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 drastic 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. While we can produce fat endogenously to fill these roles without consuming it, this doesn’t mean that we need to eliminate fat from our diet as long as carbohydrates are our primary fuel source.

References
7 Comments
  • Craig
    Posted at 13:40h, 15 June Reply

    Hey Jay,

    Thank you for my favorite article yet! Everyone is entitled to their opinions, but science is not about opinion, and this article is heavy on science and light on opinion. I intend to re-read it a few times after refreshing my detailed knowledge on the ever-so-important Krebs cycle. The article raises a couple of questions to me, on which I would love to get your feedback:

    — Everyone carrying an extra 10 or 50 pounds of weight must employ the process of lipolysis to liberate the fat from their waistlines. Elevated levels of insulin, which result from high carb intake, inhibit lipolysis. So how can an overweight person achieve fat loss without minimizing carbs as compared to fat & protein? I understand that energy balance may be negatively impacted by the low-carb regimen, but the cost-benefit analysis for the overweight person seems to favor going lower on carbs until they hit their goal.

    — The liver miraculously converts proteins and fats into glucose via gluconeogenesis (hat tip to Wikipedia) in order to maintain a stable level of blood sugar. This is evinced in people who employ ketogenic diets – they all have normal (or near normal) blood sugar levels despite the minimal levels of carb intake. Of course they all have high ketone levels. So our bodies are designed to optimize blood sugar (i.e. glucose) regardless of the level of carbohydrate consumption. In light of this, why should we choose to eat a diet consisting of elevated carbs at the risk of consisting spiking insulin output?

    Regards and thanks.
    Craig

    • Jay Feldman
      Posted at 16:25h, 17 June Reply

      Hey Craig,

      Thanks for the feedback, I’m glad to hear you liked it!

      In answer to your first question: I think the emphasis on lipolysis and fat-burning for fat loss is misplaced. Instead, I would say that fat deposition is a better focus than the oxidation of fat. For example, in this study the carbohydrate-restricted group showed large decreases in insulin secretion and large increases in fat oxidation relative to the fat-restricted group, but they lost less body fat and lost greater amounts of fat-free mass. In the context of a high-carb diet, fat deposition is decreased both due to a reduced availability of fat (the conversion of carbs to fat is inefficient and only occurs in a large excess of carbohydrates as I explained in this article) and by improving energy production (resulting in less substrate from which to produce fat and reductions in stress hormones with increases in pro-metabolic hormones). And, some amount of fat oxidation/lipolysis is always going on, even a high-carb, low-fat diet, which combined with reduced fat deposition can lead to a loss of body fat while increasing the energy supply.

      In order to answer your second question I have to break down two underlying assumptions that I don’t think are valid. The first is that supplying blood sugar via gluconeogenesis is equivalent to supplying blood sugar via carbohydrates, and the second is that increases in insulin secretion are inherently harmful.

      While gluconeogenesis does allow for the maintenance of blood sugar, it’s far from ideal. Gluconeogenesis is primarily activated by glucagon, although adrenaline and cortisol also play major roles. These hormones are released under times of stress, or a lack of energy, and low blood sugar is one of those times (this is why hyperglucagonemia is a key feature of diabetes/insulin resistance). In other words, gluconeogenesis is activated by stress. A similar process regulates ketogenesis, with glucagon, adrenaline, and cortisol being the primary regulators.

      In other words, gluconeogenesis and ketogenesis are brought out by a low-energy stress state. This is the environment that occurs in starvation, and it’s also mimicked by removing carbohydrates from the diet. In this state, both energy production and usage are further reduced to conserve energy (this is brought out through hormonal changes, including the ones I mentioned in relation to blood sugar as well as a reduction in thyroid hormones and other pro-metabolic hormones).

      There are other related issues that the low-carb/ketogenic diet brings up. In this state, ketones and glucose are mostly reserved for the brain while the rest of the body uses fatty acids for fuel, which I’ve outlined my issues with in this article. In this context, any increased need for fuel, which in this case would be glucose or ketones, must be made up for by stress-induced gluconeogenesis or ketogenesis, rather than being able to be fueled by increased carb intake (or the release of stored glycogen) in the context of higher-carb diets. This stress further adds to the feedback mechanisms that reduce fuel usage in order to conserve energy as I mentioned earlier. I know you acknowledged in your first question that this cost exists, but I felt it was worth elaborating on.

      To summarize all of this, I would say that low-carb/ketogenic diets cause a low-energy stress state, and this is represented throughout all aspects of our physiology. Gluconeogenesis as a means of blood sugar regulation is a feature of this low-energy stress state and is not equivalent to blood sugar regulation in the context of a high-carb diet.

      As far as the “insulin is harmful” hypothesis goes, I would say that simply put, it’s not supported. Increases in insulin secretion don’t cause insulin resistance or diabetes (I explain this here and here). And increases in insulin by increasing carbohydrates don’t cause fat gain, as is evidenced by the study I posted earlier and others like this one. I do agree that low blood sugar is a problem as it reduces fuel availability and therefore energy production, which leads to stress, so regulating blood sugar on a high-carb diet is important (I explain this here). Also, as far as spiking insulin goes, insulin sensitivity increases on high-carb diets (reducing the amount of insulin secreted) and consuming carbs that have both glucose and fructose is also important for preventing large spikes in insulin output and excessive fluctuations in blood sugar.

      Man that was a long-winded answer but I hope I explained my thoughts clearly. I appreciate you bringing up these questions as it allows me to further explore my thoughts on this topic. I think I’ll turn this ridiculously long response into an article on the hormonal effects of fat vs. carbs in the near future.

      Thanks again for the comments!

      Jay

  • leo
    Posted at 10:54h, 14 July Reply

    Hi! What suggest minimum fat intake for fat Loss ? 20gr Thanks!

    • Jay Feldman
      Posted at 12:23h, 14 July Reply

      Hi Leo! I don’t recommend a specific amount because it’s entirely individual and depends on many factors. I would suggest experimenting and seeing what works best for you.

  • Elaine
    Posted at 14:12h, 05 August Reply

    Hi Jay,
    I love your articles! I was wondering if you are familiar with Lore of Nutrition: Challenging conventional dietary beliefs by Tim Noakes. His is a professor in south Africa who introduced the keto/low carb way of eating to his patients who all got well. But he was ridiculed by is colleagues and this resulted in a year long inquiry by the South African council which he won. I got his book from the library (I’m a lay person) and there are tons of in depth scientific info. I was wondering what you thought if you are familiar with his book and why these people continue to do well long term.

    Thanks.
    Elaine

    • Jay Feldman
      Posted at 10:05h, 06 August Reply

      Hi Elaine,
      Thanks, I’m glad to hear that!
      I haven’t read any of Tim Noakes’s books but I am familiar with the diet he’s recommending and his perspective on health (I’ve experimented quite a bit with low-carb and ketogenic diets). I have quite a few disagreements with him, especially when it comes to carbohydrates and PUFA (specifically omega-3s).
      He doesn’t consider the bioenergetic perspective that I present in this article, which I think is the biggest flaw, and his focus on “carbohydrate resistance/intolerance” is evidence of this. Carbohydrate resistance/intolerance is simply inhibited glucose oxidation, and he proposes avoiding carbohydrates rather than fixing the underlying issue.
      And, the low-carb/ketogenic diet that he’s suggesting as a solution can cause many problems because it’s not ideal from a bioenergetic view, as I explained in this article. I think the reason that people can feel better on those diets is that the low-carb/ketogenic state is better than a state where both glucose and fat oxidation are inhibited (I mention this at the end of the article). But, it’s still far from ideal. I also explain the hormonal implications of this in my earlier response to Craig in the comments.
      I hope that’s helpful!
      Jay

    • Jay Feldman
      Posted at 17:40h, 07 August Reply

      Another reason that people often feel better on low-carb/ketogenic diets is that carbohydrate-containing foods can be hard to digest. Gut function is impaired when metabolic function is impaired, and eating foods that are hard to digest leads to the production of excessive amounts of endotoxin which further inhibits metabolic function. So, by avoiding these foods the production of endotoxin is drastically reduced.

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