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Biomedical subjects

O G Cameron

Publications and source records attributed to O G Cameron.

At least 37 records · Page 2Linked to original sources

Symptoms of insulin-induced hypoglycemia in normal subjects.

In order to better characterize the psychobiology of hypoglycemic symptom production, six normal subjects had physiological/biochemical and symptom ratings at 20, 30 and 40 min after six different doses of intravenous regular insulin (0.0, 0.5, 1.0, 2.0, 3.0 and 4.0 units, in a Latin-square design); subjects also indicated after each dose whether they believed they had received an active or an inactive substance. Choice response switched from inactive to active substance when plasma glucose fell to the mid to high 50s mg/dl (i.e. whole blood glucose of approximately 50), and plasma epinephrine levels rose to between 100 and 200 pg/ml. Adrenergic symptoms and 'weakness' were most strongly associated with choice; other symptom variables had weaker associations. Symptoms were more strongly correlated with epinephrine than glucose levels, but anxiety was not strongly correlated with the epinephrine increases.

Adult↗

Chronic caffeine consumption and the dexamethasone suppression test in depression.

Acute caffeine administration increases cortisol and converts the dexamethasone suppression test (DST) to nonsuppression in normal humans; data concerning chronic administration as well as effects in depressed patients are minimal. To determine whether caffeine intake influenced DST results in depression, we retrospectively studied the relationship between regular daily caffeine consumption and pretreatment DST status in major depressives. Daily intake was not correlated with either post-DST cortisol levels or symptom ratings. These data suggest that chronic caffeine use is unlikely to be a major factor in dysregulation of the hypothalamic-pituitary-adrenal axis in depression, perhaps because of the development of tolerance.

Adult↗

Systemic hormonal and physiological abnormalities in anxiety disorders.

Among the studies of systemic hormonal and physiological abnormalities associated with anxiety disorders, the most consistent and extensive findings suggest (a) peripheral adrenergic hyperactivity (including increases in norepinephrine but not epinephrine) and functional dysregulation, (b) increased incidence of mitral valve prolapse in panic patients, and (c) normal suppressibility of the hypothalamic-pituitary-adrenal cortical endocrine system with dexamethasone in panic patients. Other less-certain findings include (a) increased circulating concentrations of plasma ACTH and/or cortisol, and prolactin, in panic patients, (b) increased platelet monoamine oxidase activity in generalized anxiety and/or panic patients, (c) decreased gonadal axis activity in some anxious individuals, (d) decreased nighttime melatonin plasma concentrations in panic patients, and (e) peripheral alpha 2 and beta-adrenoreceptor down-regulation, with normal serotonin binding parameters. These findings, taken together, provide tentative support for dysfunction in adrenergic and GABAergic central nervous system mechanisms in people with anxiety disorders. Abnormal anxiety and normal stress both show evidence of adrenergic hyperactivity; however, there appear to be differences in hormonal profiles, especially the apparent lack of increase of epinephrine during panic attacks, as well as differences in the reactivity of the system, and in the "trigger" mechanisms which determine when the response occurs.

Animals↗

Anxiogenic effects of caffeine on panic and depressed patients.

Caffeine increases anxiety in people with anxiety disorders. To determine whether caffeine exerts a similar effect in depression, the authors compared retrospective reports of caffeine intake and symptoms produced by caffeine ingestion in patients with panic disorder, patients with major depression, and control subjects. Panic patients consumed less caffeine and reported more symptoms than depressed or control subjects. Although depressed patients did not differ from control subjects in caffeine intake or most symptoms, more depressed patients reported that caffeine induced anxiety. These data support prior reports that panic patients have increased sensitivity to caffeine; some depressed patients may also have increased sensitivity.

Adult↗

Circadian fluctuation of plasma epinephrine in supine humans.

Previous studies have demonstrated circadian fluctuations of systemic catecholamines in man. However, methodological differences and conflicting results with epinephrine are apparent. In the present study, plasma and urinary epinephrine and norepinephrine and plasma cortisol were studied in healthy young adult males over 24 hr with 20 min plasma sampling and EEG monitoring of sleep. Plasma epinephrine did not have a circadian variation in supine subjects. Urinary epinephrine levels and small urinary circadian variations were increased by normal posture and activity. Sleep and sleep stage were not associated with different plasma epinephrine levels, and no ultradian fluctuation was observed. Levels of norepinephrine and cortisol were normal. Based on all studies to date, it appears that basal plasma epinephrine has either a very small amplitude or no circadian rhythm, but that changes in posture and activity or the rest/activity cycle may modify this pattern.

Activity Cycles↗

Endocrine and physiological changes during "spontaneous" panic attacks.

Eight patients with DSM-III-defined panic attacks were compared to four normal subjects on hormonal and physiological variables measured at six predetermined times through 24 hr and also during nine "spontaneous" attacks. Levels at predetermined times were not different, other than a reduction of urinary unconjugated epinephrine in patients. Plasma prolactin was elevated at the peak of most of the attacks and correlated with attack severity. Plasma cortisol and growth hormone, and heart rate, were elevated during some attacks, and plasma norepinephrine showed small increases. Significant plasma epinephrine and MHPG changes were not observed.

Adult↗

Ethanol retards desensitisation of simple phobias in non-alcoholics.

Twenty non-alcoholic patients with DSM-III defined simple phobias for small animals received behavioural approach tests and exposure therapy while under the influence of a moderately intoxicating dose of ethanol or after placebo administration. Ethanol did not demonstrate any acute anti-anxiety effect, but retarded the rate of behavioural in vivo desensitisation, without changing the final treatment outcome. State-dependent effects of ethanol on anxiety were not demonstrated. This study supports prior research indicating no anti-anxiety or 'tension-reducing' effects of ethanol for simple phobias.

Adult↗

Symptom profiles of patients with DSM-III anxiety disorders.

The authors used symptom profiles, demographic data, and other variables to compare 316 patients representing all specific DSM-III anxiety disorders except posttraumatic stress disorder to each other and to published norms for both an unselected psychiatric outpatient population and normal subjects. The results support the grouping of these disorders, with the possible exception of obsessive-compulsive disorder, into one general diagnostic category of "anxiety disorders." The distinction between the specific diagnoses of simple phobia and social phobia was also supported; however, the differentiation between panic disorder, agoraphobia, and generalized anxiety was only weakly supported.

Adolescent↗

Anxiety and caffeine consumption in people with anxiety disorders.

Forty-three anxiety disorder patients (DSM-III) who completed the Hopkins Symptom Checklist (SCL-90-R) and a caffeine questionnaire were compared to 124 medical inpatients. Eighty-four percent of the anxious patients were low caffeine consumers (0-249 mg/day) compared to 41% of medical inpatients; 65% of anxiety patients consumed less than 100 mg/day. In anxiety patients, there were no significant correlations between subscale scores of the SCL-90-R and amount of caffeine consumption. Patients who consumed less than 100 mg/day did not differ on anxiety subscale scores of the SCL-90-R from those who consumed more. However, patients who reported becoming anxious in response to drinking coffee had higher SCL-90-R anxiety subscale scores than patients who did not, even though their daily consumption was not different. It appears that anxiety disorder patients have increased caffeine sensitivity which leads to decreased consumption.

Adult↗

Urinary catecholamines and mitral valve prolapse in panic-anxiety patients.

Free norepinephrine and epinephrine were measured in two consecutive 12-hour urine collections gathered during normal activity and sleep from 23 panic-anxiety patients and 9 normal subjects. Mitral value prolapse (MVP) was found in 7 of 20 patients who had echocardiograms. Mean nighttime norepinephrine and epinephrine excretion in panic-anxiety patients without MVP was significantly higher than that of control subjects, and was significantly higher than that of anxiety patients with MVP. In the daytime, all groups had higher catecholamine (CA) levels, but the differences between the groups were less pronounced. Medication significantly relieved symptoms and was associated with decreased CA levels. Elevated basal CA levels may characterize the subgroup of panic-anxiety patients who do not have MVP.

Adult↗