or, "kids do the darnedest things"...
KTLA News (Los Angeles)
Dangerous 'Vodka Eyeballing' Popular with College Students
Eyeballing can cause damage to the optic nerve, leading to blindness.
9:11 AM PDT, May 20, 2010
LOS ANGELES -- A dangerous drinking fad known as "Vodka eyeballing" is growing in popularity on college campuses in the UK and the United States, and experts say it could leave students blind.
So-called "eyeballers" claim it's an instant high with a splash of alcohol giving them a buzz, literally, in the blink of an eye.
But, doctors say, it's a dangerous trend that could cause permanent vision damage.
Dr. Elise Brisco of the Hollywood Vision Center told KTLA that the practice creates an almost instant buzz "because it's going into the central nervous system into the brain."
The alcohol can damage the optic nerve, creating spotty vision and even complete blindness.
"If it's severe enough and there's a lot of optic nerve damage, your vision may not return," Brisco said.
Some eyeballers have posted videos of themselves online, and there are even "fan" pages for the practice on Facebook.
It's believed the dangerous trend started in the United States, but it is quickly gaining popularity at British universities, according to the UK Daily Mail.
Tuesday, May 25, 2010
Wednesday, May 19, 2010
Why do you think they call it DOPamine?
More on that infamous substance we all seem to be trying to maximize day to day:
U.S. Department of Health and Human Services
National Institutes of Health
NIH News
National Institute on Alcohol Abuse and Alcoholism (NIAAA) http://www.niaaa.nih.gov
EMBARGOED FOR RELEASE: Tuesday, May 18, 2010 @ 9:00 AM EDT
Contact: NIAAA Press Office, 301-443-3860, NIAAAPressOffice@mail.nih.gov<
Receptor Variant Influences Dopamine Response to Alcohol
A genetic variant of a receptor in the brain’s reward circuitry plays an important role in determining whether the neurotransmitter dopamine is released in the brain following alcohol intake, according to a study led by researchers at the National Institute on Alcohol Abuse and Alcoholism (NIAAA), part of the National Institutes of Health. Dopamine is involved in transmitting the euphoria and other positive subjective effects produced by alcohol.
A report of the findings, which help explain the diverse genetic susceptibility for alcohol use disorders, will appear online in Molecular Psychiatry on May 18, 2010.
“By advancing our understanding of the neurobiology that underlies the addictive properties of alcohol, this finding helps us understand why alcohol affects people in very different ways,” says NIAAA Acting Director Kenneth R. Warren, Ph.D. “This kind of information also aids the development of personalized medications for alcohol problems.”
Receptors for brain molecules known as opioid peptides help initiate the neurochemical reactions that underlie the positive effects produced by alcohol. Activation of the mu-subtype of opioid receptor following alcohol consumption triggers the release of dopamine from the forebrain.
“But there is much variation in alcohol-induced responses that are thought to be related to dopamine,” explains Markus Heilig, M.D., Ph.D., NIAAA clinical director and the study’s senior author. “Previous studies by our group and others suggest that variants of opioid genes may contribute to the observed variation, possibly through effects on alcohol-induced dopamine release.”
He notes, for example, that people who carry the mu-opioid receptor variant designated as 118G report increased euphoria following alcohol consumption. Dr. Heilig’s group has reported that a similar mu-opioid receptor variant in monkeys heightened the stimulating effects of alcohol and increased their alcohol consumption.
In the current study, first author Vijay A. Ramchandani, Ph.D., an investigator in NIAAA’s Laboratory of Clinical and Translational Studies, Dr. Heilig, and their colleagues explored whether the 118G mu-opioid receptor variant influences dopamine release from a forebrain region called the ventral striatum in response to alcohol.
Using human positron emission tomography (PET), an imaging technique that allowed the researchers to analyze dopamine activity in the brain, they compared dopamine release in two groups of people that had been given a dose of alcohol. The groups consisted of those who carried a copy of the gene for the 118G mu-opioid receptor variant, and those who carried only genes for the more common 118A variant. They found that only people with the 118G variant had a dopamine response to alcohol – no such response happened in subjects with the 118A receptor variant.
In a separate experiment, they inserted genes for the human 118G or 118A mu-opioid receptor variants into mice and then directly measured the animals’ dopamine response to a dose of alcohol. Mice with the 118G variant showed a fourfold higher peak dopamine response to the alcohol challenge compared to mice with the 118A variant.
“Taken together, our data strongly support a causal role of the 118G variant of the mu-opioid receptor to confer a more vigorous dopamine response to alcohol in the ventral striatum,” says Dr. Ramchandani. “The findings add further support to the notion that individuals who possess this receptor variant may experience enhanced pleasurable effects from alcohol that could increase their risk for developing alcohol abuse and dependence. It may also explain why these individuals, once addicted, benefit more from treatment with blockers of endogenous opioids.”
Additional Information
Why Meds Work for Some People, but Not for Others<http://nihrecord.od.
NIH Record, 5/14/2010
Alcohol’s effects on endogenous opioids in the brain<http://www.niaaa.nih.
The National Institute on Alcohol Abuse and Alcoholism, part of the National Institutes of Health, is the primary U.S. agency for conducting and supporting research on the causes, consequences, prevention, and treatment of alcohol abuse, alcoholism, and alcohol problems. NIAAA also disseminates research findings to general, professional, and academic audiences. Additional alcohol research information and publications are available at www.niaaa.nih.gov<http://www.
The National Institutes of Health (NIH) — The Nation's Medical Research Agency — includes 27 Institutes and Centers and is a component of the U. S. Department of Health and Human Services. It is the primary Federal agency for conducting and supporting basic, clinical, and translational medical research, and it investigates the causes, treatments, and cures for both common and rare diseases. For more information about NIH and its programs, visit http://www.nih.gov.
U.S. Department of Health and Human Services
National Institutes of Health
NIH News
National Institute on Alcohol Abuse and Alcoholism (NIAAA) http://www.niaaa.nih.gov
EMBARGOED FOR RELEASE: Tuesday, May 18, 2010 @ 9:00 AM EDT
Contact: NIAAA Press Office, 301-443-3860, NIAAAPressOffice@mail.nih.gov<
Receptor Variant Influences Dopamine Response to Alcohol
A genetic variant of a receptor in the brain’s reward circuitry plays an important role in determining whether the neurotransmitter dopamine is released in the brain following alcohol intake, according to a study led by researchers at the National Institute on Alcohol Abuse and Alcoholism (NIAAA), part of the National Institutes of Health. Dopamine is involved in transmitting the euphoria and other positive subjective effects produced by alcohol.
A report of the findings, which help explain the diverse genetic susceptibility for alcohol use disorders, will appear online in Molecular Psychiatry on May 18, 2010.
“By advancing our understanding of the neurobiology that underlies the addictive properties of alcohol, this finding helps us understand why alcohol affects people in very different ways,” says NIAAA Acting Director Kenneth R. Warren, Ph.D. “This kind of information also aids the development of personalized medications for alcohol problems.”
Receptors for brain molecules known as opioid peptides help initiate the neurochemical reactions that underlie the positive effects produced by alcohol. Activation of the mu-subtype of opioid receptor following alcohol consumption triggers the release of dopamine from the forebrain.
“But there is much variation in alcohol-induced responses that are thought to be related to dopamine,” explains Markus Heilig, M.D., Ph.D., NIAAA clinical director and the study’s senior author. “Previous studies by our group and others suggest that variants of opioid genes may contribute to the observed variation, possibly through effects on alcohol-induced dopamine release.”
He notes, for example, that people who carry the mu-opioid receptor variant designated as 118G report increased euphoria following alcohol consumption. Dr. Heilig’s group has reported that a similar mu-opioid receptor variant in monkeys heightened the stimulating effects of alcohol and increased their alcohol consumption.
In the current study, first author Vijay A. Ramchandani, Ph.D., an investigator in NIAAA’s Laboratory of Clinical and Translational Studies, Dr. Heilig, and their colleagues explored whether the 118G mu-opioid receptor variant influences dopamine release from a forebrain region called the ventral striatum in response to alcohol.
Using human positron emission tomography (PET), an imaging technique that allowed the researchers to analyze dopamine activity in the brain, they compared dopamine release in two groups of people that had been given a dose of alcohol. The groups consisted of those who carried a copy of the gene for the 118G mu-opioid receptor variant, and those who carried only genes for the more common 118A variant. They found that only people with the 118G variant had a dopamine response to alcohol – no such response happened in subjects with the 118A receptor variant.
In a separate experiment, they inserted genes for the human 118G or 118A mu-opioid receptor variants into mice and then directly measured the animals’ dopamine response to a dose of alcohol. Mice with the 118G variant showed a fourfold higher peak dopamine response to the alcohol challenge compared to mice with the 118A variant.
“Taken together, our data strongly support a causal role of the 118G variant of the mu-opioid receptor to confer a more vigorous dopamine response to alcohol in the ventral striatum,” says Dr. Ramchandani. “The findings add further support to the notion that individuals who possess this receptor variant may experience enhanced pleasurable effects from alcohol that could increase their risk for developing alcohol abuse and dependence. It may also explain why these individuals, once addicted, benefit more from treatment with blockers of endogenous opioids.”
Additional Information
Why Meds Work for Some People, but Not for Others<http://nihrecord.od.
NIH Record, 5/14/2010
Alcohol’s effects on endogenous opioids in the brain<http://www.niaaa.nih.
The National Institute on Alcohol Abuse and Alcoholism, part of the National Institutes of Health, is the primary U.S. agency for conducting and supporting research on the causes, consequences, prevention, and treatment of alcohol abuse, alcoholism, and alcohol problems. NIAAA also disseminates research findings to general, professional, and academic audiences. Additional alcohol research information and publications are available at www.niaaa.nih.gov<http://www.
The National Institutes of Health (NIH) — The Nation's Medical Research Agency — includes 27 Institutes and Centers and is a component of the U. S. Department of Health and Human Services. It is the primary Federal agency for conducting and supporting basic, clinical, and translational medical research, and it investigates the causes, treatments, and cures for both common and rare diseases. For more information about NIH and its programs, visit http://www.nih.gov.
Wednesday, May 12, 2010
More on "process addictions"
This new study found that the same brain mechanisms that are dysregulated in drug addiction are also dysregulated in binge eating. This is not surprising, of course, since behavior is dysregulated in similar ways in both disorders. That is, the behavior already tells us that the same underlying brain regulatory systems are not working properly, so these studies help confirm what we already suspected. However, these findings are not profound or startling unless one starts with the assumption that behavior can become consistently dysregulated without the corresponding systems in the brain also becoming dysregulated. To put it simply: dysregulated behavior<=>dysregulated brain. In addition, social interactions also have a correlary dysfunction, and there are additional corresonding changes at other levels of analysis, such as gene function, metabolism, and so forth. In other words the system changes at all levels at once. The other thing to keep in mind is that a study such as this does not mean that compulsive behaviors are just and only "brain diseases," since there are correlary changes up and down the system chain of events. It also does not mean the the only appropriate place to intervene is by directly manipulating neurotransmitters, e.g. medication therapy. Although that might be a useful tool, because all of these subsystems are interconnected, it is also possible to change the brain by changing the environment, or to focus on changing behavior and so forth. In addition, the study does not demonstrate that "obese people really cannot help it," or at least it is not news that this is true. We already knew that, with hundreds of studies showing that 95% of weight loss is regained after 5 years. Finally, remember that, as technically impressive as this study is, it is still a short-term study of rodents, and humans are not rodents. Rodent models give us clues, but findings in rodents do not directly translate to humans.
MW
Compulsive Eating Shares Addictive Biochemical Mechanism With Cocaine, Heroin Abuse, Study Shows
ScienceDaily (Mar. 29, 2010) — In a newly published study, scientists from The Scripps Research Institute have shown for the first time that the same molecular mechanisms that drive people into drug addiction are behind the compulsion to overeat, pushing people into obesity.
The new study, conducted by Scripps Research Associate Professor Paul J. Kenny and graduate student Paul M. Johnson, was published March 28, 2010 in an advance online edition of the journal Nature Neuroscience.
The study's startling findings received widespread publicity after a preliminary abstract was presented at a Society for Neuroscience meeting in Chicago last October. Articles heralding the new discovery appeared in news publications around the world, focusing on the point obese patients have been making for years -- that, like addiction to other substances, junk food binging is extremely difficult to stop.
The study goes significantly further than the abstract, however, demonstrating clearly that in rat models the development of obesity coincides with a progressively deteriorating chemical balance in reward brain circuitries. As these pleasure centers in the brain become less and less responsive, rats quickly develop compulsive overeating habits, consuming larger quantities of high-calorie, high-fat foods until they become obese. The very same changes occur in the brains of rats that overconsume cocaine or heroin, and are thought to play an important role in the development of compulsive drug use.
Kenny, a scientist at Scripps Research's Florida campus, said that the study, which took nearly three years to complete, confirms the "addictive" properties of junk food.
"The new study, unlike our preliminary abstract, explains what happens in the brain of these animals when they have easy access to high-calorie, high-fat food," said Kenny. "It presents the most thorough and compelling evidence that drug addiction and obesity are based on the same underlying neurobiological mechanisms. In the study, the animals completely lost control over their eating behavior, the primary hallmark of addiction. They continued to overeat even when they anticipated receiving electric shocks, highlighting just how motivated they were to consume the palatable food."
The scientists fed the rats a diet modeled after the type that contributes to human obesity -- easy-to-obtain high-calorie, high-fat foods like sausage, bacon, and cheesecake. Soon after the experiments began, the animals began to bulk up dramatically.
"They always went for the worst types of food," Kenny said, "and as a result, they took in twice the calories as the control rats. When we removed the junk food and tried to put them on a nutritious diet -- what we called the 'salad bar option' -- they simply refused to eat. The change in their diet preference was so great that they basically starved themselves for two weeks after they were cut off from junk food. It was the animals that showed the "crash" in brain reward circuitries that had the most profound shift in food preference to the palatable, unhealthy diet. These same rats were also those that kept on eating even when they anticipated being shocked."
Lethally Simple
What happens in addiction is lethally simple, Kenny explained. The reward pathways in the brain have been so overstimulated that the system basically turns on itself, adapting to the new reality of addiction, whether its cocaine or cupcakes.
"The body adapts remarkably well to change -- and that's the problem," said Kenny. "When the animal overstimulates its brain pleasure centers with highly palatable food, the systems adapt by decreasing their activity. However, now the animal requires constant stimulation from palatable food to avoid entering a persistent state of negative reward."
After showing that obese rats had clear addiction-like food seeking behaviors, Johnson and Kenny next investigated the underlying molecular mechanisms that may explain these changes. They focused on a particular receptor in the brain known to play an important role in vulnerability to drug addiction and obesity -- the dopamine D2 receptor. The D2 receptor responds to dopamine, a neurotransmitter that is released in the brain by pleasurable experiences like food or sex or drugs like cocaine. In cocaine abuse, for example, the drug alter the flow of dopamine by blocking its retrieval, flooding the brain and overstimulating the receptors, something that eventually leads to physical changes in the way the brain responds to the drug.
The new study shows that the same thing happens in junk food addiction.
"These findings confirm what we and many others have suspected," Kenny said, "that overconsumption of highly pleasurable food triggers addiction-like neuroadaptive responses in brain reward circuitries, driving the development of compulsive eating. Common mechanisms may therefore underlie obesity and drug addiction."
Consistent with common mechanisms explaining addiction and obesity, levels of the D2 dopamine receptors were significantly reduced in the brains of the obese animals, similar to previous reports of what happens in human drug addicts, Kenny noted. Remarkably, when the scientists knocked down the receptor using a specialized virus, the development of addiction-like eating was dramatically accelerated.
"This addiction-like behavior happened almost from the moment we knocked down the dopamine receptors," Kenny noted. "The very next day after we provided access to the palatable food, their brains changed into a state that was consistent with an animal that had been overeating for several weeks. The animals also became compulsive in their eating behaviors almost immediately. These data are, as far as we know, the strongest support for the idea that overeating of palatable food can become habitual in the same manner and through the same mechanisms as consumption of drugs of abuse."
The study was supported by a Bank of America Fellowship, The Margaret Q. Landenberger Research Foundation and the National Institutes of Health.
MW
Compulsive Eating Shares Addictive Biochemical Mechanism With Cocaine, Heroin Abuse, Study Shows
ScienceDaily (Mar. 29, 2010) — In a newly published study, scientists from The Scripps Research Institute have shown for the first time that the same molecular mechanisms that drive people into drug addiction are behind the compulsion to overeat, pushing people into obesity.
The new study, conducted by Scripps Research Associate Professor Paul J. Kenny and graduate student Paul M. Johnson, was published March 28, 2010 in an advance online edition of the journal Nature Neuroscience.
The study's startling findings received widespread publicity after a preliminary abstract was presented at a Society for Neuroscience meeting in Chicago last October. Articles heralding the new discovery appeared in news publications around the world, focusing on the point obese patients have been making for years -- that, like addiction to other substances, junk food binging is extremely difficult to stop.
The study goes significantly further than the abstract, however, demonstrating clearly that in rat models the development of obesity coincides with a progressively deteriorating chemical balance in reward brain circuitries. As these pleasure centers in the brain become less and less responsive, rats quickly develop compulsive overeating habits, consuming larger quantities of high-calorie, high-fat foods until they become obese. The very same changes occur in the brains of rats that overconsume cocaine or heroin, and are thought to play an important role in the development of compulsive drug use.
Kenny, a scientist at Scripps Research's Florida campus, said that the study, which took nearly three years to complete, confirms the "addictive" properties of junk food.
"The new study, unlike our preliminary abstract, explains what happens in the brain of these animals when they have easy access to high-calorie, high-fat food," said Kenny. "It presents the most thorough and compelling evidence that drug addiction and obesity are based on the same underlying neurobiological mechanisms. In the study, the animals completely lost control over their eating behavior, the primary hallmark of addiction. They continued to overeat even when they anticipated receiving electric shocks, highlighting just how motivated they were to consume the palatable food."
The scientists fed the rats a diet modeled after the type that contributes to human obesity -- easy-to-obtain high-calorie, high-fat foods like sausage, bacon, and cheesecake. Soon after the experiments began, the animals began to bulk up dramatically.
"They always went for the worst types of food," Kenny said, "and as a result, they took in twice the calories as the control rats. When we removed the junk food and tried to put them on a nutritious diet -- what we called the 'salad bar option' -- they simply refused to eat. The change in their diet preference was so great that they basically starved themselves for two weeks after they were cut off from junk food. It was the animals that showed the "crash" in brain reward circuitries that had the most profound shift in food preference to the palatable, unhealthy diet. These same rats were also those that kept on eating even when they anticipated being shocked."
Lethally Simple
What happens in addiction is lethally simple, Kenny explained. The reward pathways in the brain have been so overstimulated that the system basically turns on itself, adapting to the new reality of addiction, whether its cocaine or cupcakes.
"The body adapts remarkably well to change -- and that's the problem," said Kenny. "When the animal overstimulates its brain pleasure centers with highly palatable food, the systems adapt by decreasing their activity. However, now the animal requires constant stimulation from palatable food to avoid entering a persistent state of negative reward."
After showing that obese rats had clear addiction-like food seeking behaviors, Johnson and Kenny next investigated the underlying molecular mechanisms that may explain these changes. They focused on a particular receptor in the brain known to play an important role in vulnerability to drug addiction and obesity -- the dopamine D2 receptor. The D2 receptor responds to dopamine, a neurotransmitter that is released in the brain by pleasurable experiences like food or sex or drugs like cocaine. In cocaine abuse, for example, the drug alter the flow of dopamine by blocking its retrieval, flooding the brain and overstimulating the receptors, something that eventually leads to physical changes in the way the brain responds to the drug.
The new study shows that the same thing happens in junk food addiction.
"These findings confirm what we and many others have suspected," Kenny said, "that overconsumption of highly pleasurable food triggers addiction-like neuroadaptive responses in brain reward circuitries, driving the development of compulsive eating. Common mechanisms may therefore underlie obesity and drug addiction."
Consistent with common mechanisms explaining addiction and obesity, levels of the D2 dopamine receptors were significantly reduced in the brains of the obese animals, similar to previous reports of what happens in human drug addicts, Kenny noted. Remarkably, when the scientists knocked down the receptor using a specialized virus, the development of addiction-like eating was dramatically accelerated.
"This addiction-like behavior happened almost from the moment we knocked down the dopamine receptors," Kenny noted. "The very next day after we provided access to the palatable food, their brains changed into a state that was consistent with an animal that had been overeating for several weeks. The animals also became compulsive in their eating behaviors almost immediately. These data are, as far as we know, the strongest support for the idea that overeating of palatable food can become habitual in the same manner and through the same mechanisms as consumption of drugs of abuse."
The study was supported by a Bank of America Fellowship, The Margaret Q. Landenberger Research Foundation and the National Institutes of Health.
Tuesday, May 11, 2010
Parkinson's Medications and Impulsive Behavior
There have now been several studies documenting an increase in impulse control disorders such as compulsive gambling, sexuality, shopping and other similar behaviors in people taking medications for Parkinson's Disease. These studies demonstrate that the brain, which regulates thinking, feeling and behaving, can become disordered in certain ways. In this case it is from a medication to treat Parkinson's Disease. These medications increase dopamine release, thus they add evidence to the dopamine hypothesis of impulse control disorders, including addiction to drugs. What I find interesting about them is that these were not previous drug or sex addicts or compulsive gamblers. But once their dopamine balance became dysregulated, their behavior became dysregulated. Thus, if our brain is dysregulated in certain ways, it constrains our ability to exercise choice or will. This complicates questions about responsibility, moral blameworthiness, and criminal liability. But what is becoming ever more clear as I work with many patients again is that there is a dysregulation of the ability to control behavior. The ethical and political arenas will simply have to deal with that. Here is a recent study:
Impulse Control Disorders in Parkinson Disease
A Cross-Sectional Study of 3090 Patients
Daniel Weintraub, MD ; Juergen Koester, PhD ; Marc N. Potenza, MD, PhD ; Andrew D. Siderowf, MD, MSCE ; Mark Stacy, MD ; Valerie Voon, MD ;Jacqueline Whetteckey, MD ; Glen R. Wunderlich, PhD ; Anthony E. Lang, MD, FRCPC
Arch Neurol. 2010;67(5):589-595.
Context An association between dopamine-replacement therapies and impulse control disorders (ICDs) in Parkinson disease (PD) has been suggested in preliminary studies.
Objectives To ascertain point prevalence estimates of 4 ICDs in PD and examine their associations with dopamine-replacement therapies and other clinical characteristics.
Design Cross-sectional study using an a priori established sampling procedure for subject recruitment and raters blinded to PD medication status.
Patients Three thousand ninety patients with treated idiopathic PD receiving routine clinical care at 46 movement disorder centers in the United States and Canada.
Main Outcome Measures The Massachusetts Gambling Screen score for current problem/pathological gambling, the Minnesota Impulsive Disorders Interview score for compulsive sexual behavior and buying, and Diagnostic and Statistical Manual of Mental Disorders research criteria for binge-eating disorder.
Results An ICD was identified in 13.6% of patients (gambling in 5.0%, compulsive sexual behavior in 3.5%, compulsive buying in 5.7%, and binge-eating disorder in 4.3%), and 3.9% had 2 or more ICDs. Impulse control disorders were more common in patients treated with a dopamine agonist than in patients not taking a dopamine agonist (17.1% vs 6.9%; odds ratio [OR], 2.72; 95% confidence interval [CI], 2.08-3.54; P < .001). Impulse control disorder frequency was similar for pramipexole and ropinirole (17.7% vs 15.5%; OR, 1.22; 95% CI, 0.94-1.57; P = .14). Additional variables independently associated with ICDs were levodopa use, living in the United States, younger age, being unmarried, current cigarette smoking, and a family history of gambling problems.
Conclusions Dopamine agonist treatment in PD is associated with 2- to 3.5-fold increased odds of having an ICD. This association represents a drug class relationship across ICDs. The association of other demographic and clinical variables with ICDs suggests a complex relationship that requires additional investigation to optimize prevention and treatment strategies.
Impulse Control Disorders in Parkinson Disease
A Cross-Sectional Study of 3090 Patients
Arch Neurol. 2010;67(5):589-595.
Context An association between dopamine-replacement therapies and impulse control disorders (ICDs) in Parkinson disease (PD) has been suggested in preliminary studies.
Objectives To ascertain point prevalence estimates of 4 ICDs in PD and examine their associations with dopamine-replacement therapies and other clinical characteristics.
Design Cross-sectional study using an a priori established sampling procedure for subject recruitment and raters blinded to PD medication status.
Patients Three thousand ninety patients with treated idiopathic PD receiving routine clinical care at 46 movement disorder centers in the United States and Canada.
Main Outcome Measures The Massachusetts Gambling Screen score for current problem/pathological gambling, the Minnesota Impulsive Disorders Interview score for compulsive sexual behavior and buying, and Diagnostic and Statistical Manual of Mental Disorders research criteria for binge-eating disorder.
Results An ICD was identified in 13.6% of patients (gambling in 5.0%, compulsive sexual behavior in 3.5%, compulsive buying in 5.7%, and binge-eating disorder in 4.3%), and 3.9% had 2 or more ICDs. Impulse control disorders were more common in patients treated with a dopamine agonist than in patients not taking a dopamine agonist (17.1% vs 6.9%; odds ratio [OR], 2.72; 95% confidence interval [CI], 2.08-3.54; P < .001). Impulse control disorder frequency was similar for pramipexole and ropinirole (17.7% vs 15.5%; OR, 1.22; 95% CI, 0.94-1.57; P = .14). Additional variables independently associated with ICDs were levodopa use, living in the United States, younger age, being unmarried, current cigarette smoking, and a family history of gambling problems.
Conclusions Dopamine agonist treatment in PD is associated with 2- to 3.5-fold increased odds of having an ICD. This association represents a drug class relationship across ICDs. The association of other demographic and clinical variables with ICDs suggests a complex relationship that requires additional investigation to optimize prevention and treatment strategies.
Monday, May 10, 2010
Useful information about opioid misuse in chronic pain
With all the concern recently about misuse of prescription opioids in pain patients, this study offers additional information about risk factor evaluation when considering one's approach. The study also adds further to the large body of knowledge concerning different patterns and reasons for using intoxicants between men and women. There's an old adage about this: Men go to the bar, women go to the doctor.
MW
From Medscape Medical News
Risk Factors for Opioid Misuse Among Pain Patients Differ by Sex
|
INFORMATION FROM INDUSTRY
Therapeutic Goals in Major Depressive Disorder (MDD)
In a survey published in JAMA, <22% of respondents received adequate treatment for 12-month MDD. Explore pharmacotherapy for patients in therapy for depression.
Click here
In a survey published in JAMA, <22% of respondents received adequate treatment for 12-month MDD. Explore pharmacotherapy for patients in therapy for depression.
Click here
May 4, 2010 — A new study published in the April issue of theJournal of Pain reveals men and women with chronic pain who misuse opioid medications — including taking these medications at a dose frequency unsanctioned by treating physicians — do so for different reasons.
Women with chronic pain are more likely to misuse opioids because of emotional issues and psychological distress, whereas men who do the same are more likely to report social and behavioral problems, such as associating with friends who use drugs or alcohol, having a bad temper, or having legal difficulties.
"We found from our analysis that women tend to misuse pain medications for mood problems — when they are anxious or depressed — while men misuse them for euphoric or behavioral reasons that are less associated with mood," lead researcher Robert Jamison, PhD, associate professor in the Department of Anesthesia and Psychiatry at Brigham and Women's Hospital, Boston, Massachusetts, told Medscape Psychiatry.
"So these may be important markers for clinicians that can help identify patients who might have trouble with opioid misuse — and it's important to provide these patients with interventions that might be helpful. For women, the characteristics to look for are whether they are depressed or anxious, and for men, past history would be a marker," Dr. Jamison added.
Pain Severity Similar Between Sexes
In the study, 662 patients with chronic noncancer pain who take opioid medications were recruited from medical centers in 5 states and surveyed with pain assessment questionnaires to examine rates and characteristics of problematic opioid use.
The investigators also examined predictive associations between risk factors for abuse and misuse by patients of their prescription medications. At baseline, patients completed a series of questionnaires, including the revised Screener and Opioid Assessment for Pain Patients and the Brief Pain Inventory, a multidimensional pain questionnaire.
After 5 months, they underwent a structured prescription drug use interview with a clinician, the Prescription Drug Use Questionnaire (PDUQ), and their clinicians completed the Physician Opioid Therapy Questionnaire (POTQ) — an 11-item scale used to assess misuse of opioids.
Patients were asked to undergo a urine toxicology screen and were classified by the Aberrant Drug Behavior Index (ADBI) concerning their opioid medication abuse based on a combination of self-report in the PDUQ, the physician-reported POTQ, and urine toxicology results. Because some patients had missing data on 2 or more variables, they were excluded from the final analyses — leaving a total of 455 patients or 74.2% of those who began the study.
Results indicated that there was little difference between men and women in the severity of their pain or their rate of opioid misuse — the ADBI indicated prescription opioid misuse in 31% of males and 36.7% of females in the final analysis, a difference that was not statistically significant.
Yet results from both patient self-reports and clinician evaluations indicated that women who misused their opioid medications were more likely to report a history of physical and sexual abuse, psychiatric diagnoses, or a history of psychiatric illness and family concerns. Counting pain pills was also predictive of opioid misuse among women.
High Rate of Misuse
By contrast, men who misused opioids were more likely to have close friends who used alcohol or drugs, to have a bad temper, to have legal problems, and to have a history of drug and/or alcohol abuse.
Other research by Dr. Jamison and colleagues, based on satisfaction questionnaires of chronic pain patients who misuse prescription medications, have suggested that women may benefit most from clinical interventions such as antidepressant and individual and group cognitive or behavioral therapy that addresses the psychological risk factors for misuse. Education about avoiding the use of opioids as a way of dealing with anxiety or sleep disturbances due to stress may also be helpful, he said.
Yet, men may benefit more from monthly urine screens, pill counts, and compliance monitoring to reduce opioid misuse, as well as behavioral consequences of misuse such as more frequent dosing and clinic visits, he added.
Certainly, the study calls attention to the problem of opioid misuse among chronic pain patients. And although only a small percentage of these patients actually develop dependence or addiction, clinicians at the pain management center of Brigham and Women's Hospital have found through urine screens that up to 42% of pain patients misuse their medications, he said.
"These folks have terrible pain as well as clinical history issues that make them very difficult to manage. It really is very challenging to treat these patients, and the idea of the study was to help piece together the puzzle of how to best help them," he said.
"Opioid misuse is a growing concern for chronic pain patients," commented Larissa Mooney, MD, assistant professor of psychiatry at the University of California–Los Angeles. "The vast majority of patients with chronic pain don't develop a problem, but there are vulnerable subgroups," she said.
"This study adds to an emerging literature on gender differences in addiction — how men and women are different in terms of etiology, consequences, and the mechanisms of drug misuse," she said.
Dr. Mooney cautioned that the study's conclusions may not be applicable to all patients with chronic pain. Many of the patients in the study were older (older than 50 years), had long-standing chronic pain, and were often disabled by their pain conditions. "It would be interesting to see if these findings apply to younger patients with less chronic pain history," she said.
She noted that counseling, as well as careful monitoring, for pain patients who misuse prescription opioids or have risk factors for prescription abuse may be helpful for both men and women, she said.
"I don't think that these treatment recommendations are applicable only to men or women," she added.
The study was supported by grants from the National Institute on Drug Abuse and the Arthritis Foundation. Dr. Jamison reported research support from Inflexxion Inc. Dr. Mooney has disclosed no relevant financial relationships.
J Pain. 2010;11:312-320
Sunday, May 9, 2010
Study: Viagabatrin not effective for cocaine addiction
Here is the latest in a long series of studies that have failed to demonstrate a single medication with efficacy in treating cocaine dependence. In some ways this is surprising because cocaine is a single receptor focused drug, so it simplifies the search for medications that have activity at that receptor. Alcohol, on the other hand, is highly complex and affects many areas of the brain at once. It is not receptor focused. Yet, there are proven effective treatments for alcohol dependence.
From Medscape Medical News
Vigabatrin Fails to Achieve Efficacy for Cocaine Dependence in Phase 2 US Trial
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April 23, 2010 (San Francisco, California) — A double-blind, placebo-controlled phase 2 clinical trial of the anticonvulsant agent vigabatrin for cocaine dependence in the United States failed to show that the drug was effective for achieving abstinence, according to research presented here at the American Society of Addiction Medicine 41st Annual Medical-Scientific Conference.
The trial's results contradict those of a similar phase 2 Mexican trial, published in the American Journal of Psychiatry in 2009, which showed a significant difference between subjects given vigabatrin vs placebo for cocaine addiction.
Yet researchers who conducted the US trial said the negative results may have been the result of problems with study design, rather than failure of vigabatrin to achieve efficacy in treating cocaine dependence.
"The take-home message from our trial is that it didn't work," said Eugene Somoza, MD, PhD, from the University of Cincinnati College of Medicine and the Veteran's Administration Medical Center in Cincinnati, Ohio. "But it's not that vigabatrin doesn't work — the study didn't work."
High Drop-Out Rate
In the US trial, 186 participants from 11 medical centers were randomly assigned either to 3 g/day vigabatrin daily by mouth in 2 divided doses or to placebo for 12 weeks. All patients received computerized behavioral therapy and counseling once a week, and urine specimens were collected 3 times a week to test for cocaine use.
There was a high drop-out rate — 61 patients dropped out of the study and only 125 completed at least 12 weeks of treatment. Abstinence was defined as not having used cocaine for the last 2 weeks of the study treatment period, validated by self-report and levels of benzoylecgonine in urine samples. Treatment adherence was evaluated through pill counts and self-reports.
The study failed to meet its primary endpoint — a significantly greater rate of drug abstinence in the vigabatrin group. However, the researchers found that patients receiving vigabatrin used consistently less cocaine than placebo during the 12-week treatment phase (P = .006), as measured by benzoylecgonine levels.
In a secondary analysis, the researchers also examined patient compliance with their medication regimens by reviewing urine vigabatrin concentrations in the treatment group. They found that 47.6% of the 61 patients who had completed the study in the vigabatrin group were not compliant with their medication regimens. Compliers were considered to be those with vigabatrin concentration of 630 μg/mL or more, and partial compliers were defined as those with levels of 158 μg/mL or more in urine samples. Secondary analysis indicated that those in the complier vigabatrin group used cocaine for fewer days than those in the noncomplier group (P = .084).
Although concerns have been raised about visual field defects with long-term use of vigabatrin, the researchers did not observe this adverse effect in either the treatment or placebo group. Adverse events included headache, nasopharyngitis, diarrhea, nausea, and back pain.
Lack of Adherence
So why did the US study fail while the Mexican trial showed that vigabatrin was effective for achieving abstinence? "The 2 main reasons are that patients didn't take their medications in the American study, and those in the Mexican study may have been a lot more motivated to abstain from cocaine," Dr. Somoza said in an interview with Medscape Psychiatry.
He noted that in the Mexican study, patients were observed taking their medication for 2 of 7 days. The subjects in the Mexican study were also parolees from prison, and showing up at least once per week at the vigabatrin study treatment center satisfied requirements for parole. In contrast, the American study consisted of patients who had been recruited by academic medical centers through radio and TV ads and who were paid for their participation. Dr. Somoza said.
The 9-week phase 2 Mexican trial of 103 patients randomly assigned to either vigabatrin or placebo used a treatment dosage similar to that administered in the US trial, and cocaine use was also determined with twice-weekly urine toxicology tests. In that trial, 28% of vigabatrin-treated patients vs 7.5% of participants in the placebo group achieved abstinence, defined as 3 weeks without using cocaine.
In an accompanying editorial to the publication of the Mexican trial in the American Journal of Psychiatry in November 2009, Kathleen Brady, MD, PhD, from the Medical University of South Carolina, Charleston, noted that the results were "not tremendously robust." She also cautioned that vigabatrin can cause visual field defects in 30% to 50% of patients who take it for more than 12 months. The question of whether this adverse effect could affect those with cocaine dependence who use the drug for a shorter time remains open, she said.
"We've been looking for a medication for cocaine addiction for 35 years, and to date we have no [US Food and Drug Administration]-approved medications. We haven't found anything that works," commented Timothy Fong, MD, assistant professor of psychiatry and codirector of the addiction medicine clinic at the University of California–Los Angeles.
Whether or not the differences in the Mexican and US trial results could be the result of dissimilarity in the 2 studies' population characteristics is difficult to assess, Dr. Fong noted. "But when we have used advertisements to recruit people for cocaine trials in Los Angeles, we find that their motivations are pretty high to quit — even though it's sometimes difficult to get them to stay and finish the experiment," he said.
New Trial Planned
One problem with studies on cocaine dependence is that cocaine addiction is a complicated disease, and cocaine addicts are not all the same, Dr. Fong said. "The differences between those who use crack vs powder and those who inject vs snorting need to be teased out a little more," he added. "There may be people with cocaine addiction who may respond to vigabatrin, but I don't think we've figured out who that would be yet," he said.
Although Dr. Fong noted that, in his clinical experience, vigabatrin is not that effective for treating cocaine addiction, the investigators working on the US trial plan to continue studying the drug.
A new trial funded by the National Institute on Drug Abuse is planned, Dr. Somoza said. The investigators hope to address some of the problems in the US trial by using more observed doses, by adding a marker substance to vigabatrin and placebo formulations to better assess adherence, and by enrolling patients who might be more motivated to quit cocaine, such as those in substance abuse treatment centers, Dr. Somoza added.
The study was supported by Catalyst Pharmaceutical Partners. Dr. Fong disclosed being on speakers' bureaus for Reckitt-Benckiser, Pfizer Pharmaceuticals, and Lilly Pharmaceuticals. Dr. Somoza has disclosed no relevant financial relationships.
American Society of Addiction Medicine 41st Annual Medical-Scientific Conference: Abstract 4. Presented April 16, 2010.
Friday, May 7, 2010
Is addiction a brain disease?
A blog reader recently sent me this message:
First, it still seems like the act of drinking, smoking or doing other drugs is behavior and over time this behavior can lead to real health problems. Even by your own analogy, if someone were predisposed to heart disease because their father and grandfather had heart attacks because they smoked, never exercised and were overweight does not mean that you will have a heart attack especially if you exercise, eat properly and don't smoke. So, because someone is predisposed does not mean they are diseased. It would seem reasonable to suggest that addiction is a behavior that taken to the extreme over time can lead to very real organ and organ system impairment. This distinction I think is important because doctors that subscribe to the disease model and who state that addiction is a chronic progressive brain disease which you have clearly pointed out is not necessarily the case, imply this then with addiction is general. The person addicted to the Internet has a brain disease? The person addicted to their relationship has a brain disease? Studies on addiction are mainly about drinking which makes sense because substances do effect the brain. But, if I was a chronic Blackberry user, would I be damaging my brain and need rehab? The answers to these questions would be a great follow up to your response which you stated would require further responses any way.
There is a lot of confusion about the concept of a disease, especially when it comes to behavior. I think the primary problem is that we are not used to thinking of the brain as an organ, and we don't usually associate behavioral disturbances with brain dysfunction. A second problem is that of biological reductionism, where certain classes of phenomena (e.g., genomics, cell function, neurotransmission, etc.) are considered more real or important than other classes, such as thinking, feeling or behaving. We are used to thinking that if we are retaining too much fluid there might be something wrong with our kidneys, or if we have trouble breathing there might be something wrong with our lungs. We have no trouble believing that a brain tumor can produce seizures or paralysis. However, when it comes to more functional disturbances of the brain, our brains can't handle the idea. We think the mind and will are disembodied, existing in the ether out there somewhere, not attached to flesh and blood.
But this isn't true. Our minds, our wills, our thoughts, our feelings and our behavior all involve and depend upon proper function in the physical brain. For example, try thinking, feeling or doing something without a brain. It doesn't get you very far. Does this mean that these things are just biological machinations of this organ inside our heads? No, not at all. Does it mean that we are simply computer-controlled organisms living out our programmed lives? No. Does this mean that existential meaning, relationships, and spiritual striving are merely chimera? No, absolutely not. That's just it: Just because we require a brain for those things (and we do) does not mean that they are simply reducible to brain activity. To conclude so is to fall victim to biological reductionism.
I have been thinking about and studying these things for many years, and this is one of the toughest things I have ever struggled with. Here is my conclusion: one can study a living being at a multitude of levels, from genes to cells to organs to individual organisms to collections of living organisms such as a hive or city. Each level of analysis is valid in its own rite. None are fundamentally more valid than another, and they all influence each other constantly. These are systems of parts where the system is more than the sum of its parts, it is its own thing. A person, for example, or more than a collection of organs. A heart is more than a collection of cells, etc.
So, is addiction a brain disease? Well, addiction is a disorder of behavior so clearly the brain is involved. Are compulsive gambling, sexual activity or shopping brain diseases? They involve disordered behavior, so yes, the brain is involved. Are panic attacks or schizophrenia or depression brain diseases? Again the answer is that the brain is involved, and it must be dysfunctional in some ways for the disordered behavior to occur (by definition.) BUT, are they only and simplistically brain diseases? No they are not. Does brain involvement imply that they are pre-determined, not alterable, and not amenable to social influences, psychotherapy, will and effort or medication? No it does not.
You see, taken to its extreme, all disordered behavior involves the brain. Not only that, but the definition of “disordered behavior” is heavily culturally determined. For example, in Saudi Arabia drinking alcohol at all is “disordered” (except among the royalty), while cannabis or opiate use is much more normative. The opposite holds true for North America. Compulsive sexuality in the US might be considered normal male behavior in many other cultures. Drunkenness is almost a requirement in some Asian business environments whereas it has increasingly become stigmatized in the US. Another prime example is the gradual disapproval and stigmatization of smoking tobacco in the US. What was once a symbol of sophistication has become a symbol of lower class behavior, of “inferior” people who can't quit smoking and put on Lycra for their bike ride or run after eating granola and yogurt for breakfast. Now, the same is happening for obesity.
So the bottom line is that disordered behavior necessarily involves the brain because it cannot otherwise be possible. Ergo, the brain is disordered if behavior is disordered. However, brains can become disordered by hostile environments, extreme stress and many other outside influences. To say that disordered behavior is only the product of an individually “diseased” brain is to blame the victim in many cases. One cannot separate the internal environment, the brain, and the external environment. They are all part of the same organic system. Biological reductionism is therefore inherently politically reactionary: it places the problem squarely in a disordered individual, perhaps genetically inferior, while ignoring larger social influences that have substantial effects on individuals and therefore individual brains. More on this to come.
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