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Medical effects of detransition
Those who have medically transitioned and later detransition face lasting bodily changes. Part of those changes is completely irreversible. The term "reversible", often used in information given before and during transition, is not correct for a large part of the effects described here. This page describes the medical reality as it is increasingly being documented — including aspects that have been structurally under-exposed in pre-transition information.
Irreversible voice change (FTM)
Testosterone causes lengthening and thickening of the vocal cords. The effect occurs within a few months to a year. On stopping testosterone, the voice does not recover. The lowered, masculine-sounding voice is permanent. For someone who started as a young woman and later detransitions, this is one of the most prominent, daily-experienced consequences: on the phone, in shops, with every new acquaintance she is taken for a man. Speech therapy can to a limited extent help stretch the voice range, but the physical change in the vocal cords themselves is permanent.
Loss of fertility
Loss of fertility is a core risk that has often been presented too lightly in pre-transition information. For those who, as a child or young teenager, started with puberty blockers followed by cross-sex hormones without ever going through their own puberty, functional gamete tissue was in fact never developed. Fertility preservation is then impossible: there are no eggs or sperm to freeze.
In adults using hormones long-term, fertility can decrease or disappear. In FTM, testosterone can lead to anovulation and atrophy of ovarian tissue; how far this is reversible after stopping is uncertain on an individual basis and not guaranteed. In MTF, oestrogen can lead to lasting decline of spermatogenesis. Those who have undergone gonadectomy (removal of ovaries or testicles) are permanently infertile.
For young people who at the time of treatment simply could not oversee the consequences of childlessness, this is a far-reaching and growing point of criticism of the existing care model.
Sexual dysfunction
Sexual function is profoundly affected by hormone therapy and surgery. In MTF, after long-term oestrogen + anti-androgens, erectile function and libido are often greatly reduced or absent; recovery after stopping is variable and not always complete. After vaginoplasty, genital sensitivity is sometimes reduced; orgasm is possible but different from before.
In FTM, testosterone changes the genital anatomy (clitoral hypertrophy remains permanent) and sexual experience. After phalloplasty or metoidioplasty, complications such as nerve damage, loss of sensation and functional limitation are well documented.
A particularly serious category concerns young people started on puberty blockers before sexual maturation. They never developed adult sexual function. International testimonies — including in the Cass documents — describe anorgasmia and lasting sexual dysfunction as a realistic consequence, not as a rare exception.
Breast tissue: lasting changes
A performed mastectomy (in FTM) cannot be reversed. Breast reconstruction with implants and fat injections is possible but never restores the original tissue; nipple sensitivity remains limited or absent. For someone who as a young teenager underwent a mastectomy and later detransitions, this is a lifelong consequence of an intervention for which fully informed consent could not possibly have been given at that age.
In MTF, breast formation after oestrogen is often partly permanent. Full return to pre-treatment anatomy is usually not possible; surgical removal always leaves traces.
Complications after genital surgery
Genital surgery has a significant complication profile that is rarely explicitly mentioned in public information. Vaginoplasty can lead to fistulas (urethral or rectovaginal), stenosis of the neovaginal canal (necessitating lifelong dilation to keep the canal open), bleeding, granulation tissue and chronic pain. Phalloplasty has one of the highest complication profiles in plastic surgery: urethral stricture or fistula occur frequently, repeat revision surgery is the rule rather than the exception, and functional outcomes vary widely.
In detransition these interventions cannot be undone. Reconstructive surgery can to a limited extent contribute to a body that looks more like the original sex, but full restoration is anatomically impossible.
Bone, metabolic and heart
Long-term use of puberty blockers in a phase in which bone density is normally built up produces structurally lower peak bone mass. This gives an increased risk of osteoporosis later in life. For young people who later detransition this is a lasting metabolic legacy. Cross-sex hormones bring their own risks: oestrogen increases the risk of thrombosis, testosterone affects lipid profile and possibly cardiovascular risk. After stopping this normalises in part, but the damage done during the blocker period can no longer be caught up.
Endocrine dysregulation after stopping
Abruptly stopping hormone therapy can cause complaints: mood swings, hot flushes, fatigue, change in libido. Endocrinological support on stopping is medically indicated. In practice this is poorly organised in the Netherlands — there is no fixed care pathway for detransitioners — and many patients stop on their own, with all the associated risks.
After-care: a gap in the system
Dutch care is set up for transition, not for detransition. Specialised clinics for detransitioners do not exist. Endocrinologists, gynaecologists, urologists and plastic surgeons outside the specialised gender centres rarely have experience with this specific patient group. The gender centres themselves are for many detransitioners no longer a safe place.
The Cass Review (United Kingdom, 2024) has explicitly named this gap and recommended that structural, non-stigmatising after-care be set up, separate from the affirmative clinics. For the Netherlands that recommendation remains almost entirely open. At the same time, Cass — together with the Swedish SBU and Finnish COHERE evaluations — emphasises that the evidence base under the original treatments is much weaker than has long been presented: short follow-up, high loss to follow-up, no control groups.