The Feasting Mimicking Diet For Carnivores

By Brad Marshall

I am starting a trial of a mostly carnivorous version on The Feasting Mimicking Diet.  Maybe some of you will join me?  The original trial was quite a success – I lost 15 lbs in 20 days and lowered my fasting insulin by nearly half!  

Many have asked about a carnivore version of this diet so I’ve decided to try it.  The key thing for me is finding palatable ways of incorporating lots of long chain saturated fats in a carnivore context – in my previous trials I used starch to absorb the fat.  

I’ve included a very simple recipe below but there are more to come!

The Diet

I recently published The Feasting Mimicking Diet on my blog, Fire In A Bottle.  The basic idea is to alternate periods of feasting and fasting with the goal of rapid weight loss.  The feasting keeps your metabolism high while the periods of fasting provide times where you are burning your own body fat.  I came up with the idea for the diet not out of a theory I’d been working on, but just from noticing what worked for me during my Croissant Diet experiment – when I ate enough highly saturated fat, and especially stearic acid, I wasn’t hungry again for a good long while.

Croissants are, of course, a classic French pastry made by layering butter and dough.  The best croissants are relatively low-carb, providing two thirds of their calories as fat.  The flour is really just there to hold the butter.  I made my croissants extra satiating by doping them with something called stearic acid – a long chain saturated fat (much more about LCSF further in this article).

For this diet I thought, why not just eat as much saturated fat as I can and see how long I can go. I made this drawing to illustrate the theory because obviously I’m really good at art.

In contrast to my feasting mimicking diet, an extended multi-day fast slows your metabolic rate down. Even though caloric intake falls, the amount of calories you burn does too…so you end up not losing much weight. Instead, I alternated a feasting day with a fasting day in a 48 hour cycle because it keeps metabolic rate high (I assumed) and I could do it without much hunger.  I typically eat the feast meal around 4PM and then no solid food the next day.

To test the metabolic rate idea I bought a fancy metabolic rate analyzer and used it over the course of the experiment.  Sure enough, my metabolic rate remained unchanged despite the fact that I was “fasting” (wine fasting) every other day. 

Let me explain more about why this works. 

Physiological Insulin Resistance 

Insulin resistance is not always a bad thing.  In fact, cells regularly cycle between insulin sensitive and insulin resistant states in response to meals, fasting, etc.  This is normal human physiology.

One of the things that drives physiological insulin resistance is the production of ROS (Reactive Oxygen Species) in the mitochondria.  You can read the whole story behind the science of this in my blog if you’d like to dig deeper, start with the Intro To Oxidation series and then read The ROS Theory of Obesity.

In short, though, when energy is being burned in the mitochondria, the electrons are transported by two molecules, NADH and FADH2.  Both of these molecules feed their electrons into the electron transport chain to produce ATP.  There is a bottleneck effect.  When cells are burning glucose, electrons are mostly transported on NADH, the bottleneck is not overwhelmed and very little ROS is produced.  When cells are burning long chain saturated fats. Much more FADH2 is used, the bottleneck is overwhelmed and maximal ROS is produced.  This ROS blocks insulin signalling. 

The problem with unsaturated fats is that for each unsaturated bond, one less FADH2 is produced.  Unsaturated fats don’t overwhelm the bottleneck and don’t produce much ROS and therefore leave the fat cells in an insulin sensitive state.  

This type of physiological insulin resistance is targeted at a few tissues which produce a hormone called LPL (lipoprotein lipase).  That enzyme can offload the fat cargo of the triglycerides from your meal.  LPL activity is highest in abdominal fat.  So abdominal fat is the most responsive tissue with regard to dietary fat. If dietary fat is highly saturated, the abdominal fat cells remain insulin resistant and continue to feed the body (fat burning mode).  If the meal is mostly unsaturated fat, the abdominal tissues listen to insulin, shut down lipolysis and start storing fat (fat storage mode).

The traditional carb-insulin model suggests that carbohydrates raise insulin levels which leads to continued energy storage.  But it only looks at one side of the equation in the context of the standard american diet – starch with vegetable oil.  Targeted physiological insulin resistance in fat cells is the other side of the equation.  It prevents fat storage in the presence of insulin.  This explains why mice fed starch and stearic acid, the French in 1970 eating croissants and Americans in 1940 eating cream and potatoes all were lean.  They were producing insulin but fat storage mode was in the off position due to ROS generation in the fat cells due to the high FADH2:NADH ratio of the fats in the diets.

The converse scenario – starch in the presence of vegetable oil – explains why modern Americans and the entire Middle East are now facing an obesity epidemic.

Hunger

My working hypothesis is that a major trigger for hunger is low circulating energy.  Potential energy sources include blood glucose, free fatty acids, ketones, triglycerides (really chylomicrons – more on this later) and ethanol, among others.  When one or several of these drop, hunger is spiked.  

A question I’ve always had is, “If I’m fat then why am I hungry?”  I certainly don’t need the energy.  The thing is that most cells of the body cannot use the body fat as a fuel source unless fat cells are releasing their stored fat as Free Fatty Acids through a process called lipolysis.  One way to prevent hunger is to have a high supply of Free Fatty Acids.  

A major effect of insulin signalling to fat cells is to stop lipolysis.  Insulin is telling your body that dietary calories are coming in and therefore fat cells no longer need to feed the body.  So in a healthy person, Free Fatty Acids drop after a meal.  A major determinant of hunger, then, is how quickly Free Fatty Acids rebound.

The last piece of this puzzle is that a necessary component of satiety is ROS production in the hypothalamus. The hypothalamus is an organ that plays a huge role in regulating appetite.  It is really responsible for sensing low blood energy levels and signalling hunger. The more highly saturated a fat is, and therefore the higher the FADH2:NADH ratio is, the more ROS will be generated in the hypothalamus and it will signal satiety.  So if you’ve eaten butter, you’ll have higher circulating free fatty acids for a long period of time which are producing ROS in the hypothalamus which is signalling satiety.

In fact, the hypothalamus is one of the other tissues that produces LPL, the enzyme that causes chylomicrons (AKA triglycerides in the Spanish butter example) carrying dietary fat to release their cargo, so the hypothalamus is monitoring the amount of circulating triglycerides in addition to circulating free fatty acids, blood glucose ketones, etc.  

You may be thinking that in metabolic syndrome, people have high triglycerides and so shouldn’t that be causing them to reduce intake due to ROS generation in the hypothalaumus?  The problem with this is that the triglycerides in those individuals is mostly from body fat, as opposed to dietary fat, and the body fat of obese people is highly unsaturated.  So these triglycerides will not generate sufficient ROS for satiation.

How This Looks in Real Life

When you eat, insulin is produced.  A mixed meal of starch and fat causes the most insulin release, but insulin is also released when you eat a steak.  At normal physiological levels, in an insulin sensitive person, a primary role of insulin is to tell fat cells to stop doing lipolysis, which is when fat cells release Free Fatty Acids (FFA) to feed the rest of the body. 

The chart at the left is from a study done in Spain.¹  All participants were fed 800 calories of mostly fat (160 calories of starch) and their blood levels of blood glucose, insulin, triglycerides and Free Fatty Acids (FFA) were tracked over time.  The fats given were butter, olive oil (ROO) high palmitic sunflower oil (HPSO)  or a mixture of vegetable and fish oil (VEFO).

All groups have an insulin spike.  In response, FFAs drop in all groups.  But the Free Fatty Acids (bottom chart)  drop less in the group given butter than the others.  The fat cells of the group given butter are less sensitive to insulin!  Those fat cells are burning butter, which is creating a high FADH2:NADH ratio, which is driving ROS production which lowers insulin signalling.  Their Free Fatty Acids never dip as low and they rebound to higher than baseline levels by 4 hours.  None of the unsaturated fats have the same effect.

If my theory is correct, that a hunger trigger is low levels of circulating energy, this is very important.  In all of the groups blood glucose returns to baseline within 3 hours.  

Therefore the ONLY group that had circulating energy levels higher three hours after the meal is the group given butter due to higher levels of Free Fatty Acids.  In every other group, at the three hour point, they have lower circulating energy and therefore are likely to be hungry.  Those groups have less available energy due to the fact that they’ve eaten.  I’ll say it again.  BECAUSE they’ve eaten they have less energy availability.  The ONLY group that has more circulating energy due to the meal is the group that ate butter.  This is due to the fact that butter has a very high ratio of long chain saturated fats to unsaturated fats and therefore has a high FADH2:NADH ratio, which makes their fat cells physiologically insulin resistant which means that their fat cells continue to feed the body.

Now let’s look at triglycerides – this is fat being absorbed in the intestine and released into the blood as chylomicrons which hasn’t yet been stored or burned.  They are a circulating energy reservoir.  In all the unsaturated fat groups they drop to baseline by hour six but the butter group has elevated triglycerides even after 8 hours!  

Ok, so I’m saying a lot of scary things.  Insulin resistance, triglycerides, high free fatty acids, reactive oxygen species…  It sounds like perhaps I’m describing metabolic syndrome?!  

Each of these things has a normal physiological role that when things become dysregulated become pathological.  There is a lot of context to it.  For instance, a type two diabetic doesn’t reduce circulating free fatty acids in response to insulin at all.  This is pathological.  Free Fatty Acids SHOULD drop in response to insulin, we just don’t want them to drop TOO FAR and for TOO LONG.  And triglycerides are just the body’s way of moving dietary fat through the body.  So high fasting triglycerides could be a sign that something is wrong metabolically but high triglycerides after a meal is just normal biology. Don’t worry, after an overnight fast, your triglycerides will return close to your baseline value.

So let’s think for a second about the triglycerides in the groups eating unsaturated fats.  In all of those groups, the triglycerides disappear from the bloodstream after 6 hours.  WHere did they go?  They were taken up by insulin sensitive fat cells and stored.  The butter group at 8 hours is still running on fat form the meal.  All of the other groups are a little fatter and hungry.

So how do we avoid post meal hunger?  By consuming enough highly saturated fat in a meal so that Free Fatty Acids will rebound to ABOVE baseline by the time triglycerides return to baseline.  In the study above, with every fat that was less saturated than butter this didn’t happen.

Insulin Release and Fat Ratios for Carnivores

You might be thinking that on a carnivore diet you won’t produce a lot of insulin and therefore hunger following a meal won’t be a problem..  But in fact protein combined with saturated fat DOES produce a significant insulin release.  In fact, calorie for calorie, beef stimulates more insulin release than pasta!³  So the same principle applies with or without the starch.  It is very possible for a steak to leave you with less circulating energy three hours after a meal.

You may also be thinking that if you’re a carnivore, all of your dietary fat is highly saturated.  In fact there is quite a spectrum!  Here’s a table of the ratios of long chain saturated fats to unsaturated fats (polyunsaturated fats count double) excerpted from Introducing The Croissant Diet.

	Ratio SFA/UFA	Stearic Acid
Butter	1.47	10%
Beef Suet (Kidney Fat)	~1.5	~35%
Beef Tallow (USDA)	1.00	19%
Beef fat from a Ribeye Steak	0.80	13%
Lard (From a pig I raised, wheat finished)	0.73	??
Corn Finished Lard	0.59	13%
Lard fed 16% Distiller’s Grains	0.32	8%
Chicken Fat	0.34	5%

As you can see, the range is huge!  Can we be sure that ribeye fat down at 0.8 will have the same effect as butter, way up at 1.47?  But beef suet has as high a ratio as butter and more than three times as much stearic acid!

Pork fat is all over the map!  It all depends on the breed of the pigs and what you feed them.  There’s more info about this topic in my article Disastrous Trends In American Bacon, and (shameless plug) I am offering Low-PUFA pork CSA shares at Firebrand Meats to combat these trends.

So if you’re eating a lot of bacon and chicken fat, you may not be able to drive the level of ROS production in your fat cells and hypothalamus to maintain physiological insulin resistance and satiation.  Those fats might just simply get stored in your fat cells, leaving you hungry.

Feasting and Fasting

After I posted The Feasting Mimicking Diet I received several comments that the cycle of feasting and fasting was an unnatural way of eating.  Soon thereafter, Amber O’Hearn posted in the thread on Twitter: Especially if you were using the traditional Carnivore principle of eating until “Thanksgiving full” at every meal and then not eating again until hungry.

Especially if you were using the traditional Carnivore principle of eating until "Thanksgiving full" at every meal and then not eating again until hungry.

— L. Amber O'Hearn (@KetoCarnivore) August 8, 2020

Then while researching an entirely different topic I stumbled onto this passage about Native Americans: “they will eate till their bellies stand forth, ready to split with fullness; it being their fashion to eate all at some times, and sometimes nothing at all in two or three dates”²

The more I look into things, I start to think that maybe this weird diet I came up with isn’t so weird after all.

Fasting Cheats

I define fasting days as days where you don’t consume anything that will spike insulin.  It doesn’t necessarily mean zero calories but a fast day will be a low calorie day.  The only macromolecules that really don’t spike insulin are ethanol and pure fat.  The Catholics were way ahead of us on this one.  During strict following of lent, in weeks two thru six, on Saturdays and Sundays wine and oil are permitted and nothing else!  Of course, your mileage might vary on this biohack.  If you’re not a regular consumer of ethanol, you can experience a drop in blood sugar and get the munchies.  I’m wine adapted and this is not a problem for me.  I’ve tested my blood sugar before and after a bottle of wine with zero change.

I personally just drink some dry red wine to ease me through the fasting days, but as a strict carnivore, I suspect something like a fatty beef broth would work just fine.

Another thing that could help the fast day is eating a small amount of Carnivore Aurelius’s beef liver crisps. They’re packed with nutrients and low calorie. Yes, because of the protein they’ll spike insulin — but because they’re low in fat, the spike will be minimal and short lived. His customers have also found that they’re very satiating because of the high protein and nutrient content.

Putting It Together

The concept of The Feasting Mimicking Diet is that you maximize the amount of long chain saturated fats you can consume in a single feast meal while minimizing unsaturated fats with the goal that hunger is pushed off for as long as possible.  The reason this works is that the long chain saturated fats cause your fat cells to become relatively unresponsive to insulin and therefore the fat cells continue to release Free Fatty Acids to feed the body.  You’re not hungry because your fat stores are being released.  You are now living on your own fat!  In fact, the longer the fasting part of the cycle continues the higher blood levels of Free Fatty Acids you will have, blunting hunger.

Carnivore fats to avoid:  Most pork and chicken fat.

Carnivore fats to aim for: beef suet (kidney fat).

Other fats to consider:  butter, cocoa butter, fats enhanced with stearic acid.

While fasting, you can use alcohol or pure fats (or fat with a little broth)  to blunt any hunger pangs while minimizing insulin release so that your fat cells continue to release their cargo.  Of course, I’ve used starch as a vessel to consume large of amounts of beef suet and/or stearic acid enhanced butteroil.  I’ve also used wine as a fasting tool.  In principle, you shouldn’t have to do either.  If you can find beef suet, I know some people who consume it raw and some who sautee it and eat it.  

I’m Going To Try The Carnivore Feasting Mimicking Diet

Since I’ve been asked the question a lot now, I’m going to try a carnivore (ish) version of The Feasting Mimicking Diet – mostly beef plus black coffee, red wine, butter and some spices.  One problem with this is that I don’t really LIKE eating beef suet or stearic acid enhanced butteroil straight up.  The mouthfeel is waxy and just eating straight fat doesn’t work for me.  My primary concern with this is not getting enough fat and calories at the feast meal to make it through the fast period without hunger.

The good news is that in my past life I was a meat scientist. I’m developing a couple of recipes to make consuming highly saturated fats more palatable for carnivores.  Here’s an easy one to get started with.  Check back in at Fire In A Bottle for more recipes!

Steak with a Stearic Acid Enhanced Butteroil Pan Sauce

1. Start with your favorite cut of steak.  If this is meant to be a feast meal, you should start with a large portion!
2. (Optional) Season the steak with salt and pepper.
3.  Cook the steak to your liking in a large skillet and remove from the heat.
4. (Optional) Add some minced garlic, onions or shallots to the pan plus a sprig of thyme and sautee briefly.
5. Deglaze the pan by adding a half cup or so of beef broth, water or wine and using a which or wooden spoon to dissolve the brown bits that are stuck to the pan.
6. (Optional)  Add a tablespoon of mustard to the water and whisk it in.  The mustard acts as an emulsifier and will give you a creamier sauce in addition to a tangy flavor.
7. Add 4 tablespoons of butter, Stearic acid enhanced butteroil or rendered beef suet to the skillet.  Once it has melted, whisk it all together and serve with the steak.  Magnifique!

References

1. Sergio López, Beatriz Bermúdez, Yolanda M Pacheco, José Villar, Rocío Abia, Francisco JG Muriana.  01 September 2008.  Distinctive postprandial modulation of β cell function and insulin sensitivity by dietary fats: monounsaturated compared with saturated fatty acids.  The American Journal Of Clinical Nutrition.  Volume 88, Issue 3, September 2008, Pages 638–644.
2. William Wood, New England’s Prospect (London, 1634), pp.75-77, 105-08.
3. Susanne HA Holt, Janette C Brand Miller, and Peter Petocz. 01 November 1997. An insulin index of foods:the insulin demand generated by 1000-kJ portions of common foods.  The American Journal of Clinical Nutrition.  Volume 66, Issue 5, November 1997, Pages 1264–1276.