One of the lessons that comes across most clearly from the studies that Weston Price documented in Nutrition and Physical Degeneration is that, although traditional diets all emphasized nutrient-dense foods, the specific mix of animal and plant foods was widely variable. Since it is primarily plant foods that provide carbohydrate, the carbohydrate content of traditional diets was also widely variable. In groups that lived in the Arctic, it was very low; in groups that lived close to the equator or that relied on grains, it was much higher.
This observation implies that humans can thrive on a wide range of carbohydrate intakes, but it does not imply that anyone in any circumstance can live on a diet that is virtually free of carbohydrate, and it does not imply that carbohydrate is not important. In fact, carbohydrate is essential to our physiology. In this article, I will discuss the essential roles of carbohydrate in the body,1 and then derive some practical conclusions about how we can manage our own carbohydrate intake.
STRUCTURAL ROLES OF CARBOHYDRATE
Carbohydrates play a variety of essential structural roles in our cells. Each repeating unit of DNA and RNA contains the sugars deoxyribose or ribose, which we make from glucose. These sugars are also essential structural components of the energy carriers we derive from niacin (vitamin B3), riboflavin (vitamin B2), and pantothenic acid (vitamin B5), which we use throughout every aspect of energy metabolism. They are also an essential structural component of ATP, the main energy currency of the cell.
Our tissues are composed of cells that reside within an infrastructure known as the extracellular matrix. All extracellular matrices are built largely from proteoglycans, which consist of a core protein that binds to glycosaminoglycans. In less technical terms, these are combinations of carbohydrate and protein that heavily favor carbohydrate. They are typically 95 percent carbohydrate and 5 percent protein. Popular supplements to support joint health typically contain the predominant glycosaminoglycans in joint fluid, chondroitin sulfate and glucosamine sulfate.
Glycoproteins are another way in which carbohydrates and proteins can be combined. Compared to proteoglycans, they tend to have less carbohydrate and more protein. Nevertheless, the carbohydrate content is widely variable. Antibodies such as IgG are glycoproteins, and contain as little as 4 percent carbohydrate, whereas mucin, the main constituent of mucus, is a glycoprotein that contains 80 percent carbohydrate. Cells are often coated in a glycoprotein structure known as the glycocalyx that allows cells to recognize one another, and to communicate and interact with one another.
The health value of these roles is obviously vast: without them, energy metabolism would fail, and with it, the vast array of energy-dependent processes within the body; without them, our ability to read our own genetic information or to pass it on to our offspring would fail; without them, immunity and digestion would suffer. We could expand the list of such negative health consequences endlessly. Most of the carbohydrate we take in each day is used for energy, and the role of carbohydrate in energy metabolism is a more productive area of focus if we are trying to understand the potential consequences of consuming too little of it.
CARBOHYDRATE AND ENERGY METABOLISM
Like proteins and fats, we break carbohydrates down into two-carbon units known as acetyl groups that then enter the pathways we use to break them down fully into the carbon dioxide that we exhale and the hydrogen ions and high-energy electrons that we use to synthesize ATP.
Since carbohydrate is richer in oxygen than fat, its metabolism requires 25 percent less water and generates 50 percent more carbon dioxide. Protein is intermediate. The more carbon dioxide we make, the more we need to breathe. A low-carbohydrate, high-fat diet is a useful way to decrease the stress on the lungs in patients requiring artificial ventilation. Outside of that context, however, carbon dioxide plays valuable roles. For example, it facilitates the delivery of oxygen to our tissues, and it activates vitamin K-dependent proteins. It is possible, then, that dietary carbohydrate could assist oxygenation of tissues for such purposes as healing from injury or enhancement of athletic performance, and it is possible that dietary carbohydrate could be an important synergist with vitamin K.
In the presence of oxygen, there is little difference between fully breaking down carbohydrate for energy and fully breaking down fat for energy. They each have an advantage over protein in that their breakdown does not require us to manage the disposal of leftover nitrogen, but this is just as true of fat as it is of carbohydrate.
Carbohydrates, however, have a unique advantage over the other macronutrients in that we can break them down for energy even in the absence of oxygen. We do this by splitting glucose in half and converting it to two molecules of lactate, which is known as anaerobic glycolysis.
Anaerobic glycolysis only generates a small amount of energy compared to fully oxidizing glucose to carbon dioxide. However, tissues that use anaerobic glycolysis can utilize the Cori cycle to greatly amplify the energy produced. In the Cori cycle, a lactate-producing tissue sends the lactate to the liver; the liver uses energy to convert the lactate back to glucose, and sends the glucose back to the lactate-producing tissue. The net result is that energy is transferred from the liver to the lactate-producing tissue and that the lactate-producing tissue meets its energy needs even in a relative absence of oxygen.
There are a few cases where anaerobic glycolysis is especially useful. Red blood cells lack mitochondria and are thus completely unable to fully break down macronutrients for energy using oxygen. This requires them to rely exclusively on anaerobic glycolysis. A small collection of other tissues rely substantially on anaerobic glycolysis simply because they do not take up enough oxygen from the blood, and these include the lens and cornea of the eye, the kidney medulla and the testes. In acute stress and high-intensity exercise our demand for energy temporarily exceeds the oxygen supply, and the deficit is made up with anaerobic glycolysis.
The brain uses oxygen to produce about 90 percent of its ATP and uses anaerobic glycolysis for the other 10 percent.2 Cells known as astrocytes perform most of the anaerobic glycolysis. Rather than delivering the lactate to the liver, however, they deliver it to neurons. Neurons burn the lactate for energy and that helps them conserve glucose for antioxidant defense.
ANTIOXIDANT DEFENSE AND NUTRIENT RECYCLING
In addition to anaerobic glycolysis, there is a second pathway that has an absolute demand for glucose known as the pentose phosphate pathway. In this pathway, instead of using the energy from glucose to make ATP, we use it for the synthesis of larger molecules, for antioxidant defense, and for nutrient recycling.
With the help of thiamin (vitamin B1), niacin (vitamin B3), and riboflavin (vitamin B2), this pathway takes energy from glucose and uses it for the following processes: the synthesis of fatty acids, cholesterol, neurotransmitters and nucleotides; the recycling of glutathione, the master antioxidant and detoxifier of the cell; and the recycling of vitamin K and folate.
GLUCONEOGENESIS, CORTISOL AND THYROID
Since we have an absolute need for glucose to support anaerobic glycolysis and the pentose phosphate pathway, we have a very robust system for ensuring we always have enough glucose even under conditions of dietary carbohydrate deprivation: gluconeogenesis. This is the production of glucose from non-carbohydrate precursors. Gluconeogenesis is primarily supported by protein but is also supported to a minor degree by fat.
While it is conceivable that someone on an extremely low-carbohydrate intake could suffer from a deficiency of total glucose, particularly if subsisting on a diet that is also very low in protein and deficient in nutrients needed for gluconeogenesis, this is likely to be very rare. When we chronically restrict carbohydrate, our bodies will naturally do everything in their power to conserve glucose, and in most cases gluconeogenesis will be sufficient to meet these lower needs.
The potential downside to chronic carbohydrate restriction is in the set of compensations we make to prevent a deficiency of glucose. Gluconeogenesis is primarily stimulated by the adrenal hormone cortisol. Cortisol antagonizes thyroid hormone and, when chronically elevated, impairs immunity. As we move away from burning glucose and toward greater reliance on fat, free fatty acids elevate. Cortisol augments this rise even further by causing us to release free fatty acids from adipose tissue. High levels of free fatty acids can impair thyroid hormone’s ability to carry out its physiological functions within our cells even if blood levels of thyroid hormones remain normal.
Interpreting blood, saliva, and urinary hormone testing is complicated and should be done under the supervision of a qualified practitioner. Nevertheless, we can note a few useful guidelines here.
Elevated cortisol could be a sign of inadequate carbohydrate intake. However, prolonged chronic elevation of cortisol can ultimately lead to long-term changes that bring cortisol to normal or low levels. Additionally, the rise in cortisol may occur at times that are difficult to detect. For example, if carbohydrate stores are inadequate to maintain stable blood sugar through the night, cortisol could spike in the early morning hours to stimulate gluconeogenesis. Cortisol normally spikes once you wake up and are exposed to light, and you cannot measure your cortisol when you are asleep, so it would be difficult to detect an early pre-waking rise in cortisol in this context.
If blood levels of thyroid hormone are affected, low T3 is the most likely result.3 However, T3 can be normal and elevated free fatty acids could still be impairing its cellular function.
If thyroid hormone activity is low, whether from low T3 or from interference with its activity by elevated cortisol and free fatty acids, one of the likely consequences is high LDL-cholesterol with low sex hormones. I consider the combined pattern of total cholesterol in substantial excess of 220 mg/dL, a high total-to-HDL-cholesterol ratio in substantial excess of 3.0, and total or free sex hormones toward the lower ends of the reference ranges to be a potential sign of low thyroid activity regardless of blood levels of thyroid hormones.3
HOW MUCH CARBOHYDRATE SHOULD WE EAT?
Carbohydrate demand is going to vary from person to person and is going to depend on physical activity level, but we can derive some general guidelines. The liver stores about 90 grams of carbohydrate, skeletal muscle stores 300 grams, and bodily fluids contain 30 grams.5 A completely sedentary person will primarily be tapping into the liver’s glycogen stores in order to stabilize blood sugar between meals. In the absence of physical activity, then, it makes sense to use about 100 grams per day as an initial target.
Someone whose physical activity is no more intense than walking is unlikely to begin tapping into their muscular glycogen supply. Greater intensities, however, such as running or weight lifting, will do so. It is almost impossible for someone to more than guestimate how much muscular glycogen they would burn through with any particular physical activity pattern, but it is reasonable to say that a very active person could add another 300 grams of carbohydrate on top of the initial 100 grams. In fact, the primary metabolic consequence of consuming 500 grams of carbohydrate in an otherwise healthy person, regardless of physical activity, is to shift that person’s metabolism almost entirely toward burning carbohydrate for energy.
These numbers should not provide more than an initial guideline. If someone wishes to restrict carbohydrates to less than 100 grams per day for a specific purpose, a prudent approach to safety would be to monitor stress, thyroid, and sex hormones, to ensure they all remain in optimal range. Physically active people should be aware that they may need considerably more than 100 grams to prevent these hormones from going out of range.
We may be left wondering, but what about the Inuit? Didn’t they eat far less than 100 grams of carbohydrate per day?
When we look at traditional diets, we have to be careful of emulating the tails of the distribution. Most traditional diets contained plenty of carbohydrate. Diets traditional to the Arctic are the exception, and they are adaptations to that specific environment. The inhabitants of the Arctic most likely adapted to that environment with a suite of genetic and cultural adaptations that may have to work in concert to produce optimal health.
Consider what Price himself wrote of the reproductive diets in the Arctic:
For the Indians of the far North [reinforcement of fertility] was accomplished by supplying special feedings of organs of animals. Among the Indians in the moose country near the Arctic circle, a larger percentage of the children were born in June than in any other month. This was accomplished, I was told, by both parents eating liberally of the thyroid glands of the male moose as they came down from the high mountain areas for the mating season, at which time the large protuberances carrying the thyroids under the throat were greatly enlarged.
It could well have been that consumption of moose thyroid was an important means of maintaining fertility in the face of the level of carbohydrate restriction that the Arctic environment forced on its inhabitants.
We know that there are genetic variations in fat metabolism common to Arctic populations that likely lead their fat metabolism to be different than other populations,6,7 but it is too early to fit these into a coherent explanation of how these populations adapted to the specific demands of the Arctic environment.
It is safer ground to emulate the preponderance of traditional diets that contained plenty of carbohydrate than to emulate the lower tail of the carbohydrate distribution found in the Arctic because we don’t fully understand how the particular suite of genetic and cultural adaptations allowed Arctic populations to thrive on such a low carbohydrate intake.
Nevertheless, we do as humans contain a remarkable degree of metabolic flexibility. It makes the most sense to emphasize nutrient density above macronutrient composition, but to also be conscious of the need for carbohydrate to minimize hormonal dysregulation and support athletic performance. This will allow us to gravitate intuitively toward the amount of carbohydrate that works best for us, and to modify our carbohydrate intake as needed to best support our health.
For athletes,4 the potential downside of chronic excessive carbohydrate restriction is impaired performance or impaired performance gains for activities that require anaerobic glycolysis.
There are three energy systems that fuel activity during exercise: creatine phosphate, anaerobic glycolysis and oxidative phosphorylation. Oxidative phosphorylation refers to the complete oxidation of carbohydrates, fats or proteins.
During a bout of continuous high-intensity physical activity, we fuel the first fifteen to thirty seconds with energy from creatine phosphate. The period from thirty to ninety seconds is dominated by anaerobic glycolysis. Anaerobic glycolysis remains significant through the first thirty minutes, but diminishes in importance after ninety seconds when oxidative phosphorylation begins to take over. Oxidative phosphorylation becomes the overwhelming factor after thirty minutes.
Chronically restricting carbohydrate will shift the body toward using fatty acids and ketones (small, water-soluble derivatives of fatty acids) for fuel. This can shift the post-ninety-second demand for fuel from the oxidation of carbohydrate to the oxidation of fat, but it cannot reduce the demand for glucose in the thirty to ninety-second mark. We rely on anaerobic glycolysis during this period because our demand for energy temporarily exceeds the delivery of oxygen to our tissues, and eating a high-fat diet is not going to increase the speed at which we can suddenly drive oxygen to our muscles during the acute onset of intense activity.
Athletic training itself could reduce the demand for glucose in the thirty-to-ninety-second mark by making us more effective at oxygenating our tissues and more efficient in our use of energy. But all athletes train, so no athlete can rely on this alone for a competitive edge. Even after ninety seconds, glucose will be the limiting factor for maximum intensity simply because any intensity above and beyond what the supply of oxygen can accommodate can only be met through anaerobic glycolysis.
Many athletes supplement with creatine in order to boost the amount of energy available in the first thirty seconds or extend the creatine supply somewhat beyond thirty seconds. This is especially valuable for weight training, where a set often lasts thirty to sixty seconds. Consuming a large amount of creatine from meat or supplements might reduce the demand for anaerobic glycolysis by extending the use of creatine beyond the thirty-second mark. Nevertheless, it is not going to extend the dominance of the creatine phosphate system through ninety seconds or provide the edge needed for maximal intensity thereafter.
Sprinting, track-and-field events, gymnastics and most team sports rely on short bursts of energy that depend on anaerobic glycolysis. There is currently a paucity of controlled studies investigating the degree to which these sports can maximally adapt to fat-burning on carbohydrate-restricted diets.
It is important to realize, however, that the primary variables at risk are maximal performance and stress hormone adaptation. Maximal performance is primarily important in a competitive context, where a marginal increase in speed in a particular instant could make the difference of winning or losing. Stress hormone adaptation is relevant to everyone regardless of athletic status, but since athletes have a greater need for carbohydrate, they would be more likely to experience negative adaptations than someone enduring a similar level of carbohydrate restriction but living a sedentary lifestyle.
1. Unless otherwise cited, information in this article comes from Ferrier, DA. Lippincott’s Illustrated Reviews: Biochemistry. 6th Edition. Lippincott Williams and Wilkins (Philadelphia) 2014.
2. Schoenfeld P, Reiser G. Why does brain metabolism not favor burning of fatty acids to provide energy? Reflections on disadvantages of the use of free fatty acids as fuel for brain. J Cereb Blood Flow Metab. 2013;33(10):1493-9.
3. Masterjohn C. The Daily Lipid Podcast Episode 11: Paleof(x) Grab Bag: Carbs Sex Hormones, Diabetes, and More.http://chrismasterjohnphd.com/2016/06/02/the-daily-lipid-podcastepisode-11_2/ Published June 2, 2016. Accessed September 7, 2016.
4. Hunter, GR. “Physical Activity, Fitness, and Health.” In Ross AC, et al., Eds. Modern Nutrition in Health and Disease: Eleventh Edition. Lippincott Williams and Wilkins (Philadelphia) 2014.
5. Keim NL, et al. “Carbohydrates.” In Ross AC, et al., Eds. Modern Nutrition in Health and Disease: Eleventh Edition. Lippincott Williams and Wilkins (Philadelphia) 2014.
6. Greenberg CR. The paradox of the carnitine palmitoyltransferase type Ia P479L variant in Canadian Aboriginal populations. Mol Genet Metab. 2009;96(4):201-7.
7. Zhang, JY. Desaturase and elongase-limiting endogenous long-chain polyunsaturated fatty acid biosynthesis. Curt Opin Clin Nutr Metab Care. 2016; 19(2):103-10.
This article appeared in Wise Traditions in Food, Farming and the Healing Arts, the quarterly journal of the Weston A. Price Foundation,Fall 2016🖨️ Print post