Fasting Blood Glucose Level
The finding from the present study suggests that the FBS level of cases was higher when compared to the controls. However, it still remained in the normal range for almost all users. Similar findings have been published in England [12] on the effect of different formulations of COC agents on lipid and carbohydrate metabolism. The analysis showed that increased plasma glucose, which was (40–60%) higher in cases than controls. The percent of the increment is much higher than our findings. Another similar study in 1992 revealed the same result [13]. A study in Finland [14] found that consumers of COC pills had significantly higher mean serum glucose levels compared to their baseline values, with an increased risk of developing glucose metabolism abnormalities. In the present study, it is important to note that even though the FBS level has increased, only small number of COC pills user demonstrated abnormally high glucose level. We observed that only 4.5 percent of users of COC pills had FBS level of ≥ 110 mg/dL. This is significantly lower than the figure reported in Godsland et al cross-sectional study [12]. The mechanism through which hormonal contraception causes blood glucose levels to rise has yet to be elucidated. One possible mechanism as demonstrated in rats [15] investigated the influence of estradiol on the insulin receptor of ovariectomized rats treated with different hormonal doses. Results showed that high doses of estradiol decreased the sensitivity of insulin by the carbohydrate mechanism. Contrary to the findings of the present study, a cohort study conducted in Texas[16] reported changes in mean blood glucose level of users of COC pills were not significantly different from controls. This result was supported by a study [17] which recommended best practice in the prescription of hormonal contraceptives in women, especially those with diabetes mellitus.
This disparity may be due to the variation in the study protocol used in the previous and current research. Berenson's and co-workers ' study is a cohort study involving 703 participants, whereas the current cross-sectional study involved a comparatively small sample size of 220 people. The discrepancy may also be due to the age difference between the studies. Unlike the other study [16] whose age bracket is between 25 and 33 years, the participants in this study were aged between 18–45 years. Because the women in our sample also include subjects reaching menopause that are predicted to show high blood glucose level correlated with age. The disparity in gender, food habits and behaviors can also lead to the discrepancy.
Use of COC Pills and Blood Pressure
This study revealed that mean SBP and MAP values showed a statistically significant increment in cases as compared to their matched controls and among pill users in relation to the duration of use. Diastolic blood pressure was not different when compared to controls, but, it was significantly different among users in relation to the duration of use. Such results from this research were consistent with a study in Pakistan [18] that found significantly higher SBP and DBP among pill users than controls. A related follow-up analysis by Azima and Mousavi [19] found that one year after pills intake, SBP was significantly higher compared to the baseline level. Likewise, the study conducted in Korea [20] found similar results with current research that is prolonged use of oral contraceptive related to increased blood pressure than non-users. A cross-sectional study on blood pressure in women using COC pills in England [21] found that blood pressure among users was significantly higher than the controls. The Chronic use of COCs, irrespective of estrogen concentration, can increase blood pressure in both normal and hypertensive women [22]. A similar study of hypertension among users of oral contraceptive pills conducted in Texas showed an increased blood pressure in both over the counter and clinic users of the pill [23]. Contrary to the present study, a follow-up study conducted in Minnesota, (24) reported that pill-users had a decrease in SBP and DBP after the 3rd, 6th, and12th month of follow-up. Earlier studies have shown the relationship between use of the contraceptive pill and raise of blood pressure [25]. Recent research also highlighted that, estrogen containing hormonal contraceptives always changes the blood pressure by increasing hepatic production of angiotensinogen, which in turn causes the renin-angiotensin-aldosterone system to elevate the blood pressure [26, 27].
COC use, Body weight and BMI
Results from this study showed that users of pills had significant weight gains and increased BMI compared to control groups. This is in line with a study carried out in Thailand [28] on the effect of the use of COC pills on BMI and blood pressure, according to which the use of pills containing estrogen and progestin tends to increase BMI and body weight. Another study of the effect of COC pills on lipid profile, blood pressure and BMI in Pakistan [18] also showed similar results with this report. While another study in Minnesota indicated that pills users pose increased body weight in comparison to their controls, however, changes were not statistically significant [24]. The disparity found between the studies could be attributed to the difference in race associated with a genetic weight gain predisposition, where black women had a higher mean weight gain compared to white [29]. However, the existing literature does not provide a clear picture of the mechanism of COC pills use related weight gain. Theoretically, the biological mechanism for contraceptive-induced weight gain could be attributed to fluid retention secondary to the activation of the mineralocorticoid and/or renin-angiotensin-aldosterone system and/or an increase in subcutaneous fat secondary to an increase in appetite and food intake caused by hormones [30,31].
Table 3
Mean Changes in Serum FBS Level, SBP, DBP, MAP, Weight, and BMI in COC Users with Relation to the Duration of Use, in Chencha South Ethiopia.
Parameters | Duration use (Month) | N = 110 | M ± SD | P-value |
Change in mean FBS (mg/dL) | 3–12 13–24 ≥ 25 | 42 50 18 | 87.3 ± 6.40 89.9 ± 5.96 87.7 ± 13.73 | 0.27 |
Change in mean SBP (mm Hg) | 3–12 13–24 ≥ 25 | 42 50 18 | 115.2 ± 5.52 125.6 ± 6.44 126.7 ± 6.86 | 0.000** |
Change in mean DBP (mm Hg) | 3–12 13–24 ≥ 25 | 42 50 18 | 70.0 ± 9.37 74.6 ± 7.62 74.4 ± 7.84 | 0.024* |
Change in mean MAP(mm Hg) | 3–12 13–24 ≥ 25 | 42 50 18 | 83.3 ± 9.45 91.1 ± 6.16 91.4 ± 6.47 | 0.000** |
Change in mean Weight (kg) | 3–12 13–24 ≥ 25 | 42 50 18 | 56.5 ± 4.98 56.1 ± 3.88 57.8 ± 6.87 | 0.46 |
Change in mean BMI (kg/m2) | 3–12 13–24 ≥ 25 | 42 50 18 | 21.3 ± 2.16 20.9 ± 1.93 22.6 ± 3.13 | 0.03* |
Where: BMI = Body mass index, FBS = fasting blood sugar, DBP = diastolic blood pressure, MAP = mean arterial blood pressure, SBP = systolic blood pressure, *=statistically significant, **=highly significant (P < 0.001), variables statistically significant at P < 0.05 and P-values were obtained by one-way ANOVA. |