Etonogestrel

Etonogestrel is a synthetic progestin, the active metabolite of desogestrel. In the Nexplanon implant, it is released continuously under the skin and prevents pregnancy through three actions that work together. It suppresses ovulation, so the ovary no longer releases an egg each cycle. It thickens the cervical mucus, the fluid that closes off the entrance to the uterus and blocks the passage of sperm. Finally, it alters the endometrium, the lining that covers the inside of the uterus.

Once in the bloodstream, etonogestrel circulates bound to transport proteins, about 32 % to SHBG (the globulin that binds sex hormones) and 66 % to albumin. The liver breaks it down using a specific enzyme, cytochrome P450 3A4, often shortened to CYP3A4. Its elimination half-life is around 25 hours, which explains the slow, steady release provided by the implant. This enzymatic pathway is also the key to the drug interactions described further on.

The implant is indicated to prevent pregnancy, with an effectiveness that lasts up to five years. It is a single small rod, inserted under the skin on the inner side of the upper arm by a healthcare professional. It then releases etonogestrel continuously, without any surge. Insertion is ideally done within the first five days of the menstrual cycle, which ensures protection right away.

Its great advantage lies in how simple it is to use. There is no tablet to swallow every day, no strict schedule to keep, no constraint tied to meals. Contraception therefore no longer depends on the regularity of a daily dose. Removal, like insertion, is a matter for the healthcare professional: you do not handle the implant yourself, and any decision to stop is discussed during a consultation.

The most common effect concerns bleeding. The menstrual pattern changes: irregular and unpredictable bleeding, light spotting between periods, or on the contrary a complete absence of periods. This change in bleeding is the leading reason for stopping the implant, since it led 11.1 % of users to have it removed in clinical trials. The other reasons for discontinuation remain far rarer: emotional lability and weight gain at 2.3 % each, headaches at 1.6 %, acne at 1.3 %, depression at 1.0 %.

Among the effects reported by at least 5 % of users are headaches, in nearly one woman in four (24.9 %), then vaginitis (14.5 %), weight gain (13.7 %), acne (13.5 %), breast pain (12.8 %), abdominal pain (10.9 %) and pharyngitis (10.5 %). Most of these effects remain tolerable and do not require removal of the implant. It is the discomfort linked to bleeding, more than these symptoms, that weighs most heavily in the decision to stop.

Weight gain comes up often in questions. In the American studies, it averaged around 1.3 kg after one year and around 1.7 kg after two years. These are averages: individual variation can be wider, in either direction. The order of magnitude remains modest over time.

On the metabolic side, the implant can induce slight insulin resistance and small changes in blood sugar, whose clinical significance is not established. The summary of product characteristics therefore recommends closely monitoring women who are prediabetic or diabetic, on the sugar side as well as the lipid side. As for blood pressure, hypertension that develops during treatment, or a rise that antihypertensive treatment fails to control, leads to removing the implant. These points fall under regular medical follow-up.

Since the liver breaks down etonogestrel via CYP3A4, anything that stimulates this enzyme speeds up its elimination and can lower contraceptive effectiveness. These inducers are numerous: rifampicin, rifabutin, phenytoin, barbiturates, carbamazepine, oxcarbazepine, topiramate, felbamate, griseofulvin, bosentan, efavirenz, aprepitant, rufinamide, as well as products containing St John’s wort. This last plant, sold over the counter, deserves particular vigilance because it is often wrongly associated with the idea of harmlessness. Conversely, CYP3A4 inhibitors such as itraconazole, voriconazole, fluconazole, ketoconazole or grapefruit juice can increase etonogestrel concentrations.

Breastfeeding is compatible with this contraception. Etonogestrel passes into milk in very small amounts, on the order of 178 ng/L at one month and 131 ng/L at four months, and no difference in milk volume or composition has been observed compared with a non-hormonal IUD. Expert opinion considers progestin-only contraceptives acceptable for a breastfeeding woman. Follow-up mainly consists of assessing how well the bleeding is tolerated, checking blood pressure and staying attentive to sugar metabolism in women at risk.

A diet rich in micronutrients supports the body whatever the method of contraception. Folate, vitamin B9, is plentiful in lentils, chickpeas and spinach, as well as in broccoli. Vitamin B6 is found in bananas, salmon and sunflower seeds. Zinc is well represented in pumpkin seeds and red meat, while magnesium is concentrated in almonds, dark chocolate and again spinach. These four reference points cover a real share of daily needs.

One point of vigilance deserves to be stated precisely. The literature describing a drop in folate, B6, zinc and magnesium under contraception concerns combined pills, those that pair an estrogen with a progestin. The etonogestrel implant, for its part, delivers only a progestin alone, and this effect on micronutrients is neither established nor demonstrated with it. A targeted intake therefore does not correct a presumed deficiency: it simply completes a plate that, in practice, rarely reaches every reference point. That is the meaning of a supplement conceived in addition to your contraception, never in its place.