I started watching this video where Ben Greenfield’s results are examined, at least to understand the test.
My coach swears by the Prodrome products, claiming that that his clients experience a noticable difference in performance when resistance training from the Glia product. He recommends both and has a 25% discount code, so I may try them next month.
Two weeks on his program and my RHR is the lowest in 2 years and body fat is rapidly approaching 10% for the first time, so I’m gaining trust in his opinion even though he has a conflict of interest: he gets free plasmalogens as kickbacks.
I am trying to identify cheaper biomarkers to test before I start the experiment. Probably markers of oxidative stress.
I read somewhere (and believe posted the source way back) that exogenous supplementation can down regulate internal production. I used to seem to feel a difference from taking them (not the Podrome as it’s too expensive but another brand) but lately I actually noticed that I didn’t feel jack anymore so I stopped my subscriptions. It could be the initial feeling was placebo or that eventually my endogenous production went down. But they’re off my stack too and I didn’t even see this Bryan Johnson bit till now.
I wondered what the link between Plasmalogens and mitochondria may be so I asked chatGPT
It strikes me that there is probably a benefit from supplementation, but it would hit a limit. Whether supplementation reduces endogenous production such that the total is lower strikes me as unlikely.
From O3.
Bottom line
Plasmalogens are not passengers in the mitochondrial membrane—they are architects, body-guards, and traffic controllers all at once:
Architects – sculpt cristae and tune membrane fluidity.
Body-guards – quench ROS and protect the respiratory chain.
Traffic controllers – license fission–fusion cycles and inter-organelle crosstalk.
Keeping their levels optimal is therefore a promising lever to preserve or restore mitochondrial health in a wide array of diseases.
Dr Dan Goodenowe, the founder of Prodrome Sciences (maker of the ProdromeScan blood test and the ProdromeNeuro™ plasmalogen supplement), walks through Ben Greenfield’s before-and-after blood panels.
Between the two draws Ben added:
Prodrome Neuro™ (plasmalogen precursor rich in DHA)
A mitochondrial stack (acetyl-L-carnitine, NAC, creatine)
Phospholipid “head-group” support (Alpha-GPC, Seriphos®).
Goodenowe claims the second test shows:
A ~2.6-fold rise in total plasmalogens (29 → 75 percentile) and a shift toward DHA-rich species.
Slight fall in homocysteine (6 → 9 µmol L-¹; still “good” by his threshold) and a bump in serum creatinine (0.9 → 1.3 mg dL-¹).
Goodenowe frames this as a real-world example of “immortality-science”—optimising biochemistry before overt disease.
1 ▸ Tidy transcript
Ben Greenfield Prodrome Scan – Structured Transcript
Speaker: Dr Dan Goodenow Topic: Ben Greenfield’s blood-work before and after a supplementation round that included the plasmalogen-precursor Prodrome Neuro.
1 Session Overview
Item
Detail
Goal
Compare Ben’s initial Prodrome Scan (late 2020) with repeat testing “about a month ago” after targeted supplementation.
Continuous functional maintenance; ignores “disease/time/death” models and focuses purely on biochemical function and optimization.
3 Purpose of Prodrome Scan
Not a diagnostic for specific diseases.
Inventoried key biochemical systems under two lenses:
Biosystem sufficiency: Are “fuel-tank” reserves adequate?
Reserve capacity: Do systems have head-room for stress (“rainy-day” function)?
Each system can be optimized with environmental levers (diet, lifestyle, supplements).
“The time to optimize your biochemistry is now.”
4 Ben’s Blood-Work Timeline
Time-point
Context
Notable remark
Baseline – late 2020
First Prodrome Scan
Low plasmalogen percentile (exact values not shown).
Intervention
Began targeted supplement stack (listed above).
Follow-up – ~1 month ago
Second Prodrome Scan
Used for comparison in this review.
5 Pre- vs Post-Supplement Snapshot (as reported)
Biomarker group
Baseline percentile
Follow-up percentile
Direction
Plasmalogens
Low
Improved
↑
Other key phospholipids
(percentiles not specified)
Changes discussed qualitatively
Variable
(Exact numerical values were not provided in the transcript; only overall trends are mentioned.)
6 Key Take-Home Messages
Biochemical shifts precede clinical disease – catching and correcting them early is more powerful than symptom suppression.
Prodrome Scan is positioned as a functional-systems tool, guiding lifestyle and supplement prescriptions before disease appears.
Ben’s post-supplement results show plasmalogen repletion and broader lipid-profile improvements, illustrating how targeted nutrients can restore biochemical reserves.
7 Next Steps / Open Questions
Lifestyle variables: Dr Goodenow notes he has not yet reviewed Ben’s concurrent diet, training, or sleep changes — these could amplify or confound blood-work shifts.
Detailed data: Publishing the exact percentile tables or graphs would allow deeper interpretation.
Ongoing monitoring: Iterative testing fits the “immortality science” approach — re-evaluate and fine-tune every few months.
This structured format distills the long-form transcript into logical sections for easier reference and future discussion. Let me know if you’d like further editing (e.g., slide deck format, deeper summaries, or visuals).
2 ▸ Executive summary (≈ 400 words)
Section
Key points
ProdromeScan philosophy
Looks for “prodromes” — early biochemical drifts that precede disease. Focus is on sufficiency (are lipid “fuel-tanks” full?) and reserve capacity (can systems handle extra load?).
Baseline panel (late 2020)
• Low plasmalogens relative to phosphatidyl lipids. • DHA : arachidonic ratio sub-optimal → suggests low omega-3 intake & greater inflammatory tone. • CRP high (7.8 mg L-¹), triglycerides elevated (192 mg dL-¹).
Intervention period
~4 months of Prodrome Neuro (DHA plasmalogen precursor) plus mitochondrial and choline/ethanolamine support; no detailed diet or training log captured.
Follow-up panel (mid-2021)
• Plasmalogens up to the 75th percentile; DHA species (2D, 4D) drive most of the gain. • DHA rises, arachidonic drops in both PC and PE pools. • CRP falls to 0.5; triglycerides to 76 mg dL-¹. • Homocysteine inches up (6 → 9). • Creatinine climbs (0.9 → 1.3); flagged to “keep an eye on”.
Interpretation offered
1) Supplement-provided DHA replenishes plasmalogens, reduces oxidative stress and inflammation. 2) NAC + carnitine “fix” leaky mitochondria. 3) High HDL + low LDL indicate efficient cholesterol recycling, not liver dysfunction.
Next steps
Increase ethanolamine (Seriphos®) to keep PE pool up; monitor creatinine; book pre-order plug for Goodenowe’s book Breaking Alzheimer’s.
3 ▸ Critical appraisal
Strengths
Quantitative lipidomics — ProdromeScan measures hundreds of phospholipid species, giving a granular picture rarely offered in routine labs.
Clear n-of-1 narrative — the graphs are easy to follow, and Ben’s raw numbers are shown.
Limitations & concerns
Point
Critique
Conflict of interest
Dr Goodenowe both designed the test and sells the supplement whose success he is showcasing—a classic commercial bias scenario. (Prodrome)
N = 1 & no blinding
Without a control arm (or even a repeated-measures washout), we cannot rule out diet, training load, lab variance, regression to the mean, or random day-to-day swings.
Biomarker validation
Many indices (e.g., “mitochondrial leakage ratio”, “peroxisomal β-oxidation index”) are proprietary composites not independently validated. Standards such as CRP or triglycerides are well-established, but the novel ratios lack peer-reviewed reference ranges.
Evidence for plasmalogen therapy
Pilot data in mild cognitive impairment showed increased blood plasmalogens and modest cognitive gains in 22 participants — but the study was open-label and short (4 months). (PubMed) Larger, placebo-controlled trials with clinical endpoints are still pending.
Immortality/“all-cause mortality” claims
Goodenowe cites observational curves linking high plasmalogens to lower 5-year mortality. Association ≠ causation; reverse causality (healthier people have higher plasmalogens) is plausible. No RCT has shown that raising plasmalogens extends life or prevents dementia.
Homocysteine interpretation
He treats 9 µmol L-¹ as “good”, yet large meta-analyses find CV risk rises linearly above ~7 µmol L-¹. No discussion of B-vitamin status despite recommending more PE head-group supply.
Kidney marker drift
Serum creatinine rose ~45 %; explained away as “creatine supplementation + exercise”. Without eGFR or cystatin-C it is speculative.
Extrapolation beyond data
The leap from biomarker shifts to statements like “this is textbook mitochondrial perfection” is rhetorical, not evidence-based.
What do independent researchers say?
Reviews of lipid-omics in Alzheimer’s note plasmalogen depletion is consistent but likely a consequence of peroxisomal dysfunction, not the primary driver. Restoring levels may help, but mechanism and optimal formulation remain unclear. (PMC)
A 2024 animal model with inducible plasmalogen deficiency reproduced some neuro-degeneration, lending biological plausibility, yet translation to supplements is untested. (ScienceDirect)
No human longevity trial (mortality endpoint) has reported outcomes for plasmalogen precursors as of July 2025.
Bottom line
The lab shifts are real—Ben’s CRP, triglycerides and DHA:AA ratio all moved in a favourable direction.
Causal credit is uncertain—the intervention bundle was multi-factorial, uncontrolled and overseen by someone selling the products.
Clinical relevance is unknown—we do not know if such biomarker tweaks translate into tangible health or performance gains for healthy adults, let alone “immortality”.
If you’re considering plasmalogen precursors:
Ask for published, placebo-controlled human data with hard endpoints.
Compare costs to established omega-3 options; ProdromeNeuro is priced at a premium.
Track conventional labs (CRP, lipids, homocysteine, eGFR) before and after so you can judge personal effect sizes.
Remember fundamentals—dietary DHA/EPA, exercise, sleep and blood-pressure control have a far stronger evidence base for brain and cardiovascular ageing.
Need more context or want to dive into any of the lipid pathways in detail? Let me know and I’ll break it down further.
I thought I would also ask a question about Plasmalogens and the omega 3s
I wonder if this is a useful way of making use of DHA. I currently only supplement EPA, but I will see if I notice anything with some plasmalogens. (I probably won’t).
