Biomedical subjects

C C Tay

Publications and source records attributed to C C Tay.

6 recordsLinked to original sources

PubMed1996

Twenty-four hour patterns of prolactin secretion during lactation and the relationship to suckling and the resumption of fertility in breast-feeding women.

In breast-feeding women prolactin released in response to suckling is essential for the maintenance of lactation. This physiological hyperprolactinaemia is also associated with lactational infertility. However, it is not clear whether there is any direct relationship between changes in prolactin per se and the duration of infertility. To address this question, our study determined the pattern of prolactin secretion in relation to suckling and the return of ovarian activity in the same cohort of breast-feeding women. Blood samples were withdrawn at 10 min intervals for 24 h from 09:00 to 09:00 h at either 4 (n = 9) or 8 weeks (n = 11) post-partum when the women had completely suppressed ovarian activity, at the time of the introduction of supplements to the baby (n = 17), a time associated with reduction of suckling activity, at first menses while still breast-feeding (n = 13) and in the follicular phase (n = 9) of the first menstrual cycle after weaning. During sampling, mothers and babies continued their normal pattern of suckling activity. The pattern of prolactin release was very variable at each stage of lactation, depending on the pattern of suckling. Frequent suckling was associated with elevated prolactin concentrations during the 24 h period throughout lactation. When suckling was less frequent, prolactin concentrations fell to baseline values between breast-feeds, but prolactin was released in response to all suckling episodes. An increase in prolactin concentrations at night, independent of suckling, was only evident once breast-feeding had ceased. The prolactin response to suckling declined significantly only after the return of menses at 33.6 +/- 3.5 weeks post-partum. There was no relationship between the duration of amenorrhoea and the plasma concentrations of prolactin over 24 h, or day or night separately, throughout lactation. However, there was a strong correlation (r = 0.843; P < 0.01) between the timing of the introduction of dietary supplements to the baby and the duration of amenorrhoea. These results suggest that there may be no precise link between the release of prolactin during lactation and the duration of lactational infertility in breast-feeding women.

Adolescent↗

PubMed1994

Physiological mechanisms underlying lactational amenorrhea.

Breastfeeding delays the resumption of normal ovarian cycles by disrupting the pattern of pulsatile release of GnRH from the hypothalamus and hence LH from the pituitary. The plasma concentrations of FSH during lactation are sufficient to induce follicle growth, but the inadequate pulsatile LH signal results in a reduced estradiol production by these follicles. When follicle growth and estradiol secretion does increase to normal, the suckling stimulus prevents the generation of a normal preovulatory LH surge and follicles either fail to rupture, or become atretic or cystic. Only when the suckling stimulus declines sufficiently to allow generation of a normal preovulatory LH surge to occur will ovulation take place with the formation of a corpus luteum of variable normality. Thus suckling delays the resumption of normal ovarian cyclicity by disrupting but not totally inhibiting, the normal pattern of release of GnRH by the hypothalamus. The mechanism of suckling-induced disruption of GnRH release remains unknown. It does not appear to involve prolactin, dopamine or opiates although a combination of these factors might be involved. Prolactin is the major hormone responsible for milk production and is present in sufficient quantities in almost all women to allow the establishment of normal lactation. Oxytocin is essential for milk let down and is susceptible to inhibition of release by stress. The successful initiation of lactation which would lead to the potential of utilizing breastfeeding as contraceptive may require more attention to be paid to the establishment of non-stress release of oxytocin.

Amenorrhea↗

PubMed1993

Effect of antagonists of dopamine and opiates on the basal and GnRH-induced secretion of luteinizing hormone, follicle stimulating hormone and prolactin during lactational amenorrhoea in breastfeeding women.

The role of dopamine and opiates in the suckling-induced suppression of gonadotrophin secretion and prolactin release was investigated during lactational amenorrhoea in fully breastfeeding women at 12 weeks post-partum. A total of 26 women, 20 using non-steroidal methods of contraception and six using the progestogen-only pill, Noriday (POP), breastfed their babies on demand at a frequency of 3.6 +/- 0.2 suckling episodes during the 8 h study period while blood samples were collected at 10-min intervals. Five hours after the start of sampling six women were given the dopamine antagonist metoclopramide (10 mg, i.m.) while four women received saline. In a second experiment, six women using nonsteroidal contraception and three women on the POP received an i.v. infusion of the opiate antagonist naloxone (1.6 mg/h) for 2 h, while four women using non-steroidal contraception and three women on the POP were infused with saline. Two hours after the i.m. injection or start of infusion all women were given an i.v. injection of 10 micrograms gonadotrophin releasing hormone (GnRH) and samples were collected for a further 1 h. All samples were assayed for luteinizing hormone (LH), follicle stimulating hormone (FSH) and prolactin. Plasma concentrations of oestradiol were < 60 pmol/l in all women and they remained amenorrhoeic for at least 10 weeks after the study. Pulsatile release of LH was only observed over the 5 h pre-treatment period in 10 of the 20 non-steroid taking women (1-3 pulses/5 h), and in one of the six women (1 pulse/5 h) on POP.(ABSTRACT TRUNCATED AT 250 WORDS)

Amenorrhea↗

PubMed1993

Abnormal twenty-four hour pattern of pulsatile luteinizing hormone secretion and the response to naloxone in women with hyperprolactinaemic amenorrhoea.

OBJECTIVE: Hyperprolactinaemic amenorrhoea is associated with disturbances of pulsatile gonadotrophin secretion. The underlying mechanism remains unclear and the aim of this study was to investigate the 24-hour secretory pattern of gonadotrophins in women with hyperprolactinaemic amenorrhoea. The effect of opioid blockade using naloxone infusion on LH secretory pattern was also studied. DESIGN: The secretory patterns of LH, FSH, PRL and their responses to naloxone infusion were studied by serial blood samples collected at 10-minute intervals for 24 hours. On the following day, naloxone was infused at a dose of 1.6 mg per hour for 4 hours. PATIENTS: Eight women with hyperprolactinaemic amenorrhoea, two women hyperprolactinaemic but with normal ovarian cycles, and nine control subjects in the early follicular phase of menstrual cycle. MEASUREMENTS: Concentrations of LH, FSH and PRL were measured in plasma samples obtained at 10-minute intervals for 24 hours. In one woman, concentrations of urinary oestrone glucuronide were measured daily during treatment with pulsatile GnRH. RESULTS: The number of LH pulses per 24 hours was significantly fewer in women with hyperprolactinaemic amenorrhoea than in those with hyperprolactinaemia with normal cycles or control subjects (mean +/- SEM 4.5 +/- 2.4 vs 13.5 +/- 2.5 vs 17.3 +/- 0.8, P < 0.001). The magnitude of each episode of secretion was significantly higher in the hyperprolactinaemic amenorrhoeic women (P < 0.05) so the overall mean concentrations of LH throughout the 24-hour period was similar in the three groups (5.2 +/- 1.1, 4.8 +/- 0.8 and 5.2 +/- 0.4 U/l respectively). In women with hyperprolactinaemic amenorrhoea there was no significant change in the pattern of LH secretion during sleep in contrast to the control women in whom there was a slowing in the LH pulse frequency during the night. There was no significant change in the mean concentrations of LH, FSH and PRL during the naloxone infusion. There were also no significant changes in the LH pulse frequency in response to naloxone infusion when compared with an equivalent period of time in the previous 24 hours. In one hyperprolactinaemic amenorrhoeic woman, follicular development, ovulation and pregnancy were induced when gonadotrophin releasing hormone (GnRH) was infused in a pulsatile manner at a dose of 5 micrograms every 90 minutes. CONCLUSIONS: The suppression of normal ovarian cycles in women with hyperprolactinaemic amenorrhoea is due to a significant reduction in frequency of LH (GnRH) secretion which is not due to an increase in hypothalamic opioid activity. As normal ovarian cycles can occur or be induced by exogenous GnRH in hyperprolactinaemia, it is unlikely that a high level of prolactin by itself inhibits follicular development and ovulation.

Adult↗

PubMed1992

The 24 h pattern of pulsatile luteinizing hormone, follicle stimulating hormone and prolactin release during the first 8 weeks of lactational amenorrhoea in breastfeeding women.

In women, breastfeeding results in a variable period of ovarian inactivity which is apparently related to suppression of the normal pulsatile release of luteinizing hormone (LH). However, pulse profiles had only been studied during the daytime. Since resumption of pulsatile LH secretion during puberty is initiated at night, the present study determined the pattern of pulsatile LH secretion in relation to that of follicle stimulating hormone (FSH) and prolactin, and suckling and ovarian activity at 4 and 8 weeks postpartum in 20 fully breastfeeding women with lactational amenorrhoea. Blood samples were withdrawn at 10 min intervals for 24 h from 0900 h to 0900 h at either 4 weeks (n = 9) or 8 weeks (n = 11) postpartum, while the mothers and babies continued their normal pattern of suckling activity. At 4 weeks postpartum, no LH pulses occurred over 24 h in six of the nine women while one (n = 1) or two (n = 2) LH pulses occurred in three of the nine women. In contrast, LH pulses were present in nine of the 11 women at 8 weeks postpartum. The pulse frequency varied considerably from two to eight pulses over the 24 h and there was no influence of the time of day or sleep on the time of the pulse release. Lactational amenorrhoea was maintained for at least 10 weeks afterwards and there was no relationship between the time of resumption of ovarian activity and the presence or absence of pulsatile LH secretion at 4 or 8 weeks postpartum.(ABSTRACT TRUNCATED AT 250 WORDS)

Amenorrhea↗

PubMed1991

Mechanisms controlling lactational infertility.

Despite the important role breastfeeding plays in regulating a mother's fertility, the mechanisms controlling lactational infertility remain to be fully elucidated. Breastfeeding suppresses fertility for a period which varies widely among individuals and within different communities. Suckling stimulus is the key factor in controlling the duration of infertility. Suckling by the infant appears to inhibit luteinizing hormone secretion by inhibiting the pulsatile release of gonadotrophin-releasing hormone from the hypothalamus. The exact mechanism remains unclear but a suckling-induced increase in hypothalamic opioid tone may be involved. Prolactin does not appear to play a major role, other than being essential for maintenance of milk production, in lactational infertility.

Breast Feeding↗