Can pharmacotherapists be too supportive? A process study of active medication and placebo in the treatment of depression.

BACKGROUND: This study examined therapist-patient interactions during clinical management with antidepressant medication and pill-placebo. METHOD: The sample consisted of 80 patients on active medication and 40 patients in a pill-placebo condition from a randomized controlled trial for moderate to severe depression. Pharmacotherapist-patient interactions were characterized using observer ratings of the therapeutic alliance, pharmacotherapist-offered facilitative conditions, pharmacotherapist adherence to clinical management treatment guidelines and pharmacotherapist competence. Patients, therapists and raters were blind to treatment condition and outcome. RESULTS: Provision of greater non-specific support (facilitative conditions) in early sessions predicted less subsequent improvement in depressive symptoms for patients receiving pill-placebo but not those receiving active medications, for which none of the process ratings predicted subsequent change. Early symptom change predicted later alliance and adherence in both conditions and therapist competence in the active condition. CONCLUSIONS: Higher levels of support in early sessions predict poorer subsequent response among placebo patients. It remains unclear whether patients who are likely to be refractory elicit greater non-specific support or whether the provision of such support has a deleterious effect in unmedicated patients. Differences in treatment process variables between conditions late in treatment are likely to be largely a consequence of symptom relief produced by active medications.

Insulin-like growth factor 1 and its binding protein 1 during normal and diabetic pregnancies.

Investigations of circulating insulin-like growth factor 1, hPL, and infant size during pregnancy in normal and insulin-dependent diabetic women have yielded conflicting results and have not been analyzed longitudinally. We studied serial changes in maternal serum insulin-like growth factor 1 levels (measured by radioimmunoassay after acid ethanol extraction) throughout pregnancy in 22 normal women and in 38 with insulin-dependent diabetes. The diabetic women had significantly lower serum insulin-like growth factor 1 concentrations than normal women throughout pregnancy and after delivery, although the rates of change in both groups of women were similar. Within-patient analysis showed a significant decrease in serum insulin-like growth factor 1 between 6-12 weeks' gestation and a significant increase between 24-32 weeks, followed by a significant decrease from 36 weeks' gestation to 12 weeks after delivery. Incremental changes in insulin-like growth factor 1 between 24-32 weeks' gestation correlated significantly with incremental changes in hPL (r = 0.40; P less than .001) and with birth weight (r = 0.37; P less than .01), but not with ultrasound measurements of fetal growth. The correlation of increments in insulin-like growth factor 1 and birth weight became nonsignificant when the association of hPL with both insulin-like growth factor 1 and birth weight was taken into account. Neither insulin-like growth factor binding protein 1 (placental protein 12) nor its ratio to insulin-like growth factor 1 showed any association with infant size. The physiologic changes in maternal serum insulin-like growth factor 1 in pregnant diabetic women do not appear related to the increased birth weight of their infants.

Some endocrinological events associated with early pregnancy failure.

Serial measurements of serum progesterone, oestradiol, human chorionic gonadotrophin (hCG) and human placental lactogen (hPL) have been determined in 33 women experiencing early pregnancy failure and compared with the values of the same hormones in 72 healthy women having uncomplicated pregnancies. Steroid production by the corpus luteum seemed similar in both groups up to 6 weeks gestation but thereafter placental steroidogenesis was not evident in those women in whom spontaneous pregnancy losses occurred. Placental production of the two protein hormones, hCG and hPL, did take place, and whereas the circulating levels were not as high as in normal pregnancies, levels did usually increase before clinical evidence of miscarriage occurred. hCG was not a sensitive discriminator of subsequent failure. In these women there were no significant hormone differences between those with evidence of a fetus and those without.

A longitudinal study of circulating progesterone, oestradiol, hCG and hPL during pregnancy in type 1 diabetic mothers.

Serum progesterone, oestradiol, human chorionic gonadotrophin (hCG) and human placental lactogen (hPL) were determined serially throughout 27 pregnancies in insulin-dependent diabetic patients from Newcastle (UK), 15 such patients from Stockholm (Sweden) and in 69 normal women having uncomplicated pregnancies. Mean progesterone, oestradiol and hCG concentrations were somewhat higher in the diabetic women during the third trimester but hPL values were not different from normal. The increased hormone concentrations did not relate to the increased birthweights or placental weights in the diabetic women. It is suggested that the usual physiological endocrine changes during normal pregnancy are relatively undisturbed by insulin-dependent diabetes or the degree of diabetes control achieved.