What did @paula_rastrick actually say?
Paula argued that hormonal sensitivity is not the same as oestrogen deficiency. Her framing: "that's not the same as estrogen deficiency" and the real driver is "an imbalance in excitation and inhibition" in the nervous system, with elevated glutamate, cortisol and adrenaline crowding out inhibitory signals like GABA, allopregnanolone and progesterone. She also linked this nervous system state to early life stress, PTSD, ADHD and autism diagnoses that often surface around perimenopause.
This is a specific mechanistic claim, not just vibes. She is saying the problem is a dysregulated excitatory/inhibitory balance, not a simple hormone deficiency you can fix by topping up oestrogen. That distinction matters clinically, and it is worth examining whether the evidence actually supports it.
Does the science back this up?
Mostly, yes, though the picture is more complicated than the video lets on. The excitatory/inhibitory imbalance model has real support, but separating it cleanly from oestrogen levels is harder than Paula implies.
Allopregnanolone, a progesterone metabolite and potent GABA-A receptor positive allosteric modulator, does fluctuate with the cycle and drops during perimenopause. Research by Bäckström et al. (2014, Epilepsia) showed that women with severe premenstrual dysphoria had paradoxical sensitivity to allopregnanolone, meaning the same molecule that calms most nervous systems actually increased anxiety in this group. This supports the "sensitivity" model rather than a simple deficiency model. Separately, Lupien et al. (2009, Nature Reviews Neuroscience) documented how early life stress durably alters HPA axis reactivity and glucocorticoid signalling, which is consistent with Paula's trauma link. The glutamate angle is less established in this specific hormonal context, though glutamate dysregulation in PMDD has been explored by Epperson et al. (2002, Neuropsychopharmacology).
What did they get wrong (or right)?
Paula gets the core architecture right. The idea that some women have a sensitised nervous system response to normal hormonal fluctuations, rather than simply "low" hormone levels, is supported by the PMDD and allopregnanolone literature. The trauma and neurodivergence connection is also clinically plausible and increasingly discussed in perimenopause research.
What she oversimplifies: oestrogen is not a neutral bystander here. Oestrogen directly modulates serotonin receptor expression, GABA-A receptor subunit composition, and glutamate signalling. You cannot fully separate nervous system sensitivity from oestrogen's neuroactive effects. Studies by McEwen (2002, Annual Review of Neuroscience) showed oestrogen shapes synaptic plasticity in ways that directly affect excitatory/inhibitory tone. So while Paula is right that the problem is not "just low oestrogen," framing oestrogen as separable from nervous system function is its own oversimplification. The two are tangled by design.
She also mentions allopregnanolone by name, which is accurate and specific. Credit where it is due, most social media content does not get that granular.
What should you actually know?
If you have PMDD, a trauma history, ADHD or an autism diagnosis and are entering perimenopause, the relevant clinical question is not just your hormone levels on a blood test. It is how your nervous system responds to hormonal change, which can be pathological even when levels are technically "normal."
That said, this does not mean hormone therapy is irrelevant. For some women, stabilising hormone fluctuations reduces the amplitude of nervous system dysregulation. For others, especially those with paradoxical allopregnanolone sensitivity, progestogen components of HRT can worsen symptoms. This is why the clinical conversation is genuinely complex and why a blanket "just take HRT" or "HRT won't help" stance misses the point.
Trauma-informed care and somatic therapies addressing HPA axis dysregulation are legitimate additions to the toolkit, not alternatives to medical assessment. If perimenopause is surfacing old trauma or triggering ADHD symptoms, that warrants a multidisciplinary assessment, not just a single prescription or a single framing.
Bottom line: useful framing, but incomplete
Paula is pushing back against reductive hormone discourse in a way that is broadly justified. The sensitivity model is real. The trauma link is real. The allopregnanolone detail shows genuine subject knowledge. But presenting oestrogen and the nervous system as separable systems is a clean narrative that does not quite match the biology. Oestrogen is neuroactive. Its fluctuations are part of what drives the excitatory/inhibitory shifts she is describing. The two explanations are not opposites, they are parts of the same mechanism.