As I suggested in my last post, you should watch the embedded video to study up for this post.  In case you didn’t watch the video, or if you came to this post without having seen the previous one, I’ll embed the video below.  I hate to do so, because the way YouTube shows the video caught me in an expression or whatever that makes me look 400 years old when the reality is that I’m only 300 years old. (If you would like to see how old I look in person, I’m speaking at Low-Carb Denver 2020.  It’s not just for docs.  Come by and say Hi.  I would love to meet you.)

Let me explain a little about this video.  I gave this talk at the big Low-Carb summit in Breckinridge, CO almost two years ago.  I was given 30 minutes for the presentation, and I ran over.  I had gone through the thing a few times before presenting, but for some reason, when I got going on the talk it went long by about 10-12 minutes.  The organizer of the conference was in the front row going nuts.

Which I understand.  I hate it when speakers go over, and I usually make it a point not to.  When presenters go over their allotted time, they end up throwing the whole schedule off, and the people who get shafted are the attendees, because invariably the time is made up by cutting into the break time or lunch time or bar time at the end.  I realized I was going to run over about halfway through, and so I picked up the pace.  Had I not, the thing would have run over a lot longer.

Wasn’t that fun?

I’ve agonized over how to present all this more understandably.  But it’s tough, because is complex biochemistry.  After some reflection, I’ve decided to present it from the final result backwards to the precipitating cause.  So, here goes.

How we get fat

This is going to sound simplistic, but we get fat by increasing the amount of fat in the fat cells.*  What drives fat into the fat cells?  Insulin.  If the fat cells are sensitive to insulin, insulin will drive the processes that move fat into those cells.  If the cells are insulin resistant, then the fat is turned away.

We’ve come to think of insulin resistance is a bad thing–and body wide, it surely is–but maybe it is part of the system that regulates how much fat gets into the fat cells. And maybe the shifting from insulin sensitivity to insulin resistance is a gateway controlling the amount of fat entering and staying in the fat cells.

I say maybe as this entire idea is hypothetical, not a proven fact.  But the underlying physiology and biochemistry are pretty damn compelling.

If the insulin resistance is the gateway, what is the switch for the gateway? It could be ROS, which stands for reactive oxygen species, which is the scientific term for free radicals.  As it turns out, free radicals are not the monsters they’ve been made out to be, at least not in all situations.  It’s well known that ROS (which we’ll call them from now on) are signaling molecules.  And they are an integral part of our immune system as well as contributors to many physiological functions.

ROS released from the mitochondria (the sausage-shaped organelles within the cells responsible for producing 85-90 percent of the energy required for life) accumulate and are converted to hydrogen peroxide, which then (also acting as a signaling molecule) induces insulin resistance in that cell.

How and why are the ROS that stimulate insulin resistance released from the mitochondria?

Well, this is where it gets a bit complicated, so hang in there

The energy of life

The currency of life is called adenosine triphosphate, aka ATP. Almost all of the billions of chemical reactions required to sustain life require energy to drive them and would never happen without it.  ATP is that energy source.  ATP breaks down and releases the energy needed to catalyze these life-maintaining reactions.  Since these chemical reactions are happening constantly, we need a ready source of ATP to provide the needed energy.  Fortunately, we are constantly synthesizing this ATP in our mitochondria.  In fact, we produce about our own body weight in ATP every single day.  Ponder that for a minute.  If you weigh 160 pounds, your mitochondria produce about 160 pounds of ATP each and every day to power all your ongoing chemical reactions.

ATP is produced primarily via a process called oxidative phosphorylation.  This is a term describing the addition of a phosphate group (a specific chemical structure) to a molecule of adenosine diphosphate, ADP.  The molecule ADP has two phosphate groups hooked on to it; when a third phosphate group is hooked on, ADP becomes ATP.  The DIphospate becomes TRIphospate.  It goes from two to three phosphate groups.  The bond that attaches the third phosphate group onto the other two is a high-energy bond.  When that bond is broken to release energy to fuel a chemical reaction, the ATP loses the phosphate group and becomes ADP again, which is ready to be recycled back to ATP.

It requires energy to add this third phosphate group onto ADP to make it ATP.  Where does this energy come from?

In short, it comes from the breakdown of the food we eat.  What we refer to as our metabolism breaks down the chemical bonds of the foods we eat and uses the energy released to drive the conversion of ADP to ATP.

The electron transport chain, Part 1

The electron transport chain is composed of five molecular complexes and a kind of complicated traffic interchange called the CoQ couple.  These five complexes are called, simply enough, Complexes I, II, III, IV, and V, they are usually denoted by Roman Numerals (don’t ask me why).  They are strung out along the inner mitochondrial membrane, which is extremely important, but not that important in your developing an understanding of this process, so I’m not going to go into it.  Just know that there is a membrane with space on both sides that contain the Complexes I through V and the CoQ couple.

When the metabolic processes that are initiated when we eat (or when we don’t and are breaking down stored fat and/or stored glucose/glycogen) tear apart the molecules making up the food we eat, the carbon chains making up the fats and sugars are stripped of their hydrogens and oxygens, and the energy stored in these foods is released as high-energy electrons. These electrons are grabbed by high-energy-electron-transport molecules and are carted to the electron transport chain.  This is similar to picking up coal or wood and carrying it to a furnace to be burned.  These high-energy-electron-transport molecules tote the electrons to different parts of the electron transport chain and dump them there.

Some specific electron carriers dump the electrons in Complex I, while others dump them into Complex II.  To make it even more complicated, some electron carriers dump their electrons into a structure (also in the membrane) called the electron transport flavoprotein, ETF. The ETF is not often shown in graphics of the electron transport chain, but it is there and is important to our theory.

All these structures then send their electrons through the CoQ couple, which is where the magic happens.  But before we get to that, let’s look at how the process produces ATP.

The high-energy-electrons that are dumped into the various complexes and the ETF are eventually shuttled down the line from one complex to the next, much like a bucket brigade.  As each complex hands off an electron to the next in line, a bit of energy is released.  This released energy powers the pumping of hydrogen ions (called H+) across the membrane.

As more food (or stored fat or sugar) is broken down, more high-energy-electrons are fed into the complexes and handed off down the line.  So, more energy pumps H+ across the membrane.  As the pumping continues and the H+ increases on one side, the pressure on that side builds.  (It’s not really pressure, per se, as in the air pressure in a tire, but it’s both chemical and electrical pressure.

When more H+ are on one side of the membrane, there is a difference in concentration of hydrogen and a difference in the electrical charge due to the positive or + charge on the hydrogen.  Consequently, there are two different forces pushing on the membrane: a chemical concentration one and an electrical one.  The pressure difference across the membrane is called the chemiosmotic gradient, a term you can immediately forget.)

When there is an inequality of pressure across a membrane, there is a force trying to equalize the pressure.  Just like in a tire filled with air, the air wants to get out to equalize with the air in the atmosphere, but the rubber of the tire prevents it.  If you puncture the tire, the air rushes out until the pressure inside the tire is equal to the pressure outside, an unfortunate situation we call a flat tire.

Same situation exists across the membrane in the mitochondria, except, like the air blowing through the puncture in the inflated tire, this pressure is released by the H+ zipping through Complex V.  Complex V is like a tiny turbine.  As the H+ go through it, they provide the energy to turn the turbine, which adds a phosphate group to an ADP converting it to an ATP and releasing it to go out and work to drive chemical reactions.

The Complexes

When your body metabolizes your food (or when your body turns to stored reserves), the fats and sugar are sent down different pathways.  The glucose (sugar) goes into the Krebs cycle, also called the TCA cycle and a couple of other names just to keep it confusing for medical students who are trying to learn about it.

Fats are broken down via a process called beta-oxidation, which chops the fats into two carbon segments, then feeds them into the Krebs cycle.

As glucose and fats are processed through the Krebs cycle, high-energy electrons are removed and attached to high-energy-electron carriers to be transported to the electron transport chain.

Glucose and fat

There are two types of high-energy-electron-transport molecules that carry these electrons.  They are called FADH2 and NADH.  It’s a function of where in the Krebs cycle these electrons are handed off as to which of the two carriers grabs them.  For each turn of the Krebs cycle three NADH are used and one FADH2. (NADH and FADH2 are the abbreviations of the names of these molecules.  You don’t need to know their actual names for our purposes.  Hell, I’m so used to using their initials that I can’t even remember their real names without looking them up.)

As mentioned above the process of beta-oxidation involves lopping two-carbon segments of fat off at a time and sending them to the Krebs cycle.  The process of chopping these fats involves four steps.  During the first step, an electron is thrown off and is captured by FADH2.  During the third step, another is thrown off and grabbed by NADH.  For purposes of this discussion, the first of the four steps is the important one, because it varies depending upon whether the fat is saturated or unsaturated.  The more unsaturated the fat, the less FADH2 is generated, which is crucial to the generation of ROS, which determine the amount of insulin resistance.  And, ultimately, the amount of fat stored in the fat cell.

Why are fewer electrons thrown off, requiring fewer FADH2 to carry them, from unsaturated fats than saturated fats in the first step of beta-oxidation?  Because in the first step, a double bond is inserted into a saturated fat going through the process. (See red circle in graphic below.)  This double-bond addition strips off an electron that is captured and transported to the ETF in the electron transport chain by FADH2.  Unlike a saturated fat, an unsaturated fat already has one or more double bonds, so it basically misses this step and no high-energy electron is released.  For every double bond in an unsaturated fat, one fewer electron is released and one fewer FADH2 is sent on its way as compared to a saturated fat of the same length.  So the greater the unsaturation of the fat, the greater the difference in the production of FADH2, which, as we shall see, is consequential in the storage of fat in the fat cells.

Let’s bear this in mind as we go back to the electron transport chain.

Electron transport chain, Part 2

The first complex in the electron transport chain is Complex I. NADH thrown off from beta-oxidation and the Krebs cycle enters the electron transport chain through Complex I. FADH2 enters via two different pathways. The FADH2 generated in the Krebs cycle enters via Complex II, which is actually part of the Krebs cycle that resides in the membrane.  FADH2 generated by beta oxidation enters through EFT, which is also embedded in the membrane.  This is the crucial step in understanding the difference between the effects of saturated versus unsaturated fat on the development of insulin resistance.  Here’s why.

Complex I and Complex II and ETF all feed their electrons into the CoQ couple.  After going through the CoQ couple, the electrons are handed off to Complex III, which hands them off to Complex IV, pumping H+ across the membrane all the while.  The final complex, Complex V (also called ATP synthase, just to keep things complicated), is the turbine described above (and shown in an animation in my video presentation) that churns out the ATP as the H+ flow back through in an effort to equalize ‘pressure’ on both sides of the membrane.

Electron Transport Chain

Since electrons are coming into the CoQ couple from multiple directions (Complex I, Complex II, and ETF), it is like an intersection of streets.  If traffic is moving, then everyone gets through the intersection with little delay.  If, however, it is rush hour on the Friday before a long weekend, traffic can back up, and it can take forever to get through.

We’ve all had the experience of driving somewhere and hitting such a traffic backup.  Most of the drivers of the cars wait patiently and inch their way through the long line of traffic until they make it through the intersection and are on their way.  In these situations, however, there are always impatient drivers who tire of the wait, say Screw it, pull out of the line and make a U-turn and head back up the road in the opposite way to find a faster route.

The same thing happens with electrons getting backed up going through the CoQ couple.  Most of them make it through to Complex III, but if the electron traffic is congested enough, some of them turn around and go back through Complex I backwards.  When this happens, it is called, logically enough, reverse electron transport (RET), which is a major part of our hypothesis.

When electrons go backwards in Complex I, the complex releases them as free radicals, ROS.

Reverse electron transport

These ROS then are a signal that the cell is full (which makes sense given that the CoQ Couple is jammed up with electron traffic.  The ROS end up as hydrogen peroxide and increase localized insulin resistance, which turns fat and glucose away.  And now we’re back to where we started in the earlier part of this essay.


The electrons that end up clogging the CoQ Couple are carried by the FADH2 coming from beta-oxidation of fat through ETF.  More FADH2 means more electrons means more of a traffic jam.  Which drives electrons backwards via RET through Complex 1 and pops them off as ROS, driving localized insulin resistance and preventing more fat being moved into the fat cells.

What drives more FADH2 through ETF?  Saturated fat.

What drives less through?  Polyunsaturated fat (PUFA).

Why does it matter?  That’s the question that goes to the heart of the hypothesis.

If you want to keep your fat cells from expanding beyond a certain level, and you want yourself to keep from expanding along with them (i.e., getting fat), then you want to block entry of fat into the fat cells.  Which is what localized insulin resistance does.  And this localized insulin resistance is driven by FADH2.  And what makes more FADH2?  Saturated fat.  What makes less?  PUFA.

The obesity epidemic

For decades the level of obesity in the United States stayed pretty level.  All of a sudden in about 1980 the rate of obesity began to rise.  And it hasn’t stopped since.

What happened?

You can get all kinds of answers from people.  If you look at the statistics, you’ll see that caloric intake has increased by about 240-250 calories per capita per day.  If you break this down and look at the macronutrient content of this caloric increase, you find that protein has increased a tiny bit, fat has gone up a little, while the majority of the caloric increase comes from carbohydrate.

So, there you have your answer.  More carbohydrate is making us fatter.  Seems pretty logical, but…


We can’t just say that the fact that we are eating more carbs is making us fat. Reason demands that we ask the question: Why? Why after decades of consistent carb intake, did we suddenly start eating more carbs in 1980?

Did carbs suddenly become tastier in 1980?  Did Snack food and junk food first arrive on the scene in 1980? Did people just spontaneously start stuffing their faces with carbs in 1980? Or did something else happen?

Let’s take a look at protein intake.  It rose slightly, but didn’t really change in quality.

How about fat?

Fat intake increased a little since 1980.  If you look at the change in the type of fat we ate starting in 1980, you see an enormous difference.  Although total fat didn’t change much, the amount of PUFA in the diet skyrocketed, while the amount of saturated fat fell.

So, maybe the type of fat has something to do with it.  My early hypothesis was that PUFA somehow drove the increase in obesity and maybe the fall off of saturated fat intake contributed.

In other words, maybe PUFA is driving the obesity epidemic while saturated fat is protective.  So, I started looking for a biochemical or physiological mechanism that could explain this.

I came across the work of Peter Dombromylskyj, (see his Proton Series in his Hyperlipid blog) who had gone back the basic biochemistry of fat metabolism and noticed that saturated fat increased the production of FADH2 while PUFA decreased it. So, the ratio of the two, the FADH2/NADH ratio, may act as a switch to control the storage of fat.  As the ratio goes up—more FADH2 to NADH—the storage of fat goes down.

If this were true, then it would help explain the enormous increase in obesity since around 1980.  Since then—thanks to the widespread fear of saturated fat—we’ve all been reducing saturated fat and replacing it with PUFA.

By advocating the substitution of PUFA, provided mainly in the form of industrial seed oils, for saturated fat, which we have all eaten for millennia, in a misguided attempt to reduce the rate of heart disease, the nutritional authorities unwittingly set us up for the massive obesity epidemic we’re now in the midst of.

A diet high in PUFA, by the decrease in production of FADH2, inhibits the rate of RET, allowing the fat cells to continue to take up calories beyond a certain set point. Adding saturated fat increases the RET and signals that the fat cells are full.

While the fat cells are open for stuffing, both fat and glucose go in. Since PUFA brings this about, PUFA ends up acting as a sort of supercharged carb in that it continues to flood into the fat cells like glucose, but it has over twice as many calories per gram as glucose.

Could explain a lot.

Before I end, I want to propose an experiment.  Maybe someone out there has the contacts to get it going.

McDonald's French fries

Back in the old pre-let’s-all-quit-eating-foods-of-animal-origin days, McDonald’s fries were cooked in beef tallow.  Since the CSPI and other groups of slow-witted dolts came down on them, they’ve switched to cooking them in vegetable oil. Vegetable oil doesn’t flavor them in the same way beef tallow does, so they had to do all kinds of food-technology wizardry to make them taste the same. Some people still don’t think they taste the same.  Listen to this podcast by Malcolm Gladwell, who got to eat some McDonald’s fries cooked the old way.

Vegetable oils are primarily PUFA whereas beef tallow is primarily saturated fat and mono-unsaturated fat with a little (a very little) PUFA thrown in.

If we could recruit, say, 30 people who would agree to eat McDonald’s fries till they were full, we could do a nice study.  We would use them as their own controls.  We would randomize them into two groups.  One group would eat McDonald’s fries cooked in vegetable oil until full, while the other group would eat the fries cooked in beef tallow.  We would measure the amounts of fries eaten by those in each group and record it.  Then, a couple of weeks later, we would reverse the situation.  Those who had eaten the beef-tallow cooked fries the first time, would eat until full of the vegetable cooked one.  And vice versa.

If this FADH2/NADH ratio hypothesis is valid, then it would be expected that the subjects would have eaten less of the fries cooked in beef tallow and more of those cooked in vegetable oil.

Any readers out there have a contact at McDonald’s who could help us out here? I will totally volunteer my time to oversee the experiment.

In the next post, I’ll introduce you to someone who has sort of done this experiment on himself.  And tell you the results.  And give you many, many links you can go through to learn more and maybe try it yourself.

*The fat mass can also increase by increasing the number of fat cells, but I don’t want to complicate the issue with that right now.  It’s already complex enough.)

Just in case you haven’t had enough, here are a few references you can take a look at. And, finally, if you scroll down below the references, you’ll find a way to get what I think are three of the best of these three papers.


Fisher-Wellman, K. H. & Neufer, P. D. (2012). Linking mitochondrial bioenergetics to insulin resistance via redox biology. Trends Endocrinol Metab, 23(3), 142-153.

Guarás, A. et al (2016) The CoQH2/CoQ ration serves as a sensor of respiratory chain efficiency. Cell Reports 15, 1-13.

Persiyantseva, NA (2013) Mitochondrial H2O2 as an enable signal for triggering autophosphorylation of insulin receptors in neurons. J Mol Signal 8(1) 11.

Pomytkin, IA. (2012) H2O2 Signalling pathway: A possible bridge between insulin receptor and mitochondria. Curr Neuropharmacol 10(4) 311-320.

Sato, K. et al (1995). Insulin, ketone bodies, and mitochondrial energy transduction. FASEB J, 9(8), 651-658.

Scialò, F. et al (2016) Mitochondrial ROS produced by reverse electron transport extend animal lifespan. Cell Metab, 12;23(4), 725-734.

Speijer, D. (2011). Oxygen radicals shaping evolution: why fatty acid catabolism leads to peroxisomes while neurons do without it: FADH(2)/NADH flux ratios determining mitochondrial radical formation were crucial for the eukaryotic invention of peroxisomes and catabolic tissue differentiation. Bioessays, 33(2), 88-94.

Speijer, D. (2014). How the mitochondrion was shaped by radical differences in substrates: what carnitine shuttles and uncoupling tell us about mitochondrial evolution in response to ROS. Bioessays, 36(7), 634-643.

Speijer, D. et al (2014). How to deal with oxygen radicals stemming from mitochondrial fatty acid oxidation. Philos Trans R Soc Lond B Biol Sci, 369(1646), 20130446.

Speijer, D. (2019) Can all major ROS forming sites of the respiratory chain be activated by high FADH(2)/NADH ratios?: Ancient evolutionary constraints determine mitochondrial ROS formation. Bioessays, 41(1), e1800180.

Stein, L. R., & Imai, S. (2012). The dynamic regulation of NAD metabolism in mitochondria. Trends Endocrinol Metab, 23(9), 420-428.


If you’re interested in learning more about all this, I’ve put together a packet of three papers I’ll be happy to email you.  Put in your email address and click the button below, and you’ll have them in 10 seconds.



  1. If you are talking about Brad Marshall of Fire in a Bottle, I’ve been trying his stearic acid and butter oil, along with cacoa butter (also high in stearic acid). It’s been revelatory. Though I’ve been low carb since 1/1/14, since I’ve tried eating a diet higher in stearic acid, I am amazed at the lack of hunger this causes. Not only that, but the “heat” that sometimes I’ll generate. Sometimes, I feel as if I’m burning up. I can actually eat one meal a day with high stearic acid intake, which I’ve never been able to do before.

    I am trying to keep in ketosis for health reasons, so I have been eating high stearic acid within the confines of that. I have tried some mashed potatoes with high stearic acid butter oil, but only for my first meal post-workout. Unfortunately, mashed potatoes and I don’t seem to get along, so I’ve only tried this 4 times. I do not know if there is a benefit to combining stearic acid with starch or not (relative to eating high stearic acid and keto/low carb). I would like to continue testing, though, assuming I can find a starch that does not affect me.

    Anyway, based on my experiments, I think we went horribly awry in ways we could not have imagined when we demonized saturated fat.

    1. I’ve been following Brad’s work too and added stearic acid, too and for the first time I’m able to do omad without too much bother. I have discovered, after 2 months of homemade bread loaded with butter that wheat flour causes joint inflammation and possibly mood instability, too, so none of that for me. I seem ok with a turnip/carrot/parsnip mash, though. I trying to remain fairly low carb, too.

      1. I think the effect of potatoes is variable depending upon the individual. I’ve been experimenting with a continuous glucose monitor (CGM), which has been an interesting experience. Three or four small potatoes (cherry tomato size) eaten along with a steak and a few actual cherry tomatoes don’t even give me a blip on my blood sugar curve. I haven’t tried them alone, so don’t know what they are by themselves. Also tried a bowl of ice cream (full fat) for dessert with the above meal (which I eat almost every evening – the steak meal, not the ice cream) and found the same thing. Not a blip. But when I ate the ice cream by itself after not eating for several hours the following afternoon, my blood sugar curve went up. What the CGM experience has shown me beyond the shadow of a doubt is that the glycemic index is pretty much worthless when you’re looking at the response to a mixed meal, which is what most everyone eats.

    2. As Brad explains in his description of the diet, he only included the starch to prove that ketosis was not causing the weight loss benefits. I’ve been increasing stearic acid also, but I am not adding any extra starch.

    3. I went to Brad Marshall's site and found it quite interesting. However, an obvious question I had when reading about his notion that the French eat lots of saturated fat in the form of butter, cheese is that they also eat plenty of olive oil and nuts — the nuts in general contain plenty of PUFA. Thoughts?

  2. Thanks Dr. Eades. I met you in Clearwater Fl in 2000 at a Robert Crayhon seminar. Loren Cordain and Ron Rosedale were also there. I’ve heard or read where you put significant emphasis on PUFA’s role in obesity.

    Thanks, Dan Butterfield

    1. Hi, Doc. I used to live down the doc from you in Santa Barbara. As I mentioned on Twitter I had gone on a strict keto diet last summer and fall and lost 40 lb and got down to my target weight of 200 at 6-3, feeling pretty good almost all through that and I’ve stayed at that stable weight for 6 months, still mostly Keto. I added stearic acid and stearic acid butter oil based on Brad’s articles. I wasn’t trying to lose weight. I felt pretty good where I was. But in about 10 days I was down 5 lb without trying, and I’m fairly sure that was primarily fat as I can feel it around my middle. I had already dropped a couple of pants sizes and it looks like I’m about to drop another one. I have the feeling this would help you lose weight without losing muscle as I know I lost some muscle in that keto phase. It’s hard to argue with the theoretical basis especially since I’m not a physiologist! But my N=1 has convinced me as it was a result I wasn’t expecting. Thanks for this very detailed and clear explanation. I kind of understood it before but now it’s much more transparent. I also believe that thinking about these processes so much in terms of signaling really helps understand what’s going on.

      1. I saw your tweet. Thanks for the more comprehensive update. Did you live down the doc from us on a boat in the marina?

    1. Thanks for that excellent presentation. And please, No, DON’T make things much simpler, because your detailed information was perfectly fine to follow and I will certainly love to get more information like that, so please don’t water it down. Complex situations require complex description without a lot of simplification and I think you got it perfectly right in your post.
      It was a pleasure to read it and I am looking forward to whatever you will post next.

  3. Brilliant. Thank you for this informative post. You presented the information that I, as a lay person, could easily follow. I am not sure how or from where I subscribed to your email list, been reading so much in my quest to step away from the old dogma and lead a healthier life, but I so grateful that I did. Always enjoy the thought-provoking articles/blogs you share.

  4. You begged for feedback so here it is. First, understand that I couldn’t be a bigger fan of Protein Power or more grateful to you for sending it my way. Diagnosed 40 years ago with Type II, statistically I’m long since dead, yet still plugging along, not only not obese (any more) but not even in the overweight category (double handful of belly fat notwithstanding). So why the preface? Unfortunately because I barely understood a word of the post, which is so dense with chemistry (not at all within my skill set) and acronyms that I couldn’t even read it all, had a nearly violent reaction to even trying. So I skipped to the end for the here’s what it all means in lay person’s terms part, and it wasn’t there.

    I’m looking forward to the next one, still fervently hoping to find it, and thank you for doing this work.

    1. I was worried that it was going to be a little tough to follow. The take home lesson is that probably the vast increase in vegetable oil and the reduction of saturated fat intake starting back around 1980 played a large role in the current obesity epidemic.

      1. You have beautiful graphics in your written discussion, but they are still way too complicated. WHY do readers need to know the complex biochemistry in such detail in the first place? They want to know HOW to change their diet NOW in order to prevent premature death and morbidity.

        Only those who have had some exposure to biochemistry can even begin to understand it but there is still too much detail getting between the fundamentals (simplest) and full blown research (most complicated). This leaves all the readers who haven’t been exposed to biochemistry in the “still very confusing” basket. Aren’t these the main readers you want to reach?

        May I suggest that you make it MUCH simpler including simpler graphics and have links to “subsections” in your website that have subdivisions of the original discussion for those who want to know more details (which I think will always be a minority).

        1. Thanks for the feedback. A few years ago I asked readers of my blog what they wanted to read about in my posts. One of the most common suggestions was more science. If I pile the science on too heavily, some people complain. If I try to water it down, others complain. I don’t think I’ve ever written a post this complex, so it’s kind of a one off. But I actually left a lot out. The crux of the whole process is what happens during beta oxidation. I wrote a long explanation of that that I intended to link to for those wanting more info. MD read and said You’re out of your mind if you post that. There won’t be two people who will read it. So, I’m in kind of a damned if you do, damned if you don’t situation.

          The bottom line is, assiduously avoid industrial seed oils and vegetable oils, and replace them with saturated fat when at all possible.

          1. I actually really appreciated the detail in this post. Thank you for going there and please continue. I’m looking forward to the next post.

          2. Ditto. I love the nitty gritty science stuff. I have no doubt that you’ll balance it out with some relatively easygoing posts with barbecue recipes, but this one was an intellectual steak, medium rare, and a bone to gnaw on for later.

          3. Maybe I'm in the minority, but your post was very readable and outlined the processes involved in a very useful way. I do have a biochemundefinedcell biol background, but your explanation made your thesis come alive with guideposts to cogitate on. In a different life, my faculty thesis advisor worked out the Glycogen Cycle in part by isolating the players in the process from beef heart harvested as close as possible to the moment of slaughter to minimize and or maximize the impact of stress on the reactions. (The limit of my understanding at the time). I wondered if your thesis includes the effects of stressors, chemical or otherwise, other than PUFAs vs. Sat. on fat accumulation.

          4. No, my thesis does not include stressors of any kind at this point. Simply the FADH2 to NADH ratio at this point.

        2. I always feel like this info needs 2 presentations- the uncomplicated executive summary and the nerd’s show-me-your-cards version. I love the latter and really got something out of the video; about to read the bulk of his post now. Knowing the deep nitty gritty “why” can help some really believe in advocating for the changes it suggests.

      2. I thought this was excellent. Not too over the top and you tied up a few loose ends. Thank you Dr eades I look forward to more of these!

      3. I’m also an avid reader of Hyperlipid, of which I read every word and all the comments, even though much of the chemistry is over my head. Every once in a while Peter will include a TL;DR summary that helps a lot. I think doing this gives you the best of both worlds — the details for those who want them, and the summary for those who want to skip to the chase.

  5. Dr Eades, so glad you’re back! I had viewed the video a few months ago when I found it after trying to determine where you went! The blog post reminded me of what I had seen in the video and I understand what you’re saying (sort of :-)). I hope it proves to be true and it can get out there among the so-called experts and maybe they’ll start to pay attention. Sure seems like a viable hypothesis to me! Thanks again.

  6. What happened in 1980? How about cable TV, especially ESPN 1979, CNN 1980 and MTV 1981.? The birth of couch potatoes.

    1. A multitude of studies have shown that exercise doesn’t do squat for weight loss. The late 70s and 80s also launched the jogging craze. Diet makes vastly more difference in weight loss or gain than does the level of exercise. As many have pointe out, you can’t outrun a bad diet.

  7. This brings much hope! Most of it sunk in….couldn’t repeat any of it back to anybody tho. So technical for me but you explained it well enough for a layperson. Going to watch the video next having read it. Looking forward to the next blog and really looking forward to the next Protein Power book. Thank you for all you do!
    (btw, you do NOT look anywhere near 300!) 😉

  8. I am so glad you are back! You have been missed. The way I would sum up your article is: read food labels; don’t eat anything with soybean oil or canola oil, etc; just eat real food, nothing manufactured.
    Can’t wait for your book list.

  9. Thank you Dr Eades. Great info and the video was entertaining. You can be very funny. I’ve been melting grass fed and finished beef tallow over my salads for a dressing and it’s delicious. It gets a bit waxy. Would that be as good as the bacon grease you like to use? Looking forward to your next post. Cheers.

    1. Beef tallow is always going to be a little waxy unless it’s hot. You might want to cut it with a little macadamia nut oil (a little hard to find and kind of expensive), which contains almost no PUFA. Or even a little olive oil. Bacon grease isn’t as waxy, because it has a bit of PUFA in it.

  10. I’m so glad that you are back to blogging. Too technical for me but I do get the jist about PUFA. I’ve been a follower of the Weston A. Price foundation and they’ve been vilifying PUFA for many years. Gotta make your own mayo, salad dressings, and avoid eating out.

  11. I’m a biologist of the 1980 and I was wondering how olive oil heavy in the monosaturated fat fared out in stopping fat accumulation in cells?
    Thanks in advance for your reply

    1. It’s in the middle. It does end up generating a little local insulin resistance, but not nearly as much as saturated fat. But a lot more than PUFA generates.

      1. [olive oil] ” It does end up generating a little local insulin resistance, but not nearly as much as saturated fat. But a lot more than PUFA generates.”

        So, given your response above, olive oil generates MUCH more insulin resistance than PUFA, and saturated fat also generates more insulin resistance than olive oil??? Scratching my head.

        1. I think I may have been playing fast and loose with my terminology.

          Olive oil contains some saturated fat, a lot of monounsaturated, and even a fair amount of polyunsaturated fat. As a consequence olive oil acts as a combo of these fats. It probably produces a medium amount of local insulin resistance. Pure saturated fat, such as stearic acid, produces a lot of localized insulin resistance, while PUFA (linoleic being the most common) produces little to none. Kind of a Goldilocks and the three bears situation.

          1. Well, the cat’s out of the bag now. Prior to this blog post, you could have just advertised for “30 individuals willing to stuff themselves with french fries.” But if they’re going to have serum drawn, how would they be able to influence the results by knowing or guessing the fat that was used to fry the fries? Or is that not how FADH2/NADH ratio is determined?

          2. It’s not a matter of checking the FADH2/NADH ratio–that would be impossible to check anyway. If the theory is correct, those subjects eating the fries cooked in beef tallow would not eat as many as those eating the fries cooked in vegetable oil, because the FADH2/NADH ratio would be higher with the beef tallow and therefore shut off the cells sooner, and, presumably hunger. If subjects knew what they were bing tested for, their own actions could influence the study.

          3. Waa-ah! I promise I won’t post again! Insomnia is sucking away my ability to critically analyze. But my understanding is insulin resistance = bad . If saturated fat and PUFA produce more insulin resistance than olive oil, then we should reject both sat fat and PUFA in favor of olive oil.

          4. Total body insulin resistance is bad. That’s the insulin resistance everyone talks about when they talk about insulin resistance. What I’m talking about is a transient insulin resistance that basically signals that the cells if full. It doesn’t hang around long, and doesn’t really influence total body insulin resistance.

          5. “What I’m talking about is a transient insulin resistance that basically signals that the cells if full.”

            Is this in whole or part the “physiological insulin resistance” commonly seen in people following a ketogenic diet or fasting?

          6. No. At some point, I need to do a post on physiological insulin resistance. Peter has a couple of good ones if you look at his Proton series.

          7. Peter (Hyperlipid) calls local insulin resistance “physiological insulin resistance”. This explains why low carb eaters often test higher for blood glucose in the morning. As Dr. Eades says, it’s different from the kind of whole body insulin resistance that is a hallmark of T2D. It took me quite a while to wrap my head around that.

  12. Thanks Dr Eades,

    Not just for this mind-opening video and post, but for all your work from the original Protein Powder, which I treasure.
    I’d be very interested to read about what you typically eat, or what you tell your patients to eat, and what to avoid.
    I’d also be interested to know your thoughts on how this hypothesis reconciles with Ted Naiman’s P:E Diet.
    It would be great to see you down under (Australia). I’ll give Dr Rod Tayler of Low Carb Down Under the suggestion.

    You’ve opened a great big can of worms. Fantastic! Greetings from Brisbane.

    1. I need to read up on Ted Naimen’s P:E Diet before I can comment on it. Do talk to Rod. I would love to visit Australia. He and I have discussed it a bit, but nothing came of it. I’m putting you on the case. 🙂

      As to what I typically eat…
      Mainly meat of one kind or another. Maybe 50g of carb per day, maybe. All in the form of vegetables.

  13. I am so, so glad that you are back to blogging. I like the science. And I think it is important that it is included. Readers can skip over what doesn’t totally compute, and as well, ask questions. Keep at it! You’ve been missed!!!!

  14. I’ve been making my own stearic acid butter oil for the past few days, but haven’t seen any Earth shattering results yet. I do notice that my blood sugar spikes are moderated by consumption of the oil.

    1. Interesting about your blood sugar spikes. I wore a continuous glucose monitor for almost a month, testing everything I ate. My normal evening meal is a chunk of meat, a few sliced cherry tomatoes a few tiny potatoes (potatoes the size of cherry tomatoes), and a lass of red wine. Such a meal doesn’t even give me a blip of a glucose increase. I decided to have a bowl (a small one) of ice cream for dessert to see what happened. Nada. No change in glucose. Then I tried the same bowl of ice cream after not having eaten for several hours. A little blip up, but not what you would expect. Of course, the ice cream was full fat.

  15. We have a great fish and chip shop here that people come to from 200 km away because the chips are so good. The reason they are so good is that they are cooked in beef tallow every single time. Little old New Zealand

  16. Really interesting. Thanks for your efforts to make this info available in an understandable form. I’m a 60 year old nurse and I get it. I regret the many years of following the government nutrition rules only to find that grandma knew what she was talking about. Would have saved me and my patients a lot of health problems if we had not followed the diet pyramid.

  17. I thought this post was excellent. I could only wish that Baylor College of Medicine had made biochem this understandable back in 1979…..

    Please continue to blog and record videos.

  18. Welcome back ! I really missed your blogs .

    I have just started using beef tallow and mix it with coconut oil , due to its waxy content. It works well for me.

    Beef tallow is a good source of stearic acid. which I am lead to believe, does not seem to raise serum cholesterol concentrations and I have just started to research how the length of the fatty acid influences the process of its digestion and absorption within the gastrointestinal tract. . The learning process never ends. !

  19. I’ve been researching a lot regarding the ROS theory of obesity and the one question I keep running into that I can’t seem to find an answer to is this- I understand how that “bottleneck” and subsequent reverse electron transport cause localized insulin resistance which prevents FA’s and glucose from getting into cells. The part of that equation that’s missing is if a cell is undergoing localized insulin resistance, how could the energy that’s already being stored in that cell be released? Low insulin is required for stored energy to be utilized- but if the result of the RET is that additional energy can’t get into the cell, the assumption is that stored energy also cannot get out of the cell…which to me means this theory doesn’t account for how one would lose stored body fat- low basal insulin levels are necessary for that to happen. I’d love some explanation of how increasing saturated fat (stearic acid in particular) would not only generate ROS that prevent additional energy from being stored but also how it facilitates the release of energy that’s “locked” away inside a cell.

    1. The local insulin resistance driven by stearic acid is transient. It’s there only when the food is being broken down and oxidized, which is when energy would normally be going into the cell, not out. It signals that the cell is full. During the post meal fasting state, the situation reverses, insulin falls, and fat escapes the fat cell to be used to fuel the body’s needs.

      1. That is exactly the information I was looking for!! Obviously if one is eating a low carb high fat diet insulin levels are low in general. But in the context of using an approach like “The Croissant Diet,” where starch is being consumed, I’d imagine insulin levels are going to be higher in general so I assumed that would affect the ability of stored energy to be released from cells.

  20. Thanks for another great post! More that I read about this theory, the better I understand it. Still dont fully understand and sorry for a silly question but if the fat cells no longer take in that energy because they’re full. Where does that energy go? Is it just sent out to be used by other cells, assuming the person isnt insulin resistant everywhere else? Can that unused energy be problematic?

    1. It goes to other cells and equilibrates among them all and when those are full is basically kept in the circulation till used. The fullness of the cells and the nutrients remaining in circulation doubtless send an ‘I”m full’ signal to the brain so you quit eating.

      1. So, under this theory we come back to weight loss being triggered by Calories-in Calories-Out, CICO, where CI is triggered by satiation, which is triggered by saturated fat intake?

        1. I think there is another component to this hypothesis. It’s true that saturated fat should increase satiety, but also the turning away of fat from the cells should, by a couple of different pathways increase energy expenditure.

  21. Love the details about bio-mechanisms. People who don’t like it can skim or skip to the conclusion. Thanks so much! So very happy you are back. Not to be greedy, but am waiting for some book reviews :).

    1. I’ve read a lot of books over the past couple of years. I guess I’ve got to pick a handful that are review worthy and write them up.

      1. Yes, please, more book reviews.

        No thanks to you, though, (just kidding) for writing about something that created another internet rabbit hole for me to lose myself in! The science was a bit much for my post-menopausal brain but the mental gymnastics were good for me. I do believe it all helped me to better understand your hypothesis, and look forward to more information on this. I always love hearing what you have to say.

        Also, as I read all the 61 comments I see you replied to one that you greatly have reduced your nut intake. In another of your replies where someone asked of your type of fat intake one fat you said you utilize is macadamia oil. This makes me wonder about how consuming macadamia nuts may fit into all this.

        1. Most of the fats we use are solid at room temp: butter, beef tallow, lard. When we want a liquid fat, we use macadamia nut oil because it has almost no linoleic acid. Mainly monounsaturated fat. It’s expensive, but we don’t use it often. And we sometimes use olive oil, but not a lot.

          Macadamia nuts are fine. It’s just easy to overeat them. I have no off switch when it comes to nut, so I don’t like to keep them around.

          1. In terms of stearic acid, which is the long-chain saturated fat you want to drive the FADH2/NADH ratio, beef has the most followed by lard, then butter. Coconut oil doesn’t have a lot of stearic acid. Butter and coconut oil have plenty of saturated fat, but the particular saturated fats are shorter chain sat fats, which generate a greater ratio than PUFA, but not as much as stearic acid.

          2. Cocoa butter might also be a good option? 36% stearic acid, roughly the same Oleic acid and a little less Palmitic acid.. Smells amazing although maybe too strong for some. I love the “wafers” you can find for sale (amazon, etc) as they’re so easy to use and I can just put one on my tongue – tastes like chocolate just without the sugar.

  22. I appreciate you never talk down to your audience. Sometimes I can wade through, sometimes not. But I ALWAYS have takeaways. Loved your book reviews forever, and now look forward to whatever you bring to the table. So there! Suzie

  23. I see some criticism here for the biochemistry. If you have an hypothesis about something, and you want to establish some credibility, you have to take it a step further. You need to present some kind of underlying plausible mechanism based on basic scientific principles. This is a check I use, and look for, to decipher the validity of medical claims. There are all kinds of anecdotal claims by people that do not appear to be lying or have conflicts of interest, but should you believe the claims to be generally true, and would apply to you? If they cannot take it to the next level, in terms of basic science, then it is probable that you should dismiss the claims, at least for the time being. And of course more anecdotes beg for an underlying scientific explanation.

    This is the problem with epidemiology and the majority of nutrition/chronic disease advice. They never offer a plausible and tested underlying mechanism. You could still be wrong of course, but at least you provided a plausible next step.

    The biochemistry here serves to reinforce your plausibility, and I say, keep up the good work.
    You may still be wrong, but at least you moved it up a notch as compared to the other 99% of nutrition science which has long since become an oxymoron.

    1. There is no question that obesity has skyrocketed since ~1980. There is no question that the per capita carb consumption has increased since ~1980. There is no question that saturated fat intake has fallen while PUFA intake has markedly increased since ~1980. This hypothesis proposes a mechanism that ties those facts together and makes sense of them. May be totally wrong. Hypotheses are like that.

  24. It is SO WONDERFUL to have you back!!!!
    Two questions: 1) Could you give us a list of the exact fats you and Mary Dan use in order of preference and about how much you consume each day? 2) When will you Protein Power 2.0 be published this year?
    Thank you, thank you, thank you for returning to your grateful fold.

    1. I asked MD about the amounts and types of fat we eat. She has no idea as to the amounts, because she doesn’t keep track of it. But we eat butter, beef tallow, lard, Macadamia nut oil, and a bit of olive oil. That’s about it as to the types of fat.

      Protein Power 2.0 is being worked on. I’m hoping it will be published late summer/early fall.

  25. Two Burning Questions:

    1. Avoid PUFAs in fish, nuts? (I read your Omega3/6 rationale for not worrying so much about eating NON-grass fed beef, if you are still eating nuts, as nuts contain obscenely high Omega 6s.)

    2. Does this sat/unsat fats explain females’ blindingly difficult time losing weight despite low carb? Are females more sensitive to PUFA oils than our male counterparts? Or just too sensitive to oils? (Okay, three questions.)

    1. I used to eat nuts like a chicken eating corn. But now I have backed way off on that, primarily because of the omega-6 PUFA content. Unlike males, females have menopause to contend with, which makes losing weight more difficult. I have no information that would lead me to believe females are more sensitive to PUFA than males. As compared to males of the same weight, females do have a lot less lean body mass, which is the engine for burning calories. And, in general, although females tend to eat less than males, they tend to consume the same if not more alcohol, which, sadly, inhibits weight loss. I weigh substantially more than MD, but she matches me glass of wine for glass of wine and drink for drink. But she doesn’t eat nearly as much food as I do.

  26. I’m not a doc, but I appreciate the discussion of the low-level mechanism. At least for me, you made this complicated topic (w/ all the FADH2/NADH and the various Complexes) easier to follow by starting with “how do we get fat?” and working backwards. Without an explanation of mechanism, it’s difficult for engineering types like me to be convinced why “X could cause Y”.

    On ROS-induced local insulin resistance, I keep wondering “What happens to the energy once the fat cell rejects it (by temporarily shutting down insulin reception)? That energy doesn’t just disappear from the body.” A hypothesis that Brad Marshall gave was that rejected energy (because it is circulating rather than being taken up by the fat cells) provides a greater satiety signal. Seems plausible to me, but would like to hear your thoughts on that.

    1. I agree that it can signal satiety and the fullness of the cells probably signals satiety. Also, the fat can recycle through the oxidative processes and send electrons to the ETC, most of which will move on through. The increased electron flow through the ETC ends up pumping more hydrogen ions across the membrane, increasing the chemiosmotic gradient. When this happens, some of the hydrogen ions seep back through the membrane to help equalize pressure instead of driving ATP production. This is called uncoupling. It uncouples the oxidative process from the actual formation of ATP. It releases heat without producing any work, i.e., production of ATP.

      1. Thank you for this explanation of uncoupling! I was going to request it. Peter has talked about uncoupling for years and I’ve never understood what it was.

        On the subject of seepage, I’ve also read that polyunsaturated fats can get incorporated into mitochondrial (and other) membranes. Membranes are normally built from saturated fats which form straight lines, like pickets in a fence. Polyunsaturated fats have kinks in them (from the double bonds I think; these kinks are what make PUFAs liquid at room temperature, unlike saturated fats). This essentially makes a fence with holes in it that allows unintended seepage. My understanding of this is no doubt imperfect and I’d love to see it addressed in a future blog post.

        1. I’ll be happy to address PUFA in cell membranes in a future blog. What you need to know is that researchers can break down membranes and calculate the amount of PUFA in them, then score it using what is called the Unsaturation Index. The larger the Unsaturation Index, the more double bonds in the membrane. People used to think it was good to have a high Unsaturation Index, because it made the membranes more supple, which was thought to improve the activity of the various proteins within the membrane. But, as it turns out, the higher the Unsaturation Index, the lower the longevity. More double bonds are more prone to free radical attack, resulting in a free radical cascade and damage to the membranes. Longevity can be graphed as a function of the Unsaturation Index. Barja and Pamplona have done a ton of work on this if you want to track it down and read it. It’s really interesting to me. They have been able to decrease the Unsaturation Index in lab animals by feeding them more saturated fat.

  27. The McD’s experiment would not be difficult to replicate in an environment of your choosing. You could even set it up at Low Carb 2020 if you thought a break of just a few days between the two fries fest would work instead of two weeks. The hotel kitchen could be coerced (paid) to produce the fries. Volunteers wouldn’t be difficult to line up, given a shout out in your blog and your twitter feed.

    1. I might volunteer myself.:)

      The subjects of the experiment you propose would already know what we’re trying to do. They would be trying to guess which fries were tallow fried and which were cooked in PUFA. You’ve got to hide what you’re looking for from the subjects, so they can’t fiddle with the results.

      1. I do see one problem with this experiment: there are two variables involved. One is the type of fat; the other is the assumption of how satiety works.

        Does that mean it’s not a worthwhile experiment, especially because it seems relatively simple and inexpensive—since all you’re measuring is how many french fries people are willing to eat. No expensive technology or testing required.

  28. Hey. Loved it.

    My only question is do you believe this is an addition to the carbohydrate insulin hypothesis or replaces it? There is examples of populations suffering from obesity pre seed oil manufacturer.

    1. It’s an addition. There was plenty of obesity before 1980, it’s just that that level of obesity had held steady for decades. All of a sudden, it jumped in the early 80s and has been on the rise since. I’m sure historically a percentage of people have been sensitive to carbs. Those are the people who were overweight prior to 1980. Their percentage of the population remained pretty steady for years and years. Once the per capita consumption of carbs jumped by about 250 calories per day, it snared another group of people who hadn’t exceeded their threshold of carb sensitivity at the lower levels of consumption. As per the hypothesis, the extra 250 calories per day of carb consumption may have been driven by the increase of PUFA consumption (recommended by the ‘authorities’ in a misguided effort to lower cholesterol levels) and the decrease in saturated fat (driven by the same misguided ‘authorities’).

      1. Something to be aware of with historical populations like the Pima Indians and other primitive peoples who got switched to a westernized diet: many of them were provided lard. Starting in the 1850s or 1860s, lard started being adulterated with cheaper, recently invented cottonseed oil.

  29. Hi Dr. Mike,
    So glad you are writing again. I have you to thank for curing my heartburn over 25 years ago and I still own my (very battered and dog eared) copy of PP. In the book you made an association of wheat and GERD. Every time I tried to add gluten grains back to my diet my GERD added itself back as well. Finally in 2002 or so with the advent of Agatston’s publication of his South Beach Diet book I gave up bread forever. I also eventually shied away from his notions about saturated fats, but now, he’s released a new work with an admission of oops, I was wrong. Once again, he’s right. Carbs in an of themselves have a place in an active person’s diet but they must come from underground vegetables and not refined grains or genetically modified fruit. But it’s the PUFAs that kill. And they are so hard to avoid unless you spend a lot of money on avocado oil and never eat out.

    I read the text of your talk and I was reminded that what we learned in biochemistry and human physiology class in the 80s was not the full picture. Thanks for going over 15 min. This is seminal material. You’ve earned a huge big gold star from me!

  30. A number of us jumped on The Croissant Diet over a month ago, increasing saturated fat intake, adding stearic acid and avoiding or reducing PUFAs (including chicken, pork and bacon which are high PUFA due to corn-fed diets and animal physiology. Beef and other ruminants do does not have this issue due to the nature of ruminant stomachs.)

    Some of us, especially women, have seen no weight loss whatsoever, unfortunately, so there is more information to be developed. The good news? After 18 months of keto, switching to a higher carb diet heavy in saturated fats including bread, rice and potatoes we saw no WEIGHT GAIN!

    So this may be good for maintenance, still looking to unlock the key to PERMANENT weight loss. On KETO and intermittent and extended fasting I lost 50# over 10 months but when I stopped extended fasting and kept to 2 meals a day in an8 hour period I gradually added back 20.

  31. Thanks for the post, Dr. Eades. Very informative! I am a low carber, and after seeing one of your presentations on youtube, I became interested in learning more about F/N. One of the pertinent blogs from Peter D states that an F/N of 0.46 from PUFA doesn’t produce much ROS , while an F/N of 0.49 from a long chain length SFA does. I became curious as to why such a small change would cause such a large result. I dug deeper into David Speijer’s articles, and found that he has been hypothesizing that higher F/N will release more ROS, but I only saw him compare F/N of glucose with SFA, where the shift in F/N is quite large. So I am not understanding the mechanism behind how such a small shift in F/N can have such a large impact on ROS. I am thinking maybe this is speculation from Peter D? I can follow the theory behind proton pumping, electron transfer and chemical over-potential across the mitochondrial membrane because I have a background in PEM fuel cells, but I can’t see any mechanistic reason why a small shift in F/N in going from PUFA to SFA can change ROS so dramatically. Any further information or insight would be greatly appreciate. Sincerely, John Fagley

    1. It’s pretty much hypothetical at this point. But the work done so far does seem to show that PUFA do not generate the same degree of RET as does saturated fat, despite a small difference in FADH2/NADH ratio. That small difference could be a switch flipping the RET off and on.

      Returning to the analogy of cars in traffic, back when I was in engineering school taking courses in highway design (which I hated BTW), I learned that it doesn’t take much slowing down to create a huge traffic jam if the overall traffic flow has reached a certain steady state. For instance, something as innocuous as a banged up car sitting well off the highway can, if the traffic flow is high enough, create a tremendous slowdown in traffic. Just the momentary slowing as one driver after another glances at the car on the way by can generate an enormous effect on overall traffic. Which is why sometimes you find yourself in a traffic jam and wonder what in the #%@*# is causing it, then cars ahead of you slowly speed up and everyone then starts moving. You then wonder what caused the slowdown in the first place.

      I suspect the ‘switch’ for RET works much the same way. Electrons are flowing smoothly through the CoQ couple, then saturated fat starts running more through EFT (as compared to PUFA), which are enough to cause the jam up. So, I would say biologically that 0.49 could make a big difference compared to 0.46.

      1. Thanks for the explanation and the analogy. I was on that same road yesterday! Data showing increased RET with saturated fat definitely shores up the hypothesis. Another question I had – if fat cells become insulin resistant because of high saturated fat concentration and low PUFA concentration in the blood stream supplying nutrients to the fat cell, won’t the same nutrient concentration be seen by other cells in the body, such as muscle cells, and if so, wouldn’t those other cells also become equally insulin resistant due to ROS being generated by their mitochondira? This would be counter to the effects that we want to see, i.e. insulin resistance local to the fat cells, while other cells are free to process as many nutrients as they need to do their jobs.

        1. The process should equilibrate among the cells, but it’s a transient effect. And I’m sure there is a satiety signal when this happens, not to mention uncoupling (wasting energy as heat) as a response.

          1. If the mitochondria in both fat and non-fat cells react the same way to saturated fats, then saturated fats would shut down the flow of fuel into non-fat cells as well as fat cells. It seems that if saturated fat shut down the influx of fuel to all cells, then AMP kinase would take over, and saturated fat consumption would make us feel cold, tired and hungry. Are you saying that only fat cells have a satiety signal, or that only fat cells have heat generation by uncoupling, or that only fat cells have a transient effect?

          2. I’m saying the whole thing is a plausible sounding hypothesis as to why both carb consumption and obesity suddenly started to spike in the late 1970s/early 1980s. As such, all the details haven’t been worked out. The RET process has been shown in mitochondrial preparations, which may not the same as mitochondria residing and working in the cells. Remember, the RET occurs inside the mitochondria when fat already in the mitochondria are broken down first by beta-oxidation, then by the Krebs cycle. Since the mitochondria are inside the cell, and the processes take place in the mitochondria, the fat driving the action is already inside the cell. The rest of the fat that doesn’t make it into the mitochondria are the fats that end up being stored. The RET and consequent ROS release and localized insulin resistance simply equilibrate the fat throughout the adipose tissue. When one adipocyte reaches its limit, the fat is stored in others until all are filled to capacity. The fat remaining in the circulation is taken up by working muscle and other tissues that burn fat. In the adipose cell, which is designed to expand to a certain degree to accommodate fat beyond that needed for current use by the muscle and other tissues (the adipose cell acts as a battery), saturated fat will generate the RET as a function of the amount of saturated fat in the meal just consumed. Remember, based on the graph in the post of food consumption trends, TOTAL fat consumption is around 75-80g per day, which didn’t change much till ~1980. At that time, PUFA replaced a portion of the saturated fat in the diet, but not all of it. So, what we’re talking about here is a moderate increase in saturated fat while the PUFA intake falls off. You’ll have a bit more saturated fat throwing off a higher FADH2/NADH ratio, but will still store fat, both saturated and PUFA. With elevated amounts of dietary PUFA, there will be a lower FADH2/NADH ratio, which will allow more fat to be taken up into the adipose cells and distend them. When adipose cells distend to a certain point (which is a function of ATGL and perilipin A, probably genetically determined), then these cells become insulin resistant irrespective of saturated fat content. So, basically, dietary fat in the circulation gets taken out and some is run through the mitochondria, which via RET & ROS distribute it throughout the adipose cells. Probably the same thing happens in muscle cells–some is taken up by mitochondria and burned for energy and some is stored as intramuscular lipid. That fat that isn’t stored or burned probably signals satiety and is sooner or later picked off by the mitochondria and oxidized. It’s an ongoing process. I don’t really see AMPK jumping into the fray as it is a signal that the fuel tanks are empty. It wouldn’t make sense to send that signal when the fat cells are full and fat is being turned away and remaining in the circulation.

  32. Hello, I appreciated the article! I have been trying to figure out a link between my hashimotos, low heart rate and blood pressure, and beta thalassemia minor ever since I had total knee replacement and had a very difficult recovery.

    I have always been “fluffy” and was on the ill fated low fat craze when I started getting fatter even though I was active (I have always been physically fit and fat-to-fattish). I managed to get leaner with a higher protein, lower carb approach and maintained that for about 8 years until I went back to a stressful job, although I maintain my muscle and am considered very strong.

    The TKR and the complications revealed to me that I build up excessive scar tissue very quickly and easily and when I asked why the answer was “some people just do”. I was doing some research that made me wonder if a lack of oxygen was contributing and whether the dysregulated inflammatory response was autoimmune related. Thalessemia minor is an anemia characterized by very small red blood cells (low oxygen) and of course hashimotos is autoimmune and with low heart rate (resting gets as low as 28 and is usually around 35) and blood pressure. I wonder if all of that is connected to a “slow metabolism” . I have never had any indications of high blood sugar or diabetes so I don’t believe I am insulin resistant , but I am working now on becoming more fat adapted with my diet to manage inflammation and lose weight.

    I am not a scientist and I am certainly not super self aware or very methodically in tune to my body, but the TKR (at age 50 but being advised since age 40 to do it) really made me wonder why my knees got so bad to need it so young and why the recovery was so horrible. I have never written in to a blog like this and normally am wary sharing personal info on the www, but this blog post is reinforcing a hunch I have that led me to research about mitochondria and I felt compelled to ask if you had any insight.

    My other knee is in bad shape too but but I am not going to have it done until I know how to preempt some of the calamity of the first. And of course, getting to the bottom of this “slow metabolism” and getting leaner is a big piece of that. Thanks for any response even if it is to tell me I am grasping at straws or afflicted with confirmation bias.

    1. I can’t really respond to your specific medical question, because I can’t give medical advice online to a patient I’ve never seen or examined. The law works that way.

      But I can give general advice. A low-carb diet, low in PUFA is generally anti-inflammatory. TKR are usually as a result of osteoarthritis, which can occur early in some folks. Here is a terrific post on the subject by an orthopedist who understands.

  33. Based on my testing of eating a high saturated fat (mainly, concentrating on stearic acid) diet, this might take a while:

    “One group would eat McDonald’s fries cooked in vegetable oil until full, while the other group would eat the fries cooked in beef tallow.”

    What I mean is that when I first started trying the high saturated fat diet, say at “lunch” (I usually eat two meals a day), when I got home, I usually was not hungry. However, if my family was eating at that time, I would have dinner. That dinner, as far as I could tell, was a “normal” sized dinner.

    Now, after several weeks of trying the saturated fat diet, it’s different. If I get home and the family is having dinner, what I eat is dramatically less. For instance, we had “tacos” last night, which means ground beef+seasonings, cheese, sour cream, salsa in a bowl for me (and the same for everyone, as we don’t eat chips or flours). Before, I would have multiple — at least 2 — bowls of meat. Last night, I had one. And was completely FULL after that.

    I also think that carbs still play a role. Some believe that it’s ONLY PUFAs that cause obesity. That is, as long as you stay below some limit of PUFAs, no matter what you eat, you won’t get fat.

    I don’t think that tells the whole picture, as I got fat drinking beer, eating pizza and ice cream. Not a lot of PUFAs there. I did not eat fried food, out (other than pizza) very often, etc. And when I did eat without beer, I’d eat a very low fat, high carb diet (which made me depressed…so I’d drink beer).

    So, I think carbs (and of course protein) still play some role. How much of a role, is now questionable. But under the theory that it’s only PUFAs that are to blame, I should not be able to each much ice cream., since it’s low in PUFAs and high in saturated fat (not bad for protein, either). But I am a bottomless hole when it comes to ice cream. And the stuff makes me gain weight just thinking about eating it. Which is why I limit my ice cream intake to vacations and some holidays, and then we buy small ice cream cakes that the family can eat in one sitting with no leftovers.

    Do you have any thoughts about the importance of PUFAs relative to anything else (carbs, protein,…)?

    1. If you’re asking if I think PUFA’s are the driving force behind all obesity, the answer is no. Obesity rates stayed the same for decades. But that changed in ~1980. PUFA in truckload lots came on the scene starting in 1980, so I’m attributing the increase in obesity to the addition of large amounts of PUFA. But at this point, that’s theoretical. Baseline obesity is, in my view, a carbohydrate sensitivity problem.

      1. Is it possible that the Ancient Egyptians were obese and ill because they combined high starch and PUFA undefined MUFA diet, whereas East Asians eat high starch with pork and lard (Okinawa, South China)?
        If the Egyptian had animal fat instead of olive oil, could they have avoided their "civilization" disease?

        1. Hard to say. I think the carbs had a lot to do with it, but they did consume a lot of safflower oil, which is one of the oils containing the largest amount of linoleic acid. I suspect they probably would have done better had they consumed their carbs with less linoleic acid.

    2. Doesn’t milk (in ice cream etc.) contain oestrogens and other anabolic (growth) peptides/hormones? Could that explain why many people seem to experience weight gain and weight loss stalling on dairy products? Also, doesn’t the milk protein casein metabolize into casomorphin, an opioid peptide, which might affect body composition indirectly? Looking at (, also shows some interesting iodine value (a measure of unsaturation) in milk varies over the year in a cyclical fashion. Seems that the unsaturation index increases during summer months, and decreases in winter months.

  34. Interesting!
    But … isn’t “PUFA” abit general?
    I mean There are many different PUFAs.

    What do you mean exactly by PUFA? Do you mean w-6? Which is mainly 18:2?

    What about the w-3 FAs, which we are told, are sooo healthy.

    And what about 18:1?

    1. Yes, w-6 in this case. The w-3 you’re referring to are longer-chain FA. Those are broken down in the peroxisomes. I didn’t go into that because the whole hypothesis is way to complex as it is for the general reader. Didn’t want to add further complexity to an already difficult to fathom post.

  35. Possible typo? Shouldn’t this sentence read “… fewer FADH2 …”

    “Why are fewer electrons thrown off, requiring fewer NADH2 to carry them, from unsaturated fats than saturated fats in the first step of beta-oxidation?”

  36. What kind of oil do you and Mary Dan recommend for making your own mayonnaise? I have been mixing avocado oil with light olive oil, but now, I’m wondering if I should switch. Thanks for any help you can offer.

    1. We like Macadamia nut oil for most of our oil uses, which are primarily limited to salad dressing. But MD has been unable to get Macadamia nut oil to hold together well in making mayonnaise. When she makes mayonnaise, which isn’t often, she uses light olive oil or avocado oil. As of yet, she hasn’t tried a mixture of either one of those oils with Macadamia nut oil, so the jury is still out on that one. Why don’t you try it and let us know. 🙂

  37. I couldn’t find a button to click at the end of the post to get the packet of three papers. Is that offer no longer available?

    1. I just checked, and it still works for me. I’m using a Chrome browser on a Mac. And I checked it on a Safari browser, and it works there. Sometimes these things are browser dependent upon whether they show or not. What kind of browser are you using?

    2. Often it’s a content blocker (ads, trackers, pop-ups) that renders these things invisible. Recent versions of Safari have content blocking built in (Safari menu/settings for This Website). Try turning off all your blockers.

  38. Curious (maybe not answerable but more questions to ponder) how this plays out when a fat person is trying to lose.

    What fatty acid profile lives inside our full adipocytes? I assume the kinds that we ate when getting fat, but if the body goes through trouble to change them perhaps this doesn’t apply as much.

    As one begins metabolizing their own fat, if PUFAs and MUFAs make up the majority of it, does this mean our adipocytes and other cells receiving previously-stored FFAs may “cancel” or fail to develop the H2O2 signal to grow more mitochondria et al as we lose weight due to the lower average FADH2/NADH ratio from burning stored fat?

    Is this a mechanism by which folks losing weight sabotage themselves, and perhaps the metabolism slows? Could supplementing periodically with stearic acid throughout the day help “tune” that?

  39. Another point to consider:
    Nature uses saturated fat to detect over energisation of the mitochondria.
    Poly unsaturated fats do not signal energisation.
    So energy is gained, and the “Wood pile” builds up
    Kinda like the Ozzie bushfires and Climate Luvvies!

  40. I’ll admit the diagrams and biochemistry are over my head, but I understand how they support the conclusion.

    What is interesting to me is I have kind of demonized “insulin resistance” in my head for a lot of years (I first met you and Dr. Mary Dan when you filmed me for your Pentabosol infomercial around 2000 or so), which is a big part of my I am still consistently low-carb all these years later. Was very proud that my fasting insulin levels dropped dramatically over the years and my A1c from 12.5% to 5.1%. Took all of those markers to mean my improved insulin sensitivity was a good thing.

    So when I first read your section, “How We get Fat”, it was the first time I thought that improved insulin sensitivity implied fat cells accepting more fat. Woah, I panicked for a moment! What if 20 years of low-carb habit had been wrong! And I was worried you were going to conclude saturated fats were causing the obesity issue.

    Have to say I was quite relieved by the end of the paper! The only PUFA’s I eat regularly are my daily Carlson’s cod liver oil or sardines. Other than that, I steer clear of PUFA’s, including industrial seed oils.

    Great to read your thoughts again. Been following you for decades (literally).

    1. Hey Bob, great to hear from you.

      It’s a weird situation. Insulin sensitivity encourages fat storage and obesity, whereas insulin resistance prevents obesity. But you want to retain your insulin sensitivity yet not get obese. This is where the transient insulin resistance driven by the increase in FADH2/NADH ratio comes in. It prevents some fat storage, yet doesn’t affect overall whole body insulin sensitivity. It’s actually more complicated than this, but this helps to understand it better.

      Keep in touch.

  41. Ray Peat has been writing about the perils of PUFA for many years so it’s good to hear more corroboration on this topic. I’m in Canada and most restaurants fry with canola oil due to the public brainwashing that saturated fats are dangerous to health. Thanks for the very informative post.

    1. Plenty of saturated fat, but mostly short chain. Won’t throw off as much FADH2 relative to NADH as a longer chain fat such as stearic acid would do.

  42. Went to a restaurant that had fries cooked in smoked beef fat served with duck fat hollandaise. Ordered the fries, one other appetizer, and one plate to split. The fries showed up first, my wife and I split them and we we were full. It was not a lot of fries either.

    1. @Eric—in his original blog post about the Croissant Diet, please note that Brad said he included the starch for two reasons: first, to prove that it was not a ketogenic effect that caused the weight loss; and second, because the starch soaks up a lot of fat and makes it palatable and easier to consume.

      So the starch is not a necessary part of the diet in terms of metabolic chemistry—at least in my reading. It will be interesting to see what Dr. Eades has to say.

      1. Good to know – I have been including starch a bit in my own diet (mostly toast, sometimes couscous, but not a lot and mostly to sop up excess fat from the plate). Recently this week, using toast + lots of butter as an “appetizer” tends to curb my remaining intake. I can barely eat more than 2 eggs’ worth of omelette after that, and if I do (cooked in beef tallow fwiw) I am stuffed beyond all hope with my eyes bugging out of my head. Pants are fitting a bit looser and I’m about 3-4lbs heavier after 1 week but I’m reserving judgment until I have spent more time with it…

  43. I listened to Gladwell’s podcast. Amazingly, he ends up blaming McDonald’s, not Sokolof. Ridiculous. I have to agree with Taleb, Gladwell is an idiot.

      1. Well, Taleb’s right again, they are both idiots. Where does that leave us? History teaches us that 3rd way, middle-of-the-road, trying-to-be-reasonable characters don’t win. The Buddha lost to Devadatta (according to the laity) every time, again and again, including on veganism. In other words, you can’t win by dialectics, nor by being conciliatory like Gladwell is doing. And we need to win, or plant-based will become mandated sooner rather than later.

  44. Glad to see you back blogging Dr Eades! I would definitely be keen for your podcasts when you get up and running.
    I recall reading in your book The 6 week solution for the middle aged middle (before I was middle aged!) something about theoretically being able remove stored pufa’s via plasma donations.
    I have moved many houses since then and have subsequently lost the book and never stumbled upon another copy to validate this. I believe that suggestion was the trigger for me donating plasma on a regular basis many years back so thanks for that! I then had 1 bad experience and gave it up a couple of years ago…. are your thoughts on the potential effectiveness of this further evolved since then? I’m considering taking it back up (been following Ray Peat recommendations re Pufa’s for a while now)

    1. Yep. Donating blood (whole or red cells) and/or plasma is a true win-win situation for all. Gets rid of bad stuff from you and may save the life of someone else.

  45. Perhaps my 9yo typical breakfast of hash brown potatoes fried in tallow has been superior to sugar/vegetable oil infused convenience foods

  46. Haven’t seen it mentioned here yet, but I heard from Brad Marshall’s interview with Biohackers, about Stearic acid causing mitochondrial fusion –

    I did not know mitochondria can “fuse” together, reconstructing themselves into long tubes or networks, I always assumed they were like individual specialized bacteria-ish units floating around our cells… always fun to learn something new.

    Secondarily, after googling more about mitochondrial fusion, I see-

    I wonder if part of the benefits here, and probably unrelated to the ROS, is the fact that stearic acid seems to induce a “repair” mechanism in the mitochondria every time it’s consumed?

    1. I was intrigued by that also. Wikipedia wasn’t a lot of help. In all my years of reading hyperlipid I don’t remember it ever being mentioned. Thank you for the links.

  47. Dr. Eades
    The Randle cycle incorporated into this : my take is the following
    – hormonal control i.e. insulin overrules: switches the system to use glucose and store FFA
    – Randle cycle: automatic perpetuation of the existing status quo, be it glucose or fat oxidation (in the low insulin situation ie. no hormonal control or glucagon presens)
    – ROS transient control: I the Cell am burning sat fat, leave me alone for a moment.

    So, insulin disappears but you continue to burn glucose until it is available in the cell (enter into fasting). points 1 and 2 above. After that you can/must start burning fat, and continue until insulin hits you (point 2). If you the cell are burning sat fat, you decline transiently the insulin command (point 3). Is this how it works…?

    The point 3 should make you feel satiety and make you eat less, utilizing the reserves instead (croissant diet / low carb with sat fat).

    While I have not seen this context fully explained, it botheres me a bit.
    Rgds JR

    1. I’m not sure I understand your question exactly. I think I’m getting confused with all the Points 1-3 that don’t correlate with any numbers on the actual points. Here is a link to a nice paper on the Randle cycle, which I’m very familiar with. My only problem with this paper is that late in the paper, the authors state

      Switching from glucose to fatty acid oxidation leads to a greater proportion of electrons being transferred to complex 2 rather than to complex 1 of the respiratory chain.

      Which is not really true. Even with long-chain saturated fats, you’ve got over twice as many electrons going to Complex I than to Complex II. But the conclusions they draw are accurate.

  48. On behalf of everyone, I would like to take this opportunity to thank you for being so gracious as to take the time and making the effort to answer just about everyone’s questions. You’re a helluva guy!
    I just hope it doesn’t turn you away from blogging, again.

    1. Thanks.

      It does take a ton of time to answer all the comments. Time that could be spent creating new content, but I don’t know which people prefer: new content or answers to comments?

      I while back I happened to be reading an article on blogging. In the Q&A some blogger had asked if it was legitimate to send in comments to his own blog using a junk email address and a pseudonym. Apparently he had been blogging for a while and hadn’t gotten any comments and wanted to more or less seed his comment section. I almost wrote and offered him some of mine. 🙂

  49. When I was a kid my favorite food to eat was potato pancakes (Latkes). My grandmother would make them for me as a treat (1x/mo) using 5lbs of Russet potatoes fried in Wesson corn oil. I would eat all five lbs of potato pancakes with sour cream in one sitting. My grandmother and mother couldn’t believe how as a kid I could eat that many. Needless to say, I was a chubby kid back then.
    Fast forward to a few years ago. I decided to make a batch of potato pancakes for my wife to try. I used 5 lbs of potatoes, but knowing the dangers of industrial seed oils I fried some in coconut oil, some in ghee, and some in beef tallow to see if they tasted any different. I was stuffed after eating about a pound of potato pancakes. I wondered why I could eat so many when I was a kid but couldn’t eat as many now as a full-grown adult. Now I understand why!

    1. Thanks for the interesting history. There may be another reason, too. When kids are growing, they convert excess energy to that growth. Adults convert it to fat. I just read a recipe yesterday for Rösti, which is a potato dish made from day-old boiled potatoes mixed with fat and fried. Rösti could be an interesting food to try for a couple of reasons. First, of course, the saturated fat mixed in with the potatoes and used to cook them. And, second, the fact that the starch in day-old potatoes allegedly converts to resistant starch. could be a two-fer.

      But, the more anecdotes I hear about this phenomenon, the more I think it is a valid mechanism.

      1. I read a lot on Free The Animal and other sites during the original resistant starch discussions. I distinctly remember that cooked-potato starch is only resistant as long as it’s cold. Reheating changes it again. Is there contradictory info now?

        1. Not that I know of. I never paid that much attention to the resistant starch movement back when, so I’m not completely familiar with it.

    1. That’s a controversial question. I think so, though. Since Denton Harmon came up with the free radical theory of aging decades ago, people have tried giving vitamins to all kinds of experimental subjects to make them live longer. As far as I can tell, it hasn’t work. One study giving beta-carotene to lung cancer patients had to be terminated early because the subjects getting the beta-carotene were dying at significantly greater rates than those on placebo.

  50. Haven’t had time to read all the comments, but wanted to say this was an excellent post and look forward to more detailed posts like it. I can’t wait to look over the citations. I will forward this to most everyone I know. This is exactly the type of stuff I demand from my doctors. If they don’t provide it I don’t use them, unless it is an emergency or I need some prescription. My current doctor is always giving me stuff like this. It is great to see you are blogging again, I just noticed this today. Welcome back and hope you can keep it up (blogging or podcasting). You also expected Protein Power 2.0 to come out back then, any news on an update?

    1. We are working diligently on PP 2.0 in between all the other time-gobbling stuff we have going on.

  51. I am looking forward to PP 2.0.
    I do find it interesting that Banting, back in the late 1800s was reported obese at 200 pounds. We wouldn’t even sniff at that weight these days. (similar to your images of sorority sisters over the ages in one of your presentations).
    On another note, I have not been able to get a good consistency with steaks with Sous Vide. The idea makes sense (I even got one for my parents), but when I try this on steaks, the inside is more soupy than ‘medium rare’. Any ideas?

    P.S. I do like the detail of these presentations. One either end, a summary was given, but going deep into this, and giving a proposed mechanism to support a theory, is very useful. Just like reading Taube’s Good Calorie, Bad Calorie. Some people thought it was too detailed, but I like the connected dots.


  52. I enjoy your blogs and enjoyed PP back in the last century.

    It would help if your blogposts were dated, so if one comes across a post, one would know if it was old when you didn’t have access to newer information or if it was last week.

  53. Wondering if you experimented with drinking PUFA’s and monitoring with a CGM? Would that change BG levels?

    1. We wouldn’t recommend drinking PUFAs. It’s an interesting idea to see if something would happen to BG, but we’d be surprised if it would do much peripherally.

      1. Based on thinking the last couple of years by Peter at Hyperlipid and Tucker Goodrich, I'm avoiding vegetable oils like the plague (including olive oil), and almost completely avoiding pork and poultry. Peter is kind of on the fence about grassfed versus commercial meat but then he's in the UK, while here in the US commercial meat is raised in pretty appalling conditions.

        Rather than stress about the ratio of omega-3 to omega-6, I figure eating the best quality possible real food pretty much takes care of that automatically. I went through the supplement phase, but now I believe that taking supplements is either worthless or provides supraphysiological amounts of things which can unbalance the system. Except I do take D3 in the wintertime.

        For me this is in the context not of weight loss, although that's a benefit, but rather autoimmune disease and a recent blip with cancer. FWIW I also avoid all grain, minimize carbs, and increase stearic acid by using tallow and cacao butter for cooking. I make a point of eating organ meat regularly and making my own fermented natto, kefir, yogurt, kombucha, and vegetables. And just eat one meal a day which is fairly effortless.

  54. I started eating low carb and I lost a substantial amount of weight. I still had more to lose, but the weight loss stalled. I had probably dropped 5 pounds since the beginning of the year. Along the way, I cut out the oil that you talked about after finding it in dressing, vitamin d supplements, and with almonds/pecans made in bad oils. I saw your video and applied the concept to nuts. I eat a lot of nuts and more than what is recommended. I realized that when I was first losing weight, I was eating macadamia nuts. Then, I switched to more to almonds, pecans, and walnuts. From your video, I realized that they had more linoleic acid and discovered my blind spot for Omega-6 PUFAs. I switched back to macadamia nuts. Now, I probably lost about 7 pounds in the last 3 weeks without trying. Macadamias have lower carbs but I think that I am probably also eating fewer calories since I get the signal that I am full. It has probably had a more cascading effect by getting me to delay or reduce meals.

    I did see a video where someone was recommending 1 part macadamia nut oil to 3 parts olive oil to balance the omega-3 to omega-6 ratio. If olive oil is borderline, the combination may put the two on the better side for reverse electron transport. Maybe it does not work that way. I just received my macadamia nut oil in the mail.

    Thank you.

  55. Thank you!

    I have been low carb now for over a year, and close to carnivore, and I have lost 40+ lbs. My health became important when I was diagnosed with NAFLD, along with a host of other chronic health conditions last year. Now upon learning of your hypothesis, I am incorporating significantly more stearic acid in my diet, via tallow, cocoa butter, and just plain old pure stearic acid, and reducing my linoleic acid as much as I can. It’s not been a week since I have started so I’m not expecting any radical changes just yet. I suppose my days of wolfing down deep fried everything are over 🙂

    Again, Thank You!!

  56. Dr. Ray Peat has been writing about the health dangers of PUFA for many years ( Hopefully this knowledge becomes more accepted and mainstream.

  57. I’ve been recommending your lecture on you tube to zillions of people. I find it the most comprehensive explanation on the subject. Even more so than peters various podcasts. Thankyou for that lecture.
    I am wondering what your take is on eating fatty fish andundefinedor fish oils. The msm push about essential omega 3 as healthful and necessary has me confused. Even the highly respected wapf recommends fish oil supplementation. But since it is polyunsaturated fat I am confused as to why it would’ve healthful for the mitochondria. Can you help me understand this..?

    Also, I’ve been recommending and pushing for getting you onto shawn bakers morning interview on meatrx where I actively volunteer my time to support people.
    Will you consider this?
    Thankyou once again for all your goodness and the work you do.
    In health,
    Brooke erdman

    1. I’m kind of in a state of flux about fish oil myself, for all the same reasons you are. And Peter is, too. Until it gets sorted, I’ve adopted the position that a little is good, but a lot probably isn’t. That’s my default state right now till I learn more.

      I would be delighted to be on Shawn’s podcast. In fact, I think I saw an email come through about it a day or so ago. I’ve been avoiding dealign with emails until I got the last newsletter out and finished my most recent blog post.

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