The Evolutionary Context of the Ketogenic Diet

The ketogenic diet has gained significant traction in the news, on social media, and even documentary production.  With its rising popularity, it’s hard not to wonder if this might be the answer we have all been waiting for to settle the never-ending diet war. 

The truth is, “dieting” is not an eating behavior that is natural to human evolution and is an extension of our industrialized way of life.  Industrialization has significantly impacted food availability, work required for preparation, and even the social construct around acceptable types of food. In the western world, we experience no shortage of food, not even needing to get out of our car to acquire it. Then there are the “food-like” substances that we have socially accepted as food but are full of additives, preservatives and refined ingredients, most of which were foreign to the human diet 100 years ago. These factors are important to consider because evolutionary speaking, we also went through seasons of limited availability and seasons of abundance, subsisting on a rough diet of small game, fish if near water, and seasonally available roots and berries (1). For the last 10,000 years, these patterns were hard wired into our genetics, and ultimately our biology as humans (2).

Understanding what factors strongly influenced the evolution of human biology is helpful to comprehend how particular eating patterns may be seemingly effective for modern-day human. When humans were in periods of food scarcity, or during winter months, with limited availability to plant foods (carbohydrates), they had to be able to rely on alternative fuel sources to avoid starvation. In states of limited food intake, reduced carbohydrates, or prolonged physical activity the human body begins to release fatty acids from fat stores to build ketone bodies, which like glucose, can be used to make ATP, the energy currency for the body. Interestingly, fatty acids are more efficient than glucose for energy production, and in tissues with high-energy requirements, such as the heart, 50-70% of energy comes from fatty acids (3,4).

In the 1920s the medical community adopted the ketogenic diet after it was observed that fasted states induced seizure control in epileptic patients (5). The goal of the diet was ketogenesis (the generation of ketones) and sustained ketosis (the state of elevated ketones in the blood) without fasting.  To achieve this, therapeutic ketogenic diets consisted of high ratios of fat to carbohydrates, some upwards of 90% fat. The most common therapeutic range was between 75-80% fat, 15-20% protein, and 5% or less carbohydrate. After the development of pharmaceuticals, the dietary intervention fell out of favor, except for treatment-resistant cases. 

With a resurgence of interest in research, the use of a ketogenic diet has been found useful in many conditions including Alzheimer’s disease, Parkinson’s disease, brain tumors, autism spectrum disorders, migraines, traumatic brain injuries and strokes, and more recently diabetes, weight loss, and hormonal imbalances (5,6). It has been proven to reduce inflammation, aid weight loss, boost energy, improve brain health, increase insulin sensitivity, and increase leptin sensitivity, our satiety hormone (5,6). 

For some, a ketogenic diet approach can be useful to “jump-start” their metabolic ability to utilize fat as fuel. The standard American diet relies heavily on carbohydrates which leads to high insulin states. Insulin is a hormone that helps with glucose utilization. But by nature, it’s a storage hormone that signals the body to store incoming glucose as glycogen, or fat, for utilization in times of energy deprivation. This turns off the body’s ability to release fat from cells (aka burn fat), relying solely on glucose for energy production. This is considered a loss of “metabolic flexibility” and can be experienced by blood sugar instability, insulin resistance, weight loss resistance, the inability of going 4 to 6 or more hours without food, becoming “hangry”, needing to eat before bed, or waking in the night to eat. (note* not a complete list of symptoms). To effectively lower insulin, carbohydrates need to be limited to 15-20 grams per day for women and 20-30 grams per day for men, with roughly 60-70% fat initially. This will force the body to burn through its glucose stores (glycogen) and eventually it will begin to burn fat, mobilizing fatty acids to make ketones, which are then brought to the cells to make energy. Since ketone bodies are more foreign sources of energy in individuals consuming a high carbohydrate diet, this process will be inefficient at first, and can often result in the symptoms coined as the “keto flu”. The period knows as “fat–adaptation”, is when the body is re-training the cells to switch over its energy machinery to use fatty acids when it’s used to glucose. This period can often last up to 2-3 weeks. Some of the symptoms one might experience when transitioning from a high-carb to a high-fat diet include mild hypoglycemia (low blood sugar), increased appetite, constipation, fatigue, reduced strength, and physical performance, frequent urination, drowsiness and dizziness, muscle cramps, heart palpitations, mood swings and irritability, and cravings. 

Some common and sometimes harmful mistakes that can be made when adopting a ketogenic diet include consuming the wrong sources of fat leading to inflammation, not eating enough fiber leading to constipation, not drinking enough water, leading to dehydration, and not carefully planning vegetables into meals leading to micronutrient deficiencies. Those who are struggling to reach a ketogenic state should consider their levels of stress and sleep quality. Poor sleep; high stress (think over-training, personal and work life, or illness) all result in increased cortisol, which ultimately leads to insulin release, which as described, inhibits ketosis. 

Once the body becomes fat-adapted and effectively utilizes ketones for energy, participants can experience improved mood, a sharper mind, and a natural increase in fat loss. Once this state is reached and maintained for a period of time, those who are not using the diet for treatment or management of a disease or condition should consider transitioning from strict adherence. This may include adopting a rotational pattern of ketosis, or utilizing strategies such as fasting and movement to generate ketones, while keeping carbohydrates low/moderate (75-100g), but not restricted, which aligns closer to our evolutionary pattern. Although there were indigenous cultures that consumed primarily a high-fat diet, such as the Inuit and Maasai, further research on their genetics demonstrate particular adaptations that explain their need for a chronic high fat. These adaptations/variations in genetics are absent in the majority of the population (ie. individuals who did not derive from those lineages), which would suggest that a long-term, high-fat diet, may not be best suited in most cases (7). These findings help in understanding why some individuals may experience varying responses to the diet over time, such as initial weight loss and increased energy followed by an unexpected plateau of both. Rotational patterns and metabolic flexibility are most consistent with the evolution of human biology.

Those interested in the use of the ketogenic diet should consult with their health care provider to be assessed appropriately for any circumstances in which it could be harmful. Blood work can also be ordered to help monitor the safety and efficacy of diet over time. Working with a certified coach or practitioner, who is knowledgeable about human nutrition and the biochemistry of the ketogenic diet, is recommended for diet personalization based on goals, activity level, diet history, and necessary modifications over time. 

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References

1. Fox, R. (2003). Food and eating: an anthropological perspective. Social Issues Research Centre, 1-21.
2. Jew, S., AbuMweis, S. S., & Jones, P. J. (2009). Evolution of the human diet: linking our ancestral diet to modern functional foods as a means of chronic disease prevention. Journal of medicinal food, 12(5), 925-934.
3. Bing, R. J. (1961). Metabolic activity of the intact heart. The American Journal of Medicine, 30(5), 679-691.
4. Kolwicz Jr, S. C., Airhart, S., & Tian, R. (2016). Ketones step to the plate: a game-changer for metabolic remodeling in heart failure?.
5. Barañano, K. W., & Hartman, A. L. (2008). The ketogenic diet; uses in epilepsy and other neurologic illnesses. Current treatment options in neurology, 10(6), 410–419. 
6. Branco, A. F., Ferreira, A., Simoes, R. F., Magalhães‐Novais, S., Zehowski, C., Cope, E., … & Cunha‐Oliveira, T. (2016). Ketogenic diets: from cancer to mitochondrial diseases and beyond. European journal of clinical investigation, 46(3), 285-298.
7. Senftleber, N., Jørgensen, M., Imamura, F., Forouhi, N., & Albrechtsen, A. (2019). Traditional Diet Influences Erythrocyte Fatty Acids Deferentially Across Genetic Variants of Fatty Acid Metabolism: The Greenlandic Inuit Health in Transition Cohort (FS11-02-19).