1. Study looks at neurological aspects of quitting cocaine addiction

    September 25, 2017 by Ashley

    From the Mount Sinai Hospital / Mount Sinai School of Medicine press release:

    Cocaine-addicted individuals say they find the drug much less enjoyable after years of use, but they have great difficulty quitting. A new brain imaging study led by researchers at the Icahn School of Medicine at Mount Sinai reveals why this might be so, as well as why a common psychological therapy may not work in addicted cocaine users.

    Their study, published September 5 in Addiction Biology, finds that chronic users have a “global impairment” in the ventromedial prefrontal cortex (VMPFC), an area of the brain that is linked to impulse and self-control, and is responsible for the kind of learning that assigns value to objects and behaviors.

    The Mount Sinai study investigated a specific type of learning called extinction — the process by which a new, affectively neutral, association replaces an old, affectively arousing association — to identify the neurobiological mechanism that underlies the persistence of drug seeking in addiction despite negative consequences and a reduction in the drug’s rewarding affects.

    To investigate these questions, the research team collected functional magnetic resonance imaging (fMRI) data on a three-phase classical conditioning paradigm in individuals with a history of chronic cocaine use and healthy control individuals without the drug habit. They found that in drug-addicted individuals, there was a VMPFC-mediated impairment in forming and maintaining new associations for stimuli that were previously, although no longer, predictive of both drug and non-drug related outcomes.

    “Our study data suggests that it will be hard for longtime cocaine users to unlearn what once was a positive experience if this ‘unlearning’ or new learning relies on this brain region to be effective,” says the study’s lead investigator, Anna Konova, PhD, who worked on the study while at the Icahn School of Medicine, but who is now a postdoctoral fellow at the Center for Neural Science at New York University.

    Extinction forms the basis for exposure therapy, which is often used to treat anxiety disorders like phobias.

    “There is a strong impetus for extinction-based therapy in addiction, but our findings highlight potential limitations of these existing therapies in their reliance on the VMPFC to achieve therapeutic benefits,” says the study’s senior investigator, Rita Z. Goldstein, PhD, who directs Mount Sinai’s Neuropsychoimaging of Addiction and Related Conditions research group.

    Dr. Goldstein is an international expert in the use of functional neuroimaging methods to examine the neurobiological basis of impaired cognitive and emotional functioning in human drug addiction and other disorders of self-control. Dr. Konova was a graduate student in Dr. Goldstein’s lab.

    A well-known example of the kind of learning that Dr. Konova and the research team studied in this study is the famous “Pavlov’s dog” experiment in which dogs learned to associate a food treat with the sound of a bell. Dogs soon started salivating when the bell rang. But if the bell rang enough times without being followed by the treat the salivation response of the dogs was reduced or extinguished.

    “The idea behind extinction learning as a therapeutic intervention is that a user can learn to substitute a relaxing thought — such as taking a nature stroll — for the thought of procuring cocaine when walking by their neighborhood park where they might have previously purchased or consumed the drug. By relying on these new associations, an addicted individual may be able to control their habit,” says Dr. Konova.

    Fear-based extinction learning is now widely used to treat anxiety, such as in phobias and post-traumatic stress disorder (PTSD). In this technique, a person is exposed to the thing that makes them afraid until the fear response to that thing (which is no longer associated with any real harm) is reduced and eventually extinguished, perhaps by forming a new, neutral or positive, association with their originally feared object or situation.

    While previous experiments have suggested VMPFC impairment in addicted individuals who have long used stimulants such as cocaine — a consistent finding is that the gray matter (a marker of neuronal morphological integrity) is altered in that brain area in these individuals — this is the first experiment to examine if these changes have implications for extinction learning in drug users and non-users using functional magnetic resonance imaging (fMRI) brain scans.

    The study participants — 18 chronic cocaine users and 15 control individuals from the same community — completed three rounds of learning over two days. The cocaine-using individuals had an average lifetime history of 17 years of cocaine use and currently used cocaine about twice a week. None were seeking treatment to stop.

    On the first day, while in the fMRI scanner, participants were shown, say, a colored square (a neutral cue) followed by a picture of a pleasant stimulus (such as a puppy), a different colored square this time followed by a drug-related picture (such as a crack pipe), and a third one followed by a picture of a household item. Like Pavlov’s dogs, the control individuals learned to anticipate the corresponding picture once they saw the specific square (anticipating the puppy, the drug item, or the household item). Their VMPFC also responded accordingly. They had learned the first association.

    Next, the groups were shown just the cues (squares) repeatedly and depending on the picture that had been linked to them before, their brain responses again responded accordingly: VMPFC responses now were not as high to the cues that predicted the picture of the puppy (a pleasant stimulus) and not as low as to the cues that predicted the crack pipe (an unpleasant stimulus). This was the first extinction phase, when extinction learning should occur. That is, new learning was taking place that the affectively charged pictures no longer followed the cues.

    Participants stayed overnight, and the next morning, they were shown the cues again. The extinction response was even more pronounced this time due to retention of some of the extinction association from the previous day.

    However, VMPFC signals in the cocaine-using group did not resemble that of the control group. Their data revealed that extinction learning did not engage the VMPFC to the same degree, which could result in failures in extinction learning, Dr. Konova says.

    “It may be possible to train other areas of the brain, such as the striatum, which we found did have normal responses in the drug users, to update the strong and well-established drug associations,” she says. “Or there could be ways to increase VMPFC function through cognitive retraining or pharmacologically. But our findings suggest that neither extinction learning for positive outcomes — anticipating seeing a cute puppy when this is no longer likely — or drug-related outcomes — anticipating seeing a crack pipe when this too is no longer likely — using that critical brain area will help longtime cocaine users quit.”

    “This really highlights the importance of neuroscience-informed treatment development for addiction, as this study and others like it can help speak to why some current approaches might fail or discover new, more effective ways to intervene,” says Dr. Goldstein.


  2. What makes alcoholics drink? Research shows it’s more complex than supposed

    September 20, 2017 by Ashley

    From the European College of Neuropsychopharmacology press release:

    What makes alcoholics drink? New research has found that in both men and women with alcohol dependence, the major factor predicting the amount of drinking seems to be a question of immediate mood. They found that suffering from long-term mental health problems did not affect alcohol consumption, with one important exception: men with a history of depression had a different drinking pattern than men without a history of depression; surprisingly those men were drinking less often than men who were not depressed.

    “This work once again shows that alcoholism is not a one-size-fits-all condition,” said lead researcher, Victor Karpyak (Mayo Clinic, MN, USA). “So the answer to the question of why alcoholics drink is probably that there is no single answer; this will probably have implications for how we diagnose and treat alcoholism.”

    The work, presented at the ECNP congress by researchers from the Mayo Clinic*, determined the alcohol consumption of 287 males and 156 females with alcohol dependence over the previous 90 days, using the accepted Time Line Follow Back method and standardized diagnostic assessment for life time presence of psychiatric disorders (PRISM); they were then able to associate this with whether the drinking coincided with a positive or negative emotional state (feeling “up” or “down”), and whether the individual had a history of anxiety, depression (MDD) or substance abuse.

    The results showed that alcohol dependent men tended to drink more alcohol per day than alcohol dependent women. As expected, alcohol consumption in both men and women was associated with feeling either up or down on a particular day, with no significant association with anxiety or substance use disorders. However, men with a history of major depressive disorder had fewer drinking days (p=0.0084), and fewer heavy drinking days (p=0.0214) than men who never a major depressive disorder.

    Victor Karpyak continued: “Research indicates that many people drink to enhance pleasant feelings, while other people drink to suppress negative moods, such as depression or anxiety. However, previous studies did not differentiate between state-dependent mood changes and the presence of clinically diagnosed anxiety or depressive disorders. The lack of such differentiation was likely among the reasons for controversial findings about the usefulness of antidepressants in treatment of alcoholics with comorbid depression.

    This work will need to be replicated and confirmed, but from what we see here, it means that the reasons why alcoholics drink depend on their background as well as the immediate circumstances. There is no single reason. And this means that there is probably no single treatment, so we will have to refine our diagnostic methods and tailor treatment to the individual. It also means that our treatment approach may differ depending on targeting different aspects of alcoholism (craving or consumption) and the alcoholic patient (i.e. man or a woman) with or without depression or anxiety history to allow really effective treatment.”

    Commenting, Professor Wim van den Brink (Professor of Psychiatry and Addiction at the Academic Medical Centre, University of Amsterdam) said:

    “This is indeed a very important issue. Patients with an alcohol use disorder often show a history of other disorders, including mood and anxiety disorders, they also often present with alcohol induced anxiety and mood disorders and finally the may report mood symptoms that do not meet criteria for a mood or anxiety disorder (due to a failure to meet the minimal number of criteria or a duration of less than two weeks). All these different conditions may influence current levels or patterns of drinking.

    The current study seems to show that the current presence of mood/anxiety symptoms is associated with more drinking in both male and female alcoholics, whereas a clinical history of major depression in male alcoholics is associated with lower current dinking levels. Although, the study does not provide a clear reason for this difference, it may have consequences for treatment. For example, antidepressant treatment of males with a history major depression may have no effect on drinking levels. However, these findings may also result from residual confounding, e.g. patients with a history of major depression might also be patients with a late age of onset of their alcohol use disorder and this type of alcohol use disorder is associated with a different pattern of drinking with more daily drinking and less heavy drinking days and less binging. More prospective studies are needed to resolve this important but complex clinical issue.”


  3. Brain injury in kids might lead to alcohol abuse

    August 28, 2017 by Ashley

    From the Frontiers press release:

    Researchers at Ohio State University have surveyed previous studies to investigate the relationship between traumatic brain injuries and alcohol abuse. They found evidence that traumatic brain injuries in children and adolescents could be a risk-factor for alcohol abuse in later life.

    When we think of the link between alcohol and traumatic brain injuries, we probably think of a person’s increased risk of injury while drunk. Alcohol intoxication is indeed a significant risk factor for traumatic brain injuries, and one study has reported that alcohol use is involved in as many as 50% of emergency department admissions for traumatic brain injuries in the US.

    Intriguingly, an animal study conducted by Zachary Weil, a researcher at Ohio State University, made him suspect that the converse might also be true, particularly in young people. “We recently reported that mice that experience a traumatic brain injury as juveniles drink significantly more alcohol as adults,” says Weil. “When we started to look at the human literature it became clear that alcohol and traumatic brain injuries were very connected. There were some hints that brain injuries might actually make someone more susceptible to alcohol abuse.”

    Weil was inspired to look more closely at the past literature, and what he and his team found was recently published in Frontiers in Behavioral Neuroscience. The researchers found that it was difficult to tell if their hypothesis was true in adults. “So many adults that have brain injuries are already heavy drinkers and therefore it’s really hard to tell for sure if a brain injury has affected their drinking,” explains Weil.

    However, for people who suffer a traumatic brain injury in childhood or adolescence, there was a clearer link to alcohol abuse problems in later life. For example, children under 5 years of age who suffer a traumatic brain injury are over 3.6 times more likely to exhibit substance abuse as teenagers, compared with uninjured children.

    So, why would a traumatic brain injury potentially lead to alcohol abuse? The team found evidence in the literature that brain injury can negatively affect factors that are associated with reducing alcohol abuse. For example, forming stable romantic relationships, getting involved in extracurricular activities and maintaining full-time employment are all associated with a reduced risk of substance abuse, but all are less likely in brain injury survivors.

    Traumatic brain injuries can also make people more impulsive and less aware of the consequences of their actions, and there is also evidence that brain injury survivors may use alcohol to help deal with the negative consequences of their injury.

    Beyond its psychological effects, traumatic brain injury can cause significant inflammation in the brain. Alcohol also generates neuroinflammation, and evidence from animal studies suggests that this inflammation might drive further drinking.

    Finally, traumatic brain injuries can damage specific neurochemical systems in the brain that are vulnerable during childhood development, such as the dopaminergic system. A dysfunctional dopaminergic system is a risk factor for substance abuse, suggesting another potential link between childhood brain injury and alcohol abuse in adulthood.

    So, how can we address the problem? “This is an important issue because drinking after brain injury is associated with health problems and poorer outcomes. Specifically targeting substance abuse problems in the brain-injured population could do a lot of good,” says Weil.

    The researchers caution that the link between brain injuries and alcohol abuse has not yet been completely established and more work is needed. “This has not been completely confirmed in humans, but there is a lot of suggestive evidence,” explains Weil.


  4. Study suggests gamblers more likely to have suffered childhood traumas

    August 16, 2017 by Ashley

    From the University of Lincoln press release:

    Men with problem and pathological gambling addictions are more likely to have suffered childhood traumas including physical abuse or witnessing violence in the home, according to new research.

    Psychologists examined responses in a survey of more than 3,000* men on a variety of life factors, and found that just over a quarter who had probable pathological gambling problems had witnessed violence in the home as a child. Ten per cent also reported being physically abused in childhood, and a further seven per cent said they had suffered a life-threatening injury.

    Problem gamblers — those who have not yet escalated to a pathological problem, but are deemed to have a more serious addiction than non-problem gamblers — also reported higher rates of childhood trauma, with just under 23 per cent saying they had witnessed violence at home, and nine per cent experiencing physical abuse. In comparison, just eight per cent of non-problem gamblers witnessed domestic violence when they were a child, and less than four per cent had suffered abuse.

    The study, led by the University of Lincoln, UK, also found that 35 per cent of pathological gamblers had suffered serious money problems as adults, 29 per cent had been convicted of a criminal offence, and almost 20 per cent had experienced relationship breakdowns. In comparison, for non-problem gamblers the figures came in at just 12, 9, and 10 per cent respectively.

    The pattern of people who had previously suffered traumas in childhood or stressful events as an adult becoming pathological and problem gamblers remained even when other associated risk factors, such as substance abuse and homelessness, were accounted for. Interestingly, the more serious the gambling problem, the higher the percentage of reported childhood trauma or life stressors as an adult in all but two questions.

    Researchers say the findings highlight a need for gambling treatment services to include routine screening for traumatic life events or substance abuse, so that treatments can be better tailored.

    Forensic psychologist Dr Amanda Roberts, from the University of Lincoln’s School of Psychology, led the study. She said: “The links between gambling problems, trauma and life stressors have been known to exist for some time, but understanding the extent of these relationships will help early intervention and better treatment.

    “We have found that among men in the United Kingdom, disordered gambling remains uniquely associated with trauma and life stressors in childhood and adulthood after adjusting for alcohol and drug dependence.

    “Probable pathological gamblers and problem gamblers reported injuries, marital difficulties, homelessness, money problems and criminality more often than non/non-problem gamblers. Taken as a whole, this suggests that disordered gambling does not occur on its own, but that it is perhaps symptomatic of other social, behavioural and psychological problems of some individuals.

    “General experiences of stressful life events, such as job loss or homelessness in adulthood are not usually characterised by the same extreme psychological responses; this distinction is important, since associations with traumatic events might indicate increased vulnerability to developing gambling problems, while associations with other types of stressful life event, such as job loss, might indicate consequential harms associated with gambling.”

    The results build on Dr Roberts’ previous study which found that men who gamble are more likely to act violently towards others, with the most addicted gamblers the most prone to serious violence.

    The new findings have been published in the journal Addictive Behaviors.


  5. Trauma-informed, mindfulness-based intervention significantly improves parenting

    August 12, 2017 by Ashley

    From the Thomas Jefferson University press release:

    Researchers at Jefferson’s Maternal Addiction Treatment Education & Research (MATER) program found significant improvement in the quality of parenting among mothers who participated in a trauma-informed, mindfulness-based parenting intervention while also in medication-assisted treatment for opioid use disorder. Results of the study, the first to scientifically test a mindfulness-based parenting intervention with this population, were published July 27 in the Journal of Addiction Medicine.

    “Our results validate a powerful intervention when it is needed most,” said senior author Diane Abatemarco, Ph.D., MSW, principal investigator, Director of MATER and Associate Professor of OB/GYN and Pediatrics in the Sidney Kimmel Medical College at Thomas Jefferson University. “By improving parenting through mindfulness, we may be able to change the intergenerational trajectory of trauma and improve children’s and families’ lives.”

    A total of 160 women participated in a 12-week mindful parenting intervention at Jefferson’s Family Center, an outpatient and intensive outpatient treatment center that cares for women who are pregnant, parenting or working toward reuniting with their child. The mindfulness-based program included mother/baby education and practice, education on the impact of trauma, and mindfulness meditation. Themes included non-judgment, full attention and compassion.

    “We designed the mindfulness-based parenting program to give women the resources and tools to be great parents. Our program supports moms, building their self-efficacy and self-confidence,” said Abatemarco.

    The research team conducted pre- and post-tests with the women using three validated instruments to measure observed parenting quality, the mother’s childhood trauma exposure and self-reported mindful parenting. Women who participated in the mindfulness-based parenting program experienced a clinically significant increase in parenting quality, from “low” at baseline to “moderate” at completion.

    “We also found that attendance matters,” said Meghan Gannon, Ph.D., MSPH, first author and research project manager at MATER. “For women who experienced high levels of childhood trauma, attendance was key to improving parenting.”


  6. Why does prenatal alcohol exposure increase the likelihood of addiction?

    July 21, 2017 by Ashley

    From the University at Buffalo press release:

    One of the many negative consequences when fetuses are exposed to alcohol in the womb is an increased risk for drug addiction later in life. Neuroscientists in the University at Buffalo Research Institute on Addictions are discovering why.

    Through a research grant from the National Institute on Alcohol Abuse and Alcoholism (NIAAA) of the National Institutes of Health (NIH), Senior Research Scientist Roh-Yu Shen, PhD, is studying how prenatal alcohol exposure alters the reward system in the brain and how this change continues through adulthood.

    The key appears to lie with endocannibinoids, cannabis-like chemicals that are produced by the brain itself.

    “By understanding the role endocannibinoids play in increasing the brain’s susceptibility to addiction, we can start developing drug therapies or other interventions to combat that effect and, perhaps, other negative consequences of prenatal alcohol exposure,” Shen says.

    Prenatal alcohol exposure is the leading preventable cause of birth defects and neurodevelopmental abnormalities in the United States. Fetal Alcohol Spectrum Disorders (FASD) cause cognitive and behavioral problems. In addition to increased vulnerability of alcohol and other substance use disorders, FASD can lead to other mental health issues including Attention Deficit Hyperactivity Disorder (ADHD), depression, anxiety and problems with impulse control.

    After the prenatal brain is exposed to alcohol, the endocannibinoids have a different effect on certain dopamine neurons which are involved in addicted behaviors than when brain is not exposed to alcohol,” Shen says. “The end result is that the dopamine neurons in the brain become more sensitive to a drug of abuse’s effect. So, later in life, a person needs much less drug use to become addicted.”

    Specifically, in the ventral tegmental area (VTA) of the brain, endocannibinoids play a significant role in weakening the excitatory synapses onto dopamine neurons. The VTA is the part of the brain implicated in addiction, attention and reward processes. However, in a brain prenatally exposed to alcohol, the effect of the endocannabinoids is reduced due to a decreased function of endocannabinoid receptors. As a result, the excitatory synapses lose the ability to be weakened and continue to strengthen, which Shen believes is a critical brain mechanism for increased addiction risk.


  7. Brain region that affects drug use habits identified

    July 16, 2017 by Ashley

    From the University of Iowa press release:

    The human brain is nimble. It can reorganize itself to learn new things, catalog memories, and even break old habits. So, what if our brains could be taught to suppress cravings, especially the destructive impulse to use drugs?

    University of Iowa researchers studying the infralimbic cortex — a region of the brain that controls addictive behavior — performed a series of experiments in which rats were given cocaine, then taken off the drug. The scientists found that, generally speaking, this region of the brain can be reprogrammed to ease the rats’ cocaine urges.

    The finding could help users kick the habit with the help of drugs that target the infralimbic cortex — or with improved behavioral treatment for substance addiction and relapse, according to Andrea Gutman, a postdoctoral researcher in the UI Department of Psychological and Brain Sciences and corresponding author on the paper, published in the Journal of Neuroscience.

    The infralimbic cortex, a part of the prefrontal cortex located toward the front of the head, is responsible for forming habits and regulating behavior. Think of it as a mental green light or a check on destructive or embarrassing tendencies.

    Researchers already knew about that role, but they were unsure how it controlled cravings and other habit-forming behaviors — or whether the infralimbic cortex could be manipulated to temper impulses. The UI team worked with a group of rats that were administered cocaine when they pressed a lever with their paws; the rats did so for two hours per day over the course of two weeks.

    Over the next two weeks, the rats received no cocaine when they pressed the lever. When they realized they were no longer getting the drug, the rats pressed the lever less frequently, until, by the end of the two-week period, “they hardly pressed the lever at all,” Gutman says. In other words, at least some of the rats learned to curb their addiction.

    A second group of rats followed the same regimen as the control group and were allowed to use cocaine for two weeks. However, in this second group, the researchers turned off neurons in the rats’ infralimbic cortex just as the animals pressed the drug-dispensing lever. By silencing those neurons for a period of 20 seconds every time the rats pressed the lever, the researchers in effect prevented the rats from learning to curb their drug appetite. The rats’ cravings remained as intense as in the beginning of the experiment, even though they weren’t receiving the drug.

    “They’re failing to learn to inhibit their cocaine craving,” says Gutman, who works in the lab of Ryan LaLumiere, assistant professor in the UI Department of Psychological and Brain Sciences. “They want the cocaine just as much.”

    The researchers silenced the neurons in the rats’ brains for the first five days of the cocaine-less two-week period. They found that these five days had a major impact on how effectively rats learned and began to adapt to the drug’s absence. The rats whose neurons were silenced were more likely to relapse than those that underwent withdrawal, the study found.

    The results strengthen the hypothesis that the infralimbic cortex plays an important role in the suppression of addictive behavior. It also points to when the region could best be “taught” to curb a habit.

    “No study has looked intensively at exactly how the infralimbic cortex functions, nor the importance of the first five days of treatment when it comes to curtailing drug-seeking behavior,” says LaLumiere, the paper’s co-author. “And while our experiments involved cocaine, we think the results could hold true for the infralimbic cortex’s role in conditioning withdrawal and relapse from other addictive substances, including opioids.”

    Kelle Nett, Caitlin Cosme, Wensday Worth, and Subhash Gupta, all from the UI, helped perform the research and are contributing authors on the paper. John Wemmie, UI professor of psychiatry, also is a contributing author.

    The National Institute on Drug Abuse (a branch of the National Institutes of Health), the Department of Veterans Affairs, and the Brain & Behavior Research Foundation funded the research.


  8. Anxiety study shows genes are not fixed: Experience and exposure can change them

    July 14, 2017 by Ashley

    From the Research Society on Alcoholism press release:

    Epigenetics refers to how certain life circumstances can cause genes to be silenced or expressed, become dormant or active, over time. New research shows that adolescent binge drinking can lead to epigenetic reprogramming that predisposes an individual to later psychiatric disorders such as anxiety. These data will be shared at the 40thannual scientific meeting of the Research Society on Alcoholism (RSA) in Denver June 24-28.

    “Adolescence is an important period of growth,” said Subhash C. Pandey, Ph.D., professor and director of the Alcohol Research Center at the University of Illinois at Chicago. “This is when the brain is maturing, and consistent epigenetic programing occurs. This is also a period when binge drinking is prevalent. Adolescent binge drinking can disrupt epigenetic programing in key brain regions by changing certain key molecular targets within the epigenome.”

    Pandey explained that early life exposure to alcohol can have not only long-lasting effects on brain chemistry but also induce a predisposition to psychiatric problems such as alcohol abuse and anxiety disorders. “Anxiety disorder is highly comorbid with alcoholism,” he said, “and adolescent alcohol exposure can lead to the development of high anxiety and alcohol intake in adulthood.” Pandey will elaborate on these findings at the RSA meeting on June 25.

    “More specifically, our data indicate that the enzymes histone deacetylases and demethylases — which are responsible for the regulation of histone acetylation and methylation — are altered in adulthood due to previous adolescent alcohol exposure. This alteration causes specific genes involved in regulating synaptic events to become suppressed, leading to high anxiety and high alcohol drinking behavior.” In other words, adolescent alcohol exposure can change the architecture where certain genes reside, and thus modify how the genes perform.

    “In short,” said Pandey, “epigenetic reprogramming in the brain due to early life experiences or exposure to alcohol can lead to the changes in gene functions and predispose an individual to adult psychopathology.”


  9. Drinking makes you older at the cellular level

    by Ashley

    From the Research Society on Alcoholism press release:

    The more alcohol that people drink, the more their cells appear to age. In a new study that will be shared at the 40th annual scientific meeting of the Research Society on Alcoholism (RSA) in Denver June 24-28, researchers found that alcoholic patients had shortened telomere lengths, placing them at greater risk for age-related illnesses, such as cardiovascular disease, diabetes, cancer and dementia..

    Telomeres, the protein caps on the ends of human chromosomes, are markers of aging and overall health,” said Naruhisa Yamaki, M.D., a clinical fellow at the Kobe University Graduate School of Medicine. Yamaki explained that every time a cell replicates, a tiny bit of telomere is lost, so they get shorter with age. But some groups may have shorter telomeres for reasons other than aging.

    “Our study showed that alcoholic patients have a shortened telomere length, which means that heavy drinking causes biological aging at a cellular level,” he said. “It is alcohol rather than acetaldehyde that is associated with a shortened telomere length.” Yamaki will present this research at the RSA meeting on June 25.

    Yamaki and his co-authors recruited 255 study participants from alcoholism treatment services at Kurihama National Hospital in Yokosuka, Japan: 134 alcoholic patients and 121 age-matched controls or non-alcoholics, ranging in age from 41 to 85 years old. DNA samples, as well as drinking histories and habits, were collected from all participants.

    “We also found an association between telomere shortening and thiamine deficiency (TD),” said Yamaki. “TD is known to cause neuron impairments such as Wernicke-Korsakoff Syndrome. Although how exactly TD can cause neural impairments is unclear, it is well known that oxidation stress cause telomere shortening and, thus, it is possible that oxidation stress may also cause neuron death.”

    Yamaki added that it’s important for the public to understand that heavy drinking causes telomere shortening because “awareness of this fact provides important information necessary for people to live healthier.”

    Yamaki will present these findings during the RSA 2017 meeting on Sunday, June 25 at 3:15 during “A Multifaceted View of Alcoholism in Older Adults” at the Hyatt Regency Denver.


  10. Study shows childhood psychiatric disorders increase risk for later adult addiction

    July 12, 2017 by Ashley

    From the Elsevier press release:

    Children’s health and well-being while growing up can be indicators of the potential health issues they may encounter years later. A study published in the July 2017 issue of the Journal of the American Academy of Child and Adolescent Psychiatry(JAACAP) suggests that a childhood psychiatric disorder increases the risk of developing addiction later in life. Based on a large amount of data from previous studies on these participants, the researchers identified a correlation between various psychiatric disorders among children and later risk of developing addictions.

    The team, led by researchers from the Child Study group at the Vrije Universiteit in Amsterdam and Accare, the Center for Child and Adolescent Psychiatry at the University Medical Center Groningen, the Netherlands, found that individuals diagnosed in childhood with attention-deficit/hyperactivity disorder (ADHD), oppositional defiant disorder (ODD)/conduct disorder (CD), and depression had an increased risk of developing addictions. Interestingly, results concerning anxiety were less clear. The risk may depend on the specific type of anxiety disorder, but to date, no studies have focused on this topic.

    “We know that ADHD in childhood increases the risk for later substance-related disorders, but until now, no systematic evaluation of other childhood psychiatric disorders had been conducted,” said Dr. Annabeth P. Groenman, researcher at Accare, Center for Child and Adolescent Psychiatry, University Medical Center Groningen, the Netherlands. “Our findings show that not only ADHD increased the risk of addictions, but that other childhood psychiatric disorders also increased risk. This indicates the importance of early detection of mental health problems in a wider group. Addiction is a major cause of immense personal, familial, and societal burden, and prevention is therefore an important goal.”

    The study re-analyzed data of 37 previous studies containing a total of 762,187 individuals, of whom 22,029 had ADHD, 434 had disruptive behavior disorders (such as ODD/CD), 1,433 had anxiety disorder, and 2,451 had depression. The researchers identified studies looking at childhood psychiatric disorders and later addiction.

    Disruptive behaviors (ODD/CD) frequently co-occur with ADHD, in approximately 30% of cases. This so-called “comorbidity” is often thought to be the main cause of addictions in individuals with ADHD. However, the results suggest that co-occurring ODD/CD in ADHD does not fully explain the risk of addictions in this group.

    Professor Jaap Oosterlaan, principal investigator of the Child Study Group at the Vrije Universiteit in Amsterdam and the Emma Children’s Hospital AMC, the Netherlands, said: “Now that we have firmly established children with psychiatric disorders as a high-risk group for later substance-related disorders, the next step is to make parents, clinicians, and the government aware of these risks and work together in reducing the risks for addiction and its debilitating consequences.”