Liver is evil but need not be punished. SFAs.

What to serve with a liquid lunch, and a recipe for chocolate.

It’s like a feed forward downward spiral.  If you don’t eat saturated fat & MCTs prior to imbibing, then liver intentionally makes more PUFAs for the alcohol-induced burning ROS to molest.  Liver is evil but need not be punished.  SFAs.

Brief background: (Kirpich et al., 2011 & 2013)

Researchers studying alcohol in rodents know where they’re going and like to get there fast.  70 drinks per day fast.  Granted, rats metabolize faster than humans so it’s likely a little less… but a little less than 70 is still a lot of sauce.

The intervention:  Corn oil vs. Medium Chain Triglycerides (MCTs).  FTR MCTs are saturated fat and are abundant in MCT oil (duh) and coconut oil.Kirpich diets

The bender lasted 10 weeks, and well, a 35% alcohol diet bodes poorly for just about everything.Leaving Las Vegas

Especially liver.  Except if you’re on a PUFAless diet rich in MCTs.Kirpich liver data

Intestinal inflammation, endotoxin, and subsequent 3-alarm liver fire:intestine TNF

LPS and liver TNF

They were all pair-fed, but alcohol-fed rats weighed less because alcohol induces its own burning, on top of everything else (maybe some MEOS too, but to a similar effect).BW data

ie, excess alcohol ingestion results in higher TEETrogdor

More burning = more ROS = more bad news

Saturated fat is less susceptible to oxidative stress than PUFAs.  Corn oil is PUFAs.

Increases in dietary saturated fat increased liver membrane resistance to oxidative stress…” by replacing PUFAs with SFAs.

It works with cocoa butter too (You et al., 2005):cocoa butter

The absence of corn oil or presence of cocoa butter and/or MCTs is protective against alcohol-induced liver damage.  VERY protective.

It’s like a weird [cruel] trick – I’m led to think all alcohol ingestion is bad unless on a chocolate & coconut PUFAless diet.  Don’t get any ideas; I meant unsweetened or very dark chocolateI say ‘very’ dark because it just doesn’t seem prudent to carb-load prior to bending (insulin, SCD, etc., etc.).

“Fatty acid profiling demonstrated that alcohol feeding dramatically increased hepatic unsaturated long chain faty acyl species, particularly linoleic acid and oleic acid, which was attenuated by dietary MCT” (Li et al., 2013).  Huh?

It’s like a feed forward downward spiral.  If you don’t eat saturated fat & MCTs prior to imbibing, then liver intentionally makes more PUFAs for the alcohol-induced burning ROS to molest.  Liver is evil but need not be punished.  SFAs.


It probably takes a while to comprehensively remodel liver FA saturation, but why not pre-game with homemade dark chocolate?

8 oz. unsweetened chocolate
2 tbsp (1 oz.) Coconut oil

Sweeten to taste with either:
Erythritol (virtually calorie-free, provides bulk, non-laxative, and anti-diabetic),
Stevia (anti-diabetic, antioxidant, & renal-protective),
or Sucralose.

Optional: heavy cream (similar saturated fat quantity as cocoa butter, but a little more like MCT oil [some shorter chains]).

Gently melt chocolate, stir in other ingredients, pour into cupcake molds, refrigerate, and ¡voila!  Optional: sprinkle some sea salt on top prior to refrigeration.

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  • I imagined the following conversation:
    Person 1: Who wrote the study “Role of adiponectin in the protective action of dietary saturated fat against alcoholic fatty liver in mice.”?
    Person 2: You.
    Person 1: No I didn’t!

    • lol good one, Nigel. “Me?”

      • No, not you. You! …and so on, ad infinitum.
        Luckily, Hu wasn’t a co-author! 😀

  • Carole Sampson

    I once gave up alcohol for a month and all my friends suddenly became VERY BORING! So now I drink and my friends are interesting again. Guess I could just get more interesting friends, then I wouldn’t need to drink so much.

  • When people insist that a calorie is a calorie they tend to forget than an alcohol calorie is also a calorie.
    Some say that this PUFA-elongating effect of alcohol is being exploited at the hormetic level when a little wine with a meal puts more DHA into membranes.
    Here in NZ there was an old folk remedy of eating a mutton pie (stiff with mutton fat) before a night of beer drinking.

    • Hi George,

      Thanks for the comment, I hadn’t heard of that proposed hormetic mechanism before – need to think on it a bit – still seems like part of the downward spiral, no?

      And mutton pie prior to a bender, that’s great! I was wondering how long it would take for SFAs to exert their protective effect, how much of liver FA needed to be remodeled, but that anecdote sheds a little insight.

      all best,

      • A quick search dug up this. Maybe the alcohol increases the HUFA then the polyphenols spare the n3. And this helps with the putative (small) cardiovascular benefit from (small) amounts of wine.

        Red wine polyphenols protect n?3 more than n?6 polyunsaturated fatty acid from lipid peroxidation

        • Just to clarify what I mean by hormetic, which is often abused to mean “mysterious”; hormesis might mean that although we have evolved an improved detoxification capability in regard to some ancient toxin, we still retain some of the compensatory or repair responses that our ancestors evolved previously, to recover from the damage the toxin caused back when detoxification was less effective.

        • Thanks for the link. Perhaps I should’ve considered the doses we’re talking about: 2-3 vs. 70 drinks/d. Probably not too much in common between the two.

      • As for the pie, well in those days in NZ they drank beer every night and ate mutton pies every day. You needed a doctor’s prescription to buy margarine here up until 1974. Not much fear of PUFA overexposure.

  • Fantastic post!!! I do enjoy a nice rum on the rocks

    • Hi Anna, thanks! Perhaps some dark chocolate with that rum on the rocks?

      • Absolutely. I’ve been ‘supplementing’ with sat fat and dark choc prior to heading out for years (i.e.: dinner). Perhaps that’s why I’m such a high-functioning drinker..

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  • Thomas Hemming Larsen

    This review seems says “On the basis of the small amount of studies undertaken it would seem logical to recommend an iso-caloric diet (if weight loss is not a goal) of moderate total fat intake and low (<10%TE) in SFA to lower the risk of NAFLD development."
    Do you think it has merit as it goes against what you're saying? Or is it more about total calories?

    • I still don’t really see a need to limit long-chain SFAs – the physiological range of intake isn’t that high… you’d have to try hard, like eating a lot of cocoa butter, to really push it beyond some theoretical upper limit… and even then, would be limited by satiation – couldn’t do it for many days in a row, long enough to really impact lipid membranes, etc..

      • Thomas Hemming Larsen

        Ah okay, so its more about long chain SFA than SFAs in general?

        Cocoa butter is quite palatable – I could down quite a lot of it 🙂 I do agree that it gets boring for many days in a row.

        • “Ah okay, so its more about long chain SFA than SFAs in general?”

          yup. We don’t store medium chain fatty acids very well… like coconut oil

          • Thomas Hemming Larsen

            Yeah, I just wasn’t sure if that mechanism was valid in this case.

            Regarding the MCTs, is it possible to set a percentage of how much of it just passes through?

          • “Regarding the MCTs, is it possible to set a percentage of how much of it just passes through?”

            not much. Fatty acid absorption is very efficient (even for MCTs). Even if you ingest enough to cause diarrhea, I’m not sure if that much passes through…

          • Thomas Hemming Larsen

            That’s what I thought too. It was just in the way you wrote it sounded like there was a big difference since long chain SFA seemed to be a problem and not medium chain.