07 Jun 2018 Carbs vs. Fats: Which is the Better Fuel?

It’s time for the age-old debate: carbs vs. fats.

There’s a ton of disagreement on this topic with poorly supported arguments on both sides.

Most of the current recommendations are now favoring the low-carb “fat-burning approach.” This is “supported” by all sorts of nonsense, such as that “carbohydrates aren’t essential to our diets,” “carbohydrates cause blood sugar dysregulation,” “burning fat leads to fat loss,” and “our ancestors didn’t eat carbohydrates,” among others.

While I’m tempted to go through each of these ridiculous arguments right now and explain why they aren’t at all valid, I’ll have to save that for another time.

There are many differences between the effects of consuming carbohydrates and fats that can be explored, including their interactions with various hormones, effects on blood sugar, distribution throughout the body, and many other differences, as well as the variations between the different types of carbohydrates and fats. However, while these are important topics, the answer to this debate becomes quite clear when you consider it from a bioenergetic point of view.

So in this article, I’m going to focus solely on the usage of carbs and fats as fuel to produce energy. There’s quite a bit of misinformation out there about “fat-burning” versus “sugar-burning” and their effects on energy production and mitochondrial function, and I’m going to clear that up.

In order to do that, I’m going to dive into the biochemistry of carbohydrate and fat oxidation. If you want a general overview of this topic without all the biochemistry, check out this article.

Also, I’d like to preface this article by pointing out that we’re never burning only carbs or only fats, there’s always some combination of these fuels being used, but which fuel we predominantly use does make a difference.

Carbohydrate Oxidation vs. Fat Oxidation

When considering the oxidation of carbohydrates and fats through mitochondrial respiration, a majority of the process is the same – once each of these substrates is converted to acetyl-CoA (ACoA), the rest is identical.

But, there are several important differences between carbohydrate and fat oxidation that occur before they become ACoA. While these differences may seem small, they’re responsible for the significantly increased efficiency of glucose oxidation over fat oxidation.

The oxidation of carbohydrates begins with glycolysis, where glucose is eventually converted into pyruvate and then either lactate or ACoA. For each molecule of ACoA that’s produced through this process, 1 net molecule of ATP, 2 molecules of NADH, and 1 molecule of carbon dioxide (CO₂) are produced.

The oxidation of fats, on the other hand, begins with beta-oxidation, where the fatty acid is converted to ACoA. For each molecule of ACoA that’s produced through this process, on average, 1 molecule of NADH and 1 molecule of FADH₂ are produced.

There are two key differences here that have significant effects on mitochondrial respiration:

• The additional CO₂ production in glucose oxidation, and
• The replacement of 1 molecule of NADH with 1 molecule of FADH₂ in fat oxidation

Let’s explore each of these differences more closely.

Carbon Dioxide, Simply A Waste Product?

CO₂ is often considered a waste product of mitochondrial respiration, but this couldn’t be farther from the truth. In fact, CO₂ is one of the most protective compounds in our bodies.

The oxidation of carbohydrates produces 50% more CO₂ than the oxidation of fat, which is a major difference that has a dramatic effect on the efficiency of mitochondrial respiration for a couple reasons.

For one, CO₂ production is vital for the proper oxygenation of our cells.

Our cells require oxygen (O₂) for efficient energy production, as oxygen acts as the final electron acceptor in the electron transport chain. In order to be delivered to our cells from our lungs, oxygen is carried through our blood in our red blood cells via a protein called hemoglobin, which is able to bind with both O₂ and CO₂.

In low CO₂ environments, hemoglobin releases CO₂ and binds with O₂, which is called the Haldane effect. This allows our red blood cells to drop off CO₂ and pick up O₂ at our lungs. In high CO₂ (or acidic) environments, hemoglobin releases O₂ and binds with CO₂, which is called the Bohr effect. This allows our red blood cells to offload O₂ at our tissues, where it’s needed to produce energy.

So, when our cells produce more CO₂, as they do from glucose oxidation, our tissues receive more O₂ (1). When our cells don’t produce enough CO₂, preventing enough oxygen from entering the cell, glucose is converted to lactate as opposed to ACoA and the function of the electron transport chain is impaired, drastically inhibiting energy production and increasing reactive oxygen species production (2, 3, 4, 5).

(Note: CO₂ is also a potent vasodilator, which further increases oxygen delivery to our tissues.)

Second, CO₂ acts as a powerful protector against reactive oxygen species (ROS), reactive nitrogen species (RNS), and lipid peroxidation (6, 7, 8).

These compounds all damage our cells and inhibit energy production, making protection against these compounds extremely important.

Considering these factors, the increased CO₂ production as a result of glucose oxidation results in significantly more efficient mitochondrial respiration than fat oxidation.

NADH vs. FADH₂

NADH and FADH₂ are both electron carriers that donate electrons at the electron transport chain (ETC), allowing for the production of ATP. NADH donates electrons at complex I of the ETC, whereas FADH₂ donates electrons at complex II, and these complexes compete for the same electron acceptor, ubiquinone.

Glucose oxidation produces around 25% more NADH and half as much FADH₂ as fat oxidation. Together, this leads to a ratio of FADH₂ to NADH that is around 2.5 times lower than that of fat oxidation (9, 10). This difference has substantial effects that extend throughout the processes of mitochondrial respiration.

Because FADH₂ donates electrons at complex II, downstream of complex I, it reduces the amount of ubiquinone available to accept electrons at complex I, leading to a buildup of electrons at complex I. This results in two major problems.

For one, this increases the electron leakage at complex I, which increases the production of ROS, specifically superoxide (9, 10, 11).

ROS are a major cause of cellular oxidative stress, and as I’ve already mentioned, damage the cell and inhibit energy production.

Second, the buildup of electrons at complex I reduces the donation of electrons by NADH, leading to a buildup of NADH and a decrease in the ratio of NAD⁺ to NADH (9, 10, 11, 12).

The ratio of NAD⁺ to NADH is a major controller of mitochondrial respiration and is also tied to aging, cancer, diabetes, neurodegeneration, and many other diseases (13, 14, 15).

A low NAD⁺/NADH ratio inhibits isocitrate dehydrogenase (IDH), the rate-limiting step of the TCA cycle (aka Krebs or citric acid cycle). This slows down the activity of the TCA cycle and leads to a buildup of citrate, which inhibits phosphofructokinase (PFK), the rate-limiting step of glycolysis, while also causing a buildup of ACoA (11).

The low NAD⁺/NADH ratio also inhibits pyruvate dehydrogenase (PDH), the rate-limiting-step that connects glycolysis to the TCA cycle, and the buildup of ACoA further inhibits PDH (11). This directs pyruvate towards lactate rather than ACoA.

The inhibition of glucose oxidation by fat oxidation through these mechanisms is a feature of the Randle cycle and is responsible for the insulin resistance seen in response to high-fat meals and diets (16). This is, of course, an adaptive response to using fat for fuel and is not a problem per se.

However, in this state, glycolysis is inhibited to a lesser degree than PDH, resulting in an increased production of lactate which can cause problems of its own (11, 17, 18). And, the decrease in the NAD+/NADH ratio still reduces the activity of the TCA cycle through the inhibition of IDH, which slows energy production.

Overall, fat oxidation drastically reduces the efficiency of energy production, causing much less energy to be produced while increasing ROS production, which has a damaging and destabilizing effect (11, 19).

What Does This Mean For Our Health?

Fat is our backup fuel, reserved for times when carbohydrates aren’t available, such as in a state of famine or starvation. This is evidenced by the fact that the presence of carbs, or lack thereof, is what determines the relative amount of fat oxidation (20). So, when relying on fat for energy production, it’s no wonder why there are mechanisms in place to slow our energy production – it allows us to survive longer during these sorts of stressful times.

However, it’s clear that for our brain, our most energy-intensive organ, fats simply cannot efficiently provide enough energy for proper function, which is why sugars or ketones are required as fuel. Many of our other tissues, however, can still function using solely fat as fuel.

But is this ideal for health?

As I postulated in this article, energy lies at the foundation of our health and allows our bodies to properly function. And, energy deficiencies underlie virtually all the chronic health conditions we’re seeing in epidemic proportions, as well as fat gain.

Although, it’s worth pointing out that fat oxidation isn’t the most common cause of energy deficiencies.

Energy deficiencies are most commonly a result of the various factors that impair the oxidation of glucose, like PUFA or endotoxin, even in the context of adequate glucose availability. In this context, fatty acid oxidation is also partially inhibited due to the presence of high amounts of glucose and insulin.

This results in the inhibition of both glucose and fat oxidation, leading to severe energy deficiencies and extreme stress.

This is why it’s common for health to improve when switching to a low-carb or ketogenic diet, at least at first. By reducing the amount of glucose available, insulin is suppressed and fatty acid oxidation and ketone production can increase to supply enough energy to improve function.

While this is a much better situation than when both glucose and fat oxidation are inhibited, it’s still not ideal. Considering that carbohydrate oxidation provides more energy more efficiently, and energy is the driving force behind our health, providing as much energy as we can from carbohydrate oxidation is probably ideal.

But, this doesn’t mean we need to avoid fat altogether. Fat serves many purposes in our body beyond its use as a fuel source, such as its function as a structural component of our cells and its antimicrobial effects. Plus, it’s an adequate fuel source for tissues that have very low energy demands, like our muscles at rest. While we can produce fat endogenously to fill these roles without consuming it, this comes at a cost, so we’re better off consuming some dietary fat while maintaining carbohydrates as our primary fuel source.

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