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Biomedical subjects

R M Nesse

Publications and source records attributed to R M Nesse.

At least 37 records · Page 2Linked to original sources
PubMed1994

Pentagastrin infusions in patients with panic disorder. II. Neuroendocrinology.

Cholecystokinin (CCK) has well-documented anxiogenic effects in animals and normal people, and panicogenic effects in patients with panic disorder, but little is known about its neuroendocrine profile. We examined neuroendocrine responses to intravenous infusions of pentagastrin, a selective CCK-B receptor agonist, in 10 patients with panic disorder and 10 normal control subjects. Pentagastrin potently activated the hypothalamic-pituitary-adrenal (HPA) axis, but did not release growth hormone or any of several vasoactive peptides (neurokinin A, substance P, vasoactive intestinal peptide). The HPA axis response was unrelated to increases in symptoms. Panic patients did not differ from controls in neuroendocrine responses to the CCK agonist. Differential sensitivity to novelty stress accounted for the only patient-control differences in neuroendocrine profiles. The data suggest that CCK may help modulate normal HPA axis activity, but its anxiogenic effects are unrelated to its stimulatory effects on the HPA axis. Pentagastrin provides a safe and readily available probe for further study of CCK receptor systems in humans.

Adrenocorticotropic Hormone↗
PubMed1994

Risk perception by patients with anxiety disorders.

Studies by social psychologists have recently shown that normal people have systematically distorted perceptions of risk. We extend these studies to patients with anxiety disorders to see how they differ from normal subjects, and, more specifically, to test the hypothesis that anxiety disorders might result from excessively objective risk assessments. Fifty patients with anxiety disorders and 50 matched controls estimated the likelihood that 22 events would happen to the average person or to the self. On both measures, and on accuracy, the groups were essentially identical. In confirmation of previously reported patterns of risk distortion, both groups overestimated rare risks, underestimated common risks, and consistently underestimated the relative risks to self. These results suggest that cognitive estimates of specific risks are normal in patients with anxiety disorders.

Adult↗
PubMed1992

Evolutionary biology: a basic science for psychiatry?

Evolutionary biology has much to offer psychiatry. It distinguishes between ultimate and proximate explanations of behavior and addresses the functional significance of behavior. Subtheories, frequently voiced misconceptions, specific applications, testable hypotheses and limitations of evolutionary theory are reviewed. An evolutionary perspective is likely to improve understanding of psychopathology, refocus some clinical research, influence treatment and help integrate seemingly unrelated findings and theoretical explanations.

Behavior↗
PubMed1991

A standardized behavioral group treatment program for obsessive-compulsive disorder: preliminary outcomes.

This paper provides outcome data about the efficacy of a behavioral group therapy program for obsessive-compulsive disorder (OCD). Thirty-six patients completed a 7-week outpatient treatment program which provides: (1) education about OCD and its treatment, (2) instruction in a cognitive and behavioral approach to the self-treatment of OCD and (3) guided behavioral treatment. Significant improvement in obsession, compulsion, and depression scores were observed at completion of the group and at 3 month follow-up. Significant improvement in obsessions and compulsions was observed for both patients taking anti-obsessional medications and those who did not.

Adult↗
PubMed1991

The dawn of Darwinian medicine.

While evolution by natural selection has long been a foundation for biomedical science, it has recently gained new power to explain many aspects of disease. This progress results largely from the disciplined application of what has been called the adaptations program. We show that this increasingly significant research paradigm can predict otherwise unsuspected facets of human biology, and that it provides new insights into the causes of medical disorders, such as those discussed below: 1. Infection. Signs and symptoms of the host-parasite contest can be categorized according to whether they represent adaptations or costs for host or parasite. Some host adaptations may have contributed to fitness in the Stone Age but are obsolete today. Others, such as fever and iron sequestration, have been incorrectly considered harmful. Pathogens, with their large populations and many generations in a single host, can evolve very rapidly. Acquisition of resistance to antibiotics is one example. Another is the recently demonstrated tendency to change virulence levels in predictable ways in response to changed conditions imposed incidentally by human activities. 2. Injuries and toxins. Mechanical injuries or stressful wear and tear are conceptually simpler than infectious diseases because they are not contests between conflicting interests. Plant-herbivore contests may often underlie chemical injury from the defensive secondary compounds of plant tissues. Nausea in pregnancy, and allergy, may be adaptations against such toxins. 3. Genetic factors. Common genetic diseases often result from genes maintained by other beneficial effects in historically normal environments. The diseases of aging are especially likely to be associated with early benefits. 4. Abnormal environments. Human biology is designed for Stone Age conditions. Modern environments may cause many diseases-for example, deficiency syndromes such as scurvy and rickets, the effects of excess consumption of normally scarce nutrients such as fat and salt, developmental diseases such as myopia, and psychological reactions to novel environments. The substantial benefits of evolutionary studies of disease will be realized only if they become central to medical curricula, an advance that may at first require the establishment of one or more research centers dedicated to the further development of Darwinian medicine.

Adaptation, Physiological↗
PubMed1990

Treatment of panic-like attacks with a long-acting analogue of somatostatin.

Psychiatric evaluations were completed on four patients who were treated for "idiopathic flushing" with a long-acting analogue of somatostatin. All four patients had symptom profiles consistent with a diagnosis of panic disorder. All four experienced clinically significant relief from panic-like attacks while on the experimental medication. These findings suggest a possible role for somatostatin in the pathophysiology and treatment of panic disorder.

Adult↗
PubMed1988

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↗
PubMed1988

Life table tests of evolutionary theories of senescence.

The phenomenon of senescence requires both evolutionary and proximate explanations. The most widely accepted evolutionary explanation for senescence is that it never gets exposed to natural selection because environmental hazards kill all individuals before the age at which senescence causes decreased fitness. If this explanation is sufficient, wild populations should not demonstrate senescence, and their mortality rates should therefore remain constant during adult life, except when environmental causes of mortality have recently decreased. The alternative explanation for the persistence of the genes that cause senescence is that they have been selected for because they have pleiotropic effects that are beneficial early in life when the force of selection is strongest. Where this is the case, mortality rates should increase with age in wild populations. A method is described for using life table data to calculate an estimate of the intensity of selection acting on senescence in wild populations. This method is applied to a variety of life tables. The results suggest that pleiotropic genes may be important causes of senescence in some populations, but not in others. This has implications for research on the proximate mechanisms of senescence.

Aging↗
PubMed1986

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↗
PubMed1985

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↗
PubMed1985

Psychobiology of anxiety and anxiety disorders.

New techniques for studying receptor pharmacology, neurotransmitter activity, and neuroendocrine function in affective illness have made it possible to carry out sophisticated neurochemical and neuropharmacologic investigations of the anxiety disorders. Some important reasons for pursuing these strategies have been the high frequency of depression in anxious patients, the effectiveness of antidepressants in the treatment of panic disorder, and the availability of probes for studying the physiologic changes that occur during anxiety states in human subjects. In addition, the ability reliably to induce anxiety states in man has made it possible to study at least some clinical forms of anxiety under laboratory conditions. Although animal models for simple phobia have been developed, there are currently no adequate animal models of panic disorder in man. If valid, reliable animal models, for panic disorder and other human anxiety disorders can also be identified, then a much better understanding of the nature and causes of anxiety and more effective diagnosis and treatment of clinically important anxiety disorders may be possible.

Animals↗