Take a loooong breath out
Feeling overwhelmed, panicked or distressed? Rectangular breathing can help. Breathe in for 3 and out for 6. Repeat until you feel calm.
Ask any late‑discovered neurodivergent woman "When were you diagnosed?". She will likely tell you after pregnancy or menopause. Turns out almost every mental health condition fluctuates with our hormones. This is called premenstrual exacerbation (PME). For neurodivergent women it can be a monthly rollercoaster.
What is more, research shows we are more likely to struggle with menstrual disorders and hormonal mood disorders, particularly premenstrual dysphoric disorder (PMDD), than our neurotypical peers.
PME is the exacerbation of an existing physical or mental health condition caused by changes in hormones during the luteal phase of your cycle. Conditions that worsen with PME include:
ADHD symptoms and sensory sensitivity in autism worsen with hormonal fluctuations related to the menstrual cycle, pregnancy and menopause. Neurodivergent girls are at higher risk of developing anxiety, depression and eating disorders during the onset of puberty.
Neurodivergent women are more likely to seek a diagnosis during hormonal transitions such as after the birth of a child and menopause when sex hormones drop and the risk of depression and anxiety increases. Stress, anxiety and depression can exacerbate undiagnosed ADHD or increase sensory sensitivity in autistic women, unmasking underlying neurodivergence.
PMDD is a lesser known hormonal mood disorder that affects neurodivergent women at elevated rates. PMDD is triggered by the fluctuations of hormones in the luteal phase of your cycle and sometimes the first few days of menstruation. Symptoms include:
PMDD is caused by the brain reacting to changes in hormone levels, particularly progesterone and oestrogen. PMDD is not caused by a hormonal imbalance.
GABA (gamma-aminobutyric acid) is a neurotransmitter that has a calming effect on the body and mind. In people with PMDD the GABA receptors are thought to be different, leading to dysregulation during the luteal phase of a woman's cycle.
Distinguishing between PME and PMDD can be tricky. You will need to track symptoms for three months in order to support a differential diagnosis.
The monthly rollercoaster is the rise and fall of your hormones across your cycle, and the ride your brain takes with them.
Oestrogen boosts dopamine, the brain chemical behind focus, motivation and reward.1 It works alongside vitamin D, which helps switch on the enzyme your brain uses to make dopamine,2 and vitamin D needs magnesium to become active.3 Run short of any of the three and your dopamine supply suffers. When oestrogen is high, an ADHD brain gets extra support. When it falls, ADHD symptoms rise,4 and your ADHD medication can feel like it has stopped working.5
In the first half of your cycle, oestrogen climbs towards ovulation, and energy, confidence and focus often climb with it. So can sensory distress: many women find smells, sounds and touch far stronger around ovulation. Oestrogen also prompts mast cells to release histamine, so allergies can flare.6 If you have bipolar disorder, your mood episodes may follow your cycle too.7 Migraines are most likely in the days around the start of your period, when oestrogen falls.8 ADHD women are more likely to get migraines in the first place, and early research suggests the same may be true for autistic women.9,10
After ovulation, your body makes progesterone, which turns into allopregnanolone, a calming hormone that works through GABA, your brain's main brake.11 If you don't ovulate, you don't make progesterone, and the brake never arrives. In PMDD, the brain responds differently to allopregnanolone, so even a regular cycle can leave you without it.11 With nothing to calm your body down, everything turns up: sensory distress, chronic pain, IBS, asthma and emotional dysregulation.
Emotional dysregulation and impulsivity go hand in hand. This is part of why women are more likely to lose control in the second half of their cycle. Emotional eating peaks after ovulation,12 binge drinking rises as progesterone falls,13 and self-injurious behaviour becomes more likely.14 It is a nervous system running without its brakes.
The days just before your period, and the first few days of it, are the danger zone. Oestrogen is at its lowest, and research shows suicide attempts are more common at this point in the cycle.14,15 But your cycle is predictable. When you track it, you can see the danger zone coming, plan for it and take back some control. Uma can help you do that.
Try our free anonymous PMDD mini‑screen. Real-time scoring - no email sign up necessary.
Discover if your symptoms describe PMDD. Questions relate to the days before your period.
There is no official screening questionnaire for PMDD. The questions that follow are based on the DSM-5 diagnostic criteria for premenstrual dysphoric disorder, written in the first person and simplified to a yes or no answer. A diagnosis needs symptoms tracked daily across at least two cycles.
American Psychiatric Association. (2013). Diagnostic and Statistical Manual of Mental Disorders (5th ed.). Premenstrual Dysphoric Disorder. https://doi.org/10.1176/appi.books.9780890425596
These questions ask about low mood, hopelessness and feeling out of control. Some people might find these questions triggering. Use the SOS button for crisis signposting.
In the few days before my period, I have marked mood swings, sudden sadness or tearfulness, or I become much more sensitive to rejection.
In the few days before my period, I am irritable or angry, or I have more conflict with the people around me.
In the few days before my period, my mood is low, or I feel hopeless, or I have self-critical thoughts.
In the few days before my period, I feel anxious, tense, keyed up or on edge.
In the few days before my period, I lose interest in my usual activities.
In the few days before my period, I find it harder to concentrate.
In the few days before my period, I feel lethargic, tire easily, or have a marked lack of energy.
In the few days before my period, my appetite changes, with overeating or specific food cravings.
In the few days before my period, I sleep much more than usual, or I cannot sleep.
In the few days before my period, I feel overwhelmed or out of control.
In the few days before my period, I have physical symptoms such as breast tenderness or swelling, joint or muscle pain, bloating or weight gain.
These symptoms cause me real distress, or they get in the way of my work, studies, social life or relationships.
In most of my cycles these symptoms start to improve within a few days of my period starting, and are gone in the week after.
PMDD is not a hormone imbalance. Your nervous system is more sensitive to the hormone changes of an ordinary cycle.
Feeling overwhelmed, panicked or distressed? Rectangular breathing can help. Breathe in for 3 and out for 6. Repeat until you feel calm.
You don't need to deal with these thoughts alone. Talking to a human being and putting your feelings into words can help.
Call 116 123 to talk to a Samaritan. They have volunteers trained to offer empathy, compassion and emotional support 24 hours a day.
In a shutdown or struggling to verbalise how you're feeling? In the UK you can text SHOUT to 85258 for free text support.
In crisis? Call 111 or visit your local A&E. In Scotland, you can ask for the Distress Brief Intervention (DBI) service via 111 or your GP.
Signposting
The International Association for Premenstrual Disorders is trusted worldwide as a lifeline of support, information, and resources for those affected by PMDD and PME. They offer free symptom tracking tools and PMDD screening.
Signposting
The UK's first PMDD-focused charity. They run online and in person support groups, publish free resources on getting a diagnosis and on PMDD at work, and signpost to local services.
The hypothalamic-pituitary-gonadal (HPG) axis is the two-way conversation between your brain and your ovaries that controls the production of sex hormones including oestrogen, progesterone, and testosterone. It is initiated by the release of Gonadotropin-Releasing Hormone (GnRH) from the hypothalamus, which signals the pituitary gland to release Luteinizing Hormone (LH) and Follicle-Stimulating Hormone (FSH), which in turn regulate the ovaries and trigger ovulation.16
Constantly elevated cortisol suppresses GnRH and can delay or prevent ovulation entirely. This can cause anovulatory cycles (when you do not release an egg) or amenorrhea (where your periods stop).16,17
Without ovulation, your body does not produce a corpus luteum and therefore does not produce progesterone. Progesterone is converted into allopregnanolone, which is important for signalling GABA during the luteal phase of your cycle. GABA is the body's main calming neurotransmitter. When GABA is suppressed, pain, sensory distress, emotional dysregulation, and impulsivity increase, which contribute to severe PMS, PME, or PMDD.11,18
Increased cortisol demand reduces the production of DHEA, which is essential for maintaining healthy levels of sex hormones. When DHEA is suppressed, oestrogen and progesterone levels fall.19,20 Chronic stress can also elevate blood sugar. In women, this reduces oestrogen and can elevate testosterone, creating insulin resistance and increasing the risk of type 2 diabetes and polycystic ovary syndrome (PCOS) or polyendocrine metabolic ovarian syndrome (PMOS).21–23
Oestrogen is a sex hormone that regulates mood, brain function and the menstrual cycle. It acts as a natural antidepressant by supporting serotonin and dopamine production.
That is not a metaphor. Estradiol, the main form of oestrogen in your reproductive years, acts directly on the serotonin, dopamine and glutamate systems in the brain through several different routes.24 Sex hormones shape the adult female brain across every hormonal transition, not just at puberty.1
Progesterone is a sex hormone that calms the nervous system and supports sleep. It is essential for GABA production.
Most of that calming effect is not progesterone itself. Progesterone is converted into other molecules, and those metabolites are what act on the brain's calming system.25 Progesterone rises after ovulation and falls again before your period, so the second half of your cycle is the part where this chemistry is doing the most.
Allopregnanolone is a calming brain chemical made from progesterone. It activates GABA receptors and supports nervous system stability in the second half of the cycle.
It is the single most useful idea on this page, because it connects two things that look unrelated. Progesterone goes up, allopregnanolone goes up with it, and the brain's brake pedal gets pressed harder. Progesterone falls, and it lets go.25
In PMDD, the leading explanation is not that allopregnanolone levels are unusual. It is that the brain responds differently to the ordinary rise and fall of it.26
GABA is the body's main calming neurotransmitter. It is what quietens activity in the brain, the counterweight to the systems that excite it.
The GABA system is not fixed. It is remodelled at every point in life where your hormones shift: puberty, across each menstrual cycle, in pregnancy, after birth, and through the menopause transition.27 That is why the same person can have a different tolerance for noise, light and pressure at different points in a month or a decade.
The follicular phase is the first half of the cycle, from the first day of your period to ovulation. An egg is maturing and oestrogen is climbing.
It is also the part that varies most. An analysis of more than 600,000 cycles found that cycle length varies far more than the textbook 28 days suggests, and that almost all of the variation sits in the follicular phase rather than the second half.28
The luteal phase is the second half of the cycle, from ovulation to your period. Progesterone and allopregnanolone are at their highest, then drop away in the days before you bleed.25
Unlike the follicular phase, this half is fairly consistent in length from person to person.28 If something happens to you at the same point every month, this is usually where it sits.
Rising oestrogen is the trigger, but not directly. Oestrogen acts on a group of brain cells called kisspeptin neurons, and those cells are what set off the surge of luteinising hormone that releases the egg.29
This matters for the rest of the page, because those same neurons are sensitive to stress, weight and illness. Ovulation is a brain event before it is an ovary event.
A cycle in which ovulation does not happen. You can still bleed. That is the part most people do not know, and it is why a regular-looking cycle is not proof that everything underneath it is happening.
Chronic stress is one recognised route to it, acting on the same brain signalling that sets ovulation off.30 No ovulation means no corpus luteum, which means no proper progesterone rise, which means no allopregnanolone rise either.
Periods stopping without pregnancy or menopause has several recognised causes, and the most common in otherwise healthy women is functional hypothalamic amenorrhoea: the brain turns the reproductive system down in response to energy shortage, weight loss, heavy exercise or sustained stress.16,31
It is described in the literature as a stress-based condition, not a failure of the ovaries.17 This is one to take to a doctor rather than wait out, because the consequences of low oestrogen over time reach beyond fertility.
PMS, premenstrual syndrome, is physical and emotional symptoms in the luteal phase that ease once your period starts. It is common and it is real, and it is less severe than PMDD.
A meta-analysis of menstrual cycle effects on mental health found the pattern is genuine rather than imagined, and also that the size of the effect is smaller than popular accounts suggest.15 Both of those things can be true at once.
PMDD, premenstrual dysphoric disorder, is a severe form of premenstrual disturbance with significant mood disruption in the luteal phase. It is recognised in the Diagnostic and Statistical Manual of Mental Disorders (DSM-5).
The leading explanation is not unusual hormone levels. It is an altered sensitivity in the brain to the ordinary rise and fall of allopregnanolone across the cycle.26 Women with PMDD are not producing the wrong hormones. Their brains respond differently to the right ones.
It is also more common in ADHD women. A cross-sectional survey of 715 people found a raised rate of provisional PMDD among ADHD women.32
Premenstrual exacerbation, PME, is when something you already have gets worse in the luteal phase. PMDD is a condition in its own right that appears in the luteal phase and lifts when you bleed.33
That distinction is the most useful thing on this page for neurodivergent women, and it is routinely missed. If your ADHD, autistic experience, anxiety or depression gets louder every month rather than being replaced by something new, that is PME, not PMDD.33
The review that sets this out also says plainly how much is not yet known about it.33 It is an under-researched area, not a settled one.
Yes. That is exactly what premenstrual exacerbation describes.33
Reproductive steroid levels across the cycle have been linked to ADHD symptom levels.4 A narrative review of cycle-related hormonal change in ADHD reports attention and executive function worsening in the luteal phase, particularly in the days before a period.34
The evidence base is small and the studies are heterogeneous, which the systematic review of ADHD and sex hormones says directly.35 The pattern is reported consistently. The size of it is not established.
Autistic adults report that menstruation and menopause matter to them in ways the research had largely ignored until recently, including changes in how they cope with sensory input and with everyday demands.36
A plausible mechanism sits in the GABA system, which is remodelled at each hormonal transition and is the system that decides how much incoming signal gets damped down.27 That is a mechanism worth knowing about, not a proven explanation, and nobody has yet measured sensory thresholds across the cycle in autistic women.
Your sensory sensitivity and the distress it causes can shift. Your autistic traits are not getting worse.
Migraine attacks cluster around menstruation. A study tracking incidence against cycle phase found the risk highest in the two days before bleeding and the first three days of it, the window where oestrogen drops most steeply.8
It is the withdrawal rather than the level that matters. A steady low level of oestrogen does not provoke attacks in the same way that a fall does.
Migraine is also more common in ADHD people than in the general population, which a systematic review and meta-analysis established.9
Because oestrogen acts on mast cells, the immune cells that release histamine. Estradiol activates them through a rapid, non-genomic route involving calcium, and mast cells from animals lacking the relevant oestrogen receptor do not respond to it.37,38
That mechanism comes from cell and animal work. The human side is observational: oestrogen is known to affect allergy and asthma, and a substantial proportion of women with asthma report their symptoms worsening around menstruation.6,37
So the mechanism is established in the laboratory and the monthly pattern is an observed association in women. Those are two different strengths of evidence and Uma will not merge them.
The honest answer is that cognitive change across the cycle is reported and the mechanism is not pinned down.
In ADHD women, a narrative review describes attention and executive function worsening in the luteal phase.34 The candidate mechanisms are oestrogen's effect on dopamine and serotonin signalling24 and the remodelling of the GABA system at hormonal transitions.27
Both are established as mechanisms in their own right. Neither has been shown to be the cause of what you experience as fog.
Perimenopause is the transition towards menopause, when cycles become irregular and hormone levels swing rather than decline smoothly. It commonly begins in the forties and can start earlier, and it is defined by that instability rather than by an age.18
The swinging is the point. Perimenopause is not a slow fade. It is a period of large, unpredictable fluctuation, which is why symptoms can be worse during it than after it.
This is one of the most common things late‑discovered women describe, and the research has only recently caught up with it.
A 2025 review by a large international group sets out how hormonal change across a woman's life interacts with mood, cognition and health in ADHD, and says plainly that research into the later transitions is almost entirely absent.39 The systematic review of ADHD and sex hormones reaches the same conclusion: symptoms appear to shift across hormonal life stages, and the evidence is sparse and mostly from small studies.35
So: widely reported, mechanistically plausible given what oestrogen does to dopamine signalling24, and not yet properly studied. Anyone who tells you it is settled science is overstating it, and anyone who tells you it is imaginary is ignoring both the reports and the mechanism.
Each of these is a hormonal transition, and the brain's calming system is remodelled at every one of them.27
In ADHD specifically, symptoms appear to shift across puberty, the menstrual cycle and pregnancy, but the evidence is sparse and the studies are small.35 The 2025 review of female ADHD describes the whole lifespan picture as under-researched, with the gaps largest exactly where women report the biggest changes.39
If it feels as though nobody has studied what happened to you after your baby was born, that is because, largely, nobody has.
This comes up constantly and it deserves a careful answer rather than a confident one.
Reviews of cycle-related hormonal change in ADHD report that some women describe their medication feeling less effective in the luteal phase.34 Female-specific pharmacotherapy in ADHD has been written about as an open question rather than an established practice.5 The systematic review of ADHD and sex hormones concludes that the evidence across all of these questions is limited and heterogeneous.35
Uma is not going to tell you what that means for your prescription, because that is a conversation with the person who prescribes it. What Uma will say is that if you have noticed a pattern, it is a pattern many women report.
This is the question most likely to be answered badly in either direction, so here is what the studies found.
A Danish national cohort of 1,061,997 women, followed over 6.8 million person-years, found a raised rate of first antidepressant use among users of hormonal contraception: a relative risk of 1.23 for combined pills and 1.34 for progestogen-only, rising to 1.8 and 2.2 in 15 to 19 year olds.40 A second Danish study by the same group looked at more serious outcomes and reported a raised risk there too.41
Later work complicates it rather than confirming it. A Finnish nationwide case-control study and a Swedish prospective cohort both examined the same association and found the picture varies considerably across different groups of women.42,43 A 2022 review sets out where the evidence currently sits.44
Relative risk is not the same as likelihood. A raised relative risk on a low baseline is still a low absolute chance for most people. And none of this is a reason to change or stop anything without talking to the person who prescribed it.
Mood does track the cycle, and it has been measured. A meta-analysis of menstrual cycle effects on mental health outcomes found real effects and also found them smaller than popular accounts imply.15
The reason this page exists is that for neurodivergent women the pattern is often not a small wobble but everything already there getting louder every month, which is premenstrual exacerbation rather than ordinary premenstrual change.33
Tracking it across two or three cycles is what turns a feeling into information you can take to an appointment.
1. Barth, C., Villringer, A., & Sacher, J. (2015). Sex hormones affect neurotransmitters and shape the adult female brain during hormonal transition periods. Frontiers in Neuroscience, 9, Article 37. https://doi.org/10.3389/fnins.2015.00037
2. Cui, X., Pertile, R., Liu, P., & Eyles, D. W. (2015). Vitamin D regulates tyrosine hydroxylase expression: N-cadherin a possible mediator. Neuroscience, 304, 90–100. https://doi.org/10.1016/j.neuroscience.2015.07.048
3. Uwitonze, A. M., & Razzaque, M. S. (2018). Role of magnesium in vitamin D activation and function. The Journal of the American Osteopathic Association, 118(3), 181–189. https://doi.org/10.7556/jaoa.2018.037
4. Roberts, B., Eisenlohr-Moul, T., & Martel, M. M. (2018). Reproductive steroids and ADHD symptoms across the menstrual cycle. Psychoneuroendocrinology, 88, 105–114. https://doi.org/10.1016/j.psyneuen.2017.11.015
5. de Jong, M., Wynchank, D. S. M. R., van Andel, E., Beekman, A. T. F., & Kooij, J. J. S. (2023). Female-specific pharmacotherapy in ADHD: Premenstrual adjustment of psychostimulant dosage. Frontiers in Psychiatry, 14, Article 1306194. https://doi.org/10.3389/fpsyt.2023.1306194
6. Bonds, R. S., & Midoro-Horiuti, T. (2013). Estrogen effects in allergy and asthma. Current Opinion in Allergy and Clinical Immunology, 13(1), 92–99. https://doi.org/10.1097/ACI.0b013e32835a6dd6
7. Teatero, M. L., Mazmanian, D., & Sharma, V. (2014). Effects of the menstrual cycle on bipolar disorder. Bipolar Disorders, 16(1), 22–36. https://doi.org/10.1111/bdi.12138
8. MacGregor, E. A., Frith, A., Ellis, J., Aspinall, L., & Hackshaw, A. (2006). Incidence of migraine relative to menstrual cycle phases of rising and falling estrogen. Neurology, 67(12), 2154–2158. https://doi.org/10.1212/01.wnl.0000233888.18228.19
9. Salem, H., Vivas, D., Cao, F., Kazimi, I. F., Teixeira, A. L., & Zeni, C. P. (2018). ADHD is associated with migraine: A systematic review and meta-analysis. European Child & Adolescent Psychiatry, 27(3), 267–277. https://doi.org/10.1007/s00787-017-1045-4
10. Vetri, L. (2020). Autism and migraine: An unexplored association? Brain Sciences, 10(9), Article 615. https://doi.org/10.3390/brainsci10090615
11. Gao, Q., Sun, W., Wang, Y.-R., Li, Z.-F., Zhao, F., Geng, X.-W., Xu, K.-Y., Chen, D., Liu, K., Xing, Y., Liu, W., & Wei, S. (2023). Role of allopregnanolone-mediated γ-aminobutyric acid A receptor sensitivity in the pathogenesis of premenstrual dysphoric disorder: Toward precise targets for translational medicine and drug development. Frontiers in Psychiatry, 14, Article 1140796. https://doi.org/10.3389/fpsyt.2023.1140796
12. Klump, K. L., Keel, P. K., Racine, S. E., Burt, S. A., Neale, M., Sisk, C. L., Boker, S., & Hu, J. Y. (2013). The interactive effects of estrogen and progesterone on changes in emotional eating across the menstrual cycle. Journal of Abnormal Psychology, 122(1), 131–137. https://doi.org/10.1037/a0029524
13. Martel, M. M., Eisenlohr-Moul, T., & Roberts, B. (2017). Interactive effects of ovarian steroid hormones on alcohol use and binge drinking across the menstrual cycle. Journal of Abnormal Psychology, 126(8), 1104–1113. https://doi.org/10.1037/abn0000304
14. Saunders, K. E. A., & Hawton, K. (2006). Suicidal behaviour and the menstrual cycle. Psychological Medicine, 36(7), 901–912. https://doi.org/10.1017/S0033291706007392
15. Jang, D., & Elfenbein, H. A. (2019). Menstrual cycle effects on mental health outcomes: A meta-analysis. Archives of Suicide Research, 23(2), 312–332. https://doi.org/10.1080/13811118.2018.1430638
16. Fourman, L. T., & Fazeli, P. K. (2015). Neuroendocrine causes of amenorrhea: An update. The Journal of Clinical Endocrinology & Metabolism, 100(3), 812–824. https://doi.org/10.1210/jc.2014-3344
17. Podfigurna, A., & Meczekalski, B. (2021). Functional hypothalamic amenorrhea: A stress-based disease. Endocrines, 2(3), 203–211. https://doi.org/10.3390/endocrines2030020
18. Nappi, R. E., Cucinella, L., Bosoni, D., Righi, A., Battista, F., Molinaro, P., Stincardini, G., Piccinino, M., Rossini, R., & Tiranini, L. (2022). Premenstrual syndrome and premenstrual dysphoric disorder as centrally based disorders. Endocrines, 3(1), 127–138. https://doi.org/10.3390/endocrines3010012
19. Ahmed, T., Qassem, M., & Kyriacou, P. A. (2023). Measuring stress: A review of the current cortisol and dehydroepiandrosterone (DHEA) measurement techniques and considerations for the future of mental health monitoring. Stress, 26(1), 29–42. https://doi.org/10.1080/10253890.2022.2164187
20. Tang, J., Chen, L.-R., & Chen, K.-H. (2021). The utilization of dehydroepiandrosterone as a sexual hormone precursor in premenopausal and postmenopausal women: An overview. Pharmaceuticals, 15(1), Article 46. https://doi.org/10.3390/ph15010046
21. Benjamin, J. J., K., M., Koshy, T., K. N., M., & R., P. (2021). DHEA and polycystic ovarian syndrome: Meta-analysis of case-control studies. PLOS ONE, 16(12), Article e0261552. https://doi.org/10.1371/journal.pone.0261552
22. Ding, H., Zhang, J., Zhang, F., Zhang, S., Chen, X., Liang, W., & Xie, Q. (2021). Resistance to the insulin and elevated level of androgen: A major cause of polycystic ovary syndrome. Frontiers in Endocrinology, 12, Article 741764. https://doi.org/10.3389/fendo.2021.741764
23. Marschalek, M.-L., Marculescu, R., Schneeberger, C., Marschalek, J., Dewailly, D., & Ott, J. (2023). A case-control study about markers of stress in normal-/overweight women with polycystic ovary syndrome and in controls. Frontiers in Endocrinology, 14, Article 1173422. https://doi.org/10.3389/fendo.2023.1173422
24. Bendis, P. C., Zimmerman, S., Onisiforou, A., Zanos, P., & Georgiou, P. (2024). The impact of estradiol on serotonin, glutamate, and dopamine systems. Frontiers in Neuroscience, 18, Article 1348551. https://doi.org/10.3389/fnins.2024.1348551
25. Stefaniak, M., Dmoch-Gajzlerska, E., Jankowska, K., Rogowski, A., Kajdy, A., & Maksym, R. B. (2023). Progesterone and its metabolites play a beneficial role in affect regulation in the female brain. Pharmaceuticals, 16(4), 520. https://doi.org/10.3390/ph16040520
26. Hantsoo, L., & Epperson, C. N. (2020). Allopregnanolone in premenstrual dysphoric disorder (PMDD): Evidence for dysregulated sensitivity to GABA-A receptor modulating neuroactive steroids across the menstrual cycle. Neurobiology of Stress, 12, 100213. https://doi.org/10.1016/j.ynstr.2020.100213
27. Gilfarb, R. A., & Leuner, B. (2022). GABA system modifications during periods of hormonal flux across the female lifespan. Frontiers in Behavioral Neuroscience, 16, Article 802530. https://doi.org/10.3389/fnbeh.2022.802530
28. Bull, J. R., Rowland, S. P., Scherwitzl, E. B., Scherwitzl, R., Danielsson, K. G., & Harper, J. (2019). Real-world menstrual cycle characteristics of more than 600,000 menstrual cycles. npj Digital Medicine, 2(1), 83. https://doi.org/10.1038/s41746-019-0152-7
29. Uenoyama, Y., Inoue, N., Nakamura, S., & Tsukamura, H. (2021). Kisspeptin neurons and estrogen–estrogen receptor α signaling: Unraveling the mystery of steroid feedback system regulating mammalian reproduction. International Journal of Molecular Sciences, 22(17), 9229. https://doi.org/10.3390/ijms22179229
30. Vigil, P., Meléndez, J., Soto, H., Petkovic, G., Bernal, Y. A., & Molina, S. (2022). Chronic stress and ovulatory dysfunction: Implications in times of COVID-19. Frontiers in Global Women's Health, 3, Article 866104. https://doi.org/10.3389/fgwh.2022.866104
31. Gordon, C. M., Ackerman, K. E., Berga, S. L., Kaplan, J. R., Mastorakos, G., Misra, M., Murad, M. H., Santoro, N. F., & Warren, M. P. (2017). Functional hypothalamic amenorrhea: An Endocrine Society clinical practice guideline. The Journal of Clinical Endocrinology & Metabolism, 102(5), 1413–1439. https://doi.org/10.1210/jc.2017-00131
32. Broughton, T., Lambert, E., Wertz, J., & Agnew-Blais, J. (2025). Increased risk of provisional premenstrual dysphoric disorder (PMDD) among females with attention-deficit hyperactivity disorder (ADHD): Cross-sectional survey study. The British Journal of Psychiatry, 226(6), 410–417. https://doi.org/10.1192/bjp.2025.104
33. Kuehner, C., & Nayman, S. (2021). Premenstrual exacerbations of mood disorders: Findings and knowledge gaps. Current Psychiatry Reports, 23(11), 78. https://doi.org/10.1007/s11920-021-01286-0
34. Wynchank, D., Sutrisno, R. M. G. T. M. F., van Andel, E., & Kooij, J. J. S. (2025). Menstrual cycle-related hormonal fluctuations in ADHD: Effect on cognitive functioning. A narrative review. Journal of Clinical Medicine, 15(1), 121. https://doi.org/10.3390/jcm15010121
35. Osianlis, E., Thomas, E. H. X., Jenkins, L. M., & Gurvich, C. (2025). ADHD and sex hormones in females: A systematic review. Journal of Attention Disorders, 29(9), 706–723. https://doi.org/10.1177/10870547251332319
36. Groenman, A. P., Torenvliet, C., Radhoe, T. A., Agelink van Rentergem, J. A., & Geurts, H. M. (2021). Menstruation and menopause in autistic adults: Periods of importance? Autism, 26(6), 1563–1572. https://doi.org/10.1177/13623613211059721
37. Zierau, O., Zenclussen, A. C., & Jensen, F. (2012). Role of female sex hormones, estradiol and progesterone, in mast cell behavior. Frontiers in Immunology, 3, 169. https://doi.org/10.3389/fimmu.2012.00169
38. Zaitsu, M., Narita, S.-I., Lambert, K. C., Grady, J. J., Estes, D. M., Curran, E. M., Brooks, E. G., Watson, C. S., Goldblum, R. M., & Midoro-Horiuti, T. (2007). Estradiol activates mast cells via a non-genomic estrogen receptor-α and calcium influx. Molecular Immunology, 44(8), 1977–1985. https://doi.org/10.1016/j.molimm.2006.09.030
39. Kooij, J. J. S., de Jong, M., Agnew-Blais, J., Amoretti, S., Bang Madsen, K., Barclay, I., Bölte, S., Borg Skoglund, C., Broughton, T., Carucci, S., van Dijken, D. K. E., Ernst, J., French, B., Frick, M. A., Galera, C., Groenman, A. P., Kopp Kallner, H., Kerner auch Koerner, J., Kittel-Schneider, S., Manor, I., Martin, J., Matera, E., Parlatini, V., Philipsen, A., Ramos-Quiroga, J. A., Rapoport, I. L., Remnélius, K. L., Sénéquier, A., Thorell, L., Wittekoek, J. M. E., & Wynchank, D. (2025). Research advances and future directions in female ADHD: The lifelong interplay of hormonal fluctuations with mood, cognition, and disease. Frontiers in Global Women's Health, 6, Article 1613628. https://doi.org/10.3389/fgwh.2025.1613628
40. Skovlund, C. W., Mørch, L. S., Kessing, L. V., & Lidegaard, Ø. (2016). Association of hormonal contraception with depression. JAMA Psychiatry, 73(11), 1154–1162. https://doi.org/10.1001/jamapsychiatry.2016.2387
41. Skovlund, C. W., Mørch, L. S., Kessing, L. V., Lange, T., & Lidegaard, Ø. (2018). Association of hormonal contraception with suicide attempts and suicides. American Journal of Psychiatry, 175(4), 336–342. https://doi.org/10.1176/appi.ajp.2017.17060616
42. Toffol, E., Partonen, T., Heikinheimo, O., But, A., Latvala, A., & Haukka, J. (2022). Associations between use of psychotropic medications and use of hormonal contraception among girls and women aged 15–49 years in Finland: A nationwide, register-based, matched case-control study. BMJ Open, 12(2), e053837. https://doi.org/10.1136/bmjopen-2021-053837
43. Zettermark, S., Khalaf, K., Perez-Vicente, R., Leckie, G., Mulinari, D., & Merlo, J. (2021). Population heterogeneity in associations between hormonal contraception and antidepressant use in Sweden: A prospective cohort study applying intersectional multilevel analysis of individual heterogeneity and discriminatory accuracy (MAIHDA). BMJ Open, 11(10), e049553. https://doi.org/10.1136/bmjopen-2021-049553
44. Mu, E., & Kulkarni, J. (2022). Hormonal contraception and mood disorders. Australian Prescriber, 45(3), 75–79. https://doi.org/10.18773/austprescr.2022.025