “small population-level changes in lung function may lead to significant public health benefits, and the improvements in lung function reported here could be associated with future benefit.”

In their paper, the researchers conclude: “Vitamin C supplementation in pregnant smokers may be an inexpensive and simple approach (with continued smoking cessation counseling) to decrease some of the effects of smoking in pregnancy on newborn pulmonary function and ultimately infant respiratory morbidities, but further study is required.”

Pregnant women should not smoke, and quitting is by far the healthiest option.  As Hall writes: “By preventing her developing fetus and newborn infant from becoming exposed to tobacco smoke, a pregnant woman can do more for the respiratory health and overall health of her child than any amount of vitamin C may be able to accomplish.”

McEvoy C.T.,  Nakia Clay,  Keith Jackson,  Mitzi D. Go,  Patricia Spitale,  Carol Bunten,  Maria Leiva,  David Gonzales,  Julie Hollister-Smith &  Manuel Durand &  (2014). Vitamin C Supplementation for Pregnant Smoking Women and Pulmonary Function in Their Newborn Infants, JAMA, 311 (20) 2074. DOI: http://dx.doi.org/10.1001/jama.2014.5217

Graphics Credit: http://www.quitguide.com/


Friday, June 27, 2014

Gone in June


Alcohol takes a friend.

What good does it do: You write about addiction, research it, think about it, formulate new ideas about it. You try to be of service.

What good does it do: One of your best friends ever, a talented writer you have talked to and argued with and smoked with and paddled with for more than two decades, lies dead this morning of alcohol-related liver failure at 62.

What good does it do: I couldn’t save him, couldn’t turn the head of that runaway horse, not through encouragement, shame, praise, incentive, disgust, indifference, furious anger. Not through any of that.

What good does it do: His doctor, with my help, presented a program of 30-day detox and Ativan for the rough parts. He ordered the pills, never picked them up at the pharmacy. He never went back to the doctor, claiming a lack of health insurance. He never quit. He tried, like so many deluded alcoholics, to cut back on his drinking. He kept the phone number for the local AA group in a desk drawer, but never called. When his girlfriend told him it was either her or the bottle, he picked the bottle.

What good does it do: We cajoled, we watched him, we tripped over bags of empties in the basement and he didn’t care. We couldn’t save him. I couldn’t save him. I know more about alcoholism than most addiction therapists, and I couldn’t save him. I saved myself, 25 years ago, but could not save him.

What good does it do: I don’t know how to treat alcoholism, and save alcoholics, and neither do you. And if anybody tells me today, the day of my friend’s death, that alcoholism is a lifestyle choice, I promise to throw a swift right cross and knock them out on the spot.

The only possible light on the horizon is continued scientific research aimed at better elucidating the mechanisms behind addiction. Without that, one idea is about as good as another.

Sunday, June 15, 2014

NIDA’s Dark View of Teen Marijuana Use


Federal study also discusses medical marijuana.

Considering the impasse on marijuana policy between state and federal governments in the U.S., the primary government agency in charge of drug research—NIDA, the National Institute on Drug Abuse—would seem to be caught between a rock and a hard place. Neuroscientists and other marijuana investigators who do research under NIDA grants have a fine line to walk in their efforts to disseminate research findings on cannabis.

From a public health point of view, NIDA is expected to keep up the pressure against drug legalization, or at least keep out of the fight, while also researching the medical pros and cons of cannabis. So it was with some interest that drug policy officials took in a recent article in the New England Journal of Medicine by NIDA director Nora Volkow titled “Adverse Health Effects of Marijuana Use.”

While the press has understandably centered on the risk of marijuana use among teens, which is the focus of the study, the report also contains some surprising admissions about marijuana’s health benefits as well as its addictive potential.

The teen risk emphasis comes from recent studies on two fronts—impaired driving and impaired brain function. The first is seriously confounded by dual use with alcohol, and the second is based, at least in part, on a controversial long-term study showing that marijuana use in the early years demonstrably lowers adult IQs.

No one would suggest that heavy marijuana smoking is good for developing teen brains, and there is sufficient evidence to worry about impairment to memory and to certain so-called “executive” cognitive functions. It is not clear how lasting these effects can be, but lead author Volkow is confident enough to say in a prepared statement that “Physicians in particular can play a role in conveying to families that early marijuana use can interfere with crucial social and developmental milestones and can impair cognitive development.” 

That these negative effects can be the outcome of heavy pot smoking in the teen years seems established beyond reasonable doubt. The extent and duration of these negative outcomes remain the topic of vociferous debate—although it is increasingly clear that the body’s endogenous cannabinoid system plays a key role in synapse formation during early brain development.

Meanwhile, the report re-emphasized the fact that marijuana is an addictive drug for some users—a fact that should not need re-emphasizing, but, lamentably, does. As Volkow and her co-authors write: “The evidence clearly indicates that long-term marijuana use can lead to addiction. Indeed, approximately 9% of those who experiment with marijuana will become addicted.”

Moreover, as regular readers of Addiction Inbox already know, “there is also recognition of a bona fide cannabis withdrawal syndrome (with symptoms that include irritability, sleeping difficulties, dysphoria, craving, and anxiety), which makes cessation difficult and contributes to relapse.” And, in line with the report’s overall theme, “those who begin in adolescence are approximately 2 to 4 times as likely to have symptoms of cannabis dependence within 2 years after first use.”

To their credit, the investigators decline to endorse the claim that marijuana use exacerbates or initiates episodes of illness in patients with schizophrenia and other psychoses, noting that “it is inherently difficult to establish causality in these types of studies because factors other than marijuana use may be directly associated with the risk of mental illness.” Furthermore, while early marijuana use is associated with an increased risk of dropping out of school, “reports of shared environmental factors that influence the risks of using cannabis at a young age and dropping out of school suggest that the relationship may be more complex…. The relationship between cannabis use by young people and psychosocial harm is likely to be multifaceted, which may explain the inconsistencies among studies.”

Indeed. The report also declares that the effects of long-term pot smoking on the risk of lung cancer are “unclear,” and that “the smoking of cigarettes containing both marijuana and tobacco products is a potential confounding factor with a prevalence that varies dramatically among countries.”

In conclusion, the strict demands of causality mean that the long-term effect of chronic marijuana exposure is not known with any certainty. It is possible, even likely, that these effects can vary dramatically from one smoker to another. But the equally persuasive demands of common sense dictate that inhaling dried, super-heated vegetable matter on a regular basis is likely to degrade your health, the more so if you are young and healthy to begin with.

As for other health issues: “The authoritative report by the Institute of Medicine, Marijuana and Medicine, acknowledges the potential benefits of smoking marijuana in stimulating appetite, particularly in patients with the acquired immunodeficiency syndrome (AIDS) and the related wasting syndrome, and in combating chemotherapy-induced nausea and vomiting, severe pain, and some forms of spasticity. The report also indicates that there is some evidence for the benefit of using marijuana to decrease intraocular pressure in the treatment of glaucoma.”

A detailed section titled “Clinical Conditions with Symptoms That May Be Relieved by Treatment with Marijuana or other Cannabinoids” brought additional research to light:

—Glaucoma: “More research is needed to establish whether molecules that modulate the endocannabinoid system may not only reduce intraocular pressure but also provide a neuroprotective benefit in patients with glaucoma.”

—Nausea: “THC is an effective antiemetic agent in patients undergoing chemotherapy, but patients often state that marijuana is more effective in suppressing nausea…. Paradoxically, increased vomiting (hyperemesis) has been reported with repeated marijuana use. [See various blog posts by Drugmonkey and me, starting with this and this.]

—AIDS-associated conditions: “Smoked or ingested cannabis improves appetite and leads to weight gain and improved mood and quality of life among patients with AIDS.”

—Chronic pain: “Studies have shown that cannabinoids acting through central CB1 receptors, and possibly peripheral CB1 and CB2 receptors, play important roles in… various models of pain. These findings are consistent with reports that marijuana may be effective in ameliorating neuropathic pain, even at very low levels of THC.”

—Inflammation: “Cannabinoids (e.g., THC and cannabidiol) have substantial anti-inflammatory effects…. Animal models have shown that cannabidiol is a promising candidate for the treatment of rheumatoid arthritis and for inflammatory diseases of the gastrointestinal tract (e.g., ulcerative colitis and Crohn’s disease).”

—Multiple sclerosis: “Nabiximols (Sativex, GW Pharmaceuticals), an oromucosal spray that delivers a mix of THC and cannabidiol, appears to be an effective treatment for neuropathic pain, disturbed sleep, and spasticity in patients with multiple sclerosis. Sativex… is currently being reviewed in phase 3 trials in the United States in order to gain approval from the Food and Drug Administration.”

—Epilepsy: In a recent small survey of parents who use marijuana with a high cannabidiol content to treat epileptic seizures in their children, 11% reported completed freedom from seizures…. Although such reports are promising, insufficient safety and efficacy data are available on the use of cannabis botanical for the treatment of epilepsy. However, there is increasing evidence of the role of cannabidiol as an antiepileptic agent in animal models.”

Volkow N.D., Baler R.D., Compton W.M. & Weiss S.R.B.  Adverse health effects of marijuana use., The New England journal of medicine,    PMID:

Monday, June 2, 2014

Tripling the Tax on Alcohol


Would it do any good?

A recent article in Slate by Reihan Salam, a sort of modest proposal on behalf of a big boost in alcohol excise taxes, caught considerable flack from free market advocates and conservative bloggers last week.

Salam says Americans agree on the fact that marijuana is not as dangerous a drug as alcohol, and that this agreement offers us an opportunity to “regulate alcohol more stringently than we regulate marijuana.” In fact, Salam argues, why not push the envelope: “Raise the alcohol tax to a point just shy of where large numbers of people will start making moonshine in their bathtubs.”

Salam tries to head off some of the usual criticisms by noting that Prohibition was an unmitigated disaster, but that “what most of us forget is that the movement for Prohibition arose because alcohol abuse actually was destroying American society in the first decades of the 20th Century," and that companies like Anheuser Busch and MillerCoors are plotting with national retail chains as you read this, scheming to make alcohol as cheap and easy to buy as humanly possible.

Salam further justifies a tripling of alcohol taxes by viewing it as a tactical offset to the efforts of liquor companies to focus on their best customers: “the small minority of people who drink the most.” Salam says that right now, it costs about two bucks per inebriated hour to get your drink on. Can we really argue that this price level is just too unsustainably high? Drug expert Mark Kleiman, Professor of Public Policy at UCLA, agrees.  In his book Marijuana Legalization: What Everyone Needs to Know, Kleiman and co-authors argue that “tripling the tax would raise the price of a drink by 20 percent and reduce the volume of drinking in about the same proportion. Most of the reduced drinking would come from heavy drinkers, both because they dominate the market in volume terms and because their consumption is more price-sensitive…."

Minnesota legislators recently passed a bill that opponents say would increase state excise taxes on alcoholic beverages to six times the current levels. Supporters of the alcohol tax say it means an extra $200 million per year to the state, at a cost to drinkers of about seven cents per drink. Or, in Salam's example: “Charging two-drink-per-day drinkers an extra $12 per month seems like a laughably small price to pay to deter binge drinking…. If you’re going to tax tanning beds and sugary soft drinks, why on earth wouldn’t you raise alcohol taxes too?”

Why wouldn’t you? Because it doesn’t accomplish what you want to accomplish, writes Michelle Minton at openmarket.org, the blog of the Competitive Enterprise Institute.  After a bit of throat clearing about the Nanny State, Minton writes that “fortunately, a society’s relationship with alcohol isn’t based solely on the price of alcohol…. Research shows that alcohol price is not an effective means of achieving lower total consumption or reducing binge drinking.” As evidence, Minton points to studies showing that Luxembourg and the Czech Republic “have both the highest priced alcohol and the highest rates of consumption in Europe.”

As for a comparison favored by Salam—New York’s anti-smoking campaign—Minton admits that the new higher cost of cigarettes cut the adult smoking rate dramatically, but points out that “New York is now the number-one market for smuggled cigarettes—which account for more than half of all cigarettes smoked in the state.” This is a powerful argument. If we triple the taxes on alcohol, do we risk a black market of dangerous home-brew bootlegger booze?

In my view, such threats are real, but they are theoretical. The current costs of alcohol in socioeconomic terms are enormous and undeniable. Tripling the alcohol tax might be asking for trouble, but we could get there in stages if Americans saw it as a desirable goal. Arguments against tax increases tend to ignore the fact that alcohol is a different kind of product, capable of addicting a significant minority of users, in addition to killing a certain percentage of drinkers outright through alcohol poisoning and traffic accidents. If we ignore the issue of drug dependence, and the health and legal costs of assorted alcohol-related mayhem, and simply lean on the fact that most people who drink use alcohol responsibly, then it gets easier to argue against increases in alcohol and cigarette taxes. Alcohol is not like other household products, and needn't be regulated like them.

Monday, May 26, 2014

Smoking Is Over If You Want It


Happy World No Tobacco Day

It’s one of the annual days of note concocted by the World Health Organization (WHO). The motive is undeniably noble, and the goofy negative title makes it a favorite of mine: Saturday, May 31, is the annual World No Tobacco Day.

This year, WHO and its partner organizations around the world are focusing on the economics of the global tobacco trade by urging nations to raise taxes on tobacco products. Raising taxes has two potential effects: It drives down consumption and it provides revenue for government health spending on tobacco-related illness and prevention. This latter concern will only grow in the U.S., as the aging boomer cohort reaches the decade of maximum ravagement from smoking-related diseases.

A tax increase that boosts the price of tobacco by 10% “decreases tobacco consumption by about 4% in high-income countries and by up to 8% in most low- and middle-income countries,” according to the organization. And this sweetener: “The World Health Report 2010 indicated that a 50% increase in tobacco excise taxes would generate a little more than US$ 1.4 billion in additional funds in 22 low-income countries. If allocated to health, government health spending in these countries could increase by up to 50%.”

What is the alternative? A bleak epidemic that will be killing more than 8 million people every year by 2030. “More than 80% of these preventable deaths will be among people living in low-and middle-income countries,” says WHO. The tax hammer is not as widely used for tobacco control as common sense might suggest. WHO says that “only 32 countries, less than 8% of the world's population, have tobacco tax rates greater than 75% of the retail price.” Even so, tobacco tax revenues are on average 175 times higher than spending on tobacco control, WHO data shows.

WHO also urges continued ad bans as a means of lowering consumption. “Only 24 countries, representing 10% of the world’s population, have completely banned all forms of tobacco advertising, promotion and sponsorship. Around one country in three has minimal or no restrictions at all on tobacco advertising, promotion and sponsorship.”

For more info, write the WHO Media Centre at mediainquiries@who.int.


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