The Noonday Demon (88 page)

220
A description of the use of SSRIs to bring alcoholics off alcohol is in David McDowell and Henry Spitz’s
Substance Abuse,
page 220. Mark Gold and Andrew Slaby, however, disagree with this position in their book
Dual Diagnosis in Substance Abuse.
They write, pages 210–11, “Antidepressant medication should not be prescribed for active alcoholics because the appropriate treatment is much more likely to be a period of sobriety.”

220
Increased REM latency has long been established as a hallmark sign of depression. See Francis Mondimore’s
Depression: The Mood Disease,
pages 174–78, for a good general discussion of depression and sleep. The work on REM sleep, alcoholism, and depression is taken from two studies: D. H. Overstreet et al., “Alcoholism and depressive disorder,”
Alcohol & Alcoholism
24 (1989); and P. Shiromani et al., “Acetylcholine and the regulation of REM sleep,”
Annual Review of Pharmacological Toxicology
27 (1987).

221
The statement on early-onset alcoholism and depression is taken from Mark Gold and Andrew Slaby’s
Dual Diagnosis in Substance Abuse,
pages 7–10.

221
On work with tests to diagnose primary versus secondary depression, see
Ibid.,
108–9.

221
The figures on the proportion of depressives who suffer from secondary alcoholism
and vice versa I take from Barbara Powell et al., “Primary and Secondary Depression in Alcoholic Men: An Important Distinction?”
Journal of Clinical Psychiatry
48, no. 3 (1987). For more on this complicated topic, see Bridget Grant et al., “The Relationship between
DSM-IV
Alcohol Use Disorders and
DSM-IV
Major Depression: Examination of the Primary-Secondary Distinction in a General Population Sample,”
Journal of Affective Disorders
38 (1996).

221
That substance abuse often begins in adolescence is discussed in Boris Segal and Jacqueline Stewart, “Substance Use and Abuse in Adolescence: An Overview,”
Child Psychiatry and Human Development
26, no. 4 (1996). They write lucidly: “Considering the epidemiological factors further, one must notice that adolescence is the primary risk period for the initiation of use of substances; those who have not experimented with licit or illicit drugs by age twenty-one are unlikely to do so after.” Page 196.

221
That substance abusers are more likely to relapse when depressed is indicated in Mark Gold and Andrew Slaby’s
Dual Diagnosis in Substance Abuse:
“Alcoholics reporting depression during periods of sobriety return to drinking more frequently than those with normal mood,” page 108.

221
R. E. Meyer’s views here quoted come from
Psychopathology and Addictive Disorder,
pages 3–16.

221
The remission of apparently schizophrenic symptoms (paranoia, delusions, hallucinations, etc.) in patients with depression and stimulant-abuse problems is related to the fact that mania can often be precipitated by excess dopamine. Abstinence from stimulant use may help to control such excesses. For more on the relationships among stimulants, mania, and psychosis, see Robert Post et al., “Cocaine, Kindling, and Psychosis,”
American Journal of Psychiatry
133, no. 6 (1976), and John Griffith et al., “Dextroamphetamine: Evaluation of Psychomimetic Properties in Man,”
Archives of General Psychiatry
26 (1972).

221
The severity of each illness in dual-diagnosis cases is reviewed in Mark Gold and Andrew Slaby’s
Dual Diagnosis in Substance Abuse.

222
On the depression-engendering effects of withdrawal from cocaine, sedatives, hypnotics, and anxiolytics, see
Ibid.,
105–15.

222
Work on the capacity of substances, especially alcohol, to exacerbate suicidality is summarized in Ghadirian and Lehmann’s
Environment and Psychopathology,
page 112. Mark Gold and Andrew Slaby’s
Dual Diagnosis in Substance Abuse
says “rates of self-reported suicide attempts increase progressively with increased use of licit and illicit substances.” Page 14.

222
That depression often remits because of abstinence can be adduced from a number of studies. Mark Gold and Andrew Slaby’s
Dual Diagnosis in Substance Abuse
says, “For the majority of these primary alcoholics, secondary depressive symptoms tend to remit by the second week of treatment and continue to decrease more gradually with three to four weeks of abstinence,” pages 107–8.

222
Alcohol, in fact, causes all medications to be absorbed more rapidly; and it is a primary principle of antidepressant therapy that peaks of absorption exacerbate side effects.

222
Howard Shaffer’s pithy remark about addictive dice was published in Craig Lambert, “Deep Cravings,”
Harvard Magazine
102, no. 4 (2000). Bertha Madras’s comments appear in the same article.

223
Work on endorphin levels and alcohol use has been published in J. C. Aguirre et al., “Plasma Beta-Endorphin Levels in Chronic Alcoholics,”
Alcohol
7, no. 5 (1990).

224
The four origins of addiction I take from David McDowell and Henry Spitz’s
Substance Abuse.

224
The statistics on Irish and Israeli teetotalism were discussed in an oral interview with Dr. Herbert Kleber, March 9, 2000.

225
The quotation from Eliot appears in his poem “Gerontion,” in
The Complete Poems and Plays,
page 22.

225
These remarks on substitution come from Mark Gold and Andrew Slaby’s
Dual Diagnosis in Substance Abuse,
page 199.

225
The story of chili in the elephant’s eye I take from Sue Macartney-Snape, who has spent much time in Nepal and has interviewed numerous howdah drivers.

225
Work on decreased oxygenation of the blood of smokers is reviewed in Marc Galanter and Herbert Kleber’s
Textbook of Substance Abuse Treatment,
page 216.

225
Work on smoking and serotonin may be found in David Gilbert’s
Smoking,
pages 49–59.

226
For a fuller account of my life with Russian artists, see
The Irony Tower: Soviet Artists in a Time of Glasnost.

227
That the rationale behind alcohol taxes in Scandinavia includes the benefits of reduced suicide was discussed with Håkan Leifman and Mats Ramstedt of the Swedish Institute of Social Research on Alcohol and Drugs (SoRAD). Statistical information is provided in a study to be published in a forthcoming supplement of
Addiction
entitled “Alcohol and Suicide in 14 European Countries,” by Mats Ramstedt. For more information on the relationship between alcohol consumption and suicide, see George Murphy,
Suicide in Alcoholism,
and I. Rossow, “Alcohol and suicide—beyond the link at the individual level,”
Addiction
91 (1996).

228
On serious alcoholism and cognitive impairment, see David McDowell and Henry Spitz’s
Substance Abuse,
pages 45–46.

228
For alcohol’s toxic effects on the liver, the stomach, and the immune system, see
Ibid.,
46–47.

228
That the mortality rate is higher among alcoholics than among nonalcoholics is stated in Donald Goodwin’s
Alcoholism, the Facts,
page 52.

228
The statistic that 90 percent of Americans have had alcohol and the figures on physiological addiction to alcohol in the United States are from David McDowell and Henry Spitz’s
Substance Abuse,
pages 41–42.

228
The role of serotonin and cortisol in resisting alcohol consumption is discussed in Marc Galanter and Herbert Kleber’s
Textbook of Substance Abuse Treatment,
pages 6–7 and 130–31.

228
Information on the GABA receptors I take from personal correspondence with Steven Hyman and David McDowell. For an in-depth discussion on alcohol, GABA, and other brain neurotransmitters, see Marc Galanter and Herbert Kleber’s
Textbook of Substance Abuse Treatment,
pages 3–8. Work on serotonin’s reinforcing alcohol consumption is in R. J. M. Niesink et al.’s
Drugs of Abuse and Addiction,
pages 134–37.

228
The superiority of psychodynamic therapies for dual-diagnosis patients seems more a clinical reality than a well-studied fact. Most of the clinicians I’ve spoken with have espoused a belief that for real recovery a dual-diagnosis patient must understand how the abuse affects the depression and vice versa. Marc Galanter and Herbert Kleber write in their
Textbook of Substance Abuse Treatment
that for “patients for whom affect regulation is an issue, psychodynamic psychotherapy may be especially valuable.” Page 312.

228
The Columbia practice is in the S.T.A.R.S. (Substance Treatment and Research Service) Program.

229
A great deal has been published on Antabuse. For a detailed description of its mode of action, see David McDowell and Henry Spitz’s
Substance Abuse,
pages 217–19.

229
On use of Naltrexone for withdrawal from alcohol and heroin, see
Ibid.,
48–51.

229
For information on the history of marijuana, see
Ibid.,
68.

230
Marijuana’s lung toxicity is discussed in Marc Galanter and Herbert Kleber’s
Textbook of Substance Abuse Treatment,
pages172–73.

230
The work on depression in the families of stimulant abusers is from Mark Gold and Andrew Slaby’s
Dual Diagnosis in Substance Abuse,
page 18.

230
The percentage of cocaine users who become addicted is in David McDowell and Henry Spitz’s
Substance Abuse,
page 93.

230
Work on lab rats choosing stimulants over food and sex is in R. A. Yokel et al., “Amphetamine-type reinforcement by dopaminergic agonists in the rat,”
Psychopharmacology
58 (1978). There have also been numerous studies involving rhesus monkeys, with the same results. See, for example, T. G. Aigner et al, “Choice behavior in rhesus monkeys: Cocaine versus food,”
Science
201 (1978).

230
The neurophysiology of the cocaine crash is expounded in Mark Gold and Andrew Slaby’s
Dual Diagnosis in Substance Abuse,
pages 109–10.

230
The general effects of amphetamines and cocaine on the neurotransmitters are described in R. J. M. Niesink et al.’s
Drugs of Abuse and Addiction,
pages 159–165.

230
That acute craving can last for decades is indicated in Mark Gold and Andrew Slaby’s
Dual Diagnosis in Substance Abuse,
page 110.

230
The use of a ten-week course of antidepressants to endure the drug crash is described in Bruce Rounsaville et al., “Psychiatric Diagnoses of Treatment-Seeking Cocaine Abusers,”
Archives of General Psychiatry
48 (1991).

231
The permanent effect of amphetamines and cocaine on the dopamine system is described in Mark Gold and Andrew Slaby’s
Dual Diagnosis in Substance Abuse,
page 110. They write, “Animal studies have documented occasional dopaminergic neuronal degeneration with chronic stimulant administration.”

231
The work on cocaine and CRF is in Thomas Kosten et al., “Depression and Stimulant Dependence,”
Journal of Nervous and Mental Disease
186, no. 12 (1998).

231
The figures on depression among opiate abusers comes from Ghadirian and Lehmann’s
Environment and Psychopathology,
pages 110–11.

232
The high rate of depression among people on methadone is described in Mark Gold and Andrew Slaby’s
Dual Diagnosis in Substance Abuse,
page 110.

232
The statistics on Vietnam veterans and heroin addiction are in Craig Lambert, “Deep Cravings,”
Harvard Magazine
102, no. 4 (2000): 67.

233
The work on ecstasy and serotonin axons is summarized in R. J. M. Niesink et al.,
Drugs of Abuse and Addiction,
pages 164–65. That ecstasy reduces serotonin levels 30 to 35 percent may be found in U. McCann et al., “Serotonin Neurotoxicity after 3,4-Methylenedioxymethamphetamine: A Controlled Study in Humans,”
Neuropsychopharmacology
10 (1994). For more on ecstasy and the monoamines, see S. R. White et al., “The Effects of Methylenedioxymethamphetamine on Monoaminergic Neurotransmission in the Central Nervous System,”
Progress in Neurobiology
49 (1996). For a lively and varied discussion of ecstasy and neurotoxicity, see J. J. D. Turner and A. C. Parrott, “ ‘Is MDMA a Human Neurotoxin?’: Diverse Views from the Discussants,”
Neuropsychobiology
42 (2000).