Transcription
All right guys, this is Swamp Living, the French Diet. I got a lot of questions after last week's video where I talked about two ends of the macronutrient spectrum and the advantages and the sort of magic of eating a very low-fat diet, and also the magic of eating a very low-carb, ketogenic diet, a very high-fat diet. I got a lot of questions about the middle ground, about the swamp.
I've talked on my blog a lot about the traditional French diet, which is of course very high in butter, and they're eating cheese and bread, cheese and baguettes, butter and baguettes. Um, and why does that diet work? In a subtitle of this video, we're going to talk about how PPAR Alpha controls fat composition, and what I mean by that is how PPAR Alpha controls your body fat composition. So this is pretty cool. This is actually a theory I've sort of been working on for a while. Uh, it's theoretical, but I think you'll see there's a lot of basis to what we're going to say here.
And so, just a recap, in the last video, I introduced, uh, this slide from that I stole from Denise Minger's "In Defense of Low Fat," and she told me she liked the video, so I don't think she's too mad that I stole it. Here's, here's the magic on the low-fat end of the swamp. Here's the magic on the high-fat end of the swamp. If you want to check out that video from last week, it's called "Keto vs. The Potato Hack" on Fire a Bottle YouTube.
In this video, we're going to talk about how it is that the French can live in the middle, in the macronutrient swamp land. And that means that calories from fat might be 40%, calories from carbohydrates might also be 40%, and yet, uh, the tra, the traditional French are lean. I also made a video about that called "Metabolic Challenge: France, Spain, Italy," looking at the difference between, uh, health statistics in France versus the neighboring countries, Italy and Spain, on a Mediterranean diet. So let's get into it.
This is taken from Julia Child's "Mastering the Art of French Cooking." This is the first recipe in the chapter about how to cook chicken. You can see this is, is roast chicken. I picked this recipe because I'm going to argue that if you are going to eat in the swamp, you have to consume highly saturated fats. Examples of cultures where they ate, uh, carbohydrates with fat and remain lean are a lot of the European countries like France and Switzerland, eating a lot of dairy products, which are very saturated, with baguettes. The traditional American diet, um, where people were lean up until 1960 or 1970 or so. There's also the diet of Tokelau and the Pacific Islands where they ate a lot of fat from coconuts, which is very saturated, along with things like breadfruit, which was a source of carbohydrates.
But the French have been doing this a long time, and they have a lot of tricks, and it's built right into the, in France, they have this long tradition of the French chefs and this handing down of knowledge, and you do things a specific way. There's a lot of tradition based around their cooking, and meals are served a certain way. And so this book, this chapter, or this recipe really dials in on a lot of that.
Chicken fat is highly unsaturated. So it would seem that if you are living in the swamp, you don't really want to be eating a lot of chicken because chicken is mainly monounsaturated fat, and it has a lot of polyunsaturated fat. It's only the fat in a chicken is only around 30% saturated. Uh, that is a lot less saturated fat than I would recommend if you're living in a cuisine where you're combining fat, fat, and starch and trying to maintain your metabolic health.
What do they do in France? You can see the recipe is roast chicken, and the first thing in the recipe is the wine suggestion to go along with it. So, of course, they're consuming wine with their chicken. This over here in red, uh, this is the sauce that goes on the final chicken. You can see they're using a chicken stock or chicken broth. So in addition to consuming muscle meats, the French are consuming gelatin-rich broths with most of their meals in the form of these sauces. And so those are kind of previews because I probably will have upcoming videos about wine and also about, uh, consuming broth and gelatin.
But for the purpose of this video, I want to focus on what is going on with fat composition. The recipe starts with a three-pound ready-to-cook roasting or frying chicken. Those chickens back when this book was written took a lot longer to grow than they do today, and they weren't as fatty in the first place. And she says to rub the chicken with butter, then she says is to baste the chicken, add more butter, and oops, even a tablespoon of cooking oil. Julia Child does not use a lot of cooking oil in, uh, "The Joy of French Cooking," but it is, but it does show up here and there. I'm not trying to minimize that, right? It's in the recipe.
But you've probably already noticed if you're watching this, uh, this step that I have highlighted in green. So we're roasting a chicken, we're basting it in this, uh, in in butter and oil, but then when we get to this step, we're going to remove all but two tablespoons of fat from the pan in which we cook the chicken, and we never come back to that. That presumably gets discarded. And then we're going to add our broth to that, and we're going to add more butter. We're essentially going to double the amount of oil.
Now, when we think about the composition of these drippings, remember that we've added four tablespoons of butter already. This is going to be more saturated. This oil that we're removing is going to be more saturated than probably what came out of the chicken normally, because butter is that much more saturated than chicken fat, and we'll show that. And then we're going to add more butter to that. So, so the final, and this is going to be a sauce that we're going to serve on the chicken, this butter and the stock and the salt and pepper. And so the chicken is going to be served with this very buttery sauce of very saturated fat. And of course, a lot of the fat that's started on that chicken is going to be rendered out of the bird.
Furthermore, you can see, uh, her vegetable suggestion is one of the potato casserole recipes on page 523. And so I went ahead and grabbed one of those recipes. This is, uh, scalloped potatoes. You can see you've got two pounds of boiling potatoes, and you're adding to those potatoes four tablespoons of butter, a cup of grated Swiss cheese, and a cup of boiling milk. So even though this meal is based on eating a chicken, the final fat composition of this meal in total is going to be very saturated when you consider the butter that's added to that sauce that the chicken was served with, and the butter that is added to the potato dish.
And so here I have these numbers are from, uh, the USDA Food Data Central. The fat numbers never added up to 100, so I've adjusted them, uh, into percentages based on what's being reported. And you can see chicken fat is about 32% saturated, butter is about 70% saturated. Uh, monounsaturated, uh, the chicken is about 48%, so that's the chicken is plurality monounsaturated, and it's got about 21% PUFA, whereas the butter is only 26% monounsaturated and three and a half percent PUFA in this case. And so if you were to combine them, if you assume that roughly in this meal, what you actually eat is about half chicken fat and butter, that means that your saturated fat consumption is going to be up to 51% of the meal. Monounsaturated fat is going to be down to 36%, and polyunsaturated fat is going to be down to 12%. And it might even really be 65% butter and 35% chicken fat when you actually figure out all of the fat in the recipe.
Now, again, you can check out my videos from, uh, the last couple of weeks if you want to learn more about PPAR Alpha. But this slide is pointing out what does PPAR Alpha do? I talked about it in the last video, but so PPAR Alpha is a nuclear receptor. What it's doing is it's looking for signals from the outside world, and then it's upregulating different genes in the cell, and it's making things happen by controlling the expression of other genes. Mostly what PPAR Alpha is looking for is different fats. It's looking for dietary oleic fat that gets triggered by something called OEA that's produced when you eat it. It's looking for alpha-linolenic acid and other long-chain omega-3 fats.
When PPAR Alpha gets triggered by those types of fats, is it turns on genes involved both in breaking down fat and in making fat at the same time. Now, that seems like a weird thing to do. It would be like setting up a factory that's breaking down Honda Civics and rebuilding them into Honda Accords, and you're spending a lot of time and energy and money to do this when you've already got perfectly good cars. The only reason you would do that is if for some reason you really preferred Honda Accords to Honda Civics, right? And it looks like that's what PPAR Alpha is doing, right?
And so here's the chart of things that trigger PPAR Alpha. You see, uh, this is alpha-linolenic acid, like in flaxseed oil. So this can massively activate PPAR Alpha if it's around in high enough quantities. This is, uh, this is in coconut oil, actually. This is 12-vol. This is lauric acid. It's a short-chain or it's a medium-chain fatty acid, really. It's a medium-chain saturated fatty acid. And these are monounsaturated fats. So this is oleic acid, like in olive oil. You can see that palmitic acid actually activates PPAR Alpha at very low levels. PPAR Alpha is not particularly triggered by linoleic acid either.
When you look at, at human fat composition or fat composition in livestock, so I raised pigs for a long time, and I went through great pains to give them great pasture. We rotated them to fresh pastures every day. We were feeding them a diet of mostly barley, which is low in linoleic acid. So I was trying to create a, a pork fat that was balanced in linoleic acid and alpha-linolenic acid, which comes from the pasture. So I made sure that their diet was, they were getting more or less 50/50. And I did some fat testing, and it actually didn't matter. The pork fat from those pigs still had something like a 12:1 ratio of linoleic acid to alpha-linolenic acid, even though I was strictly limiting their linoleic acid and giving them as much alpha-linolenic acid as I had.
Because look what happens. The alpha-linolenic acid triggers PPAR Alpha, and the linoleic acid doesn't. This is the one that sticks around. This is the one that accumulates. There's a study somewhere, sorry I didn't clip it for this video, where people fed pigs sunflower seeds. They had extra sunflower seeds. They just wanted to see what happened. So they fed pigs like 40% of their diet was these sunflower seeds, and the fat in those pigs went all the way up to 50% linoleic acid. That was in pig fat that was 50% linoleic acid. And so you can absolutely accumulate, uh, linoleic acid to a much greater degree than you can alpha-linolenic acid.
This is just another view at how all of this works, and so you can see these fats here that I say that are that I'm saying break it down at the right concentration, they're all activating PPAR Alpha. And since the primary end product of de novo lipogenesis is palmitic acid, when that palmitic acid level starts to build, that then inhibits PPAR Alpha and it shuts down this whole process of converting unsaturated fats into saturated fats. So PPAR Alpha controls fat composition, and the way that it does that is that unsaturated fats and medium-chain saturated fats trigger it to break down fats and rebuild them, which it rebuilds them into mostly palmitic acid, some stearic acid, and oleic acid. And the target we can see by looking at traditional cultures is probably something around 40% saturated, 50% monounsaturated, and 10% polyunsaturated.
Okay, so that was my little nerd out about PPAR Alpha and how what it's doing is it's recognizing unsaturated fats, and that is the trigger to break them down, rebuild them into saturated fats. Let's bring that back to that French meal. What you saw in that recipe was that the saturated fats, remember the keeper fats that don't activate PPAR Alpha, went from 32% of the fat in the chicken to more than half, probably more like two-thirds of the fat in the final meal. And so the chef in France is removing the less saturated fats, the ones that are more likely to trigger PPAR Alpha, and they're replacing it with more saturated fats at the table so that your body doesn't have to do it.
And why does that happen? Well, let's look at what causes de novo lipogenesis, which is the process of building new fat. And so this is the Krebs cycle. I've talked about it in a lot of the videos. Krebs cycle is how we get ATP from our food. First, you can see what I have written down here at the bottom is beta-oxidation of fat. So this is a scenario where if PPAR Alpha is in control, you're going, what happens is you, you lower your metabolism of carbohydrates and you increase your metabolism of fats. So that's what the oleic acid in that chicken would do is it would, um, it would activate PPAR Alpha. You would oxidize more fat, and so you would have a lot of acetyl-CoA because, uh, beta-oxidation of fat produces acetyl-CoA directly.
Now, I talked a lot about this in the last video, "Keto vs. The Potato Hack," but beta-oxidation of fat and increases the concentration of acetyl-CoA in the cell, and it increases the amount of NADH. And those two things, in both inhibit the activity of pyruvate dehydrogenase. Pyruvate dehydrogenase is the enzyme that breaks down pyruvate. Pyruvate comes from the glucose that we eat or the starch that we eat. And so if we don't have pyruvate dehydrogenase activity, we cannot use pyruvate dehydrogenase to break down incoming glucose. And there's a lot of benefits to pyruvate dehydrogenase. I've talked about it in a ton of my videos, including "The Redux Case for Carbs in 10 Minutes." So check that out.
As I said in the last video, the fact that pyruvate dehydrogenase is inhibited might be fine if you're living in a ketogenic diet context. However, if you're consuming a fat that's high in oleic acid, which is activating PPAR Alpha and pushing up acetyl-CoA, what happens is the glucose still comes in from your food. It still gets converted to pyruvate, but now the pyruvate is going to go through this alternate, uh, pathway called pyruvate carboxylate. And this is important because again, if you watch the last video, you will have seen that oxaloacetate is absolutely crucial for doing de novo lipogenesis.
If all that you have is acetyl-CoA coming in from fat, what happens is this is a whole cycle, and it goes around in citrate becomes oxaloacetate. And in a genic context, this oxaloacetate becomes limiting because this is what your body steals away to make blood glucose. It does gluconeogenesis. In ketogenesis, what happens is you run out of this oxaloacetate and you start just dumping these acetyl-CoA groups as ketones. However, if you have a steady supply of incoming glucose, and if pyruvate dehydrogenase is deactivated because you have an active PPAR Alpha, you can use this incoming glucose in pyruvate to steadily replenish oxaloacetate.
And this beta-oxidation of fat is continuously replenishing acetyl-CoA. And if that happens, acetyl-CoA and oxaloacetate can combine to make citrate. Citrate is the starting product of de novo lipogenesis. Citrate gets exported from the mitochondria, and we use the citrate to do de novo lipogenesis. So in this way, you can use the carbon coming in from beta-oxidation of fat to make acetyl-CoA, and you can use the carbon coming in from glucose to make oxaloacetate, and you can combine the fat calories and the carbohydrate calories to do de novo lipogenesis, and you can rebuild new fats.
So if you're in the swamp, and if you're activating PPAR Alpha, so you can actually take both your fat and your carbs and you can repackage them into shiny new fat that you just made in your cell from de novo lipogenesis. This is a boring molecular biology slide. I'm not going to make you think too much about it, but PPAR Alpha also directly inhibits pyruvate dehydrogenase.
Okay, so let's recap. What the French are doing is they're minimizing activation of PPAR Alpha by changing the types of fats that they're eating to more saturated ones. Saturated fats don't activate PPAR Alpha, and in high quantities, they inhibit PPAR Alpha. And therefore, this whole cycle of breaking down fats into acetyl-CoA at at accelerated levels, and then rebuilding them through the process of de novo lipogenesis, is inhibited. When you're not doing that cycle, that means that you're not rebuilding all of your dietary fat and your dietary carbohydrate back into fat via de novo lipogenesis.
The French are also consuming wine with their meal. Uh, that's also supposed to say "glass of Cinsault" with the L in the T swapped. It's a type of fancy red wine grape that's grown in France. Anyway, this is another study, and I'm just going to, I'm just going to point this out real quick because we're going to have another video about it. But interestingly, PPAR Alpha is actually directly inhibited by ethanol. When you consume ethanol, it's broken down in the liver into acetaldehyde, and the acetaldehyde directly inhibits PPAR Alpha. And so you can see what they're looking at is fatty acid binding protein. Protein is a target gene of PPAR Alpha. What they're doing is they're trying to produce fatty liver disease in these mice, and a good way to produce fatty liver is to feed mice a lot of PUFA, a lot of polyunsaturated fat, and ethanol at the same time. And so they're feeding them either corn oil plus ethanol or fish oil plus ethanol. And in this specific case of fatty liver in a mouse, there are reasons to upregulate PPAR Alpha, but what happens is the ethanol prevents the activation of PPAR Alpha.
You know, in the French case, since they're not consuming a lot of corn oil or a lot of fish oil, they don't have to worry so much about the fatty liver from the ethanol. It's preventing this whole cycle of breaking down fats and doing de novo lipogenesis. And so this sounds pretty simple. The keys to actually living in the macronutrient swamp is almost simply to keep your fat saturated. Don't do anything that is going to activate PPAR Alpha. You know, and I say, avoid unwanted fat. Well, what does that mean? I mean, avoid those fats that, that are unwanted by PPAR Alpha, that PPAR Alpha is not trying to break down, right? It, it wants to get rid of the oleic acid. It wants to get rid of the oleic acid. So you want to reduce those things.
Then perhaps consider having wine with your meals. If, if you're not an alcohol drinker, I'm not saying you should add wine just for this reason, but if you're already someone who consumes some wine with meals, this is an argument to to keep doing that if that's something that you find enjoyable. Lastly, I say broth. I have broth-based sauces. This is a thing that the French do. We're going to have a whole video about this topic about gelatin and how that helps with insulin sensitivity and how that prevents the insulin insensitivity caused by PPAR Alpha activation.
I know I teased at the end of the last video that I was going to dig into longer-term changes in fat composition due to ketogenic diet versus high-starch diet. We're still going to do that. I didn't have time to get to it this week. Uh, that one is going to take a lot of research. It is going to happen. In the meantime, I think next week I really want to talk about gelatin and broth, branched-chain amino acids, and the effects of different amino acids on insulin sensitivity. And I'm very excited about that video because I'm going to kind of tease this new diet concept that I have that is really, um, bringing together a lot of ideas, a lot of these about these other videos, uh, that I'm going to kind of float to you guys next week. So look forward to that.