PART 2 of 2: The Evolving Hypothesis of Obesity – how polyunsaturated fat makes us fat

This content of this post is based largely on a presentation titled “A New Hypothesis for Obesity” given by Dr. Michael Eades at the Low Carb Breckenridge Conference, Breckenridge Colorado, Sunday, March 4, 2018 with some details filled in from his website. Dr. Eades has been in full time practice of bariatric, nutritional and metabolic medicine since 1986 and is the Director of Medi-Stat Medical Clinics, a chain of ambulatory out-patient family care clinics in central Arkansas. I have added the Canadian data for the benefit of my readers. This article is Part 2 in the two-part series The Evolving Hypothesis of Obesity. Part 1, which lays the groundwork for this article can be read here.

In the 1970’s the Dietary Guidelines in both the US and Canada advised us to eat more grains, vegetables and fruit and to eat vegetable fat, instead of saturated fat in butter, eggs, whole milk and red meat.

The US has dutifully complied, as indicated by the following graph;

US per capita consumption of grains, vegetables and fruit and vegetable oils compared to red meat, whole milk, eggs, animal fats and butter – Nina Teicholtz via – Dr. Michael Eades – A New Theory of Obesity, Low Carb Breckenridge, March 4 2018

Similar types of increases and decreases have been observed in Canada. According to Statistics Canada;

“In the past two decades, Canadians have shifted towards a diet which includes more fruits and vegetables, cereal products, and nuts and beans. During this time, poultry consumption has increased, while beef and pork consumption has continued to decline.”

In 2016, per capita consumption of beef, pork, lamb and veal in Canada was 47.7 kg (105 lbs) per person per year down from the 73.2 (161 lbs) per person per year it was in 1980. Egg consumption also dropped from 21.96 dozen per person per year in 1980 to 19.93 dozen in 2016. The last time it was measured nationally in 2009, total fresh vegetable intake (excluding potatoes) rose to a record 40.7 kg (89.7 lbs) per person and the amount of potatoes including as french fries was 27.9 kg (61.6) per person, making total vegetable consumption 68.6 kg (151 lbs) per person per year. Total fresh fruit consumption also rose to a record 39.3 kg per person.

The Canadian Canola Growers Association reported that in 2012, 600,000 tonnes of canola oil and soybean oil was consumed by Canadians either as grocery store items or food-service products, including margarine, cooking oil, mayonnaise and salad dressing. In the twelve months ending July 2012, 2.8 million tonnes of Canadian vegetable oil was exported to the US and China, accounting for another 2.4 million tonnes.

In 2012, Sean McPhee, President of the Vegetable Oil Industry of Canada said;

”The vegetable oil industry is an important part of Canada’s growing agri-food sector. The industry’s processing capacity in 2012 is nearly double the capacity of 2007, and it is anticipated that further expansion will increase capacity 50 per cent by 2015.”

As saturated fat intake has declined, carbohydrate intake has continued to increase from the mid-1960s onward.

Decrease in saturated fat consumption, increase in carbohydrate consumption (US data) – Dr. Michael Eades – A New Theory of Obesity, Low Carb Breckenridge, March 4 2018

The Evolving Hypothesis of Obesity

The most significant change since 1976-1980 is that we are eating a great deal more linoleic acid found in soybean, canola and corn oil while simultaneously eating significantly less saturated fat and overall eating more calories.

Three factors together are thought to have produced the “perfect storm” which has resulted in the massive increase in obesity from 1980 until the present;

(1) the vilification of saturated fat
(2) the encouragement to eat industrially produced vegetable oils
(3) the increased consumption of refined carbohydrates.

Simply put, the evolving hypothesis of obesity states that in addition to the (a) increasing amount of carbohydrate in the diet since ~1980, things are made significantly worse by (b) large amounts of industrially-produced  polyunsaturated fats which promote obesity simultaneous to the (c) decrease in naturally occurring saturated fats which protect against obesity.

Dr. Eades credits much of the mechanism for the linoleic hypothesis to Dr. Petro Dobromylskyj, whose is a doctor of veterinary medicine and who writes a technical blog called Hyperlipid which I referred to in order to fill out my understanding in writing this article.

The difference between how the body processes saturated fats versus polyunsaturated fats

To understand the mechanism, the only chemistry you need to understand is the difference between a saturated fat and an unsaturated fat.

Saturated fats are ones where all the carbons in the chain are saturated with hydrogen atoms and there are no double bonds in the middle of the fatty acid chain. Palmitic acid (a 16 carbon fat) is an example of a saturated fat – and is one that our body synthesizes.

Saturated fat – palmitic acid

When a saturated fat is broken down (called “beta oxidation”), 2 carbons are cleaved off at a time, until the fat is completely broken down.

Beta Oxidation of a Saturated Fat – e.g. palmitic acid

Glucose is processed anaerobically in the cytosol of cell, but fatty acids are metabolized inside organelles called mitochondria (the ‘powerhouse of the cell’). All our food (regardless what it is) is metabolized to a combination of FADH2 and NADH.

The NADH and FADH2 enter the Electron Transport Chain at different complexes. NADH enters at Complex I (CI), while FADH2 enters at Complex II (CII).


Saturated fat has a feedback mechanism called the Reverse Electron Transport which keeps the cell from taking in too much energy – – Dr. Michael Eades – A New Theory of Obesity, Low Carb Breckenridge, March 4 2018

The lower the FADH2:NADH ratio is, the lower the local insulin resistance is and the higher the FADH2:NADH ratio, the higher the local insulin resistance.

A saturated fat generates a higher FADH2:NADH ratio, so saturated fat increases local insulin resistance which serves to keeps more carbs in the blood.  A process called Reverse Electron Transport is initiated which results in the making of a signalling molecule known as a superoxide (SO) molecule. This signalling molecule tells the body to stop insulin signalling by inducing local insulin resistance. This way, the cell doesn’t take up too much energy.

An unsaturated fat, on the other hand (such as palmitoleic acid or linoleic acid) has double bonds in the middle of the chain which changes the way the body processes it.

Beta oxidation of Palmitoleic acid (unsaturated fatty acid)
Polyunsaturated fat provide NO feedback mechanism (no Reverse Electron Transport) so there is nothing to keep the cell from taking in too much energy – Dr. Michael Eades – A New Theory of Obesity, Low Carb Breckenridge, March 4 2018

When fat cells (and other cells) are metabolizing an unsaturated polyunsaturated fat (PUFA) such linleoic acid from soybean oil, corn oil or canola oil, they generates a lower FADH2:NADH ratio, so an unsaturated fat reduces local insulin resistance, which means they allow plenty of glucose into the cells along with the PUFA.

These n-6 PUFAs generate energy all the way through the Electron Transport Chain and the Reverse Electron Transport is not triggered, so NO (superoxide) signalling molecule to tell the body to stop insulin signalling (i.e. there is no localized insulin resistance caused). The cell just keeps taking in more and more energy even though it doesn’t need any more!  This means the fat gets driven into the fat cells and is stored there, making it unavailable for use for energy.

Once fat gets stored in the fat cells, the body can only break it down when no more energy is coming in (such as when fasting), so the only way the body can get more energy is to eat more. The glucose is driven into the cells because of the decreased insulin resistance caused by the n-6 PUFAs oils, which results in glucose level falling. This causes the body to produce a strong signal to eat; in other words, it makes you hungry.

Along with carbohydrates, n-6 PUFA vegetable oils have increased dramatically in the typical American and Canadian diet since the 1970s and this mechanism explains why we’ve been getting fatter and fatter since then.

So much of our eating now takes place away from home, or with food made away from home, that much of the fat intake in the diet is n-6 PUFA vegetable oils that signal glucose to come right in along with them.

French Fries then and now

In the 1960’s French fries were fried in beef tallow (which is a saturated fat), and the stearic acid from the beef fat and the glucose (from the broken down potato) would be processed by the fat cell (adipocyte).

When the cell had enough energy, Reverse Electron Transport would kick in and create the signalling molecule (superoxide molecule), which would tell the body that it didn’t need any more energy. This would result in a decrease in hunger and an increase in energy expenditure.

Think of the superoxide molecule as a “bouncer” at a night club.  When there are enough people inside, the “bouncer” simply won’t admit any more people until some leave.

When French fries are fried in polyunsaturated vegetables oil, the linoleoic acid (from the soybean oil or canola oil) and glucose (from the broken down potato) are processed by the fat cell. The problem is, that even when the cell has more than enough energy, Reverse Electron Transport does NOT kick in and there is NO signalling molecule (superoxide) produced. The body doesn’t get any message that it doesn’t need any more energy, and the person doesn’t get any signal that they’re full, so they just keep eating.

In the case of eating foods made with polyunsaturated fat, it would be like a night club that has no “bouncer”.  Even when the club is jam-packed with people, everybody is admitted until there is no room to move!

The absence of a feedback mechanism in processing unsaturated polyunsaturated fats results in fat cells getting bigger and bigger – Dr. Michael Eades – A New Theory of Obesity, Low Carb Breckenridge, March 4 2018

The mechanism simply explained

Fat cells (adipocytes) bind more insulin at a given level of exposure when eating polyunsaturated fats such as soybean oil, canola oil and corn oil, than fat cells bind when eating saturated fat such as butter, lard or beef tallow.

Since insulin has to bind to its receptor to work and more insulin is bound when eating a diet rich in polyunsaturated fats, significantly more glucose is taken up into a fat cell in a diet high in polyunsaturated fats than in a diet rich in saturated fat. That is, the cells are more sensitive to insulin when eating a diet rich in polyunsaturated fats than a diet rich in saturated fat, so polyunsaturated fats allow too much glucose in to cells.

When fat cells and other cells are metabolizing saturated fat they make a superoxide (SO) molecule as a result of Reverse Electron Transport which is used to stop insulin signalling. When fat cells and other cells are metabolizing polyunsaturated fats, there is NO Reverse Electron Transport, so they are unable to generate the  superoxide molecule that is needed to stop insulin signalling. This is because there is too little FADH2 being delivered to ETF.

Saturated fats, such as Palmitic acid have a higher FADH2: NADH ratio and it is believed that this is what drives Reverse Electron Transport (RET).

The FADH2 to NADH Ratio (also called the F:N ration – different with saturated fats and unsaturated fats – Dr. Michael Eades – A New Theory of Obesity, Low Carb Breckenridge, March 4 2018

Oleic acid, the monounsaturated fat found in olive oil drives Reverse Electron Transport (RET) somewhat, but to a lesser degree than a saturated fat.

Unsaturated polyunsaturated fats such as Linoleic acid (found in soybean oil, corn oil and canola oil) have too small a FADH2: NADH ratio which prevents it from initiating Reverse Electron Transport (RET). It is thought that because polyunsaturated fats have such a low FADH2: NADH ratio, they are treated by the body similarly to glucose.

There are two consequences to eating fats with this low FADH2: NADH ratio.

  1. the fat cells (adipocytes) get over-stuffed with fat (because there is no “off switch”)
  2. When these fat cells get over-full they are unable to keep the fat contained as they should, and as a result free fatty acids are released and eventually find their way into other places where fat is not supposed to be found, such as in the liver, pancreas, even muscle and bone cells.  This is known as ectopic fat and the condition that results is called metabolic syndrome.


What happened after the 1950s and 1960s that caused overweight and obesity to suddenly explode in the 1970’sand just keep rising?

The answer is the types of fat we started eating.

Even though we were eating the same total amount of fat as before, these new industrially-produced polyunsaturated fats (such as soybean oil, canola oil and corn oil) do NOT provide the feedback mechanism that natural fats (such as butter, lard and beef tallow) do, so there is nothing in these manufactured fats to signal us that we are “full”.

This is why we began eating 240 more calories per day in carbohydrates –because the polyunsaturated fat that accompanied the carbs don’t tell us we’ve had enough!

The (1) the vilification of saturated fat, the (2) encouragement to eat and our acceptance and adoption of industrially produced vegetable oils and the (3) increased consumption of refined carbohydrates created the “perfect storm” and which taken together, certainly provide a reasonable mechanism with explains the massive increase in obesity from 1980 until the present.

Final Thoughts…

The different way the body processes natural saturated fats (such as butter, lard and beef tallow) versus the way it processes industrially-produced polyunsaturated fats (such as soybean oil, canola oil and corn oil) explains the mechanism by which the prevalence of obesity graph so closely mirrors the consumption of vegetable oil graph.

Trends in obesity among US Adults Aged 20-74 – Dr. Michael Eades – A New Theory of Obesity, Low Carb Breckenridge, March 4 2018
Added fats and oils compared with trends in obesity among US Adults Aged 20-74 – Dr. Michael Eades – A New Theory of Obesity, Low Carb Breckenridge, March 4 2018

Given that (1) total fat consumption has not changed since the 1960’s, only the type of fat we are eating has and (2) given that the body manufactures saturated fat in the form of palmitate, these naturally occurring saturated fats should not be thought of as “dangerous” or to underlie obesity.

As occurred late in the game with trans fats, it is time that these industrially-produced polyunsaturated fats be examined much more closely.

We ought to ask ourselves if we should even be eating oil from crops not thought of as fat-containing. If we squeeze an olive and fat comes out or we crush a nut and oil comes out, these are natural fats. Fats such as cold pressed olive oil, macadamia nut oil and walnut oil (to name a few) are natural sources of largely monounsaturated fats that are foods our ancestors (or other people’s ancestors) knew.

If “oil” needs to be produced under high pressure, high heat and with the use of solvents and deodorizers, is this even “food”? I think not.

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Dr. Michael Eades – A New Theory of Obesity, Low Carb Breckenridge, March 4, 2018 (NOTE: here is a similar talk given a Low Carb Down Under on August 11, 2018 and published on YouTube, called A New Hypothesis of Obesity.)