The purpose of this study was to explore women’s subjective food and eating experiences from childhood through to adulthood and the ways in which these experiences either connected or disconnected them from their appetites for food and eating. The present study used a qualitative life history methodology, the goal of which is to assess individuals’ lived experiences to construct broader contextual meaning. In-depth interviews were used to investigate food and eating experiences among twelve women between ages 25 and 44, representing diverse social and cultural backgrounds as well as current and past eating problems. Participants took part in an open-ended interview, using a series of guided questions about their food and eating experiences from childhood through to adulthood. The interviews were transcribed and analyzed for themes using the constant comparison method. Two models emerged from the data in this study that described the social factors that connected and disconnected women from their appetites and eating. The Regulating Discourses Model which outlines current ways women negotiate appetite and desire through food and eating experiences, and the Socialization through Food and Eating Model which delineates socialization processes related to food and eating during women’s development. This research may be useful for counselors, health care professionals, as well as the larger community to increase awareness on ways to maintain girls’ and women’s connection to their bodily appetites and desires throughout the lifespan.

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This thesis addresses the effects of pharmacological manipulations of brain 5- hydroxytryptamine (5-HT, serotonin) and it's precursor, tryptophan, on appetite and mood in humans. Chapter 1 is a presentation of the literature reviewed in order to carry out the studies contained within this thesis. General methods are described in Chapter 2; these include biochemical methods for analysis of plasma tryptophan, and measures and assessment methodologies for analysis of appetite and mood. This chapter also contains a pilot study of the methodology adopted for lowering plasma tryptophan levels. The first experiment (Chapter 3) examines the effects of calorie controlled dieting on plasma tryptophan, mood and appetite using a longitudinal design. Dieters were compared with a matched control group, and the results demonstrated that whilst dieting does not appear to alter mood or responses to food in a laboratory setting, it does lower levels of plasma tryptophan compared with baseline and with controls. In view of the confounding variables of dieting on mood and appetite, the second experiment (Chapter 4) examined the effects of an acute, laboratory based depletion of plasma tryptophan on these parameters in healthy female volunteers acting as their own controls. Significant depletion of plasma tryptophan was not associated with alterations in mood or appetite. The third experiment (Chapter 5) addresses the issue of predisposing factors in the effects of tryptophan depletion on mood and appetite. This was carried out with a group of women who had recovered from an eating disorder (bulimia nervosa). These subjects were acting as their own controls but were also compared directly with the non-clinical group of subjects from the previous experiment. This experiment demonstrated interesting differences in the eating behaviour of the two groups, and a significant difference in baseline levels of total plasma tryptophan. There were, however, no effects of tryptophan depletion on mood or appetite in the women who had recovered from bulimia nervosa. In view of the apparent lack of effect of tryptophan depletion on mood or appetite, the remaining two experiments examine the role of specific 5-HT receptor subtypes in the control of appetite. Chapter 6 examines the effect of meta-chlorophenylpiperazine (mCPP), a 5-HT_2C receptor agonist on appetite, and Chapter 7 examines the effect of 5-HT₃ receptor blockade on amphetamine anorexia. Whilst the data from these experiments do not support a role for these receptor subtypes in appetite, it is suggested that this is a potentially fruitful area for future research. The results generated by the above experiments are discussed in Chapter 8 in the light of other research findings. The methodologies adopted for these experiments and the implications of these studies for future research are discussed.

Thesis (M.S.)--Rutgers University, 2007. / "Graduate Program in Nutritional Sciences." Includes bibliographical references (p. 38-45).

Thesis (Ph. L.)--Catholic University of America, 2005. / Includes bibliographical references (leaves 100-104).

Thesis (M.A.)--West Virginia University, 2004. / Title from document title page. Document formatted into pages; contains v, 50 p. : ill. Includes abstract. Includes bibliographical references (p. 30-35).

Thesis (Ph. L.)--Catholic University of America, 2005. / Includes bibliographical references (leaves 100-104).

Bibliography: pages 159-173. / Previous research into the families of eating disordered individuals appears to have focused almost exclusively on the families of anorexics. In view of the problems associated with the conceptualization of bulimia as a syndrome distinct from anorexia nervosa, it seems possible that research into the families of anorexics may have included the families of bulimics. Following the introductory overview of some of the literature on bulimia, highlighting the lack of diagnostic clarity in this area, previous research into the families of both anorexics and bulimics is reviewed. In view of the lack of documented research into the families of bulimics from a systems perspective, the present study aimed to explore these families' functioning. Family functioning was assessed according to the McMaster Model of Family Functioning (Epstein and Bishop, 1981): clinical interviews with 13 bulimics provided qualitative data on their families' functioning: quantitative data were elicited from the family members of 10 of these bulimics by means of the Family Assessment Device (Epstein and Bishop, 1983). Clinical assessment of the families of bulimics reveals unhealthy family functioning. The ratings of all family members as well as those of the researcher indicate that there is familial dysfunction on all dimensions of family functioning. The main emphases in these families appears to be on instrumental issues, while affective issues are inappropriately handled. Discussion centres on the findings of the present study, which show some variance with the results of previous research into the families of anorexics; and an understanding of bulimia from a systems perspective is presented.

Several feeding-related factors can affect taste sensitivity or preferences and therefore may be part of a homeostatic regulatory mechanism. Cholecystokinin (CCK), a hormone which reduces food intake in several species, has also been postulated to interact with the orosensory characteristics of food. To test this hypothesis, the effects of CCK-8 and food deprivation on the short-term intakes of water, sucrose solutions (0.05 to 1.0 M), and saline solutions (0.05 and 0.15 M) were determined. In most cases, CCK (2 μg/kg) reduced sucrose intake when measured either as the amount consumed or the number of licks in a short period (nine minutes). Additionally, CCK reduced the intake of 0.15 M NaCl in satiated rats and water intake in both hungry and satiated rats. Rats usually consumed more sucrose when hungry than when satiated or fed ad libitum; CCK-induced suppression of intake, however, was generally greater in the satiated or ad libitum conditions than in the hungry condition. There was no systematic effect of sucrose concentration on the amount of CCK-induced suppression of intake, which suggests that CCK regulates rather than interferes with ingestion. To determine whether the CCK-induced suppression is due to a change in the peripheral taste signal, the integrated chorda tympani responses to sucrose and NaCl tastes were recorded in rats anesthetized with either urethane, Innovar-Vet, or a combination of urethane and alpha-chloralose. The only significant effect of CCK was the slight increase in the initial response to 0.3 M sucrose after the infusion of a total of 10 μg of CCK-8 into rats anesthetized with Innovar-Vet. In general, therefore, the effect of CCK on sucrose intake does not appear to be due to a peripheral taste change; an analysis of single taste fibers, however, would be more conclusive. An examination of the effects of CCK on central gustatory and reward areas might yet provide a mechanism for the CCK effect on taste-motivated ingestion.