Posts tagged addiction
Articles and news from the latest research reports.
Study uncovers surprising differences in brain activity of alcohol-dependent women
A new Indiana University study that examines the brain activity of alcohol-dependent women compared to women who were not addicted found stark and surprising differences, leading to intriguing questions about brain network functions of addicted women as they make risky decisions about when and what to drink.
The study used functional magnetic resonance imaging, or fMRI, to study differences between patterns of brain network activation in the two groups of women. The findings indicate that the anterior insular region of the brain may be implicated in the process, suggesting a possible new target of treatment for alcohol-dependent women.
"We see that the network dynamics of alcohol-dependent women may be really different from that of healthy controls in a drinking-related task," said Lindsay Arcurio, a graduate student in the Department of Psychological and Brain Sciences. "We have evidence to suggest alcohol-dependent women have trouble switching between networks of the brain."
The research is part of a larger new effort to understand the differences between men and women with respect to alcohol. Arcurio said most of the research on alcohol dependence has been conducted with men or groups of men and women. Yet several factors make looking at women “really important.”
One such factor is that the physiological effects of drinking alcohol, which include liver damage, heart disease or breast cancer, set in much earlier in women than in men. For this reason, the suggested limit on the number of drinks per week that women can safely consume is eight, whereas for men, it is 14. Secondly, binge-drinking in women is on the rise. One in five adolescent girls is binge-drinking three times a month. In women between the ages of 18 and 54, that number is one in eight.
A ‘sledgehammer’ approach to defining differences in brain network activation
Research on decision-making mechanisms in alcohol-dependent individuals typically involves a general risk-taking situation in which money or points are at stake. In this study, participants were placed in the fMRI brain scanner and asked to consider low-risk and high-risk situations specifically related to alcohol — what the researchers describe as “ecological” tasks. Participants were then asked to make decisions regarding control stimuli — food as well as a presumably neutral stimuli, a stapler — to observe whether risky behavior was greater with respect to drinking than with these other items. The same picture cues were used to present high-risk and low-risk scenarios, and these two extremes were as follows:
For the low-risk situation, participants were told: Imagine you are at a bar. You are offered a drink, already paid for, with two shots of alcohol, and you have a safe ride home. For the high-risk, they were told: You are at a bar and are offered a drink already paid for, with six shots of alcohol, but you do not have a safe ride home.
The reason for such an extreme contrast between the two situations, Arcurio said, is that “as one of the first ecological tasks used in the scanner, we wanted to take a sledgehammer approach to really find the differences between cases that are definitely high-risk and those that are definitely low-risk.”
The findings, however, reflect an equally sharp contrast in differences between the brain network activation in alcohol-dependent women versus the controls.
For the control group, high-risk decisions to drink led to the deactivation of regions associated with “approach behavior,” deciding to take the drink in a risky situation. Conversely, women in the control group activate regions associated with the default mode network, a region traditionally thought to involve resting-state behavior or inactive or relaxed mental state, but which some now speculate plays a role in conceptualizing one’s future.
"It gets really interesting," Arcurio said, "comparing this pattern of activation to those in alcohol-dependent women, who behaviorally say they’re more likely to take the high-risk drink compared to the controls. They don’t deactivate anything. In contrast to the controls, alcohol-dependent women activate all three regions in question. They activate regions associated with reward (which release dopamine). They also activate frontal control regions involved in cognitive control and regions associated with the default mode network, involved in resting-state behavior. They are activating everything."
The investigators infer from these findings that alcohol-dependent women have trouble switching between networks. Being unable to activate one region and deactivate another in response to an alcohol-related situation means they are unable to use one strategy over another.
Furthermore, Arcurio said, “a lot of evidence suggests that switching between networks is influenced by the anterior insular and anterior cingulate regions of the brain, and we did find major differences in the insula between the alcohol-dependent women and controls. We’re thinking the issue is pinpointed to that region.”
The researchers are now running analyses to test the hypothesis that the insula helps in this process, which could offer new possibilities for intervention, with both behavioral therapy and medication.
The research is part of a whole research program, both planned and in the works, to further explore the questions about risky decision-making in alcohol-dependent women: studies of adolescent drinking, risky sexual behavior in alcohol-dependent women, the interaction of visual networks with decision-making networks, as well as the way music (or auditory networks) interacts with decision-making mechanisms in alcohol-dependent women. In the latter experiment, college-age participants choose a song that they associate with drinking and one with quiet reflection.
"There’s a lot of Miley Cyrus in the first category," Arcurio said.
(Source: news.indiana.edu)
Molecule discovered that protects the brain from cannabis intoxication
Two INSERM research teams led by Pier Vincenzo Piazza and Giovanni Marsicano (INSERM Unit 862 “Neurocentre Magendie” in Bordeaux) recently discovered that pregnenolone, a molecule produced by the brain, acts as a natural defence mechanism against the harmful effects of cannabis in animals. Pregnenolone prevents THC, the main active principle in cannabis, from fully activating its brain receptor, the CB1 receptor, that when overstimulated by THC causes the intoxicating effects of cannabis. By identifying this mechanism, the INSERM teams are already developing new approaches for the treatment of cannabis addiction.
These results are to be published in Science on 3 January.
Over 20 million people around the world are addicted to cannabis, including a little more than a half million people in France. In the last few years, cannabis addiction has become one of the main reasons for seeking treatment in addiction clinics. Cannabis consumption is particularly high (30%) in individuals between 16 to 24 years old, a population that is especially susceptible to the harmful effects of the drug.
While cannabis consumers are seeking a state of relaxation, well-being and altered perception, there are many dangers associated to a regular consumption of cannabis. Two major behavioural problems are associated with regular cannabis use in humans: cognitive deficits and a general loss of motivation. Thus, in addition to being extremely dependent on the drug, regular users of cannabis show signs of memory loss and a lack of motivation that make quite hard their social insertion.
The main active ingredient in cannabis, THC, acts on the brain through CB1 cannabinoid receptors located in the neurons. THC binds to these receptors diverting them from their physiological roles, such as regulating food intake, metabolism, cognitive processes and pleasure. When THC overstimulates CB1 receptors, it triggers a reduction in memory abilities, motivation and gradually leads to dependence.
Increase of dopamine release
Developing an efficient treatment for cannabis addiction is becoming a priority of research in the fiend of drug addiction.
In this context, the INSERM teams led by Pier Vincenzo Piazza and Giovanni Marsicano have investigated the potential role of pregnenolone a brain produced steroid hormone. Up to now, pregnenolone was considered the inactive precursor used to synthesize all the other steroid hormones (progesterone, estrogens, testosterone, etc.). The INSERM researchers have now discovered that pregnenolone has quite an important functional role: it provide a natural defence mechanism that can protect the brain from the harmful effects of cannabis.
Essentially, when high doses of THC (well above those inhaled by regular users) activate the CB1 cannabinoid receptor they also trigger the synthesis of pregnenolone. Pregnenole then binds to a specific site on the same CB1 receptors (see figure) and reducing the effects of THC.
The administration of pregnenolone at doses that increase the brain’s level of this hormone even more, antagonize the behavioral effects of cannabis.
At the neurobiological level, pregnenolone greatly reduces the release of dopamine triggered by THC. This is an important effect, since the addictive effects of drugs involve an excessive release of dopamine.
This negative feedback mediated by pregnenolone (THC is what triggers the production of pregnenolone, which then inhibits the effects of THC) reveal a previously unknown endogenous mechanism that protects the brain from an over-activation of CB1 receptor.
A protective mechanism that opens the doors to a new therapeutic approach.
The role of pregnenolone was discovered when, rats were given equivalent doses of cocaine, morphine, nicotine, alcohol and cannabis and the levels of several brain steroids (pregnenolone, testosterone, allopregnenolone, DHEA etc..) were measured. It was then found that only one drug, THC, increased brain steroids and more specifically selectively one steroid, pregnenolone, that went up3000% for a period of two hours.
The effect of administering THC on the pregnenolone synthesis (PREG) and other brain steroids
This increase in pregnenolone is a built-in mechanism that moderates the effects of THC. Thus, the effects of THC increase when pregnenolone synthesis is blocked. Conversely, when pregnenolone is administered to rats or mice at doses (2-6 mg/kg) that induce even greater concentrations of the hormone in the brain, the negative behavioural effects of THC are blocked. For example, the animals that were given pregnenolone recover their normal memory abilities, are less sedated and less incline to self-administer cannabinoids.
Experiments conducted in cell cultures that express the human CB1 receptor confirm that pregnenolone can also counteract the molecular action of THC in humans.
Pier Vincenzo Piazza explains that pregnenolone itself cannot be used as a treatment “Pregnenolone cannot be used as a treatment because it is badly absorbed when administerd orally and once in the blood stream it is rapidly transformed in other steroids”.
However, the researcher says that there is strong hope of seeing a new addiction therapy emerge from this discovery. “We have now developed derivatives of pregnenolone that are well absorbed and stable. They then present the characteristics of compounds that can be used as new class of therapeutic drugs. We should be able to begin clinical trials soon and verify whether we have indeed discovered the first pharmacological treatment for cannabis dependence.”
Silencing Synapses: Research Team Finds Hope for Pharmacological Solution to Cocaine Addiction
Imagine kicking a cocaine addiction by simply popping a pill that alters the way your brain processes chemical addiction. New research from the University of Pittsburgh suggests that a method of biologically manipulating certain neurocircuits could lead to a pharmacological approach that would weaken post-withdrawal cocaine cravings. The findings have been published in Nature Neuroscience.
Researchers led by Pitt neuroscience professor Yan Dong used rat models to examine the effects of cocaine addiction and withdrawal on nerve cells in the nucleus accumbens, a small region in the brain that is commonly associated with reward, emotion, motivation, and addiction. Specifically, they investigated the roles of synapses—the structures at the ends of nerve cells that relay signals.
When an individual uses cocaine, some immature synapses are generated, which are called “silent synapses” because they send few signals under normal physiological conditions. After that individual quits using cocaine, these “silent synapses” go through a maturation phase and acquire the ability to send signals. Once they can send signals, the synapses will send craving signals for cocaine if the individual is exposed to cues that previously led him or her to use the drug.
The researchers hypothesized that if they could reverse the maturation of the synapses, the synapses would remain silent, thus rendering them unable to send craving signals. They examined a chemical receptor known as CP-AMPAR that is essential for the maturation of the synapses. In their experiments, the synapses reverted to their silent states when the receptor was removed.
“Reversing the maturation process prevents the intensification process of cocaine craving,” said Dong, the study’s corresponding author and assistant professor of neuroscience in Pitt’s Kenneth P. Dietrich School of Arts and Sciences. “We are now developing strategies to maintain the ‘reversal’ effects. Our goal is to develop biological and pharmacological strategies to produce long-lasting de-maturation of cocaine-generated silent synapses.”
(Source: news.pitt.edu)
Synthetic alcohol substitute could eliminate health risks – and hangovers
A drug that mimics some effects of alcohol but lacks its harmful properties would have real benefit for public health, a leading scientist has argued.
Professor David Nutt, the Edmond J. Safra Professor of Neuropsychopharmacology at Imperial College London, has identified candidate molecules that reproduce the pleasurable effects of alcohol but are much less toxic. He is looking for investors to help develop the product and bring it to the market.
Alcohol mimics a chemical called GABA which is produced in the brain, but it also acts on receptors for other brain chemicals. The alcohol substitute would be designed to target GABA receptors very selectively, avoiding undesirable side effects such as hangovers and loss of coordination. An antidote could also be made to block the receptor, allowing drinkers to sober up quickly.
Professor Nutt told the Today programme on BBC Radio 4 that he first tested such a compound many years ago, but even better substitutes could be developed.
“There’s no question that you can produce a whole range of effects like alcohol by manipulating this system in the brain,” he said. “In some experiments, the effect is indistinguishable from alcohol.
“What we want to do is get rid of any the unwanted effects of inebriation, like aggression and memory impairment, and we just want to keep the pleasure and the sense of relaxation.
“We think by clever molecular modelling we can get rid of the risk of addiction as well.”
Professor Nutt hopes to make a range of cocktails containing his synthetic alcohol substitute. He has spoken to investors about taking the product to market, but many are wary that the drug might be controlled by legislation.
“I would like the government to make a recommendation that we try to improve on the health of our people by allowing these kind of substitute alcohols to be legal.”
Alcohol is responsible for 2.5 million deaths worldwide each year. Making safer alternatives available could reduce the harms significantly, Professor Nutt argued.
“I think this would be a serious revolution in health benefits, just as the e-cigarette is going to revolutionise the smoking of tobacco. I find it weird that we haven’t been talking about this before because it’s such an obvious target for health improvement.”
(Source: www3.imperial.ac.uk)
Scientists reduce behaviours associated with problem gambling in rats
With the help of a rat casino, University of British Columbia brain researchers have successfully reduced behaviours in rats that are commonly associated with compulsive gambling in humans.
The study, which featured the first successful modeling of slot machine-style gambling with rats in North America, is the first to show that problem gambling behaviours can be treated with drugs that block dopamine D4 receptors. The findings have been published in Biological Psychiatry journal.
“More work is needed, but these findings offer new hope for the treatment of gambling addiction, which is a growing public health concern,” says Paul Cocker, lead author of the study and a PhD student in UBC’s Dept. of Psychology. “This study sheds important new light on the brain processes involved with gambling and gambling addictions.”
For the study, rats gambled for sugar pellets using a slot machine-style device that featured three flashing lights and two levers they could push with their paws. The rats exhibited several behaviours associated with problem gambling such as the tendency to treat “near misses” similar to wins.
Building on previous research, the team focused on the dopamine D4 receptor, which has been linked to a variety of behavioural disorders, but never proven useful in treatment. The study found that rats treated with a dopamine D4 receptor-blocking medication exhibited reduced levels of behaviours associated with problem gambling.
While findings suggest that blocking the D4 dopamine receptor may help to reduce pathological gambling behaviours in humans, the researchers note that further research is needed before the drugs can be considered a viable pharmaceutical treatment for pathological gambling in humans.
BACKGROUND
“Pathological gambling is increasingly seen as a behavioural addiction similar to drug or alcohol addiction, but we know comparatively little about how to treat problem gambling,” says Cocker. “Our study is the first to show that by blocking these receptors we might be able to reduce the rewarding aspects of near-misses that appear to be important in gambling.”
Methods: In the 16-month study,a cohort of 32 laboratory rats responded to a series of three flashing lights before choosing between two levers. One combination of lights (all lights illuminated) signaled a win and seven combinations (zero, one or two lights) signaled a loss. A “cash-out” lever rewarded the rat with 10 sugar pellets on winning trials, but gave a 10-second “time out” penalty on losing trails. The “roll again” lever allowed the rats to begin a new trial without penalty, but provided no sugar pellets.
Interestingly, the rats showed a tendency towards choosing the cash-out lever when two lights (near-miss) illuminated, suggesting that rats, like people, are susceptible to the near-miss effect. By blocking the D4 receptors with drugs, the researchers were successfully able to reduce the rat’s choice of the “cash-out” lever on non-winning trials.
The D4 blocker drug used in the study has previously been tested on humans in attempts to treat behaviour disorders like schizophrenia but appeared to have no effect.
Near misses: This common cognitive bias is considered an important factor in the development of pathological gambling problems. The fact that slot machines tend to have a relatively high proportion of near-misses in comparison to other gambling games may be the reason that slot machines are such a particularly addictive form of gambling.
Study authors: Paul Cocker and Prof.Catharine Winstanley (UBC Dept. of Psychology), Bernard Le Foll (University of Toronto, Centre for Addiction and Mental Health) and Robert D. Rogers (Bangor University). The study, A Selective Role for Dopamine D4 Receptors in Modulating Reward Expectancy in a Rodent Slot Machine Task, is available upon request.
UBC’s Laboratory of Molecular and Behavioural Neuroscience, led by Psychology Prof. Catharine Winstanley, focuses on understanding the biological mechanisms of functions such as impulse control and gambling, leading to new and improved treatments for disorders like attention deficit hyperactivity disorder, bipolar disorder, personality disorders, and drug addiction.
Problem gambling: Compulsive gambling affects between three and five percent of North Americans, according to recent statistics.
New study shows promise for first effective medicine to treat cocaine dependence
New research published in JAMA Psychiatry reveals that topiramate, a drug approved by the U.S. Food and Drug Administration (FDA) to treat epilepsy and migraine headaches, also could be the first reliable medication to help treat cocaine dependence.
The study, led by Bankole A. Johnson, DSc. MD., MB.ChB., MPhil., chairman of the Department of Psychiatry at the University of Maryland School of Medicine and head of the School’s new Brain Science Research Consortium Unit, with support from the National Institutes of Health and Agency for Healthcare Research and Quality, is one of the first to establish a pharmacological treatment for cocaine addiction, for which there are currently no FDA-approved medications.
Addiction affects 13.2 to 19.7 million cocaine users worldwide. Cocaine is responsible for more U.S. emergency room visits than any other illegal drug. Cocaine harms the brain, heart, blood vessels, and lungs — and can even cause sudden death.
Professor Johnson, one of the nation’s leading neuroscientists and psychopharmacologists, had previously found that topiramate was a safe and effective treatment for alcohol dependence compared with placebo.
In releasing the new study, Professor Johnson, who conducted the research when he was with Department of Psychiatry and Neurobehavioral Sciences at the University of Virginia, provided full disclosures, which follow the text of this news announcement.*
The study enrolled 142 participants, aged 18 years or older, seeking treatment for cocaine dependence. Following enrollment, participants were randomly assigned into a topiramate group or placebo group. Neither the participants nor the healthcare professionals administering the treatment knew who was in which group (double-blinded study).
Using an intent-to-treat analysis, the researchers found that topiramate was more efficacious than placebo at increasing the participants’ weekly proportion of cocaine nonuse days and in increasing the likelihood that participants would have cocaine-free weeks. Furthermore, compared with placebo, topiramate also was significantly associated with a decrease in craving for cocaine and an improvement in participants’ global functioning.
The study investigators also observed few side effects due to drug treatment. In general, participants in the topiramate group experienced mild side-effects, including abnormal tingling skin sensations, taste distortions, anorexia, and difficulty concentrating.
"Our findings reveal that topiramate is a safe and robustly efficacious medicine for the treatment of cocaine dependence, and has the potential to make a major contribution to the global health crisis of addiction," Professor Johnson said. "However, topiramate treatment also is associated with glaucoma, and higher doses of the drug can increase the risk of side effects; therefore, caution must be exercised when prescribing the drug, especially when given in high doses."
These results build upon earlier work from Professor. Johnson’s group which indicated that individuals dependent on cocaine, but not seeking treatment, who took topiramate were more likely to experience reduced cravings and preference for cocaine, compared with placebo. The findings of the current study indicate that topiramate may be even more effective in treating people with addiction who actively want to quit using cocaine.
"Because topiramate is the first medication to demonstrate a robust therapeutic effect for the treatment of cocaine or alcohol dependence, its fundamental neurochemical effects provide important clues as to common links in the neurobiological basis of the addictive process in general," remarked Professor Johnson. "These findings also add to our understanding of how addiction affects the brain because it demonstrates the unique concept that dual neurotransmitter modulation, by simultaneously augmenting the inhibitory action of gamma amino butyric acid and inhibiting the excitatory effects of glutamate, can result in therapeutic effects that reduce the propensity to use cocaine."
*Editor’s Notes:
A. Statement of Disclosure
Professor Johnson reported serving as a consultant for Johnson & Johnson (Ortho-McNeil Janssen Scientific Affairs, LLC) the manufacturer of topiramate, from 2003-2008 and currently has no affiliation with that Company, Transcept Pharmaceuticals, Inc. from 2006-2008, Eli Lilly and Company from 2009-2010, and Organon from 2007-2010. He currently consults for D&A Pharma, ADial Pharmaceuticals, LLC, (with which he also serves as chairman), and Psychological Education Publishing Company (PEPCo), LLC. Topiramate is currently available as a generic medicine in the USA, and Professor Johnson has no commercial affiliation with any generic manufacturer of topiramate. Dr. Liu reported serving as a consultant for Celladon Corporation. No other disclosures were reported.
B. Funding/ Support
This study was supported by NIH grants 501 DAO17296-04 and 5 RC1AA019274-02, and Agency for Healthcare Research and Quality grant 7 RO1 HS020263092.
Research attributes high rates of smoking among mentally ill to addiction vulnerability
People with mental illness smoke at much higher rates than the overall population. But the popular belief that they are self-medicating is most likely wrong, according to researchers at the Indiana University School of Medicine. Instead, they report, research indicates that psychiatric disease makes the brain more susceptible to addiction.
As smoking rates in the general population have fallen below 25 percent, smoking among the mentally ill has remained pervasive, encompassing an estimated half of all cigarettes sold. Despite the well-known health dangers of tobacco consumption, smoking among the mentally ill has long been widely viewed as “self-medication,” reducing the incentive among health care professionals to encourage such patients to quit.
"This is really a devastating problem for people with mental illness because of the broad health consequences of nicotine addiction," said R. Andrew Chambers, M.D., associate professor of psychiatry at the IU School of Medicine. "Nicotine addiction is the number one cause of premature illness and death in the United States, and most of that morbidity and mortality is concentrated in people with mental illness."
In a report published recently in the journal Addiction Biology, the research team lead by Dr. Chambers reported the results of experiments using an established animal model of schizophrenia in which rats display a neuropsychiatric syndrome that closely resembles the disease.
Both the schizophrenia-model rats and normal rats were given access to intravenous self-administration of nicotine.
"The mentally ill rats acquired nicotine use faster and consumed more nicotine," Dr. Chambers said. "Then when we cut them off from access to nicotine, they worked much harder to restore access to nicotine than did the normal ‘control’ rats."
In additional testing, the researchers found that administration of nicotine provided equal, but minimal, cognitive benefits to both groups of rats when performing a memory test. When the nicotine was withdrawn, however, both groups of rats were more cognitively impaired, so that any cognitive benefits to nicotine administration were “paid for” by cognitive impairments later.
“These results strongly suggest that what has changed in mental illness to cause smoking at such high rates results in a co-morbid addiction to which the mentally ill are highly biologically vulnerable. The evidence suggests that the vulnerability is an involuntary biological result of the way the brain is designed and how it develops after birth, rather than it being about a rational choice to use nicotine as a medicine,” Dr. Chambers said.
The data, he said, point to neuro-developmental mechanisms that increase the risk of addiction. Better understanding of those mechanisms could lead to better prevention and treatment strategies, especially among mentally ill smokers, Dr. Chambers said.
A video interview of Dr. Chambers discussing his research is available here.
(Source: news.medicine.iu.edu)
Seeking new methods to treat heroin addiction
“Heroin itself is an inactive substance,” explains Jørg Mørland, Norwegian forensic medicine and toxicology researcher. “The substances that heroin forms in the body are mainly what enter the brain and cause the narcotic effects.”
The heroin high and feelings of pain relief manifest themselves almost immediately after the drug has been injected. Yet it was shown many years ago that heroin is inactive at the opioid receptors in the brain.
So what is it about heroin that brings about such a pronounced effect? A number of research projects funded under the Programme on Alcohol and Drug Research (RUSMIDDEL) at the Research Council of Norway may help to solve the mystery.
“Gaining a thorough understanding of the effects of heroin and of the neurobiological mechanisms involved will be a valuable basis for the development of new treatments for addiction,” states Jørg Mørland, who is the project manager of an ongoing project on this important subject, the most recent in a long line of such Norwegian projects which he has headed.
Dr Mørland is a senior researcher at the Norwegian Institute of Public Health and Professor emeritus at the University of Oslo. Through studies on rats and mice, he and his colleagues have come up with new findings that may be significant to the development of new treatment methods.
Heroin metabolises rapidly
One widely-held theory has been that heroin passes quickly into the brain where it is converted into morphine, and that what users are actually experiencing are the effects of morphine. As it turns out, however, heroin undergoes a number of important transformations on its way to the brain. Just a few minutes after injection, the conversion of heroin into the metabolite 6-MAM is almost complete.
“Our research shows that it is primarily 6-MAM that crosses the blood-brain barrier and that heroin as such only enters the brain to a small degree. Thirty minutes after injecting heroin, 6-MAM is the predominant substance both in the blood and in the brain,” Dr Mørland explains.
The presence of 6-MAM also results in a sharp increase in the signalling molecule, dopamine, in certain areas of the brain. This plays a pivotal role in the rewarding effect.
“This points towards 6-MAM as the main substance behind all the acute effects of heroin,” says Dr Mørland.
“After about an hour, most of the 6-MAM has been converted into morphine. Morphine acts rapidly on the body and is the dominant component for the next hours, but from six to twelve hours after injection the effects observed are mostly consequences of a metabolite formed from morphine, morphin-6-glucuronide.
Looking for a new treatment
“We are working to understand the roles of all these metabolites and to investigate potential treatments to counter their effects,” Dr Mørland states.
The current approach to treating heroin addiction in Norway is pharmacotherapy – using methadone, subutex or subuxone. These are synthetic substances that all work in the same way as heroin, however, and are addictive in their own right.
“The treatment method involves administering these substances over the course of a day to reduce the rewarding effect. The intent is to diminish the patient’s preoccupation with finding heroin in order to lead a more normal life,” Dr Mørland points out.
Researchers at the Norwegian Centre for Addiction Research (SERAF) in Oslo are examining sustained-release naltrexone – a non-addictive opioid antagonist that blocks the effects of opiates in the brain. Dr Mørland is hopeful that his research will make it possible to affect opiates even before they reach the brain.
An opiate roadblock
“It may be possible to block these substances from ever entering the brain, thereby modifying the effect of heroin,” Dr Mørland adds.
As part of a new project, he and his colleagues will study the effect of a 6-MAM antibody developed by a Norwegian company. The antibody binds to the 6-MAM in the blood, making the 6-MAM molecule too large to cross the blood-brain barrier.
“If we succeed in getting this antibody to work it could block much – and maybe even all – of the effect of heroin,” the researcher concludes.
Researchers Identify Risk-Factors for Addictive Video-Game Use among Adults
New research from the University of Missouri indicates escapism, social interaction and rewards fuel problematic video-game use among “very casual” to “hardcore” adult gamers. Understanding individual motives that contribute to unhealthy game play could help counselors identify and treat individuals addicted to video games.
“The biggest risk factor for pathological video game use seems to be playing games to escape from daily life,” said Joe Hilgard, a doctoral candidate in the Department of Psychological Sciences in the MU College of Arts and Science. “Individuals who play games to get away from their lives or to pretend to be other people seem to be those most at-risk for becoming part of a vicious cycle. These gamers avoid their problems by playing games, which in turn interferes with their lives because they’re so busy playing games.”
Problematic video game use is more than just excessive use of video games; it also includes a variety of unhealthy behaviors, such as lying to others about how much time is spent playing games and missing work or other obligations to play games.
“People who play games to socialize with other players seem to have more problems as well,” Hilgard said. “It could be that games are imposing a sort of social obligation on these individuals so that they have to set aside time to play with other players. For example, in games like World of Warcraft, most players join teams or guilds. If some teammates want to play for four hours on a Saturday night, the other players feel obligated to play or else they may be cut from the team. Those play obligations can mess with individuals’ real-life obligations.”
Problematic video game use isn’t all that different from other types of addictive behavior, such as alcohol or drug abuse, which can be spurred by poor coping strategies, Hilgard said.
“Gamers who are really into getting to the next level or collecting all of the in-game items seem to have unhealthier video-game use,” Hilgard said. “When people talk about games being ‘so addictive,’ usually they’re referring to games like Farmville or Diablo that give players rewards, such as better equipment or stronger characters, as they play. People who are especially motivated by these rewards can find it hard to stop playing.”
Understanding individuals’ motives for playing video games can inform researchers, game developers and consumers about why certain games attract certain individuals, Hilgard said.
“Researchers have suspected that Massively Multiplayer Online Role-Playing Games (MMORPGs) are the most addictive genre of video games,” Hilgard said. “Our study provides some evidence that supports that claim. The games provide opportunities for players to advance levels, to join teams and to play with others. In addition, the games provide enormous fantasy worlds that gamers can disappear into for hours at a time and forget about their problems. MMORPGs may be triple threats for encouraging pathological game use because they present all three risk factors to gamers.”
“Consistent with previous research, we did not find a perfect relationship between total time spent playing games and addictive video game behaviors,” said study co-author Christopher Engelhardt, a postdoctoral research fellow in the Department of Health Psychology in the MU School of Health Professions and the MU Thompson Center for Autism and Neurodevelopmental Disorders. “Additionally, other variables, such as the proportion of free time spent playing video games, seem to better predict game addiction above and beyond the total amount of time spent playing video games.”
The open-access journal, Frontiers in Psychology, published the article, “Individual differences in motives, preferences, and pathology in video games: the gaming attitudes, motives, and experiences scales (GAMES),” earlier in September.
Addiction: Can You Ever Really Completely Leave It Behind?
A new study in Biological Psychiatry suggests the answer is no
It is often said that once people develop an addiction, they can never completely eliminate their attraction to the abused substance. New findings provide further support for this notion by suggesting that even long-term abstinence from cocaine does not result in a complete normalization of brain circuitry.
Scientists are currently trying to answer some of the ‘chicken and egg’ questions surrounding the abuse of drugs. In particular, one of those questions is whether individuals who abuse psychostimulants like cocaine are more impulsive and show alterations in brain reward circuits as a consequence of using the drug, or whether such abnormalities existed prior to their drug use. In the former case, one might expect brain alterations to normalize following prolonged drug abstinence.
To address these questions, Krishna Patel at Institute of Living/Hartford Hospital and colleagues compared neural responses between three groups of people who were asked to complete a task that resembles bidding on eBay items. The 3 groups consisted of 47 healthy controls, 42 currently drug-abusing cocaine users, and 35 former cocaine users who had been abstinent an average of 4 years. They also compared all three groups on their levels of impulsivity and reward responding.
They found that active users showed abnormal activation in multiple brain regions involved with reward processing, and that the abstinent individuals who were previously cocaine dependent manifested differences in a subset of those regions. Both current and former cocaine users displayed similarly elevated impulsivity measures compared to healthy controls, which may indicate that these individuals had a pre-existing risk for addiction. Indeed, the degree of impulsivity correlated with several of the brain activation abnormalities.
These findings suggest that prolonged abstinence from cocaine may normalize only a subset of the brain abnormalities associated with active drug use.
"The knowledge that some neural changes associated with addiction persist despite long periods of abstinence is important because it supports clinical wisdom that recovery from addiction is a lifelong process," says Dr. John Krystal, Editor of Biological Psychiatry. "Further, it is the start of a deeper question: How do these persisting changes develop and how can they be reversed?"
The authors agree that further studies will be needed to investigate such questions, including the continued attempt to determine the extent to which differences in former cocaine users reflect aspects of pre-existing features, exposure to cocaine, or recovery.
(Image: Shutterstock)