Also see: Bisphenol A (BPA), Estrogen, and Diabetes
The longer a woman stays on hormones, the more each cell in her body is poisoned. Does poison sound like too strong a word? A woman must decide for herself. As the years pass, her sugar metabolism may test out like a diabetic’s. -Drs. Barbara and Gideon Seaman
Am J Obstet Gynecol. 1990 Jul;163(1 Pt 2):382-7.
Effects of oral contraceptives on carbohydrate and lipid metabolisms in a healthy population: the Telecom study.
Simon D, Senan C, Garnier P, Saint-Paul M, Garat E, Thibult N, Papoz L.
In a cross-sectional study that aimed to identify risk factors for diabetes, 1290 consecutive, healthy, nonpregnant women of child-bearing age were examined in a center for preventive medicine. An in-depth interview about menses, use of oral contraceptives, and menopause was performed. Plasma glucose at fasting and 2 hours after a 75 gm glucose load, glycated hemoglobin A1c, fasting plasma insulin, total plasma cholesterol, and triglycerides were measured. Compared with nonusers taking no progestogens, oral contraceptive users (n = 431; 33.4%) were younger (p less than 0.001) and leaner (p less than 0.001). After adjustment for age and body mass index, oral contraceptive users had higher 2-hour plasma glucose (p less than 0.001), higher fasting plasma insulin (p less than 0.01), and higher triglycerides levels (p less than 0.01). Fasting plasma glucose, glycated hemoglobin A1c, and total cholesterol did not significantly differ between the two groups. In relation to dosage and types of steroid components, few differences have been found between high-dose and low-dose oral contraceptives or according to the estrogen-progestogen balance of the preparations. Use of oral contraceptives appears to induce an increase of insulin-resistance markers, which have recently been cited as risk factors for ischemic vascular diseases. These markers should be carefully monitored in oral contraceptive users.
J Hypertens. 1998 Mar;16(3):357-68.
A study of the interactive effects of oral contraceptive use and dietary fat intake on blood pressure, cardiovascular reactivity and glucose tolerance in normotensive women.
Straznicky NE, Barrington VE, Branley P, Louis WJ.
OBJECTIVE:
To investigate the interactive effects of oral contraceptive pill use and dietary fat intake on cardiovascular haemodynamics and metabolic parameters in young normotensive women.
DESIGN:
Thirty-two women participated, of whom 16 were taking oral contraceptive pills (ethinyl-oestradiol plus levonorgestrel) and 16 were age-matched and weight-matched controls not taking such pills. Subjects consumed either a high-fat or a low-fat diet for 2 weeks in an open, randomized, crossover study lasting 6 weeks. Investigations were performed at the end of each diet during the luteal phase of the menstrual cycle.
METHODS:
Blood pressure was measured by 24 h ambulatory recording; cardiovascular reactivity was determined by examining blood pressure responses to systemic infusions of noradrenaline and angiotensin II and to the cold pressor test; and carbohydrate metabolism was investigated by an intravenous glucose-tolerance test.
RESULTS:
Plasma triglyceride levels were significantly higher in women taking oral contraceptive pills compared with non-users on both diets; however, responses of lipoprotein levels to the two diets did not differ between study groups (total and low-density lipoprotein cholesterol levels decreased by 15 and 17% in oral contraceptive pill users and by 14% each in non-users, on the low-fat compared with the high-fat diet). Fasting plasma insulin levels, the insulin-production response to administration of glucose (insulin area under the curve) and resting clinic and night-time systolic blood pressures were all significantly reduced on the low-fat diet, but only in non-users. Blood pressure responses to noradrenaline and maximal heart rate response to cold were significantly attenuated during the low-fat diet in oral contraceptive pill users. During the low-fat diet, resting systolic, 24 h systolic and diastolic blood pressures and insulin area under the curve were all significantly higher for women taking the oral contraceptive pills. Users of these pills also exhibited a greater systolic sensitivity to administration both of noradrenaline and of angiotensin II and had a higher plasma renin activity irrespective of dietary phase.
CONCLUSIONS:
These results confirm that oral contraceptive pills have the potential to cause adverse effects on blood pressure, cardiovascular reactivity and the insulin-production response to administration of glucose and suggest that some of the beneficial effects of a low-fat diet on these parameters may be negated in women taking oral contraceptive pills.
PIP:
The interactive effects of combined oral contraceptive (OC) use and dietary fat intake on cardiovascular hemodynamics and metabolic parameters were investigated in a comparative study of 16 normotensive OC users from Australia and 16 age- and weight-matched nonuser controls. The 6-week study’s crossover design allocated women to consume either a high- or low-fat diet for 2-week periods. Analyses were performed at the end of each diet during the luteal phase of the menstrual cycle. Plasma triglyceride levels were significantly higher in OC users than nonusers in both diet groups; however, responses of lipoprotein levels to the 2 diets did not differ between study groups. Total and low-density lipoprotein cholesterol levels decreased by 15% and 17%, respectively, in OC users, and by 14% each in non-OC users on the low-fat, compared to the high-fat, diet. Fasting plasma insulin levels, the insulin production response to administration of glucose, and resting clinic and night-time systolic blood pressures were all significantly reduced on the low-fat diet, but only in nonusers. In OC users, blood pressure responses to noradrenaline and maximal heart rate response to cold were significantly attenuated by the low-fat diet. During the low-fat diet, resting systolic, 24-hour systolic, and diastolic blood pressures and areas under the curve were significantly higher in the OC group. OC users also demonstrated a greater systolic sensitivity to administration of both noradrenaline and angiotensin II, and had a higher plasma renin activity, regardless of diet. Overall, these findings confirm that OCs can cause adverse effects on blood pressure, cardiovascular reactivity, and the insulin production response to glucose administration, and negate some of the beneficial effects of a low-fat diet.
Proc Soc Exp Biol Med. 1996 Jul;212(3):243-7.
Effect of estrogen on hyperprolactinemia-induced glucose intolerance in SHN mice.
Matsuda M, Mori T.
The effects of prolactin (PRL) on circulating levels of glucose and insulin, and of estradiol on hyperprolactinemia-induced glucose intolerance of tissues were studied in pituitary-grafted SHN mice (PG mice) and sham-operated controls. Pituitary grafting (PG) decreased blood glucose levels in male mice at 1 and 3 months after the operation but did not alter those in females. PG had little effect on serum insulin levels in males, but increased those in females. In female mice at 2 months after PG, blood glucose levels were significantly higher at 1, 2, and 4 hr after glucose load when compared with those in controls. In contrast, there was no significant difference in blood glucose levels after glucose load between male PG and control mice. The rate at which blood glucose levels decreased was slower in female PG mice than in controls during the 30 min after insulin injection, whereas there was no difference in the rate after insulin injection between male PG and control mice. In ovariectomized (Ovx) mice, no significant difference was found in the blood glucose levels after a glucose load between PG and control groups at 2 months after PG. In Ovx mice treated daily with estrogen, however, a PG-dependent high level of blood glucose was observed after glucose load. These results suggest that hyperprolactinemia decreases glucose tolerance via an increase in insulin resistance in female SHN mice and that estrogen is essential to the expression of the PRL effect.
