Every post in this series so far has ended with some version of "we sell nothing for this." Epilepsy is different. We sell two things that appear in the epilepsy literature, and neither of them appears well. One is ineffective. The other is an interaction risk.
So this page does two jobs: it explains the condition, and it tells you plainly what that evidence means for our own products. We are not doctors, and nothing here is treatment advice.
This is the second post in our series on the neurological conditions beyond dementia, after Parkinson's disease.
Epilepsy is a tendency to recurrent unprovoked seizures — bursts of abnormally synchronised electrical activity in the brain. It is one condition by name and many by cause: genetic, structural (after a stroke, injury, tumour or malformation), metabolic, immune, infectious, or unknown.
The most useful thing a non-specialist can know is that most seizures are not convulsions.
Antiseizure medications control seizures in the majority of people who take them. Around 30% do not respond to initial pharmacological treatment and are classed as having drug-resistant epilepsy — a figure that recurs consistently across the literature, and which comes up again below.
SUDEP — sudden unexpected death in epilepsy — is the commonest directly epilepsy-related cause of death. A 2026 review sets out the scale:1
The mechanism, as currently understood, runs like this: a bilateral tonic-clonic seizure, often nocturnal, is followed by pathologically impaired arousal, then apnoea, then bradycardia, progressing to fatal asystole. Established risk factors include frequent bilateral tonic-clonic seizures — especially nocturnal ones — living alone, long epilepsy duration, and drug-resistant epilepsy.
A 2026 update on the field adds newly identified risk factors from prospective studies: peri-ictal apnoea, disrupted sleep homeostasis, extratemporal epilepsies and elevated BMI.2 It also reports something that matters more than any of them: multiple surveys highlight substantial gaps in SUDEP communication, with many people with epilepsy and their carers remaining insufficiently informed. And alongside that, accumulating evidence that optimising seizure control is likely to reduce SUDEP risk.
In the severe childhood epilepsies the numbers are concrete. A Bayesian meta-analysis of 37 randomised trials and 15 extension studies covering 3,757 patients with developmental and epileptic encephalopathies estimated all-cause mortality at 8.76 per 1,000 person-years (95% credible interval 5.50–13.89) and SUDEP at 4.32 per 1,000 person-years (2.66–6.64). In Dravet syndrome specifically, SUDEP ran at 7.59 per 1,000 person-years.3
We are including this because the research itself says people are not being told, and because the practical implications are things a person can act on: taking medication consistently, not sleeping alone where that is avoidable, and treating nocturnal convulsions as a specific thing to raise with a neurologist rather than a general worry.
Note what two of those risk factors are: nocturnal seizures, and disrupted sleep homeostasis. Sleep is not a peripheral wellness concern in epilepsy. It sits inside the mechanism of the condition's main cause of death.
That is precisely why it is not a sales opportunity, and the next two sections explain why.
Ketogenic diet therapy is one of the few non-drug interventions anywhere in neurology with randomised evidence behind it. A 2026 systematic review of randomised controlled trials screened 1,193 articles and included 17 RCTs — 11 in children, 6 in adolescents and adults, with follow-up from 6 to 24 months:4
A 2025 umbrella review of 18 meta-analyses, appraised with AMSTAR 2, found the same direction with a different diet coming out on top.5 Dietary therapies — particularly the Low Glycemic Index Treatment — significantly increased the chance of a ≥50% reduction (relative risk 1.95, 95% CI 1.58–2.33) and a ≥90% reduction (RR 3.33, 1.51–5.14).
But not seizure freedom. The pooled estimate for becoming seizure-free on dietary therapy was RR 0.68, with a published interval of 0.00–1.36 — which is to say no effect, reported with an interval wide enough to be uninformative. Fewer seizures, not no seizures.
This is the part that gets left out of every enthusiastic article about keto and the brain. The same umbrella review found that dietary therapies and antioxidants together significantly increased the overall incidence of adverse events (RR 1.56, 1.19–1.92). Broken out for the ketogenic diet specifically:5
A separate 2026 review of micronutrient risk on ketogenic therapy adds that the diet's restrictive nature drives falling adherence over time, with gastrointestinal problems, potential for malnutrition and a high risk of micronutrient deficiencies — concluding that a registered dietitian monitoring growth and adjusting the plan is central to doing it safely.6
So the honest summary of the one dietary intervention with real evidence in a neurological disease: it works, modestly; it does not produce seizure freedom; it roughly quintuples kidney stone risk; and it requires a dietitian. That is medical nutrition therapy prescribed and monitored by clinicians. It is the opposite of something you start yourself because an article said keto is good for the brain.
Now the part that applies to our shelf.
Antioxidants do not work for epilepsy. The same umbrella review tested vitamin D, vitamin E and melatonin as adjunctive antioxidant therapy. In the subgroup analysis of ≥50% seizure reduction, antioxidants did not demonstrate significant efficacy, and the authors' stated conclusion is that current evidence does not support the use of antioxidants as effective adjunctive therapy for epilepsy.5
Melatonin specifically was ineffective at reducing seizure frequency (reported as RR 0.30, 95% CI 0.00–0.63 — an interval running to zero, which is itself a sign the pooled estimate is imprecise, and which we are printing as published rather than tidying).5
We sell melatonin. It is in Sleep Support at 10 mg and Sleep Formula at 2 mg. We have written about what the melatonin dose-response evidence actually shows for sleep onset, which is a real if modest literature. None of it extends to seizures, and the pooled epilepsy evidence says it does not reduce them. If you have epilepsy, melatonin is not a seizure intervention and should not be treated as one.
St John's Wort is an interaction risk, and it is in Sleep Support. A 2026 systematic review of cytochrome P450 herb-drug interactions, grading evidence from in-vitro work through human pharmacokinetic studies and documented case reports, assessed Hypericum perforatum among its herbal candidates and found clinically relevant induction or inhibition of CYP activity — particularly CYP3A4 — with the potential to alter drug exposure, reduce therapeutic efficacy or increase toxicity.7
Antiseizure medications are among the most interaction-dense drug classes in medicine; several are themselves enzyme inducers, and several have narrow margins where a drop in blood level means a breakthrough seizure. Reduced therapeutic efficacy of an antiseizure medication is not an inconvenience. Given what the section above says about seizure control and SUDEP risk, it is a safety matter.
We already carry an interaction warning on Sleep Support's product page and we have written the ingredient up in full in St John's Wort: real efficacy, real interaction risk and in our products and mental health medication interactions. Stating it here as plainly as we can:
If you have epilepsy, do not take Sleep Support without clearing it with the doctor who prescribes your antiseizure medication. That is not a formality and it is not a legal disclaimer. The full ingredient list is in inside Sleep Support so you can take it to the appointment.
Several of the older antiseizure medications induce cytochrome P450 enzymes, which accelerates the breakdown of vitamin D. An observational study of 226 patients on long-term carbamazepine measured the effect: serum vitamin D fell from a mean of 45 nmol/L before treatment to 36.6 nmol/L after (95% CI for the difference −14.47 to −2.37, P = 0.007), with calcium and sodium also significantly reduced.8
That is a genuine, mechanistically coherent reason for someone on an enzyme-inducing antiseizure medication to have their vitamin D checked and, if low, corrected. It is also a monitoring and prescribing decision for a clinician who knows which drug you are on, not something to self-administer off the back of a blog post.
We do not sell a vitamin D product. We are pointing at it anyway, because it is the honest answer to "is there any supplement that matters in epilepsy?" — and the answer is one we have no commercial interest in.
For the roughly 30% with drug-resistant epilepsy, the options are surgery, devices, or dietary therapy. The device evidence is worth seeing precisely because of the gap between two numbers that are often reported as if they were one.
A systematic review of 88 studies and 3,068 children with drug-resistant epilepsy treated with invasive neuromodulation found vagus nerve stimulation produced a pooled responder rate — meaning a 50% or greater seizure reduction — of 54% (95% CI 51–58%). Pooled seizure freedom was 6% (4–8%).9
A separate meta-analysis of 19 studies and 149 children on deep brain stimulation, at a minimum 12 months' follow-up, found a responder rate of 63.3% (53.2–72.3%, I² = 3%) and seizure freedom of 13.8% (8.2–22.3%). Age at implantation did not predict response, and differences between stimulation targets were not significant.10
"More than half respond" and "one in sixteen becomes seizure-free" describe the same intervention. Both are true, and which one a family hears changes what they expect.
We sell nothing that treats or prevents epilepsy, and two things we do sell need the cautions above. That is the least flattering position we have taken on this blog, and printing it is cheaper than the alternative, which is a reader with epilepsy taking our sleep product without mentioning it to their neurologist.
The broader pattern is the same one we found in Parkinson's disease, where mitochondrial antioxidants engaged their targets without changing the disease. Epilepsy tests the antioxidant thesis directly, in a condition whose biology genuinely involves oxidative stress, and the pooled answer is no. Our standing argument about why mechanism is not evidence is in why we don't sell brain blends.
This article is for informational purposes only and has not been evaluated by the FDA. It is not intended to diagnose, treat, cure, or prevent any disease. We are not doctors. Epilepsy requires specialist diagnosis and management. Nothing here is a reason to start, stop or change any prescribed medication — abruptly stopping an antiseizure medication can cause status epilepticus, which is a medical emergency. Do not start a ketogenic or other therapeutic diet for epilepsy without medical and dietetic supervision. If you have epilepsy and take or are considering any supplement, including ours, tell the clinician who prescribes your antiseizure medication.