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Literature and Clinical Research Related to American Indian Health Problems
By Ann Dapice, Ph.D. 2004

Literature Review. Food and tobacco are connected to other addictive substances in important evolutionary and physiological ways.  Processes formerly necessary for our safety and well being, 1) the so-called “thrifty gene” and 2) mechanisms for fight and flight, now serve to make and keep us ill.  Our bodies and brains continue to function according to hunting and gathering needs appropriate thousands of years ago.

 

While tobacco use remains in first place with respect to fatal forms of substance abuse, obesity is rapidly moving ahead as the number one killer (Tanner, L., 2004).  Recent research released this April demonstrates that “brain circuits involved in drug addiction are also activated by the desire for food… (T)he right orbital-frontal cortex is involved in compulsive behaviors characteristic of addictive states and that this  brain region is activated when addicted individuals crave drugs such as cocaine.” Food stimulation increases levels of dopamine and when obese individuals were examined they were found to have fewer dopamine receptors—as in addiction to other substances Brookhaven National Laboratory, 2004.  It is, of course, important that food be satisfying for the survival of the species.   Having fewer receptors increases the level of food intake, when possible, and this was once adaptive to prepare for winter months, or times of famine—and still is in some parts of the world today.

 

Research shows hypoglycemia affects up to 95% of alcoholics causing them to become irritable, angry, depressed, hostile, and crave carbohydrates in the form of food or alcohol.  Consuming carbohydrates in various forms serves to relieve symptoms temporarily. With surges of insulin the cycle continues.  This is known as “dry drunk” in the alcoholic community and may be observed whether or not individuals have ever used alcohol.  Diabetics often experience these same hypoglycemic symptoms and are taught how to respond appropriately with diet (Mathews-Larson, 1991, Bell, L. and Martin K., 2002; Dapice, A., et al, 2001).

 

The American Cancer Society notes that while a third of the nation’s 50 million smokers attempt to quit each year, not unlike statistics in alcohol and drug addiction (Mathews-Larson, 1991; NIAAA Match Findings, 1997; Polick, V., D. Aarmor and H. Bracker, 1980), fewer than five percent succeed.  And, as we had already observed and reported (Morgan, Kendall, 2003), smokers who try to stop tobacco use through patches and gum become addicted to these as well (Bartosiewicz, P., 2004).  This information becomes even more important with the recognition that continued use of nicotine is the leading cause of relapse to alcohol and other drugs (Mathew-Larson, 1991).  Research has demonstrated how this can be, since drinking alcohol improves the enjoyment of tobacco.  On the average, more than 85 percent of adults with a history of alcohol abuse smoke, and they may be more addicted to nicotine than are smokers without a history of drinking (Abrams, David B.; Monti, Peter M.; Niaura, Raymond S.; Rohsenow, Damaris J.; Colby, Suzanne M., 1996).   Further, individuals with such mental illnesses as depression and schizophrenia often self medicate with tobacco.  A recent study at Duke University documents that “prenatal nicotine inflicts lasting damage leaving the brain vulnerable to further injury and addiction upon later use of the drug” (2004).

 

The fight/flight physiological process protected out ancestors from predators.  It becomes destructive when such actions are inappropriate to the situation or the stress or danger becomes chronic. Cortisol, produced during these times, becomes toxic to cells in the body and the brain, killing brain cells and leaving depression in its wake (Sapolsky, R., 1996).  Especially important is the relationship of stress, cortisol and predispostion to self medication.  As noted by the National Institute of Drug Abuse (NIDA, 2002), studies in the Journal Psychoneuroendocrinology indicate: 1) Stress and cortisol sensitize animals for drug-seeking behaviors and facilitate self-administration. 2) Animals that are under-aroused and have low levels of cortisol are more prone to develop drug-seeking behaviors. 3) Severe stress early in life induces a series of physiological, neurobiological, and hormonal events that result in dysregulation of biological reward pathways in the central nervous system and in stress response systems; these changes seem to prompt self-administration of drugs and alcohol later in life. 4) Prenatal exposure to stress and drugs predispose animals to drug-seeking behaviors in adulthood. 5) Post traumatic stress disorder is a risk factor for substance abuse.  6) The administration of cocaine to humans causes similar physiological reactions such as secretion of adrenalin and cortisol, and psychological reactions similar to arousal caused by stress. 

 

Post traumatic stress disorder (PTSD) resulting from traumatic events continues the effects of the stress over time, with a cycle of cortisol production resulting in depression.  PTSD patients typically continue to re-experience a trauma, demonstrate hyperarousal, irritability, insomnia and inability to concentrate (Bremner, J., Randall, P., Capelli, S., Scott, T., McCarthy, G., and Charney, D., 1995; Steinberg, D. 2001; Golier, J. and Yehuda, R., 1999; Litz, B. T. and Kean, T. M. 1989; Resnick, H., Yehuda, R., Pitman, R., and Foy, D., 1995; Stein, M., Yehuda, R., Koverola, C., Hanna, C. 1997; Yehuda, R., Southwick, S. M., Mason, J. W., and Giller, E. L. 1990; Yehuda, R., Giller, E. L., Southwick, S. M., Lowy, M. T., and Mason, J. W. 1991c; Siegfried, B., Frischknecht, H. R., and Nunez, de Souzza, R. 1990.). Cortisol may become depleted after continued stimulation. Children born to mothers with low cortisol levels related to stress, oppression and genocide have often been found to have low cortisol levels as well. (Yehuda, R., Kahana, B., Binder-Brynes, K., Southwick, S., Mason, J., and Giller, E. 1995; Yehuda, R. et al. 2002; Duran, E., and Duran, B., 1995).  Unexpectedly, children who are bullies and violent prison inmates are found to be low in cortisol (MacKeen, D., 2000).

 

Child abuse, neglect, sexual abuse and verbal abuse causes damage to the cerebellar vermis in

the brain, causing electrical irritability that the brain attempts to quell physiologically and the

individual attempts in adulthood to alleviate by abuse of alcohol and drugs.  This area of the brain is extremely sensitive to stress hormones (Anderson, C., 2002).  Brain imaging technology (Teicher, Martin H. 2002) demonstrates that there are three major changes observed in the brains of adults who were abused as children: 1) Limbic irritability with increased incidence of clinically significant EEG abnormalities.  2) Deficient development of the left hemisphere of the brain (throughout the cerebral cortex and hippocampus).  3) Deficient integration of the left and right hemispheres of the brain with diminished development of the middle portions of the corpus callosum that serves as a bridge connecting the left and right brain. These lateralization changes in the brain are similar to the work of many other researchers for PTSD. Essentially, the right brain takes control with negative affect and related behaviors (Sapolsky, R. 1996 and 2000); Bremner, J., Narayan, M., Anderson, E., Staib, L., Miller, H., and Charney, D., 2000; Bremner, J., Randall, P., Vermetten, E., Staib, L., and Bronen, R. 1997. Bremner, J. 1999; Dapice, A., Inkanish, C., Martin, B., Brauchi, P., 2002.)  Importantly, with decreased communication between left and right brain, the cerebellum has the potential architecturally to continue communication between the left and right brain (Anderson, C, 2003) and appropriate electrical stimulation of the area has removed pathological symptoms (Heath, R. G., 1977.)

 

EEG brain waves are shaped genetically and researchers have demonstrated reduced amplitude that correlates with alcohol dependence and have identified the chromosomal region that affects the P300 electrical brain wave, already correlated with alcohol craving and predisposition to relapse.  These abnormalities are true both of alcoholics as well as their “alcohol-naïve” (never used) offspring (Porjesz, B.; Almasy, L.; Edenberg, H.J.; et al. 2002; Propping, Kruger & Mark, 1981, Pollock, V.E., Volavka, J., Goodwin, D.W., Mednick, S.A., Gabrielli, W.F., Knop, J. and Schulsinger, F., 1983; Begleiter, Henri, 2001; Begleiter, H., Porjesz, B., Bihari, B., and Kissin, B., 1984. Begleiter and Porjesz, 1988, Tabakoff and Hoffman, 1988; Volavka, J., Pollock, V., W. F. Gabrielli, and S. A. Mednick. 1985). According to a report from the NIDA, 2001 studies at University of Connecticut by Dr. Lance Bauer show that relapse to alcohol, cocaine, and opioid dependence can be predicted by brain waves.  The high frequency activity on EEGs was found to far outweigh clinical and demographic variables as a predictor of relapse (NIDA).  Alcoholic P300 brain waves appear as “jagged mountains” compared to the normal appearance of gentle “foothills.”

 

Clinical Implications and Research.  In our American Indian non-profit outpatient counseling facility we utilize research-based practice to respond to the ills that most affect American Indians: stress, depression; PTSD; suicide; alcohol, nicotine and drug abuse; irritability; anger; hostility; and violence.  Related to the research above, treatment includes appropriate nutrition to lessen  symptoms and disease (Bennett, A. E., et al, 1970; Bachmanov, A., et al, 1996; Drewnoski, A., et al, 1992; Forsander, O. and Poso, A., 1987; Kampov-Polevoy, A, et al, 1997; Mathews-Larson, J, 1991; Stewart, R.B., et al, 1994; and Yung, L., et al, 1983). 

 

Also based on research, we utilize cranial electrotherapy stimulation or CES (FDA sanctioned treatment for stress, depression, anxiety, insomnia, and treating addictions to nicotine, alcohol, prescription and street drugs.  CES is a cost-effective self-administered 9-volt battery pocket sized unit that is clipped to the ear lobes or attached by electrodes behind the ears.  Clients may use CES at home and anywhere needed.  There are no real side effects and few contraindications.  Unlike psychotropic medications, electrical treatment does not have to pass the blood brain barrier and immediately begins to act on the brain directly. Its action normalizes brain waves, stimulates endorphins and neurotransmitters.  Research is pending to assess its effects on neurogenesis as well.  CES research has been published and continued since 1970 (e.g., Braverman, E., et. Al, 1990; Gomez, E. and Mikhail, A, 1974; Grinenko, A., et al, 1988; Jarzembski, W. B., 1985; Klawanski, S., et al, 1995; Krupitski, E. M., et al, 1991; Marshall, A. G. and Izard, C., 1974; O’Conner, M. E., et al, 1991; Patterson, M., et al, 1984; Schmitt, R., et al, 1986; Smith, R., 1975; Smith, R., 1982; Smith, R. and Shiromoto, F, 1992;Yudofski, S, 1999).

 

The use of nutrition and CES greatly facilitate other treatment that includes counseling and education.  The long time alcohol drug and licensed counselors at our facility attest to the differences these two additions make to successful treatment for both addictions and mental health issues.  Since we have numerous diabetic clients as well, treatment of their illnesses are also facilitated.

 

 

 

 

 

References

 

Abrams, David B.; Monti, Peter M.; Niaura, Raymond S.; Rohsenow, Damaris J.; Colby, Suzanne M. 1996. Interventions for alcoholics who smoke. Alcohol Health & Research World; March 01.

 

Anderson, C. M. 2003.  Invited Lecture, Ninth Annual Zarrow Mental Health Symposium, Tulsa, OK, September 19th. "Early Abuse, ADHD, and Addiction: A Developmental-Cerebellar Connection?" Unpublished.

 

Anderson, C.M., Teicher, M.H., Polcari, A., and Renshaw, P.F. 2002. Abnormal T2 relaxation time in the cerebellar vermis of adults sexually abused in childhood: Potential role of the vermis in stress-enhanced risk for drug abuse.  Psychoneuroendocrinology,    

 

Bachmanov, A. A., M. G. Tordoff and G. K Beauchamp, 1996. Ethanol consumption and taste preferences in CF7BL/6ByJ and 129/J mice. Alcoholism and Experimental Research. 20(2):201-206.

 

Bartosiewicz, Petra. 2004. A quitter’s dilemma: Hooked on the cure.  New York Times.  http://www.nytimes.com/2004/05/02/business/yourmoney/02smok.html.

 

Begleiter, Henri. 2001. Brain imbalance linked to alcoholism.  Alcohol Clin Exp Res (25): 330-337.

 

Begleiter, H., Porjesz, B., Bihari, B., and Kissin, B. 1984. Event-related brain potentials in boys at risk for alcoholism.  Science 225:1493-1496. 

 

Begleiter, H. and Porjesz, B. 1988. Potential biological markers in individuals at high risk for developing alcoholism. Alcoholism: Clinical and Experimental Research 12(4), 488-493.

 

Bell, L. and Martin K. 2002. A natural prescription for addiction. Counselor, 3(4), 40-44.

 

Bennett, A. E., R. Doll and R. W. Howell. 1970. Sugar consumption and cigarette smoking.  The Lancet, 1970 (May 16):1011-14.

 

Braverman, et al. 1990. Modification of P300 Amplitude and Other Electrophysiological Parameters of Drug Abuse by Cranial Electrical Stimulation. Current Therapeutic Research, 48(4):586-596.

 

Bremner, J., Narayan, M., Anderson, E., Staib, L., Miller, H., and Charney, D. 2000. Hippocampal volume reduction in major depression. Am. J. Psychiatry, 157:115-127.

 

Bremner, J., Randall, P., Vermetten, E., Staib, L., and Bronen, R. 1997. Magnetic resonance imaging-based measurement of hippocampal volume in posttraumatic stress disorder related to childhood physical and sexual abuse—a preliminary report. Biol. Psychiatry, 41:23-27.

 

Bremner, J. 1999. Does stress damage the brain? Biol. Psychiatry, 45:797-804.

 

Bremner, J., Randall, P., Capelli, S., Scott, T., McCarthy, G., and Charney, D. 1995.  Deficits in short term memory in adult survivors of childhood abuse. Psychiatry Res., 59:97-105. 

 

Brookhaven National Laboratory, 2004.  Exposure to food increases brain metabolism. http://www.bnl.gov/bnlweb/pubaf/pr/2004/bnlpr041904.htm.

 

Dapice, A., Inkanish, C., Martin, B., and Montalvo, E. 2001. Killing us slowly: The relationship between type two diabetes and alcoholism. Native American Times, June.

 

Dapice, A., Inkanish, C. Martin, B., and Brauchi, P.  2002.  Killing us lowly: When we can’t fight and we can’t run.  Native American Times, September. 

 

Drewnoski, A., et al. 1992. Taste responses and preferences for sweet high-fat foods: Evidence for opioid involvment.  Physiology and Behavior. 51(2):371-79.

 

Duke University, 2004. Prenatal nicotine primes adolescent brain for addiction. 

http://www.sciencedaily.com/releases/2004/04/040420214434.htm

 

Duran, E., and Duran, B., 1995. Native American postcolonial psychology. Albany, NY: State University of New York Press.

 

Forsander, O. A. and A. R. Poso. 1987. Is carbohydrate metabolism genetically related to alcohol drinking? Alcohol and Alcoholism, 1:357-59.

 

Gianoulakis, C., et al. 1989. Different pituitary beta-endorphin and adrenal cortisol response to ethanol in individuals with high and low risk for future development of alcoholism. Life Sciences (England). 45(12):1097-109.

 

Golier, J. and Yehuda, R. 1999. The HPA axis in Gulf War veterans with PTSD: Preliminary findings. Int. Soc. Traumatic Stress Studies, Annual Meeting, Ab. 1662.

 

Gomez, Evaristo and Mikhail, Adib R. 1974. Treatment of methadone withdrawal with cerebral electrotherapy (electrosleep).  Paper presented at the annual meeting of the American Psychiatric Association, Detroit.

 

Grinenko A., Drupitsky, E. M., Lebedev V. P. 1988. Metabolism of Biogenic Amines During Treatment of Alcohol Withdrawal Syndrome by Transcranial Electric Treatment. Biogenic Amines 5(6): 527-536. 

 

Heath, R. G., 1977. Modulation of emotion with a brain pacemaker: Treatment for intractable psychiatric illness.  J. Nerv. Mental Dis./65, 300-317.

 

Jarzembski, W. B. 1985. Electrical Stimulation and Substance Abuse Treatment. Neurobehavioral Toxicology and Teratology, 119-123. 

 

Kampov-Polevoy, A., J. C. Garbutt and D. Janowski. 1997. Evidence of preference for a high-concentration sucrose solution in alcoholic men.  Amer. J. of Psychiatry. 154(2): 269-270.

 

Klawansky, S., Yeung, A., Berkey, C., and Shah, N., et al. 1995. Meta-analysis of randomized controlled trials of cranial electrotherapy stimulation: efficacy in treating selected psychological and physiological conditions. Journal of Nervous and Mental Diseases, 183(7):478-485.

 

Krupitsky, E.M., Burakov, G.B., Karandashova, Jas., et al. 1991. The administration of transcranial electric treatment for affective disturbances therapy in alcoholic patients. Drug and Alcohol Dependence, 27:1-6.

 

Litz, B. T. and Kean, T. M. 1989. Information processing in anxiety disorders: Application to the understanding of post-traumatic stress disorder. Clin. Psychol Review. 9:243-257.

 

MacKeen, D. 2000. Hormonal rages: A new study links decreased levels of cortisol with aggressive behavior in boys. From http://www.salon.com/health/log/2000/01/14/cortisol.

 

Marshall, Alan G. and Izard, Carrol E. 1974. Cerebral electrotherapeutic treatment of depressions.  Journal of Consulting and Clinical Psychology. 42(l):93-97.

 

Mathews-Larson, J. 1991. Seven weeks to sobriety.  NY:Villard Books.

 

Morgan, Kendall, 2003.  More than a kick. Science News, Vol. 163, No. 12, March 22, 2003, p. 184.

 

NewScan: NIDA Addiction Research News. 2002. http://www.drugabuse.gov/Med Adv/02/NS-04.html. April 8.

 

NIAAA, 1998, Alcohol Alert. No. 39, www.niaaa.nih.gov/publications/aa39.htm+NIAAA+

smoking+cessation&hl=en&ie=UTF-8.

 

NIAAA Match Findings, 1997. http://www.niaaa.nih.gov/press/1996/match.htm

 

O'Connor, Mary Ellen, Bianco, Faust, and Nicholson, Robert. 1991. Meta-analysis of cranial electrostimulation in relation to the primary and secondary symptoms of substance withdrawal. Presented at the 12th annual meeting of the Bioelectromagnetics Society, June 14, 1991.

 

Passini, Frank G., Watson, Charles G., and Herder, Joseph. 1976. The effects of cerebral electric therapy (electrosleep) on anxiety, depression, and hostility in psychiatric patients. Journal of Nervous and Mental Disease. 163(4):263-266.

 

Patterson, M. A., Firth, J. and Gardner R. 1984.  Treatment of drug, alcohol and nicotine addiction by neuro-electric therapy: analysis of results over seven years. Journal of Bioelectricity (3), 193-221.

 

Polick, V., D. Aarmor and H. Bracker. 1980. The Course of Alcoholism, Four Years after Treatment, Santa Monica: Rand Corp.:169-70.

 

Pollock, V.E., Volavka, J., Goodwin, D.W., Mednick, S.A., Gabrielli, W.F., Knop, J. and Schulsinger, F. (1983) The EEG after alcohol administration in men at risk for alcoholism. Archives of General Psychiatry 40, 857-861.

 

Porjesz, B.; Almasy, L.; Edenberg, H.J.; et al. 2002. Linkage disequilibrium between the beta frequency of the human EEG and a GABAA receptor gene locus. Proceedings of the National Academy of Sciences of the U.S.A. 99:3729–3733, 2002.

 

Propping, P., Kruger, J. and Mark, N. (1981) Genetic disposition to alcoholism. An EEG study in alcoholics and their relatives. Human Genetics 59, 51-59.

 

Resnick, H., Yehuda, R., Pitman, R., and Foy, D. 1995. Effects of previous trauma on acute plasma cortisol level following rape. Am. J. Psychiatry, 152: 1675-1686.

 

Sapolsky, R. 1996. Why stress is bad for your brain. Science, 273:749-750.

 

Sapolsky, R. 2000. Glucocorticoids and hippocampal atrophy in neuropsychiatric disorders. Archives of General Psychiatry, 57:925-935.

 

Schmitt, Richard, Capo, Thomas, Boyd, Elvin.  1986. Cranial electrotherapy stimulation as a treatment for anxiety in chemically dependent persons. Alcoholism: Clinical and Experimental Research. 10(2):158-160.

 

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Smith, Ray. 1982. Confirming Evidence of an Effective Treatment for Brain Dysfunction in Alcoholic Patients. J of Nervous and Mental Disease:275-277. 

 

Smith, Ray B., Shiromoto, Frank N. 1992. The use of cranial electrotherapy stimulation to block fear perception in phobic patients. Journal of Current Therapeutic Research.  51(2):249-253.

 

Stein, M., Yehuda, R., Koverola, C., Hanna, C. 1997. Enhanced dexamethasone suppression of  plasma cortisol in adult women traumatized by childhood sexual abuse. Biol. Psychiatry, 42:680-690.

 

Steinberg, D. 2001. Understanding stress disorders takes on urgency. The Scientist, 15(22)1.

 

Stewart, R.B., et al. 1994. Consumption of sweet, salty, sour, and bitter solutions by selectively bred alcohol-preferring and alcohol-nonpreferring lines of rats. Alcoholism: Clinical and Experimental Research. 18(2):375-381.

 

Tabakoff, B. and Hoffman, P.L. (1988) Genetics and biological markers of risk for alcoholism. Public Health Reports 103(6), 690-698.

 

Tanner, L., 2004.  Study: We’re eating ourselves to death.  Associated Press.

 

Teicher, Martin H. 2002. Scars that won’t heal: The neurobiology of child abuse.  Scientific American.  March, 68-75. 

 

Volavka, J., Pollock, V., W. F. Gabrielli, and S. A. Mednick. 1985. The EEG in Persons at Risk for Alcoholism.  Recent Developments in Alcoholism 3 (1985): 21-36. 

 

Yehuda, R., Southwick, S. M., Mason, J. W., and Giller, E. L. 1990. Interactions of hypothalamic-pituitary adrenal axis and the catecholaminergic system in posttraumatic stress disorder. In Giller, E. L. Ed. Biological Assessment and Treatment of PTSD. Washington, DC: American Psychiatric Press.

 

Yehuda, R., Giller, E. L., Southwick, S. M., Lowy, M. T., and Mason, J. W. 1991c. Hypothalamic-pituitary adrenal dysfunction in posttraumatic stress disorder.  Biol. Psychiatry, 30:1031-1048.

 

Yehuda, R., Kahana, B., Binder-Brynes, K., Southwick, S., Mason, J., and Giller, E. 1995. Low urinary cortisol excretion in Holocaust survivors with posttraumatic stress disorder. Am. J. Psychiatry, 152:982-990.

 

Yehuda, R. et al. 2002. Low cortisol and risk for PTSD in adult offspring of Holocaust survivors.

Am. J. Psychiatry,157:1252-1259.

 

Yudofsky, Stuart C. 1999. Parkinson's disease, depression, and electrical stimulation of the brain. The New England Journal of Medicine, 340 (19), pp. 1500-1502.

 

Yung, L., E. Gordis and J. Holt. 1983. Dietary choices and likelihood of abstinence among alcoholic patients in an outpatient clinic. Drug and Alcohol Dependence, 12:355-62.

 

 

   

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