Are there downsides to eating too many MUFAs/nuts?

#28

Some nuts with high oxalates (like almonds) can potentially cause kidney stones. I dealt with that for a bit.

However, I personally am on a MUFA-centric diet… and it’s helped my lipids, etc better than any other diet. There are areas of Italy where they avg around a liter of EVOO a week, and they tend to have abnormally long lifespans.

I currently get about 65% of my fats from MUFAs… and then try to split the remainder with saturated & polyunsaturated. It’s not an easy task, but I’ve done it through a daily smoothy that’s half EVOO, half vegies.

#29

Even respected researchers debate macros and fat types, but it does seem from research that the majority of issues coming from specific macro or fat mixes come from caloric excess. When the body needs energy and food supplies that energy, nothing is sticking around particularly long. It gets used to power daily energy needs. When you have a caloric surplus, now things start to get hairy. The body has to decide how to store away that energy and now you’re making longer-lasting changes to the body.

#30

I’ve significantly reduced my nut consumption over the past few weeks (ONLY over the past few weeks!!) b/c I’ve finally started properly using acarbose for once [why this took so long, I don’t know] and beans I can eat with zero BG increase (+I discovered other fruits that dont increase it much)

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#31

OIL, ~1.18 g/kg (they used canola oil for their MUFA…)

45*1.18/4.44 = 12 teaspoons roughly (this is comparable to what happens when I overeat MUFAs)

Upon OIL intervention, preclamp hepatic and whole-body insulin sensitivity markedly decreased by 28% and 27%, respectively, along with 61% higher rates of hepatic gluconeogenesis and 32% lower rates of net glycogenolysis, while hepatic triglyceride and ATP concentrations did not differ from VCL. During insulin stimulation hepatic and whole-body insulin sensitivity were reduced by 21% and 25%, respectively, after OIL ingestion compared with that in controls.

CONCLUSION

A single MUFA-load suffices to induce insulin resistance but affects neither hepatic triglycerides nor energy-rich phosphates. These data indicate that amount of ingested fat, rather than its composition, primarily determines the development of acute insulin resistance

==
I binged on a lot of olive oil lately (I remember binging on chia seeds last year) => both seeemed to be followed by unusually high resting BG.

There are papers that say the opposite (MUFAs reducing insulin resistance) but I’m interested in cases where one eats > 1000 calories of MUFA per day.

image

Both high-fat diets produced obesity and insulin resistance. EVOO-fed rats showed smaller increases in total cholesterol and arterial lipid peroxidation when compared with M-fed rats. Vascular reactivity to phenylephrine and sodium nitroprusside was not modified, but the vasodilating effect of carbachol was especially reduced in the M-fed rats compared with the EVOO-fed or control groups. Metformin addition to the incubation media decreased the vascular response to phenylephrine; decrease that was lower in rats fed with both high fat diets, and increased the carbachol and nitroprusside effects, but the metformin-enhanced response to carbachol was lower in the M group.

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#32
#33

I read somewhere that walnuts are the healthiest nuts. But walnuts also have way more PUFAs than most nuts

Tbf it’s consistent with everything else I’ve seen about PUFAs decreasing heart disease and overall mortality more than MUFAs.

Maybe the “soybean/vegetable oil = bad” studies show up because of the CHEMICAL PROCESSING used on it, rather than the linoleic acid/PUFAs themselves (processing is especially bad on linoleic acid/PUFAs). Chemical processing also makes soybean oil (and most seed oils) WAY less healthy than canola oil b/c of PUFA vs MUFA content.

Anyways I figured that my solution to the “overeating” nuts problem (even when still primarily going low-carb) is to just eat olives + nut milks, which have way lower calorie densities, making it MUCH harder for me to binge over 2000 calories than it is on nuts/avocados. Or add a bit of olive oil to coleslaw

Chocolate - I’ve found that unsweetened bare chocolate is the easiest chocolate to not overeat (just 2 Ghirardelli bars for the low lead/cadmium cocoa flavonols)

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#34

I over eat when I have macadamia nuts. I’m probably going to just have to stop buying them all together sadly. Even if they are raw and unsalted I will still eat too many unfortunately. :frowning:

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#35

What studies?

Walnuts tend to go rancid easily because of the PUFAS and the low amount of processing, altering the taste, etc.

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#36
#37

It’s a mice study. Very low quality evidence.

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#38

Lipid droplets and peroxisomes are co-regulated to drive lifespan extension in response to mono-unsaturated fatty acids

https://www.nature.com/articles/s41556-023-01136-6

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#39

They decrease mitochondrial oxidation and do not increase fragmentation, UNLIKE SFA

Screenshot_20230623_113550_YouTube
Screenshot_20230623_113550_YouTube1080×2400 172 KB

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#40

For so long I had the intuition that MUFA calories are not the same as calories from any other source, and so angry that all the fat (and even calorie restriction) research was on palmitate rather than on MUFAs. These last few studies/videos all but vindicate a large fraction of this intuition.

I almost ate an entire box of raw mixed nuts today (after a long MUFA break mostly b/c of beans). It’s >> 2500 calories, but I know from previous nut binges that I never seem to have detrimental effects (well, I had a very extended period [2 weeks] of binging in early 2022 and it resulted in some weight/BP gain that was reversible but I wouldn’t do that again].

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#41

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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#42
#43

"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

  1. 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.

  2. 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.

  3. 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.
#44

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

  1. 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.
  2. Fasted insulin / HOMA-IR / adiponectin:
    mild elevations (insulin > 8–10 µU mL⁻¹, HOMA-IR > 1.5) would corroborate lipid-induced insulin drag.
  3. 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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My iollo reports 2023 vs 2024
#45

" 60–80 g fat

…that… isn’t even that much… like… one box of blue diamond almonds…

#46

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.

#47

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

  1. SFA → MUFA conversion by SCD-1 lowers the FADH₂ : NADH ratio delivered to complex II of the ETC, reducing mitochondrial ROS.

  2. Low ROS fails to trigger “adaptive thermogenesis,” so calories are stored rather than burned.

  3. 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.

  4. Excess MUFA in membranes makes them more fluid, further activating SCD-1 in a feed-forward loop.

  5. 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.