Judith DeJong

Factors associated with recidivism in a criminal population

The present study is a follow-up of a sample of 348 men convicted of manslaughter, attempted manslaughter, or arson who were released from incarceration. Multiple factors assessed at the time of incarceration, including demographic, behavioral, family history, and biochemical variables, and psychiatric diagnoses were used in an attempt to discriminate between those who became recidivists during the follow-up period and those who did not. Violent recidivism was most strongly associated (sensitivity of 90%) with impulsivity of the original crime in killers and attempted killers; for arsonists, having made a suicide attempt was the strongest predictor (68% sensitivity). For predictive purposes, both single factor associations and multiple entries into discriminant analysis produced too many false-positives, i.e., the high rate of false designation as recidivist remained a problem.

CSF GABA in depressed patients and normal controls.

: The inhibitory neurotransmitter gamma-aminobutyric acid (GABA) has been implicated in the pathophysiology of depression. Therefore, we examined cerebrospinal fluid (CSF) levels of GABA in depressed patients (N = 25) and normal controls (N = 20). There was no significant difference between the groups. However, among the depressed patients the subgroup of unipolar melancholic patients (N = 13) had significantly lower CSF levels of GABA than the rest of the depressed patients (N = 12). There was no significant difference for CSF levels of GABA between depressed patients who were (N = 14) or were not (N = 11) cortisol non-suppressors. It was of interest that among the controls there was a significant negative correlation between CSF levels of GABA and CSF levels of norepinephrine.

CSF GABA and neuropeptides in pathological gamblers and normal controls

We previously reported that pathological gamblers may have increased central noradrenergic activity. Neurons releasing gamma-aminobutyric acid (GABA) are known to be a part of an inhibitory system regulating the activity of central noradrenergic neurons. Therefore, we examined cerebrospinal fluid (CSF) levels of GABA in pathological gamblers and normal controls. There was no significant difference between the groups. Also, depressed and nondepressed gamblers did not differ significantly in their CSF levels of GABA. Among controls, however, there was a significant negative correlation between CSF levels of GABA and the norepinephrine metabolite 3-methoxy-4-hydroxyphenylglycol (MHPG) and a significant positive correlation between CSF levels of GABA and corticotropin releasing hormone (CRH). Also, CSF levels of CRH showed a significant positive correlation with CSF levels of adrenocorticotropic hormone in both pathological gamblers and controls.

CSF diazepam-binding inhibitor in alcoholics and normal controls

Diazepam-binding-inhibitor (DBI) and gamma-aminobutyric acid (GABA) are colocalized in neurons in the brain. This system has been implicated in anxiety and in the regulation of corticotropin-releasing hormone (CRH) secretion. Alcohol has direct and indirect effects on the functioning of GABAA receptors. Abstinent alcoholics are, on the average, more anxious than controls. In tests of animal behavior, DBI has anxiogenic, and alcohol has anxiolytic potency. Therefore, we compared alcoholic patients and healthy controls for cerebrospinal fluid (CSF) levels of DBI, and looked for a correlation between CSF levels of DBI and CRH. There was no significant difference in CSF concentrations of DBI between the two groups and no significant correlation between CSF DBI and our measure of anxiety. However, there was a significant positive correlation between CSF levels of DBI and CRH in both the alcoholic and control groups.

Cerebrospinal fluid variables among alcoholics lack seasonal variation

Seasonal influences on indices of serotonergic function, including cerebrospinal fluid (CSF) concentrations of the serotonin metabolite 5‐hydroxyindoleacetic acid (5‐HIAA), have been reported in psychiatric patients and healthy volunteers. We examined seasonal differences in CSF concentrations of 5‐HIAA among 135 alcoholics admitted to a research ward who had a lumbar puncture. No significant seasonal differences were found for either CSF concentrations of 5‐HIAA or CSF concentrations of other monoamine metabolites or peptides. The possible explanations for these negative findings are discussed.

Cerebrospinal fluid thyrotropin-releasing hormone concentrations in alcoholics and normal controls

Alterations in hypothalamic-pituitary-thyroid axis function have been reported in alcoholism. Blunting of the thyroid-stimulating hormone (TSH) response to thyrotropin-releasing hormone (TRH) occurs in approximately 25% of alcoholic patients. Using a sensitive radioimmunoassay that allows TRH itself to be measured in cerebrospinal fluid (CSF), CSF concentrations of TRH were measured in alcoholics and normal controls. There was no significant difference in TRH concentrations between the groups. However, among the controls there was a significant correlation between CSF concentrations of the major serotonin metabolite 5-hydroxyindoleacetic acid (5-HIAA) and CSF concentrations of TRH. This correlation was lacking in the alcoholics. These findings are of interest because basic neurobiological studies have reported that TRH and serotonin are co-localized in certain neurons in the rat central nervous system.

Cerebrospinal fluid levels of somatostatin, corticotropin-releasing hormone and corticotropin in alcoholism

Reduced brain and cerebrospinal fluid (CSF) levels of somatostatin, corticotropin‐releasing hormone (CRH) and corticotropin (ACTH) have been reported among neuropsychiatric patients with cognitive dysfunction. Alcoholism is a disorder in which associated neuropsychiatric disorders occur. Therefore, we compared CSF levels of somatostatin, CRH and ACTH in alcoholics (n= 100) and normal controls (n= 30). There were no significant differences between the groups in concentrations of the 3 peptides. Moreover, there were no significant correlations between concentrations of the peptides in CSF and computed tomographic measures of the size of brain ventricles. There were, however, significant correlations between CSF concentrations of CRH and ACTH and between CSF concentrations of CRH and somatostatin in both the alcoholic and control groups.

CSF neuropeptide Y in alcoholics and normal controls

Neuropeptide Y is found in brain tissue. In dogs it has been shown to enhance activation of the hypothalamic-pituitary-adrenal axis by corticotropin-releasing hormone. It is localized in certain catecholamine neurons and to some extent colocalized with somatostatin. Disturbances of the central noradrenergic system may underlie some forms of alcoholism. Therefore, we compared male alcoholics and normal controls on cerebrospinal fluid (CSF) levels of neuropeptide Y. There was no significant difference between the two groups for neuropeptide Y. There was also no significant difference for CSF levels of growth hormone releasing hormone. However, there were significant positive correlations between CSF levels of neuropeptide Y and CSF levels of corticotropin-releasing hormone, somatostatin, and growth hormone releasing hormone.

Substance abuse among subjects screened out from an alcoholism research program

Three hundred and eight subjects were screened over the phone for admission to an inpatient alcohol treatment research unit. Using a structured interview, the prospective patients were asked questions regarding demographics, drinking history, previous treatments, physical health, family history, and a detailed history of past and present substance use. Drug use was studied as regular use versus no use or brief experimental use of five drug categories: cannabinoids, stimulants, sedatives, opiates, and hallucinogens. Fifty-one percent of the men and 48% of the women reported regular use of one or more of the drugs in addition to alcohol. For women, the amount of alcohol intake was positively correlated with use of stimulants (r = .32, p = .001), cannabinoids (r = .24, p = .019), sedatives (r = .30, p = .003), and hallucinogens (r = .30, p = .003). For men, correlations between the amount of alcohol intake and drug use were weaker but significant for stimulants (r = .21, p = .002), opiates (r = .15, p = .028), and hallucinogens (r = .15, p = .029). Women with alcoholic mothers displayed higher alcohol intake than women with nonalcoholic mothers (p = .02) and also showed more frequent use of most drugs. Although men with alcoholic fathers also showed greater alcohol intake compared to men with nonalcoholic fathers, the two groups did not differ in drug use. Younger subjects of both sexes were more likely to use cannabinoids, stimulants, opiates, and hallucinogens. Alcohol and sedative use was relatively constant across all age groups.

CSF 5-HIAA and suicidal behavior among adult psychiatric patients and alcoholics

398 older suicide attempters (age > 55) and age-matched diagnostic controls without a history of suicide attempts indicates a significant difference in levels of 5-HIAA. As with younger populations, CSF 5-HIAA levels in the attempter group were lower (X = 18.96; SD = 6.7; N = 12) than the nonattempter group (X = 25.68; SD = 7.2; N = 9) (t = 2.2; df = 19; p < .04). Lower levels of CSF 5-HIAA were characteristic of aged attempters not only in comparison with aged diagnostic controls, but also in comparison with age-matched normals (X2 = 8.1, p < .02). Levels of the dopamine metabolite, homovanillic acid (HVA) in CSF were also significantly different in older patients with a history of suicide attempts (X = 29.93; SD = 14.3; N = 12) than diagnostic controls with no history of attempts (X = 49.00; SD = 21.0; N = 9); (t = 2.48; df = 19; p < .02). The relationship between behavioral measures, such as impulsivity and biochemical indices will also be reported.