Follow-up of a cohort of alcoholic patients through 12 months of comprehensive biobehavioral treatment

Journal ofSubstance Abuse Treatment, Vol. 8, pp. 133-142, 1991

0740-5472/91 $3.00 + .OO

Printed in the USA. All rights reserved.

Copyright 0

1991 Pergamon Press plc

Follow-Up of a Cohort of Alcoholic Patients Through 12 Months of Comprehensive Biobehavioral Treatment JOSEPH D. BEASLEY, MD, MPH, DTM&H (Land.),* ROGER C. GRIMSON,phDt BICKER, phD,* WILLIAMJ. CLOSSON,phD,$ CATHERINEA. HEUSEL, MA,* AND F. INGE FAUST, MA, MS, PhD (Cand.)*

ALVIN A.

*Institute of Health Policy and Practice, Bard College Center, Amityville, New York; tSchooI of Medicine, State University of New York at Stony Brook; SClinical Chemistry Laboratory, Brunswick Hospital Center, Amityville, New York

Abstract-One hundred and eleven socially stable alcoholic patients were subjected to a comprehensive diagnostic and treatment protocol based on a biobehavioral model of alcoholism. Physical pathology, malnutrition, and toxicity were prevalent throughout the sample. After a period of inpatient care, subjects were treated for a period of 12 months with a combination of medical, nutritional, behavioral, and psychological support and care. At the end of the study period, 91 subjects (81.90/,) remained in treatment contact. Sixty seven subjects (60.40/o) were abstinent and physically stable at the Ibmonth date. Elevations of three scales of the MMPI were significantly predictive of treatment outcome.

Keywords-alcoholism; allergy;toxicity;treatment;nutrition.

of the medical problems that continue to plague alcoholics in recovery. These difficulties include substitute addictions, tremors, anxiety, depression, memory difficulties, and interpersonal problems (De Soto, O’Donnell, Allred, & Lopes, 1985; Gerard, Saenger, & Wile, 1962; Mossberg, Liljeberg, & Borg, 1985; Vaillant & Milofsky, 1982). The mortality rates of recovered alcoholics run two to three times higher than those of controls (Costello, Parsons-Manders, & Schneider, 1978; De Lint & Levinson, 1975; Tashiro & Lipscomb, 1963), and the incidence of suicide among them is also higher (Berglund, 1984). In fact, one group of researchers (Pell & D’Alonzo, 1973) found that the mortality rate of recovered alcoholics did not differ significantly from that of active alcoholics. These persistent difficulties may contribute to the high attrition rates that are characteristic of most alcoholism treatment programs. Reported attrition rates after one year of treatment range from 20% to 70% or higher (Alford, 1980; Cole, Lehman, Cole, & Jones, 1981: Hoffman & Harrison, 1986; Welte, Hynes,

INTRODUCTION

medical problem that has been sorely neglected in the modern war on drugs. It has been estimated that between 30% and 50% of hospital inpatients suffer from undiagnosed alcoholism (Breitenbucher, 1976; McCusker, Cherubin, & Zimberg, 1971; Moore et al., 1989) and up to 40% of emergency room visits are alcohol related (Zimberg, 1979). Nonetheless, approximately 87% of alcoholics are not in touch with alcoholism treatment facilities (Pokorny & Solomon, 1983), and one extensive survey of such facilities found that only 9% of patients had been referred there by a physician (Mendelson, Miller, Mello, Pratt, & Schmitz, 1982). The lack of significant physician involvement in alcoholism treatment is particularly regrettable in light

ALCOHOLISM IS A PERVASIVE

Requests for reprints should be addressed to Dr. Joseph D. Beasley, Institute of Health Policy and Practice, 221 Broadway, Suite 301, Amityville, NY 11701.

133

134

Sokolow, & Lyons, 1979). One analysis of an urban hospital-based program found that 45% of patients were lost to follow-up within 30 days (Gordis, Dorph, Sepe, & Smith, 1981). More than two decades of clinical and experimental research on alcoholism have revealed that the biological complexity of this disease matches (and may even exceed) its behavioral complexity. Early evidence of a genetic predisposition to alcoholism (Cadoret, Cain, & Grove, 1980; Goodwin, Schulsinger, Hermansen, Guze, & Winokur, 1973; Hrubec & Omenn, 1981) has been supplemented by data that indicates that the children of alcoholics have unique biological and neurological responses to ethanol (Begleiter, Porjesz, Bihari, & Kissin, 1984; Gabrielli et al., 1982; Pollock et al., 1983; Schuckit, 1980; Schuckit & Rayses, 1979). In alcoholic patients, alcohol’s toxic effects are manifested in a variety of serious and chronic syndromes. The nutritional impact of alcoholism goes beyond poor dietary habits to severe disruptions of the organ systems that absorb, metabolize, and utilize nutrients. In the gastrointestinal tract, alcohol directly injures the mucosa of the small intestine (Bjarnason, Ward, & Peters, 1984; Goldstein, 1987), leading to a generalized malabsorption of nutrients, including fat, xylose, folate, and thiamine (Winick, 1980). Alcoholinduced liver damage impairs nutrient metabolism and utilization, causing altered amino acid metabolism, decreased fatty acid oxidation with increased fatty acid synthesis, and depleted hepatic stores of folate, pyridoxine, Bi2, and niacin (Geokas, Lieber, French, & Halsted, 1981; Lieber, 1981; Prasad, Oberleas, & Rajasekaran, 1970). The combined effects of decreased nutrient intake, increased excretion, and impaired absorption/metabolism/utilization of nutrients lead to pancellular malnutrition with marked vitamin, mineral, and protein deficiencies (Leevy, Cardi, Frank, Gellene, & Baker, 1965; Sherlock, 1984; Sinclair, 1972). It is also known that alcoholism causes widespread suppression of immune responses (Flavin, 1987; MacGregor, 1986) with increased susceptibility to invasive organisms (Rajkovic & Williams, 1985), atherosclerotic disorders (Fraser, Day, & Fernando, 1986), and cancer (Glassman, Bennet, & Randall, 1985). Alcoholism, particularly with liver disease, has also been associated with increased synthesis of serum immunoglobulins (Nouri-Aria et al., 1986; Van de Weil et al., 1987). The increased permeability of the intestinal lining may contribute to the high percentage of positive reactions to allergens -both environmental and food -that has been observed in alcoholic patients (Closson, 1985; Sugerman, Southern, & Curran, 1982). Alcohol’s effect on glucose metabolism, and the possible relationship between glucose metabolism and brain serotonin levels, have been investigated by several researchers. Evidence of acute reactive hypogly-

J.D. Beasley et al.

cemia after alcohol “priming” (Dornhost & Ouyang, 1971; Marks, 1975; Metz, Berger, & Maka, 1969; O’Keefe & Marks, 1977; Serenyi & Endrenyi, 1978) has been augmented by evidence of abnormal glucose tolerance tests in abstinent incarcerated alcohol abusers, with a pattern of hypoglycemic responses characterized by high peak insulin levels followed by below-base blood glucose levels (Virkkunen, 1982). Serotonin metabolism is also disrupted by alcohol abuse (Ballenger, Goodwin, Major & Brown, 1979; Davidson, Lipper, Kilts, Mahorney, & Hammett, 1985; Dolinsky, Shaskan, & Hesselbrock, 1985; Kent et al., 1985; von Knorring, Bohman, von Knorring, & Oreland, 1985), and it has been hypothesized that there is a link between abnormal GTTs and serotonergic deficits in alcoholics-perhaps as a result of a dysfunction of the suprachiasmatic nuclei (Roy, Virkkunen, Guthrie, Linnoila, 1986; Yamamoto, Nagai, & Nakagawa, 1985). If so, these dysfunctions may contribute to the depressive syndromes common in alcoholism, and to the high rate of attempted and successful suicide among alcoholic individuals (Asberg, Thoren, Traskman, Bertilsson, & Ringberger, 1976; Asberg, Traskman, & Thoren, 1976; Berglund, 1984; Brown et al., 1982). All this work has clearly illustrated that alcoholism is a complex disorder requiring sophisticated, long-term treatment, since alcoholic patients exhibit cognitive impairment and inability to retain treatment-relevant information for as long as three weeks into rehabilitation (Becker & Jaffe, 1984). Treatment programs that have integrated nutritional concepts into a longterm protocol have proven successful in controlled studies (Guenther, 1983; Mathews-Larson & Parker, 1987). The following study was designed to document the existence and extent of medical pathology in a cohort of socially stable alcoholic patients and to monitor their progress during a 1Zmonth program of comprehensive biobehavioral care. It is not meant as an evaluation of the comparative efficacy of this treatment approach, since it was felt that it would be inappropriate to withhold any aspect of care from these patients. Instead, multivariate discriminant analysis was used to identify significant discriminators between subjects in recovery and those who are actively drinking or lost to follow-up.

MATERIALS AND METHODS Subjects were selected from the patient population of Brunswick House, a private alcoholism treatment hospital located in Amityville, Long Island, New York. For 7 months, all admissions were screened for possible inclusion in the study. Patients were considered if they:

Biobehavioral Treatment of Alcoholism

met the National Council of Alcoholism criteria for the diagnosis of alcoholism, with alcoholism as the primary dependency l were staying for the full 5 days of detoxification and 14 to 28 days of rehabilitation . were employed or employable with insurance coverage for treatment l were residents of the Long Island/metropolitan New York area (to facilitate follow up). Thus, the targeted population consisted of socially and economically stable alcoholic patients, rather than disenfranchised individuals such as the homeless. Patients who met the initial criteria were further evaluated through detailed histories, physical examinations, and, where appropriate, neurological and/or psychological evaluations. Grounds for exclusion at this point were: l Organic brain syndrome with impaired self-care, decision making, and learning skills. l Absence of a significant other who could be contacted during the study. l Refusal to participate in an aftercare program. Of approximately 180 patients deemed eligible for the study, 111 agreed to participate. A comparative analysis of those who declined found no apparent demographic differences between nonparticipants and participants. Upon admission to the study group, each participant underwent a detailed medical diagnostic protocol consisting of: l Comprehensive histories: - medical - nutritional - family medical - allergy and toxic exposure - drug and alcohol use l 24hour dietary recall for the time prior to admission l Physical examination l EKG and chest x-ray l Complete laboratory work-up, including: - CBC - platelet count - chemical profile: glucose, BUN, serum creatinine, sodium, potassium, chloride, carbon dioxide, total protein, albumin, LDH, bilirubin, cholesterol, uric acid, ALP, AST, ALT, GGT, magnesium, amylase, calcium, phosphorus - urinalysis: drug and alcohol screen, pH, specific gravity, sugar, albumin, acetone, bile, blood, and microscopic - lipoprotein electrophoresis - serological test for syphilis - vitamin assays: A and E (high-performance liquid chromatography) Bi, BZ, and Bs (functional assay) C and l

135

carotene (spectrophotometry) B,, and folate (radioimmunoassay) - mineral assays: copper, zinc, chromium, iron, magnesium, calcium, selenium - toxic metal screen (serum and whole blood): arsenic, aluminum, cadmium, mercury, lead - RAST test of circulating, allergen-specific IgE in serum for: milk, wheat, corn, peanut, shrimp, tomato, orange, cocoa, whole egg - hemoccult on feces as indicated - 6-hour glucose tolerance test (in subjects without known diabetes mellitus) approximately 2 weeks after detoxification; insulin levels were measured at fasting state, 1 hour, 2 hours, and 3 hours - special diagnostic tests as indicated. Three weeks after detoxification, 99 subjects (89.1070) underwent psychological testing using the Minnesota Multiphasic Personality Inventory (MMPI). Three subjects withdrew from the study and 9 others were released from rehabilitation prior to testing. The MMPI was used to identify factors to be included in analysis for reliable predictors of treatment success or failure, not for clinical diagnosis. The inpatient phase of treatment, both detoxification and rehabilitation, emphasized the physiological as well as the psychological aspects of the disease of alcoholism. Vitamin and mineral supplementation began upon admission to detoxification, and consisted of: l Lymphomed Injectable B-complex plus C, 2 cc IM q.i.d. x 4 days l Alpha Nutrient Supplement, 3 tablets t.i.d. l Calcium-magnesium supplement, 1 tablet b.i.d., consisting of 375 mg calcium, 150 mg magnesium. The inpatient dietary plan was designed to provide a steady supply of high-nutrient foods that would maintain blood glucose levels and reduce possible adverse reactions to additives and preservatives. Candy, donuts, refined sugar products, and caffeinated beverages were not served. Fruit and vegetable snacks, fruit juices, and decaffeinated drinks were available at all times. Meals were kept as unprocessed and additive-free as possible. Whole grain breads, fresh vegetables, dairy products, and unprocessed meats, fish, and poultry were dietary staples. Salt was used only during food preparation, and then sparingly. Modifications were made for subjects with diabetes or specific adverse food reactions. Subjects were detoxified from all addictive medications, including physician-prescribed drugs. Medications were reevaluated and adjusted as individual medical problems were resolved. For example, subjects with hypertension secondary to alcoholism were weaned off medication as their condition improved. During detoxification, pharmacological interven-

136

tions were modified depending on the subject’s substance abuse history: l Alcohol alone - chlordiazepoxide hydrochloride (Librium) or hydroxyzine (Vistaril) l Alcohol and benzodiazepine - equivalent longacting benzodiazepine or phenobarbital l Alcohol and narcotics-clonidine or, when necessary, clonidine and methadone. Other drug addictions were managed on an individual basis. Subjects were transferred to rehabilitation when judged medically stable by the supervising physician, usually after 5 days of detoxification. All subjects were seen by a physician at least once a week throughout the rehabilitation period. Counseling and education began during rehabilitation and included weekly classes on the nutritional effects of alcohol abuse and the basics of proper nutrition. Other classes dealt with the metabolic, immunological, and physiological effects of alcohol abuse and the genetics of alcoholism. The education program was designed to provide subjects with the information and skills needed to take an active part in their physical recovery. In addition to the above classes, subjects in rehabilitation were required to participate in: l group therapy l individual counseling l role-play workshops l nightly Alcoholics Anonymous (AA) and Narcotics Anonymous (NA) meetings, including step meetings and assignment of a temporary sponsor l job counseling (where needed) l family counseling (where needed) l vocational counseling l physical activities and exercise sessions (geared to individual subjects’ cardiac status). Shortly before discharge from rehabilitation, the outpatient treatment plan was reviewed with each subject, his or her significant other, and his or her employer (where applicable). Subjects signed releases allowing contact with these corroborative sources. Contact was maintained via phone interviews and questionnaires, and all subjects and corroborative sources were free to call the treatment team at any time. The goal of the 1Zmonth follow-up period was to maintain treatment contact and to help the subjects continue the healthy lifestyle begun during hospitalization. Subjects were enrolled in weekly aftercare or group sessions and were strongly encouraged to participate in their local AA groups. Contact was made with local groups prior to discharge, and AA involvement was monitored during the follow-up period. The importance of dietary modification and nutritional supplementation were strongly stressed during the outpatient phase, and nutritional counseling was

J.D. Beasley et al.

an integral part of all follow-up visits. A detailed diet plan was provided for each subject, including a listing of foods and medications to avoid. Upon discharge from rehabilitation, each subject received a one-month supply of the following supplements: l Bronson Fortified Insurance Formula, 2 tablets t.i.d. l Calcium-magnesium supplement, 1 tablet b.i.d., consisting of 375 mg calcium, 150 mg magnesium l L-glutamine powder, 1000 mg p.o. b.i.d. First medical follow-up was 2 weeks after discharge and about once a month thereafter. During each visit the physician reviewed the subject’s progress and dealt with actual or anticipated medical, social, or psychological problems. The next month’s supply of nutrient supplements was also provided. Contact was maintained through aggressive followup. Those who missed appointments were immediately contacted by phone and mail for rescheduling. Home visits were arranged for subjects with transportation problems. When direct communication with the subject was difficult, contact was established through the significant other or employer. Records were kept of all missed visits. Relatives or friends who had agreed to participate in the program filled out three follow-up questionnaires during the year and were telephoned monthly to verify the subject’s progress-drinking status, AA attendance, adherence to the diet/supplement regimen, and mental state. Where appropriate, contact was also maintained with an employee assistance counselor at the subject’s workplace. The subjects themselves filled out monthly questionnaires that assessed substance use, dietary habits, sleeping patterns, AA attendance, and general health. Physical status was monitored throughout the year, by both clinical evaluation and laboratory testing. Blood profiles consisted of CBC, glucose, BUN, serum creatinine, sodium, potassium, chloride, carbon dioxide, total protein, albumin, LDH, bilirubin, cholesterol, uric acid, ALP, AST, ALT, GGT, magnesium, amylase, calcium, and phosphorus. Urine samples were randomly collected. Outcome was judged at the end of the 1Zmonth follow-up period, and was based on (in descending order of priority): l sequential urine and drug screen results l laboratory results (CBC and SMA 25) l longitudinal evaluation of clinical pathology l clinical evaluation by counselors and physicians l report of employer (if applicable) l report of significant other l subject’s self-report. Subjects were considered to be in recovery if they were abstinent and physically/emotionally/socially stable 12 months after their discharge from rehabili-

Biobehavioral

137

Treatment of Alcoholism

tation. Physical findings-sequential liver function tests, other blood work, and urine screens-had to indicate steady physical improvement over time. Psychosocial status was determined on the basis of the treatment team’s assessment and corroborative information from significant others, employers, and the subjects themselves. While total abstinence was the ideal goal, one or more “slips” (defined as any alcohol or drug intake) did not in itself exclude a subject from the recovering group, if he or she was physically stable and abstinent at the 1Zmonth date. Statistical analysis was performed in stages. The descriptive univariate analysis employed means, medians, and standard deviations as measures. Bivariate analysis was used to search for initial relationships between independent and dependent (outcome) variables and to identify discriminators between recovering and nonrecovering groups. The variables that were considered are listed in Table 1. Continuous independent variables were compared between the two groups using the student’s t and Mann-Whitney tests, while categorical variables were analyzed with the chi square. Multivariate assessment was then performed with discriminant analysis to determine which variables related to group distinctions between recovering subjects and those who were actively drinking or lost to follow-up. RESULTS Initial Findings All 111 study participants completed 5 days of detoxification and a minimum of 14 days of rehabilitation. Demographic and historical evaluation of the study participants revealed that in comparison with the population of Suffolk County the study population was disproportionately male, with fewer unmarried individuals (Table 2). The subjects’ ages ranged from 20 through 60 years, with a median age of 40. Although alcohol was the primary drug of abuse, 42 subjects (37.8%) reported regular use of other drugs, including 21 (18.9%) who reported daily use. Marijuana, cocaine, and Valium or other tranquilizers were the most frequently cited cross-addicting drugs. Eighty-one subjects (72.9%) were cigarette smokers. Most subjects had long histories of substance abuse with frequent treatment attempts. One individual reported going through 20 detoxification programs. Another reported 15 previous rehabilitation programs. Patterns of frequent heavy drinking were common: 20 subjects (18%) said they drank “continuously,” 54 (48.6%) said they drank every day, and 14 (12.6%) reported binge drinking. Seventy-seven subjects (69.3%) said they consumed a pint or more of alcohol per day during their drinking episodes.

TABLE 1 Variables Analyzed Continuous (f 8 Mann-Whitney) Age Height Weight MMPI scores G-l-f hourly insulin values hourly glucose values Lab results allergy screens blood values Categorical (chi square) Race Gender Religion Marital status # Children Ethnicity Medical history Medical condition upon admission # Previous detoxes # Previous rehabs Quantity of drinking Frequency of drinking Activities to relieve stress Drinking-related problems Reasons for entering treatment Physical effects of alcohol use Psychological effects of alcohol use Reasons for drinking Family history Drug use history Eating patterns Cravings

Many subjects revealed a propensity for solitary and furtive drinking, often beginning early in the day. Sixty-six (59.4%) hid bottles, 81 (72.9%) drank surreptitiously, and 94 (84.6%) drank alone. Twenty-nine subjects (26.1 vo) had been jailed due to intoxication. Family medical histories showed patterns of alcoholism dating back two generations in some cases. Eighty-nine subjects (80.1070)reported alcoholism in at least one blood relative. Paternal alcoholism was indicated more frequently than maternal (45.5% versus 17.9%), while 12 subjects (10.8%) said both parents had a drinking problem. Drinking-related physical problems were common: 80 subjects (72%) reported blackouts, 67 (60.3%) sickness, and 14 (12.6%) delirium tremens. Alcohol consumption also had a generally negative impact on nutritional status. The subjects’ 24hour dietary recalls revealed diets well below the Recommended Dietary Allowances, and 91 (81.9070)were diagnosed as clinically malnourished. Thirty-five subjects (3 1.5%) reported skipping one or more meals daily because of

J.D. Beadey et al.

138

TABLE 3 Nutrient Deficiencies, Metal Toxicity, and Adverse Food Reactions (N = 108)

TABLE 2 Demographic Profiles (N = 111)

Patients n

%

Deficiencies

Suffolk Co. %

n

%

Vitamin E Zinc Calcium Magnesium Vitamin B6 Vitamin A

64 36 21 17 15 12

59.2 33.3 19.4 15.7 13.9 11.1

Thiamine Folate Carotene Protein Copper Vitamin B2

12 11 10 5 5 4

11.1 10.2 9.2 4.6 4.6 3.7

4 3 2 2 1 1

3.7 2.8 1.9 1.9 0.9 0.9

Nutrient Sex Male Female

77 34

69.4

30.6

47.8 52.2

Race White Black Other

94 9 8

84.7 8.1 7.2

92.4 5.6 2.0

Marital Status Married Single Separated Divorced Widowed

64 18 8 9 4

57.7 16.2 7.2 8.1 3.6

60.3 27.2 2.2 3.7 6.7

Children Yes No

70 41

63.1 36.9

-

Previous Detoxification Yes No

87 24

78.4 21.6

-

84 27

75.7 24.3

-

Previous Detoxification Rehabilitation Yes No

Phosphate Vitamin B, 2 Potassium Vitamin C Chloride Chromium

Metal Toxicity

8. Subjects with Excessive Values

-

drinking, and another 44 (39.6%) said they skipped meals “occasionally” for this reason. Laboratory testing and detailed medical evaluations were carried out on 108 (97.2%) of the original 111 subjects. (Three subjects withdrew from the study prior to full medical evaluation.) All 108 were found to have extensive physical pathology, from mild gastritis to advanced liver disease. Most exhibited a constellation of physical problems in which malnutrition, abnormal carbohydrate metabolism, macrocytosis (enlarged erythrocytes indicative of anemia) and disorders of lipid metabolism were common. Forty-eight subjects (44.4%) displayed abnormal lipoprotein electrophoresis. Ninety-three subjects (86.1 (r/o) suffered from five or more physical disorders in addition to the primary diagnosis of alcoholism. In addition to their generally poor nutritional status, blood work-ups revealed specific nutrient deficiencies and metal toxicity in many of the subjects, as delineated in Table 3. RAST allergen profiles also revealed extensive food sensitivities in the study population. Of 108 tested subjects, 106 (98.1%) reacted to one or more of nine food antigens. One of the most striking features of this population was the prevalence of atypical carbohydrate metabolism, as evidenced by dramatic fluctuations of insulin

Metal

Normal Range

Cadmium Aluminum Mercury Lead

<5 O-l 3 O-5 O-30

ng/mL ng/mL ng/mL fig/dL

n

%

15 6 3 1

13.9 5.5 2.8 0.9

Adverse Food Reactions Tested Population n

%

Corn Milk Peanut Cocoa Whole egg

82 80 73 72 65

75.9 74.1 67.6 66.7 60.2

Orange Tomato Shrimp Wheat

62 57 52 50

57.4 52.8 48.1 46.3

Allergen

and glucose levels during the 6-hour glucose tolerance test. Forty-seven subjects (43.5%) displayed hyperinsulinism, and abnormally high, delayed peaks of insulin release were common throughout the sample. Forty-four subjects (39.6%) also reported cravings for sweets. The subjects’ MMPI profiles were markedly elevated

Biobehavioral

139

Treatment of Alcoholism

on several scales, notably Depression (D), Hysteria (Hy), Psychopathic Deviancy (Pd), Psychasthenia (Ps), and Hypomania (Ma). 1ZMonth Outcomes At the end of the study period, contact had been maintained with 91 (81.9Vo) of the original 111 subjects. Three subjects dropped out of the study group prior to discharge from rehabilitation, stating that they planned to move out of the study area. The remaining 17 subjects were lost to follow-up at various points in the study period. Table 4 summarizes the 1Zmonth status of the study population. Of the original study group, 67 subjects (60.4%) were sober and stable 12 months after discharge. The course of recovery varied widely among these subjects. Forty-two (37.8%) were abstinent throughout the treatment year, and another 10 subjects (9.0%) had a single drinking episode. Of the 6 subjects with more than 2 drinking episodes during the year, 4 had had relapses within the last 2 months. Nonetheless, laboratory data and corroborative reports indicated that these individuals had steadily improved physically and were stable and abstinent at 12 months. Eight of the subjects who were lost to follow-up were know to be drinking at the time of last contact, bringing the number of subjects drinking or presumed so to 32 (28.8% of the original sample). The condition of the remaining 12 patients (10.8%) could not be determined. Physical examinations and laboratory results at 12 months showed a marked decrease in physical pathology among recovering subjects. Of the 67, only 17 (25.4%) exhibited residual pathology. Macrocytosis was the most common medical problem, still present in 6 subjects. Of the MMPI scales, three were statistically significant in discriminating between recovering and non-

TABLE 4 12-Month Status (N = 111)

n

%

42 10 9 6

37.8 9.0 8.1

recovering patients who were still in treatment contact. Moderate to high elevations on the F, Hypochondriasis, and Hypomania scales were significant at p values of c.05, <.05, and <. 10, respectively. Average scores on these predictive scales are noted in Table 5. Elevations of all three scales were predictive of unsuccessful outcome with 78% accuracy. This finding was significant at a level of .009. Compliance with the treatment protocol -defined as abstinence from alcohol and all psychoactive drugs, adherence to dietary guidelines, continuation of vitamin and nutrient supplementation, and aftercare attendance (where applicable) - was significantly correlated with recovery at a p value of <.Ol . Reliability, as measured by the number of missed and rescheduled physician’s appointments, was also significantly correlated with recovery at a p value of .Ol . AA attendance data, with confirmation by the significant other, were obtained for 52 (78%) of the 67 patients in recovery and for 13 (57%) of the 23 patients in treatment contact and actively drinking. While there was a correlation between regular attendance (one or more meetings a week) and recovery, the numbers reporting were insufficient to assure statistical significance. DISCUSSION The findings of the present study illustrate several of the more neglected aspect of the disease of alcoholism, as well as offering some support to existing theories of its pathogenesis. The relatively low attrition rate (18%) at the end of the 1Zmonth study period demonstrates that it is possible to maintain long-term treatment contact with alcoholics, although the process is sometimes difficult. It is encouraging that more than 73% of the patients who remained in treatment for the full 12 months were sober and stable at the end of the study period, and that more than 60% of these (37.8% of the original sample) had been abstinent throughout. The use of sequential blood tests and urine screens to evaluate progress proved to be a crucial component in getting an accurate picture of the patients’ status. On several occasions laboratory data (either positive urine screen or elevated liver enzymes) alerted the physician to a relapse before the corroborative sources

In Contact (n = 91) Abstinent throughout 1 drinking episode* 2 drinking episodes* 2-5 drinking episodes Drinking

l

Lost to Follow-Up (n = 20) Moved, status unknown Lost to follow-up, status unknown Lost to follow-up, drinking at last contact l

Includes readmissions

24

3 9 8

5.4 21.6

2.7 8.1 7.2

TABLE 5 Average Scores on Predictive MMPI Scaler (Recovery versus Return to Drinking)

Posttreatment Status In Recovery Drinking Again p-Value

F

Hs

Ma

61.6 67.0 < .05

59.2 66.7 < .05

61.8 67.2 < .lO

140

were aware of the patients’ drinking behavior. Laboratory evidence of decompensation was a powerful tool in addressing relapses and intervening with patients in crisis. Sequential testing throughout the study period allowed the treatment team to monitor subtle changes in the patients’ conditions and, by integrating corroborative reports with patients’ self-reports, to arrive at reliable final assessments. From a treatment perspective, the prevalence of physical pathology, disordered metabolism, and malnutrition in this ostensibly stable population is indicative of the medical severity of the disease of alcoholism. More than 80% of the study population were clinically malnourished, with specific nutrient deficiencies, and poor dietary habits. The majority of these individuals were consuming diets high in refined carbohydrates, fats, additives, and preservatives, and relied on a very small variety of foods. These dietary habits undoubtedly contributed to the disorders of lipid and carbohydrate metabolisms that were common throughout the sample. Other research’ ers have hypothesized that there is a link between abnormal glucose metabolism and poor impulse control, depression, and violent behavior, which may be triggered or exacerbated by alcohol use (Virkkunen, 1982; Virkkunen, 1983). The initial psychological profiles of this study group showed extensive depression and impulsivity, as measured by the Depression and Psychopathic Deviancy scales of the MMPI. Fifty-one percent of subjects also indicated that alcohol consumption made them angry, while 32.7% reported that their drinking was usually followed by fights. Seventeen percent reported injuries as a result of fighting while intoxicated, and 26.1% had been jailed as a result of their drinking behavior. The interrelationship of these behavioral/psychological factors and abnormalities in glucose metabolism bears further investigation and research. It is apparent that the glucose disorder is not limited to active alcoholics, and requires treatment during the recovery process. It is possible that treatment, in the form of dietary modification, may alleviate some of the mood swings that afflict alcoholics in recovery. Compliance with the dietary protocol was correlated with recovery in this study group, and many patients reported feeling less anxious and moody than they had in years, but it is difficult to infer the significance of this data. A surprising and potentially significant finding was the prevalence of metal toxicity in the study population. Cadmium toxicity, which has been linked to alcohol-seeking behavior in animal studies (Nation et al., 1987), was detected in 15 (13.9%) of tested subjects, and unusually high levels of aluminum were found in another 6 (5.5%). Toxic levels of mercury (3 subjects) and lead (1 subject) were also detected. There is evidence that cadmium toxicity has an inverse effect on

J.D. Beusley et al.

the rewarding effects of alcohol, prompting craving and increased intake (Nation, Von Stultz, Frye, & Bratton, 1989). Toxic metal screens are therefore advisable when evaluating alcoholic patients, particularly those who are long-term smokers, since cadmium is a component of tobacco smoke. Another finding with important treatment ramifications was the prevalence of adverse food reactions, as measured by RAST allergen profiles. While the exact cause of this reactivity is subject to debate, the prevalence of allergic responses to environmental and food antigens in alcoholic patients has been noted by other researchers (Closson, 1985; Sugerman et al., 1982) and should be further investigated. The extensive testing and demographic analysis performed on this population was for the dual purpose of designing a comprehensive medical follow-up protocol and detecting factors that might discriminate between subjects who maintained their recovery and those who returned to drinking. Of all the factors analyzed, only the F, Hypochondriasis, and Hypomania scales of the MMPI proved to have any predictive value in discriminating between patients in treatment who were in recovery and those who were actively drinking. The MMPI has generally not been effective as a predictive tool in alcoholism (Krasnoff, 1977; O’Leary, Rohsenow, & Chaney, 1979; Clopton, 1978), and the value of this particular combination of scales can be undermined by extreme elevations in F scores, which would cast doubt on the validity of the entire profile. However, the elevations found in this population were not generally in the extreme range. At the end of 12 months, the recovering subjects all showed marked physical improvement, although 17 subjects still exhibited residual pathology. We feel this finding indicates that alcohol-induced pathology, though extensive, can be resolved with proper treatment. However, this treatment must continue for an extended period of time to insure recovery. The 17 patients with residual pathology continued in treatment contact for up to a year after the close of the study, as did many of the other recovering subjects. This study focused on an economically and socially stable group of patients, and documented the extent of pathology, malnutrition, and dysfunction throughout this population. These problems will only be compounded in patients from less stable environments. The nutritional, immunological, toxicological, and metabolic disorders that accompany alcoholism require additional research and clinical attention. The 12-month outcomes of our subjects in recovery indicate that it is possible to correct these conditions, although the process of maintaining treatment contact often requires heroic efforts on the part of the treatment team. The most commonly cited predictors of treatment

Biobehavioral

Treatment

of Alcoholism

outcome, such as previous treatment history and extent of physical pathology, did not prove predictive in this group. Instead, a pattern of elevations in the F, Hypochondriasis, and Hypomania scales of the MMPI seems to point to the existence of a subgroup of alcoholic patients whose negative expectations and fear/distrust of treatment impede successful outcomes. Further investigation of this finding and of less cumbersome diagnostic instruments to identify these higher-risk patients may help in addressing this treatment problem. Additional analysis also needs to be done on the characteristics of subjects who were lost to follow-up.

REFERENCES Alford, G.S. (1980). Alcoholics Anonymous: An empirical outcome study. Addictive Behaviors, 5, 359-370. Asberg, M., Traskman, L., & Thoren, P. (1976). S-HIAAA in the cerebrospinal fluid: A biochemical suicide predictor? Archives of General Psychiatry, 33, 1193-l 197. Asberg, M., Thoren, P., Traskman, L., Bertilsson, L., & Ringberger, V. (1976). ‘Serotonin Depression’- A biological subgroup within the affective disorders? Science, 191, 478-480. Ballenger, J., Goodwin, F., Major, L., & Brown, G. (1979). Alcohol and central serotonin metabolism in man. Archives of General Psychiatry, 36, 224-227. Becker, J.T., & Jaffe, J.H. (1984). Impaired memory for treatmentrelevant information in inpatient men alcoholics. Journal of Studies on Alcohol, 45, 339-343. Begleiter, H., Porjesz, B., Bihari, B., & Kissin, B. (1984). Event related brain potentials in boys at risk for alcoholism. Science, 225, 1493-1496. Berglund, M. (1984). Suicide in alcoholism, a prospective of 88 suicides: 1. The multidimensional diagnosis at first admission. Archives of General Psychiatry, 41, 888-891. Bjarnason, I., Ward, K., & Peters, T.J. (1984). The ‘leaky gut’ of alcoholism: Possible route of entry for toxic compounds. Lancer, 1, 179-182. Breitenbucher, R.B. (1976). The routine administration of the Michigan Alcoholic Screening Test to ambulatory patients. Minnesota Medicine, 59, 425-429. Brown, G.L., Ebert, M.H., Coyer, P.F., Jimerson, D.C., Klein, W.J., Bunney, W.E., & Goodwin, F.K. (1982). Aggression, suicide, & serotonin: Relationships to CSF amine metabolites. American Journal of Psychiatry, 139, 741-746. Cadoret, R.J., Cain, C.J., & Grove, W.M. (1980). Development of alcoholism in adoptees raised apart from biologic relatives. Archives of General Psychiatry, 31, 561-563. Clopton, J.R. (1978). Alcoholism and the MMPI: A review. Journal of Studies on Alcohol, 39, 1540-1558. Closson, W. (1985). Levels of IgE antibodies in hospitalized alcoholics vs. nonalcoholic elective-surgery controls. Unpublished paper, Brunswick Hospital Center, Amityville, NY. Cole, S.G., Lehman, W.E., Cole, E.A., & Jones, A. (1981). Inpatient vs. outpatient treatment of alcohol and drug abusers. American Journal of Drug and Alcohol Abuse, 8, 329-345. Costello, B.M., Parsons-Manders, P., & Schneider, S.L. (1978). Alcoholic mortality: A 12-year follow-up. American Journal of Drug and Alcohol Abuse, 5, 199-210. Dahlstrom, W.G., Welsh, G.S., & Dahlstrom, L.E. (1982). An MMPI Handbook, (Vol. I). Minneapolis: University of Minnesota Press. Davidson, J., Liper, S., Kilts, C.D., Mahorney, S., & Hammett, E.

141 (1985). Platelet MAO activity in post-traumatic stress disorder. American Journal of Psychiatry, 142, 1341-1343. De Lint, J., & Levinson, T. (1975). Mortality among patients treated for alcoholism: A 5-year follow-up. CMA Journal, 113, 385-387. De Soto, C.B., O’Donnell, W.E., Allred, L.J., & Lopes, C.E. (1985). Symptomatology in alcoholics at various stages of abstinence. Alcoholism: Clinical and Experimental Research, 9, 505-512. Dolinsky, Z.S., Shaskan, E.G., & Hesselbrock, M.N. (1985). Basic aspects of blood platelet monoamine oxidase activity in hospitalized men alcoholics. Journal of Studies on Alcohol, 46(l), 81-85. Dornhorst, A., & Ouyang, A. (1971). Effect of alcohol on glucose tolerance. Lancet, 2, 957-959. Flavin, D.K. (1987). Alcohol and the human immune defense system. Medical and Scientific Advisory, January 20, 1987, National Council on Alcoholism, New York. Fraser, R., Day, W.A., & Fernando, N.S. (1986). Review: The liver sinusoidal cells. Their role in disorders of the liver, lipoprotein metabolism and atherogenesis. Pathology, 18, 5-l 1. Gabrielli, W.F., Jr., Mednick, S.A., Volavka, J., Pollock, V.E., Schulsinger, F., & Itil, T.M. (1982). Electroencephalograms in children of alcoholic fathers. Psychophysiology, 19, 404407. Geokas, M.C., Lieber, C.S., French, S., & Halsted, C.H. (1981). Ethanol, the liver, and the gastrointestinal tract. Annals of Internal Medicine, 95, 198-211. Gerard, D.L., Saenger, G., & Wile, R. (1962). The abstinent alcoholic. Archives of General Psychiatry, 6, 99-l 11. Classman, A.B., Bennett, C.E., & Randall, C.L. (1985). Effects of ethyl alcohol on human peripheral lymphocytes. Archives of Pathology and Laboratory Medicine, 109, 540-542. Goldstein, D.B. (1987). Ethanol-induced adaptation in biological membranes. Annals of the New York Academy of Sciences, 492, 103-111. Goodwin, D.W., Schulsinger, F., Hermansen, L., Guze, S.B., & Winokur, G. (1973). Alcohol problems in adoptees raised apart from alcoholic biological parents. Archives of General Psychiatry, 28, 238-243. Gordis, E., Dorph, D., Sepe, V., & Smith, H. (1981). Outcome of alcoholism treatment among 5578 patients in an urban comprehensive hospital-based program: Application of a computerized data system. Alcoholism, Clinical and Experimental Research, 5, 509-522. Guenther, R.M. (1983). The role of nutritional therapy in alcoholism treatment. International Journal of Biosocial Research, 4(l), 5-18. Hoffman, N.G., & Harrison, P.A. (1986). CATOR 1986 report: Findings two years after treatment. St. Paul, MN: The Chemical Abuse/Treatment Outcome Registry. Hrubec, Z., & Omenn, G.S. (1981). Evidence of genetic predisposition to alcoholic cirrhosis and psychosis: Twin concordances for alcoholism and its biological end points by zygosity among male veterans. Alcoholism, Clinical and Experimental Research, 52, 207-215. Kent, T.A., Campbell, J.L., Pazdernik, T.I., Hunter, R., Gunn, W.H., & Goodwin, D.W. (1985). Blood platelet uptake of serotonin in men alcoholics. Journal of Studies on Alcohol, 46, 357-359. Krasnoff, A. (1977). Failure of MMPI scales to predict treatment completion. Journal of Studies on Alcohol, 38, 1440-1442. Leevy, C.M., Cardi, L., Frank, O., Gellene, R., & Baker, H. (1%5). Incidence and significance of hypovitaminemia in a randomly selected municipal hospital population. American Journal of Clinical Nutrition, 17, 250-270. Lieber, C.S. (1981). Metabolic effects of ethanol on the liver and other digestive organs. Clinics in Gastroenterology, 10, 315-342.

142 MacGregor, R.R. (1986). Alcohol and immune defense. Journal of the American Medical Association, 256, 1474-1479. Marks, V. (1975). Alcohol and changes in body constituents: Glucose and hormones. Proceedings of the Royal Society of Medicine, 68(6), 377-380. Mathews-Larson, J., & Parker, R.A. (1987). Alcoholism treatment with biochemical restoration as a major component. International Journal of BioSocial Research, 9(l), 92-106. McCusker, J., Cherubin, C.E., & Zimberg, S. (1971). Prevalence of alcoholism in general municipal hospital population. New York State Journal of Medicine, 71, 751-754. Mendelson, J.H., Miller, K.D., Mello, N.K., Pratt, H., & Schmitz, R. (1982). Hospital treatment of alcoholism: A profile of middleincome Americans. Alcoholism, Clinical and Experimental Research, 6, 377-383. Metz, R., Berger, S., & Maka, M. (1%9). Potentiation of the plasma insulin response to glucose by prior administration of alcohol: An islet-priming effect. Diabetes, 18, 517-522. Moore, R.D., Bone, L.R., Geller, G., Mamon, J.A., Stokes, E.J., & Levine, D.M. (1989). Prevalence, detection, and treatment of alcoholism in hospitalized patients. Journal of the American Medical Association, 261, 403-407. Mossberg, D., Liljeberg, P., & Borg, S. (1985). Clinical conditions in alcoholics during long-term abstinence: A descriptive, longitudinal treatment study. Alcohol, 2, 551-553. Nation, J.R., Baker, D.M., Bratton, G.R., Fantasia, M.A., Andrew, K., & Womac, C. (1987). Ethanol self-administration in rats following exposure to dietary cadmium. Neurotoxicology and Teratology, 9, 339-344. Nation, J.R., Von Stultz, J., Frye, G.D., & Bratton, G.R. (1989). Effects of combined lead and cadmium exposure: Changes in schedule-controlled responding and in dopamine, serotonin and their metabolites. Behavioral Neuroscience, 103, 1108-I 114. Nouri-Aria, K.T., Alexander, G.J.M., Portmann, B.C., Hegarty, J.E., Eddleston, A.L.W.F., &Williams, R. (1986). T and B cell function in alcoholic liver disease. Journal of Hepatology, 2, 195-207. O’Keefe, S.J.D., & Marks, V. (1977). Lunchtime gin and tonic a cause of reactive hypoglycaemia. Lancet, 1, 1286-1288. O’Leary, M.R., Rohsenow, D.J., & Chaney, E.F. (1979). The use of multivariate personality strategies in predicting attrition from alcoholism treatment. Journal of Clinical Psychiatry, 40, 190-193. Pell, S., & D’Alonzo, C.A. (1973). A five-year mortality study of alcoholics. Journal of Occupational Medicine, 15, 120-125. Pokomy, A.D., & Solomon, J. (1983). A follow-up survey of drug abuse and alcoholism teaching in medical schools. Journal of Medical Education, 58, 316-321. Pollock, V.E., Volavka, J., Goodwin, D.W., Mednick, S.A., Gabrielli, W.F., Knop, J., & Schulsinger, F. (1983). The EEG after alcohol administration in men at risk for alcoholism. Archives of General Psychiatry, 40, 857-861. Prasad, A.S., Oberleas, D., & Rajasekaran, G. (1970). Essential micro-nutrient elements: Biochemistry and changes in liver disorders. American Journal of Clinical Nutrition, 235, 581-591.

J.D. Beasley et al. Rajkovic, I.A., &Williams, R. (1985). Mechanisms of abnormalities in host defenses against bacterial infection in liver disease. Clinical Science, 68, 247-253. Roy, A., Virkkunen, M., Guthrie, S., Linnoila, M. (1986). Indices of serotonin and glucose metabolism in violent offenders, arsonists and alcoholics. Annals of the New York Academy of Sciences, 487, 202-220. Schuckit, M.A. (1980). Biological markers: Metabolism and acute reactions to alcohol in sons of alcoholics. Pharmacology, Biochemistry & Behavior, 13, 9-16. Schuckit, M.A., & Rayses, V. (1979). Ethanol ingestion: Differences in blood acetaldehyde concentrations in relatives of alcoholics and controls. Science, 203, 54-55. Serenyi, G., & Endrenyi, L. (1978). Mechanism and significance of carbohydrate intolerance in chronic alcoholism. Metabolism, 27, 1041-1046. Sherlock, S. (1984). Nutrition and the alcoholic. Lance& 1, 436-439. Sinclair, H.M. (1972). Nutritional aspects of alcohol consumption. Proceedings of the Nutrition Society, 31, 117-123. Sugerman, A.A., Southern, L., Curran, J.F. (1982). A study of antibody levels in alcoholic, depressive and schizophrenic patients. Annals of Allergy, 48, 166-171. Tashiro, M., & Lipscomb, W.R. (1963). Mortality experiences of alcoholics. Quarterly Journal of Studies on Alcohol, 24(10), 203212. Vaillant, G.E., & Milofsky, E.S. (1982). Natural history of male alcoholism: 4. Paths to recovery. Archives of General Psychiatry, 39, 127-133. Van de Weil, A., Seifert, W.F., Van der Linden, J.A., GmeligMeyling, F.H.J., Kater, L., & Schuurman, H.-J. (1987). Spontaneous IgA synthesis by blood mononuclear cells in alcoholic liver disease. Scandinavian Journal of Immunology, 25, 181-187. Virkkunen, M. (1983). Insulin secretion during the Glucose Tolerance Test in antisocial personality. British Journal of Psychiatry, 142, 598-604. Virkkunen, M. (1982). Reactive hypoglycemic tendency among habitually violent offenders. Neuropsychobiology, 8, 35-40. von Knorring, A.L., Bohman, M., von Knorring, L., & Oreland, L. (1985). Platelet MAO activity as a biological marker in subgroups of alcoholism. Acta Psychiatrica Scandinavika, 72, 51-58. Wehe, J., Hynes, G., Sokolow, L., & Lyons, J. (1979). Outcome Study of Alcoholism Rehabilitation Units. New York: New York Research Institute on Alcoholism, New York State Division of Alcoholism and Alcohol Abuse. Winick, M. (1980). Nutrition in Health andDisease, pp. 183-186. New York: Wiley. Yamamoto, H., Nagai, K., & Nakagawa, H. (1985). Lesions involving the suprachiasmatic nucleus eliminate the glucagon response to intracranial injection of 2-deoxy-D-glucose. Endocrinology, 117, 468-473. Zimberg, S. (1979). Alcoholism: Prevalence in general hospital emergency room and walk-in clinic. New York State Journal of Medicine, 7, 1533-1535.