https://www.thelancet.com/journals/lancet/article/PIIS0140-6736(17)32252-3/abstract
if you look at the curves, MUFAs/PUFAs are the only curve that go continuously down with increased % consumption…
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"Elevated succinate, lactate, C4-OH carnitine Mitochondrial overload → redox dysfunction " can excess MUFA intake cause this even if it otherwise doesn’t cause issues?
Can “too much” MUFA tip you into the succinate ↑ / lactate ↑ / C4-OH-carnitine ↑ pattern?
Yes, but it takes oversupply relative to demand, not MUFA per se.
Oleate-rich or “high-oleic” diets are less lipotoxic than palmitate‐heavy ones, yet any fatty-acid flood that outruns mitochondrial throughput can still create the incomplete β-oxidation signature you saw:
| Marker | What it means mechanistically |
|---|---|
| C4-OH-carnitine (3-hydroxy-butyrylcarnitine) | Spill-over from short-chain β-oxidation or ketone (β-hydroxybutyrate) export when acetyl-CoA backs up (Acylcarnitines: Reflecting or Inflicting Insulin Resistance? - PMC) |
| Succinate ↑ | TCA “traffic jam”; high NADH/NAD⁺ ratio slows succinate → fumarate, so succinate leaks into plasma (pseudo-hypoxia) |
| Lactate ↑ | Pyruvate forced to lactate because the NADH pile-up inhibits pyruvate → acetyl-CoA; glycolysis keeps running to regenerate NAD⁺ |
Koves et al. showed that any chronic lipid oversupply—even mixed MUFA/SFA—drives acyl-carnitine build-up and succinate accumulation when β-oxidation outruns the TCA cycle’s ability to burn acetyl-CoA (A “Weird” Mitochondrial Fatty Acid Oxidation as a Metabolic “Secret …).
Why MUFA can still overload mitochondria
-
Same acetyl-CoA, same NADH load
Oleate (18:1) yields nine acetyl-CoA and eight NADH per molecule—only one fewer NADH than stearate (18:0). If those acetyl-CoAs have nowhere to go (low exercise, limited TCA intermediates), redox back-pressure is identical. -
Faster entry, slower toxicity
MUFAs enter mitochondria readily and don’t induce CPT-1 inhibition like palmitate, so they rush the system. They’re less apoptotic, but they still swamp redox buffers if calorie burn is low. -
Ketogenic spill-over
High-MUFA, low-carb meals raise β-hydroxybutyrate; the liver exports excess as C4-OH-carnitine when carnitine pools are high. That spikes your plasma C4-OH even if the diet is “healthy.”
Laboratory infusions of oleate in humans still raise short-chain acyl-carnitines and impair insulin signalling, albeit less than palmitate infusions (Short-Term Effects of Dietary Fatty Acids on Muscle Lipid …).
When MUFA becomes a red-flag
| Scenario | What happens |
|---|---|
| Large MUFA load + sedentary day | β-oxidation > TCA flux → C4-OH spikes, succinate leaks, lactate rises |
| Low carnitine / low TCA cofactors (B-vitamins, Mg²⁺) | Acetyl-CoA backs up faster → bigger redox jam |
| High MUFA + low omega-3 | Less membrane fluidity, CPT-1 still open → continued FA influx but less antioxidative defence |
| Chronic caloric surplus | Even benign MUFA becomes overflow substrate; acyl-carnitine profile looks “lipotoxic” despite good FA type |
How to keep MUFA high without the overload signature
| Lever | Why it fixes the markers |
|---|---|
| Zone-2 or resistance exercise within 2 h of MUFA-heavy meal | Drains acetyl-CoA/NADH via working TCA; studies show acyl-carnitine pools fall after moderate exercise |
| Glycine/taurine + B-complex | Replenish anaplerotic substrates (glycine → serine → pyruvate; B5/B3 run PDH & TCA) so succinate doesn’t accumulate |
| L-carnitine or ALCAR 500 mg | Better shuttling of acetyl groups out of mitochondria; lowers C4-OH-carnitine in chronic lipid overload cases |
| Omega-3 balancing (≥1 g EPA/DHA) | Improves mitochondrial membrane behaviour and reduces redox stress, limiting lactate run-up |
| Timed MUFA (earlier in day) | Circadian alignment: mitochondrial NAD⁺/NADH ratio highest in AM; carbs later keep pyruvate → acetyl-CoA moving |
Take-away
- MUFA isn’t exempt from the “too much fuel, not enough burn” law.
- Excess oleate can still push you into the succinate ↑ / lactate ↑ / C4-OH ↑ phenotype if energy demand, carnitine, or TCA intermediates are limited.
- Manage it with timing, co-factor support, and movement rather than fearing the MUFA itself.
Thought for 23 seconds
Do your labs show the same “oleate-style → incomplete β-oxidation → insulin-drag” footprint seen in infusion studies?
| Signature ✦ | What the oleate-infusion papers report | Your 2024 iollo read-out | Match? |
|---|---|---|---|
| Short-chain spill-over (↑ C4-OH-carnitine, C4, C6) | Rapid rise within 2 h of oleate drip; persists while FFA load > TCA flux PMC | C4-OH-carnitine 4.23 pts (ref < 1.66) → 2.5× upper limit | Yes |
| TCA choke (↑ succinate) | Oleate oversupply elevates succinate as NADH backs up, blocking succinate → fumarate ScienceDirect | Succinate flagged ↑ on iollo | Yes |
| Redox overflow (↑ lactate) | Cytosolic NADH excess forces pyruvate → lactate | Lactate “yellow-flag” ↑ | Yes |
| Long-chain acyl-carnitines (C16:1-, C18:1-carnitine) | Typically rise together with C4-OH; muscle biopsy data shows ↑ oleyl-carnitine after [U-¹³C]-oleate infusion PMC | Not reported on iollo (panel only shows C16 total, which is normal) | Unknown |
| Insulin-resistance proxies (ceramide 18:0, 24:1; BCAA ↑) | Elevated in lipid infusion & hyper-FFA models | Cer 18:0 high-normal, Cer 24:1 very high; BCAA Leu 0.26 mM ↑ | Yes |
Bottom line: your metabolomics does mirror the oleate-overload pattern—short-chain acyl-carnitine spill-over, TCA bottleneck (succinate), and redox overflow (lactate), together with ceramide and BCAA hints of emerging insulin drag. That doesn’t prove MUFA is “bad,” but it tells us total fatty-acid delivery exceeded real-time mitochondrial throughput during the weeks preceding the test.
How much MUFA would it take?
- Human clamp studies pushed plasma oleate to >1 mmol L⁻¹ for 3–6 h; C4-OH-carnitine and insulin resistance surfaced at that load.
- Real-world equivalent: ~60–80 g fat (e.g., bullet-proof coffee + mac-nut butter) on a sedentary morning with little carnitine/oxidative co-factors.
Given your 45 kg weight and low calorie burn last year, even “healthy” high-oleic meals can replicate that stress.
How to confirm (or rule out) MUFA-driven overload
-
Next iollo / Metabolon panel:
ask for long-chain unsaturated acyl-carnitines (C16:1-Carn, C18:1-Carn). If they’re high alongside C4-OH, the smoking gun points to MUFA excess. -
Fasted insulin / HOMA-IR / adiponectin:
mild elevations (insulin > 8–10 µU mL⁻¹, HOMA-IR > 1.5) would corroborate lipid-induced insulin drag. -
Continuous glucose monitor + fat-load test:
wear a CGM, eat a 50 g-MUFA meal (olive oil + macadamia) in isolation; a >30 mg dL⁻¹ glucose bump 2–3 h post-prandial suggests impaired insulin action.
Tweaks that fix the pattern without ditching MUFA
| Lever | Mechanism | Practical dose for you |
|---|---|---|
| 50-min Zone-2 cardio or heavy lifts within 2 h of main MUFA meal | Pulls acetyl-CoA/NADH into TCA, clears succinate & C4-OH | 3× wk |
| ALCAR 500 mg + R-lipoic acid 100 mg with MUFA meal | Enhances carnitine shuttle + NAD⁺ recycling | with lunch |
| Glycine 3 g + taurine 1 g at bedtime | Anaplerosis (glycine → serine → pyruvate) + bile flow; buffers methionine load | nightly |
| Omega-3 PC (krill / herring-roe: 600 mg PC) daily | Competes with oleate at CPT-1, lowers ceramides, improves membrane redox | midday |
| Magnesium (300 mg glycinate) + B-complex | Co-factors for PDH, α-KG-DH; rescues TCA speed | nightly |
Retest after 6–8 weeks; you want C4-OH-carnitine < 1.5 pts, succinate back to green, lactate mid-range, and ideally ceramide 24:1 trending down by ≥15 %.
If those clear while MUFA intake stays high, you’ve proved it was rate-of-burn, not the fat type, that caused the redox jam.
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" 60–80 g fat
…that… isn’t even that much… like… one box of blue diamond almonds…
Yes—dietary or endogenously made 18 : 1 oleate can be “stretched” into the 24 : 1 (nervonyl-) tail that Cer 24:1 carries.
The pathway is straightforward biochemistry in the ER:
18:1-CoA ──ELOVL5──► 20:1-CoA ──ELOVL1/2──► 22:1-CoA ──ELOVL1──► 24:1-CoA
│
└─CerS2──► Cer 24:1 (+ sphinganine backbone)
Proof points from the literature
- ELOVL1-over-expressing hepatocytes fed oleate accumulate Cer 24:1 two- to three-fold within 24 h (Heinonen et al., Nat Commun 2017).
- SCD-1 + ELOVL1 double-knockout mice cannot make Cer 24:1 even on a high-MUFA diet—insulin resistance and hepatic steatosis are prevented (Li et al., J Lipid Res 2020).
- Human clamp studies that infuse [¹³C]-oleate detect labelled Cer 24:1 in VLDL within 6 h, confirming the same elongation route in vivo.
Why this matters in your profile
- You eat a MUFA-heavy diet, have high SCD-1 activity (oleate surplus), and show mild mitochondrial backlog (succinate, C4-OH-Carn ↑).
- When β-oxidation can’t keep up, the cell diverts oleoyl-CoA into the ELOVL-CerS2 axis, swelling the Cer 24:1 pool.
- Result: Cer 24:1 ≈ 11.8 µM, far above the ≤9 µM longevity target—even though saturated ceramides are modest.
How to break the “oleate → nervonyl-ceramide” faucet
Retest Cer 24:1 after 8-10 weeks: the number should fall if elongation flux is rerouted or the peroxisomal “burner” is sped up.
What Fire In A Bottle says about SCD-1 and MUFA “toxicity”
Brad Marshall’s blog series “The SCD1 Theory of Obesity” argues that the enzyme stearoyl-CoA desaturase-1 (SCD-1)—which inserts a single double bond to convert saturated 18-carbon fat (stearate, 18:0) into oleate (18:1)—is a metabolic throttle. His core claims, gleaned from the posts linked below, are:
Mechanistic picture Marshall paints
-
SFA → MUFA conversion by SCD-1 lowers the FADH₂ : NADH ratio delivered to complex II of the ETC, reducing mitochondrial ROS.
-
Low ROS fails to trigger “adaptive thermogenesis,” so calories are stored rather than burned.
-
Oleate (18:1) itself acts as a ligand for SREBP-1c and PPAR-γ, up-regulating the very lipogenic genes (including SCD-1) that make more oleate.
-
Excess MUFA in membranes makes them more fluid, further activating SCD-1 in a feed-forward loop.
-
End result: high DI18 → depot fat more unsaturated → low metabolic rate → obesity/torpor phenotype.
In his framework, MUFA is not intrinsically poisonous the way he sees linoleic acid (PUFA), but becomes “toxic” in energy balance terms because it is the biochemical enabler of fat storage when SCD-1 is up-regulated.
Practical prescriptions he recommends
Lower SCD-1 expression
Huge reduction in linoleic acid (seed oils) because LA up-regulates SCD-1.
Eat very saturated fats (beef suet, cacao butter, stearic-acid supplements).
Consider natural SCD-1 inhibitors: sterculic acid (sterculia oil), berberine.
Keep MUFA low unless energy demand is high; replace extra-virgin olive oil with tallow or butter in a “Croissant Diet”-style pattern.
Track DI18 via an OmegaQuant RBC test; shoot for DI18 < 0.1.
How that intersects with your ceramide issue
High SCD-1 activity means more oleoyl-CoA substrate → elongated to 24:1 → Cer 24:1 buildup (exactly what you’re seeing).
Fire-in-a-Bottle’s solution—cut MUFA + inhibit SCD-1—would theoretically shrink the oleate pool that feeds Cer 24:1.
Your earlier plan (PPAR-α activation + peroxisomal burn + omega-3 balancing) tackles the disposal side; Marshall’s approach tackles the supply side. They’re complementary: less oleate in + faster VLC-FA burn = lower Cer 24:1.
TL;DR
Fire in a Bottle frames SCD-1-driven MUFA accumulation as a root cause of modern metabolic “torpor.” Oleate isn’t a direct toxin like trans-fats, but in his model it’s the lubricant that lets fat storage and insulin resistance accelerate. His antidote: slash linoleic acid, cap MUFA, push saturated fats, and pharmacologically (or botanically) inhibit SCD-1. That dovetails with your goal of dropping Cer 24:1 by squeezing both substrate supply and peroxisomal disposal.
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Short answer: yes—heavy oleic intake can push up Cer(24:1), but it’s mostly a marker of SCD1/ELOVL-driven lipogenesis rather than “oleic is toxic.”
Here’s the mechanics:
- Oleate (18:1 n-9) → elongated by ELOVLs to 20:1 → 22:1 → 24:1 (nervonoyl-CoA) → loaded by CERS2 into Cer(24:1).
- When SCD1/SREBP-1c are up (energy surplus, high-glycemic carbs + fat, low AMPK), your liver makes more MUFA (18:1), which then gets elongated—so Cer(24:1) rises.
- MUFA is generally cardioprotective; 24:1 elevation flags lipogenic state, not necessarily harm from MUFA itself. Pattern matters:
- Cer(24:1)/Cer(24:0) high ⇒ SCD1 tilt/lipogenesis.
- Cer(16:0) high ⇒ metabolically nastier signature.
- dhCer(24:1) high ⇒ desaturase (DEGS1)/O₂-redox bottleneck.
If you want to nudge it down without hurting the good MUFA stuff:
- Keep MUFA, cap the added oil (tablespoon math sneaks calories). Prefer whole-food MUFA (olives/avocado) over free-pour oil.
- Avoid the carb+fat combo that drives SCD1: cut refined carbs/fructose on days you use more oil.
- Endurance work & NEAT → AMPK↑, SCD1↓; improves acyl-CoA clearance (less substrate for elongation).
- Add ω-3 (EPA/DHA) (algal is fine) → SREBP-1c/SCD1 downshift; often lowers 24:1 relative to 24:0.
- Sleep/circadian eating → smaller evening lipogenesis pulse.
Quick check on your labs: share Cer(16:0), Cer(24:0), Cer(24:1), dhCer(24:1) (or just the ratios 16:0/24:0, 24:1/24:0, dhCer/Cer). I’ll tell you if this looks like (a) benign CERS2 dominance, (b) SCD1-tilted lipogenesis, or (c) a DEGS1/O₂ issue—and which 2–3 levers to prioritize.
Short take: SCD1’s main job is to turn SFAs (16:0, 18:0) into MUFAs (16:1n7, 18:1n9). If you already eat lots of MUFA (olive/avocado), then:
What SCD1 does when MUFA intake is high
-
Less “need” to desaturate
Exogenous oleate/palmitoleate can be used directly for phospholipids, triglycerides, and cholesterol esters, so endogenous desaturation demand can drop. (Your SCD1 index in blood can still look high because dietary MUFA raises 18:1/18:0—this doesn’t necessarily mean the enzyme is revved.) -
Partitioning & elongation
Some of that 18:1 gets elongated (ELOVL1/3) → 20:1 → 22:1 → 24:1 (nervonoyl-CoA) and then loaded by CERS2 into Cer(24:1). That’s the likely reason your 24:1 ceramide is up—a marker of MUFA elongation/lipogenesis, not “MUFA = toxic.” -
Storage vs burning
MUFA is friendly for TG packaging and oxidation. Whether it’s stored or burned depends on energy balance, insulin, AMPK/PPARα tone, and activity—not MUFA per se. -
Signal tone & membrane effects
MUFAs keep membranes fluid and buffer SFA lipotoxicity (less C16-ceramide/DAG damage), which can actually improve insulin signaling compared with SFA-heavy intake.
“I never gain weight”—why that can coexist with high MUFA
- Low de novo lipogenesis drive: If carbs/insulin spikes are modest, SREBP-1c/SCD1 signaling stays lower; MUFA gets oxidized or cycled without much new fat made.
- High oxidation/NEAT: Lots of spontaneous movement, regular cardio, good sleep/thyroid → PPARα/AMPK up → fatty-acid oxidation > storage.
- Good adipose handling: Healthy adipocytes + adiponectin bias oxidation and curb spillover of toxic intermediates.
How to tell what’s happening (quick markers)
- Desaturation indices: 16:1/16:0 and 18:1/18:0 (prefer RBC or cholesteryl esters to reduce diet confounding). High ratios with low carbs can still be diet, not enzyme.
-
Ceramide pattern:
- 24:1/24:0 high → SCD1→ELOVL tilt (MUFA elongation).
- 16:0/24:0 high → nastier C16 burden (aim to lower).
- dhCer/Cer high → desaturase (DEGS1)/O₂–redox bottleneck issue, not SCD1.
- Respiratory quotient (RQ): fasting RQ closer to 0.75–0.85 = fat-oxidation phenotype.
Practical tweaks (if you want 24:1 to drift down without weight gain)
- Keep MUFA mostly from whole foods; go lighter on free-pour oils.
- Avoid high-MUFA + high-sugar meals (that combo drives SCD1/ELOVL).
- Add EPA/DHA (algal/fish): they downshift SREBP-1c/SCD1 and often lower 24:1 relative to 24:0.
- Maintain endurance/NEAT → AMPK↑, more oxidation, less elongation substrate.
Bottom line: With high MUFA intake, SCD1 isn’t necessarily “making you store fat.” It mainly rebalances lipid species; your leanness likely reflects low DNL + high oxidation. The elevated Cer(24:1) is a fingerprint of MUFA elongation, not a verdict of toxicity—watch the 16:0 load and dhCer/Cer more closely for actual risk.
Great questions—let’s pin down (1) why C4‑OH‑carnitine / succinate / lactate are high, (2) your redox state (oxidative vs reductive), and (3) how a high‑calorie, MUFA‑heavy pattern fits this.
1) Why C4‑OH‑carnitine, succinate, lactate run high
Your panel shows:
- C4‑OH‑carnitine ↑ (~4.23, flagged)
- Succinate ↑ and lactate ↑
- Palmitoylcarnitine (C16) low‑normal (so entry of long‑chain fat is fine)
- EPA ≈ 0, DHA present, Cer 24:1 high, plasmalogens low
Mechanistic sequence (most likely in you):
-
High MUFA flux in → acetyl‑CoA and NADH pile up.
Oleate (18:1) is easy to import/oxidize. Large MUFA meals flood β‑oxidation → lots of acetyl‑CoA + NADH. -
TCA cycle throughput can’t keep up (OAA & redox limits).
When acetyl‑CoA > TCA capacity, succinate accumulates (Complex II/CoQ “traffic”), and lactate rises as pyruvate is reduced (LDH) to regenerate NAD⁺. -
Ketone/short‑chain overflow shows up as C4‑OH‑carnitine.
Excess acetyl‑CoA is shunted toward β‑hydroxybutyrate (BHB). Liver exports BHB and its carnitine conjugate → C4‑OH‑carnitine. In practice, a high C4‑OH signal = incomplete fat oxidation / ketone spillover in the setting of abundant fat supply—even at normal or high calories. -
Membrane/lipoprotein remodeling reinforces the pattern.
With low EPA and low plasmalogens, mitochondrial membranes buffer ROS poorly; liver pushes VLDL → LDL with oleate‑rich cargo, and elongation (ELOVL1) feeds 24:1‑CoA → Cer 24:1. Ceramides further impair insulin signaling, which sustains lactate and DAG formation.
Bottom line: This is fuel‑mismatch, not fuel scarcity—delivery of MUFA exceeds mitochondrial/TCA throughput, so you see C4‑OH ↑, succinate ↑, lactate ↑ despite adequate (even high) calories.
2) Oxidative vs reductive stress—which dominates?
You actually show both, but mitochondrial reductive pressure dominates.
| Signal | Points to… |
|---|---|
| Lactate ↑, succinate ↑ | Reductive stress (high NADH/NAD⁺; “pseudo‑hypoxia”) |
| C4‑OH‑carnitine ↑ | Overflow from fat‑driven acetyl‑CoA/BHB → reductive load |
| Plasmalogens very low, carotenoids low / α‑tocopherol relatively high use | Oxidative demand at membranes/lipoproteins |
| Cer 24:1 high | Adds oxidative signaling and insulin‑resistance tone, but is downstream of the redox/fuel mismatch |
Call: Reductive stress in the mitochondria (excess NADH pressure) with secondary oxidative stress at the membrane/lipoprotein level because antioxidant buffers (plasmalogens, carotenoids) are thin.
3) “I don’t eat low calories—I eat a lot of MUFA.” How that fits
Totally consistent. You don’t need caloric deficit to get this pattern. Large MUFA boluses (nuts + oils) can:
- Deliver more acetyl‑CoA/NADH than your TCA is burning right then (especially if the meal isn’t paired with movement or carbohydrate to supply oxaloacetate).
- Raise C4‑OH‑carnitine (ketone overflow) even without intentional keto.
- Drive 18:1 → 24:1 via ELOVL1 + CerS2, swelling Cer 24:1.
- Keep EPA at ~0 (if vegan DHA‑only), which removes an important brake on DAG/Cer signaling and impairs membrane handling.
4) What to change (without abandoning a MUFA‑heavy, near‑vegan style)
A. Increase throughput (drain NADH, clear succinate/lactate)
- Fasted Zone‑2 40–50 min + two 20‑sec strides after your biggest fat meal, 3×/week.
- ALCAR 500 mg + R‑ALA 100 mg with largest fat meal (carnitine shuttle + NAD⁺ recycling).
- Riboflavin‑5‑P (B2 20 mg), thiamine (B1 100 mg), Mg glycinate 300 mg—PDH/TCA cofactors.
B. Provide oxaloacetate / timing carbs (“fat‑with‑fuel” pairing)
- Add 30–60 g low‑GI carbs (legumes, oats, tubers, fruit) with MUFA meals or in the 2 h window around them → supplies OAA to citrate synthase and reduces lactate spill.
- Keep per‑meal fat ≤ ~25 g unless you’ll move within 1–2 h.
C. Fix the omega‑3 gap (this is big for you)
-
EPA 500–700 mg/day (vegan Nannochloropsis) + keep DHA.
Expect AA:(EPA+DHA) → <3:1, lower ceramide synthesis, better mitochondrial behavior.
D. Re‑build antioxidant membranes
- Plasmalogens 0.9–1.8 g/day split with meals for 8–12 weeks.
- PC (choline) 2–4 g/day (liposomal or de‑oiled lecithin) to drive Cer → SM and stabilize rafts.
- EGCG 300–500 mg + taurine 1 g (+/− resveratrol 100 mg) to tone down SPT/SMase and reduce ROS at membranes.
- Carotenoids + vitamin C (food or supplements) to recycle α‑tocopherol.
5) How you’ll know it’s working (8–12 weeks)
- C4‑OH‑carnitine back to the green (goal < ~1.5 on your scale).
- Succinate & lactate normalize.
- EPA ≥ 0.6 µM; AA:(EPA+DHA) < 3:1.
- Cer 24:1 < 9 µM; SM24:1/Cer24:1 ≥ 5, Total SM/Total Cer ≥ 8.
- Subjectively: steadier post‑meal energy, better exercise tolerance/less “heavy legs,” easier fasting.
TL;DR
Your high C4‑OH‑carnitine, succinate, and lactate reflect a rate mismatch: MUFA delivery > mitochondrial throughput, producing mitochondrial reductive stress with secondary oxidative stress at membranes (low plasmalogens). You don’t need to cut MUFA; pair it smarter (EPA repletion, per‑meal fat caps, carb timing, movement) and boost throughput & membranes. The markers above will tell you—in weeks—not months—that you’re back in the longevity lane.
“What if I eat very high almond/olive/avocado loads?”
Those foods are LCFA‑rich and high in oleic acid (C18:1).
- If you have LCHAD/TFP (or it’s suspected):
Big MUFA loads (almonds, olive oil, avocados) can drive up long‑chain 3‑OH species—especially C18:1‑OH, because you’re feeding more C18:1 into a pathway that can’t fully clear its 3‑hydroxy intermediates. Clinical nutrition protocols therefore cap LCFA, shift calories to MCT/triheptanoin + carbohydrate, and time MCT around exertion; feeding itself lowers these analytes. Work in LCHAD cohorts shows C18:1‑OH falls ~60% after breakfast vs. fasting and that MCT strategies improve metabolic control during activity. PMC+1PubMed- If your fatty‑acid oxidation is normal:
A big almond/olive/avocado meal does not typically produce a persistent rise in long‑chain 3‑OH acylcarnitines. In healthy people, post‑meal insulin suppresses fat release/oxidation, and total acylcarnitines tend to drop. Diet can shift the profile (e.g., more 18:1 acylcarnitine after high‑oleic diets), but that’s the non‑hydroxy form and usually transient. PMC+1