The Croissant Diet FAQ

Are you serious? Is this some type of ruse or joke?

Of course it is!! When I was explaining the diet to a good friend doing the carnivore diet I was laughing uproariously. I amuse myself and yes, it’s meant to be cheeky.

BUT! I have done experimental science in a past life and I designed the diet to prove my point that “A primary regulator of whole body energy flux is the ratio of saturated to unsaturated fat.” If I did a modified keto diet with a specific fat ratio how would I know if the diet was working because of the keto diet or the fat ratios? Or something else like maybe the keto diet was low in food reward? It was important to establish that this diet is NOT based on macro ratios (fat, carb, protein) but that it is based on fat quality. Long chain saturated fat is the king of fats.

Perhaps more importantly, there are clearly millions of people out there who are never going to take the plunge into true low carb eating. I think the existence of a proven diet where people can lose weight eating pasta with butter is a good thing for the population in general. I love my carnivore friends and my keto friends and they can argue that those diets are more optimal than the croissant diet and they may be right. But I would argue that the croissant diet is based on the traditional diet of many groups of people around the world and that it’s clear that it is a safe, nutritious diet. And it certainly is very good for your metabolism.

You understand that this diet flies in the face of conventional wisdom, the Mediterranean Diet, the keto diet, the carnivore diet, the Atkins diet, recommendations from the American Heart Association and what I read in Redbook?

I understand that. I’m not terribly worried about it.

Is this a high fat diet?

It is! Croissants achieve their flaky texture because the starch is nearly saturated with fat. Croissants are a type of pastry that deliver well over half of their calories as fat, the majority of it saturated. The croissant recipe I’ve been following from Sally’s Baking Addiction is about 66% of calories from fat with 30% coming from carbohydrate and 4% from protein. I fill them with eggs and cheese and ham to make sure I’m getting protein.

Maybe the French are onto something? People have actually written books on this topic.

Are there other types of traditional French pastries that deliver such a high saturated fat content?

Of course there are! Pate a choux is the basic dough that makes creampuffs, eclairs and beignets! It is similarly high in fat. So is any “laminated dough”, the very flaky doughs that make fruit tarts and croissants. All of these are made from butter and flour. What about a butter pie crust or crumble? Pretty much the same macros.

The general term for these pastries enhanced with butter and eggs is viennoiserie. You’ll have to spell that for the quiz.

Sausage, egg and cheese on a homemade stearic acid butter oil scone, a British form of viennoiserie.

It was good.

Are there traditional foods other than pastries that deliver the same macros?

Sure. Pasta with Butter. Macaroni and cheese. Potato Chips or tortilla chips fried in beef tallow. Pasta Alfredo.

I’m sorry, you’re suggesting that insulin resistance is a GOOD THING?!

I’m suggesting that there are multiple types of insulin resistance and that the long term, irreversible type of insulin resistance that happens in type 2 diabetes is VERY different from the short term, physiological insulin resistance that should happen after every meal to shut off energy shuttling into fat cells and to help signal satiety. This is the “good” insulin resistance and it’s what the croissant diet is based on.

The mitochondrial electron chain is designed very specifically to generate ROS when saturated fat is being metabolized. This is an evolutionary strategy to let the cell know what the mitochondria is doing (metabolizing fat). ROS is the signal. When too many unsaturated fats are consumed and SCD1 is upregulated, not enough ROS is produced in the mitochondria and even if the mitochondria is metabolising fat the rest of the cell has no way of knowing what fuel is being burned and it can’t act appropriately.

In short, ROS production by mitochondria in response to saturated fat metabolism is an evolutionarily conserved signal that tells the rest of the cell what the fuel supply is like at any moment and what the cellular energy level is so that the cell can respond appropriately. The recent rise in PUFA consumption means that our mitochondria don’t produce enough ROS when we are burning fat and our cells therefore don’t know what fuel is being burned. This dysregulates our energy metabolism. The only way to fix our metabolism is to fix the fat ratios.

What are SFA, MUFA, PUFA and Stearic Acid?

  • SFA: Saturated Fatty Acids, AKA Saturated fat like in butter
  • MUFA: Monounsaturated Fatty Acids, like in olive oil
  • PUFA: Polyunsaturated Fatty Acids, like in soybean oil
  • STEARIC ACID: The second most prevalent saturated fat, found in large amounts in chocolate and beef tallow

So you’re saying olive oil is bad?! What about avocado oil??!

I’m saying those oils are bad IF you need to lose weight and if you prefer to continue to eat some starch. I know that a lot of keto dieters lose weight eating olive and avocado oil.

My argument is this: keto and croissants cause you to lose weight via a related mechanism, which is by reducing the signal from insulin. In the case of keto, by avoiding carbs you are reducing the amount of insulin that you produce in the first place. In the case of croissants, you are producing (probably) more insulin but you are shutting down insulin signalling further down the chain.

The mechanism that the croissant diet is based on is ROS production at the bottleneck in the mitochondrial electron transport chain. Unsaturated fats simply don’t produce enough ROS to shut down insulin signalling.

You may be thinking that there are traditional cultures that consume olive oil without becoming fat and you’re right. Interestingly, the body compensates for the consumption of monounsaturated fat by producing less SCD1 and when you eat saturated fat more SCD1 is produced. The body is trying to keep a balance of saturated and monounsaturated fats and that ratio is typically around 50:50. But when you grow up in a PUFA drenched world, I think you may need to compensate that by not eating large amounts of MUFA. The MUFA fed mice were fatter than the starch fed mice, after all.

Did the alcohol and flour help me to lose weight or would the stearic acid butter work just as well in a keto diet without the wine?

I don’t really know but I’ll speculate a little. A fat cell that has lots of ATP and is oxidizing saturated fat should be somewhat or entirely resistant to insulin due to ROS production in the mitochondria. Since insulin signalling is the thing that flips the switch to turn off fat metabolism, the fat cells should continue metabolizing stored saturated fat.

There is evidence that increasing the saturated to unsaturated fat ratio increases a protein in fat cells called GLUT1. GLUT1 is a glucose transporting molecule that works INDEPENDENTLY of glucose. So those fat cells WILL increase their metabolism of glucose as blood glucose rises. Not as much as if they were responding to glucose, but there will still be an increase. Cytoplasmically generated NADH from glycolysis is (sometimes, it’s tissue dependent) transported to the mitochondrial electron transport chain through something called the glycerophosphate shuttle, which delivers the electrons directly to Coenzyme Q. If this is the case, the glucose being metabolized would increase traffic at the bottleneck in the electron transport chain and therefore increase ROS production.

Lastly, alcohol doesn’t need to be transported into cells, it just diffuses through the membrane. Alcohol is known to cause ROS production, acute insulin resistance and lipolysis (the beginning point of fat metabolism).

So there is an argument to be made that one hour post Croissant and wine meal, the fat cells are metabolising saturated fat, alcohol and glucose at the same time which would presumably generate maximum insulin resistance and lead to continuous fat burning. Maybe.

What does the ratio of saturated fat to unsaturated fat have to be to cause weight loss?

This is a complicated question. I would say that the ratio of FADH2 to NADH produced in the mitochondria needs to be above 0.47, but 1) that number is non-trivial to calculate (it will be the subject of a future post), 2) that’s kind of assuming a simple system where fat is the only thing being metabolised and 3) there’s no way to know what percent of fat sent to the mitochondria is from stored, PUFA laced body fat VS from our pristine, low-PUFA croissant fat. I WILL say that a higher ratio of saturated to unsaturated is probably better and that your results may vary.

Is the total amount of fat important or just the ratio?

This is another question I don’t have a direct answer to. In the mice fed stearic acid, a 17% fat (as calories) diet didn’t produce fat loss and a 40% fat diet did. 40% is still not that much fat. I tend to lean towards a higher fat diet because I’m coming from the high fat keto world and I don’t like the idea of producing too much insulin and I like croissants and buttery potatoes.

Do you have to be very strict at each meal? If I eat a steak or god forbid a piece of skin-on chicken between meals will all hope be lost?

I cheated a fair amount and it still worked out OK. For social reasons I eat at a Mexican restaurant weekly. I’m sure everything there is cooked in vegetable oil. I also cheated with pizza once or twice a week and there is a little vegetable oil in the crust. The diet still worked for me. I was using a LOT of the stearic-acid-butter to try to overwhelm everything else. Your mileage may vary.

Is it necessary to enhance butter with stearic acid or would ordinary butter work?

I originally made the stearic acid butter because 1) the stearic acid worked so well in the mice, 2) I was worried that I would have to overwhelm the stored PUFA in my bodyfat, 3) I was worried I would have to overwhelm my presumably high production of SCD1, which unsaturates saturated fat and 4) stearic acid kicks the body into fat burning mode.

Obviously a skinny Frenchman in 1970, raised on flour and butter and steak and potatoes and low PUFA pork, didn’t need the extra stearic acid. But he didn’t damage his metabolism with years of PUFA. I can’t say whether you, personally, will need it.

Is this an overall healthy diet?

This diet is based on a traditional dietary pattern that has kept cultures in good health in Europe, Asia and Africa since the dawn of agriculture and in the Americas since 1492. Herding cultures in Asia live on starch, dairy products and meat. That’s it! They seem to be quite healthy. Dairy products provide vitamins A, D, K and E, calcium, potassium and phosphorous. Meat provides b vitamins, choline, iron, copper, selenium, etc. Starch provides calories.

Of course butter and flour isn’t a complete diet and in the specification I’ve tried to emphasize consuming nutrient dense foods like egg yolks, liver, seafood, meat, other full fat dairy products and vegetables.

You probably shouldn’t drink as much red wine as I do but I’m an adult and I can make my own choices.

Are there health benefits other than weight loss?

Everything I’m about to say is based on my understanding of the science but is also highly speculative!!!

I often say that while metabolizing saturated fat, the mitochondria generates ROS which shuts down insulin signalling. In particular, insulin carries out its role in the cell by activating a protein called Insulin Receptor Substrate (IRS1) which in turn activates a protein called PI3 Kinase. ROS blocks the activation of IRS1, which also means that if you generate enough ROS you shut down PI3 Kinase. PI3 kinase is considered a master regulator of cancer and many inhibitors of it are in clinical trials. Consider the snippet from this paper.

“PI3K inhibitors are effective in inhibiting cancer progression.” ROS generation in the mitochondria inhibits PI3K. Fat blends with a high ratio of saturated to unsaturated fat generate ROS in the mitochondria.

SCD1 is also increased by insulin signalling. If insulin signalling is shut down by ROS production, you make less SCD1. When you don’t make SCD1, your fat becomes more saturated. When your fat is more saturated, you generate more ROS, which reduces insulin signalling and lowers levels of SCD1. Which makes your fat more saturated. See the pattern?

Mice who lack SCD1 have lifetime protection against diabetes. And then there is the cancer connection.

“Studies have demonstrated the involvement of SCD1 in the promotion of cancer cell proliferation, migration, metastasis and tomur growth.” So I’d say that a diet that leads to a negative feedback loop resulting in ever lower SCD1 might not be such a bad thing.

One more benefit of ROS production is that ROS stimulates “autophagy”, which means self-eating, which is the process by which the cells break down and recycle old, worn out organelles like mitochondria. These old organelles can be a source of oxidative stress in the cell. Oxidative stress is associated with neurodegenerative diseases, cancer and inflammation, for starters. So a high saturated fat diet might induce autophagy which might reduce oxidative stress.

Overall, I feel pretty good about it.

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35 thoughts on “The Croissant Diet FAQ”

  1. Adrian Elizondo

    Are you worried aboud the methods of extration of stearic acid?
    Also, do you buy stearic acid or Stearin (
    tristearin)?

    This is a very interesting Blog!
    Thank you for the time you took writting it.

    1. I’m not really worried about it. The truth is I don’t know how they extract it so maybe I should be?? I’m not a huge worrier, I guess?

      I’ve been in a lot of food processing facilities. Although they suck at understanding scientific evidence of what is healthy, they all run very tight ships, follow GMPs (good manufacturing practices), etc.

      Brad

  2. I think I understand the overall theory. But I don’t understand why stearic is better than other saturated fats (e. g. palmitic) at mithocondrial level.

    1. It’s probably not. I mean, technically it has a higher FADH2:NADH ratio. And that’s important, but the difference is minor. There IS a whole body of research out there that says that stearic acid is somehow unique from other saturated fats, but I suspect that’s just an artifact of the anti saturated fat lobby.

      1. So the hypothesis would be that stearic acid is a supplemental approach to overwhelm the stored PUFA fat (in terms of ROS) in-order to maximize fat loss? (when the attempt it to regulate insulin beyond just low-GI diets)

        In other words, this could be effective in context of American type diet obesity/stubborn fat?

    1. It’s probably fine, it’s certainly a good source of calcium and other minerals. I guess I would say if it works for you, then don’t sweat it too much. Of course, a higher cream milk from something like a jersey cow is better and raw, unhomogenized milk is better yet if you can find it.

    1. When ordering stearic acid in larger quantities it is possible to get 90% pure but unfortunately stearic acid in smaller batch sizes rarely specifies whether its 90% or closer to 50% stearic. Either way, they’re all long chain sat fat.

      1. fireinabottle.net is now selling the 90% in one lb increments. It’s much better than most stuff out there. Much more neutral flavor and a lot less smoke.

  3. Made the New England clam chowder today. Eliminated the chicken fat and bacon fat. Made a blond roux with ghee. Malillard reaction on the garlic in ghee then sauté aromatics. Very nice flavor. Can’t wait for the delivery of my butter-oil.

    I think poor people in Italy would sauté garlic in oil and serve over spaghetti for a light dinner. I’m thinking substitute ghee and your good to go on that one.

    1. I don’t know about Italy but in upstate New York I’ve often seen garlic in butter over spaghetti. We’re working hard to make the butteroil project happen, thanks for your support!

  4. Brad, what is most important carbon chain length or degree of saturation? Recognizing that all cooking fats are a mixture should I be looking at distributions of carbon chain length?

  5. Any thoughts on how the body handles the excess insulin and glucose?

    It’s cool that the cell resists them. But, does that mean that the body remains in a high insulin/glucose state? Do other tissues use them? Does the body dispose of them? Do they just get used later (after the ROS is no longer being produced)?

    For Type 1 Diabetics, they are taught to manually inject insulin to “cover” excess blood glucose. Would you expect the blood glucose readings to remain high (which would cause the T1D to feel compelled to inject/bolus insulin for it)?

    If they did inject insulin, could it overcome the ROS signal or does ROS always win?

    I saw your reply discussing GLUT1. That makes me guess that BG would lower over time, but perhaps too slowly for the emotional comfort of a T1D who has been taught to fear high BG (and perhaps even concern a “normie” who wears a continuous blood glucose monitor for body-hacking/data-collecting purposes).

    Curious if the body would “dump” glucose through urine, etc. to “fix” the BG automatically (and how long that might take triggering fear and insulin injection/bolus by T1D).

    1. I suspect there’s not really that much excess glucose. Since I’ve been doing 65-70% of (solid) calories as fat, any given meal I consume at MOST 60g starch. It’s really not that much, so I doubt the BG response is that high. Dietary fat is preferentially delivered to fat cells so I suspect that’s where the Insulin Resistance is the most intense. Muscle cells and brain cells are probably happy to continue using glucose. Also, the decision to listen to insulin is a decision that happens individually in each cell. I suspect there is a whole spectrum of IR states on a cell to cell basis so I suspect insulin will eventually win that battle.

      Saturated Fat seems to upregulate BASAL, non insulin-dependent glucose uptake (yes, this is a thing), so that’s another mechanism to deal with the blood glucose.

      I don’t know enough about how this effect a T1D to speculate about it.

    1. Could be? I think weight loss is generally harder as you get older but I don’t think the basic principles change.

      1. Well, I shall give this a go and if I lose weight I can be your old lady poster girl. Mostly, though, I am trying this to normalize my eating and feeling about food overall. Eating should be normal; food should be good. 5 years of LCHF, Keto iterations, full-on carnivore and anymore I am afraid of food. Bet I am in a lot of company. But your points about cultures that thrive on meat, dairy and starch rang a lot of bells and so here goes. Will let you know how it goes!

        1. Me too. I’m 58 and been down the keto/carnivore route. No energy. Can’t lose that last 7lb. All older French women are skinny so I’m game for it. Then I’m switching to Peat style diet to boost metabolism.

    2. I’m a 53 year old woman and I’m giving it a try too. Similar to the other ladies I’ve just come off a month of carnivore and it was keto before that and paleo before that. I did see some success, but not to the level I’d prefer and there’s some stubborn fat that’s been resistant to coming off no matter what I’ve done. When I saw this diet originally I thought WTF? Really? That could work? Then my sense of humor kicked in and I thought how funny it would be if it did work. So I decided to give it a try for a few weeks. Yesterday was day 1. I wasn’t going to go through the hassle of making croissants. That’s way too much work. I made biscuits instead. I didn’t have stearic acid so I melted some cocoa butter and mixed it in some ghee. I’m going to have to tweak the biscuit recipe. I used way too much butter/cocoa butter and the biscuits came out crumbly. I ate them anyway because why waste the food and they did fit the regime. Regardless, it worked. It’s amazing how filling those biscuits were. I could only manage one and a half biscuits and a couple of scrambled eggs before I was so full I couldn’t eat another bite (this was lunch – I’d skipped breakfast). For dinner I had two biscuits and some shrimp ceviche. Again, I was incredibly full and felt very full for many hours afterward. The scale is lower this morning so this could actually work. Fun, fun, fun. Thanks Brad! 🙂

      1. Thanks for your post! I love the fact that you tried this because “it’s funny”. That’s why I did it in the first place. Probably I should say “paradoxical”, but funny is good, too 🙂

    1. Probably. Coconut fat is shorter in chain length. It’s probably OK, but I didn’t want to speculate.

  6. Early physiological insulin resistance (from consuming more saturated fat) would cause the adipocyte to reject further glucose/fat intake, but what happens to that glucose and fat that’s circulating in the blood outside of the fat cells? Wouldn’t that eventually be deposited as visceral fat if the fat cells keep rejecting it?

    1. This is, of course, a very interesting question and the simple answer is that I don’t know. What I suspect is that the buildup of glucose and fat in the blood is what causes the intense satiation on this diet and your body deals with it in time. Yesterday I made a flourless chocolate cake which is just butter, dark chocolate and eggs. It’s like a stearic acid bomb. I ate two slices before bed last night. I have this great meal planned for today but I don’t even want to eat. IDK when I’ll get to make it.

  7. Adriana Gutierrez

    For those of us who love salads, what would you recommend for salad dressing given the poor ranking of olive oil on the stearic acid chart?

    Where do heavy cream, sour cream and cheeses rank?

    1. I don’t recommend oil based salad dressings. In “The Croissant Diet Specification” I give my recipe for a cream and sour cream based dressing which I think is delightful. Someday, when I find a good source of lard, I will share my lard dressing recipe.

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