Journal of Youth andAdolescence, VoL 12, No. 2, 1983

Diabetic Control in Children and Adolescents: Psychosocial Factors and Therapeutic Efficacy 1 P. B a r g l o w , 2 D . V. E d i d i n , 3 A . S. B u d i o n g - S p r i n g e r , 4 D . Berndt s R. P h i l l i p s , 6 and E. D u b o w 7

ReceivedAugust 3, 1982

Forty4wo insulin-dependent latency and adolescent age diabetics were studied over a four-month period. H a l f o f the population received a multicomponent intervention designed to enhance diabetic regulation. Psychological and demographic variables and glycosylation o f hemoglobin were correlated in order to investigate the interaction between personality factors and metabolic control. Number o f life event changes predicted initial values o f glycohemoglobin, while ego development predicted the magnitude o f improved diabetic control.

'A version of this article was presented at the meeting of the American Psychiatric Association, April 1983. 2Clinical Director, Psychosomatic and Psychiatric Institute, Michael Reese Hospital and Medical Center; Associate Professor, Department of Psychiatry, Pritzker School of Medicine, University of Chicago. 3Attending Physician, Division of Endocrinology, Michael Reese Hospital and Medical Center; Assistant Professor, Department of Pediatrics, Pritzker School of Medicine, University of Chicago. 4Nurse Coordinator, Pediatric Model Unit, Diabetes Research and Training Center, University of Chicago/Michael Reese Hospital and Medical Center. sSenior Clinical Psychologist, Department of Psychiatry, Michael Reese Hospital and Medical Center; Research Associate (Assistant Professor), University of Chicago. ~Staff Social Worker, Children's Hospital, Boston, Massachusetts. "Graduate student, Department of Psychology, University of Illinois. 77 0047-2891/8310400-0077503.00/0

© 1983 Plenum Publishing C o r p o r a t i o n ~

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INTRODUCTION Recent evidence indicates that educational programs and optimal psychological care enhance metabolic control of juvenile diabetes. 8 Furthermore, many major studies support the assumption that excellent diabetic control correlates with a lowered incidence of chronic degenerative complications of diabetes mellitus (e.g., Pirart, 1978a, 1978b; Knowles, 1979; Brown et al., 1982). Optimal diabetic control is also a desirable goal because it minimizes the risk of acute metabolic decompensation by widening the margin between the patient's present status and that of ketoacidosis. Many clinical studies have provided evidence that emotional and physical stresses are related to deterioration of control in juvenile diabetics. Marigo et al. (1977) reported increased urinary glucose and acetone following parental visits to children with diabetes. Weil and Sussman (1961) determined that stress correlated with glycosuria in summer camp diabetic children. Vandenbergh (1966) and Sanders et al. (1975) noted a correlation between poor diabetic control and emotional lability. Ack (1974), Kaufman and Hersher (1971), and K~Jnmerer and Reindell (1977) found high anxiety to be characteristic of adolescent diabetics; the same conclusion has been reached by many investigators in psychiatry and medicine (e.g., Swift et al., 1967; Stearns, 1959; Minuchin, 1977). In addition to evidence suggesting a relationship between poor control and stress, Nabarro (1965) and Cohen et al. (1960) maintained that up to 20°70 of episodes of acute diabetic ketoacidosis in an adolescent population was precipitated by emotional disturbances. Stearns (1959), Peck and Peck (1956), and Minuchin eta/. (1975) also have related repetitive episodes of ketoacidosis to emotional factors and family conflict. Simonds et a/.(1981), investigating control in adolescence using glycohemoglobin measurement, have reported that better control correlates positively with active parental supervision and negatively with increased self-care. Daneman et al. (1981) suggests that this factor could explain poorer control with increasing age during adolescence. K/immerer and Reindell (1977) have argued that metabolic decompensation associated with anxiety is mediated by the sympathetic nervous system. Considerable evidence supports the hypothesis that stress can influence diabetic control adversely through a number of neuro-endocrine mechanisms. Several hormones related to stress have been demonstrated to counteract some metabolic actions of exogenous insulin given diabetic patients and of endogenous insulin produced by the pancreas. One iraThe term "juvenile" is used to designate Type I (insulin-dependent) latency and adolescent age diabetics.

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portant effect of insulin is to reduce the hyperglycemia that seems to be linked to chronic medical sequelae of insulin-dependent diabetes. Simply stated, stress, by stimulating secretion of hormones with a counterregulatory function (i.e., opposing the glucose-reducing effect of insulin), can exert its action through several different mechanisms: (1) through the pituitary-adrenal cortex a x i s - b y increasing cortisol levels, which in turn elevate blood glucose; (2) through the adrenal medulla--sympathetic nervous system--by increasing levels of catecholamines (epinephrine or norepephrine) that increase blood sugar by opposing insulin action and stimulating hepatic glycogenolysis and gluconeogenesis; (3) by stimulating glucagon secretion, which also acts to increase blood sugar (elevations of growth hormone and prolactin have also been correlated with increased glucose levels during stress). Cortisol, catecholamines, and glucagon have many physiological functions other than increasing blood sugar or mediating the impact of stress. But physiological attributes less related to glucose metabolism will not be discussed, for the sake of clarity. In this article these substances with a blood glucose-increasing capacity will be designated by the term "stress hormones." Improvement in techniques of measuring stress hormones has permitted more precise quantification of fluctuations in these hormones' concentrations during periods of poor control. Baker et ai. (1967) had already demonstrated a brisk ketonemic response to epinephrine stimulation of diabetic children. Using sensitive assay methods, Christensen (1970, 1974) reported higher levels of plasma catecholamines in poorly controlled diabetics, compared to patients with good control. L i n n e t al. (1980) reported high stress scores to be associated with accelerated response to a cold pressor test in diabetic males. MacGillivray et ai. (1981) measured plasma glucose, glucocorticoids, and other hormones during the onset of diabetic ketoacidosis in children who had received their usual insulin injection. No physical stress (such as infection) was present. Several children had elevated levels of cortisol, epinephrine, growth hormone, and glucagon. MacGillivray et al. concluded that in their population the effect of the administered insulin was nullified by the "glycogenolytic, lipolytic and ketogenic action of stress hormones" elevated in these patients. Schade and Eaton (1980) proved that the stress of pyrogen administration could produce a rapid increase in plasma growth hormone, catecholamines, and cortisol. Furthermore, these elevations occurred before the subsequent rise in free fatty acids and ketone body concentrations. They continuously infused insulin during these measurements, proving that a patient need not have absolute insulinopenia to develop such metabolic alterations. Such data provide evidence that stress hormones can be elevated before

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metabolic decompensation, and indicate that such increases are not just a result of poor control. Zadik et al. (1980) compared 24-hour integrated plasma glucose, catecholamines, cortisol, growth hormone, and aldosterone levels in insulin-dependent diabetic children with glucosuria but without ketonuria with levels in matched nondiabetic controls. The diabetic children had an increase in catecholamine, growth hormone, and aldosterone levels in comparison to controls. The preceding studies show that stress hormones may be elevated before or after metabolic decompensation, and that they may play a role both in initiating and exacerbating episodes of hyperglycemic ketoacidosis. Glucagon is another important hyperglycemic hormone which is produced by the alpha cells of the pancreas. These alpha cells are relatively uninvolved in the destruction that characterizes the beta cells of insulindependent diabetics, particularly in response to stress. The effects of stress through increased glucagon production may be potentiated by catecholamines, which also decrease endogenous insulin levels. This latter effect of catecholamines on insulin release is not a factor in Type I (insulin-dependent) patients, in whom only negligible endogeneous insulin production occurs. It has become increasingly clear that hormone action is not only dependent upon the local concentration (which may or may not be reflected by systemic concentrations) but also upon sensitivity of the target tissue to the hormone. Shamoon et al. (1980) have shown that insulin-dependent diabetics exhibit increased sensitivity to cortisol and catecholamines in comparison to normal individuals, accounting for the former's heightened hyperglycemic response to these hormones. Although no single personality type can be associated with diabetes mellitus (Dunn and Turtle, 1981), Hauser and Pollets (1979) clearly demonstrated that diabetic youth differed from controls on measures of self-esteem and ego development. One of the co-authors of the present study noted in a pilot study (Edidin et a/., 1979) that children with above average self-esteem tended to have increased knowledge of diabetes mellitus, which in several instances could be correlated with excellent diabetic control. The self-esteem influence upon control has also been implicated by Sullivan (t978). Chase and 'Jackson (1981) in a study of diabetic children demonstrated that high stress scores on the Coddington checklist (1972) were correlated with decreased short-term and long-term glucose control as measured by fasting serum glucose and HbA1 (hemoglobin AI). However, this relationship between increased stress and decreased metabolic control could not be demonstrated through measures of serum triglycerides or cholesterol (Chase and Jackson, 1981). Wellcontrolled adolescents have been found to have less anxiety, less family

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conflict, and a better self-concept than poorly controlled subjects (Anderson et aL, 1981). If stress does affect metabolic control through the intermediate influence of stress hormones, the contributing effect of diminished compliance with the medical regimen in stressed youthful diabetics cannot be ruled out. The senior author of this study has reported an apparent relationship between compliance and general psychosocial risk factors in pregnant adolescent diabetics (Barglow etal., 1981). In summary, juvenile diabetics represent a population of individuals with the following characteristics relevant to diabetic control: 1. Their personality configurations differ from nondiabetic youth as shown by clinical manifestations of increased anxiety and family conflict, decreased self-esteem, impaired ego development, and other psychological test results. 2. The above psychological traits may affect their metabolic control adversely. 3. They respond to stress with elevations of stress hormones that have hyperglycemic and ketogenic effects. 4. Stress can affect their metabolic control either through a neurohumoral mechanism or by diminishing adherence to the medical regimen. But considerable contrary evidence and conclusions also exist. Some investigators maintain that metabolic control is unrelated to personality variables in insulin-dependent diabetics (e.g., Jenkins and Webb, 1980), and others consider cause-effect connections to be inadequately demonstrated by empirical statistical study. Jacobs and Marrero (1981), for instance, have called attention to the inability of retrospective studies of diabetes mellitus to produce clear-cut answers to causal questions. Kravitz et al. (1971) have noted the paucity of physiological measurements in stress-control research, and have pointed out the necessity to measure the relative contribution to diabetic control of social and medical factors that do not involve stress factors. Some physiological findings have been negative. For instance, Chase and Jackson (1981) did not find a relationship between increased stress and better metabolic control using serum triglyceride levels as an indicator. Other results have been contradictory. Fallstrom (1974) correlated emotional pressure not with hyperglycemia, but with hypoglycemic convulsions. Simonds et aL (1980), Olataware (1972), and Sterky (1963) have found psychopathology in diabetic youth unrelated to diabetic control. Simonds et al. (1981), in a carefully controlled recent study of juvenile diabetics, reported that no significant psychological measurements differentiated

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subjects with good control from subjects with poor control as measured by HbA, levels. The presence of residual beta cell function as determined by C-peptide in juvenile diabetic patients with briefer durations of illness has been inadequately taken into account (Goldstein et al., 1980; Tarnow and Silverman, 1981-1982). Individuals with significant insulin secretory capacity must either be matched or excluded from control studies of Type I insulin-dependent diabetic patients. Furthermore the exact determination of the existence of good or bad control is controversial. In the Northwestern University Diabetes in Pregnancy Center, measurement of 17 separate metabolic substances was considered necessary to comprehensively describe diabetic control (Hatcher, 1981). Moreover, the definition and measuring instruments used to identify stress have varied widely in the research literature. Family conflict (Anderson et al., 1981) and patients' depression (Depuis et al., 1980), immaturity, and low self-esteem have all been considered indicators of stress. One recent publication has criticized the validity of stress scales such as the Coddington scale (Kimball, 1982). The adherence variable which could explain the effect of the emotions upon diabetic control is poorly defined (Surwit et aL, 1982), difficult to measure, and probably varies with age in populations of youthful diabetic patients (e.g., Hauser and Pollets, 1979; Daneman et al., 1981; La Greca, 1981). But there has been Sufficient demonstration of stress-control correlations in recent years to guide specific efforts to improve metabolic control by diminishing the stress impact or by reinforcing coping capacity. Interventions have been designed to counteract or enhance the activity of psychosocial or hormonal factors which the researchers consider most important in regulating diabetic control. Baker et aL (1967), for instance, assert that in labile adolescent patients emotional stress leads to mobilization of free fatty acids and ketoacidosis mediated by counterinsulin stress hormones, especially catecholamines and cortisol. Although positive proof of this mecahnism is lacking, Baker et aL (1969) used the beta adrenergicblocking agent propanalol to treat juvenile diabetics with severe ketoacidosis. Recently, however, Baker has found psychological therapies to be even more effective (Tarnow and Silverman, 1981-1982). Minuchin et al. (1975) have reported 13 cases of very labile juvenile diabetes who had had an average of 12 hospitalizations per year. Family therapy reduced the number of hospitalizations to 1 per year, with an average of three years' follow-up. Citrin et al. (1981) have demonstrated the success of multifamily group therapy in improving control. A number of other interventions have been proposed. Warren-Boulton et al. (1981) have successfully used a group approach to reduce glucose levels in a small group of young diabetic women. Etzwiler (1981) has studied the use of written

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contracts and specific rewards. La Greca (1981) and Surwit et al. (1982) advocate behavioral treatment, and others (e.g., Donohue et al., 1981; Hoffman et aL, 1978; Epstein et al., 1981; Rudolf et al., 1982; McNeal et aL, 1981; Marigo et aL, 1977) recommend educational methods. Tarnow and Silverman (1981-1982) propose a flexible multiple modality therapeutic approach utilizing a detailed juvenile diabetic stress-metabolic response paradigm. Accumulating evidence that "tight" metabolic control may mitigate the extent of chronic diabetic complications and evidence of the importance of personality, stress, compliance, and family factors for achieving and maintaining optimal diabetic regulation has motivated recent investigators to begin to identify more precisely the specific variables through which the psychosocial milieu influences the metabolic control of Type I diabetics. Grossman et aL (1981) have demonstrated in youthful diabetics that a "self-efficacy" construct correlated positively with improved metabolic control. Marrero et al. (1981) have related good juvenile control to reliance upon parental, rather than peer group, social support networks. Family "competence" has predicted better metabolic control measured by HbAl in studies by Minuchin et aL (1978) and Anderson et aL (1981). Hauser and Pollets (1979), Drash (1979), and Daneman et al. (1981) have emphasized relative emotional immaturity as a negative factor in adolescent diabetic regulation. Simonds et aL (1981), on the other hand, could not relate control to a variety of personality characteristics. A major critical review of the subject of personality and juvenile diabetes (Butch and Phillips, 1967) mandated "further carefully designed conceptually based systematic empirical research" to clarify psychosomatic interactions, a view echoed by Hauser and Pollets in 1979. The present study attempts to identify more precisely significant personality variables that predict both initial diabetic control and changes in this control resulting from caregiver intervention with a population of insulin-dependent juvenile diabetics.

METHOD Subjects

Subjects were 42 juvenile diabetics who either received standard care or were assigned to an intensive multicomponent treatment group. The treatment group was preselected for geographic proximity and willingness to adhere to the treatment protocol. Subjects, however, were not preselected on the basis of previous compliance. The two groups were not

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Barglow, Edidin, Budiong-Springer,Berndt, Phillips, and Dubow Table I. Demographic and Descriptive Information for the Study Population Treatment group Standardcare group (n = 21) (n = 21) Age (years) x-= 13.4, SD = 3.3 x = 12.2, SD = 2.5 Duration of illness x"= 59.0, SD = 45.4 x"= 38.6, SD = 35.4 (months) Initial HbAxevalues x-= 12.2, SD = 2.3 x-= 12.1, SD = 3.5 Gender 57~/0female, 43°'/omale 76% female, 24% male Race 62% Black, 38% White 43% Black, 57% White

significantly different on initial glycohemoglobin values or with regard to age, gender, duration o f illness, or race (see Table I). Procedures Subjects were recruited from the Pediatric Model Unit o f the University of Chicago/Michael Reese Diabetes Research and Training Center. All subjects were given a psychological test battery and a psychosocial questionnaire designed to assess demographic data, compliance, and knowledge about diabetes. Hemoglobin A1 levels were measured at three intervals, approximately six to eight weeks apart, during routine visits to the clinic. Glycohemoglobin assay measures the amount o f hemoglobin nonenzymatically bound to glucose and indicates the net level of glycemia that occured during the six weeks prior to sampling (Gonen and Rubenstein, 1978; Koenig et al., 1976). The method permits better monitoring o f diabetic control over longer time segments than does infrequent fasting or random glucose determination, which may reflect periodic or unsustained episodes of deterioration in control caused by stress, infection, or changes in dietary and exercise routines. Since few subjects had a duration o f diabetic illness less than one year, C-peptide determinations were not considered necessary. The treatment group participated in the above protocol and also received a multicomponent treatment package.

Multicomponent Treatment Package An intensive multicomponent treatment was developed, with the goal o f maximizing the achievement o f metabolic control. The current study was not designed to evaluate efficacy o f treatment components, but to evaluate the impact o f psychosocial variables. At the initial treatment visit, baseline data on dietary, medication, and exercise patterns

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were obtained and subjects were given psychological tests. Deficits in technical skills and/or basic knowledge of diabetes and its management were identified at this visit. An individually designed therapeutic alliance was promulgated between medical caregiver and the child and his/her family to counteract information gaps and to change poor medical selfcare habits. Children chose available prizes that would be provided for attainning a normal glycohemoglobin value by the end of a four-month period. Progress was recorded on a prominently displayed large glycohemoglobin chart. The patients were identified by a symbol known only by the participants and researchers to ensure confidentiality. Daily telephone contact with the nurse educator (A.S.) or physician (D.E.) was initiated for each participant and maintained on weekends and holidays. One practical aspect of the dally contact was to monitor daily glucose readings, which the children were obtaining through the use of glucose oxidase strips. The phone contact simultaneously served as a personal reinforcement for the children and clarified any problems or issues that sometimes resulted from tight diabetes management. Insulin adjustments were made by the medical caregivers based on home glucose monitoring results and subjective and objective data relayed by the child and/or parent. The rapport developed with the nurse educator and physician maximized compliance and provided a milieu in which teaching, clarification, and reinforcement of progress were possible. More concentrated behavioral reinforcement intervention occurred during every two-week clinic visit, at which self-monitoring records, diet, exercise, and insulin self-administration were reviewed and interpreted in terms of progress in metabolic control by the physician or nurse educator. School and social problems of an individual child were discussed, praise often given, and the parents encouraged to participate actively in the program. When necessary, consultations were requested, utilizing a dietitian, psychiatrist, or social worker. One group discussion meeting was held. Additional assessments not relevant to the current study (lipid profiles, echocardiograms) were also obtained once a month.

PSYCHOLOGICAL TEST BATTERY Coddington Scale

The Coddington (1972) Social Readjustment Rating Scale is an adaptation of the Holmes and Rahe (1965) scale for children and ado-

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Barglow,Edidin, Budlong-Springer,Berndt,Phillips,and Dubow

lescents. The method involves asking the subject to check from a list of age-relevant items the events that occurred during the prior 12 months. Life changes of any sort have been reported to demand both physiologic and psychological adaptation. To account for the differential adaptational demands associated with incidents such as "divorce of parents" or "move to a new school district," weights referred to as "life change units" are ascribed to each event by Coddington (1972), using the method described by Holmes and Rahe (1967). The life change unit weights associated with items checked by the patient were summed to provide a measure of the adaptational demands of environmental factors that impinged upon the subject. Another method, simply summing the number of events without the weights (a procedure frequently used with the adult version), was also employed. Psychopathology Scale

The psychopathology scale from the Offer Self-Image Questionnaire for Adolescents (OSIQ; Offer, 1982) is an 11-item self-report scale extracted from the longer questionnaire. The OSIQ has been used with over 10,000 teenagers in many countries since it was introduced in 1962. Extensive reliability and validity are presented in the manual (Offer, 1982). The scale was designed to measure overt or severe psychopathology. Washington University Sentence Completion Test

The Washington University Sentence Completion Test (WUSCT) was administered in order to assess level of ego development, as operationalized by Loevinger (1976). The WUSCT has been demonstrated to have good reliability and validity (Loevinger and Wessler, 1970; Hauser, 1976; Loevinger, 1979). It consists of 36 sentence stems that subjects complete to form whole sentences. Subjects' responses to each stem are analyzed independently for stage of ego development. An item sum score, derived by summing the ratings of each stem, yields a continuous score suitable for multiple regression analysis (Cox, 1974). In addition, a formula is used to type subjects at a particular stage of ego development. According to Loevinger, the WUSCT assesses the individual's general flame of reference toward self and world. Loevinger conceptualizes ego development as the attainment of increasingly more mature levels of functioning in the realms of impulse control, moral development, and quality of interpersonal relations. The responses were scored by a rater (E.D.) blind to the treatment group, HbA, levels, and all other variables except gender.

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Adequate reliability with another experienced rater (0.76) had been established in a previous study.

Rosenberg Scale The Rosenberg (I965) Self-Esteem Scale was developed originally in 1965 as a 10-item Guttman-type scaling instrument. Subsequent users (e.g., Berndt and Berndt, 1980) have employed a true-false format to improve reliability. Kaplan (1975), on the basis of factor analysis, recommends using only 7 of the 10 items. In a pilot study by one of the present authors (Edidin et al., 1979), Kaplan's modification was useful with a juvenile diabetic population. The 7-item true-false format was utilized in the current study. RESULTS To test the effect of the treatment intervention compared to the routine clinic group over time, a repeated measures analysis of variance was performed, with the three HbA, measures as the dependent variable. Figure 1 illustrates the effects across time for the two groups. Selection 1S.S~

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effects in the initial group assignments obviously limit the inferences from the finding of different outcomes in the two groups. The results indicate a significant main effect for time, F(2, 80) = 9.61, p < .01, and for the interaction between treatment and time, F(2, 80) = 3.69, p < 0.05. As Figure 1 illustrates, the time x treatment interaction is primarily the consequence of a linear decrease in HbA, (greater control over time) for the treatment group, while the standard care group demonstrated only a minor decrease over time. In order to assess the relationship between the psychosocial variables and decreases in HbAt across time, change scores were computed, subtracting HbA~ levels at the final period from the initial reading. Delta (representing changes in the direction of increased control) was correlated with the psychosocial measures and demographic variables and was significantly related to the number of life changes on the Coddington, r(40) = 0.29, p < 0.05, and the item sum measure for the Loevinger WUSCT, r(40) = 0.37, p < 0.01. There was no significant relationship for age, psychopathology, or self-esteem. Similarly, using nonparametric correlation between respondents' stage of ego development and change in glycohemoglobin level, Kendetl's nonparametric statistic of relationship was not significant. More variables were related to initial readings of HbAI, a measure of control at the first assessment, prior to treatment intervention. These comparisons showed a relationship between control and age, r(40) = 0.31, p < 0.05; duration of illness, r(40) = 0.34, p < 0.05; the number of life events, r(40) = 0.72, p < 0.001; and the WUSCT item sum score, r(40) = 0.69, p < 0.001. Self-esteem and psychopathology were not significantly related. In order to assess which psychosocial variable was most useful in predicting (a) initial glycohemoglobin levels and (b) change in control (as measured by the change scores), stepwise multiple regression analyses were performed on all 42 subjects. For the change scores (increasing control over time), the total item sum of the Loevinger WUSCT, the number of endorsed items of the Coddington, the psychopathology scale, and the self-esteem measures were entered in a stepwise manner. Only the Loevinger WUSCT significantly predicted change, F(1, 39) = 6.34, p < 0.05. The standardized regression coefficient was 0.29, and the predictor accounted for 14% of the variance. By the usual standards of social science research this is considered to be adequate prediction, but 860/0 of the variance remained to be accounted for. Other measures used in the current study did not significantly contribute to the prediction of increased control. When the same predictors were regressed on the initial glycohemoglobin values of all 42 subjects, the only significant predictor was the number of

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life event changes on the Coddington, F ( I , 39) = 41.33, p < 0.001. The standardized regression coefficient for the Coddington was 0.75, and the predictor accounted for a surprisingly high 51°70 of the variance. None of the other variables contributed significantly to predict initial control as measured by initial glycohemoglobin values.

DISCUSSION The interaction in Figure 1 between treatment and time was not unexpected. Several studies (e.g., Minuchin et al., 1975; Depuis et al., 1980; Etzwiler, 1981; Fairclough et al., 1981; Gardner et al., 1981; Surwit et al., 1982; Rudolf et al., 1982) have indicated that treatments ranging from home monitoring to family therapy to behavior management could significantly improve diabetic control. Consequently, the treatment results were not of primary importance. The data did not permit speculation as to which components of the treatment program may have been effective. The results did indicate that the intensive intervention strategy was successful over time. Although this conclusion might be explained by nonrandom assignment to routine or intensive intervention group, this explanation is less tenable, since the two populations were comparable on most relevant variables, including the initial HbA~ level. The most pertinent results focused on two separate questions. The first question asked which major variables accounted for good diabetic control as indicated by HbA, at the time of initial assessment. This question was raised by Simonds et al. (1981), who were unable to find psychosocial or demographic variables related to HbA, levels. In contrast, the current results found several variables significantly related to initial measurement of diabetic control: age, duration of illness, life events changes, and ego development. However, several differences must be noted between the current study and that by Simonds et al. (1981), which used a homogeneous group of White rural middle class adolescents who had had diabetes for at least five years. Our population was more heterogeneous in age, race, and duration of illness. Perhaps the psychological measures selected by Simonds et al. (1981)--anxiety level, locus of control, self-concept, and personality traits--were less relevant to the question. As the regression analysis indicated, the number of life event changes on the Coddington scale was the most important predictor of initial control. Other variables did not significantly increase the ability to predict HbA~ levels. The current results provide further evidence of the validity of social readjustment rating scales such as the Coddington. These results are consistent with the results obtained by Chase and

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Jackson (1981). They also support the hypothesis that chronic adaptation to life changes affects diabetic control. It would be of interest to identify specific life changes relevant to diabetic control. However, the current study sample size is too small to adequately examine this question. Future research should consider which events are most crucial, since specific interventions might then be indicated. The second question asked by this study was, Are changes of HbA1 over time (indicative of progressive, relatively stable improvements in control) related to predisposing psychological variables within the individual? Although both ego development on the Loevinger WUSCT and life event changes on the Coddington were related to improved control over time, only the Loevinger significantly predicted the change scores. Neither the Coddington nor any of the other psychological variables contributed appreciably to the ability to predict improvement in diabetic control. The results, in some respects, complement the report by Hauser and Pollets (1979) that ego development was impaired in diabetics relative to a comparable nondiabetic sample. The current study is, however, the first to relate good ego development to improved control (decreases in HbA1 over time). The Loevinger WUSCT scores, although related to improved control, accounted for only a small portion of the variance. Consequently, many other factors--ranging from changes in neurohumoral homeostasis to family s u p p o r t - m a y have been important to achievement of longrange diabetic control. The failure of either psychopathology scale items or self-esteem scores to relate significantly to diabetic control may have been an artifact of the choice of measures of the current study, since both measures may have relatively low reliability. Hauser and PoUets (1979) reported the Coopersmith (1959, 1967) inventory to be an effective measure of selfesteem for diabetics; although it is slightly longer, the Coopersmith is the more widely used measure of self-esteem for youths. The current study is a first step towards identifying predisposing factors in individuals which lead to increased diabetic control. Life event changes and ego development appear to be promising variables for future research. Since our analysis of the data used correlational techniques, including regression analyses subject to sample-specific error, a crossvalidation study would be necessary to establish further validity of these results. More investigation is also necessary to clarify whether the effect of life changes or treatment interventions upon diabetic control is mediated by increased adherence to treatment or changes in neurohumoral homeostasis. One might predict, for example, that ego development primarily affects adherence to treatment, while the increased life changes reflected by the Coddington scale influence diabetic control through the catecholamine

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stress axis or by affecting the secretion of adrenal glucocorticoids. Failure to maintain the diabetic control achieved through the efforts of medical caregivers may be explained by the same variables we have identified or by an entirely different group of factors. Such considerations remain to be examined in future studies.

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