Prodrome Science™ — Webinar Series

Dr. Goodenowe’s Multiple Sclerosis Webinar

Why does traditional MS treatment stop relapses but fail to halt disease progression? Dr. Dayan Goodenowe explains the biochemical truth behind MS — and what that means for treatment.

⚠️ Never change MS medication on your own. This webinar is critical of B‑cell depletion therapy, and it is worth knowing that the pivotal trials of those drugs did find a significant reduction in disability progression — see the note below. Disease-modifying therapy should never be stopped, reduced, or altered without the supervision of your own neurologist. Nothing on this page is medical advice.

Dr. Dayan Goodenowe, PhD — MS & Brain Repair

Excerpt — full video on Dr. Goodenowe’s website.

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Watch the Full Webinar

Dr. Goodenowe presents the complete Multiple Sclerosis webinar — the biochemistry of impaired myelin repair, why relapse-focused therapy leaves progression untouched, and Lisa’s full case with two years of neuroimaging.

Watch on DrGoodenowe.com ↗

1 hour 17 minutes · Free to watch · Opens in a new tab

About This Presentation

Dr. Goodenowe opens with a challenge to the standard MS narrative. Go online, he says — visit the Mayo Clinic, the Cleveland Clinic, Harvard — and you will find the same information reproduced everywhere. “You get bombarded and drowned out by this common speak and you don’t really understand.” His goal in this webinar is to go deeper: to explain what MS actually is at the biochemical level, why conventional treatment stops relapses but not the disease, and what a genuinely restorative approach looks like in practice.

The webinar was recorded in Saskatchewan — a global hotspot for MS — and includes a live case study from Lisa Grillo, a fifty-three-year-old woman who was told she would develop MS at age twenty-one. After thirty years of relapsing MS — optic neuritis in 1992, a cluster of relapses in 2007, drop foot in 2021 — and legal blindness in her right eye, Lisa began Dr. Goodenowe’s protocol in March 2023. Within eight months, she reports, she was reading with an eye she had been legally blind in for thirty-two years. Her neuroimaging, according to Dr. Goodenowe, tells the rest of the story.

Key points from the webinar — in Dr. Goodenowe’s own words

MS symptoms come from grey matter loss, not white matter lesions. As Dr. Goodenowe explains: “Loss of grey matter is what causes your symptoms in MS.” According to Dr. Goodenowe, study after study shows no meaningful statistical association between white matter damage and how a patient actually feels. In his view, the lesions that show up biggest and brightest on an MRI are often the ones causing the least harm.
Relapses are a symptom of the disease, not the disease itself. “Relapses are not the disease. Relapses are intermittent biomarkers of an underlying chronic neurodegeneration process.” In Dr. Goodenowe’s analogy, a relapse is the fire alarm going off — not the fire. Treating relapses without addressing the underlying damage is, in his words, “really smoke and mirrors.”
B-cell depletion therapy reduces relapses but not disease progression. Dr. Goodenowe cites large published clinical trials showing B-cell therapies cut relapse rates significantly — but when researchers measured actual disability progression and brain volume loss, he reports “there is no difference” compared to older therapies. In his words: “B cell depletion has no effect on brain shrinkage.” This one is contested, and the disagreement matters: the pivotal OPERA I and OPERA II trials (1,656 patients, published in the New England Journal of Medicine) found that ocrelizumab, a B-cell depleting therapy, reduced confirmed disability progression by 40% compared with interferon — a statistically significant result on the exact measure at issue. Dr. Goodenowe cites a more recent comparison reaching a different conclusion. If you are weighing this therapy, this is a question for your neurologist rather than a settled point.
The root cause is an inability to repair damaged myelin. “The impaired myelin repair process is the root cause of the chronic immune reactivity in MS. It’s trying to fix itself and it can’t.” According to Dr. Goodenowe, the immune system isn’t attacking randomly — it’s reacting to oxidized phospholipids produced by damaged, unrepaired myelin. Remove that trigger, he argues, and there is nothing left for the immune system to attack.
The brain can repair itself when given the right materials. “If you supply your brain with the appropriate materials and energy it can win this battle and it can repair itself.” Dr. Goodenowe describes two types of plasmalogen precursors he has developed — omega-nine for myelin structure and omega-three for synaptic function — as the raw materials the brain can no longer obtain from diet alone. Lisa’s neuroimaging, he reports, showed a fifty percent increase in the fibre connectivity measured in her occipital cortex, and a twenty percent increase in thalamus volume over two years.
Dr. Goodenowe argues an underlying mitochondrial weakness sits beneath MS. “In MS you have a mitochondrial weakness to begin with, which is why the fatigue is associated with MS.” In his framing, that weakness is what leaves a cell unable to resolve an oxidative insult that a healthy neighbour would handle — which is why he considers supporting mitochondrial function a core part of any restorative approach. This is his hypothesis rather than an established finding, and one supporting claim he makes for it does not hold: the strongest genetic risk factor for MS is HLA‑DRB1*15:01, an immune gene carrying roughly a threefold increase in risk, identified more than forty years ago. Of the 200-plus genetic variants since linked to MS, the great majority are immune-related, not mitochondrial. Mitochondrial dysfunction is genuinely studied in MS — it is simply not what the genetics point to.

Why Lisa’s Case Matters

According to Dr. Goodenowe, Lisa’s results are validated by advanced MRI taken at multiple points over two years. At baseline, he reports, eighteen regions of her brain showed cortical thinning two standard deviations below normal. After two years on his protocol, none did. Where published MS clinical trials show patients losing roughly half a percent of cortical thickness per year, Dr. Goodenowe reports Lisa gained one point three percent — and her total brain volume increased by two percent.

Most striking, according to Dr. Goodenowe, is what happened to her vision. He reports that the fibre connectivity measured in her occipital cortex grew from approximately six thousand to nine thousand — a fifty percent increase. “We did not anticipate this fibre growth,” Dr. Goodenowe admits. “There’s no way we would have predicted that she actually regained vision to that level and that the fibre networks would just burst like that. That’s brand new stuff.”

A note on what that number is: these counts come from tractography, an MRI technique that models the likely paths of white matter bundles. The “fibres” it counts are reconstructed pathways, not individual axons, and the total shifts with the scanner settings and software used — so a change between scans is not a direct count of new wiring. It is a real measurement of something; it is not a headcount of nerve fibres.

The mechanism, as Dr. Goodenowe explains it: plasmalogens make up around eighty percent of the ethanolamine content of the myelin sheath. When plasmalogen levels fall, he argues, the brain cannot repair damaged myelin fast enough, oxidized phospholipids accumulate, and the immune system reacts to them. In his view, the slow smoldering fire of MS continues regardless of whether B cells are suppressed. Restore the plasmalogen levels and remove the immune trigger, and the brain — given the right raw materials — can begin to repair itself. As he puts it: “If there are no new oxidized phospholipids, you shouldn’t have to get rid of your B cells.”

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