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Dive into the research topics where Bonnie Spring is active.

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Featured researches published by Bonnie Spring.


Journal of Abnormal Psychology | 1977

Vulnerability: A new view of schizophrenia.

Joseph Zubin; Bonnie Spring

Although descriptive and etiological approaches to psychopathology have made notable advances, they seem to have reached a plateau. After reviewing the six approaches to etiology that now preempt the field—ecological, developmental, learning, genetic, internal environment, and neurophysiological models—a second-order model, vulnerability, is proposed as the common denominator, and methods for finding markers of vulnerability are suggested in the hope of revitalizing the field. It is assumed that exogenous and/or endogenous challengers elicit a crisis in all humans, but depending on the intensity of the elicited stress and the threshold for tolerating it, that is, ones vulnerability, the crisis will either be contained homeostatically or lead to an episode of disorder. Vulnerability and episode stand in a trait-state relation, and markers for each must be provided to distinguish between them.


Journal of Applied Psychology | 1994

Bias Against Overweight Job Applicants in a Simulated Employment Interview

Regina Pingitore; Bernard L. Dugoni; R. Scott Tindale; Bonnie Spring

This study assessed whether moderately obese individuals, especially women, would be discriminated against in a mock employment interview. Potential confounding factors were controlled by having 320 Ss rate videotapes of a job interview that used the same professional actors appearing as normal weight or made up to appear overweight by the use of theatrical prostheses. Results suggested that bias against hiring overweight job applicants does exist, especially for female applicants. Bias was most pronounced when applicants were rated by Ss who were satisfied with their bodies and for whom perceptions of their bodies were central to self-concept. The decision not to hire an obese applicant was, however, only partially mediated by personality attributions. Implications and limitations of these results are discussed.


Journal of Psychiatric Research | 1982

Effects of protein and carbohydrate meals on mood and performance: Interactions with sex and age

Bonnie Spring; Owen Maller; Judith J. Wurtman; Larry Digman; Louis Cozolino

Normal adult subjects (n = 184) consumed a high-protein or high-carbohydrate meal. Two hours later their mood and performance were tested. The effects of meal composition on mood were different for men and women, and for older and younger subjects. Females, but not males, reported greater sleepiness after a carbohydrate as opposed to a protein meal. Male subjects, but not females, reported greater calmness after a carbohydrate as opposed to a protein meal. Older subjects responded differently to meals depending upon the time of day when these were consumed. When meals were eaten for breakfast (but not for lunch) individuals 40 yr of age or older felt more tense and less calm after a protein than after a carbohydrate meal. Although older subjects reported subjective discomfort after a morning protein meal, they displayed objective performance impairments after a carbohydrate lunch. Subjects 40 yr of age or older were impaired on a test of sustained selective attention (dichotic shadowing) after consuming a high-carbohydrate lunch. The shadowing impairment after carbohydrate consumption was as pronounced without distraction as with distraction and resulted mostly from increased omission errors. Our findings suggest negative effects on concentration when older subjects consume a high-carbohydrate, low-protein lunch. These negative effects of carbohydrate consumption appear to arise predominantly from lapses of attention rather than from intrusion of distractors.


International Journal of Eating Disorders | 1998

Correlates of binge eating in Hispanic, Black, and White women

Marian L. Fitzgibbon; Bonnie Spring; Mary E. Avellone; Lisa R. Blackman; Regina Pingitore; Melinda R. Stolley

OBJECTIVEnWe sought to compare the severity and correlates of binge eating in White, Black, and Hispanic women.nnnMETHODnOur sample consisted of 351 (55 White, 179 Black, and 117 Hispanic) women who were assessed on three proposed factors associated with binge eating (weight, depression, and ideal body image).nnnRESULTSnOur results showed that binge eating symptoms were more severe in our sample of Hispanic versus Black or White women. Across all ethnic groups, women who binged more were heavier, more depressed, and preferred a slimmer body ideal. Binge eating severity was predicted by weight and depression in Hispanics and by depression in Whites. None of the proposed factors significantly influenced binge eating in Blacks.nnnDISCUSSIONnThese results show ethnic differences in the correlates of binge eating and highlight the need for further comparative research on aberrant eating patterns.


Journal of Psychiatric Research | 1982

Mood, performance, and pain sensitivity: changes induced by food constituents.

Harris R. Lieberman; Suzanne Corkin; Bonnie Spring; John H. Growdon; Richard J. Wurtman

We examined the behavioral effects of the dietary constituents tryptophan and tyrosine on human mood, sensorimotor performance and pain sensitivity. Tryptophan and tyrosine are neurotransmitter precursors present in varying amount in protein-containing foods. Tryptophan (50 mg/kg) increased subjective drowsiness and fatigue but unlike many hypnotics did not impair sensorimotor performance. Tryptophan also decreased human pain sensitivity in a manner that was more specific than certain analgesic drugs.


Health Psychology | 1991

Weight Gain and Withdrawal Symptoms After Smoking Cessation: A Preventive Intervention Using d-Fenfluramine

Bonnie Spring; Judith J. Wurtman; Ray Gleason; Richard J. Wurtman; Kenneth Kessler

Directly measured food intake in 31 overweight female smokers to test whether (a) calorie and carbohydrate intakes increase after smoking cessation and (b) double-blind d-fenfluramine (30 mg), a serotonin-releasing drug, suppresses weight gain, overeating, and dysphoric mood associated with stopping smoking. Placebo-treated patients grew dysphoric after smoking withdrawal and ate 300 kcal/day more from 2 to 28 days after, showing a 3.5-lb weight gain. Fat and protein intakes did not change, but carbohydrate intake increased (30% to 40%). D-fenfluramine prevented postcessation dysphoria. Although drug-treated patients ate more carbohydrate snacks just after quitting, they returned to baseline by 4 weeks, showing a 1.8-lb weight loss. Agents that enhance brain serotonin-mediated neurotransmission may help prevent weight gain, overeating, and dysphoric mood after smoking withdrawal.


Journal of Psychiatric Research | 1978

Attention and information processing as indicators of vulnerability to schizophrenic episodes

Bonnie Spring; Joseph Zubin

As A DESCRIPTIVE model, we find it useful to distinguish between vulnerability to schizophrenia which is a relatively permanent, enduring trait, and episodes of schizophrenic disorder that are waxing and waning states. According to this model, episodes of schizophrenia ensue when endogenous and exogenous challengers surpass a threshold set by the individual’s dispositional level of vulnerability. When such challenging events subside, the patient shows at least some degree of recovery, and sometimes even reattains his premorbid level of functioning. However, even when a schizophrenic’s state has normalized, his vulnerability persists and leaves him at risk for future episodes of schizophrenia. The various etiological models of schizophrenia have been presented elsewhere.1 Here it will suffice to suggest that vulnerability to schizophrenia may originate in many ways. Biological models emphasize etiological forces arising from an individual’s internal makeup: his genes, biochemistry, and neurophysiology. Field theory models stress the role of exogenous forces impinging on the maturation, learning and immediate behavior of the individual. The different etiological models often agree in predicting that a particular group of individuals will be vulnerable to schizophrenia, although these predictions are based on different rationales. Most models predict that siblings of schizophrenics represent a group at some risk for schizophrenia, since they share numerous possible sources of vulnerability with the schizophrenic probands. These include a shared gene pool, similar intrauterine environments, common family and community interaction experiences, exposure to the same diseases, die s, physical environments, etc. Because of the evidence that disturbed sensation, perception and attention may be central characteristics of the schizophrenic syndrome,2-4 our selection of potential vulnerability indicators has been influenced by the neurophysiological model of schizophrenia, This model seeks the causes of schizophrenic symptoms in disorders of central nervous system functioning and the capacity to take in and process information. Disturbances of information processing have a prima-facie link with schizophrenic psychopathology because


Journal of Behavioral Medicine | 1991

Tryptophan and high-carbohydrate diets as adjuncts to smoking cessation therapy

Deborah J. Bowen; Bonnie Spring; E.A. Fox

Treatments that reduce the immediate effects of smoking withdrawal have potential for helping smokers quit. Serotonin-enhancing substances, such as tryptophan and high-carbohydrate diets, have been used in clinical disorders to relieve negative affect, a classic symptom of cigarette withdrawal. This research project investigated the use of tryptophan (50 mg/kg/day) and high-carbohydrate diets, together with more traditional smoking cessation treatment techniques, to ameliorate the smoking withdrawal syndrome and to improve abstinence rates. Subjects were randomly assigned to receive either tryptophan (n=16) or placebo (n=15). Standard smoking cessation treatment was identical for the experimental and control groups and consisted of four 2-hr weekly sessions of multicomponent group therapy. Smoking behavior, symptoms of nicotine withdrawal, and negative affect were assessed during a 2-week withdrawal period. Tryptophan-treated subjects who could not fully abstain were able to smoke fewer daily cigarettes. Reported anxiety and other withdrawal symptoms were lower in the tryptophan group compared with control subjects. These data suggest that serotonin-enhancing substances show promise for use as an adjunct to existing smoking cessation programs.


Psychopharmacology | 1992

Amitriptyline, clovoxamine and cognitive function: a placebo-controlled comparison in depressed outpatients

Bonnie Spring; Alan J. Gelenberg; Rob Garvin; Sheri Thompson

No longer prescribed only for vegetative signs of depression, tricyclic antidepressants also lessen depressive cognitive distortions. Less clear is whether they ameliorate depressed patients other cognitive deficits in memory, information processing speed, and psychomotor performance. We tested the alternative hypothesis that amitriptyline, because of its anticholinergic and sedative properties, would exacerbate depressed patients cognitive disturbances. Depressed outpatients received double-blind placebo (n=15), amitriptyline (n=10), or clovoxamine fumarate (n=10), a serotonin reuptake inhibitor relatively lacking in anticholinergic properties. Depression, memory, and psychomotor performance were assessed at baseline and after 7 and 28 days of drug treatment. Depression was alleviated after all treatments, including placebo. Only amitriptyline impaired performance on tests of memory, producing a significant decrement, relative to placebo, after 4 weeks of treatment. None of the treatments adversely affected performance on psychomotor tasks. These findings add to the evidence that antidepressant drugs with high anticholinergic activity can impair memory, despite alleviation of depression.


Psychopharmacology | 1984

Effects of two antidepressants on memory performance in depressed outpatients: a double-blind study

Donna L. Lamping; Bonnie Spring; Alan J. Gelenberg

Forty outpatients with primary depression were randomly assigned on a double-blind basis to treatment with amitriptyline (a tricyclic antidepressant) or clovoxamine (a nontricyclic, experimental antidepressant). Memory and depression were assessed during a pretreatment baseline period and at the end of days 4, 7, and 28 of drug treatment. A signal detection recognition memory task and conventional memory measures (including the Benton Visual Retention, Wechsler Logical Memory, and verbal learning tests) were used to assess memory.Although both drugs led to comparable clinical improvement in depression, they affected memory performance differently. The signal detection recognition memory task detected an impairment in memory after chronic amitriptyline administration, as contrasted with an improvement in memory after chronic administration of clovoxamine. The memory impairment in the amitriptyline group and improvement in the clovoxamine group were the result of changes in sensitivity [P(A)]. No changes in response bias (BO were detected. Conventional memory tests failed to detect drug-related differences in memory between the two groups. On the Benton, errors decreased over time within both drug treatment groups, whereas correct reproductions increased within the amitriptyline group only. However, between-group differences on the Benton did not reach significance.Results from the signal detection task suggest an amitriptyline-associated memory impairment. However, this interpretation is tempered by the finding that conventional memory measures failed to detect differences in memory performance between the two groups. We discuss the limitations of traditional memory measures and the utility of a signal detection approach in studies of psychopharmacologic influences on memory.

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Richard J. Wurtman

Massachusetts Institute of Technology

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Harris R. Lieberman

United States Army Research Institute of Environmental Medicine

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Joseph Zubin

University of Pittsburgh

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Judith J. Wurtman

Massachusetts Institute of Technology

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Regina Pingitore

Rosalind Franklin University of Medicine and Science

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Gail S. Garfield

Massachusetts Institute of Technology

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