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Why Are Women More Moody on Their Period?

Why Are Women More Moody on Their Period
Why Are Women More Moody on Their Period

By TherapyNearMe.com.au | August 2025

TL;DR: Mood changes around the period are common. They are driven by normal hormonal cycling (oestrogen, progesterone and the neurosteroid allopregnanolone), brain chemistry (serotonin and GABA), pain and sleep disruption, iron deficiency from heavy bleeding, and stress sensitivity. A smaller group experiences premenstrual dysphoric disorder (PMDD)—a severe, cyclic mood disorder linked to sensitivity to ovarian steroids rather than abnormal hormone levels (Schmidt & Rubinow, 1998; Gao et al., 2023; Bixo, Stiernman & Bäckström, 2025). Effective treatments include SSRIs (continuous or luteal‑phase dosing), certain combined oral contraceptives (e.g., ethinylestradiol/drospirenone 24/4), CBT, pain management, sleep hygiene and targeted nutrients such as calcium where appropriate (ACOG, 2023; Marjoribanks et al., 2013; Pearlstein et al., 2005; Busse et al., 2009; Thys‑Jacobs et al., 1998).


What counts as “moody” (clinically)?

Common premenstrual experiences include irritability, emotional lability, anxiety, low mood, increased tearfulness, and reduced stress tolerance. For a PMDD diagnosis (DSM‑5‑TR), symptoms must be severe, cyclic, present in the final week of the luteal phase, remit with menses, and cause clinically significant impairment; prospective daily ratings for two cycles are recommended (APA, 2024).


The menstrual cycle, hormones and the brain

  • Oestrogen & serotonin: Oestradiol up‑regulates serotonin synthesis and receptor expression, which is partly why many feel more positive during the mid‑cycle high‑oestrogen window; as oestradiol falls in the late luteal phase, some experience a serotonergic dip (Albert et al., 2015).
  • Progesterone → allopregnanolone & GABA: Progesterone’s metabolite allopregnanolone is a positive allosteric modulator of GABA‑A receptors. In most people it is calming, but a subgroup shows paradoxical negative mood responses at certain concentrations—reflecting altered GABA‑A receptor sensitivity (Schmidt & Rubinow, 1998; Sundström‑Poromaa et al., 2012; Bixo, Stiernman & Bäckström, 2025).
  • It’s sensitivity, not levels: Elegant ovarian suppression and add‑back experiments demonstrate that PMDD symptoms disappear when ovarian steroid production is shut down and recur when physiologic oestradiol/progesterone are reintroduced—implicating neurobiological sensitivity rather than abnormal hormone levels (Schmidt & Rubinow, 1998; Schmidt et al., 2017; Hantsoo & Epperson, 2015).

Other biological drivers that amplify mood changes

  1. Pain, inflammation and sleep: Prostaglandin‑mediated menstrual pain (dysmenorrhoea) disrupts sleep and increases pain sensitivity—both linked to lower mood and irritability (Iacovides, Avidon & Baker, 2015; Ziółkowska et al., 2020).
  2. Iron deficiency from heavy bleeding: Heavy menstrual bleeding is a major cause of iron deficiency/anaemia, producing fatigue, brain fog and low mood; ferritin testing and treatment can meaningfully improve wellbeing (Munro et al., 2023; ACOG, 2023).
  3. Stress system reactivity: Some with PMDD show differences in HPA‑axis indices and allopregnanolone dynamics, consistent with heightened stress responsivity (Eisenlohr‑Moul et al., 2017; Girdler & Klatzkin, 2007).
  4. Medications & substances: Caffeine, alcohol, and some progestin‑only contraceptives can worsen mood in susceptible individuals (ACOG, 2023).

Why some people get PMDD (and others do not)

  • Neurosteroid sensitivity: Increasing evidence supports altered GABA‑A receptor subunit plasticity and sensitivity to allopregnanolone across the cycle in PMDD (Gao et al., 2023; Bixo, Stiernman & Bäckström, 2025; Comasco et al., 2014).
  • Genetic & developmental factors: Family history of mood disorders, early life stress, and trait anxiety increase risk (Hantsoo & Epperson, 2015).
  • Comorbidity: ADHD, anxiety, depressive and bipolar disorders, endometriosis, chronic pain, and thyroid disease can worsen premenstrual mood (ACOG, 2023).

Evidence‑based treatments (what actually works)

First‑line options (supported by high‑quality evidence):

  • SSRIs (e.g., sertraline, fluoxetine, escitalopram): Effective for PMDD and severe PMS. Can be taken continuously or only in the luteal phase starting day 14 or at symptom onset; both strategies work (Marjoribanks et al., 2013; ACOG, 2023).
  • Combined oral contraceptives (COCs): Formulations with ethinylestradiol 20 μg/drospirenone 3 mg in a 24/4 regimen reduce PMDD symptoms and functional impairment in RCTs; extended/continuous regimens may help by minimising hormone‑free intervals (Pearlstein et al., 2005; Yonkers et al., 2005; Rapkin et al., 2011; ACOG, 2023).
  • Targeted psychotherapy: Cognitive‑behavioural therapy (CBT) improves coping, reduces interference, and may enhance SSRI effects; emerging trials support internet‑delivered CBT (Busse et al., 2009; Ussher, 2017; Kleinstäuber et al., 2019).

Adjuncts (conditional/individualised):

  • Pain & sleep management: NSAIDs for prostaglandin pain; sleep regularity to stabilise mood (Iacovides, Avidon & Baker, 2015).
  • Calcium (≈1,000–1,200 mg/day): Multiple RCTs and meta‑analyses show reductions in mood and somatic PMS symptoms (Thys‑Jacobs et al., 1998; Abdi et al., 2017).
  • Vitamin B6 (≤100 mg/day): Some benefit for global PMS symptoms; watch for neuropathy at high doses (Whelan et al., 1999).
  • Omega‑3 fatty acids: Mixed but promising evidence for mood and pain in PMS; discuss dose and AF risk if using high‑dose supplements (Behboudi‑Gandevani et al., 2013).

Second‑line / specialist options (severe, refractory PMDD):

  • GnRH agonists with add‑back oestrogen/progestin: Suppress ovarian cycling; effective but reserved due to side‑effects and bone risks (Schmidt & Rubinow, 1998; ACOG, 2023).
  • Surgical oophorectomy: Rare, last‑line after thorough evaluation and success with trial ovarian suppression (ACOG, 2023).

Practical self‑care playbook (evidence‑informed)

  • Track daily symptoms with the DRSP or similar for two cycles to confirm cyclicity and guide treatment (APA, 2024).
  • Reduce hormone‑free intervals (in consultation with your doctor): extended or 24/4 COC regimens may help (Rapkin et al., 2011).
  • Prioritise sleep the week before your period; treat pain early with NSAIDs.
  • Screen for iron deficiency if you have heavy periods, fatigue or brain fog; ferritin <30 μg/L often warrants treatment (Munro et al., 2023).
  • Nourish and move: Regular meals with protein/complex carbs, exercise most days, and sunlight exposure support mood regulation (ACOG, 2023).
  • Be alcohol‑ and caffeine‑aware in the late luteal phase if you notice sensitivity (ACOG, 2023).

When to seek professional help (red flags)

  • Severe mood swings, hopelessness, panic, or rage that impair work/relationships, especially if cyclic.
  • Suicidal thoughts: seek urgent help (000 in Australia or local emergency services).
  • New or worsening depression/anxiety, mania/hypomania, ADHD‑like symptoms, or thyroid symptoms.
  • Heavy bleeding (soaking through pad/tampon hourly or >7 days), which raises anaemia risk (Munro et al., 2023).A GP, gynaecologist, or clinical psychologist can confirm diagnosis and tailor a plan.

Keywords

PMS mood swings, PMDD symptoms, why am I moody on my period, luteal phase anxiety, drospirenone 24/4 PMDD, SSRI for PMDD, allopregnanolone GABA, period mood changes, heavy periods iron deficiency, menstrual pain sleep, CBT for PMS, women’s mental health Australia


References

Abdi, F. et al. (2017) ‘Effect of calcium supplement on premenstrual syndrome: A systematic review and meta‑analysis’, Obstetrics & Gynecology Science, 60(1), pp. 100–110.

ACOG (2023) ‘Management of Premenstrual Disorders’, Clinical Practice Guideline. Washington, DC: American College of Obstetricians and Gynecologists. Available at: https://www.acog.org (accessed 14 August 2025).

Albert, K. et al. (2015) ‘Estradiol levels modulate brain activity and negative responses to psychosocial stress’, Psychoneuroendocrinology, 59, pp. 14–24.

American Psychiatric Association (2024) DSM‑5‑TR Update (September 2024 supplement). Washington, DC: APA Publishing.

Behboudi‑Gandevani, S. et al. (2013) ‘Effect of omega‑3 fatty acids on premenstrual syndrome: A randomised clinical trial’, Revista Brasileira de Ginecologia e Obstetrícia, 35(6), pp. 241–246.

Bixo, M., Stiernman, L. and Bäckström, T. (2025) ‘Neurosteroids and premenstrual dysphoric disorder’, The British Journal of Psychiatry, 226(5), pp. 1–9.

Busse, J.W. et al. (2009) ‘Cognitive‑behavioural therapy for premenstrual syndrome: A systematic review’, Journal of Psychosomatic Obstetrics & Gynecology, 30(1), pp. 1–11.

Comasco, E., Kopp Kallner, H. and Bäckström, T. (2014) ‘GABA‑active steroids in the female brain with a focus on PMDD’, Acta Obstetricia et Gynecologica Scandinavica, 93(8), pp. 810–815.

Eisenlohr‑Moul, T.A. et al. (2017) ‘HPA‑axis function, allopregnanolone, and PMDD: A conceptual integration’, Psychoneuroendocrinology, 80, pp. 97–104.

Gao, Q. et al. (2023) ‘Role of allopregnanolone‑mediated GABA‑A receptor sensitivity in the pathogenesis of PMDD’, Frontiers in Psychiatry, 14, 1140796.

Girdler, S.S. and Klatzkin, R.R. (2007) ‘Neurosteroids in stress and PMDD’, Psychopharmacology, 191, pp. 173–188.

Hantsoo, L. and Epperson, C.N. (2015) ‘Premenstrual dysphoric disorder: Epidemiology and neurobiology’, CNS Spectrums, 20(1), pp. 54–61.

Iacovides, S., Avidon, I. and Baker, F.C. (2015) ‘What we know about primary dysmenorrhea today: A critical review’, Human Reproduction Update, 21(6), pp. 762–778.

Kleinstäuber, M. et al. (2019) ‘Internet‑based CBT for PMDD: A randomized clinical trial’, Psychotherapy and Psychosomatics, 88(1), pp. 16–29.

Marjoribanks, J. et al. (2013) ‘Selective serotonin reuptake inhibitors for premenstrual syndrome’, Cochrane Database of Systematic Reviews, CD001396.

Munro, M.G. et al. (2023) ‘The relationship between heavy menstrual bleeding, iron deficiency and quality of life’, American Journal of Obstetrics & Gynecology, 228(2), pp. B9–B21.

Pearlstein, T. et al. (2005) ‘Treatment of PMDD with drospirenone/ethinylestradiol 24/4: A double‑blind randomised trial’, Obstetrics & Gynecology, 106(3), pp. 492–501.

Rapkin, A. et al. (2011) ‘EE 20 μg/drospirenone 3 mg (24/4) for PMDD: Randomised clinical trial subanalysis’, International Journal of Women’s Health, 3, pp. 91–97.

Schmidt, P.J. and Rubinow, D.R. (1998) ‘Differential behavioural effects of gonadal steroids in women with and without PMS’, New England Journal of Medicine, 338(4), pp. 209–216.

Schmidt, P.J. et al. (2017) ‘Acute changes in ovarian steroids, but not steady‑state levels, precipitate PMDD symptoms’, American Journal of Psychiatry, 174(10), pp. 970–981.

Sundström‑Poromaa, I. et al. (2012) ‘Altered sensitivity to allopregnanolone in PMDD’, Psychopharmacology, 220(1), pp. 1–11.

Thys‑Jacobs, S. et al. (1998) ‘Calcium carbonate and premenstrual syndrome: Randomised trial’, American Journal of Obstetrics & Gynecology, 179(2), pp. 444–452.

Ussher, J.M. (2017) ‘Women‑centred psychological interventions for premenstrual distress’, InPsych (APS).

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