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What are the effects of blocking puberty in females?

Pubertal development in females requires the reception of sex hormones through the hypothalamic-pituitary-gonadal axis. Block this axis, as puberty blockers do, and you'll end up with a host of physical and cognitive issues.

Researchers have tested the effects of blocking this axis in female mice. For example, when puberty suppressors are given to female mice, there is reduced bone mass acquisition and bone strength; increased risk of obesity; decreased uterine and ovarian weights; completely absent follicle maturation (no mature eggs produced); and a lack of a reproductive cycle. In females, reproductive cycles create cyclical hormone levels of estrogen and progesterone that rise and fall, essential for maintaining healthy anatomy and physiology.

On the psychological and behavioral level, there is inhibition of feeding (hyponeophagia) matched with hyperactivity in the dentate gyrus of the hippocampus, signifying high anxiety; despair-like behavior; and negative mood regulation.

In other animals like sheep, it's been shown that blocking puberty also permanently impairs long-term spatial reference memory even after the drugs are stopped, reflecting a time-limited period of hippocampal plasticity where a specific window around puberty is required for its maturation. This is particularly concerning knowing that the hippocampus is essential for learning, memory, and spatial navigation.

These findings in mice and sheep match with what we see in trans-identifying females whose puberty is blocked by gonadotropin-releasing hormone (GnRH) antagonists and agonists, which reduce sex hormone levels to castration levels within 30 days and halt the reproductive cycle. In human females, GnRH analogue usage around puberty increases emotional reactivity, including emotional and behavioral responses to fearful situations; decreases long-term decision making; and it also decreases the resting heart rate. It also is associated with a higher risk of osteoporosis and cardiovascular disease.

GnRH analogues have their place in medicine, but they are not designed to be used long term at consistent doses and certainly not to block puberty, where the important physical and neurological maturation is essential for long term health.

[1] Dela Cruz, C., Kinnear, H., Hashim, P., et al. (2023). A mouse model mimicking gender-affirming treatment with pubertal suppression followed by testosterone in transmasculine youth. Human Reproduction, 38(2).

[2] Anacker, C., Sydnor, E., Chen, B., et al. (2021). Behavioral and neurobiological effects of GnRH agonist treatment in mice—potential implications for puberty suppression in transgender individuals. Neuropsychopharmacology, 46.

[3] de Tassigny, X., Fagg, L., Dixon, J., Colledge, W. (2007). Hypogonadotropic hypogonadism in mice lacking a functional Kiss1 gene. Biological Sciences, 104(25).

[4] Xu, L., Li, H., Liu, S., et al. (2022). Constitutional delay of growth and puberty in female mice is induced by circadian rhythm disruption in utero. Ecotoxicology and Environmental Safety, 241.

[5] Hough, D., Bellingham, M., Haraldsen, I., et al. (2017). Spatial memory is impaired by peripubertal GnRH agonist treatment and testosterone replacement in sheep. Psychoneuroendocrinology, 75.

[6] Novara, G., et al. (2009). Impact of Surgical and Medical Castration on Serum Testosterone Level in Prostate Cancer Patients. Urol Int, 82(3).

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