As we know all too well there has been an explosion in the incidence of obesity and type II diabetes over the past 30-40 years. Depending upon the bias involved, many people have opined as to the cause of this sudden departure from what had been fairly stable rates of obesity over the previous decades. People who are believers in the caloric theory of obesity – CICO (calories in vs calories out) – tend to believe the increase in obesity is simply a consequence of people eating more than they used to. As a corollary to that theory, those of a conspiratorial bent believe Big Food has made its spawn-of-the-devil products so tasty and addictive that they can’t be avoided. Those believing the carbohydrate – insulin theory of obesity posit that the increase in carbs in the diet since the late 1970s has driven the obesity epidemic. And all of these groups have data to back up their beliefs.
In the chart above from the dietdoctor.com site, it is clear that something happened circa 1980 that tripped the obesity trigger. Despite there being a multitude of theories as to why this happened, there is agreement across the spectrum of ideas that the obesity trigger did indeed get tripped.
All you need to do to realize how much obesity there is out there is take a look at an old movie or an old TV show. Rent Dirty Harry (which I did not long ago) and watch it for a few minutes. All the people look like stick people compared to people we see today. The contrast is startling. Or Google Woodstock and look at the images of all the folks there in 1969. Granted most are young people, but compare them to young people today on college campuses everywhere. Although there are a few mildly overweight kids sprinkled here and there in the photos, most of them look like stick figures compared to today’s college students.
Why has this happened to us?
If you look at graphs of the changes in food consumption from the 1970s till now, you’ll notice a few things. First, overall calories have gone up by around a little over three hundred per day. Second, although fat consumption has remained about the same, the percent of fat consumption as compared to total calories has fallen. Third, the amount of sugar in the diet has increased slightly. Fourth, the quality of the sugar has changed and become more fructose-laden. And fifth, as we’ll discuss shortly, the type of fat has changed. Saturated fat consumption has declined while polyunsaturated fats–i.e., vegetable oils–has increased markedly.
Importantly, most of the ~350 calorie increase has been made up of carbohydrate. Stephen Guyenet (who created the above chart), no believer in the carb-insulin hypothesis, calculates the composition of these extra calories to be as follows:
65 percent of the increase in calories can be attributed to carbohydrate, 24 percent can be attributed to fat, and 11 percent to protein.
These diverse changes in diet since 1970 allow people to hang onto their pet theories. The CICOers say it’s all because people are eating more. The anti-sugar people point to the increase in sugar. Those against fructose point to that. The low-carbers point to the fall off in fat consumption and the increase in carb consumption as the driver of all the obesity.
As you might imagine, my bias falls in with the notion that the increased carbs are a major force in the hugely increased rate of obesity. You might be surprised to learn, however, that I’ve always had a little niggling doubt that carbs alone were the cause.
Why have I had niggling doubts? Because of observations I’ve made over the course of my life.
When I was a kid growing up in the rural Ozark Mountains, everyone I knew ate sugar. A lot of it. Everyone, and I mean everyone, ate bread at every meal. As far as people then were concerned, it really was the staff of life. Same with potatoes, though they weren’t eaten at every meal. People celebrated holidays and get togethers with pies, cakes, cookies, brownies, cupcakes, etc. Most folks started off their day with a bowl (or two or three) of hot or cold cereal with milk and sugar on it.
I watched my own grandfather eat his breakfast every day while I was eating my cereal and toast. He started off with a big glass of prune juice – which I can’t abide to this day – for regularity. Then he broke into small bits two pieces of buttered toast and put them into a big glass of buttermilk. He threw a few spoonfuls of sugar on top, then mashed the whole thing around and ate it. He finished off with a cup of black coffee. Other than the coffee, it was not exactly a low-carb breakfast. But he was thin, as was most everyone at that time.
Other than the handful who were overweight at that time, people pretty much gave no thought to what they ate, other than how much they enjoyed it. I suspect the small percentage of people who were overweight back then were the group the obesity researchers of the time fingered as carbohydrate sensitive. (These are the researchers Gary Taubes wrote about in Good Calories, Bad Calories and Why We Get Fat.)
So, how did the majority of people back then eat sugar, bread, cakes, cookies, pies and potatoes and not get fat, while people today watch every carb and/or calorie and struggle?
I’ve always wondered what the change was that took place back at the inflection point in the graph at the top. Sure, we started eating more carbs then, but what else? I’ve had my suspicions that there was something else. And I think I’ve got a bead on it.
Before I reveal what I think the cause is, I’ve got to say that I always hate it when people are considered in the abstract. People aren’t abstractions; they are individuals. When we say that people are eating an extra 350 calories per day today as compared with 1970, that’s an abstraction. The reality is that some people are eating 1000 calories extra while others are eating, say, 200 fewer calories than they did in 1970. I am one of those who eat fewer calories now than I did in 1970 when I was thin and exercised almost no restraint. So, why do I always have to watch what I eat? I should be lighter than I was in 1970, not heavier. Which I am, by about 10 pounds. What’s the difference in my behavior now vs then?
Let’s look at another couple of trends besides just the caloric differences.
As you can see from the above charts, a couple of major changes have taken place besides just an increase in calories, 65 percent of which are from carbohydrate.
First, although overall fat consumption hasn’t risen by much, there has been a dramatic change in the type of fat we’ve been eating. Which to a CICOer doesn’t mean squat. Calories are calories irrespective of where they come from. In my view, as I’ll discuss shortly, this is a big mistake.
Second, we’ve been consuming more and more of our meals away from home since 1970. In other words, we have been relying on people who run restaurants to determine the fats we eat. And having been in the restaurant business and knowing a lot about it from having many friends in the biz, I can tell you that most restaurants use shelf-stable crappy oils for just about everything. So when you dine out and get a steak, salad and sautéed vegetables, you don’t have a clue as to how much vegetable oil you’re getting along with it. I, myself, am victimized by this frequently because I, like most people, eat out a lot.
When I was a kid, we always ate all of our meals at home. We never, and I mean never, went out for dinner. Or had takeout. My own kids eat out or have take out vastly more often than they cook at home.
Why does this matter?
Because we all get more vegetable oils than we should.
And why does that matter?
That question leads me to the heart of this post.
The importance of the FADH2 to NADH ratio
I have to start by saying that our metabolic machinery converts every food we eat to FADH2 and NADH. These are high-energy electron carriers that end up carting the energy of the food we’ve eaten into the mitochondria and transferring it to various complexes of the electron transport chain (ETC). The electron transport chain, in a bucket brigade sort of way, hands off these electrons from one mitochondrial ETC complex to another until they are ultimately attached to an oxygen molecule, forming H2O, water.
As these electrons make their journey through the ETC, they release energy that drives protons across a membrane creating an electrochemical gradient called the proton-motive force. This proton-motive force drives the little turbines that end up creating ATP, the energy currency of life.
The above is a simplistic explanation of an incredibly complex process. In an effort to keep this post from expanding to War and Peace length, I’ve put a couple of videos at the end. One is for beginning biochemistry students at MIT that explains in nice, but not overly complex, detail what ATP is and how it is made. It runs for about 35 minutes, but those interested need watch only the first 25 mins. The other short little video shows how NADH works.
Our metabolism converts all foods to a combination of FADH2 and NADH. It matters not whether you are eating Aunt Jemima’s Pancakes (with or without her syrup) or a New York steak cooked sous vide, it all resolves into FADH2 and NADH. Carbs convert to more NADH than FADH2 while fats, especially saturated fats, convert to a larger ratio of FADH2 to NADH.
NADH and FADH2 enter the ETC at different complexes. NADH enters at Complex 1 while FADH2 enters at Complex 2. Where these electrons enter combined with what happens to the proton-motive force determines the amount of free radicals released from Complex 1. (Complex 2 doesn’t release free radicals.)
You’ve probably been led to believe that free radicals are a bad thing. And in large amounts they are. But in small amounts, they can be signaling molecules.
In the case of the small amounts of free radicals we’re going to be discussing, they are signaling molecules. What do they signal? They determine insulin sensitivity. They determine whether the cells are sensitive to or resistant to insulin, and they do so in a brilliant way.
Basically, the lower the FADH2:NADH ratio is, the lower the insulin resistance is. Conversely, the higher the FADH2:NADH ratio, the higher the insulin resistance.
Carbs generate a low FADH2:NAHD ratio, which means carbs end up generating fewer free radicals and, consequently, lowering insulin resistance. Which makes sense when you think about it. If you eat carbs, you want to be able to move the glucose from the blood into the cells. This happens easily when insulin works well (also a function of the free radicals) and insulin resistance is low.
Since saturated fat generates a higher FADH2:NAHD ratio, saturated fat increases insulin resistance, which keeps more carbs in the blood.
Why would this be a good thing?
Well, in the event of starvation, the body ‘eats’ more fat in the sense that it extracts fat from the fat cells for energy. As the body metabolizes this fat, the FADH2:NAHD ratio increases, which increases insulin resistance and keeps the carbs available for brain function instead of being shunted into, say, muscle cells, which can function beautifully on fat.
After several days of starvation or a ketogenic diet, a similar situation prevails. Although the ketones reduce the FADH2:NAHD ratio, they also affect the proton-motive force in such a way as to both increase insulin resistance and increase the efficiency of ATP formation. So, glucose is made available for the brain while ketones become the fuel of choice for most everything else. And the ketones also power some of the brain as well, sparing glucose for those brain functions that run on glucose only. The blood sugar rises a bit, and this is what we call physiological insulin resistance. Also, understanding how this all works almost militates that there be a metabolic advantage while in ketosis, but that’s a subject for another post.
What about vegetable oils?
Omega-6 oils and other polyunsaturated fats (PUFA), the ones we want to avoid, unlike saturated fats, generate a fairly low FADH2:NAHD ratio. Which means they reduce insulin resistance. Which means they allow plenty of glucose into the cells along with the PUFA.
This means the fat gets driven into the fat cells and is sequestered there, making it unavailable for use for energy. When fat gets stuck in the fat cells, the only way the body can get more energy is to eat more. When the glucose is also driven into the cells because of decreased insulin resistance, the glucose levels fall, which is a strong signal to eat. In other words, it makes you hungry.
Which is why most processed foods filled with soybean oil (high in PUFA) and sugar make us want to keep eating them.
And it confirms, to me at least, why we’ve all gotten fatter and fatter since 1970. Along with carbohydrates, vegetable oils have increased dramatically in the typical American diet. Over the same time period, we’ve all started eating away from home more and more, so that we’ve lost control of exactly what kinds of fats we’ve been eating.
It also probably explains the situation of a friend of mine who just complained to me that he has gained 20 pounds over the past year or so despite rigid adherence to his low-carb diet. He started a new job that requires almost constant travel at the same time his unexplained weight gain started. Constant travel equates with constant restaurant food, which equates with a lot of PUFA. Which can equate with lower insulin resistance and more fat storage. I’m not sure this is what has happened, but it makes perfect sense.
If you want to read about all of this in more detail, take a look at Peter’s series on protons (especially this one) and physiological insulin resistance (Peter writes the Hyperlipid blog, which is one of my favorite blogs and listed in my list of my eight favorite blogs). Peter also has influenced my thinking on this subject greatly, and for that I owe him an enormous debt of gratitude.
Also, if you are interested, I’ll be happy to post in more depth, especially on reverse electron transport, which I managed to avoid discussing in this post. Just let me know in the comments.
Why do the new Dietary Guidelines mean we will all get fatter?
As I detailed in an earlier post, the folks responsible for the new Dietary Guidelines for Americans came under a lot of pressure for their idiotic recommendations to continue to demonize fat in general and saturated fat in particular. In an effort to appear to placate those voices demanding a reappraisal of the total fat and saturated fat limits, the powers that be ended up with recommendations guaranteed to make things worse.
According to Adele Hite (who writes in Eathropology, a blog that would make my top ten list now), the new guidelines are made to seem like they make a move toward good sense, but the reality is that they don’t. For example, most people think in the new Dietary Guidelines the limits on fat are gone.
Nope. Limits on “fat” are still there. If you’ve been hearing rumors that we are at the end of the “low-fat” era, and you thought that meant that the Guidelines were going to give the green light to fats–natural fats, fats that you could find at your local farmers market–you would be sadly, profoundly mistaken.
Just like all squares are rectangles, but only some rectangles are squares, all oils are fats, but only some fats are oils. The new Guidelines have been credited with saying, “Hey we’re okay with rectangles” but they are only okay with those rectangles that are squares. You can eat fat, but only if it’s oil.
So: Fat–as in “saturated fat”– is still evil. But lower limits on “oil” are eased–with the exception of a few oils that the DGA folks still don’t like because their fatty acids are mostly saturated. Lower limits on oils in the diet have shifted from no less than 20% of calories to no less than 25%. But make no mistake: The upper limit on dietary “oil” as a macronutrient remains at 35% of calories, as it has been since 2005. Only by keeping limits on “oil” low can we manage to cram in the Guidelines’ requisite 45%-65% of calories of carbohydrate into our diets and still have room for protein.
In other words, the USDA hasn’t discarded the “low-fat” diet. They’ve discarded the “low oil” diet and actually, not even that. Now you are allowed a whopping 27 grams (about 5 teaspoons) of highly processed and refined, probably not local or within your foodshed, oily oil. Cheers!
So, we’ve got pretty much the same old carb recommendations that we had back in 1980, when the guidelines first kicked off, but now with some added vegetable oils. Given what we know about the FADH2:NAHD ratio, how can we not get fatter?
(If you think we’re stupid here in the US, take a look at the recent New Zealand guidelines to see some real stupidity.)
One of the most common polyunsaturated fatty acids is alpha linolenic acid (actually an O-3 fatty acid) called linseed oil when used industrially and found along with O-6 oils in the PUFA we get from soybean oil, the most common oil in processed foods.
In a post about the obesogenic nature of this PUFA, Peter summarizes:
When PUFA are being oxidised in the mitochondria of adipocytes, those adipocytes are unable to resist the signal from insulin to distend with fat. The more double bonds in the PUFA has, the greater the effect. Linseed oil should be used for making varnish.
The take home message from all this is to work hard to avoid vegetable oils in any part of your low-carb diet.
Note: The above re the activity of FADH2:NAHD ratio in terms of insulin resistance is at the level of hypothesis now, but it’s the only thing that really makes sense to me. It predicts with great accuracy why we see the results we see with the consumption of different foods. And it makes sense teleologically in how glucose is made more or less available for the brain and other glucose-dependent cells and tissues during starvation or limited carbohydrate availability. The actual FADH2:NAHD ratio generated by various macronutrients is not hypothetical – it is precisely known.
In the next post I’ll explain how a food most consider a true Paleo food and a low-carb staple might not be such a great food based on the FADH2:NAHD ratio.
If you would like to read more about the mitochondria, read Peter’s blog and almost anything by Nick Lane.
Here are a few other papers as well.
All papers showing a link have full text available.
Fisher-Wellman, K. H., & Neufer, P. D. (2012). Linking mitochondrial bioenergetics to insulin resistance via redox biology. Trends Endocrinol Metab, 23(3), 142-153.
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., Kashiwaya, Y., Keon, C. A., Tsuchiya, N., King, M. T., Radda, G. K., . . . Veech, R. L. (1995). Insulin, ketone bodies, and mitochondrial energy transduction. FASEB J, 9(8), 651-658.
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., Manjeri, G. R., & Szklarczyk, R. (2014). How to deal with oxygen radicals stemming from mitochondrial fatty acid oxidation. Philos Trans R Soc Lond B Biol Sci, 369(1646), 20130446.
Stein, L. R., & Imai, S. (2012). The dynamic regulation of NAD metabolism in mitochondria. Trends Endocrinol Metab, 23(9), 420-428.
Besides Nick Lane’s Power, Sex, Suicide: Mitochondria and the Meaning of Life one other book I have found useful is Bioenergetics. But Bioenergetics is extremely technical, so if you don’t have a decent fund of knowledge on the workings of mitochondria or if you’re not used to reading technical literature, I would recommend you not spend the money on this book.