| 1. IT’S HEALTH RELATED COSTS ARE HIGHER 2. DEATH IS A GREAT BUSINESS 3. CANCER CLINICS ARE MAKING A KILLING 4. IT’S ADDICTIVE NATURE FUELS OTHER ADDICTIVE BEHAVIORS WHICH FUEL THE ECONOMY 5. IT CREATES ABUSERS AND PUTS MORE PEOPLE IN PRISON |
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| 1. IT’S HEALTH RELATED COSTS ARE HIGHER 2. DEATH IS A GREAT BUSINESS 3. CANCER CLINICS ARE MAKING A KILLING 4. IT’S ADDICTIVE NATURE FUELS OTHER ADDICTIVE BEHAVIORS WHICH FUEL THE ECONOMY 5. IT CREATES ABUSERS AND PUTS MORE PEOPLE IN PRISON |
January 17, 2015Alcoholism: Clinical & Experimental Research For individuals who drink before sleeping, alcohol initially acts as a sedative -- marked by the delta frequency electroencephalogram (EEG) activity of Slow Wave Sleep (SWS) -- but is later associated with sleep disruption. A study of the effects of alcohol on sleep EEG power spectra in college students has found that pre-sleep drinking not only causes an initial increase in SWS-related delta power but also causes an increase in frontal alpha power, which is thought to reflect disturbed sleep. For individuals who drink before sleeping, alcohol initially acts as a sedative -- marked by the delta frequency electroencephalogram (EEG) activity of Slow Wave Sleep (SWS) -- but is later associated with sleep disruption. Significant reductions in EEG delta frequency activity and power also occur with normal development between the ages of 12 and 16; likewise this is a time when alcohol is commonly consumed for the first time, with dramatic increases in drinking occurring among collage-age individuals. A study of the effects of alcohol on sleep EEG power spectra in college students has found that pre-sleep drinking not only causes an initial increase in SWS-related delta power but also causes an increase in frontal alpha power, which is thought to reflect disturbed sleep. Results will be published in the February 2015 online-only issue of Alcoholism: Clinical & Experimental Research and are currently available at Early View. "People likely tend to focus on the commonly reported sedative properties of alcohol, which is reflected in shorter times to fall asleep, particularly in adults, rather than the sleep disruption that occurs later in the night," said Christian L. Nicholas, National Health & Medical Research Council Peter Doherty Research Fellow in the Sleep Research Laboratory at The University of Melbourne as well as corresponding author for the study. "The reduction in delta frequency EEG activity we see across the ages is thought to represent normal brain maturational processes as the adolescent brain continues to develop to full maturity," said Nicholas. "Although the exact function of non-Rapid Eye Movement (NREM) sleep, and in particular SWS, is a topic of debate, it is thought to reflect sleep need and quality; thus any disruption to this may affect the underlying restorative properties of sleep and be detrimental to daytime functioning." Nicholas and his colleagues recruited 24 participants (12 female, 12 male), healthy 18- to 21-year-old social drinkers who had consumed less than seven standard drinks per week during the previous 30 days. Each participant underwent two conditions: pre-sleep alcohol as well as a placebo, followed by standard polysomnography with comprehensive EEG recordings. Results showed that alcohol increased SWS delta power during NREM. However, there was a simultaneous increase in frontal alpha power. "For individuals researching sleep in the field of alcohol studies," said Nicholas, "our findings indicate that care needs to be taken when interpreting increases in 'visually scored' SWS associated with alcohol consumption. Increases in SWS, which traditionally would be interpreted as a good thing, can be associated with more subtle changes indicating disrupted sleep, such as the increases we observed in alpha activity, which are revealed when more detailed micro-structural components of the sleep electroencephalogram are assessed." Nicholas explained that the increase in frontal alpha power that occurs as a result of pre-sleep drinking likely reflects a disruption of the normal properties of NREM slow wave sleep. "Similar increases in alpha-delta activity, which are associated with poor or unrefreshing sleep and daytime function, have been observed in individuals with chronic pain conditions," he said. "Thus, if sleep is being disrupted regularly by pre-sleep alcohol consumption, particularly over long periods of time, this could have significant detrimental effects on daytime wellbeing and neurocognitive function such as learning and memory processes." Alcohol is not a sleep aid, said Nicholas. "The take-home message here is that alcohol is not actually a particularly good sleep aid even though it may seem like it helps you get to sleep quicker. In fact, the quality of the sleep you get is significantly altered and disrupted." Story Source: The above story is based on materials provided by Alcoholism: Clinical & Experimental Research. Note: Materials may be edited for content and length. Journal Reference:
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Alcoholism: Clinical & Experimental Research
Approximately 71 percent of people in the US (adults) drink alcohol. While alcohol interacts negatively with a number of commonly prescribed medications, little is known on a population level about the use of alcohol-interactive prescription medication among US drinkers. A new study has found that almost 42 percent of drinkers in the US population have used one or more alcohol-interactive prescription medications.
While alcohol interacts negatively with a number of commonly prescribed medications, little is known on a population level about the use of alcohol-interactive (AI) prescription medication among US drinkers. A new study has found that almost 42 percent of drinkers in the US population have used one or more alcohol-interactive prescription medications.
Results will be published in the February 2015 online-only issue of Alcoholism: Clinical & Experimental Research and are currently available at Early View.
"To our knowledge there have been only four previous US population-based studies," said Rosalind A. Breslow, an epidemiologist in the division of epidemiology and prevention research at the National Institute on Alcohol Abuse and Alcoholism as well as corresponding author for the study. "Three, conducted only among elderly people, concluded that substantial numbers of seniors were both drinking and taking alcohol-interactive medications and called for increased awareness about possible harmful consequences. One, conducted among adults of all ages, had a similar conclusion based on assessment of a limited number of prescription medications. Ours is a national-level study that estimates the proportion of adult drinkers who use a wide range of prescription medications that can interact with alcohol to cause numerous harms ranging from nausea, headaches, and loss of coordination to internal bleeding, heart problems, and difficulties in breathing."
Breslow added that her group expected to find greater prevalence among older drinkers. "People develop more chronic diseases as they age," she said, "so older people are more likely to be taking medications, many of which can interact harmfully with alcohol. They also may be taking multiple medications to treat multiple diseases. In addition, older people are at particularly high risk for harmful alcohol-medication interactions. There is some evidence that, as we age, our ability to metabolize alcohol decreases so alcohol might remain in our systems longer to interact with medications. Furthermore, the metabolism of several medications that interact with alcohol slows as we get older, creating a larger window for potential alcohol/medication interactions. For instance, diazepam -- known as Valium -- hangs around in the body about three times longer in a 60-year-old than a 20-year-old, thereby creating a much longer window for potential interactions with alcohol."
Breslow and her co-authors examined data from the 1999-2010 National Health and Nutrition Examination Survey, in which 26,657 adults (13,557 men, 13,100 women) aged ?20 years had provided data on past-year alcohol consumption and past-month prescription medication use. Analyses were adjusted for age, race/ethnicity, education, marital status, and smoking, and were also weighted in order to be nationally representative.
"Almost 42 percent of drinkers in the US population used one or more AI prescription medications," said Breslow. "Among seniors, aged 65 and older, the proportion was even higher, almost 78 percent. Regardless of age, the main therapeutic classes of AI medications used in the population were cardiovascular agents such as blood pressure medications, central nervous system agents such as sleeping pills, pain medications, and muscle relaxers, metabolic agents such as medications for diabetes and cholesterol, and psychotherapeutic agents such as antidepressants and antipsychotics."
Breslow noted that her group had expected a high prevalence rate, however, she emphasized that the data referred to potential, not actual, prevalence. "The data don't tell us exactly how many people in that 41.5 percent actually drink and take their medications within a similar time frame or how often they do so," she said. "However, if someone drinks regularly and takes medications regularly, the likelihood of taking them within a similar time frame is pretty high."
According to co-author Aaron White, a neuroscientist in the division of epidemiology and prevention research at the National Institute on Alcohol Abuse and Alcoholism, the consequences of mixing prescription medications with alcohol can have a variety of effects, some deadly.
"Alcohol can increase blood pressure, which could be counterproductive if one is taking medications to control blood pressure," he explained. "Mixing diuretic medications with alcohol, which is also a diuretic, could contribute to dehydration. Mixing alcohol and other sedatives, like sleeping pills or narcotic pain medications, can cause sleepiness, problems with coordination, and potentially suppress brain stem areas tasked with controlling vital reflexes like breathing, heart rate, and gagging to clear the airway. Alcohol increases insulin levels and lowers blood glucose, so combining alcohol with antidiabetic agents that regulate glucose levels could cause an undesirable drop in blood sugar. And, over time, alcohol can contribute to insulin insensitivity."
"Our findings highlight a major gap in the literature," said Breslow. "We found no US nationally representative data that queried combined use of alcohol with a wide range of prescription medications and yet it appears that a large percentage of people who drink regularly could be at risk of serious alcohol and medication interactions."
Breslow suggested that individuals who drink, particularly the elderly, should be educated about of the risks of combining alcohol with their medications. "We suggest asking one's doctor or pharmacist whether they should avoid alcohol while taking the medications they are prescribed," she said.
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The above story is based on materials provided by Alcoholism: Clinical & Experimental Research. Note: Materials may be edited for content and length.
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Numerous studies have shown that individuals with an alcohol use disorder perform worse than those without one on multiple neurocognitive domains of function following detoxification from alcohol, although the level of impairment can vary widely among individuals. A new study of the degree of neurocognitive recovery in treatment-seeking alcohol dependent individuals (ALC) -- with varied degrees of smoking status -- during the first eight months of sustained abstinence from alcohol has found that smoking status influenced the rate and level of recovery.
Results will be published in the November 2014 online-only issue of Alcoholism: Clinical & Experimental Research and are currently available at Early View.
"There have been few longitudinal studies that have specifically studied the effects of cigarette smoking on cognitive recovery in ALC during abstinence," said Timothy C. Durazzo, associate professor in the department of radiology and biomedical imaging at the University of California San Francisco, and corresponding author for the study. "To our knowledge, there have been no previous studies that used multiple assessment points to investigate the effects of cigarette smoking on cognitive recovery over the first eight months of abstinence from alcohol. We chose to examine measures of processing speed, learning and memory, and working memory because these abilities have been shown to be adversely affected by alcohol use disorders as well as chronic cigarette smoking."
Durazzo and his colleagues examined a total of 133 ALC participants -- 30 had never smoked, 28 were former smokers, and 75 were active smokers -- as well as 39 never-smoking "control" participants. Approximately 89 percent of the participants were male. All of the participants were given standardized measures of auditory-verbal and visuospatial learning and memory, processing speed, and working memory. Assessments after one week, four weeks, and eight months of abstinence for the ALC group allowed a comparison of the rates of neurocognitive changes from one to four weeks versus one to eight months of abstinence. The controls completed a baseline assessment and a follow-up approximately nine months later.
"We found that, overall, the ALC as a group showed the greatest rate of recovery on most abilities during the first month of abstinence," said Durazzo. "Over eight months of sustained abstinence from alcohol, active-smoking ALC showed poorer recovery than never-smoking ALC on measures of learning, and both former-smoking ALC and active-smoking ALC recovered less than never-smoking ALC on processing speed measures. In addition, after eight months of abstinence, active-smoking ALC performed worse than both controls and never-smoking ALC on most measures, former-smoking ALC performed worse than never-smoking ALC on several tests, but never-smoking ALC were not different from controls on any measure. Overall, the findings indicated never-smoking ALC showed full recovery on all measures after 8 months of sustained abstinence from alcohol."
"What this new research has found is that cognitive improvements are not uniform across alcoholic patients in recovery," explained David A. Kareken, deputy director of the Indiana Alcohol Research Center, and professor in the department of neurology at Indiana University School of Medicine. "In particular, some of this variability in cognitive recovery is explained by smoking. That is, those who stopped drinking, yet continued to smoke -- or even smoked in the past -- were slower to recover some types of mental skills over a period of months as compared to those who never smoked. This was most evident in skills such as visual memory, attention, and the capacity to quickly perform motor tasks that require directed, focused mental activity."
Durazzo said he was somewhat surprised by the degree of recovery. "The average alcohol consumption for the never-smoking ALC participants was about 370 drinks per month during the year prior to study," he said. "This suggests that significant cognitive recovery is possible during sustained abstinence from alcohol."
Both Durazzo and Kareken commented on the damaging toxicity of cigarette smoke.
"Cigarette smoke contains a tremendous number of toxic compounds that affect multiple organs in the body, including the brain," said Durazzo. "The components of cigarette smoke can promote significant oxidative stress in the lungs, blood vessels, and brain in humans. Oxidative stress is cause by 'free radicals' that directly damage the various cells that constitute the brain, which may lead to impaired function; the human brain is highly vulnerable to oxidative stress. The active-smoking ALC stopped drinking, but continued to smoke, which may have damped their recovery because of continued exposure to the various chemicals in cigarette smoke that promote oxidative stress. The diminished recovery of former-smoking ALC may represent the residual effects of long-term oxidative stress; however, this is all speculative."
Kareken agreed. "What precisely it is about smoking that causes alcoholic patients to recover cognitive abilities more slowly is uncertain, as smoking involves much more than delivering a drug," he said. "Certainly, nicotine can acutely stimulate attention and mental abilities, which is one reason why many people find smoking to be reinforcing. However, smoking also involves the delivery of a very large number of toxins and gasses that ... may also interact with how alcohol damages the brain. Smoking could affect the brain indirectly, as well, by damaging other organs that interact with the brain, such as the heart and lungs. Teasing apart the precise effects will be complex."
"Our findings stress the importance of evaluating the influence of conditions/behaviors that often accompany alcohol use disorders, such as cigarette smoking, to better understand the factors that may hinder cognitive recovery during abstinence from alcohol," said Durazzo. "The frequency of cigarette smoking is much higher in those with alcohol and substance use disorders compared to the general public. It is important to emphasize that cigarette smoking alone is associated with adverse effects on multiple areas of cognitive function, such as learning and memory and processing speed. And, just like alcohol use disorders, cigarette smoking and nicotine dependence are treatable conditions. We believe our findings strongly reinforce the growing clinical movement to offer a comprehensive smoking-cessation program to individuals seeking treatment for alcohol and substance use disorders."
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The above story is based on materials provided by Alcoholism: Clinical & Experimental Research. Note: Materials may be edited for content and length.
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Alcoholism is a chronic and often progressive disease that includes problems controlling your drinking, being preoccupied with alcohol, continuing to use alcohol even when it causes problems, having to drink more to get the same effect (physical dependence), or having withdrawal symptoms when you rapidly decrease or stop drinking. If you have alcoholism, you can't consistently predict how much you'll drink, how long you'll drink, or what consequences will occur from your drinking.
It's possible to have a problem with alcohol, even when it has not progressed to the point of alcoholism. Problem drinking means you drink too much at times, causing repeated problems in your life, although you're not completely dependent on alcohol.
Binge drinking — a pattern of drinking where a male consumes five or more drinks in a row, or a female downs at least four drinks in a row — can lead to the same health risks and social problems associated with alcoholism. The more you drink, the greater the risks. Binge drinking, which often occurs with teenagers and young adults, may lead to faster development of alcoholism.
If you have alcoholism or you have a problem with alcohol, you may not be able to cut back or quit without help. Denying that you have a problem is usually part of alcoholism and other types of excessive drinking.