19 Sep 2018 Carbs vs. Fats: Hormonal Effects
It’s time to continue the debate on carbs vs. fats.
In the last carbs vs. fats article, I described the different effects of carbohydrates and fats on our health through a bioenergetic lens and how this view suggests that fats are an inferior fuel compared to carbohydrates.
But, many of the claims in favor of “fat-burning,” including that it improves blood sugar regulation, cognitive function, and libido, are directly related to the hormonal effects that result from using fat as the primary fuel source.
As I explained in a recent article, our hormones play an integral role in our adaptive response to our environment and reflect our underlying energetic state. Therefore, changes in fuel availability, or the availability of carbohydrates and fats, have major hormonal effects.
In this article, I’m going to explain exactly how these different fuels affect our hormonal state, specifically in the context of low-carb or ketogenic diets and higher carb diets.
Hormones and Fuel Availability
In my previous article on carbs vs. fats, I explained that fat is our backup fuel, reserved for times when carbohydrates aren’t available, such as in a state of famine or starvation. This is reflected on the energetic level, where using fat for fuel slows the production and usage of energy. And this is also reflected on the hormonal level, which further encourages the conservation of energy in order to prolong survival.
These hormonal effects begin with changes in the availability of glucose. Glucose is our primary fuel source and its availability dictates which fuel will be used to produced energy (1, 2). On a high-carb diet, where the glucose supply is plentiful, glucose is the primary fuel used to produce energy. Whereas on a low-carb or ketogenic diet, or if we don’t eat at all (such as when fasting or if we were starving), there’s reduced glucose availability. Our body then adapts to this situation of reduced glucose availability in several ways.
First, it begins using fats as its primary fuel, which replaces the glucose that would typically be used. However, as I explained in this article, fat is an extremely inefficient fuel, and therefore can’t be used by the brain. So, our bodies will produce glucose to fuel the brain through a process called gluconeogenesis.
Gluconeogenesis takes place in the liver and converts primarily amino acids to glucose. If there isn’t enough protein available from the diet to supply these amino acids, our bodies break down their own muscle tissue or even organ tissue to produce the amino acids needed to produce glucose.
However, regardless of the source of the amino acids, gluconeogenesis is an inefficient and energetically wasteful process (3). So, in addition to producing glucose, our bodies will produce ketones through a process called ketogenesis, which can replace as much as 60% the glucose needed for the brain (4).
All these processes are primarily regulated by the blood sugar regulating hormones, or more accurately, the acute energy regulating hormones.
When carbohydrates aren’t eaten for a few hours, the blood sugar drops which reduces the availability of fuel. This increases the production of glucagon, which leads to the release of glucose from stored glycogen in the liver, as well as the release of fatty acids from fat stores and an increase in fat oxidation.
Then, if carbohydrates still aren’t eaten, the liver will begin to run out of glycogen and adrenaline and cortisol will be released. These hormones cause the breakdown of our tissues and upregulate gluconeogenesis to provide glucose to raise the blood sugar and fuel the brain. They also further increase the usage of fat for fuel while stimulating ketogenesis in order to spare glucose and muscle tissue.
To summarize, when carbohydrates aren’t eaten or if we fast (or starve), our body begins to use primarily fat, our backup fuel, to produce energy while supplying the brain with glucose and ketones through the processes of gluconeogenesis and ketogenesis. These glucose-conserving mechanisms are almost entirely mediated by the stress hormones.
And, these processes are intensified over time on a low-carb or ketogenic diet as the glycogen stores are reduced due to a lack of available glucose, leading to an increased need for fat oxidation, gluconeogenesis, and ketogenesis (5, 6, 7).
As I explained in this article, the stress hormones downregulate our higher-level functions and reduce the production of the prometabolic thyroid and reproductive hormones in order to further conserve energy. These adaptive energy-conserving processes allow us to survive longer when we’re starving or in other extremely stressful situations, which are mimicked by low-carb and ketogenic diets (4, 8, 9).
The opposite occurs on a higher carb diet where blood sugar is effectively regulated. In this case, glucose is supplied by the diet and an adequate glycogen supply, resulting in far less need to use fat for fuel or to stimulate gluconeogenesis or ketogenesis.
So, the amount of stress hormones released to supply fuel is minimal compared to the constant production of stress hormones needed to maintain a fatty acid supply, gluconeogenesis, and ketogenesis on a low-carb or ketogenic diet. And, this difference is even further exaggerated when additional stressors come into play.
Stressors and Fuel Availability
At rest, low-carb and ketogenic diets produce a state where fats become the primary fuel and gluconeogenesis and ketogenesis supply fuel for the brain, basically resulting in constant, low-grade stress. And this effect is intensified even further when stressors are involved.
Stressors, like exercise or psychological stress, increase the energy demand, and therefore the need for additional fuel. The fuel usage hierarchy at rest is mirrored under stress, where glucose is the primary fuel, followed by fat as the backup fuel and ketones as a replacement for some of the glucose needs.
So when we’re faced with stressors on a higher carb diet, the increased fuel needs would mostly be supplied by glycogen, requiring the release of glucagon. Glucagon would also increase the release of fatty acids to supplement this glucose, and any additional fuel needs would be supplied by further increased fat oxidation and eventually gluconeogenesis through the release of adrenaline and cortisol. Glucose could also be supplied by eating carbohydrates, which reduce or completely reverse the stress response, even in severe circumstances (10, 11).
This is contrasted by the stress response that occurs on low-carb and ketogenic diets.
In this case, there’s already little glucose and glycogen available at rest, so fat is the primary fuel used which is largely mediated by the increased production of glucagon and, to a lesser extent, the increased production of adrenaline and cortisol. When faced with additional stressors, greater amounts of adrenaline and cortisol are needed to provide fuel by releasing more fatty acids from fat storage and producing greater amounts of glucose and ketones through gluconeogenesis and ketogenesis.
So, the exposure to stressors on a low-carb or ketogenic diet increases the production of stress hormones to a greater degree than on a higher carb diet (6, 7, 12, 13). This, in turn, leads to an even greater downregulation of our higher-level functions and further reductions in the production of the prometabolic hormones.
In other words, low-carb and ketogenic diets increase the amount of stress hormones produced in response to stressors and reduce our resilience to stress.
What Does This Mean For Our Health?
It’s important to mention that it’s not quite as simple as “carb-burning” vs. “fat-burning.”
Our bodies typically use some combination of carbs and fats as fuel, and this changes based on the time of day, activity level, and other factors. And, this is mirrored by our hormonal profile under these different circumstances.
But, changing the amount of carbohydrates in our diet (such as a higher carb diet vs. a low-carb or ketogenic diet) does have a large effect on which fuel is primarily used and to what extent its favored over the other, as well as on the hormones that regulate these processes. So, a higher carb diet does offer substantial benefits from this perspective.
However it’s also worth noting that, as I explained in my last article on carbs vs. fats, the energetic state produced by a low-carb or ketogenic diet is still better than that produced when both glucose and fat oxidation are inhibited. And the same goes for the hormonal effects.
It’s common for hormonal profiles and related measures and symptoms, like blood sugar regulation, cognitive function, and libido, to improve on low-carb or ketogenic diets when coming from a higher carb diet where both glucose and fat oxidation are inhibited.
But, this doesn’t make these diets ideal. Remember, they still produce a low-energy survival state that leads to adaptive responses (like increased stress hormones and fat and ketone utilization) to conserve energy. In order to attain an optimal, highly energized state, the inhibition of mitochondrial respiration must first be addressed. Then, a higher carb diet can provide the fuel needed to produce an optimal high-energy state and the hormonal state that comes with it.
But remember, 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. So, having fat in our diet doesn’t interfere with achieving an optimal high-energy state as long as carbohydrates remain our primary fuel source.
- Flatt, J. P. “Use and storage of carbohydrate and fat.” The American journal of clinical nutrition, 61, 4 Suppl, 1995, 952S-959S. doi:10.1093/ajcn/61.4.952S.
- Melzer, Katarina. “Carbohydrate and fat utilization during rest and physical activity.” e-SPEN, the European e-Journal of Clinical Nutrition and Metabolism, 6, no. 2, 2011, e45-e52. doi:10.1016/j.eclnm.2011.01.005.
- Veldhorst, Margriet A. B., et al. “Gluconeogenesis and energy expenditure after a high-protein, carbohydrate-free diet.” The American journal of clinical nutrition, 90, no. 3, 2009, pp. 519–26. doi:10.3945/ajcn.2009.27834.
- Cox, Pete J., and Kieran Clarke. “Acute nutritional ketosis: Implications for exercise performance and metabolism.” Extreme physiology & medicine, 3, 2014, p. 17. doi:10.1186/2046-7648-3-17.
- Phinney, S. D., et al. “The human metabolic response to chronic ketosis without caloric restriction: Preservation of submaximal exercise capability with reduced carbohydrate oxidation.” Metabolism, 32, no. 8, 1983, pp. 769–76. doi:10.1016/0026-0495(83)90106-3.
- Helge, Jørn Wulff. “Long-term fat diet adaptation effects on performance, training capacity, and fat utilization.” Medicine and science in sports and exercise, 34, no. 9, 2002, pp. 1499–504. doi:10.1249/01.MSS.0000027691.95769.B5.
- Helge, J. W. “Adaptation to a fat-rich diet: Effects on endurance performance in humans.” Sports Medicine, 30, no. 5, 2000, pp. 347–57.
- Boelen, Anita, et al. “Fasting-induced changes in the hypothalamus-pituitary-thyroid axis.” Thyroid : official journal of the American Thyroid Association, 18, no. 2, 2008, pp. 123–29. doi:10.1089/thy.2007.0253.
- McCue, Marshall D. “Starvation physiology: Reviewing the different strategies animals use to survive a common challenge.” Comparative biochemistry and physiology. Part A, Molecular & integrative physiology, 156, no. 1, 2010, pp. 1–18. doi:10.1016/j.cbpa.2010.01.002.
- Laugero, Kevin D. “Reinterpretation of basal glucocorticoid feedback: Implications to behavioral and metabolic disease.” Vitamins and hormones, 69, 2004, pp. 1–29. doi:10.1016/S0083-6729(04)69001-7.
- Dhar, H. L., et al. “The relationship of the blood sugar level to the severity of anaphylactic shock.” British journal of pharmacology and chemotherapy, 31, no. 2, 1967, pp. 351–55.
- Jansson, E., et al. “Diet induced changes in sympatho-adrenal activity during submaximal exercise in relation to substrate utilization in man.” Acta physiologica Scandinavica, 114, no. 2, 1982, pp. 171–78. doi:10.1111/j.1748-1716.1982.tb06969.x.
- Galbo, H., et al. “The effect of different diets and of insulin on the hormonal response to prolonged exercise.” Acta physiologica Scandinavica, 107, no. 1, 1979, pp. 19–32. doi:10.1111/j.1748-1716.1979.tb06438.x.
harrymacdonaldPosted at 13:14h, 22 September
Hi Jay. I’m really enjoying your website. Just wondering if you subscribe to the A.I. hypothesis?
Jay FeldmanPosted at 15:20h, 22 September
Hi Harry, I’m glad to hear that! I’m assuming you’re referring to the association-induction hypothesis, in which case I do but it’s a topic I’m still learning more about (I don’t have much of a physics background). My general focus on energy has, at least in part, been inspired by it.
DanaPosted at 07:02h, 20 June
I find the the raymond peat diet is very hard for me to institute. I’m having energy problems from years of dieting and using veganism to cure other health problems (which it did, but at the expense of my hormones and vitamin stores). When I was younger. eating the western diet gave me tons of energy to get the job done daily, and I dont want to go back to that, for obvious reasons, so I am really lost in what to do since my body seems to get long lasting energy from odd ways. The Peat diet does work but I struggle with getting the right combos
Jay FeldmanPosted at 17:40h, 20 June
I totally understand Dana, it can all be pretty overwhelming and difficult to navigate. Why don’t we schedule a time to talk so you can give me some more details about your situation and I can share some suggestions with you. You can sign up for a free call here.
toscaPosted at 12:39h, 08 July
Hey Jay, I really love your content and you’ve really helped me with my own health (as a recovering hormesis paradigmer!) and been a springboard for me to dive into these concepts and question the biohacking norm, as a lover of physiology myself … one question I can’t seem to wrap my mind around: there seems to be contradiction in the mainstream in your conclusion that fat is an extremely inefficient form of energy. I totally get the 50% less CO2 and less NADH per molecule of Acetyl CoA and that it takes an ATP to get the chain into the mitochondria in the first place, but wouldn’t it depend on the size of the FA that would determine whether or not it was inefficient. A LCFA could produce upwards of 7 ACoA molecules to enter the TCA cycle which would generate a whole lot more ATP per chain, surely? Is it mainly the bottleneck of electrons and decrease in NAD+:NADH at Complex I that drives your conclusion (and resulting ETC & glycolysis shutdown) …are there studies that quantify how bad this bottleneck is in comparison to the multitudes more ATP beta oxidation produces per full chain… like maybe a breakdown of 1 glucose molecule ox vs say 1 palmitic acid molecule ox (I *know I’m going to be asked that question and I want to make sure I get it!). I’m probably just not getting a fundamental concept… Thanks again so much I’m hooked on your content!
Jay FeldmanPosted at 23:40h, 15 August
Awesome to hear that Tosca!
The longer the fatty acid, the less efficient the oxidation (slower ATP production and more ROS production), due to the increase in the FADH2/NADH ratio that occurs as the a result of the longer fatty acid chain.
It’s not a matter of number of ACoA or ATP produced per molecule (in which case fat would win hands down) – it’s a matter of potential rate and efficiency of ATP production, which depend on the NAD+/NADH ratio and ROS production (at least in the context of comparing carb and fat oxidation).
“Quantitatively, it has been estimated that the rate of ATP generation based on the carbohydrate oxidation is in the range of 0.51 to 0.68 mmol per second per kg body mass. In comparison, the rate of ATP generation based on triacylglycerol fueling is approximately two- to threefold lower (0.24 mmol per second per kg body mass).” – https://pubmed.ncbi.nlm.nih.gov/23921897/