Tuesday, October 6, 2009

Marijuana Arrests Fuel Increase in Teen Drug Treatment Numbers

The number of American teenagers in drug treatment increased dramatically during the 1990s, but that jump was fueled almost entirely by teen marijuana users arrested and ordered into treatment by the courts. According to a study released earlier this fall by the Substance Abuse and Mental Health Services Administration (SAMHSA), the number of youth aged 12 to 17 placed in drug treatment programs rose from 95,000 in 1993 to 138,000 in 1998, an increase of 46% in five years. But the study, "Coerced Treatment Among Youths: 1993-1998," reported that "the increase was largely driven by marijuana-involved admissions referred through the criminal justice system."

"What an incredible waste," said retired American University law professor Arnold Trebach, founder of the Drug Policy Foundation and currently head of the Trebach Institute (http://www.trebach.org). "The idea that every teenage pot-smoker needs treatment is absurd," he told DRCNet. "I'm opposed to kids smoking pot," he added. "That could lead to tobacco use, which could be dangerous, but the notion that they need treatment is a reflection of how messed up our drug policy is at its core."

The study, which relied on data from SAMHSA's Drug and Alcohol Services Information System's Treatment Episode Data Set (TEDS), a nationwide compilation of treatment episodes in centers receiving federal funding, found that teen drug treatment referrals from other sources remained stable over the five-year period. Teens referred to drug treatment by schools have declined slightly to about 15,000 after peaking at about 20,000 in 1995. Self-referrals, where either the teen or a friend or family member arranged the intervention, hovered at about 20,000 in 1998, down slightly from the mid-1990s. All other referrals, which include health care providers and community, government or religious social service providers, increased from 20,000 to 30,000 between 1993 and 1995, but have remained at that level since then.

Criminal justice system referrals, either for marijuana alone or for marijuana and alcohol, have gone through the roof, however, increasing from about 37,000 in 1993 to more than 60,000 in 1998. According to the study, by 1998 almost half (49%) of all teen drug treatment admissions came through the courts, and people admitted for marijuana alone or marijuana and alcohol combined constituted three-quarters of all admissions. (Over the five-year period, alcohol alone and marijuana alone switched positions. In 1993, alcohol alone was named in 24.4% of admissions and marijuana alone in 11.9%. By 1998, alcohol alone had dropped to 9.3%, while marijuana alone had increased to 24.9%. Marijuana and alcohol combined grew slightly from 45.4% in 1993 to 51.2% in 1998.)

During the five-year period, in the midst of rapidly rising marijuana arrests during the Clinton administration, the number of teens forced into drug treatment by the criminal justice system increased 73%.

Despite the increases in overall marijuana arrests and in teens sent to drug treatment by courts, "there is very little evidence of a teen pot problem," said Trebach. "I just checked the data on child deaths from drug abuse from 1996-1999," he explained. "There are roughly a hundred per year, for all drugs. Kids are fairly sensible about this," said Trebach. "There is no great need for treatment [for teenagers], but there is a real need for getting honest information to the kids. Some kids do get in trouble with drugs, and they could use the help, but it has to be intelligent help, not the harsh regimen they often find in drug treatment today."

Visit http://www.samhsa.gov/OAS/coercedTX.pdf to read the study in full.

Tuesday, September 29, 2009

Everything You Need to Know About CARE Addiction Recovery

Author: Kausik Dutta

Acknowledging that you have a problem with drugs or alcohol can be stressful and upsetting. However, it’s the first step to recovering from your addiction and learning to live a fulfilling and sober life.


The next step can be frustrating as well: choosing which recovery or rehabilitation center to enroll in. There are many different options out there, and you want to find the one that will be the best for you. For many different reasons, CARE is a wonderful place for you to recover from your addiction.


CARE offers a wide variety of programs and treatments for you to participate in. This center understands that each person is different and strives to individualize each treatment program so that it will best treat the addict on a specific and individual basis. CARE also has a low client to therapist ratio, so you’re sure to get the attention and help that you need through this difficult time. The center realizes that they are not treating only an addiction—they are treating a human being as well. Therefore, each program is customized, taking into consideration your special needs, histories and reasons for becoming an addict. Each drug is different, too, and CARE takes this into consideration. Some drugs affect our bodies differently than others, and the combination of a specific drug and an individual personality can be complex to treat. This is why CARE approaches each patient with respect, care and concern. Their number one goal is to aid you to recovery.


While CARE uses a modified 12-step program such as those used through Alcoholics Anonymous and Narcotics Anonymous, the center takes it a step further and incorporates holistic healing, pain management, and the treatment and acknowledgement of underlying psychological factors that some patients may have. There are many specialty programs available such as alternative medicine, massage therapy, nutrition counseling, and herbal therapy. The combination of these alternative practices with tradition detox and recovery programs help to make CARE the successful addiction recovery center that it is.


If you or something you know has a problem with drugs or alcohol, contact CARE Addiction Treatment. The staff will do all they can to help you down the bumpy road of rehabilitation and recovery.

Author Information:
CARE Addiction Treatment is the premier source for finding information about drug rehab Florida centers. Source: http://u.article99.com.com/rkweb-solution/

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Tuesday, September 22, 2009

Signs of an Addiction

Addictions come in many forms. It's important to recognize the signs of addictions in order to seek out help before the problem becomes to large.

Some different types of Addictions are: Caffeine addiction, nicotine addiction, drug addiction, Alcohol addictions, and gambling addictions.

Like mentioned above it's very important to recognize the symptoms of addictions in order to be able to recognize and treat an addiction before it becomes to serious. There are several different symptoms, some vary on type of addiction, and others are age and gender specific. Here is a look at some of the most common symptoms:

  • Uncontrolled Craving and Desires – This symptom can be general to all types of addictions. For example: food/drink cravings, gambling cravings
  • Fatigue – Often times addictions will result in both physical and mental fatigue, as your body will often be working over time, and not resting properly.
  • Obsessive thoughts – Can you not get a thought out of your mind, is it starting to take over and effect the way you think?
  • Change in Behavior – Do you suspect that your behavior has changed? Are you more moody, or easily frightened?
  • Hyperactivity – Do you seem to be excessively active, but not getting a lot done? Do you fidget more then usual? Do you have problem sitting still for any length of time?

    These are just a few of several signs that can indicate the development or indication of an already existing addiction. If you are experiencing any of these signs, and it is unusual for you, I would recommend seeking out further existence either by a medical or mental professional.

    Be smart with your health and body. Your only given one chance with it!

    --

    Feel free to reprint this article as long as you keep the following caption and author biography in tact with all hyperlinks.

    Ryan Fyfe is the owner and operator of Addiction Area. Which is a great web directory and information center for Addiction and related topics like Rehabilitation.

  • Source: healingsteps.com
  • Tuesday, September 15, 2009

    When Alcohol Abuse Changes to Alcoholism

    By Dennis Soinski

    Changing a Person's Drinking Behavior

    Thousands of articles have been written and countless research studies have been undertaken regarding alcoholism. In spite of this, the one finding that has apparently failed to reverberate throughout the alcohol abuse and alcoholism academic and medical communities is the emphasis on the fact that alcohol addiction has its roots in alcohol abuse. While this fact has many ramifications, perhaps the key upshot of this fact is that millions of non-alcoholic individuals in our society and throughout the world who engage in abusive drinking can address their drinking consumption and make healthy and positive changes in their drinking behavior before they become alcohol dependent.

    One school of thought sees alcohol abuse in the following way: alcohol abuse takes place whenever an individual's drinking causes a problem in any aspect of his or her life.

    The areas of a person's life where alcohol abuse commonly leads to problems includes the following:

    · relationships
    · employment
    · school
    · finances
    · health
    · the law (for instance, a DUI).

    The Need for Positive and Healthy Change

    Now that we are aware of the problems that are usually associated with alcohol abuse, it can be seen that in order to overcome these difficulties and issues it is important for the alcohol abuser to look in the mirror and honestly ask himself or herself if alcohol is causing a problem in any facet of his or her life.

    As an additional component in the quest for healthy and positive change, problem drinkers need to understand that continued, repetitive, and heavy drinking can and does turn into alcohol addiction. Stated differently, millions of non-alcoholics in our society who have a drinking problem will, at some point in their lives, experience a transition from alcohol abuse to alcohol dependency. When this happens, it must be emphasized, the person will no longer simply be an alcohol abuser. Indeed, at this point, the person will be an alcohol abuser and an alcoholic.

    Signs of Alcohol Addiction

    How can a person tell if he or she is alcohol dependent? First, the experience of alcohol withdrawal symptoms when an individual suddenly stops drinking is one sign that alcoholism has reared its ugly head.

    Second, repetitive and out-of-control drinking behavior is another indication that a person has become an alcoholic. What this usually means is that after consuming the first drink, the individual lacks control over stopping his or her drinking and therefore continues to drink until he or she becomes inebriated.

    Alcohol Addiction Has Its Roots in Alcohol Abuse

    Perhaps the key in all of this is the following: most, if not all instances of alcohol addiction get their start from alcohol abuse. Stated another way, it is highly unlikely that a non-drinker will become alcohol dependent simply by having one drink or that a non-drinker will become an alcoholic by getting drunk once. Indeed, alcoholism does not result from infrequent and sporadic drinking but rather from continuous, excessive, and repeated drinking. The point: alcoholism doesn't take place in a vacuum. In short, the roots of alcoholism are found in alcohol abuse.

    Knowing this and letting this "fact" influence an individual's drinking behavior in a positive and healthy manner is perhaps the single most important health-related bit of information that a problem drinker can learn and implement in his or her life.

    Why is this so important? Research shows that alcoholics are masters of denial, deception, dishonesty, and manipulation and often blame their alcohol-related problems on situations and people outside themselves. Alcoholics also exhibit out-of-control and irresponsible drinking behavior. Not only this, but most alcoholics will lie, cheat, and steal in order to get their next drink. Why would an alcohol abuser who is not yet an alcoholic want to face such a dreary and destructive set of circumstances?

    Part One of Two

    This article is part one of a two-part article. See the "About the Author" section below for the website address of the complete article.

    About The Author:

    Denny Soinski writes about alcohol abuse, alcoholism, drug abuse, and drug addiction. The above article is part one of a two-part article. To see the full version of this article, please go to the following website: When Alcohol Abuse Changes to Alcoholism.

    Copyright 2009 - Denny M. Soinski. All Rights Reserved Worldwide. Reprint Rights: You may reprint this article as long as you leave all of the links active, do not edit the article in any way, and give the author name credit.

    Article Source: http://EzineArticles.com/?expert=Dennis_Soinski

    Tuesday, September 8, 2009

    Cocaine Use by College Students and Celebrities

    Cocaine Use Increases

    An article entitled "Cocaine Epidemic Feared As Cocaine Deaths Nearly Double In Florida Over Past 5 Years" was featured on the "Medical News Today" website on October 21, 2006. Not surprisingly, the information contained in this article was quite disconcerting. For instance, one of the key points in the article was that cocaine use is on the rise among college students with disposable income and also among high-profile celebrities. Perhaps of more importance, however, are two facts that are associated with the escalation in cocaine use: the increased cocaine-related emergency room visits and the rising cocaine-related fatalities. In fact, according to Florida drug authorities, cocaine-related deaths in Florida have almost doubled from 2000 to 2005.

    Why People Use Cocaine

    Why do various individuals use cocaine? Cocaine gives a person a feeling of euphoria, energy, and at times, an unbelievable, almost superhuman sense of control and mastery. For instance, some people who have taken cocaine have been known to leap out of windows or off rooftops, thinking that they could fly or that they could jump dozens of feet without getting injured. There is, however, a physiological reason why people continue to use cocaine after their first encounter. Cocaine exhausts the "feel-good" neurotransmitter dopamine, thus causing a need for even more use. In short, and from a physiological perspective, cocaine use perpetuates more cocaine use.

    Fatalities and Cocaine Use

    To gain a better understanding of the ultimate danger inherent in cocaine use, namely death, one needs to focus on the timeframe regarding its life-threatening effects. To accomplish this, cocaine use will be compared with prescription drug abuse.

    The abuse of prescription drugs such as Oxycontin, Vicodin, and Adderall can trigger abrupt cardiac or respiratory arrest at the time of abuse. Thus the critical and fatal timeframe when abusing prescription drugs is mostly "short-term." Conversely, due to the snowballing effects of cocaine, especially regarding the blood vessel damage that increases the risk of stroke or heart attack as a person ages, users can suddenly die years after their cocaine abuse started. Therefore, the critical and fatal timeframe for cocaine use, unlike the same measure for prescription drug abuse, is typically "long term."

    Why the Rise in Cocaine Use?

    Why is cocaine use increasing? One of the reasons is that celebrities who are addicted to cocaine have become "walking cocaine advertisements" and, as a result, have been able to adversely influence others, such as students, who have access to relatively large amounts of disposable income.

    The Need For Intervention and Education

    Florida drug experts stress that additional drug education and intervention need to take place in schools, colleges, and in local communities nationwide to help prevent a full-blown cocaine epidemic. I agree, but to be effective, I assert that the intervention and educational strategy has to include facts that challenge the lifestyles of the cocaine-using celebrities. Let me explain. Students need to be aware that they are observing a "snapshot in time" that does not reveal "the rest of the story" as Paul Harvey would say. Stated differently, college students who are impressed by cocaine-using high rollers need to learn how to see through the VIPs' facade and realize that they are getting "sold" faulty goods by the cocaine-using rich and famous.

    Many celebrities are at or approaching middle age. As a result, most, if not all, of the high-profile chronic cocaine have learned first-hand about the consequences of their drug-related lifestyles. On the other hand, most "traditional" college students are either teenagers or very young adults. Due to the cumulative effects of cocaine use, however, college students who continue to use cocaine are essentially playing Russian roulette with their near and long-term future.

    The Rest of the Story

    College students must be made aware of the fact that the cocaine-using celebrities that they are impressed with are really loose cannons that may explode into oblivion at any time because of their drug-related lifestyles. This "ultimate" and fatal consequence, however, does not tell the whole story. Indeed, the "rest of the story" also focuses on both the short-term and the long-term health consequences of cocaine use.

    Short and Long-Term Effects of Cocaine Use

    What the impressionable students have not seen are the friends of celebrities who have died from cocaine-related cardiac arrest, seizures, strokes, and respiratory failure. In addition, the vulnerable students have not been told about the "coke crash" that certainly has left some of the rich and famous depressed, irritable, and fatigued.

    Not only this, but the easily influenced students have not been informed about the loss of smell, problems with swallowing, and the nosebleeds experienced by some of the rich and famous who got their cocaine "buzz" via snorting. Moreover, the "receptive" students have not been notified about the bizarre, unpredictable, and at times violent behavior of many high rollers who took increasingly larger doses of cocaine in order to experience the desired high.

    Additionally, the suggestible students were not informed about the abdominal pain and nausea experienced by some of the cocaine-using celebrities. In a similar manner, the impressionable students were not told about the paranoid psychosis and auditory hallucinations experienced by various VIPs who experimented with binge cocaine use, i.e., taking more frequent AND higher doses of the drug at the same time.

    Moreover, the vulnerable students were not told about the fever, convulsions, blurred vision, muscle spasms, and comas experienced by some of the cocaine-using VIPs or by some of their friends who "party" with them. Similarly, the impressionable students were not told about the major weight loss, malnourishment, and loss of appetite experienced by numerous celebrities who have been chronic cocaine users. And finally, the susceptible students were not informed about the severe chest pains, coughing, shortness of breath, and bleeding in the lungs experienced by some of the celebrities who got their cocaine "buzz" via smoking.

    Conclusion

    College students need to become knowledgeable of the immediate and the long-term health problems that virtually all chronic cocaine users, even celebrities, eventually experience. In addition, they need to become aware of their vulnerability to cocaine use due to the fact that, statistically speaking, the 18 to 25-year-old age group currently has the highest rate of cocaine use compared to other age groups. Until college students can "see" the contradictions and damaging effects inherent in the questionable lifestyles of cocaine-using VIPs, however, some of them will continue to follow the destructive paths of the high-profile cocaine-using celebrities.

    Copyright 2007 - Denny Soinski. All Rights Reserved Worldwide. Reprint Rights: You may reprint this article as long as you leave all of the links active, do not edit the article in any way, and give the author credit.
    Denny Soinski

    Denny Soinski, Ph.D, writes about alcohol abuse intervention, alcohol addiction, alcohol testing, alcohol use and binge drinking, alcoholism, alcohol recovery, alcohol treatment, and alcohol rehab. For more information, please visit college and teen alcoholics right away!

    Thursday, September 3, 2009

    Careful treatment of alcohol dependency is necessary for a swift recovery by Andrew Regan

    For many people in the UK, the consumption of alcohol is merely an everyday habit. Whether it's two or three beers in the pub after work, or a few glasses of wine with your dinner, drinking alcohol is, to many, a basic social gesture. And while many individuals may binge drink to their detriment every weekend, it's important to establish the difference between people who often drink more than is good for them and those that are alcohol dependent.

    If you suffer from alcohol dependency, it means that you feel the need to have a drink to help you with certain situations. For instance, if the thought of socialising without having a few drinks first fills you with dread and anxiety, then you're likely to be alcohol dependent. Alcohol dependency isn't quite the same as alcoholism; alcoholics need alcohol to handle every situation, while alcohol dependents rely on alcohol to get them through only certain situations. But, alcohol dependency does require treatment, and may in turn develop into alcoholism if left unchecked.

    In contrast to opiate dependency, alcohol withdrawal may often present a risk to life; and acute withdrawal of alcohol in chronic alcohol dependency may lead to Delirium Tremens. Delirium Tremens is characterised by acute confusion, disorientation, vivid visual hallucinations, paranoia, marked tremors and other various symptoms and signs of alcohol withdrawal. If left untreated, Delirium Tremens can lead to a 10 per cent mortality rate, and therefore requires urgent medical admission.

    Additionally, alcohol withdrawal seizures often present a risk to life and, if observed, should be treated with a bolus of parenteral or per rectal diazepam. However, in most cases, alcohol dependent patients will not need prescriptions. Instead, following advice to cut down drinking at a gradual pace will be sufficient to manage most acute presentations of alcohol dependency. Nevertheless, it's important to keep in mind that a patient with a clear history of withdrawal seizures, who claims to have no access to alcohol supplies, may be labelled as appropriate to commence a community detoxification with chlordiazepoxide immediately - but this course of action should be avoided wherever possible.

    If you suffer from alcohol dependency, or are close to someone who does, and are looking for alcohol treatment, you might find that private residential alcohol treatment is preferable to community treatment. This method of alcohol treatment is beneficial because it allows the patient to choose their own location in which they'd like to treat their alcohol dependency. But wherever you choose to undertake a course of alcohol treatment, it's important to always keep basic alcohol treatment guidelines in order to ensure a swift and effective recovery.



    Andrew Regan is an online, freelance journalist.

    Article Source: http://www.a1-articledirectory.com

    Tuesday, September 1, 2009

    Issues for DSM-V: Internet Addiction

    Jerald J. Block, M.D.

    Internet addiction appears to be a common disorder that merits inclusion in DSM-V. Conceptually, the diagnosis is a compulsive-impulsive spectrum disorder that involves online and/or offline computer usage (1, 2) and consists of at least three subtypes: excessive gaming, sexual preoccupations, and e-mail/text messaging (3). All of the variants share the following four components: 1) excessive use, often associated with a loss of sense of time or a neglect of basic drives, 2) withdrawal, including feelings of anger, tension, and/or depression when the computer is inaccessible, 3) tolerance, including the need for better computer equipment, more software, or more hours of use, and 4) negative repercussions, including arguments, lying, poor achievement, social isolation, and fatigue (3, 4).

    Some of the most interesting research on Internet addiction has been published in South Korea. After a series of 10 cardiopulmonary-related deaths in Internet cafés (5) and a game-related murder (6), South Korea considers Internet addiction one of its most serious public health issues (7). Using data from 2006, the South Korean government estimates that approximately 210,000 South Korean children (2.1%; ages 6–19) are afflicted and require treatment (5). About 80% of those needing treatment may need psychotropic medications, and perhaps 20% to 24% require hospitalization (7).

    Since the average South Korean high school student spends about 23 hours each week gaming (8), another 1.2 million are believed to be at risk for addiction and to require basic counseling. In particular, therapists worry about the increasing number of individuals dropping out from school or work to spend time on computers (5). As of June 2007, South Korea has trained 1,043 counselors in the treatment of Internet addiction and enlisted over 190 hospitals and treatment centers (7). Preventive measures are now being introduced into schools (9).

    China is also greatly concerned about the disorder. At a recent conference, Tao Ran, Ph.D., Director of Addiction Medicine at Beijing Military Region Central Hospital, reported 13.7% of Chinese adolescent Internet users meet Internet addiction diagnostic criteria—about 10 million teenagers. As a result, in 2007 China began restricting computer game use; current laws now discourage more than 3 hours of daily game use (10).

    In the United States, accurate estimates of the prevalence of the disorder are lacking (11, 12). Unlike in Asia, where Internet cafés are frequently used, in the United States games and virtual sex are accessed from the home. Attempts to measure the phenomenon are clouded by shame, denial, and minimization (3). The issue is further complicated by comorbidity. About 86% of Internet addiction cases have some other DSM-IV diagnosis present. In one study, the average patient had 1.5 other diagnoses (7). In the United States, patients generally present only for the comorbid condition(s). Thus, unless the therapist is specifically looking for Internet addiction, it is unlikely to be detected (3). In Asia, however, therapists are taught to screen for it.

    Despite the cultural differences, our case descriptions are remarkably similar to those of our Asian colleagues (8, 1315), and we appear to be dealing with the same issue. Unfortunately, Internet addiction is resistant to treatment, entails significant risks (16), and has high relapse rates. Moreover, it also makes comorbid disorders less responsive to therapy (3).

    Footnotes
    Address correspondence and reprint requests to Dr. Block, 1314 Northwest Irving St., Suite 508, Portland, OR 97209; jblock@aracnet.com (e-mail). Editorial accepted for publication November 2007 (doi: 10.1176/appi.ajp.2007.07101556).

    Dr. Block owns a patent on technology that can be used to restrict computer access. Dr. Freedman has reviewed this editorial and found no evidence of influence from this relationship.

    Editorials discussing other DSM-V issues can be submitted to the Journal at http://mc.manuscriptcentral.com/appi-ajp. Submissions should not exceed 500 words.

    References

     TOP
     References

    1. Dell’Osso B, Altamura AC, Allen A, Marazziti D, Hollander E: Epidemiologic and clinical updates on impulse control disorders: a critical review. Eur Arch Psychiatry Clin Neurosci 2006; 256:464–475[CrossRef][Medline]
    2. Hollander E, Stein DJ (eds): Clinical Manual of Impulse-Control Disorders. Arlington, Va, American Psychiatric Publishing, 2006
    3. Block JJ: Pathological computer use in the USA, in 2007 International Symposium on the Counseling and Treatment of Youth Internet Addiction. Seoul, Korea, National Youth Commission, 2007, p 433
    4. Beard KW, Wolf EM: Modification in the proposed diagnostic criteria for Internet addiction. Cyberpsychol Behav 2001; 4:377–383[CrossRef][Medline]
    5. Choi YH: Advancement of IT and seriousness of youth Internet addiction, in 2007 International Symposium on the Counseling and Treatment of Youth Internet Addiction. Seoul, Korea, National Youth Commission, 2007, p 20
    6. Koh YS: Development and application of K-Scale as diagnostic scale for Korean Internet addiction, in 2007 International Symposium on the Counseling and Treatment of Youth Internet Addiction. Seoul, Korea, National Youth Commission, 2007, p 294
    7. Ahn DH: Korean policy on treatment and rehabilitation for adolescents’ Internet addiction, in 2007 International Symposium on the Counseling and Treatment of Youth Internet Addiction. Seoul, Korea, National Youth Commission, 2007, p 49
    8. Kim BN: From Internet to "family-net": Internet addict vs. digital leader, in 2007 International Symposium on the Counseling and Treatment of Youth Internet Addiction. Seoul, Korea, National Youth Commission, 2007, p 196
    9. Ju YA: School-based programs for Internet addiction prevention and intervention, in 2007 International Symposium on the Counseling and Treatment of Youth Internet Addiction. Seoul, Korea, National Youth Commission, 2007, p 243
    10. The more they play, the more they lose. People’s Daily Online, April 10, 2007
    11. Aboujaoude E, Koran LM, Gamel N, Large MD, Serpe RT: Potential markers for problematic Internet use: a telephone survey of 2,513 adults. CNS Spectr 2006; 11:750–755[Medline]
    12. Block JJ: Prevalence underestimated in problematic Internet use study (letter). CNS Spectr 2007; 12:14[Medline]
    13. Lee HC: Internet addiction treatment model: cognitive and behavioral approach, in 2007 International Symposium on the Counseling and Treatment of Youth Internet Addiction. Seoul, Korea, National Youth Commission, 2007, p 138
    14. Block JJ: Pathological computer game use. Psychiatric Times, March 1, 2007, p 49
    15. Ko CH: The case of online gaming addiction without other comorbid psychiatric disorders, in 2007 International Symposium on the Counseling and Treatment of Youth Internet Addiction, Seoul, Korea, National Youth Commission, 2007, p 401
    16. Block JJ: Lessons from Columbine: virtual and real rage. Am J Forensic Psychiatry 2007; 28:5–33
    Source: ajp.psychiatryonline.org

    Monday, August 31, 2009

    How To Find The Right Drug and Alcohol Rehab Center

    By: Jon Arnold

    When you, a family member or loved one is battling against the demons associated with drug and/or alcohol abuse, rehabilitation is needed to get back on a healthy track. Turning to the healing properties of a drug rehab or alcohol rehab center can bring about the lifestyle and behavioral changes associated with leaving negative influences to the wayside.

    There are numerous drug and alcohol rehab centers across the United States. Sometimes, a patient may even choose treatment outside of the country. Rehabilitation is a very emotional and a mental roller coaster that takes every ounce of restraint and focus. It is the responsibility of alcohol and drug rehab centers to find the medium and motivation for each patient to embrace recovery. Each and every individual that walks through the door of a clinic or enters a program is unique.

    Different Clinic and Program Approaches

    Since no two patients are alike, drug and alcohol rehab programs and procedures differ. While some rely heavily on prescription drugs and other medical techniques, there are other methods of treatment that utilize holistic or natural approaches. When evaluating a potential drug or alcohol rehab center, there are several different types of treatment programs to consider. Substance abuse is a delicate issue and each drug of choice is dealt with in a different manner. For instance, sleeping pill addiction will not be treated in the same way as crystal meth addiction.

    One of the main decisions regarding the type of alcohol or drug rehab center to consider is the length of necessary treatment. With short-term rehab clinics, a patient may become a resident and undergo various medical approaches for several weeks. They may also receive drug-free outpatient services. When longer-term care is needed, several outpatient treatments are available as well. A patient may also choose to live in a residential community treatment center to ensure continue drug-free success. Some residents may choose or need to spend years at these types of facilities.

    The issue of medication and other drug treatment options come into play when choosing a drug rehab clinic, as seen through what is called maintenance treatment. For example, a heroin addict may receive an oral dose of methadone to help block the effects of their abused drug of choice. The methadone helps to eliminate the cravings that many addicts encounter through physiological demands on their body. Some people are leery of methadone treatments because this drug in itself can be addicting.

    When it comes time to locate the best drug rehab and alcohol rehab centers within your grasp, doctors and other health professionals will give you what is called a referral. You may receive one or two to choose from, but they are usually the most viable options of treatment for you to consider. When budget is of no concern, some people will look into treatment options both near and wide. Some drug and alcohol rehab centers are more private than others, offering certain luxuries that state officials cannot afford. There are numerous brochures and websites to scan when you are able to pay more for your treatment options.

    What to Expect With Treatment

    Very rarely do you see drug rehabilitation without some sort of approach towards psychological repair. Even though drugs can be purged from the physical parts of the patient, it is the mental barriers and breakdowns that continue the vicious cycle of drug abuse. Most drug rehab and alcohol rehab programs will treat the mind, body and soul of a patient. This is the best approach towards increasing the success rate for when patients are released onto the world.

    It is also much healthier for the patient to receive well-rounded treatment so that they may achieve stronger, more positive outcomes. It is the goal of rehab centers to make sure patients equip themselves with the tools and strength needed to resist temptation and face the threat of relapse.

    While at a drug or alcohol rehab center, you will encounter a trained professional who knows the ins and outs of drug addictions. Physicians and therapists become important fixtures on the road to recovery. They will ask you many different questions and may even perform a series of medical tests. This will assist in the accurate assessment of your personal characteristics. It will aid in deciding on the appropriate drug rehabilitation program that you will benefit the most from. You could face inpatient, outpatient, residential, and/or short-stay treatment.

    Helping Rehabilitated Patients Succeed

    It is the responsibility of the newly rehabilitated patient to take control over the things that affect their life. Surrounding themselves with positive influences and adhering to outpatient counseling and programs is a must. Family and friends should be supportive and aware that the potential of relapse is never too far behind. A circle of support and encouragement is crucial to long term success.

    For a newly released drug or alcohol rehab patient, one day at a time never made more since than now. Each morning should be greeted with individual care and concern. They may need a lot of help to continue their success. Love, understanding, and support is all friends and family can give; the rest is up to the rehabbed individual.

    Article Source: http://www.afroarticles.com/article-dashboard

    Jon Arnold is a computer engineer who maintains many websites to pass along his knowledge and findings. You can read more about Drug and Alchohol Rehab at his web site at www.rehab-alcohol-drug.com/

    Thursday, August 27, 2009

    About Drug Rehabilitation Centers in New Jersey

    New Jersey drug rehabilitation centers assist substance abusers with detoxification and recovery from drug addiction. The term "drug" is defined here as any addictive chemical including alcohol, tobacco, prescription pharmaceuticals and illegal narcotics. The New Jersey Division of Addiction Services (DAS), a division of the Department of Human Services and the central organization for addiction recovery in the state, defines addiction as "a chronic, progressive, and often fatal disease characterized by irrational thoughts and habitual behaviors," but the DAS recognizes that the disease is treatable.

    Features

    Drug rehabilitation centers in New Jersey are as varied in scope and focus as our universities and hospitals. Facilities may specialize in substance abuse and recovery, or they may treat cases in conjunction with broader mental and behavioral health services. Many offer clinical and emotional support, while others provide only detoxification and medical attention. Treatment facilities are religious, like Catholic Charities in East Brunswick, or secular. Some centers are associated with local hospitals such as Raritan Bay Medical Center Behavior Services in Perth Amboy, but most are independent organizations providing customized recovery care.

    Function

    In addition to standard detox and recovery, New Jersey treatment facilities provide drug abuse education, occupational and life skills training, emotional and psychological support, and community reintegration. Rehab centers help patients recover physically and emotionally from the ravages of addiction, and then prepare them for a clean, productive life as fully functioning members of society. Addiction issues are approached differently based on the type of care and rehabilitation required.

    Types

    The DAS identifies 12 types of drug and alcohol abuse treatment. They are:

    1. Hospital-based detoxification--Detox services administered and managed by a licensed general or specialized hospital. Service providers are associated with a local hospital, and may offer in-patient or out-patient detoxification.

    2. Non-hospital-based detoxification--Detox services administered and monitored in a licensed residential (non-hospital) treatment facility. Service providers are not associated with a hospital, but are licensed by the state and capable of providing in-patient as well as out-patient detoxification.

    3. Residential short-term--A licensed non-hospital facility that provides a structured recovery environment and professional clinical services that address addiction and lifestyle issues for recovering addicts.

    4. Residential long-term or therapeutic community--A licensed non-hospital facility that provides a structured recovery environment and professional clinical services that address addiction and lifestyle issues for recovering addicts. This program utilizes the structure of a community to reintegrate the patient into society with specific focus on education and vocational skills.

    5. Extended care--A licensed non-hospital facility that provides room and board for 60 days or more. The structured environment addresses addiction, interpersonal skills and emotional development with an emphasis on work therapy.

    6. Partial hospitalization--A licensed freestanding, non-hospital and non-residential facility providing a structured environment 20 hours per week over a minimum of four separate occasions. Services include substance abuse counseling, education and community support.

    7. Intensive out-patient--A licensed, non-residential facility providing clinically intensive programs. Services include individual, group and family counseling, and education for a minimum of nine hours per week.

    8. Out-patient--A licensed, non-residential facility providing scheduled individual, group and family counseling for less than nine hours per week. Patients have access to medical and support services.

    9. Methadone maintenance--Also referred to as opioid pharmacotherapy. A licensed facility utilizing methadone, LAAM2 or other approved pharmaceutical to maintain patients addicted to heroin or similar opiates. These facilities also provide medical monitoring, lab testing, clinical assessment and intervention.

    10. Out-patient detoxification--Planned withdrawal implemented by gradually decreasing doses of the problem drug.

    11. Halfway house--Licensed facility providing six months or more of room, board and support services. Treatment is intended to assist patients with adjusting to regular patterns of life via education, vocation and independent self-monitoring.

    12. Group recovery homes--Not licensed by the state. Facilities are also referred to as transitional homes or three-quarter Houses. Patients rent living space and offer each other support services. A boarder must abstain from drugs and alcohol to remain a resident. Oxford House is the recommended provider in New Jersey. For a list by county of

    Benefits

    Rehab facilities are conveniently located, with multiple centers in each of New Jersey's 21 counties. Most licensed centers receive state and county funding from the DAS to offset costs and reduce rates. Payment methods and funding resources include:

    * Private health insurance
    * Military insurance (VA,TRICARE, etc.)
    * Medicaid
    * Medicare
    * Self pay/sliding scale
    * Payment assistance
    * South Jersey Initiative (SJI)
    * NJ Access Initiative (NJAI)
    * Drug Court (DC)
    * DUI Initiative (DUII)
    * Work First New Jersey (WFNJ)
    * Dept. of Youth & Family Services (DYFS)
    * MAP Program

    Considerations

    The Division of Addiction Services evaluates, regulates and licenses drug rehabilitation treatments, programs and facilities throughout New Jersey to ensure hygienic, professional care. Before beginning any treatment program, make sure the facility is licensed and current with the DAS.

    Written by John Farley

    Source: essortment.com

    The "Rock Bottom" Myth - Learn How to Raise the Bottom

    The "Rock Bottom" Myth - Learn How to Raise the Bottom
    This whole idea of "hitting bottom" is out of date. Some people will wait years-even decades-for their friend to reach this mythical point in their alcohol and drug use. But why wait for them to "hit bottom"? Why not help them by raising their bottom?

    Ezine Articles by Joe Herzanek

    Tuesday, August 25, 2009

    EEG Spectral Changes in Treatment Naïve Active Alcoholics

    G. Fein, Ph.D and J. Allen, B.A
    Neurobehavioral Research, Inc., Corte Madera, CA
    Address reprint request and correspondence to: Dr. George Fein, Neurobehavioral Research, Inc., 201 Tamal Vista Boulevard, Corte Madera, CA 94925, Tel: 415.927.7676, Fax: 415.924.2903, Email:george@nbresearch.com

    Abstract
    Background
    The present study examines the EEG spectra of actively drinking treatment naïve alcoholics (TxNA).
    Methods
    EEGs were gathered on 51 TxNA’s and age and sex-matched controls during eyes-closed conditions. Participants were excluded for lifetime diagnoses of psychiatric or substance abuse disorders. Power for the theta to high beta bands was examined across midline electrodes.
    Results
    The TxNA sample exhibited a nexus of disinhibited traits associated with the vulnerability to alcoholism, and had developed alcohol dependence, but no other diagnosable psychiatric or substance abuse disorders. The TxNA subjects evidenced higher power for all EEG bands compared to controls. The magnitude and anterior-posterior extent of the group differences varied across bands. Within the TxNA group, EEG power was negatively correlated with average and peak alcohol drinking duration and average and peak alcohol dose.
    Conclusions
    Increased EEG power across the theta to high beta bands distinguishes TxNAs without comorbid diagnoses from controls. These effects varied across bands in their magnitude and spatial extent, suggesting that there are different effects for the different EEG spectral generators. We hypothesize the increased power in these individuals is a trait difference associated with the inherited nexus of disinhibited traits and its manifestation in alcoholism.
    Based on the strong negative correlations with alcohol use variables, we speculate that decreases in EEG power are a morbid effect of long-term alcohol abuse. We acknowledge that this hypothesized effect of alcohol abuse on EEG power is opposite to the increased EEG power we hypothesize is associated with alcoholism and its inherited nexus of disinhibited traits. An implication of this model is that with continuing alcohol abuse, the increased EEG power in TxNAs will eventually be overpowered by the effects of long-term severe alcohol abuse. This model predicts that in very long-term alcoholics EEG power would be equal to or lower than that of age and sex comparable controls.
    Keywords: Resting EEG, power spectra, alcoholism, treatment naïve, aging

    INTRODUCTION
    Given the EEG’s high heritability and its dramatic response to alcohol intoxication, the EEG has been studied extensively as a trait marker for the genetic vulnerability to alcoholism. Many studies have reported increased slow alpha activity as a response to ethanol ingestion in both men and women (Cohen et al., 1993; Ehlers et al., 1989; Lukas et al., 1986; Lukas et al., 1989), and some have revealed changes in theta, and fast alpha activity as well (Ehlers et al., 1989; Lukas et al., 1986; Volavka et al., 1985). The background EEG is highly heritable (e.g., (Van Baal et al., 1996), as is alcoholism (Begleiter and Porjesz, 1999; Foroud et al., 1998; Foroud et al., 2000; Reich et al., 1998). Moreover, the heritability of the EEG recorded post alcohol administration is even higher than that recorded under resting conditions (Propping, 1977; Sorbel et al., 1996). In alcohol challenge studies, Ehlers and Shuckit reported elevated beta in FHP (family history positive) vs. FHN (family history negative) men 90 minutes post ethanol (Ehlers and Schuckit, 1990) and a decrease in fast alpha post-ethanol in FHN, but not FHP subjects (Ehlers and Schuckit, 1991).
    Several studies have examined EEG power as a trait marker for alcoholism, comparing individuals at high vs. low risk for developing alcoholism, with varying results. In a recent study, Rangaswamy et al. found increased beta power in FHP individuals (Rangaswamy et al., 2004). Pollock et al. (Pollock et al., 1995) reported increased beta power in older FHP subjects compared to age- and gender-matched controls. Ehlers and Shuckit found elevated baseline fast alpha in FHP subjects (Ehlers and Schuckit, 1991). In contrast, Finn and Justus found that the offspring of alcoholics showed reduced alpha power and elevated beta power compared to FHN controls (Finn and Justus, 1999). Finally, Cohen et al. found no alpha or beta EEG power differences between FHP vs. FHN samples (Cohen et al., 1991).
    Compared to the studies of high-risk samples, there have been relatively few studies of alcoholic samples. Rangaswamy et al. found increased theta power in alcoholics (Rangaswamy et al., 2003), as well as increased low beta power in male alcoholics, and increased mid beta power in female alcoholics (Rangaswamy et al., 2002). Pollock et al. examined the EEG spectra (delta through beta), and found increased theta amplitude for recovered alcoholics, but no differences for any other band (Pollock et al., 1992). These EEG spectral studies included large numbers of participants with comorbid substance abuse disorders, antisocial personality disorder, and depression, all factors independently associated with abnormal EEG power (Bauer and Hesselbrock, 1993; Costa and Bauer, 1997; Knott et al., 2001; Newton et al., 2003; Petersen et al., 1982).
    Finn et al. (Finn et al., 2000) reported that social deviance proneness and excitement/pleasure seeking account for a significant portion of the relationship between a positive family history of alcoholism and later alcohol abuse. Current theories propose that disinhibition is a fundamental mediator of the inherited predisposition toward alcohol dependency (Begleiter and Porjesz, 1999; Cloninger, 1987; Sher et al., 1991; Tartar et al., 1985). It has been proposed that behavioral phenomena such as psychopathy, antisocial and impulsive traits, and alcoholism, should be viewed as variable expressions of a generalized disinhibitory complex (Gorenstein and Newman, 1980). Several studies have reported that EEG power in externalizing disorder samples is similar to that seen in FHP samples. Excessive theta activity has been associated with a number of indicators of disinhibited personality, such as antisocial personality (Mednick et al., 1981), attention-deficit/hyperactivity disorder (Barry et al., 2003), borderline personality disorder (Russ et al., 1999), and criminality (Petersen et al., 1982; Raine et al., 1990). Excessive theta activity is thought to indicate cortical underarousal and has been associated with measures of low autonomic arousal (Raine et al., 1990). Some theorize that excessive theta reflects delayed cortical maturation and poor behavioral control that often leads to disinhibited behavioral syndromes such as antisocial personality and substance abuse (Ishikawa and Raine, 2002). Alpha power has been reported to be increased in persons with extroverted personality traits (Wall et al., 1990).
    The current study examines eyes-closed resting EEG power in treatment naïve actively drinking alcoholics (TxNA) compared to age- and gender-matched controls. This study excludes participants with lifetime diagnoses of comorbid psychiatric or substance abuse disorders. Participants were currently drinking, met current DSM-IV-R criteria for alcohol dependence, and had never sought treatment for alcoholism; in fact none of the TxNA participants self identified as alcoholics. This sample is more representative of alcoholic dependent individuals in the general population than are treated samples. We have shown that they come from a different population than treated samples, with less severe drinking histories in the first four to five years after meeting criteria for heavy drinking (Fein and Landman, in press). During this period, long-term abstinent alcoholic men and women drank an average of 210 and 134 drinks per month while TxNA men and women drank an average of 165 and 98 drinks per month. In the current study, we examine the TxNA sample’s EEG spectra, and its association with age and drinking variables.

    METHODS
    Participants
    All participants were recruited from respondents to postings, mailings, newspaper ads, ads on an Internet site, and referrals from other participants. The study involved a sample of treatment naïve, actively drinking, alcohol dependent (TxNA) individuals, and a control sample (C) matched on a one-to-one basis on gender and age with the TxNA sample. The TxNA group was recruited by advertising for ‘heavy social drinkers’ or ‘men and women who have a high tolerance for alcohol’. None of the TxNA participants labeled themselves alcoholics, and we never used the word alcoholism in referring to these participants, either in our advertisements or in their assessment procedures.
    The TxNA group (n= 51) was comprised of 20 women and 31 men between the ages of 19 and 50 (mean = 31.9, SD = 8.0). Table 1 presents subject demographics, alcoholism family history measures, and alcohol use variables and a measure of the number of symptoms of externalizing disorders and two personality measures of deviance proneness, the CPI (California Psychological Inventory Socialization Scale (Gough, 1994)), and MMPI-2 Pd (Minnesota Multiphasic Personality Inventory 2 Psychopathic Deviance Scale (Hathaway, 1989)).
    Table 1
    Table 1
    Characteristics of Participant Groups
    The inclusion criteria for the TxNA group was that they meet lifetime DSM-IV-R (American Psychiatric Association, 2000) criteria for alcohol dependence, that they were currently drinking, and that they have never sought treatment for alcoholism. DSM-IV criteria for alcohol dependence were assessed from an initial phone interview with the subjects. Participants were asked a series of questions taken from the DSM-IV-R criteria for alcohol abuse and dependence. If a subject answered “yes” to three or more of these questions at any time in the same twelve-month period, he/she met criteria for alcohol dependence. Similar questions were asked for all other drugs used more than experimentally to exclude individuals who met criteria for abuse or dependence on other drugs. Inclusion criteria for the C group was a lifetime drinking average of less than 30 alcohol containing drinks per month, and never having exceeded 60 drinks per month (a standard drink was defined as 12oz. beer, 1.5 oz. liquor, or 5 oz. of wine).
    All participants were given a computerized psychiatric diagnostic evaluation (Computerized Diagnostic Interview Schedule (Robins, 1998)) and psychological assessments. Separate lifetime use data was gathered for alcohol and all drugs used more than experimentally (using the timeline follow-back methodology of the Lifetime Drinking History Questionnaire (Skinner and Sheu, 1982; Sobell and Sobell, 1992)). Participants also had their medical history reviewed, had a blood draw to test liver function, and completed the Family Drinking History Questionnaire, based on the Family Tree Questionnaire by Mann et al., (Mann et al., 1985). We derived two measures from the Family Drinking History Questionnaire: the number of first degree relatives that were identified by the participant as problem drinkers, and the proportion of first degree relatives that were identified as problem drinkers. Post-alcohol withdrawal hyper-excitability (PAWH) was implemented partway through the study, after which it was administered to all TxNA subjects (n=28). PAWH was measured using a self-report questionnaire where subjects estimated (on a 0 to10 point scale) the frequency and distress caused by physical and psychological symptoms experienced during alcohol withdrawal. For the frequency estimate, a 0 meant never, 1 corresponded to 10 % of the times one ceased drinking, up to a 10 which indicated the symptom was experienced 100% of the time one ceased drinking. For the degree of distress caused by the presence of the symptom, a 0 meant not at all distressing, a score of 5 meant somewhat distressing, and a 10 meant “unbearable.” The symptoms were compiled from the Diagnostic Interview Schedule (DIS) (Robins, 1998), the alcohol dependence scale (Skinner and Allen, 1982), and SSAGA interviews (Bucholz et al., 1994). We computed the average frequency and intensity over eight symptoms that measure PAWH: i) shakes (hands tremble, shake inside); ii) feel tense, nervous or anxious; iii) feel fidgety or restless; iv) have trouble concentrating v) heart pound or beat rapidly; vi) feel hypersensitive to stimuli (e.g. light, sound, touch); vii) have difficulty sleeping; and viii) have memory problems.
    Exclusion criteria for both groups were: 1) history or presence of an Axis I diagnosis on the DIS, 2) history of stroke, diabetes, or hypertension that required medical intervention, 3) significant history of head trauma or cranial surgery, 4) clinical or laboratory evidence of active hepatic disease, 5) Wernickes-Korsakoff syndrome, 6) a history of drug dependence other then caffeine or nicotine, or 7) current substance abuse other then alcohol (aside from caffeine and nicotine). As noted above, substance abuse and dependence were determined from the phone interviews where follow-up questions were asked for all drugs (other than caffeine or nicotine) where the subject acknowledged more than experimental use.
    Each subject was informed as to the nature of the study and procedures and signed a consent form prior to their participation. Participants were to complete a total of four sessions that included clinical, neuropsychological, electrophysiological and neuroimaging assessments. All participants were to abstain from drinking for 24 hours prior to each lab visit, and a Breathalyzer was administered before each session. No participants in the current study had positive Breathalyzer results (>.000) on any of their study sessions. Other drugs of abuse were not tested for. For the purposes of this study, we are examining only the data during the eyes closed resting portion of the EEG session, which took place on the third visit. All participants who completed a session were paid for the session and any travel expenses. Participants also received a completion bonus if they completed all four sessions of the study.
    EEG Recording and Artifact Reduction
    As noted above, participants were given a Breathalyzer upon arrival at the EEG lab; a 0.000 Breathalyzer result was required to continue the session. Participants were seated comfortably in a sound attenuated room. The computer screen, used in presenting stimuli for other EEG/ERP experiments, was turned off. The participants were asked to relax with their eyes closed for five minutes. Over the course of the study, two EEG acquisition systems were used, a 40-channel system (n = 87) and a 64-channel (n = 15). Only the midline electrodes, which were common to both systems, were examined for this study. Reference was the right ear for all recordings, and ground was 4 cm above the nasion for 40-channel caps and 8 cm above the nasion for 64-channel caps. EEG data was acquired using the NuAmps (NuAmp, Neuroscan, Inc.) single-ended 40 channel amplifier and Scan 4.2 Acquisition Software (Neurosoft, Inc.) for the 40-channel recordings. The NuAmps amplifier had a fixed range of ±130 μV sampled with a 22 bit A/D converter where the least significant bit was 0.062 μV. For the 64-channel recordings, EEG data was acquired using the SynAmps2 (SynAmps2, Neuroscan, Inc.) amplifier and Scan 4.3 Acquisition Software (Neurosoft, Inc.). The SynAmps2 amplifier had a fixed range of ± 333 μV sampled with a 24 bit A/D converter where the least significant bit was 0.019 μV. Electrode impedances were maintained below 10 kΩ. The sampling rate was 250 samples per second, and activity was recorded for 5 minutes. Data from control subjects whose data was collected using the different amplifier systems (NuAmps, SynAmps2) were examined, and revealed no differences associated with the different acquisition amplifiers. Vertical eye movements were recorded by electrodes above and below the left eye for later reduction of ocular artifact.
    Raw data were processed offline using the Edit Program in Scan 4.3 (Neurosoft, Inc.). Data from the first and last minute were discarded and the analysis was performed on the middle three minutes of recordings. Ocular artifacts were removed using the ocular artifact reduction algorithm (ARTCOR) implemented in Scan4.3 (Neuroscan, 2003). Data were then bandpass filtered between 0.5 and 30Hz at 48 dB/Octave. Power spectra was computed using the Scan4.3 AVERAGE procedure which computes a standard power spectrum adapted from the Cooley-Tukey method, on 512 sample epochs (2.044 seconds in duration) using a 10% cosine taper. Average power spectra were then aggregated for six frequency bands: theta (3 to 7.5 Hz), low alpha (7.51 to 10 Hz), high alpha (10.01 to 12 Hz), low beta (12.01 to 16 Hz), mid beta (16.01 to 20 Hz), and high beta (20.01 to 28 Hz). A natural log transformation was applied to the absolute power data to normalize the distributions.
    Statistical Analysis
    This paper only examines the midline recordings common to all participants (Fz, FCz, Cz, CPz, Pz, Oz). Repeated measures ANOVA was carried out on the log power dependent variables using the General Linear Models procedure in the Statistical Analysis System (SAS Institute, 1990), with age, group and gender as between-subject effects and EEG band and electrode as repeated measures. The association of band power with age and alcohol use variables was analyzed using Spearman correlations. Because alcohol use duration is partially confounded with age (older participants have had a longer life in which to drink), associations of EEG measures with alcohol use duration and with age were examined using partial correlation analysis (i.e., association of EEG measures and age with alcohol use duration partialled out, and association of EEG measures and alcohol use duration with age partialled out).

    RESULTS
    Group Differences in Demographic and Subject Variables
    Table 1 presents the demographic, alcohol use and subject variables for men and women in each group. As noted above, the TxNA group and controls were matched for age and gender with age ranging from 19 to 50 years. The groups were also similar in education. The TxNA group had more first degree relatives who were problem drinkers (F1,98 = 6.72, p < .02), but this effect was not very large, with group membership accounting for only 6.2% of the variance of the number of first degree relatives who were problem drinkers. As expected, the groups differed on alcohol use measures (group membership accounted for 5.2% of the variation in duration of active drinking, 64.1% of the variance of average lifetime drinking dose, 59.8% of the peak dose variance, and 58.7% of the variance of the drinking dose in the 6 months immediately prior to the study. The TxNA group compared to Controls had a larger number of externalizing symptoms (the sum of Antisocial Personality Disorder and Conduct Disorder symptoms on the DIS (Robins, 1998)), with group membership accounting for 8.5% of the symptom count variance (F1,98 = 9.96, p<.003). They also showed more evidence of deviance proneness on both the California Psychological Inventory (CPI) socialization scale (Group accounting for 21.7% of the variance (F1,98 = 27.85, p < .0001) and the MMPI Psychopathic Deviance (PD) scale (Group accounting for 9.5% of the variance (F1,98 = 10.31, p < .002).
    As described above, PAWH was measured using a self-report questionnaire where participants estimated (on a 10 point scale) first, the frequency and then, the distress level of physical and psychological symptoms experienced during alcohol withdrawal. The TxNA’s mean score (± sd) for the frequency of withdrawal symptoms was 2.46 ± 1.6, meaning that, on average they experienced withdrawal symptoms after drinking 24.6% of the time. On the distress level scale (10 point scale), a zero indicated that the withdrawal symptoms bothered the participant “not at all”, a three indicated that the symptoms were “a little bothersome” and five indicated that the symptoms were “somewhat bothersome”. The mean score for distress was 2.91 ± 1.89, indicating that the participants typically found the distress of withdrawal symptoms less then “a little bothersome”. There were no significant associations between EEG power and withdrawal measures.
    EEG Power
    Analysis of between-group effects (between subject variance)
    In the between subjects analysis (power averaged across bands and electrodes), group membership accounted for 4.0 % of the log power variance (F1,93 = 4.4, p < r =" −.22,">1,93 = 5.1, p <>1,93 = 3.0, p < .09), with men having lower EEG power than women.
    Analysis of repeated measures effects
    The analysis of repeated measures indicated the well known large differences in power between the EEG bands (accounting for 33.3% of the within-subject across band variance, F5,465 = 51.43, p < .0001), and across electrode sites (accounting for 6.9% of the within-subject across electrode variance, F5,465 = 8.34, p < .0001). There were also electrode by group interactions (accounting for 5.6% of the within-subject across electrode variance, F5,465= 6.75, p < .0005), and band by electrode by group interactions (accounting for 2.5% of the within-subject across bands and electrodes variance, F25,2325 = 2.63, p < .02); both of these effects indicate that differences in power between the groups varied across bands and electrodes. Figure 1
    Fig. 1
    presents this data. The strongest group differences were observed for low alpha and mid beta, where the TxNA group had higher power at all midline electrode locations except the most frontal (Fz). The TxNA group showed higher power at the central-posterior sites (CPz, Pz, Oz) for high beta. For theta, high alpha, and low beta the TxNA group had higher power at CPz and Oz, with a trend towards higher power at Pz.
    Fig. 1
    Fig. 1
    Fig. 1
    Displays group differences in EEG power for each band at each midline electrode location. For presentation purposes the inverse of log (power) has been used to show the results as power on a natural log scale. *, **, ***: p < .05, p < (more ...)
    There were band by age interactions, electrode by age interactions, and group by band by electrode by age interactions (all F5,465 > 4.88, p < .002) indicating that the correlations with age differ across groups, bands, and electrodes. In order to better understand this data, we computed age correlations for each group at each electrode within each band. Table 2. presents these associations. In the controls, there were only a few age associations. For high alpha, there was a negative association at Fz, as well as trends for negative associations at FCz and Oz. For low beta, a positive association with age was observed at CPz, with a trend at Cz. Similarly, positive associations between age and power were observed at these same electrode locations for mid and high beta.
    Table 2
    Table 2
    Association of EEG Power with Age and Lifetime Drinking Duration
    Within the TxNA group, the age associations were consistently negative, and showed strong patterns across electrodes within specific bands. Strong negative correlations with age were observed at all midline electrode sites for theta, high alpha, and low beta power. For mid-beta power, negative associations were observed only at Oz, and for low alpha and mid beta power only a trend for a negative correlation at Oz was observed.
    Since age may potentially be confounded with lifetime drinking duration (older participants may have had a longer time to drink), we examined the association between lifetime drinking duration and power measures in the TxNA group. There were strong negative associations between power and lifetime drinking duration for theta, high alpha, and low beta at all electrode sites, and for low alpha power and mid beta power at Oz, with a trend for high beta at Oz (see Table 2). Within the TxNA group, we next examined the associations between age and power with lifetime drinking duration partialled out. These partial correlations were close to zero (see Table 2). Because negative associations with age were not seen in controls, the simplest explanation for this pattern of results is that these negative associations in the TxNA group of age with EEG power are a consequence of the negative association of abusive drinking with power.
    In a search for additional evidence supporting this hypothesis, we examined the association between lifetime drinking dose (drinks/month) and the power measures within the TxNA group. Table 3 presents these associations. There were strong negative associations at all electrode sites of the alcohol dose variables with low beta, mid beta, and high beta, as well as negative associations with low alpha power at Fz, FCz, Cz, and CPz, with a trend for an association at Pz. Negative associations were also evident for high alpha power at the frontal electrodes, with a trend for a negative association for theta power at Pz and Oz. These negative associations between alcohol dose and power measures is consistent with the hypothesis that the negative associations of power measures with age and with lifetime duration of drinking in the TxNA group are a consequence of abusive drinking rather than of age per se.
    Table 3
    Table 3
    EEG Power Associations with Lifetime Drinking Dose (Average Drinks/Month)
    The few associations observed between power and lifetime drinking dose in the controls were more sporadic, weaker, and positive rather then negative. These positive associations and trends were seen for theta power at CPz, low alpha power at Cz, CPz, Pz, and Oz, and mid beta power at Oz. It is of interest that in the controls, the effects of moderate or light drinking may have the opposite effect to that seen in the alcohol dependent sample, with alcohol use actually increasing EEG power.
    In the TxNA group, the measures of alcohol use over the six months prior to study were very highly correlated with the average lifetime dose measures (r = 0.93). For this reason, we did not examine the associations of recent alcohol dose with EEG measures since the results would have been entirely redundant with the results for average dose. Finally, we found no associations of the power measures with either of the family history of alcoholism measures (number of first degree relatives with alcohol problems and percent of first degree relatives with alcohol problems) all r’s < |.22|, p > 0.12.

    DISCUSSION
    Central Findings
    The central finding in this study was that TxNA alcoholics evidence higher power than controls across the theta to high beta bands, with the magnitude and anterior-posterior extent of these effects varying across bands. The largest and most widespread effects were for the low alpha and mid beta bands, where the effects were present for all electrodes posterior to Fz. For the other bands, the effects did not extend as anteriorly and were of smaller magnitude. These differences in the effects across bands indicate that the effects are not a simple global increase in EEG power, but rather are specific and different effects for the various bands. Given that we asked all subjects to abstain from alcohol for 24 hours prior to the EEG session, no subjects had positive breathalyzer tests on the day of their EEG study, and that on average our TxNA subjects reported experiencing withdrawal symptoms only about one quarter of the time, we believe it is highly unlikely that their EEG results reflect the effects of post alcohol withdrawal hyperexcitability.
    In the introduction, we reviewed the literature showing that there is a nexus of disinhibitory traits, deviance proneness, externalizing symptoms, and a positive family history for alcoholism that often appear together and are strongly associated with alcoholism and other substance abuse. In its more severe manifestations, this nexus is represented in alcoholics with comorbid psychiatric, other substance abuse, and antisocial diagnoses. In addition, a relatively common set of EEG characteristics has been associated with the various aspects of this nexus.
    The population studied here is unique with regard to this nexus discussed above. All participants met criteria for alcohol dependence (alcoholism), yet they had at most a minimally greater family history for alcoholism than controls. Individuals with comorbid antisocial personality disorder, conduct disorder, depression, anxiety, or other substance abuse disorders were excluded. The TxNA sample came from a population with a history of early abusive drinking (in the first five years immediately after meeting criteria for heavy alcohol consumption) that was 30–40 % less in average and peak dose than treated samples (Fein and Landmann, in press). They had an increased rate of externalizing symptoms and psychological evidence of deviance proneness compared to controls, although these rates were markedly less than those of treated samples (Fein et al., 2004). Our hypothesis is that the population studied is composed of individuals with less severe manifestations of the nexus described above who have gone on to develop alcohol dependence but no other diagnosable psychiatric or substance abuse disorders. We believe our results show that this select population is characterized by increased EEG power across the theta to high beta bands.
    While the sample studied (TxNA) was advantageous in that it is more representative of alcoholics in the general population in that it is an untreated sample free of comorbid disorders, there were limitations inherent in studying this sample. We did not examine severe active alcoholics, and although it is possible that our sample represents severe alcoholics in the relatively early stages of their alcoholism, previous examination of this population suggests that this is in fact a different population from alcoholics typically studied. Furthermore, the sample studied reported experiencing relatively minor withdrawal symptoms. Although it is beneficial to be able to show that it is highly unlikely that our results are associated with alcohol withdrawal, our results are silent on the EEG effects of more severe withdrawal that may be present in samples with greater alcoholism severity.
    There are other limitations to the current study. In hindsight, we should have assessed for caffeine or nicotine dependence or recent caffeine or nicotine use to determine the degree to which such use or dependence could have influenced our EEG results. Finally, since our TxNA sample is almost by definition in denial about their alcoholism, it is also highly likely that they would be in denial with regard to alcohol problems in their first degree relatives. Their data regarding the family history of alcoholism assessment is highly suspect and may be a gross underreporting of alcohol problems in their extended families. Therefore, the negative findings regarding the association of the EEG power measures with the family history of alcoholism should be discounted.
    Our data support the hypothesis that an effect of long-term alcohol abuse is to negatively impact the substrate underlying EEG power. Negative associations between EEG power and alcohol use variables (both dose and duration), suggests that a reduction in EEG power is a morbid effect of accumulating alcohol abuse. We acknowledge that this hypothesized effect of alcohol abuse is opposite to the increased EEG power effect that we hypothesize is associated with the inherited nexus of disinhibited traits that conveys a vulnerability to alcoholism. The current subjects were studied at the relatively early stages of this process, before these morbid effects of chronic alcohol abuse can overpower the trait-related increased EEG power present in this sample of alcoholics.
    With continuing alcohol abuse, we would expect to see the trait of increased EEG power in alcoholics overpowered by the effects of long-term severe alcohol abuse. In other words, in longer term and more severe alcoholics, we hypothesize that we would not see the increased EEG power observed in the current study. In the most severe and longest-term alcoholics, we hypothesize that we would see an actual reduction in EEG power. We have been studying a sample of long-term abstinent treated alcoholics in whom we can test these hypotheses.

    Footnotes
    This work was supported by Grants AA11311 (GF) and AA13659 (GF), both from the National Institute of Alcoholism and Alcohol Abuse. We also express our appreciation to the NRI recruitment and assessment staff, and to each of our volunteer research participants.

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