How has the Ketogenic diet evolved?

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The Ketogenic diet (KD, Keto) has become a fairly popular way in recent years to lose weight. It has become popular through the endorsement of celebrities and almost what it seems to be immediate results experienced by individuals adhering to the eating regimen.

The KD focuses on a nutritional regimen that promotes high-fat and low carbohydrate intake. The metabolic outcome of this diet induces the production of ketone bodies in the liver through fat metabolism. As a result of the higher fat intake, the body uses ketone bodies as the primary source of fuel for the central nervous system, in turn, replacing glucose as the primary fuel source.

Origins of the Keto diet

The KD was initially used in the treatment of epilepsy. Going back to the days of Hippocrates, sustained fasting was a method of treatment in controlling seizures. Starvation was the method used to treat seizures, which then evolved into the classic KD. The starvation approach was not sustainable due to the difficulty in maintaining long-term patient compliance. In 1866, Charles Radcliffe designed the high-fat, low carbohydrate diet associated with the classic KD. In developing the classic KD, many of the characteristics of the initial fasting regimen were replicated but without starvation, nutrient deprivation or persistent hunger.

The KD has evolved over time. Each variation is differentiated by slight modifications in the macronutrient allocations among fat, protein and carbohydrates. The basic tenet of maintaining the highest macronutrient allocation to fat is present in all these variations.

The primary variations of the KD include:

• Modified Atkins diet (MAD): As a method to mitigate a criticism of the classic KD, the MAD was designed to emulate the high-fat component of the KD but permitted for a higher allocation to protein in order to increase patient compliance to the overall nutritional regimen.
• Low Glycemic Index Treatment (LGIT) diet: The LGIT was created as an alternative to the classic KD due to sustained decreases in blood glucose observed in following the classic KD. The LGIT promoted stable circulating levels of glucose while still providing the initial benefit of the classic KD in controlling seizures.
• Caloric Restriction (CR) diet: The CR diet, also referred to as intermittent fasting, focused on the research supporting the positive effects of fasting on epileptic patients and the resulting seizure control. The focus of the CR diet reduced total daily caloric intake below the necessary levels but not to the levels of malnutrition. The CR diet is primarily used in cases to treat age-related and metabolic diseases.

The Keto diet

The KD in practice generally aligns with one of these four categorizations:

• Standard Ketogenic diet (SKD): Very low-carb, moderate protein and high-fat consumption. Macro allocations: 75% fat, 20% protein, 5% carbs.
• Cyclical Ketogenic diet (CKD): Periods of higher carb refeeds- 5 keto days, 2 high carb days.
• Targeted Ketogenic diet (TKD): Add carbs around workouts.
• High-protein Ketogenic diet: Similar to the SKD but includes higher protein consumption. Macro allocations: 60% fat, 35% protein, 5% carbs.

There isn’t much research on the CKD and the TKD, while the SKD and high-protein keto versions have been subject to research. Athletes adhering to the KD tend to follow the CKD or the TKD methods.

Foods to avoid on Keto include:

• Sugary foods
• Grains/starches
• Fruit (berries are ok)
• Beans/legumes
• Root veggies/ tubers
• Low-fat/ diet products
• Unhealthy fats
• Alcohol

Foods to consume on Keto include:

• Meat
• Fatty fish
• Eggs
• Butter/cream
• Cheese
• Nuts/seeds
• Healthy oils
• Avocados
• Low-carb veggies

The KD typically limits carbohydrates to 5–10% of total caloric intake, which is less than 50 g of carbs per day. The low carb intake promotes the production of ketones resulting in ketosis.

Ketosis is a metabolic state in which fat (instead of carbs) produces the majority of the fuel for the body. When the body has a limited supply of glucose, ketosis ensues.

To achieve ketosis, the carb intake is usually 20–50g/day. Some side effects of ketosis include: headache; lethargy; constipation; high cholesterol; and bad breath.

The weight loss experienced from following the KD is a result of:

• Decrease in lipogenesis (metabolic formation of fat).
• Increase in lipid oxidation.
• Increase in adiponectin (protein hormone produced by fat cells that reduces inflammation and formation of fatty deposits in the arteries).

There is mixed research on the long-term sustainability of the KD. Some literature supports an association between following a high-fat diet in the long term and negative implications in total and LDL-cholesterol but positive implications in HDL-cholesterol. A study conducted by Mohorko et al. supported the short-term benefits of the KD as a method to reduce obesity; however, also suggested the need for longer-term studies to determine longer-term effects.

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Criticisms of the Keto diet

While there may be some health benefits associated with following the KD, there are naturally criticisms of the eating regimen. Some criticisms of the KD include lack of adequate micronutrient consumption and risk of ketoacidosis.

Lack of adequate micronutrient consumption

A study conducted by Kenig et al. evaluated the micronutrient consumption in patients following a KD over a 12-week period. Overall, the findings supported the claim the KD results in lower consumption of micronutrients. The study also acknowledged the benefits of the KD in its promotion of weight loss, decreased fat mass, and decreased insulin. All of these effects resulted in improved cognitive and physical performance.

In following the KD, some food groups are eliminated which simultaneously reduces the necessary micronutrient consumption. To mitigate the reduction in micronutrient consumption, supplementation paired with regular monitoring of micronutrient levels may be a consideration while following the KD to mitigate adverse health outcomes.

Risk of ketoacidosis

Diabetic ketoacidosis occurs when the body is unable to produce sufficient insulin and the body responds by breaking down fat as fuel. This process results in the production of increased acids in the bloodstream, referred to as ketones. The KD replaces glucose as a source of fuel for the body with ketones, whereby ketone bodies are synthesized once stored glycogen has been depleted.

While much research supports the KD in the treatment of neurological disorders, the ketone bodies as the main driver of fuel for the body is not always neuroprotective. Ketoacidosis is an example of how ketone bodies may be neurotoxic. Ketoacidosis is normally a complication of type 1 diabetes. If a diabetic patient lacks the appropriate levels of insulin, the body is unable to move glucose from the blood into cells where glucose is used for energy. Ketoacidosis is treatable through insulin therapy and electrolyte replacement. While the concern of ketoacidosis is legitimate, it is more of a concern for diabetic patients.

The Keto Diet and Gut Microbiota

Dietary patterns are believed to have an impact on the gut microbiota. A typical Western diet high in saturated and trans fat, high in sugar and low in fiber results in a reduction in the production of short-chain fatty acids (SCFA). This results in the production of harmful metabolites which promotes the increase of bacteria related to chronic inflammation.

Short-chain fatty acids are important in regulating the immune function in the body and also impacts the mitigation of inflammation.

While high-fat diets have been associated with inflammation, some studies have suggested the type of fatty acids consumed is of importance in the promotion of health outcomes. Monounsaturated fatty acids (MUFAs) and polyunsaturated fatty acids (PUFAs)- our friend, omega-3!- have been hypothesized to be factors in controlling mild inflammation in the body and gut. Shorter-term studies have found diets high in fat with a focus on good quality fat, polyunsaturated fats and plant-based protein aid in the maintenance of normal gut function. The KD can alter the structure of the gut; however, this characteristic is what makes the diet successful in the treatment of neurological disorders and promotes an anti-seizure effect for epileptic patients.

Conclusion

The initial implementation of the Ketogenic diet was not for weight loss. In a follow-up blog, I will discuss some of the implementations of the KD on neurological disorders. There is interesting research supporting the implementation of the KD in treating epilepsy and Alzheimer’s disease. While individuals may experience significant weight loss in following the KD, there are concerns on the adequate consumption of micronutrients for sustainable health. The longer-term effects of the diet on overall health (in individuals not suffering from neurological disorders) are also not determined; more research is needed.

References

1. McDonald T, Cervenka M. Ketogenic diets for adult neurological disorders. Neurotherapeutics. 2018;15:1018–1031. doi:10.1007/s13311–018–0666–8.
2. Gano L, Patel M, Rho J. Thematic review series: Calorie restriction and ketogenic diets: ketogenic diets, mitochondria, and neurological diseases. J. Lipid Res. 2014;55:(11) 2211–2228. doi:10.1194/jlr.R048975.
3. Clanton RM, Wu G, Akabani G, Aramayo R. Control of seizures by ketogenic diet-induced modulation of metabolic pathways. Amino Acids. 2016;49(1):1–20. doi: 10.1007/s00726–016–2336–7.
4. Paoli et al. Ketogenic diet and microbiota: friends or enemies? Genes. 2019;10(7):1–19. doi:10.3390/genes10070534.
5. Mawer R. The ketogenic diet: a detailed beginner’s guide to keto. Healthline Web site. https://www.healthline.com/nutrition/ketogenic-diet-101. Updated July 30, 2018. Accessed August 26, 2020.
6. Mohorka et al. Weight loss, improved physical performance, cognitive function, eating behavior, and metabolic profile in a 12-week ketogenic diet in obese adults. Nutr Res. 2019;62:64–77. doi:10.1016/j.nutres.2018.11.007.
7. Kenig S, Petelin A, Vatovec TP, Mohorko N, Jenko-Praznikar Z. Assessment of micronutrients in a 12-wk ketogenic diet in obese adults. Nutrition. 2019;67–68:1–7. doi: 10.1016/j.nut.2019.06.003.
8. Diabetic ketoacidosis. The Mayo Clinic website. https://www.mayoclinic.org/diseases-conditions/diabetic-ketoacidosis/symptoms-causes/syc-20371551. Updated December 11, 2019. Accessed August 26, 2020.
9. Fedorovich S, Voronina P, Waseem T. Ketogenic diet versus ketoacidosis: what determines the influence of ketone bodies on neurons? Neural Regeneration Research. 2018;13(12):2060–2063. doi:10.4103/1673–5374.241442.
10. Villines Z. Differences between ketosis and ketoacidosis. Medical News Today website. https://www.medicalnewstoday.com/articles/324237.php. Updated January 21, 2019. Accessed October 1, 2019.