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Heavy Drinking Throughout College Could Increase Heart Attack Risk, Study Finds


By  | April 24, 2013 |

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Four years of heavy drinking between the ages of 18 and 25 could permanently increase the risk of heart attack and stroke, a new study suggests.

The study included 38 nonsmoking college students. Half did not drink, and half were binge drinkers, meaning they consumed five or more servings of alcohol in two hours, at least six times a month, for about four years, the Los Angeles Times reports.

The researchers from the University of Illinois used ultrasound imaging to examine blood vessels in the students’ arms when they were given the blood-vessel dilating drug nitroglycerin. They observed what happened when the arm’s blood flow was temporarily restricted, and then allowed to run freely.

The students who didn’t drink had blood vessels that were more elastic, and dilated more easily, compared with the vessels of binge drinkers. This could be an early indicator of blood vessel damage and heart disease, which could increase the future risk of heart problems, the researchers said.

“Regular binge drinking is one of the most serious public health problems confronting our college campuses, and drinking on college campuses has become more pervasive and destructive,” researcher Shane A. Phillips, PT, PhD, said in a news release. “Binge drinking is neurotoxic and our data support that there may be serious cardiovascular consequences in young adults.”

“It is important that young adults understand that binge drinking patterns are an extreme form of unhealthy or at-risk drinking and are associated with serious social and medical consequences,” added co-author Mariann Piano, PhD, RN. “Discoveries and advances in many different areas of medical science have cautioned against the notion that youth protects against the adverse effects of bad lifestyle behaviors or choices.”

The new study will appear in the Journal of the American College of Cardiology.

NIDA Researchers Suggest New Direction for Treating Addictions



Using optogenetics, essentially shining a light, on particular cells in the prefrontal cortex can reduce cocaine addiction in rats, according to a study published April 3 in Nature. The senior scientist was Antonello Bonci, M.D., scientific director of the National Institute on Drug Abuse (NIDA). “Our results can be immediately translated to clinical research settings with humans, and we are planning clinical trials to stimulate this brain region using noninvasive methods,” Bonci reported in a press statement. “By targeting a specific portion of the prefrontal cortex, our hope is to reduce compulsive cocaine-seeking and craving in patients.”

“This exciting study offers a new direction in research for the treatment of cocaine and possibly other addictions,” added NIDA Director Nora Volkow, M.D. “We already knew, mainly from human brain imaging studies, that deficits in the prefrontal cortex are involved in drug addiction. Now that we have learned how fundamental these deficits are, we feel more confident than ever about the therapeutic promise of targeting that part of the brain.”

Bonci and his colleagues gave cocaine to two groups of rats—those addicted to cocaine and those not addicted to cocaine—then compared the neuron-firing patterns in the prefrontal cortex in both groups. They found less firing in the deep-layer pyramidal neurons of the prefrontal cortex in the addicted rats than in the nonaddicted rats, implying that such sluggish firing might be critical for cocaine addiction. They then used optogenetics to stimulate the underperforming pyramidal neurons in the addicted rats and found that it reduced cocaine-seeking behavior. “Thus, targeted stimulation of the prefrontal cortex could serve as a promising therapy for treating compulsive drug use,” the researchers concluded.

Researcher Uses Virtual Reality to Reduce Addiction Cravings


Virtual reality 4-22-13

A Duke University researcher is studying whether virtual reality can be used to reduce cravings in people who are addicted. The goal is to help them develop coping strategies that they can use in the real world, Popular Science reports.

A person using virtual reality for addiction treatment is hooked up to a simulator, and enters a virtual environment with one of their triggers, such as a crack pipe or bottle of alcohol. Someone in the scene offers them their drug of choice. Researchers slowly add cues to the virtual environment, or change the situation, based on the patient’s history.

A voice tells the person to put down the joystick and look around the room without speaking, to allow their craving to dissipate. The voice asks them to rate their cravings periodically.

The research is spearheaded by Zach Rosenthal, who receives funding from the National Institute on Drug Abuse and the Department of Defense. He uses virtual reality to trigger a reaction, and then teaches patients to cope with it. The method is called cue reactivity, which has long been used for treating phobias.

Dr. Rosenthal believes virtual reality is more effective than showing someone a real-life trigger, such as a lighter or empty bottle, in a lab setting. His hope is that creating a virtual world that is similar to the patients’ environment will help them transfer the lessons to the real world.

Rosenthal has been using virtual reality to treat substance abuse in veterans. The soldiers have post-traumatic stress syndrome. The program trains veterans’ minds not to respond to cravings when they are faced with temptations such as alcohol or drugs. Veterans participating in the research receive cellphone calls several times daily that transmit a tone to remind them about the steps they have learned to deal with their cravings.

Vigabatrin – Not Useful For Treatment Of Cocaine Dependence:


By Will Boggs, MD

NEW YORK (Reuters Health) Apr 16 – The GABA-transaminase inhibitor vigabatrin failed to help patients with cocaine dependence in a randomized multisite study.

“Based on our clinical trial it seems unlikely that vigabatrin will ever be found to be effective in the treatment of cocaine dependence,” Dr. Eugene C. Somoza from the Cincinnati Veterans Affairs Medical Center and the University of Cincinnati in Ohio told Reuters Health.

Dr. Somoza and colleagues compared vigabatrin with placebo in a 12-week clinical trial with 186 participants at 11 U.S. sites. Everyone received weekly computerized cognitive behavioral therapy plus biweekly half-hour individual sessions with a counselor. One hundred forty-one patients completed the study, according to a report April 10th online in JAMA Psychiatry.

Cocaine abstinence was defined by two measures: self-report of cocaine use, and quantitative measurements of the cocaine metabolite benzoylecgonine and creatinine.

Overall, about 25% of urine samples were missing. Roughly 11% of samples in each group went missing during active treatment. Another 14% in each group were missing due to study dropout. And in both groups, only 55% of participants were more than 90% compliant, and only 66% were more than 70% compliant. In 39 patients the primary outcome could not be determined because of insufficient study participation.

With these shortcomings in mind, only seven of 92 vigabatrin participants met the primary endpoint of abstinence during the last two weeks of the 12-week treatment phase, compared with five of 94 placebo participants (7.6% vs 5.3%; p=0.67).

There were no significant differences between the groups in weekly fraction of cocaine use days, percentage of drug-free urine samples during weeks one through 13, or improvements in craving or global function.

“In a post hoc measure of vigabatrin in the urines of some participants it was estimated that the actual adherence may have been around 50%,” Dr. Somoza said. “Nevertheless, an analysis of just the adherent patients revealed that the medication was still not efficacious.”

Adverse event rates were similar in the two groups, except that placebo participants reported significantly more headaches.

Changes in visual acuity have been reported in association with vigabatrin use, but there were no clinically significant decreases in visual acuity during the study.

These results contrast with findings in a Mexican placebo-controlled trial in which 28% (n=14) of vigabatrin participants maintained full abstinence during the last three weeks of treatment, compared with 7.5% (n=4) of placebo participants (p=0.009).

The researchers suggest that their disappointing results may have been due to “weak efficacy of the drug” or significant nonadherence.

They also note that a third vigabatrin trial, funded by the National Institute on Drug Abuse, was designed “to more adequately address medication adherence (e.g., with once-daily dosage, observed dosing three times per week, and riboflavin level monitoring to measure compliance).”

Dr. Somoza said, “I know that this trial ended several months ago, but I do not know when the official results will be announced.” He said the results might be presented at the annual College on Problems of Drug Dependence (CPDD) meeting in San Diego in June.

“Cocaine is very different from other addictive agents, particularly because it lacks the intense withdrawal symptoms of other substances like opioids, alcohol, and benzodiazepines,” Dr. Somoza explained. “Thus, the cocaine withdrawal symptoms are so mild, non-specific, and often non-existent that they cannot be used to detect cocaine withdrawal. Note that in spite of this, DSM5 continues to assign as much importance to cocaine withdrawal symptoms as to the other addictive agents.”

“My feeling is that the scientific community and NIDA need to put a stronger emphasis on finding a better outcome variable for use in cocaine clinical trials to replace what is currently being used,” Dr. Somoza continued. “At the present time most clinical trials on cocaine employ only self-report measures of cocaine use. They generally claim that these self-reports are ‘validated’ by measuring benzoylecgonine (BE) levels in urine. However these BE measures are generally done qualitatively (and infrequently). Also, the ‘validation’ procedures tend to be quite feeble and seldom described, thereby making self-reports the de facto primary outcome variable.”


JAMA Psychiatry 2013.

Exercise May Mitigate Brain Damage Due to Heavy Drinking


Exercise May Mitigate Brain Damage Due to Heavy Drinking

Deborah Brauser (From Medscape)

Apr 16, 2013

Aerobic exercise may help prevent some of the brain damage caused by the effects of heavy alcohol consumption, preliminary research suggests.

A study of adults who drank heavily showed that those who participated in low levels of aerobic exercise had decreases in white matter integrity in the brain’s external capsule and superior longitudinal fasciculus (SLF) — areas that are important for cognitive, behavioral, and emotional functioning.

However, the association between alcohol intake and white matter health was not significant for those who reported high levels of exercise involvement.

“The results suggest a first step in better understanding the relationship between the brain, exercise, and alcohol consumption,” Hollis C. Karoly, from the Department of Psychology and Neuroscience at the University of Colorado at Boulder, told Medscape Medical News.

She noted in a release that although it is common knowledge that long-term alcohol exposure is linked to white matter damage, “little is known about how this damage could be reversed or prevented.”

On the basis of their findings, “aerobic exercise appears to be a promising candidate for decreasing alcohol-related brain damage,” said Karoly, adding that clinicians should consider prescribing this type of exercise as adjunct treatment for patients with a history of heavy alcohol use.

“We already know how good exercise is for your heart, your muscles, and your lungs. So the suggestion that it could also lead to positive changes in brain health is not all that surprising. It’s something that’s important for overall health.”

The study was published online April 2 in Alcoholism: Clinical and Experimental Research.

Protective Effect

According to the investigators, aerobic exercise has been shown to decrease cognitive decline and negative neural changes associated with aging and with several neurologic disorders.

“Engaging in regular aerobic exercise has been found to improve learning, memory, and self-control,” said Karoly, adding that this appears to be particularly true among older adults who exercise regularly.

She noted that exercise has also been shown to protect white matter from age-associated damage.

“White matter is a crucial part of the nervous system, relaying information between areas of the brain. In general, white matter damage can lead to motor deficits, sensory problems, and cognitive difficulties.”

In addition, heavy use of alcohol “is associated with a number of deleterious health outcomes, such as…widespread damage to the brain, including gray and white matter loss,” write the researchers.

Given all of this, “it seemed likely that aerobic exercise may work to reverse or prevent some of the damage to the brain caused by chronic alcohol consumption,” said Karoly.

Investigators assessed data on 60 adults between the ages of 21 and 55 years who participated in 1 of several previous studies on alcohol and nicotine use.

All had undergone a diffusion tensor imaging scan and had completed the Voluntary Aerobic Exercise Questionnaire; the Alcohol Use Disorders Identification Test (AUDIT); the Time Line Follow Back (TLFB), in which participants recorded the number of drinks consumed in the last 60 days; and the Impaired Control Scale, which is a measure of loss of control over drinking.

Relationships between these factors were assessed by measuring fractional anisotropy in the brain’s SLF, external capsule, fornix, and superior and anterior corona radiata.

“These five…tracts were selected based upon their demonstrated association with alcohol consumption in several previous studies,” report the investigators.

Results showed a significant association between level of aerobic exercise participation and alcohol consumption on fractional anisotropy in both the external capsule and the SLF (both areas, P < .05).

There was a strong link between low exercise and decreased white matter integrity in both of these brain areas, and this association did not change significantly after adjusting for use of cigarettes or cannabis.

“Both the external capsule and [SLF] connect important brain areas, so damage to these tracts may have a host of more specific implications for negatively impacting cognitive, behavioral, and emotional functioning,” said Karoly.

No Causal Claims Yet

No relationship was found between alcohol intake and white matter health for the average or above-average exercisers.

In addition, for the low exercisers, there was a stronger association between alcohol intake and loss of control over drinking than for the high exercisers (P < .01). However, this association was only found in the AUDIT measure and not in the TLFB.

Karoly pointed out that the study did not prove a causal effect or even that aerobic exercise is protective against alcohol-related white matter damage, although the results “are consistent with the notion that exercise may be protective.”

“This was more of an associational study, so making a definitive claim like that is a little too strong right now. We don’t know the mechanisms by which this effect is happening, and we didn’t look at this over time to see if it could repair damage that has already happened,” she said.

In addition, future studies “relating neural characteristics to exercise behavior” should consider lifelong exercise patterns as well as more recent participation, note the investigators. They add that a healthier diet and improved sleep that often comes with a heavy exercise lifestyle should also be examined.

Karoly added that the researchers are now planning a new study that will also assess “dose levels” of aerobic exercise (including type, duration, intensity, and frequency) on white matter effects.

Compelling Study

Susan F. Tapert, PhD, professor of psychiatry at the University of California, San Diego, and chief of psychology at the VA San Diego Healthcare System Psychology Service, said in a release that the focus of this study is highly significant because, although heavy drinking has been linked to white matter damage, “it is unclear why the effects are more prominent in some individuals than in others.”

“Although we don’t know yet if the exercise is protecting against alcohol-related damage, or if it is a sign of factors linked to brain health, this is a very compelling study,” said Dr. Tapert, who was not involved with this research.

“This suggests that individuals who have experienced alcohol-related brain problems could possibly use exercise to help recover those effects; studying people over time will tell us if this is in fact the case.”

She added that she hoped the findings “drive more research” into this topic area.

“From a neurobiological perspective, it will be very interesting to see how aerobic exercise could potentially mitigate inflammatory, oxidative, and other sources of neural injury produced by heavy alcohol use,” concluded Dr. Tapert.

The study was funded by grants from the National Institute on Alcohol Abuse and Alcoholism and the National Institute on Drug Abuse. The study authors have reported no relevant financial relationships.

Alcohol Clin Exp Res. Published online April 2, 2013.