Harry K-P | Shes Not Crazy :
📌 The list, the numbers, and where I’ve had to be careful:
🧬 Oestrogen modulates serotonin synthesis, transport and receptor sensitivity — Bethea et al., 2002, Frontiers in Neuroendocrinology; Rubinow et al., 1998
🧬 Late-luteal decline in oestradiol and progesterone, and its association with premenstrual symptoms — Rubinow et al., 1998
🧬 Symptom prevalence — up to three in four menstruating women report some premenstrual symptoms (ACOG). Symptom lists in the clinical literature vary enormously in length, and the longest run to well over a hundred
🧬 Luteal-phase basal metabolic rate rises modestly, which is part of why appetite and cravings change. The chocolate isn’t a discipline failure
🧬 Premenstrual fluid retention is well documented, commonly in the range of a couple of pounds
🧬 Palpitations, migraine, joint pain and gastrointestinal changes all appear in standard premenstrual symptom inventories
📌 Honest note on the clumsiness. It’s very widely reported and I’ve given fluid retention as the reason, which is the common explanation. It is not well established — the link between premenstrual fluid shifts and coordination hasn’t been properly nailed down. I’ve kept it because women describe it constantly, and I’d rather flag the gap than drop the symptom.
📌 On PMDD. There’s a separate and far more severe condition, premenstrual dysphoric disorder, affecting somewhere in the region of three to eight percent of women. This piece isn’t about that. If what’s described here sounds mild compared to what someone’s living with, PMDD is worth reading about and worth taking to a GP.
📌 One thing worth knowing about diagnosis. PMS is identified by symptoms appearing in the luteal phase and resolving once the period starts. Which means tracking is the whole diagnostic tool, and a lot of women have never been told that.
2026-09-09 10:22:23