|
|
|
After establishing rapport and trust, what is the next step when you suspect the client, or someone in his or her family has a problem with substance abuse? Now enters
Compassion is vital in all healing work. It is the ability to be totally present for the client in the moment, in the pain. It is not sympathy, or pity, but rather a 'feeling with' the person. This allows the therapist to not judge, but rather to hear the tears, to not fix, but rather hold the vision that we are all on this little planet struggling for wholeness. This includes neutrality, which can be difficult for therapists; we want our clients to get better, and can experience negative countertransference when they don't. The key here is to be non-judgemental, and detached as to the outcome. This breaks the cycle in which the therapist becomes the enabler. Detachment combined with caring is what 'warms up' the neutrality. The addict or enabler must know you care, but ultimately must undertake the healing journey for themselves, not to please you. Holding hope is crucial, although it may be something you never verbalize to the client. Therapists who trust that there is a core in each of us that wants us to be healed and whole transmit through the unspoken countertransference an optimism that can carry the therapy during times of despair.
for the addict and their family continues throughout the treatment, as does attention to the body-mind-spirit continuum of the disease. Our first concern as with any illness is assessing the physical needs of the addict. This is best done by a physician specializing in addiction and a nutritional consultant. Always be sure to assess for the possible necessity of an in-patient program based upon amount and length of abuse. Chronic abusers may need a more intensive intervention to assist not only their physical needs but the dismantling of their entrenched system of denial. Although many such programs are costly there are often county, state, church, or Salvation Army funded detox programs.
Chemical dependency is very hard on the body and the person's nutrition has often been their last concern. There is a paradox here in that many addicts do pay extreme attention to what they eat and how they exercise with the same type of obsessive thinking and compulsive behavior that highlights their addiction. We particularly see this with cocaine and amphetamine abusers. Eating disorders are another strand on the web of addictions, and many of the same dynamics and principles occur in these disorders as in substance abuse. The primary difference is that while an alcoholic or drug abuser can and often must learn to abstain totally from the drug, no one can go without food. If your client has an eating disorder, make sure you refer to a physician. Unfortunately, the specific methodology of treatment of anorexia, bulimia and compulsive over-eating are beyond the scope of this course.
In drug addiction, when an individual is trying to "white knuckle" recovery they may also become compulsive in their health routines. "White knuckling" refers to trying through will alone to overcome addiction. These attempts are characterized by extreme irritation, tension and nervous energy. All addicts are likely to exhibit these signs in early recovery and there is an initial honeymoon period: however, the degree of arrogance of thinking that they can do it alone without a larger support system distinguishes the "white knuckler". We often feel that "the beast has changed clothes" when the same illusions persist in this type of attempt to recover. The feeling that "I am in control" is perhaps the biggest of these. While it is a huge step for the addict to realize there is a problem, this type of quitting is often doomed to failure, setting off a new round of use and abuse, overlaid with feelings of failure and depression, guilt and shame.
When making the referral make sure the physician knows the nature of the issues of addiction. Our society underestimates the seriousness of this problem at every level and in every profession. Although things have progressed dramatically from have no alcoholism or substance abuse classes regularly required for therapists or physicians twenty years ago to having the requirements of today, these advances are fairly recent. In some ways our own professions are in the early stages of recovery from codependence! There is also increasing evidence of change in body chemistry related to long term use of drugs.
Traditionally, the long held goal has been for the addict to be totally drug free so not to trigger any cravings for the drug of choice. We are seeing in our clinical practices greatest long term success for some clients with varying prescription maintenance, particularly with antidepressants. There way be a "self-medicating" component to many addictions, particularly at the onset of the addiction, and new research is looking at the biochemistry and neurology of addiction. Be prepared for resistance, sometime more from the client's sponsor than the client, and be willing to educate the client about medication. Also, medication is no substitute for attending meetings, working the "program" and being in therapy.
Working
closely with a physician or psychiatrist is crucial in clients with a dual
diagnosis. Additionally
alternative therapies such as nutritional counseling, acupuncture and herbs
are being reported as having positive therapeutic values in this regard.
With the physical side of addiction being monitored you are then able to
concentrate on the domains of counseling: mind and spirit. Please go now
to the article 
Managing
coexisting depression calls for careful diagnosis, treatment for more
information on treating depression in addicts.
http://www.niaaa.nih.gov/publications/aa33.htm
National Institute on Alcohol Abuse and Alcoholism No. 33 PH 366 July 1996
Neuroscience Research and Medications Development
Research suggests that the processes leading to the development of alcoholism reside largely in the brain. This has led to the concept of developing medications that act on specific brain chemicals to interfere with these processes. In 1995, the U.S. Food and Drug Administration approved the use of one such medication--naltrexone, under the brand name ReVia(TM)--to help prevent relapse in recovering alcoholics. By combining results of clinical and neuroscience research, this advance signals a new era in alcoholism treatment. This Alcohol Alert shows how brain chemistry research may lead to further breakthroughs in the medical treatment of alcoholism and its effects.
Phenomena of Addiction
Reinforcement. It may seem self-evident that a person will repeat an action that brings pleasure, or reward. The process by which such an action becomes repetitive is called positive reinforcement. Normally, this process functions to sustain motivation for behaviors essential to the individual or species, such as eating, drinking, or reproductive behavior (1,2). Evidence suggests that alcohol and other drugs of abuse (AOD's) are chemical surrogates of such natural reinforcers (3). AOD's that cause a rewarding mental state (e.g., euphoria) function as positive reinforcers upon initial exposure (3). These drugs may be more powerfully and persistently rewarding than the natural reinforcers to which the human brain is accustomed (4). Thus, continued exposure to AOD's can initiate increased drug-seeking behavior and set the stage for addiction. Although the remainder of this discussion concentrates on alcoholism, the principles described are generally valid for other addictions as well.
After alcohol-seeking behavior has been established, the brain undergoes certain adaptive changes to continue functioning despite the presence of alcohol. As a consequence of this adaptation, however, certain abnormalities occur in the brain when alcohol is removed. Thus, periods of abstinence are marked by feelings of discomfort and craving, motivating continued alcohol consumption. This kind of motivation--based not on reward but on avoidance of painful stimuli--is called negative reinforcement. Both positive and negative reinforcement are involved in the maintenance of alcoholism (5,6).
Dependence. Physical dependence in alcoholism is the need for continued alcohol consumption to avoid a withdrawal syndrome that generally occurs from 6 to 48 hours after the last drink. Withdrawal symptoms include anxiety, agitation, tremor, elevated blood pressure, and, in severe cases, seizures. The withdrawal syndrome is distinct from the ongoing process of negative reinforcement described above, although both phenomena result from adaptation of the nervous system (7,8).
Alcohol and the Brain
All brain functions, including addiction, involve communication among nerve cells (neurons) in the brain. Each of the brain's neurons connects with hundreds or thousands of adjacent neurons. The points of connection between neurons are generally separated by microscopic gaps called synapses. Messages are carried across synapses by chemicals called neurotransmitters. Although there are approximately 100 different neurotransmitters, each neuron releases only one or a few different types. After its release, a neurotransmitter crosses the synapse and activates a receptor protein in the outer membrane of the "receiving" neuron.
Each receptor type responds preferentially to one type of neurotransmitter. However, most neurotransmitters can activate different subtypes of the same receptor, producing different responses in different brain cells or in different parts of the brain (9). Determining the specific neurotransmitters and receptor subtypes that may be involved in the development and effects of alcoholism is the first step in developing medications to treat alcoholism (10,11).
Receptor activation causes a change in the receiving neuron. This change may consist of a transient increase or decrease in the neuron's responsiveness to further messages (12). Alternatively, some receptors promote long-term changes that support functions such as growth; learning; or adaptation to changes in the neuron's environment, such as the presence of alcohol. The process of converting messages from other neurons into changes within the receiving neuron is called signal transduction (9). Alcohol may produce some of its effects by interfering with signal transduction (13,14).
Pharmacological treatment for alcoholism has focused on the processes described above. Other elements of message proce ssing, described below, may provide additional targets for medications development.
The brain's long-lasting adaptations to alcohol may result in part from changes in gene function (15). Genes direct the synthesis of proteins, such as receptors. By influencing gene function, alcohol may alter the structure and function of specific receptors that have roles in intoxication, reinforcement, and physical dependence (16-19). Alcohol's effects on genes may also alter proteins involved in signal transduction (14). Additional research is needed in this area before practical benefits, in the form of medications, can be realized.
Groups of neurons with similar functions extend from one brain region to another, forming neural circuits. Circuits interact with one another to integrate the functions of the brain. One important part of a circuit that has been studied for its role in reward is the nucleus accumbens, located near the front of the brain (3,20). Other circuits are involved in various aspects of alcoholism. For example, circuits involved in physical withdrawal have long been targets of medications development.
Medications Development
Any alteration in the function of message reception or transduction systems may have significant effects on the progression of alcoholism after drinking has started. An understanding of how specific changes in the function of these systems affect susceptibility to alcohol provides a starting point for medications development (21-23). Medications can theoretically be developed to block receptors or enhance their function; to increase or decrease the synthesis, release, or synaptic concentration of neurotransmitters; or to modulate signal transduction.
Medications development for alcoholism focuses mainly on two goals: treatment of withdrawal and the maintenance of abstinence (relapse prevention). Many withdrawal symptoms appear to result in part from overactivity of the sympathetic ("fight or flight") nervous system (24), which normally functions to prepare the body for stressful situations. The preferred medications for withdrawal are benzodiazepines, such as Valium¨, which "brake" the racing sympathetic nervous system while helping prevent seizures (25,26).
Medications to interrupt the process of reinforcement are being investigated. The key neurotransmitters involved in reinforcement include the endogenous opioids and dopamine. The endogenous opioids are a group of brain chemicals similar in action to morphine. They appear to amplify the pleasurable effects of rewarding activities (27,28) and have been shown to help maintain drinking behavior (29,30). Naltrexone helps prevent relapse and reduce craving by blocking certain opioid receptors, presumably reducing the pleasurable effect of alcohol (31-33).
Dopamine is involved in aspects of motivation and has been implicated in addiction to several drugs (34). Alcohol has been shown to increase levels of dopamine in the nucleus accumbens (35), although dopamine's precise role in the development of alcoholism remains unclear (34,36). Bromocriptine, a medication that activates dopamine receptors, has been thought to reduce craving in alcoholics; however, it has not been found to maintain abstinence (37).
A significant impetus to medications development has been the recognition that alcoholism and some psychiatric disorders appear to involve some of the same neurotransmitter systems (38). This presumed similarity in neural mechanisms may also be related to the substantial co-occurrence of AOD and psychiatric disorders in the same patients (39-41). For both of these reasons, researchers have investigated current and experimental psychiatric medications to treat alcoholism occurring either alone or in the presence of psychiatric symptoms. An example is buspirone, an antianxiety medication that activates certain serotonin receptors. Seroton in, a neurotransmitter that helps regulate many mental and bodily functions, helps modulate reinforcement (42,43). Extensive research has demonstrated a limited effect of buspirone on alcohol craving and consumption among anxious alcoholics (44,45). Similarly, the antidepressants imipramine (46) and desipramine (47) were found to decrease alcohol consumption among alcoholics whose co-occurring depression improved in response to the medication.
The antidepressants that have stimulated the most alcohol-related research activity include fluoxetine (Prozac¨) and related medications that increase serotonin concentrations in synapses (48,49). Clinical trials of these medications to date have not shown effectiveness in treating alcoholism (23).
In summary, medications that treat psychiatric disorders may in some cases be effective in treating co-occurring alcoholism as well. Further research is needed to determine whether such medications can improve treatment outcome in the absence of co-occurring psychopathology.
Neuroscience Research and Medications Development-- A Commentary by NIAAA Director Enoch Gordis, M.D.
Developing effective pharmacotherapies for alcoholism treatment is a top priority of alcohol research. Doing so depends on neuroscientists' continued elucidation of how alcohol acts on the brain to produce the fundamental phenomena of alcoholism--tolerance, withdrawal, impaired control over drinking, and craving--and how these phenomena can be interrupted or controlled. It also depends on clinical researchers' testing the efficacy of medications through carefully controlled clinical trials. The development of naltrexone in the United States and acamprosate in Europe is based on just such an important convergence of neurosciences and clinical research.
At the present time, clinical research indicates that the best treatment results are achieved with a combination of pharmacotherapy and skilled counseling. Research is underway to determine how alcoholism treatment medications work (the mechanism of action), the potential therapeutic value of using pharmacotherapy over a longer period of time, and which subsets of patients are most likely to benefit from new pharmacological treatments. The prospects for improved alcoholism treatment have never been better.
References
(1) Koob, G.F. Plenary address: Neural mechanisms of drug reinforcement. In: Kalivas, P.W., and Samson, H.H., eds. The Neurobiology of Drug and Alcohol Addiction. Annals of the New York Academy of Sciences 654:171-191, 1992. (2) Koob, G.F., and Bloom, F.E. Cellular and molecular mechanisms of drug dependence. Science 242(4879):715-723, 1988. (3) Di Chiara, G.; Acquas, E.; and Tanda, G. Ethanol as a neurochemical surrogate of conventional reinforcers: The dopamine-opioid link. Alcohol 13(1):13-17, 1996. (4) Hyman, S.E., and Nestler, E.J. Initiation and adaptation: A paradigm for understanding psychotropic drug action. American Journal of Psychiatry 153(2):151-162, 1996. (5) Gardner, E.L., and Lowinson, J.H. Drug craving and positive/negative hedonic brain substrates activated by addicting drugs. Seminars in the Neurosciences 5(5):359-368, 1993. (6) Koob, G.F.; Markou, A.; Weiss, F.; and Schultheis, G. Opponent process and drug dependence: Neurobiological mechanisms. Seminars in the Neurosciences 5(5):351-358, 1993. (7) Linnoila, M. Alcohol withdrawal and noradrenergic function. Annals of Internal Medicine 107(6):875-889, 1987. (8) Morrow, A.L.; Suzdak, P.D.; Karanian, J.W.; and Paul, S.M. Chronic ethanol administration alters *-aminobutyric acid, pentobarbitol and ethanol-induced 36Cl* uptake in cerebral cortical synaptoneurosomes. Journal of Pharmacology and Experimental Therapeutics 246(1):158-164, 1988. (9) Shepherd, G.M. Neurobiology . 3rd ed. New York: Oxford University Press, 1994. (10) Hunt, W.A. Neuroscience research: How has it contributed to our understanding of alcohol abuse and alcoholism? A review. Alcoholism: Clinical and Experimental Research 17(5):1055-1065, 1993. (11) Deitrich, R.A., and Erwin, V.G., eds. Pharmacological Effects of Ethanol on the Nervous System. Boca Raton, FL: CRC Press, 1996. (12) Grant, K.A. Emerging neurochemical concepts in the actions of ethanol at ligand-gated ion channels. Behavioural Pharmacology 5:383-404, 1994. (13) Alling, C.; Diamond, I.; Leslie, S.W.; Sun, G.Y.; and Wood, W.G., eds. Alcohol, Cell Membranes, and Signal Transduction in Brain. New York: Plenum Press, 1993. (14) Davis-Cox, M.I.; Fletcher, T.L.; Turner, J.N.; Szarowski, D.; and Shain, W. Three-day exposure to low-dose ethanol alters guanine nucleotide binding protein expression in the developing rat hippocampus. Journal of Pharmacology and Experimental Therapeutics 276(2):758-764, 1996. (15) Miles, M.F. Alcohol's effects on gene expression. Alcohol Health & Research World 19(3):237-243, 1995. (16) Snell, L.D.; Tabakoff, B.; and Hoffman, P.L. Radioligand binding to the N-methyl-d-aspartate receptor/ionophore complex: Alterations by ethanol in vitro and by chronic in vivo ethanol ingestion. Brain Research 602(1):91-98, 1993. (17) Charness, M.E.; Hu, G.; Edwards, R.H.; and Querimit, L.A. Ethanol increases *-opioid receptor gene expression in neuronal cell lines. Molecular Pharmacology 44(6):1119-1127, 1993. (18) Ortiz, J.; Fitzgerald, L.W.; Charlton, M.; Lane, S.; Trevisan, L.; Guitart, X.; Shoemaker, W.; Duman, R.S.; and Nestler, E.J. Biochemical actions of chronic ethanol exposure in the mesolimbic dopamine system. Synapse 21(4):289-298, 1995. (19) Hu, G.; Querimit, L.A.; Downing, L.A.; and Charness, M.E. Ethanol differentially increases *2-adrenergic and muscarinic acetylcholine receptor gene expression in NG108-15 cells. Journal of Biological Chemistry 268(31):23441-23447, 1993. (20) Koob, G.F.; Rassnick, S.; Heinrichs, S.; and Weiss, F. Alcohol, the reward system and dependence. In: Jansson, B.; Jšrnvall, H.; Rydberg, U.; Terenius, L.; and Vallee, B.L, eds. Toward a Molecular Basis of Alcohol Use and Abuse. Basel, Switzerland: Birkhaźser-Verlag, 1994. pp. 103-114. (21) Kranzler, H.R., and Orrok, B. The pharmacotherapy of alcoholism. In: Tasman, A.; Hales, R.E.; and Frances, A.J., eds. American Psychiatric Association Review of Psychiatry. Vol. 8. Washington, DC: American Psychiatric Press, 1989. pp. 359-379. (22) Litten, R.Z., and Allen, J.P. Pharmacotherapies for alcoholism: Promising agents and clinical issues. Alcoholism: Clinical and Experimental Research 15(4):620-633, 1991. (23) Litten, R.Z., and Allen, J.P. Pharmacological therapies of alcohol addiction. In: Miller, N.S., and Gold, M.S., eds. Pharmacological Therapies for Drug & Alcohol Addictions. New York: Marcel Dekker, 1995. pp. 127-141. (24) Linnoila, M. Alcohol withdrawal syndrome and sympathetic nervous system function. Alcohol Health & Research World 13(4):355-357, 1989. (25) Treiman, D.M. Treatment of alcohol withdrawal seizures with benzodiazepines: Clinical applications. In: Porter, R.J.; Mattson, R.H.; Cramer, J.A.; Diamond, I.; and Schoenberg, D.G., eds. Alcohol and Seizures: Basic Mechanisms and Clinical Concepts. Philadelphia: F.A. Davis, 1990. pp. 283-289. (26) Anton, R.F., and Becker, H.C. Pharmacotherapy and pathophysiology of alcohol withdrawal. In: Kranzler, H.R., ed. The Pharmacology of Alcohol Abuse. New York: Springer-Verlag, 1995. pp. 315-367. (27) Terenius, L. Alcohol addiction (alcoholism) and the opioid system. Alcohol 13(1):31-34, 1996. (28) Reid, L.D. Endogenous opioids and alcohol dependence: Opioid alkaloids and the propensity to drink alcoholic beverages. Alcoh ol 13(1):5-11, 1996. (29) Froehlich, J.C.; Zweifel, M.; Harts, J.; Lumeng, L.; and Li, T.-K. Importance of delta opioid receptors in maintaining high alcohol drinking. Psychopharmacology 103(4):467-472, 1991. (30) Gianoulakis, C.; De Waele, J.-P.; and Thavundayil, J. Implication of the endogenous opioid system in excessive ethanol consumption. Alcohol 13(1):19-23, 1996. (31) Volpicelli, J.R.; Alterman, A.I.; Hayashida, M.; and O'Brien, C.P. Naltrexone in the treatment of alcohol dependence. Archives of General Psychiatry 49:876-880, 1992. (32) Volpicelli, J.R.; Watson, N.T.; King, A.C.; Sherman, C.E.; and O'Brien, C.P. Effect of naltrexone on alcohol "high" in alcoholics. American Journal of Psychiatry 152(4):613-615, 1995. (33) O'Malley, S.S.; Jaffe, A.J.; Chang, G.; Rode, S.; Schottenfeld, R.; Meyer, R.E.; and Rounsaville, B. Six-month follow-up of naltrexone and psychotherapy for alcohol dependence. Archives of General Psychiatry 53(3):217-224, 1996. (34) Di Chiara, G. The role of dopamine in drug abuse viewed from the perspective of its role in motivation. Drug and Alcohol Dependence 38:95-137, 1995. (35) Wozniak, K.M.; Pert, A.; Mele, A.; and Linnoila, L. Focal application of alcohols elevates extracellular dopamine in rat brain: A microdialysis study. Brain Research 540(1-2):31-40, 1991. (36) Rassnick, S.; D'Amico, E.; Riley, E.; and Koob, G.F. GABA antagonist and benzodiazepine partial inverse agonist reduce motivated responding for ethanol. Alcoholism: Clinical and Experimental Research 17(1):124-130, 1993. (37) Powell, B.J.; Campbell, J.L.; Landon, J.F.; Liskow, B.I.; Thomas, H.M.; Nickel, E.J.; Dale, T.M.; Penick, E.C.; Samuelson, S.D.; and Lacoursiere, R.B. A double-blind, placebo-controlled study of nortriptyline and bromocriptine in male alcoholics subtyped by comorbid psychiatric disorders. Alcoholism: Clinical and Experimental Research 19(2):462-468, 1995. (38) Schatzberg, A.F., and Nemeroff, C.B., eds. The American Psychiatric Press Textbook of Psychopharmacology. Washington, DC: American Psychiatric Press, 1995. (39) Helzer, J.D., and Pryzbeck, T.R. The co-occurrence of alcoholism with other psychiatric disorders in the general population and its impact on treatment. Journal of Studies on Alcohol 49(3):219-224, 1988. (40) Regier, D.A.; Farmer, M.E.; Rae, D.S.; Lake, B.Z.; Keith, S.J.; Judd, L.L.; and Goodwin, F.K. Comorbidity of mental disorders with alcohol and other drug abuse: Results from the Epidemiological Catchment Area (ECA) study. Journal of the American Medical Association 264(19):2511-2518, 1990. (41) Kessler, R.C.; Nelson, C.B.; McGonagle, K.A.; Edlund, M.J.; Frank, R.G.; and Leaf, P.J. The epidemiology of co-occurring addictive and mental disorders: Implications for prevention and service utilization. American Journal of Orthopsychiatry 66(1):17-31, 1996. (42) Grant, K.A. The role of 5-HT3 receptors in drug dependence. Drug and Alcohol Dependence 38(2):155-171, 1995. (43) Wozniak, K.M.; Pert, A.; and Linnoila, M. Antagonism of 5-HT3 receptors attenuates the effects of ethanol on extracellular dopamine. European Journal of Pharmacology 187(2):287-289, 1990. (44) Malec, E.; Malec, T.; GagnŽ, M.A.; and Dongier, M. Buspirone in the treatment of alcohol dependence: A placebo-controlled trial. Alcoholism: Clinical and Experimental Research 20(2):307-312, 1996. (45) Malcolm, R.; Anton, R.F.; Randall, C.L.; Johnston, A.; Brady, K.; and Thevos, A. A placebo-controlled trial of buspirone in anxious inpatient alcoholics. Alcoholism: Clinical and Experimental Research 16(6):1007-1013, 1992. (46) McGrath, P.J.; Nunes, E.V.; Stewart, J.W.; Goldman, D.; Agosti, V.; Ocepek-Welikson, K.; and Quitkin, F.M. Imipramine treatment of alcoholics with primary depression: A placebo-controlled clinical trial. Archives of General Psychiatry 53(3):232-240, 1996. (47) Mason, B.J.; Kocsis, J.H.; Ritvo, E.C.; and Cutler, R.B. A double-blind, placebo-controlled trial of desipramine for primary alcohol dependence stratified on the presence or absence of major depression. Journal of the American Medical Association 275(10):761-767, 1996. (48) Naranjo, C.A.; Sellers, E.M.; and Lawrin, M.O. Modulation of ethanol intake by serotonin uptake inhibitors. Journal of Clinical Psychiatry 47(Suppl 4):16-22, 1986. (49) Gorelick, D.A. Serotonin uptake blockers and the treatment of alcoholism. In: Galanter, M., ed. Recent Developments in Alcoholism: Volume 7. Treatment Research. New York: Plenum Press, 1989. pp. 257-281.
All material contained in the Alcohol Alert is in the
public domain and may be used or reproduced without permission from NIAAA.
Citation of the source is appreciated.
Copies of the Alcohol Alert are available free of charge from the Scientific
Communications Branch, Office of Scientific Affairs, NIAAA, Willco Building,
Suite 409, 6000 Executive Boulevard, Bethesda, MD 20892-7003. Telephone: 301-443-3860
Full text of this publication is available on NIAAA's World Wide Web site at
http://www.niaaa.nih.gov
http://store.health.org/catalog/productDetails.aspx?ProductID=16579
Suicide, Depression, and Youth DrinkingAlcohol used in adolescence is associated with psychological distress and depression.The severity of behavioral problems in adolescents is significantly associated with increased likelihood of adolescent alcohol use.
There is a link between suicide and alcohol use in adolescents.Adolescents struggling with serious emotional disturbances (SED) face even greater challenges when they use alcohol.
Co-occurring disorders prompt new federal action.
1Substance Abuse and Mental Health Services Administration (SAMHSA), Office of Applied Studies. The Relationship Between Mental Health and Substance Abuse Among Adolescents. (SMA) 99-3286. Rockville, MD: SAMHSA, 1999. 2 Hanna EZ, Hsiao-ye Y, Dufour MC, et al. The relationship of drinking and other substance use alone and in combination to health and behavior problems among youth ages 12-16: Findings from the Third National Health and Nutrition Survey (NHANES III). Paper presented at the 23rd Annual Scientific Meeting of the Research Society on Alcoholism, June 24-29, 2000, Denver, CO. 3Burgdorf K, Chen X, Herrell J. The prevalence and prognostic significance of sexual abuse in substance abuse treatment of women. Center for Substance Abuse Treatment (CSAT), 2001. 4 SAMHSA. The Relationship Between Mental Health and Substance Abuse Among Adolescents. 5Ibid. 6Unpublished data extrapolated by National Institute on Alcohol Abuse and Alcoholism from State Trends in Alcohol Mortality, 1979- 1992; US Alcohol Epidemiolgic Data Reference Manual, Volume 5. Rockville, MD: National Institute on Alcohol Abuse and Alcoholism, 1996. 7Windle M, Miller-Tutzauer C, Domenico D. Alcohol use, suicidal behavior, and risky activities among adolescents. J Res Adolesc 2(4):317-330, 1992. 8SAMHSA. The Relationship Between Mental Health and Substance Abuse Among Adolescents. 9Ibid. 9Report to Congress on the Prevention and Treatment of Co-Occurring Substance Abuse Disorders and Mental Disorders, SAMHSA, 2002. |
http://www.drugabuse.gov/NIDA_notes/NNVol17N4/Depression.html
Depression, PTSD, Substance Abuse Increase in Wake of September 11 Attacks
 |
By Jill S. Williams, NIDA NOTES Contributing Writer
A survey of New York City residents in the wake of the September 11, 2001, terrorist attacks found high levels of both depression and posttraumatic stress disorder (PTSD) among respondents and documented an increase in substance abuse. The survey, conducted by NIDA-funded researchers Dr. David Vlahov and his colleagues at the New York Academy of Medicine 5 to 8 weeks after the terrorist attacks, quantifies the relationships among stress, depression, and substance abuse. The results provide insight into public health service delivery needs as well as clues to effective treatment strategies to help individuals cope with traumatic events. Stress has long been recognized as one of the most powerful triggers for drug craving and relapse to drug abuse. Research has shown that survivors of disasters are prone to stress-related problems such as PTSD and depression. People who experience major trauma and those with PTSD or depression may self-medicate with drugs or alcohol to relax, cope with stress, or relieve symptoms. "This study is one of the first to capture data on the effects of traumatic events on substance abuse patterns," says Dr. Jacques Normand of NIDA's Center on AIDS and Other Medical Consequences of Drug Abuse. "The increase in substance abuse found here was of significant magnitude. This study reminds counselors and treatment providers to be alert to increased use of alcohol, tobacco, and marijuana in the wake of such events." Survey respondents reported post-attack rates of depression and PTSD that were approximately twice the baseline levels previously documented in a 1999 benchmark national study. Some 9.7 percent had symptoms of depression, and 7.5 percent qualified for a diagnosis of PTSD compared to baseline levels of 4.9 percent for depression and 3.6 percent for PTSD. In looking at rates of new substance use among respondents, the researchers found that, of respondents who did not use these substances during the week before September 11, 3.3 percent started smoking cigarettes after September 11; 19.3 percent started drinking alcohol; and 2.5 percent began using marijuana. Overall, the percentages of respondents who smoked, consumed alcohol, and used marijuana increased 9.7 percent, 24.6 percent, and 3.2 percent, respectively, after the attacks. Almost 29 percent of respondents reported that they were smoking more cigarettes and/or marijuana and/or drinking more alcohol. Among those who were already using these substances before September 11, 41.2 percent smoked more cigarettes and 41.7 percent drank more alcohol after the attacks. Among smokers, 8.2 percent smoked at least one additional pack of cigarettes a week; 20.8 percent of drinkers had at least one additional drink a day. "The survey results are significant for the sheer numbers of people revealed to be affected by the disaster, the scope of the problem on a citywide scale, and challenges to the delivery of services," says Dr. Vlahov. He estimates that of the approximately 911,000 people in the area of New York under study, 67,000 had PTSD and approximately 87,000 had depression at the time of the study. Likewise, he estimates that 265,000 people increased their use of any of the substances in question: 89,000 smoked more cigarettes, 226,000 consumed more alcohol, and 29,000 used more marijuana. "This survey demonstrated that whole populations are affected by such disasters," says Dr. Vlahov. "The increases in use of cigarettes, alcohol, and marijuana across the population are large, making this a broad public health issue." While the initial survey goal was to perform a public health assessment to document the scope of the problems and to help authorities apply for appropriate aid, Dr. Vlahov says that other questions also drove the research. "From a scientific perspective, we knew that attention typically focuses on victims, rescue workers, and their families. But here was an event that affected everyone in a major way. We asked, how do people cope with the stress of a disaster? Do they turn to cigarettes, alcohol, or marijuana? What are the implications for public health planning and delivery?"
Survey MethodologyResearchers randomly selected 1,008 adults living south of 110th Street in Manhattan, the area closest to the World Trade Center, to take part in the telephone survey. A 35-minute questionnaire was used to assess respondents' exposure to the September 11 events, psychological symptoms after the attacks, changes in substance abuse patterns, and other factors such as demographics, levels of social support, and previous life stressors. Surveyors referred respondents for counseling services as appropriate. The overall cooperation rate for the survey was 64.3 percent; 52 percent of respondents were women, and 71.6 percent were white. The mean age of respondents was 42 years. Surveyors used a series of questions based on accepted psychological tests to diagnose both depression and PTSD. To determine levels of pre- and post-September 11 substance abuse, surveyors asked respondents to estimate how many times they had used cigarettes, alcohol, and marijuana during the week before September 11, and then asked about the number of times they had used each substance during the week before the survey was conducted. Analyses revealed that those who were most directly exposed to events were more likely to suffer PTSD; those who experienced loss -- of jobs, possessions, friends or family members -- were more likely to suffer from depression. Dr. Vlahov says that the key demographic, event experience, and other characteristics most closely related to diagnosis of either PTSD or depression provide important clues to immediate crisis intervention: "Clinicians can learn that getting a history of an individual's exposure to events can help focus or target issues and clarify how he or she may be reacting." The survey data revealed associations between specific psychological diagnoses and drug use patterns. Survey respondents diagnosed with PTSD were approximately five times as likely as other respondents to increase their use of cigarettes or marijuana. Survey respondents who were diagnosed with depression were much more likely to increase use of all three substances than were those who were not depressed. Again, Dr. Vlahov suggests that these data may be important to clinicians. "Increased use of cigarettes, alcohol, and marijuana may be an indicator of underlying psychological response issues. Clinicians should look for links between PTSD, depression, and increased use of cigarettes, alcohol, or marijuana." Followup studies will assess outcomes at 4 months, 6 to 8 months, and 12 months after the attacks. "We need a better understanding of the extent to which substance abuse complicates psychological problems," says Dr. Vlahov. "Longitudinal studies will help us determine whether increased use of substances leads to dependence, and to identify predictors of drug dependence that will help us guide intervention planning." SourcesGalea, S.; Ahern, J.; Resnick, H.; Kilpatrick, D.; Bucuvalas, M.; Gold, J.; and Vlahov, D. Psychological sequelae of the September 11 terrorist attacks in New York City. New England Journal of Medicine 346(13):982-987, 2002. [Abstract] Vlahov, D., et al. Increased use of cigarettes, alcohol, and marijuana among Manhattan, New York, residents after the September 11th terrorist attacks. American Journal of Epidemiology 155(11):988-996, 2002. [Abstract]
For More InformationHelp for those struggling with stress and substance abuse issues is available in two recent NIDA publications:
Volume 17, Number 4 (November 2002) |
|
||||||||||||||||||||||||||||||||||||||||||||||||||||||
There are also many addicts in need of other psychotropic medications; it is beyond the scope of this course to address these issues.
Early recovery is marked by a "honeymoon" of elation and feeling of omnipotence wherein the addict believes they have it all together and perhaps can even be of help to others dealing with the pain. However, one reason twelve step programs honor 'birthdays' is the recognition of the newness of the process and the need to go slow and provide support. As you would not give a one year old child great responsibilities as they learn how to walk, you also want to consider great support in not overwhelming the person in their first year of recovery.
The person with an addiction problem is already showing you how they deal with too much pressure and anxiety...by using. Therefore to bring up intrapsychic pain which produces anxiety in these early stages is doomed to failure. Although the person may be very curious as to how they have let themselves and their lives to spin out of control, it is imperative to stay with the present day recovery as a structure which will give later intrapsychic investigation a supportive foundation. It is very likely this same intrapsychic pain triggered the initial use. If you do not have a counter balance of support in recovery the old pattern of addiction will prevail. This counter balance can include teaching the substance abuser very simple forms of meditation and stress reduction techniques. One of the strongest tools against relapse is education. The more your client realizes that their addiction is not special or unique but follows the pattern of millions of others the less viable are their rationalizations.
Secondly, addiction affects people on every level of their being. Once a week therapy with a compassionate therapist will not be enough to support recovery. If the addict is active in a family the family will need counseling to understand the process with which they are dealing they are dealing and a place for their own frustrations fears and regrets surrounding the process. Will they even like the sober person? Have they even known this person sober? Do they have substance abuse issues of their own?
Loneliness is a hallmark of addiction and recovery. The person in recovery will need a new group of people with whom to socialize. Although there is a tendency to want to start over and have nothing to do with anyone who has had similar problems, this can be a setup of codependence. People who have not struggled with chemical dependency are most likely to underestimate the occasional use of an addict and overestimate the successful steps they are taking towards recovery. This is just human nature. We want to see the addict in the best light possible and are reluctant even after all this time and research to accept the lifelong nature of this struggle. Although as clinicians we do not go immediately into investigating the underlying causes for addiction we know do they exist and can be triggered at any moment.
The crazy thinking and feelings that surface during recovery are often best understood by others whom have 'been there' and done similar work. These folks are most easily found in twelve step programs: however, if the client has an equal type of support elsewhere do not negate this either. We have known many people in recovery without twelve step aid: however, those who are attending regular support groups in addition to therapy have repeatedly come faster farther. The another plus of twelve step programs is sponsorship wherein an "older" person, in terms of recovery takes the newcomer under their wing to help them struggle through the twelve steps of recovery and be a "24 and 7" (24 hours and 7 days a week) support system. We are in deep gratitude to the many sponsors of the many recovering clients with whom we have worked. Although we have never met or talked to them personally, we have been extraordinarily grateful for the dedication and commitment they have shown our clients at various times. It is a remarkably special human service. Many of those in recovery truly embody the archetypal spirit of the "wounded healer" and acknowledge that part of their continued recovery is staying in touch with those beginning this journey.
As clinicians and or family members we should not underestimate the amount of support a person in recovery will need. This often runs directly opposite to what the person in recovery presents personality wise. Many chemically dependent people have been those upon whom others have relied for support. They are not the most likely candidates to acknowledge their own needs. Once again people who have been there are more likely to recognize the signs of needing help than those of us who are just focusing on the recovery and wanting to believe the competence and displayed confidence of the addict in denial. The families of these clients may be very used to these individuals behaving like children. Part of this stems from the maturational delay engendered by the years of drug use to avoid problem solving. As therapy progresses the therapist must help this 'addict child' within the adult body acknowledge and overcome difficult situations.
One chemical dependency counselor, April Mondragon, told us "Addicts must learn to realize that disappointment, loss, anger and hurt are emotional processes that have a beginning, a middle and an end. As we move through these emotional issues we are then better able to recognize the completion of one level of learning and apply it the lessons that are inevitably around the corner. As we build a repertoire of positive resolution to life's challenges we create greater reserves for future difficulties and a stronger base of self esteem. If we started using drugs in our teens or earlier our reservoirs will be pretty shallow in early recovery and we will need guidance to help them grow. It is important to note here that if you are an "adults only" therapist that researching developmental issues and dynamics of the ages wherein your client was using and stopped problem solving will be essential."
A male in his mid forties entered therapy during his first year of recovery from alcohol abuse. In spite of being given several thousand dollars a year by his mother, he often would call her to bail him out for credit card debt following late night home shopping sprees. He would feel this to be his right since his mother was a wealthy woman. Additionally he would hide his purchases of things that his mother would disapprove. After many months of working on financial recovery, he could also identify the rush of buying and the need make his mother keep taking care of him. He came out of his denial around his debting, realizing that "the beast had changed clothes"; that the same dynamics existed in this addiction as in his alcohol use.
With these treatment considerations in mind let us now explore some of the current research in the field. Although the nature of addiction is by far one of the most complicated clinical considerations, working with a person in recovery and healing is one of the most rewarding and profound human experiences.
888-777-3773
|
©
2000 - 2010 www.psychceu.com
all rights reserved. |
PDF
Format
