October 20, 2020
A good friend of mine recently emailed me about a guy named Brad Marshall who has a fascinating take on why we get fat, which he calls the ROS (Reactive Oxygen Species) Theory of Obesity. Inspired by the French Paradox, Brad claims that ROS signaling as a result of eating saturated fats is critical for satiety. Here's what my friend had to say:
“..the more I read the more I’m pretty sure he is onto something. Joel Greene thinks Brad is crazy on this point but I have a feeling he will end up being right on most if not all of it. You can read more here: “The ROS Theory Of Obesity.“
Essentially, our entire meat supply (pork and chicken especially) is much higher in polyunsaturated fats than they should be and the only real way to change it is to change what we feed them. He is also starting to offer meats that are fed properly to ensure lower levels of PUFA. He also has been working on how eating croissants is the key to leanness. It has to be wrong but he makes VERY interesting arguments about it.”
Naturally, I just had to get in touch with this guy, and you can tune in to my podcast this Saturday to hear straight from the horse's mouth how all of this could be true.
But for today's article, Brad has graciously offered to fill you in on how The French Paradox compelled him to experiment with a “Croissant Diet,” (and the shocking results of his experiment), precisely what the ROS Theory of Obesity is, what all of this means for burning fat, and more.
The French Paradox
One often-overlooked reason you may be struggling with your weight, particularly in the abdominal area, could be the quality and ratio of the fats you’re eating.
Specifically, I’m referring to the ratio of long-chain saturated fats (which you should be eating more of, as they will make your fat cells mildly, and reversibly, insulin resistant) to unsaturated fats (which you should be eating less of).
See, insulin sends a signal to fat cells to stop releasing fat to feed the rest of your body and takes your body out of fat-burning mode. Keeping your dietary fat highly saturated prevents insulin from locking away your fat stores, thereby enabling your fat cells to continue feeding your body. This results in greater satiation immediately after a meal and less hunger hours later.
Widely varying ratios of saturated to unsaturated fats can help explain the differences in obesity rates that can be seen around the world and over time.
A perfect example of this is the case of the French remaining lean while eating butter croissants. As an off and on again keto dieter—mostly off the last 10 years as I ran a farm and butcher shop and watched my waistline swell—I’ve always been amazed and astounded that the French were able to stay thin on a diet of butter croissants, baguettes with cheese, and bonbons. While this has changed somewhat in the last 20 years as their diets have vastly changed, urban Parisians in 1970 stayed slim while combining processed white flour and white sugar with butter. Conversely, the Middle Eastern diet combines white flour, white rice, and sugar with polyunsaturated vegetable oils, and today Kuwait is one of the few countries on earth with a higher obesity rate than America.
This is all chronicled in my blog posts “The French Diet In France” and “The Anti-French Diet.”
The following table is extracted from “The Anti-French Diet” based on food disappearance data from the Food and Agricultural Organization of the United Nations. Food Disappearance is the amount of food a country “goes through.” It does not account for waste so the caloric amounts might not be accurate, but the data gives a really good snapshot of the quality of the diet by illustrating the ratios of the foods that are eaten. I’ve included the US as a reference point.
|France, 1970||Kuwait, 2013||America, 2013|
|White Wheat Flour||721 kcal/day||721 kcal/day||599 kcal/day|
|Carbs Plus Alcohol||1635||1677||1522|
|Moderately Unsaturated Vegetable Oils – Canola, Olive, Peanut||110||29||82|
|Highly Unsaturated Vegetable Oils – Soybean, Corn, Sunflower||69||248||605|
Americans are in their own category with their jaw-dropping consumption of sugar and soybean oil, but the French and Kuwaiti diets look more similar than different: total calories, total calories from carbohydrates and alcohol, and sugar consumption are all about the same.
The main difference between the French diet of 1970 and the Kuwaiti diet of 2013 is that French sources of fat were predominately from meat and dairy whereas Kuwaiti sources of fat were predominately from polyunsaturated vegetable oils.
How could this affect their waistlines so dramatically?
The main argument I hear people say when I mention this is that, “the French walk a lot.” People in New York City walk a lot, too. I lived there for two years—10 blocks to the subway, take the subway to work, 6 blocks to work, walk 12 blocks round trip for lunch to that new hip spot, do it all again in the evening. It certainly didn’t prevent me from gaining weight, and when I go to the city now the obesity epidemic (while perhaps less severe than in other parts of the US) is on full display.
Needless to say, I think there’s more to it than just walking, which brings me to the ROS Theory Of Obesity.
The ROS Theory Of Obesity
In the winter of 2019, I realized that I had gained quite a bit of weight after neglecting my diet for some time. I struggled to take the weight off using my usual fail-safe keto diet, and soon realized it wasn't as easy to lose weight at the age of 43 as it had been when I was 25. No shocker there… but it was frustrating.
So, I began re-reading the protons thread from a blog called Hyperlipid. Hyperlipid is brilliant, controversial, and extraordinarily dense with science and jargon. While absorbing it, I realized that the Protons Theory actually explains the French Paradox—why the French stay thin and the Kuwaitis become obese. Shortly thereafter, I published The ROS Theory of Obesity to explain why this was so.
Consider this graph, taken from my post “Long Chain Saturated Fat Causes Fat Loss in Mice,” that shows the amount of fat mass in mice fed a low-fat diet (10-week chow). As you can see, the low-fat chow diet mice maintained their fat mass over the ten weeks, the long-chain saturated fat stearic acid (long-chain saturated fat found in beef and chocolate) mice lost close to half of their body fat, and the mice fed oleic acid (long-chain monounsaturated fat found in olive oil and avocados) had a significant gain in body fat. What makes this more striking is that this experiment was done on wild-type (normal) mice, not some strain that had been artificially bred to become easily diabetic or obese.
The difference between the mice who lost body fat and the mice who gained body fat is a single double bond.
Stearic acid is an 18-carbon saturated fat found in foods such as beef suet and cocoa butter, and oleic acid is an 18-carbon monounsaturated fat famously found in olive oil (but even most beef fat is around half oleic acid). So the only difference between stearic acid and oleic acid is that single double bond. To learn more about all of the different fats, you can check out my primer The What’s, Why’s and Where’s of Fat.
A Billion-Year-Old Molecular Bottleneck In The Mitochondria
Mitochondria were at one point free-living organisms that were taken into other cells in an amoeba-like fashion, except that instead of being digested, they lived there. Mitochondria have their own DNA, and their job is to oxidize glucose and fat, with the ability to switch from burning one to the other.
Inside of the mitochondria is where the real action is, metabolically speaking:
- If a cell is burning glucose, the glucose is broken into two molecules of pyruvate (which are shuttled into the mitochondria) by a process known as glycolysis.
- If a cell is burning fats, they are broken down and shuttled into the mitochondria via a process known as beta-oxidation.
Ultimately, the pyruvate and the acetyl-CoA produced from beta-oxidation enter the Krebs cycle, AKA the citric acid cycle. In this cycle, electrons are steadily removed from carbon and hydrogen-rich molecules and passed through something called the electron transport chain, which is a series of protein complexes in the inner mitochondrial membrane. The electron transport chain turns the chemical energy stored in the carbohydrates and fats into adenosine triphosphate (ATP), which is used to power your muscles and other bodily activities.
The electrons are moved to the electron transport chain by two carrier molecules: nicotinamide adenine dinucleotide + hydrogen (NADH) and flavin adenine dinucleotide (FADH2). NADH hands its electrons off to Complex I (a very large enzyme catalyzing the first step of the mitochondrial electron transport chain) of the electron transport chain and FADH2 hands its electrons off to Complex II (transfers electrons from FADH2 onto Coenzyme Q).
Both Complex I and Complex II hand their electrons to Coenzyme Q, and this is the bottleneck. When ATP levels are high, and NADH and FADH2 are also both high, this bottleneck becomes overwhelmed with traffic and some of the electrons ping back out and combine with molecular oxygen (O2) to form a free radical called superoxide.
As I mentioned, one primary difference between burning glucose and fat is that glucose goes through glycolysis and the fat goes through beta-oxidation. During glycolysis, nearly all of the electrons are transported to the electron transport chain by NADH. Conversely, a saturated fat produces a molecule of FADH2 for each round of beta-oxidation, which happens one time for every two carbons in the fat. A saturated fat produces a much higher ratio of FADH2:NADH than does burning glucose. Whenever a fat has a double bond, no FADH2 is produced during that cycle of beta-oxidation. Therefore, the more unsaturated a fat is, the lower the ratio of FADH2:NADH is.
After a meal high in saturated fat, energy levels are high and ATP is high. In a cell that is burning saturated fat from said meal, FADH2 and NADH will both be trying to hand electrons off to Coenzyme Q. In this scenario, a significant number of electrons will ping back out of the electron transport chain and form superoxide. Superoxide is rapidly turned to hydrogen peroxide by a molecule called superoxide dismutase, which is a crucial part of your body's inbuilt antioxidant system. It is literally the fastest enzyme that has ever been found.
Hydrogen peroxide is unique in that it is an oxidant, but it is not a free radical. Therefore, it is not a powerful enough oxidant to damage DNA or protein. It also is soluble in water but can pass through lipid (fat) membranes. So if the fuel burning in the mitochondria produces a lot of FADH2, a lot of superoxide is produced, which is rapidly converted to hydrogen peroxide, which can diffuse out of the mitochondrial membrane. These molecules, superoxide and hydrogen peroxide are known collectively as reactive oxygen species (ROS).
If any of what I just covered is unclear, remember that I'm going to be unpacking all of this with Ben this Saturday on his podcast, which you can find here once it goes live. The takeaway message though is that when your cells are burning saturated fat, there is an electron bottleneck that produces ROS. What is ROS?
ROS Is The Signal
Despite having somewhat of a bad rap, ROS are actually crucial molecules that send a signal to the cell, from the mitochondria, that the mitochondria are burning fat. Hydrogen peroxide does its job by oxidizing the sulfur atoms of specific cysteine amino acids of what are known as “redox-sensitive proteins.” These sulfur atoms are like light switches.
Hydrogen peroxide turns these genes on or off. Some of the genes turned on by hydrogen peroxide are transcription factors, which go into the nucleus and turn on genes that are involved in fat metabolism. The nucleus of the cell responds to what the mitochondria are doing, and the messenger is ROS.
In my post, Two Elegant Experiments Demonstrating That ROS Is the Signal, I discuss a study done on C elegans, which are tiny nematodes that live in the soil and eat exudate from plant roots, typically carbohydrates. Glucose is a signal to a C elegans worm that life is good, energy is plentiful, and they should go on reproducing and pass away. (They only live for about 18 days.) The study showed that if you deprive them of glucose, they will live an additional three days, which gives them longer to find a nice source of carbohydrates. During glucose restriction, they burn their own body fat, creating ROS, which is the signal to the organism that the mitochondria are burning fat, not glucose.
Here’s the crucial point about the C elegans: If you deprive them of glucose and give them an antioxidant, the antioxidant mops up the ROS, no message is delivered to the nucleus, the worm doesn’t know that glucose is in short supply, and therefore it doesn’t live the extra three days—because ROS is the signal.
Physiological Insulin Resistance
Some of the signaling proteins that are turned off by hydrogen peroxide include those in the insulin signaling pathway. When these proteins are turned off, insulin cannot signal as strongly.
This creates a mild, reversible form of insulin resistance in tissues that are burning saturated fat.
Dietary saturated fat is targeted to tissues that produce a protein called lipoprotein lipase (LPL), which is expressed most strongly in abdominal (visceral) fat. Therefore, visceral fat is the first tissue to become physiologically insulin resistant after a fatty meal. Check out Ben's article “Your Body Fat Is Your Immune System’s Mothership: The Mysterious Relationship Between Fat Cells & Immunity.” for more on visceral fat.
One of the main functions of insulin is to shut off lipolysis, which is the process by which fat cells release their stored energy as free fatty acids, or fuel for the rest of your body. Fat cells that are physiologically insulin resistant continue to release fat in the presence of insulin and therefore tend to get smaller in time.
For every double bond in a fat, one less molecule of FADH2 is formed. Animals can only create saturated or monounsaturated fat, which is stored as a blend of around 50:50 saturated to monounsaturated (along with a little polyunsaturated fat, which has to come from the diet and is usually less than 10% and under 3% in stored adipose tissue). The system is very tightly controlled to recognize this blend of fat. If mitochondria are burning pure monounsaturated fat, like in the mouse study above, the FADH2:NADH ratio is too low to elicit a large ROS response from the mitochondria.
Polyunsaturated fats, like those in soybean or corn oil, have a second double bond and produce even less FADH2 (and therefore less ROS) than do monounsaturated fats. The predominant polyunsaturated fat in modern diets is called linoleic acid. In a tightly controlled system where small changes in FADH2:NADH ratios can have huge effects on organismal energy balance as demonstrated by the feeding study in mice, introducing an evolutionarily novel fat such as linoleic acid into the system—which dramatically lowers the FADH2:NADH ratio—can really throw a wrench into the gears of your underlying metabolism.
France Vs. Kuwait Revisited
Let’s think again about the diet of lean French people in the 1970s and obese Kuwaitis in 2013. The primary difference between their diets was the FADH2:NADH ratio.
The French ate butter croissants, which forced their visceral fat to be physiologically insulin resistant and enabled them to burn their own stored body fat throughout the day.
The Kuwaitis, on the other hand, ate pastries made out of soybean oil, which caused their fat cells to become very insulin sensitive and respond to the insulin released from the meal by shutting down lipolysis. Three hours after a meal, their blood glucose would have returned to normal, but their free fatty acids would still be below pre-meal levels and hunger would ensue. They couldn't continue to burn their stored body fat because their fat cells responded to insulin and were no longer releasing their stored energy to the rest of the body. They ended up with less circulating energy in their blood precisely because they ate. They had lots of stored energy in their fat cells, but they couldn't access it because their fat cells had become insulin sensitive.
A great experiment done in Spain illustrates this very clearly: Groups of healthy volunteers were given an 800-calorie meal comprised mostly of fat, little starch, and only 160 calories from carbohydrates. The fats were either butter, olive oil, or vegetable oils. The only group that had the same amount of free fatty acids 3 hours after the meal was the group given butter (shown as black squares in the graph). Even eight hours after the meal, the group given butter had significantly more fat available from their own fat cells than did the groups whose adipocytes were insulin sensitive.
Another reason frequently given for why the French could remain thin is that they don’t snack, to which I reply, “Maybe they don’t snack because they’re not hungry.”
After considering all of these concepts, I started to wonder if I could actually lose weight by eating croissants, so I set off on creating my very own Croissant Diet.
Real croissants get upwards of 70% of their calories from fat, all from butter. I wanted my Croissant Diet to work, so I gamed the system by doping butter with stearic acid (the same long-chain saturated fat fed to the skinny mice) before making my own croissants. My stearic acid-enhanced butteroil was VERY high in long-chain saturated fat, quite low in monounsaturated fat, and very low in polyunsaturated fat.
I started making croissants with the butteroil and eating exclusively croissants, black coffee, and red wine—it’s a diet based on French concepts, after all. Amazingly, I started losing inches off of my waist right away!
I noticed several things while eating croissants: First, they were intensely satiating. I couldn’t eat more than one and a half croissant sandwiches for dinner. For me, that’s not a lot of food! I’ve always struggled to get real satiation. I would usually go for thirds and then stop eating because my stomach hurt. This was different.
The other thing that happened was suddenly I could go longer between meals. I started skipping meals, sometimes by mistake. That is definitely something that never happened before. So I lost inches, found satiation, and went longer between meals despite the fact that I reintroduced white flour into my diet! (Admitedly not all that much as a croissant only has about 25-30g of carbohydrates, and I was eating less than three per day.)
One of the other areas of the body that expresses LPL, and therefore is targeted by dietary fat, is the hypothalamus, the gland in your brain that signals satiation. A key component of the satiety signal is ROS production in the hypothalamus. One of the reasons I was failing to feel true satiation earlier in life may have been that my dietary fat was insufficiently saturated, and I was unable to drive sufficient ROS production in my hypothalamus.
So What Types Of Fat Should You Eat?
The main premise of The Croissant Diet is that, when thinking about a weight loss or weight control diet (especially if you have excess abdominal fat), you should be thinking about fat quality in addition to macro ratios.
Independent from the amount of carbohydrates, fats, protein, and ethanol you consume is the FADH2:NADH ratio of your diet.
The table you'll see below, excerpted from The Croissant Diet Specification, lists the ratio of long-chain saturated to unsaturated fats in a variety of fat sources. It doubly penalizes polyunsaturated fats. It also lists the amount of stearic acid in each fat. The best fats would have a high ratio and be high in stearic acid. The chart also shows that some of what many in the keto community consider to be “safe” fats—such as olive oil and nuts—actually do very poorly by this metric.
|Stearic Acid Enhanced Butter Oil||2.53||27%|
|Wild Elk Backfat||1.86||23%|
|Beef Tallow (USDA)||1.00||19%|
|Beef fat from a Ribeye Steak||0.80||13%|
|Wheat Finished Lard||0.73||??|
|Corn Finished Lard||0.59||13%|
|Lard fed 16% Distiller’s Grains||0.32||8%|
So, if you've hit a weight loss plateau on a keto diet, or really any diet, consider removing olive oil, avocado oil, and nuts and swapping those fats out for butter, cocoa butter, or stearic acid-enhanced butteroil. You can also try supplementing with stearic acid.
Another trojan horse for polyunsaturated fats is pork and chicken, especially in America. You are what you eat, and this is no different for pigs and chickens. In the US, what they routinely eat is corn—a relatively oily grain. Additionally, chickens are routinely given supplemental soybean oil in their ration only because it gets them to market a few days faster. Unfortunately, this is true whether or not the chicken is pastured, non-GMO, or organic. All of the feed mills have their diets designed by university-trained animal nutritionists who tell them they have to have soybean meal in their diets. Consider sourcing chicken and pork that is low in polyunsaturated fat!
If you are struggling with your weight, especially in the abdominal area, it would surely benefit you to give some serious thought to the types of fats you're consuming.
Eating highly saturated fats will allow your fat cells to keep your body in fat-burning mode, releasing their stored energy to keep you running on your own stored energy all day.
And when you consider the fact that the traditional French way of consuming highly-saturated fats includes eating plenty of butter and chocolate, it's a fairly easy diet to get behind.
To recap, here's a list of fats, from best to worst:
- Ideal: Butter, Ghee, Pastured beef suet, Stearic acid-enhanced butteroil, Cocoa butter, Chocolate
- Good: Beef, Goat, or lamb fat, Fat from Low-PUFA pork
- Avoid: Vegetable oils, Olive Oil, Avocado Oil, Nuts, Most chicken fat, and most pork fat
If you want to geek out some more on everything I just covered, be sure to listen to my podcast with Ben this weekend, which you'll be able to find here on Saturday: “The Croissant Diet, Wine Fasting, Oodles Of Pork Lard, Keto Bricks & Much More With Brad Marshall.”
How about you? Have you tried a highly-saturated fat diet? Let me know in the comments section below your successes or failures with fats, or if you have any questions, comments, or thoughts, and I'll respond!
35 thoughts on “The Croissant Diet & The French Paradox (How Changing Your Fat Ratios Can Put You Back In Charge Of Your Waistline).”
But also look at the dates when the data was collected… 2013 for Kuwait and USA but 1970 for France… this is about activity level! In 2013 Kuwait was already a sedentary country, as was USA. But in 1970s France people would not be sedentary. And even in urban France today, many people walk everywhere, which burns calories without jacking up hunger, and controls blood sugar. This is not scientific in the least bit.
There are a few other differences per the data in the table you presented:
Kuwait consumes much, mucb more grains (rice)
while the French consume more tubers.
That is, the kind of starches consumed is different, in the same way the kind of oils is different.
The French consume a lot more milk and meat – per this data, protein consumption is considerably higher. This is going to have significant effcets on metabolism too.
It is very obvious which nation is ‘wealthier- – poor peoples tend to bulk up on rice, and have little protein in their diet…
They have vastly different weather, vastly different exposures to sunlight – which, the majority of the women are convering themselves up. That’s vitamin D.
There is a lot more going on that just the PUFAs…
How would this kind of diet – emphasizing long chain sfa’s and minimizing pufas – work in someone who is chronically insulin resistant?
Hey Caitlin –
I think carbs are still more important….for me anyway. I’ve just done a year of lots of saturated fat with carbs like potatoes and bread and getting PUFA down to less than 10g a day and I’m still insulin resistant and overweight- I am gradually gaining although it is very slow. I did keto for many years before having kids and I was eating chicken and pork and olive oil and was at a healthy weight with no insulin resistance (resolved) – I was eating saturated fat too. When I reintroduced whole food carbs I was fine for awhile then started gaining – now I’m in pretty bad shape and although not obese my blood markers aren’t good. I personally think you have to test it for yourself – some people respond really well, although it seems some of those people are in fact countinng calories and eating in a slight deficit to lose body fat. Whatever the reasons, it wasn’t the magic solution I was hoping for. Go test and see!! Maybe you will be one of the lucky ones….everybody is different.
The type of carbs is important too – not juat the type of oil.
Have you tried switching he bread and potatoes for fruit?
I’ve been on the Croissant diet since Oct 0f 2020, I have lost over 30+ lbs, and I am the leanest I have been in 30 years. I am 53 years old and have abs now. I can definitely attest to it working. I dropped PUFA as much as possible and normally consume less than 10 grams of it a day. While I eat roughly 150 grams of Fat daily with 70+ grams of that being saturated. I turned my neighbor on to it and he has lost 28 lbs since Jan. I’ve done keto several times with decent results, been strict Vegan for a full year and felt great but didn’t recomp much, and done several other diets over the years. Nothing has worked like this one for me. My blood pressure is better now 115/70 this morning, my blood glucose response is great too, 2 hours after a pint of Haagen Dazs my blood glucose was 110!
Would love to hear more from Brad again on the podcast.
Very intriguing theory!
Personally, I do subscribe to Brad’s point of view on stearic acid and overall SaFa.
Every time I introduce a solid amount of PUFAs in my diet, it’s much harder to reach a satiety point, (especially if the PUFA source is some kind of nut butter- or seed-based) and in the long term, I do notice a nice body layer of fat build-up.
P.S. On the funny side, I’ve put his theory under a good amount of sourdough bread and butter for dinner.
Seems to work perfectly, as expected, for me.
Hello, I love your content! What do you think about Keto? Any thoughts? Here are couple custom keto recipes, let me know what you think!
I’m confused as Ben has mentioned mutiple times insulin sensitivity being desirable and enhancing it via Apple cider vinegar, Ceylon cinnamon, Kion Lean etc along with meals. But this diet seems based around the opposite- decreasing insulin sensitivity temporarily, and achieving greater satiety that way.
Is there a place for both, at different times, or is this just a different theory/approach?
Great comment. I think what you are referring to here is physiological IR (ie: satiety after eating saturated fat) vs pathological IR (associated with hyperinsulinemia and conditions such as Diabetes/NAFLD/PCOS that occurs once fat threshold is exceeded).
Very interesting, especially in view of so much guidance to avoid combining simple / starchy carbs and saturated fats. I was eating avocados and protein powder for a while last year. Haha. (Was pretty lean, but already was pretty lean, and it’s hard to get fat, exactly, eating avocados and protein powder.)
As a fun anecdote, my wife and I went to western Europe a few years ago and in France, in particular, we were absolutely eating like pigs (croissants and other pastries, and everything else you could imagine), and lost weight. Tons of walking, too, but as addressed in the article, that isn’t always dispositive.
There are so many issues around food these days and it doesn’t help that much of it seems contradictory.
My personal food journey started when I was a fat 10 year old told by a doctor that no one would like me & I would die young because I was over weight and then sent by my parents to “fat” camp in Boone, NC. From there, I calorie restricted for years & thinned down a lot. By the time I reached college, my dad was following the Adkin’s plan, which seem to work well for our family genetics. I figured a moderation diet would be best, watching my carbs, calorie counting, and going easy on the fat. That is until I read Mark Hyman‘s book eat fat get thin. At that point I switched over to higher quality fat as a higher percentage of my daily caloric intake.
That all said, I can see the truth in the higher quality, even animal-based, Fatte’s has a better and more satisfying source of calories. I just wonder how some of the other food related issues play into it. For instants soy beans and corn tend to be highly genetically modified and this has got bacteria altering effects and can be highly inflammatory. And as you mentioned in the article, when you eat meats you also eat with the meat eight and if they’re eating grains or GMO products then you are eating highly inflamed materials. So it is hard to tease a part one factor in our food from another, making the whole issue very complicated. Americans do not tolerate this well. Rather, they would like someone just to tell them what to eat. Build them a meal plan and let them follow it. We are a plug and play society after all!
I wonder where duck (or goose) fat which is abundantly used in south of France in many recipes and ways to preserve ‘confit” meat would be in terms of ratio and stearic acid.
I started the diet a few weeks ago. No changes yet. Using cocoa butter in coffee (I hate coffee but putting this or butter/ghee in tea is worse), buttered/ghee rice, rice pasta, potatoes. Homemade cream of rice with heavy cream. Heavy cream in oatmeal. Saladino’s Fire Starter. I tried popcorn but it bloats me. In fact, I do get gas build up, constipated. Feel bloated and fat all the time. This makes sleep horrible.
Do you feel bloated and fat all the time, or only since you started eating like that?
I’m absolutely fascinated by this and ever since reading your blog and listening to some podcasts you’ve been on, I have eased myself out LCHF diet and have been reintroducing carbs. For the last week I’ve upped my saturated fats and dropped PUFAS (I’ve kept eggs, though I might let those go for a little while) and made sure that my fats were about equal to the amount of carbs I’m consuming, if not higher. I haven’t been weighing myself but I am tracking my waist line. I’m a big gal with a belly to prove it and found that I keep losing and regaining the same half inch. I don’t count calories but I am careful of the carb/fat balance. In fact, I worry I’ve been under eating due to the level of satiety this diet brings on. I consider myself a carb/sugar addict but this had me scratching my head whenever I call it quits in the middle of a meal that I normally would have gotten at least a second plate of, especially where sweets are concerned.
I was hoping for magical weight loss, of course, but I’ve eaten PUFAS all my life and only slowed my consumption once I became keto and carnivore intermittently for the last four or so years. I’ve got some grass fed ghee and the 90% Stearic Acid from your site and will be making my own SA butter oil to cook with. I’ll also incorporate some cocoa butter. I’ve considered lowering my carbs again if only to avoid the dreaded blood sugar crashes (I get them bad sometimes) but I’m really enjoying being able to eat ‘regular’ foods for once, and not immediately balloon the way I thought I would. I don’t mind the half inch loss and gain for now but if it creeps upwards, I guess I’ll have to make some keto-y adjustments after all.
The greatest benefit I’ve seen so far is that my cycle has returned after a 4+ month absence. So, there’s that at least! Thanks for all of the info, Brad, I’m curious to see what comes next and enjoy all of the articles and podcasts.
I do have one question if you don’t mind me asking: do you have any protein macro recommendations in the context of this way of eating?
Super excited about this! Had the most glorious year of fat loss 2017, then it stopped, then went the other direction. Looking at how I was eating then and how my diet has incrementally changed since, this could be it. Lord, let it be so.
I listened to the podcast you did with Paul Saladino and was telling a friend about it. He did a week-long experiment of adding extra saturated fats and avoiding PUFAs. He lost 6 lbs and could feel a difference in his “spare tire” fat. I think I might have him convinced. Can’t wait to hear your podcast with Ben!
Ray Peat would agree
What is the recipe for the French Connection Croissants Brad Marshall made?
This is what I used: https://sallysbakingaddiction.com/homemade-croissants/
Great article! Curious where would fat from eggs fit in? Ideal, good, or avoid?
American eggs are laced with PUFA since literally everyone – conventional, organic AND non-GMO – supplements laying hen diets with soybean oil. Having said that, eggs are so nutritious that its hard to argue they should be avoided completely. I’m torn on this issue.
This is why I started Firebrand Meats – to provide quality products but also just advocacy around this issue.
commercial eggs are going to have the same problem as commercial pork. the hens are fed a diet of corn and soy. pufas
I was wondering the same thing. I also wonder if you fried/scrambled the eggs in some nice grass fed butter or steric acid enhanced ghee if that would put the ratio in the positive? I think it would.
Now bacon… that make me sad.
Very interesting, but I am a little confused about which type of fat leads to insulin-resistant fat cells. At the very top of the article, you state:
“Specifically, I’m referring to the ratio of long-chain saturated fats (which you should be eating more of) to unsaturated fats (which you should be eating less of as they will make your fat cells mildly, and reversibly, insulin resistant).”
This sounds like we don’t want unsaturated fats because they create temporary insulin resistance in fat cells which is bad for weight loss. But later you state:
“This creates a mild, reversible form of insulin resistance in tissues that are burning saturated fat.”
This makes it sound like saturated fat creates temporary insulin resistance in fat cells and it is good for weight loss.
Can you clarify?
I think this is being fixed, thanks for the heads up!
And yes, it is SATURATED fat that causes the temporary insulin. Polyunsaturated fat prevents it.
Love the work, Brad! I think there may be a minor syntactic mistake in the first paragraph that may confuse new readers:
“Specifically, I’m referring to the ratio of long-chain saturated fats (which you should be eating more of) to unsaturated fats (which you should be eating less of as they will make your fat cells mildly, and reversibly, insulin resistant).”
The way it’s written right now, it sounds like PUFAs are what make the cell mildly/reversibly insulin resistant. If I understand the hypothesis correctly, it’s SFAs, not PUFAs, that make the cell mildly/reversibly insulin resistant. Just move the parenthesis and it should clear up the confusion.
Looking forward to the conversation on Saturday 👍
“Avoid: Vegetable oils, Olive Oil, Avocado Oil, Nuts, Most chicken fat, and most pork fat”
This is a sentence I never thought I would see on a Greenfield article. Very interesting.
Follow up: I did a DNAFit consultation based off your recommendation. They found I have a gene that said I should eat equal fats and carbs. Only 5% of those fats should be saturated fats. Apparently I have another gene that says saturated fats lead to weight gain and high cholesterol. How do I know what to believe? Everything about keto and healthy fats teaches me that saturated fats are the goto, but now my DNA results say otherwise? Could you shine some light here?
I must have the same variant and was anxiously looking to see if this was addressed. Thank you for bringing it up, as I would like to know as well.
I’m not sure why that would be. Do you know what gene the variant is in?
The only way to know for sure is to test it yourself. DNA is not the end all be all as we also have epigenetics to consider.
Go on a diet with a much higher amount of saturated fat. (say for example you try Keto or even a Paleo diet). Experiment with a minimum of 50 percent of your fat being Saturated or more if you desire. Weigh yourself over 6 weeks and see the trend that forms. As long as your Saturated fat sources are of good quality, you should get some good results.
Let’s not forget that genes can be activated and deactivated.
Let’s not forget either that your mitochondria also have DNA, and that the populations of bacteria in your gut play a large role in your health and wellbeing.
So basically, the results of your DNA test can not give the full picture.
So with this theory the, I would love to know your thoughts on Fish Oil as they are very high in PUFAs. When it comes to Cholesterol and Heart Disease, would Vitamin E then be a MUCH better option?
The answer to the fish oil question is complicated. Long chain fats – over 18 carbons, which is most fats in fish oil – are oxidized in peroxisomes as opposed to mitochondria. This generates something called malonyl-CoA, which blocks the oxidation of fat in the mitochondria. So eating a large amount of fish oil can shift the mitochondria towards burning glucose. Peter covers this the best I’ve seen in his recent post but this isn’t an easy read: https://high-fat-nutrition.blogspot.com/2020/09/protons-64-miracle-of-fish-oil-6.html