Desogestrel

Desogestrel is a synthetic progestogen. It is a prodrug: the body converts it into its active metabolite, etonogestrel, also called 3-keto-desogestrel, which carries the entire contraceptive effect. This etonogestrel binds to the progesterone receptor, the key through which it drives its effects. Its terminal half-life is around 30 hours, and the blood concentration reaches steady state after four to five days of daily intake.

Its main action is to prevent ovulation. Like other progestogens, it curbs the secretion of GnRH by the hypothalamus and the release of LH and FSH by the pituitary gland, the hormonal signal that normally drives the maturation and then the release of the egg. Added to this central blockade are local effects: desogestrel thickens the cervical mucus, which hinders the passage of sperm, slows the motility of the tubes and thins the endometrium. In trials of the 75 microgram pill, the observed ovulation rate was only 1 percent, that is one user in 103.

This progestogen-only pill is taken without a break: one tablet each day, at roughly the same time, with no interruption between packs. No dietary restriction applies, and it is swallowed with or without a meal. Regularity matters, because protection rests on a stable hormone concentration and the half-life of etonogestrel is short. This contraceptive is not stopped on one’s own initiative: any interruption is decided with the professional who prescribed it.

The margin in the event of a missed dose is narrow. If the delay stays under 12 hours, contraceptive protection is maintained: simply take the tablet as soon as possible, then continue at the usual time. Beyond 12 hours, efficacy is no longer guaranteed: take the last missed tablet, continue the pack and add a barrier method for the following seven days. This short window follows directly from the speed with which the body eliminates etonogestrel.

The most expected change affects menstruation. A change in the bleeding pattern, irregular bleeding, spotting between cycles or a complete absence of periods, concerns up to half of users. Irregular periods and amenorrhoea are indeed among the common effects, reported in at least one user in a hundred. This pattern stems from the action of the progestogen on the endometrium, which it keeps thin.

This thinning of the uterine lining, endometrial atrophy, locally extends the contraceptive mechanism. It explains why bleeding becomes unpredictable, lighter, or stops altogether. Dysmenorrhoea, that is painful periods, appears uncommonly, in fewer than one user in a hundred. An ovarian cyst may occur within this same frequency range, between one user in a thousand and one in a hundred.

Several common effects, defined as affecting at least one user in a hundred and fewer than one in ten, are worth knowing. Reported are an altered mood, a depressed mood, a drop in libido, headaches, nausea, acne, breast pain and weight gain. Their intensity varies from one person to another and none of these effects occurs systematically. Spotting them early makes it possible to raise them at the right moment with the prescriber.

Uncommon effects, between one user in a thousand and one in a hundred, include vomiting and fatigue. Rarer still, below one in a thousand, are a skin rash, urticaria and erythema nodosum. Furthermore, desogestrel lowers estradiol at the level of the early follicular phase; it is not yet known whether this decrease has a clinically relevant effect on bone mineral density.

Certain combinations reduce the efficacy of desogestrel. Inducers of liver enzymes, in particular inducers of cytochrome P450 3A4, speed up its elimination and lower its blood concentrations. Concerned are rifampicin, carbamazepine, phenytoin and St John’s wort, among others. During these treatments and for the 28 days that follow their discontinuation, a barrier method is recommended in addition to the pill.

Medical monitoring accompanies this contraceptive. It includes an annual examination with measurement of blood pressure, examination of the breasts, abdomen and pelvic organs, as well as cervical cytology. When desogestrel is combined with an oestrogen in a combined pill, other parameters shift: a decrease in glucose tolerance appears in a proportion of users, the carrier protein for sex hormones (SHBG) rises markedly, going from 150 to 230 nmol/L between the first and twenty-first day of the third treatment cycle, and HDL cholesterol may decrease. These elements guide the biological points of vigilance.

Diet meets this treatment on one precise point: folate, that is vitamin B9. Oral contraception can lower the level of folate circulating in the blood. Yet this folate comes mainly from the plate: dark green leafy vegetables such as spinach and kale, legumes such as lentils and beans, and citrus fruit, foremost among them the orange. Building meals around these foods supports the baseline intake.

Vitamin B9 holds a particular place for a woman of childbearing age, because it acts very early in a pregnancy, sometimes even before it is known. A plate rich in green vegetables, legumes and fruit covers a good part of the daily need. When this intake stays on the low side, a targeted supplement makes sense, in addition to your treatment, never in its place.