NOTE: Free essay sample provided on this page should be used for references or sample purposes only. The sample essay is available to anyone, so any direct quoting without mentioning the source will be considered plagiarism by schools, colleges and universities that use plagiarism detection software. To get a completely brand-new, plagiarism-free essay, please use our essay writing service.
One click instant price quote
... levels in spring and fall. 29 For cortisol, data indicate consistent differences between winter and summer samplings (but inconsistencies as to direction of effects, possibly attributable to geographic, meteorologic, or other differences). 30 Our own data showed trends or effects consistent with high peak prolactin levels in winter, high Bmax and cortisol levels in summer, and intermediate values on these indices in spring and fall. To control for this range of effects, we entered 2 dummy variables as covariates, which compared samplings obtained in summer (and then fall and spring) to those obtained in winter. Consistent with published findings, 31 our data showed contraceptive users to show strongly higher range of cortisol values and weakly higher peak prolactin levels.
Even though proportions of contraceptive users did not differ significantly across groups, we introduced a covariate to code for being "on" or "off" oral contraceptives. Statistical tests were 2 -tailed and conducted at the. 05 level of significance. To balance type I and type II errors, we report pairwise group comparisons with and without Bonferroni corrections. RESULTS CHILDHOOD ABUSE Abuse was reported by 26 (76 %) of 34 bulimic women and 12 (52 %) of 23 non bulimic women. Significant bulimic and non bulimic differences were indicated for physical abuse (21 [ 62 %] of 34 vs 7 [ 30 %] of 23, respectively; &# 61539; 21 = 5. 39; P = . 02), but not for sexual abuse (14 [ 41 %] of 34 vs 8 [ 33 %] of 24, respectively). Among sexually abused bulimic and sexually abused non bulimic participants, mean SD severities (3. 21 0. 89 vs 2. 75 1. 04, respectively) and ages of abuse onset (9. 50 3. 46 vs 9. 63 3. 11 years, respectively) did not differ (t 20 = 1. 11, P> . 25 and t 20 = - 0. 08, P> . 50, respectively).
Corresponding mean SD physical abuse severities (3. 62 0. 92 vs 3. 71 0. 76) and ages of onset (7. 43 3. 68 vs 5. 86 2. 19 years) did not differ (t 26 = - 0. 25, P> . 50 and t 26 = 1. 06, P> . 25, respectively). EATING SYMPTOMS AND PSYCHOPATHOLOGICAL INDICES Table 1 shows mean SD values on measures of eating and psychopathological symptoms for each of the groups. On most indices bulimic women showed expected elevations relative to non bulimic women. Abused bulimic women reported significantly more self-injuriousness than did non abused bulimic women or women who were normal eaters. Prevalence's of major depression, PTSD, and BPD obtained in different groups are shown in Table 2. (DIS 4 values were non systematically missing for 4 bulimic women and 1 non bulimic woman. ) Results (tested with Fisher exact tests) indicate lifetime major depression to co aggregate, regardless of abuse, with BN. In contrast, PTSD (lifetime or current) occurred especially often in abused bulimic women.
Statistically significant differences were not obtained on BPD. SEROTONERGIC AND NEUROENDOCRINE MEASURES Results on paroxetine-binding tests were evaluated using analyses of covariance (Rancova) to compare transporter density (Bmax) and binding affinity (Kd) indices across groups, with dummy variables for seasonal effects (Table 3 presents unadjusted means and SDs). The analysis on Bmax indicated expected winter vs summer (F 1, 50 = 7. 26, P< . 02) and spring or fall vs summer (F 1, 50 = 5. 93, P< . 03) effects, with higher Bmax in the summer. Once removed, a significant group effect remained (F 3, 50 = 4. 61, P< . 01). Covariate-adjusted group contrasts (with or without Bonferroni corrections) generally indicate lower Bmax in bulimic women, but no differences attributable to childhood abuse (Table 3). No effects were obtained on Kd.
We analyzed serial prolactin findings (Figure 1, plotting unadjusted means and SEs) using a 2 -way repeated-measures analysis of covariance (RANCOVA), with covariates for contraceptive and seasonal effects. The RANCOVA yielded a significant time x contraceptive interaction (F 8, 400 = 2. 83, P< . 01), indicative of earlier "peaking" in contraceptive users, which remained significant after Greenhouse-Geisser correction (F 2, 77 = 2. 83, P< . 05). Examination of resulting curves and proportions of contraceptive users across groups indicated that the interaction could not have confounded group and time effects of main interest. There was no main effect of contraceptives or main or interaction effects implicating season of testing. A main effect of time of sampling (F 8, 400 = 5. 17, P< . 005), showing expected stimulation of prolactin after m-CPP administration, remained significant after Greenhouse-Geisser correction (F 2. 77, 138. 63 = 5. 17, P< . 005). More important, after removal of covariates, a significant group x time interaction effect was obtained (F 24, 400 = 2. 10, P< . 005), which remained after Greenhouse-Geisser correction (F 8. 32, 138. 63 = 2. 10, P< . 04).
Simple effects of group were indicated at 180 (F 3, 50 = 4. 50, P< . 01) and 210 (F 3, 50 = 3. 52, P< . 025), and, as a trend, at 240 minutes (F 3, 50 = 2. 74, P< . 055). The pattern of results on covariate-adjusted pairwise comparisons, conducted with and without Bonferroni corrections (Figure 1), indicates "blunted" prolactin response in both bulimic and abused participants. An adjunctive analysis, conducted using 1 -way ANCOVA (with covariates controlling for seasonal effects) testing group differences on an index of change (&# 61508; -peak) on prolactin (ie, peak minus baseline at each time point for each subject), indicated no seasonal effects, but a significant overall group effect (F 3, 55 = 3. 15, P< . 04). Covariate-adjusted contrasts showed mean peak prolactin for bulimic women (5. 62 3. 95), abused bulimic women (7. 26 7. 06), and abused women who were normal eaters (5. 73 5. 19) to always be lower than the score obtained in the group of non abused women who were normal eaters (13. 57 9. 94). The combination of downward diurnal cortisol variations with upward shifts (presumably) due to m-CPP administration complicated determination of &# 61508; -peak values on cortisol. We therefore analyzed serial cortisol findings using 2 -way RANCOVA, with covariates for contraceptive and seasonal effects (Figure 2, which plots unadjusted means and SEs).
The RANCOVA indicated a significant time x contraceptive effect (F 8, 392 = 2. 58, P< . 01), even after Greenhouse-Geisser correction (F 4. 16, 203. 71 = 2. 58, P< . 04), and an even stronger main effect of contraceptive use (F 1, 49 = 27. 43, P< . 001). Average SE cortisol level was higher in contraceptive users (21. 08 1. 18) than in nonusers (11. 25 0. 99) (and downward diurnal shifts in these individuals were, correspondingly, somewhat larger). Examination of curves suggested that the interaction of time and contraceptive variables could not have confounded effects of main interest. Moreover, after removal of covariate effects, a significant group x time interaction was obtained (F 24, 392 = 2. 03, P< . 005), even after Greenhouse-Geisser correction (F 12. 47, 203. 71 = 2. 03, P< . 03). There was no main time or group effect. Simple effects of group were indicated at 210 minutes (F 3, 49 = 2. 89, P< . 05) and 240 minutes (F 3, 49 = 3. 15, P< . 04).
Covariate-adjusted pairwise group comparisons indicated significantly lower means at these time points in samples of abused bulimic women and abused women who were normal eaters (Figure 2). However, after Bonferroni corrections, pairwise differences remained significant in abused bulimic women only. COMMENT This study shows intriguing patterns of association, in bulimic and non bulimic women, between childhood abuse, on the one hand, and eating pathology, general psychopathology, and 5 -HT and cortisol functioning, on the other. Although we found no systematic association between childhood abuse and expression of eating or affective or impulsive symptoms, we did note symptoms of PTSD and self-destructiveness to be elevated in abused bulimic women compared with levels obtained in other groups. This pattern links abuse (in at least the presumably more vulnerable bulimic individuals in our sample) with symptoms that are believed to sometimes represent posttraumatic sequelae.
On neurobiological indices, different findings were obtained on different measures. We observed reduced platelet paroxetine binding (Bmax) in bulimic women relative to that in non bulimic women (with no apparent effects due to childhood abuse). These findings replicate our previous finding in 40 bulimic women (16 of whom were in the present sample) of reduced platelet [ 3 H]-paroxetine binding. 6 If paroxetine binding models the central 5 -HT transporter, then such findings would indicate reduced 5 -HT reuptake at central presynaptic sites. Regardless, our findings link reduced paroxetine binding more strongly to BN than to developmental abuse. On prolactin, we obtained further evidence of abnormal 5 -HT function in BN (Figure 1), replicating well-known tendencies for bulimic women to display smaller prolactin responses after m-CPP administration than non bulimic women. 7 Blunting of prolactin response after m-CPP administration has been interpreted as indicating down-regulation of postsynaptic 5 -HT receptors on which m-CPP acts. Whether such findings reflect "state" effects attributable to active BN (eg, due to sequelae of binge eating on 5 -HT mechanisms), "trait" effects related to some stable aspect of those who develop BN, or some combination of the 2 remains unknown, however.
Blunting effects obtained in abused women who were normal eaters at some prolactin sampling intervals are consistent with previous findings on prolactin after m-CPP administration in abused non bulimic populations. 2 Such findings would suggest that there may also be an association between childhood abuse and reduced postsynaptic 5 -HT activity. However, further work is needed to clarify causal questions, since such effects could constitute a simple correlate (vs consequence) of abuse. For example, connection between 5 -HT function and abuse could reflect association with a trait (eg, impulsivity) that might be present in the abusive parent and the vulnerable child, without implying a causal role of abuse. Results on cortisol levels contrast with our other findings. Compared with levels in non abused women who were normal eaters, we obtained unequivocal evidence of reduced plasma cortisol levels in abused bulimic women, weak evidence of such reduction in abused women who were normal eaters, but no evidence of such reduction in non abused bulimic women (Figure 2).
In other words, our data did not so much link decreased cortisol levels with BN (as was the case for 5 -HT indices such as prolactin and paroxetine binding) as with abuse. Reduced cortisol activity has been thought to represent an adaptation of the HPA axis to prolonged or particularly intense stress. 3, 4 From this perspective, abnormally low cortisol values, especially evident in our abused bulimic patients, could reflect a posttraumatic alteration of HPA axis function. Particularly strong effects in the bulimic participants might be attributed to 1 (or both) of the following. First, abused bulimic women more often reported a history of PTSD (Table 2), perhaps indicating that these participants underwent more intensely traumatic experiences than did abused women who were normal eaters.
Second, it may be that the same vulnerability that rendered abused bulimic women susceptible to BN also rendered them vulnerable to detrimental effects of abuse manifested (at a neurobiological level) as cortisol alteration and (at a behavioral level) as PTSD symptoms. Although we are unable to ascertain which of these explanations is correct, rated severities of abuse did not differ significantly across abused bulimic and non bulimic women, and this argues in favor of an explanation couched in terms of susceptibility to, rather than severity of, abuse. Regardless, it is striking to note effects, in individuals who are on average in their mid- 20 s, of events that occurred in childhood. We note various limitations of our study. Our design did not include measurement of serum estradiol levels and m-CPP concentrations to ascertain hormonal and drug effects.
It also lacked a placebo condition by which to evaluate neuroendocrine responses under neutral circumstances. Finally, without prospective measurements, we cannot interpret effects observed as either consequences of active BN or stable "trait" antecedents. Regardless, results obtained point to potentially important 5 -HT and cortisol effects. Direct and indirect effects of 5 -HT and cortisol anomalies observed might have various implications for affected individuals's tress tolerances, impulse controls, capacities for mood regulation, and abilities to control eating behavior (ie, to satiate). We therefore speculate that, here, we may be observing neurobiological mediators of the link between developmental trauma and heightened susceptibility to BN.
Free research essays on topics related to: sexually abused, physical abuse, major depression, abused women, bulimic
Research essay sample on Sexually Abused Abused Women
