Mind-boggling new blog post by Dr. Michael Eades on complex biochemistry, ROS, ATP (the energy of life) PUFAs, oh my!



"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."

“Maybe PUFA is driving the obesity epidemic while saturated fat is protective.”

"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."

And with plenty o’ humor woven in among the dizzying array of acronyms!

(Troy) #2

Fun study below

Fall off the horse :racehorse: and barely hang on to the wagon
I’m a Team player, I may take one for this team here!:weary:

"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."

(Michael - When reality fails to meet expectations, the problem is not reality.) #3

For anyone interested, there are two charts (1) of overall fat compo of various oils/fats, and (2) with Omega 6/3 breakdown here:

(Bunny) #4

What is sad :slightly_frowning_face: is that Dr. Michael Eades does not even discuss the finer points of hydrogenation (trans fats) in a clear context?

And then you have to keep in mind the supra-physiological doses used in any research on PUFA’s?

So we have no idea how to view the variables in his hypothesis about PUFAS?

If you are going to go by the hypothesis that omega 6’s are the driving force behind fat cell expansion and eating saturated fat some how reverses this process then how do we explain the shrinking of a fat cell creating more tinier fat cells (you lose body fat then re-gain it back?) when somebody decides to go back to eating how much of whatever diet?

The other problem with his hypothesis is when we eat carbohydrates we are creating saturated fats naturally in our body with out even touching a drop of saturated fat? What’s up with that?

The bigger question; does the human body create PUFA’s endogenously?

Notice below “…it requires?..”

”…The human body can produce all but two of the fatty acids it requires. Linoleic acid (LA, C18:2n-6) (precursor to the n-6 series of fatty acids) and α -linolenic acid (ALA, C18:3n-3) (precursor to the n-3 series of fatty acids) are the simplest members of each family of PUFA and are termed essential fatty acids as the body cannot synthesise these. PUFA regulate a wide variety of biological functions, depending on the location of the last double bond, which range from blood pressure and blood clotting to the correct development and functioning of the brain and nervous system [2]. In addition, lipid mediators generated from long-chain (LC-) PUFA (arachidonic acid (AA) in the n-6 series and eicosapentaenoic acid (EPA) and docosahexaenoic acid (DHA) in the n-3 series) have important roles in immune regulation and inflammation [3]. The main dietary sources of LA include plant oils such as sunflower, safflower, and corn oils (Table 1), but they are also present in cereals, animal fat, and wholegrain bread. Rich dietary sources of ALA include green leafy vegetables, flaxseed, and rapeseed oils [2] (Table 1). …” …More

Thus PUFA’s cannot be entirely responsible for obesity, of course there will be lots of supporters of this hypothesis, it is still after all, only a hypothesis?

If you look at the template below it explains Dr. Michael Eades (et al. hyperlipid’s) hypothesis much better on why people get fat than his own interpretation of his own hypothesis and the real driving force behind obesity?

Keep in mind these percentages below are calories not amounts:

1. A lipid blend, designed to increase the intramyocellular lipid level in an individual , characterized in that it contains

oleic acid of from 50-70%,

n-6 linoleic acid of from 20-35%,

n-6 linolenic acid or longer chain fatty acids of the n-6 family of from 15-25%,

stearic and palmitic acids, together in an amount of from 0-15%, and

polyunsaturated fatty acids of the n-3 family from 1-10%.

2. A lipid blend designed to decrease the accumulation of intramyocellular lipid in an individual, characterized in that it contains

medium-chain fatty acids in an amount of from 40-65%;

glycerides with long-chain saturated fatty acids of from 20-50%, and

monounsaturated or polyunsaturated fatty acids in an amount of from 0-30%. …More

My current experiment:

Dr. Doug McGuff‘s Body by Science seems to work with the above in my own experiments in purposely making myself fat and simply using my own body weight doing squats (eccentrically) to failure or exhaustion against the gluteus maximus and after weeks and months of doing this I lost the weight again without restricting carbohydrates with no problems what so ever?

And of course being my own n=1 could be placebo?

Why Don't we Get Hungry During Extended Fasting?
(Edith) #5

Tucker Goodrich is a guy who believes that PUFAs have driven the obesity epidemic around the work. This is a very interesting podcast from Peak Human.

(Utility Muffin Research Kitchen) #6

Actually, this study has been done :slight_smile: Pretty much exactly as described, using kids as subjects. They used fries in vegetable oils and (unfortunately) compared it to mashed potatos with butter and not with tallow fries. But the kids ate almost twice as much when they had fries. You have to read the full text, the authors missed the significance of this and didn’t put it in the abstract.

And wasn’t it Eades who discussed the study in this very talk? Or was it David Ludwig?

Frankly, I find it hard to grasp what exactly you are trying to say. Maybe lose the sarcasm here and try again.

Eades is saying that we will store more fat/carbs in fat cells if we eat n-6 PUFAs. That is, we will need to eat more to achieve satiety. Carb intake goes up, we get metabolic syndrome. I don’t see how your n=1 experiment relates to that. Of course, n=1 experiments can never prove a statement, they can only disprove one by giving a counterexample. But the theory here is much more complex, we know that people lose weight without carb restriction if (and only if) they are insulin sensitive. So what exactly does your experiment counter?

BTW, I really like Fungs scepticism on whether we have really understood insulin resistance, which he discusses in Peter Attias podcast https://peterattiamd.com/jasonfung/. So we should always keep in mind that we are juggling with a lot of assumptions here that may turn out to be false. I think the protons theory makes a lot of sense, but I also think there are some questions that need to be answered.

(Utility Muffin Research Kitchen) #8

I like the blog post, but frankly I don’t think it contains anything new compared to Mike Eades talk (which I watched several times but a while ago).

However, there are some things that are missing.

  1. Why should the ROS generated by the RET affect only fat cells (storage)? What’s the effect on mitochondrial ATP generation? What happens in the liver?
  2. We see high ROS levels in patients with autoimmune diseases. So basically I understand that low ROS levels work as signalling device, while high ROS levels are used as means of chemical warfare against intruders. What’s the deal there, why do autoimmune patients still get fat and diabetic? And could these high ROS levels be responsible for fatigue?
  3. What are the implications for blood glucose? Hyperinsulinemia is obviously rampant with the western diet, so if the theory is correct, PUFAs should lead to higher blood glucose levels. How?

Somehow I think the underlying mechanism must influence glucose levels, because the obesity epidemic clearly correlates with metS. Somehow n-6 PUFAs are responsible for a slower glucose processing, causing higher insulin levels and more insulin resistance (long term). Local insulin resistance at the fat cells shouldn’t be the primary mechanism. If more fat enters the fat cells directly, we should be able to process the remaining nutrients (glucose) faster, not slower. We’re missing something here.

(Bunny) #9


I really don’t know what to tell you, if you cannot see parallels or relations other than that you should read more and educate yourself on the subject?

Getting certain percentages from different fats in calories from the diet effects where they go or accumulate in the body.

In other words how can you make 80% or 70% of your caloric intake in dietary fat below (hint: requires a little math/arithmetic):

2. A lipid blend designed to decrease the accumulation of intramyocellular lipid in an individual, characterized in that it contains

medium-chain fatty acids in an amount of from 40-65%;

glycerides with long-chain saturated fatty acids of from 20-50%, and

monounsaturated or polyunsaturated fatty acids in an amount of from 0-30%. …More

What combination of foods contain these types of fats and how much should you eat to get the right combination in calories?

Not sure what the BTW: Peter Attia Fung mental gymnastics thing you are going on about, I already know that? If you want to play mental merry-go-around and go off subject, I can do that to?

(John) #10

Study I found a while back that seems to indicate the mix of fatty acids may be important. I am not sure if it is germane to this topic, but I found it interesting.

(Bunny) #11

From the study above, interesting?

”…This study tested the hypotheses that: a) body composition, inflammation and vascular function would improve with a high fat diet (HFD) when type of fat is balanced as 1/3 SFA, 1/3 MUFA and 1/3 PUFA; and b) body composition, inflammation and vascular function would improve more when balanced HFD is supplemented with 18C fatty acids, in proportion to the degree of 18C unsaturation. …”


”…Significant improvements occurred in fat oxidation rate (↑6%), body composition (%fat: ↓2.5 ± 2.1%; %lean: ↑2.5 ± 2.1%), inflammation (↓ IL-1α, IL-1β, 1L-12, Il-17, IFNγ, TNFα, TNFβ) and vascular function (↓BP, ↓PAI-1, ↑tPA activity). When compared to HFD+placebo, HFD+stearate had the greatest effect on reducing IFNγ (↓74%) and HFD+linoleate had the greatest effect on reducing PAI-1 (↓31%). …” …More

(Bob M) #12

If anyone here does not think this theory works, try it. Eat high stearic acid (or palmitic acid) foods (eg, butter, actual stearic acid/butter oil as sold on the Fire in a Bottle site, cacao butter) and limit your PUFA intake (eat beef, no chicken, no pork fat, no bacon, no olive oil, no oils really at all, EDIT: no nuts, which are very high in PUFAs; fry only in tallow).

I’ve been testing it, and I CANNOT believe how full I get. And I’ve been eating low carb/keto for 6+ YEARS. It’s been a revelation.

For instance, I just had some ground beef, ham, eggs on stearic acid infused mashed potatoes, and I added high stearic acid butter oil to it, and ate a 50/50 split of high stearic acid butter oil and cacao butter. I am so freaking full right now, it’s stunning.

Moreover, I will get “hot” eating this diet. The last time I did this (Tuesday, today is Thursday), I got hot enough to sweat.

I’m testing eating small amounts of carbs after workouts, and I’m currently using potatoes with butter/stearic acid. I’ve been able to maintain ketosis while doing this. I’m trying to determine whether “starch” is necessary or not for this to work, and also testing whether I can get better/faster recovery from my workouts. Unfortunately, potatoes and I don’t seem to get along. I had horrible stomach issues on Tuesday and my hip pain, which had disappeared, came back. So, I’ll have to look for something other than potatoes.

I’m sorry, but I can’t listen to Attia’s podcasts. I honestly dislike him as a human being. The way he treated Dave Feldman, for instance, was terrible.

(Utility Muffin Research Kitchen) #13

Cacao butter doesn’t have the same effect on me. I tried about 50g cacao butter as dessert and some more in my morning coffee, but I didn’t note any change in satiety. But then I’m still losing weight, and have certainly stored quite a lot of PUFAs in my fat cells which might make a difference. Living in Europe I would have to pay a fortune for the fire in a bottle stuff (shipping and customs can double the price).

I’m not a fan of Attia, but was interested in what Fung had to say. (This was just my second Attia podcast, and I was unimpressed by the first one.) Fung basically says it makes no sense to assume that some cells are insulin resistant (muscle) while all other cells seem to process insulin just fine (liver storing glucose and creating fatty acids for example). So he thinks that we’ve got it wrong, what we consider insulin resistance is actually a matter of cells loaded with glucose/glycogen so they can’t store any more, and we need higher insulin levels to cram the remaining glucose in. I’m not sure that I agree with him, but it’s worth thinking about.